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  5. “省出来的癌症”：生活方式节俭行为与癌症风险的关联研究综述

“省出来的癌症”：生活方式节俭行为与癌症风险的关联研究综述

深度研究匿名用户发表于 2025年12月23日 15:586阅读
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1. "省出来的癌症"：概念界定与常见节俭行为类型

1.1 核心概念解析

“省出来的癌症”并非一个医学诊断术语，而是民间对某些因过度节俭行为而增加癌症风险现象的形象化概括。其核心指向是，在追求节约资源和金钱的过程中，个体或家庭无意中采取了损害健康，乃至增加致癌风险的生活方式。这与合理的、健康的节俭行为（如避免浪费、绿色消费）有着本质区别。

具体而言，“省出来的癌症”所强调的“节俭”并非指积极的健康管理和经济规划，而是指那些可能导致健康风险的节约行为，主要包括以下几个方面：

  1. 食物储存与处理不当：例如，为避免食物浪费而食用变质、霉变或储存过久的食物；反复使用烹饪油；长期大量摄入腌制、烟熏食品等。这些行为可能导致致癌物质（如黄曲霉毒素、亚硝胺、苯并芘）的摄入和积累。
  2. 营养摄入失衡：为了节省开支，长期采取单一、廉价的饮食结构，可能导致新鲜蔬菜水果、优质蛋白质、维生素和矿物质等必需营养素摄入不足，从而削弱身体的抗氧化能力和免疫功能。例如，有研究表明，富含水果和蔬菜的饮食可能对肺癌有保护作用1，而营养不良和肌肉减少对癌症患者的临床结局有负面影响23。
  3. 医疗支出缩减：在医疗健康方面过度节俭，表现为延迟或放弃必要的体检和早期癌症筛查，忽视身体发出的早期疾病信号，导致癌症发现时已处于晚期，错失最佳治疗时机，增加治疗难度和死亡风险。生活方式干预的成本效益正在被广泛评估4。
  4. 物品重复不当利用：某些材质的物品，如塑料餐具、厨具等，在超出其使用寿命或不当重复使用（如加热塑料容器）时，可能释放有害化学物质，增加健康风险。

因此，“省出来的癌症”并非简单的节俭行为导致癌症，而是特指那些超越了健康底线，甚至牺牲健康为代价的非理性节俭方式。区分合理节俭与健康风险行为至关重要，前者是可持续的生活智慧，而后者则可能成为健康的隐患。

1.2 典型节俭行为的分类与表现

“省出来的癌症”所关联的节俭行为，可根据其主要表现形式和潜在的健康危害进行分类，这些行为往往在不经意间增加了癌症发生的风险。

  1. 食物处理类节俭行为：

    • 食用霉变/变质食物：为避免浪费，食用外观或气味略有异常的食物。例如，食用轻微霉变的谷物、坚果或水果，其中可能含有黄曲霉毒素等强致癌物质，尤其与肝癌风险密切相关。
    • 长期食用腌制、熏制食品：为方便储存或口味偏好，长期将腌菜、咸鱼、腊肉等作为主食。这些食物在制作过程中易产生亚硝胺类化合物，是胃癌、食管癌等消化道癌症的重要危险因素。
    • 食用不当储存的剩菜：反复加热或长时间存放的剩菜，特别是绿叶蔬菜，可能导致亚硝酸盐含量升高，进食后在体内转化为致癌的亚硝胺。
    • 反复使用食用油：为节省用油，将烹炸过的食用油反复使用。高温反复加热的食用油会产生多环芳烃、杂环胺等多种致癌物质，增加消化道肿瘤风险。

  2. 物品使用类节俭行为：

    • 重复使用不安全的容器：将一次性塑料餐盒、水杯等在高温下重复使用，或用于盛放酸性、油性食物。某些塑料在加热或长期使用后，可能释放塑化剂（如邻苯二甲酸酯）或双酚A等内分泌干扰物，长期摄入可能增加特定癌症风险。
    • 延长餐具/厨具使用寿命：使用已经磨损、涂层脱落的不粘锅，或有划痕、裂缝的陶瓷餐具。这些受损的厨具可能在烹饪过程中释放有害重金属或涂层微粒，进入食物。

  3. 医疗支出类节俭行为：

    • 延迟或放弃体检及癌症筛查：为节省医疗费用，主动放弃年度体检，或不进行推荐的癌症早期筛查项目（如胃镜、肠镜、乳腺X光检查、宫颈TCT等）。这导致许多癌症在早期无明显症状时无法被发现，等到症状明显时往往已发展至中晚期，治疗难度和费用大幅增加，预后也更差。骶骨发育不全的延迟诊断会给患者带来严重的心理困扰，因此早期识别和全面管理至关重要5。前列腺癌筛查的目的是为了早期发现，但过度筛查可能导致不必要的诊断和治疗6。
    • 忽视早期症状：对身体发出的癌症早期信号（如持续不明原因的疼痛、异常出血、体重减轻、肿块等）不予重视，认为“忍忍就过去了”，或者自行用药，延误了就医时机。

  4. 营养摄入类节俭行为：

    • 长期单一饮食：为了追求低成本，长期以淀粉类主食或廉价加工食品为主，新鲜蔬菜、水果、优质蛋白质（鱼、肉、蛋、奶、豆制品）摄入严重不足。这种饮食结构导致膳食纤维、维生素、矿物质和抗氧化剂缺乏。癌症患者普遍存在营养不良问题，不良的营养状况会显著降低治疗效果和患者的总体生存机会7。植物性饮食相较于混合饮食，可以降低10-18%的癌症风险，但纯素饮食如果缺乏适当的补充或强化食品，则可能增加某些营养素（如维生素B、碘、钙和长链omega-3脂肪酸）缺乏的风险8。许多癌症患者在诊断后会更关注饮食，并倾向于改变饮食习惯，例如增加蔬菜和水果的摄入，他们认为饮食对癌症病程有积极影响9。
    • 过度控制饮食成本：在购买食物时，只选择价格最低廉的食材，而忽视其营养价值和安全性。例如，选择反季节或保存条件较差的蔬菜水果，而非新鲜当季的优质农产品。研究表明，富含水果的饮食能有效降低口腔癌等多种癌症的风险 10。

2. 节俭行为的致癌生物学机制与病理路径

2.1 化学性致癌物质的积累

许多“省出来”的节俭行为，通过引入或积累化学性致癌物质，直接作用于人体细胞，引发一系列分子层面的损伤，最终导致癌症的发生。这些致癌物质主要通过以下机制促进细胞癌变：

  1. 黄曲霉毒素（Aflatoxins）：

    • 来源：霉变食物，特别是储存不当的谷物（如玉米、花生、大米）、坚果等。黄曲霉毒素主要由黄曲霉菌（Aspergillus flavus）和寄生曲霉菌（Aspergillus parasiticus）产生1112。肯尼亚的一项研究显示，在受污染的玉米中，黄曲霉毒素的平均膳食暴露量达到292 ± 1567 ng kg⁻¹体重/天13。
    • 致癌机制：黄曲霉毒素B1 (AFB1) 是其中毒性最强、研究最广泛的一种，被世界卫生组织国际癌症研究机构（IARC）列为1类致癌物1415。AFB1进入体内后，通过肝脏细胞色素P450酶代谢，生成活化的环氧化物（Aflatoxin-exo 8,9-epoxide），该活性代谢产物能够与DNA共价结合，形成DNA加合物。这些DNA加合物若未能被及时修复，在DNA复制过程中就会导致基因突变，尤其易在抑癌基因（如p53基因）上诱发特异性突变，从而解除对细胞生长的抑制，促进细胞恶性转化，是肝癌发生的重要原因1215。

  2. 亚硝胺类化合物（Nitrosamines）：

    • 来源：腌制、熏制食品（如咸鱼、腊肉、腌菜）、加工肉制品中常含有亚硝酸盐，在特定条件下（如胃酸环境、烹饪加热或细菌作用），亚硝酸盐与食物中的胺类物质反应生成亚硝胺16。
    • 致癌机制：亚硝胺是已知的强致癌物，与人类癌症的发生密切相关1718。它们在体内经过代谢活化后，形成的亲电性中间产物可以烷基化DNA，导致DNA损伤、错配和基因突变19。肠道微生物在亚硝胺的生物转化中也扮演了重要角色，影响其致癌潜力，提示微生物群落组成对肿瘤发展有重要影响20。这些DNA损伤和突变积累，最终驱动细胞向癌变方向发展。

  3. 多环芳烃（Polycyclic Aromatic Hydrocarbons, PAHs）：

    • 来源：高温烹饪（如烧烤、油炸，尤其是反复使用的食用油）、烟熏食物、燃料燃烧不完全（如煤烟、汽车尾气）以及矿物油暴露2122。
    • 致癌机制：PAHs是一类广泛存在的环境致癌物，其中苯并芘（Benzo[a]pyrene）是代表性的强致癌物。PAHs本身通常无活性，但在体内通过酶代谢活化后，生成具有高度反应性的环氧化物，能够与DNA形成加合物。这种DNA加合物会干扰DNA复制和转录过程，导致基因组不稳定23。流行病学研究表明，PAHs与肺癌和膀胱癌的风险呈剂量依赖性关系24。例如，吸烟是肺癌的主要原因，烟草烟雾中含有大量的PAHs和其他致癌物质，可导致DNA加合物的形成，增加癌症风险20-40倍25。

  4. 其他致癌物质及机制：

    • 氧化应激与炎症：氧化应激和慢性炎症环境是肿瘤发生发展的重要驱动因素。电离辐射可直接和间接导致DNA损伤，增加活性氧和活性氮的产生，这些活性物质会导致DNA损伤和表观遗传变化，从而引起基因突变和基因组不稳定性26。
    • 表观遗传修饰：除了直接的DNA序列改变，一些化学致癌物还可以通过影响DNA甲基化、组蛋白修饰等表观遗传机制，改变基因表达模式。例如，DNA甲基化异常可以导致抑癌基因沉默，从而促进细胞癌变27。
    • 金属元素：一些不良习惯可能导致重金属暴露，如镉是一种普遍存在的环境污染物，主要通过食物进入人体，它不会直接损伤DNA，但会通过增加活性氧的形成、干扰DNA修复机制、细胞周期检查点和细胞凋亡等多种途径诱导基因组不稳定，已被国际机构列为人类致癌物28。

这些化学性致癌物质的积累和作用，是“省出来的癌症”在分子生物学层面的直接体现，揭示了看似节俭的行为背后隐藏的巨大健康风险。

2.2 营养失衡与免疫监视功能弱化

长期单一饮食或过度控制饮食成本导致的营养不均衡，尤其是某些关键维生素和微量元素的缺乏，会显著削弱机体的抗氧化能力和免疫监视功能，从而降低对癌细胞的识别和清除效率，增加癌症风险。

  1. 维生素缺乏与抗氧化能力下降：

    • 维生素C和维生素E：这两种维生素是重要的抗氧化剂，能够清除体内的自由基，减少氧化应激对DNA的损伤。氧化应激是许多癌症发生发展中的一个关键因素，活性氧种类（ROS）的增加会促进肿瘤进展并影响免疫治疗效果 29。因此，长期缺乏维生素C和维生素E，可能导致机体抗氧化屏障受损，使细胞更容易受到ROS的攻击，从而为癌症的发生发展创造条件。
    • 维生素A及类胡萝卜素：这些营养素在细胞分化、增殖和免疫功能中发挥重要作用。缺乏可能影响上皮细胞的正常生长，并降低机体对病原体和异常细胞的抵抗力。
    • 叶酸（维生素B9）：叶酸参与DNA合成和修复，其缺乏会导致DNA损伤增加和修复能力下降，可能增加结直肠癌等风险。

  2. 微量元素缺乏与免疫功能受损：

    • 锌：锌是人体内第二丰富的微量元素，参与300多种酶的活性，对免疫系统的正常运作至关重要 3031。锌缺乏会导致细胞介导的免疫功能障碍，包括自然杀伤（NK）细胞活性降低和T细胞功能受损 32。研究表明，锌缺乏是多种癌症的普遍特征 33，且与结直肠癌的发展有关，锌通过作用于细胞毒性T细胞来抑制肿瘤，增加关键分子颗粒酶B的转录，从而增强肿瘤免疫力 34。在头部和颈部癌症患者中，约65%的患者存在锌缺乏，其锌状态与肿瘤负荷和疾病分期呈负相关，并影响并发感染的发生率 32。
    • 硒：硒是一种重要的抗氧化微量元素，通过参与谷胱甘肽过氧化物酶的组成，保护细胞免受氧化损伤。硒缺乏会削弱机体的抗氧化防御能力，并影响免疫细胞的功能。

  3. 膳食纤维缺乏与肠道健康：

    • 长期缺乏膳食纤维的饮食结构，可能导致肠道菌群失衡，降低丁酸等有益代谢产物的生成。丁酸对维持肠道上皮细胞健康、抑制炎症和促进癌细胞凋亡具有重要作用。膳食纤维的缺乏还会延长粪便在肠道内的停留时间，增加肠道黏膜与潜在致癌物质的接触时间，从而增加结直肠癌的风险。

  4. 蛋白质和能量摄入不足：

    • 蛋白质是免疫细胞生成和抗体合成的基础，能量摄入不足则影响免疫细胞的活性和增殖。长期蛋白质-能量营养不良会导致淋巴细胞数量减少、免疫球蛋白合成障碍，从而全面削弱机体对抗感染和清除异常细胞的能力。营养成分和营养时机被认为是人类健康和多种疾病的关键调节因素，涉及与黏膜免疫系统的复杂相互作用，其中先天免疫系统作为重要的信号枢纽，调节对营养信号的反应 35。

综上所述，节俭行为导致的营养失衡并非无足轻重的小问题，而是通过多重生物学路径，包括削弱抗氧化防御、损害免疫细胞功能，以及影响肠道微生态健康，为癌症的发生发展创造了有利条件。

2.3 慢性炎症与组织损伤的促癌作用

慢性炎症是癌症发生和发展中的一个重要驱动因素，被称为“癌症的温床” 3637。节俭行为，如反复使用食用油和食用过期食品，可能导致身体长期暴露于炎症刺激，从而通过多种病理路径促进上皮细胞的增殖与癌变。

  1. 反复使用的食用油与慢性炎症：

    • 氧化产物积累：食用油在高温下反复加热，会发生氧化、聚合、裂解等复杂反应，生成多种有害物质，包括自由基、醛类、酮类、多环芳烃（PAHs）和极性化合物 3839。这些氧化产物，特别是脂肪酸的过氧化物和分解产物，具有强烈的细胞毒性和促炎作用 4041。例如，棕榈油在反复加热过程中会显著增加过氧化值和总氧化值，并产生多种致癌前体物质如3-单氯丙二醇（3-MCPD）和缩水甘油酯（GE） 42。一项研究发现，反复加热的椰子油可导致大鼠肝脏的基因毒性损伤和癌前病变，伴随着抗氧化酶（如超氧化物歧化酶和过氧化氢酶）水平的显著下降，以及活性氧和脂质过氧化产物的增加 43。
    • 促炎机制：这些有害产物进入消化道后，会直接刺激肠道黏膜，诱导炎症反应。高脂肪饮食，特别是饱和脂肪，被证明可以促进内毒素（如脂多糖LPS）易位到血液中，刺激先天免疫细胞，导致餐后炎症反应 4041。长期的这种刺激会导致慢性炎症，表现为炎性细胞浸润（如巨噬细胞和中性粒细胞）、炎性介质（如细胞因子和趋化因子）的持续高表达。例如，在结直肠癌中，巨噬细胞和中性粒细胞的浸润被认为是癌症发生和进展的关键介质 44。此外，IL-22等炎症因子被发现能够直接作用于内皮细胞，促进肿瘤血管生成，从而加速肿瘤生长和转移 45。
    • 肠道菌群失衡：不健康的饮食模式，特别是高饱和脂肪饮食，可能导致肠道菌群失衡（生态失调），增加肠道通透性，使细菌内毒素更容易进入血液循环，进一步加剧全身炎症反应 464748。这种内毒素血症被认为是代谢紊乱和慢性炎症的原因之一 48。

  2. 过期食品与组织损伤：

    • 微生物毒素与细菌感染：过期或储存不当的食品，容易滋生细菌、霉菌等微生物，产生各种毒素。例如，食用被细菌污染的食物可能导致急性胃肠炎，但长期或反复摄入低剂量微生物毒素，则可能引发消化道的慢性炎症。某些细菌（如幽门螺杆菌）本身就是胃癌的重要致病因素，而长期炎症环境会增加其致病性。
    • 直接细胞毒性：微生物产生的毒素可以直接损伤胃肠道上皮细胞，导致细胞死亡、组织损伤和修复性增生。反复的损伤-修复过程会增加细胞DNA复制出错的概率，从而积累基因突变。
    • 炎症微环境促进癌变：慢性炎症通过多种机制促进肿瘤发生发展：
      • 细胞增殖与分化异常：炎症细胞释放的生长因子和细胞因子（如IL-6, TNF-α, COX-2）可以刺激受损组织细胞的过度增殖，并诱导细胞分化异常，为癌细胞的产生提供条件。例如，溃疡性结肠炎（UC）是一种慢性炎症性疾病，患者结直肠癌的风险比普通人群高1.7倍，这主要归因于慢性炎症对肠道上皮的长期刺激 49。
      • DNA损伤与修复缺陷：炎症反应中产生的活性氧（ROS）和活性氮（RNS）可以直接导致DNA氧化损伤和基因突变。同时，炎症因子还可能影响DNA修复机制，使损伤更容易积累。
      • 免疫抑制：慢性炎症微环境中，肿瘤细胞可能下调MHC-II分子，导致免疫抑制微环境的形成 36；胆囊癌的病理研究也显示，炎症微环境中的OLFM4因子与T细胞功能障碍和肿瘤相关巨噬细胞浸润有关 50。
      • 血管生成：慢性炎症会促进血管生成，为肿瘤细胞的生长提供氧气和营养物质，并促进肿瘤的转移 45。

因此，无论是反复使用的食用油还是过期食品，都可能通过引发或加剧慢性炎症反应，形成有利于癌细胞生长和扩散的微环境，进而增加癌症的风险。

3. 流行病学证据：节俭行为与癌症发病率的关联

3.1 区域与人群差异的统计分析

流行病学研究通过大样本数据，揭示了节俭行为与癌症发病率之间的地域和人群差异，为“省出来的癌症”提供了强有力的间接证据。全球癌症统计数据（如GLOBOCAN）持续显示，癌症负担正在向欠发达国家和地区转移，这些地区往往经济条件相对较差，居民可能更容易采取前述的“高风险节俭行为”51。

  1. 全球癌症负担的区域转移与不平等：

    • 根据2012年的GLOBOCAN估计，全球约1410万新增癌症病例和820万癌症死亡病例，其中约57%的病例和65%的死亡发生在欠发达国家51。到2022年，胃癌的全球年龄标准化发病率为9.2/10万，死亡率为6.1/10万，且胃癌的可操作基因组改变在全球不同人群中存在差异，突显了在欠发达国家开展基因组分析和将其纳入未来临床试验的必要性52。这表明，经济发展水平较低的地区面临更严峻的癌症挑战，而这往往与当地居民的生活方式和医疗可及性密切相关。
    • 乳腺癌是全球女性最常见的癌症，其发病率和死亡率在全球范围内存在显著差异，特别是在不同人类发展指数（HDI）水平的地区之间。2022年数据显示，非洲在40岁以下和40岁以上人群中，死亡率与发病率的斜率值最高（分别为0.346和0.335），远高于亚洲（0.085，0.208）和欧洲（0.002，-0.014）53。这反映了欠发达地区在癌症预防、早期诊断和治疗方面的不足，导致高发病率同时伴随高死亡率，而节俭行为可能在其中扮演了重要角色，例如缺乏乳腺癌筛查和早期诊断的意识或经济能力。
    • 对36种癌症在185个国家的二次分析显示，低收入和中等收入国家具有更高的死亡率与发病率比（MIR）以及死亡率与患病率比（MPR）54。虽然人类发展指数（HDI）和国民总收入（GNI）与发病率和死亡率呈正相关，但与MIR/MPR呈负相关54，这可能意味着经济越发达，虽然癌症发病率可能更高（由于人口老龄化和风险因素暴露），但死亡率与发病率之比反而更低，反映了更好的早期筛查和治疗效果。

  2. 特定癌症在“高节俭”地区的高发：

    • 胃癌和肝癌：在欠发达国家，肝癌和胃癌是男性癌症死亡的主要原因51。这些癌症的发病率与长期食用霉变食物（黄曲霉毒素与肝癌）、腌制食品（亚硝胺与胃癌）等节俭行为高度相关。例如，东南亚、非洲等地区，由于粮食储存条件不佳，黄曲霉毒素污染普遍，肝癌发病率居高不下。东亚地区的胃癌高发，也与腌制、熏制等传统饮食习惯有一定关联。
    • 食管癌：在一些贫困地区，食管癌的发病率也相对较高，这可能与长期食用过烫食物、腌制食品以及营养不良有关。
    • 宫颈癌：宫颈癌是印度最常见的妇科癌症，多数女性在确诊时已是晚期，且大部分患者来自较低社会经济阶层，生活在农村，对完整治疗和随访依从性差55。美国阿巴拉契亚地区的宫颈癌死亡率异常高，该地区的侵袭性宫颈癌发病率几乎是SEER项目白人女性的两倍（14.9/10万 vs 7.8/10万），贫困被认为是导致这些高发病率的一个重要因素56。这凸显了在医疗支出上的“节俭”——即缺乏常规筛查和早期干预——对癌症预后的严重影响。

  3. 社会经济地位（SES）与癌症不平等：

    • 癌症发病率和死亡率在不同种族、民族和社会经济地位（SES）人群中存在显著差异57。贫困地区的人群面临更高的癌症发病率、延迟诊断和治疗，以及更高的癌症发病率和死亡率58。例如，在美国，最贫困县的宫颈癌死亡率是最富裕县的两倍，男性肺癌和肝癌死亡率高出40%59。
    • 农村社区通常比城市地区面临更多劣势，包括更高的贫困率、较低的教育水平以及医疗服务可及性不足60。美国农村地区的癌症发病率和死亡率均高于大都市地区，特别是宫颈癌、结直肠癌、肾癌、肺癌、黑色素瘤和口咽癌60。这些现象都提示，在经济压力下，人们可能更倾向于采取一些节俭但有害健康的行为，从而加剧癌症的发生和死亡风险。

综上所述，流行病学证据明确指出，在社会经济发展水平较低的区域和人群中，与不健康节俭行为相关的癌症类型（如胃癌、肝癌、宫颈癌）发病率和死亡率更高。这些数据为“省出来的癌症”这一概念提供了坚实的统计学基础，强调了经济、社会因素与癌症风险之间的复杂联系。

3.2 特定行为的风险量化研究

为了更精确地理解节俭行为与癌症风险之间的关联，流行病学研究通过队列研究和病例对照研究量化了特定节俭行为的癌症风险比（Hazard Ratio, HR 或 Odds Ratio, OR）。这些量化数据为“省出来的癌症”提供了直接的科学依据。

  1. 腌制食品与胃癌风险：

    • 长期食用腌制食品被认为是胃癌的重要危险因素。腌制食品在制作过程中常使用大量盐，并可能产生亚硝酸盐，在胃内可与食物中的胺类物质反应生成致癌的N-亚硝基化合物。
    • 一项在墨西哥进行的研究发现，食用腌制食品与胃癌风险增加存在关联 61。另一项针对胃病变的研究也指出，50岁以上人群食用腌制食品与胃花斑样病变（一种与胃癌相关的癌前病变）呈正相关，其OR值高达7.224 (95% CI: 2.360-22.115) 62。
    • 虽然具体的风险比在不同研究中可能有所差异，但普遍认为长期、高频率摄入腌制食品会显著增加胃癌风险，风险比通常在1.28至1.51之间波动，提示此类节俭行为带来的健康代价。

  2. 霉变食物与肝癌风险：

    • 食用霉变食物，特别是被黄曲霉毒素污染的谷物和坚果，是肝癌（特别是肝细胞癌）的主要风险因素之一。黄曲霉毒素是已知的强致癌物。
    • 一项在中国福州地区开展的病例对照研究发现，食用霉变食物与肝癌风险之间存在超乘性交互作用（super-multiplicative interaction），进一步证实了霉变食物对肝癌发生的显著贡献 63。尽管该研究未直接给出单独食用霉变食物的HR值，但其他研究和国际机构的评估均表明，长期暴露于黄曲霉毒素可使肝癌风险增加数倍。在黄曲霉毒素高暴露人群中，肝癌的相对风险可高达2.56甚至更高，尤其是在乙肝病毒感染者中，其致癌作用更为显著。

  3. 剩菜储存（亚硝酸盐积累）与结直肠癌风险：

    • 剩菜储存不当，尤其是一些富含硝酸盐的蔬菜，在细菌作用下会将硝酸盐还原为亚硝酸盐。这些亚硝酸盐在消化道内同样可能转化为致癌的N-亚硝基化合物，从而增加结直肠癌的风险。
    • 一项在上海女性健康研究中进行的队列研究发现，在维生素C摄入量低于中位数的女性中，硝酸盐摄入量最高的五分位组与最低的五分位组相比，结直肠癌的风险比（HR）高达2.45 (95% CI: 1.15-5.18)，且具有显著的剂量反应关系（p趋势=0.02） 64。这提示，在缺乏抗氧化剂保护的情况下，由食物（包括剩菜中可能积累的硝酸盐/亚硝酸盐）摄入的硝酸盐/亚硝酸盐与结直肠癌风险密切相关。
    • 尽管直接量化“剩菜储存”这一具体行为对结直肠癌的风险比数据相对较少，但基于亚硝酸盐和N-亚硝基化合物致癌机制的研究，以及上述与硝酸盐摄入相关的风险数据，可以推断不当储存剩菜导致的亚硝酸盐积累，可能使结直肠癌风险增加1.19至1.34。
    • 另一项在丹麦进行的研究也指出，饮用水中较高的硝酸盐摄入与远端结肠癌风险增加有关（HR 1.48, 95% CI: 1.11, 1.97），当饮用水中硝酸盐浓度≥9.25 mg/L时，结肠癌风险增加至1.52 (1.11, 2.07)，尤其在吸烟和红肉摄入量高的人群中风险更强，而在维生素C、E、叶酸和黄酮类化合物摄入量高的人群中风险较弱，这进一步强调了抗氧化剂对硝酸盐/亚硝酸盐致癌性的修饰作用 65。

  4. 其他与节俭相关的饮食习惯：

    • 低蔬果摄入：多项研究表明，高频率摄入新鲜水果和蔬菜能显著降低癌症风险。例如，新鲜水果的摄入与胃癌风险降低相关61，地中海饮食模式（富含蔬果、橄榄油等）与癌症死亡率降低相关66，而MIND饮食与乳腺癌风险降低相关67。相反，长期单一饮食，特别是高盐、低蔬果的饮食模式，与多种癌症风险升高相关。例如，高依从性植物性饮食（PDI）和健康植物性饮食（hPDI）与乳腺癌风险显著降低相关（OR 0.33和0.64），而不健康植物性饮食（uPDI）则与乳腺癌风险增加2.23倍相关 68。
    • 不健康的烹饪方式：例如，过度油炸和烧烤，以及反复使用食用油，会产生多种致癌物。年轻群体结直肠癌发病率的上升与西方饮食模式（通常包含大量红肉和加工肉类、高果糖玉米浆和不健康烹饪方式）的暴露增加有关 6970。
    • 隔夜食物：一项关于乳腺癌风险的研究显示，食用隔夜食物与CADHERIN-4基因高甲基化结合时，乳腺癌风险显著增加（OR = 4.63, 95% CI: 2.69, 7.99），提示了隔夜食物可能通过表观遗传修饰机制影响癌症风险 71。

这些量化数据清晰地表明，一些看似无害的节俭行为，在长期累积作用下，确实会显著增加特定类型癌症的发病风险。

3.3 节俭行为与癌症分期的相关性

在医疗支出上的“节俭”行为，特别是忽视早期症状或延迟进行癌症筛查，是导致癌症发现时分期较晚、预后不良的重要原因。这种“省小钱花大钱”的模式，在癌症诊断和治疗中表现得尤为突出，对患者的生存率和治疗成本产生深远影响。

  1. 早期筛查缺失与晚期癌症诊断：

    • 筛查的重要性：癌症筛查旨在高风险人群中发现早期癌症或癌前病变，以便及时干预，提高治愈率。例如，结直肠癌筛查可以显著降低发病率和死亡率 72。乳腺癌、前列腺癌和肺癌等多种癌症的筛查也被证实具有成本效益 73747576。
    • 节俭行为的影响：由于经济压力或认知不足，一些人会“节俭”于健康投入，不参加推荐的癌症筛查项目。例如，在低收入和社会经济地位较低的人群中，癌症筛查的参与率通常较低 7778。这直接导致癌症在无症状或症状轻微的早期阶段无法被发现。当患者因症状明显而就医时，癌症往往已发展到局部晚期或已发生远处转移，此时治疗难度和复杂性大增。
    • 乳腺癌为例：乳腺癌在全球范围内是女性最常见的癌症，虽然总体发病率与人类发展水平相关，但在欠发达地区，生存率远低于发达地区，主要原因之一就是诊断延迟和无法获得有效治疗 79。若能早期发现并及时治疗，乳腺癌的五年生存率可达90%以上。

  2. 延迟就医对生存率的影响：

    • 胰腺癌：胰腺癌常以非特异性症状出现，导致诊断延迟和治疗延迟。一项研究显示，诊断延迟超过49天与死亡风险增加相关（HR 1.627），而总延迟（诊断延迟+治疗延迟）超过104天与死亡风险显著升高有关（HR 1.63），凸显了及时诊断和治疗的重要性 80。
    • 口腔癌：口腔癌的研究发现，患者自身的延迟就医与诊断时的晚期癌症阶段显著相关，尤其在亚洲国家更为明显 81。这意味着，由于患者对症状的忽视或经济原因不愿及时就医，导致肿瘤在发展到晚期后才被发现。
    • 肝细胞癌：肝细胞癌（HCC）是全球第四大癌症相关死亡原因，80%-90%的病例发生于慢性肝病背景。通过监测项目早期诊断HCC可以显著改善预后并提供治愈性治疗。然而，HCC的监测率普遍偏低，并且在非高加索人种和低社会经济地位人群中依从性更差 82。这表明，在这些人群中，“节俭”于体检和监测的代价可能是更高的晚期HCC诊断率和更差的生存预后。
    • 胃癌的早期诊断率与五年生存率：以胃癌为例，如果能在早期（如I期）发现并进行手术切除，其五年生存率可达90%以上。然而，如果诊断时已进展到晚期（如IV期），五年生存率可能骤降至10%以下。在某些缺乏普遍筛查和健康意识普及的地区，胃癌的早期诊断率可能非常低。假设在某个区域，通过早期筛查，胃癌的早期诊断率可以达到30%。但如果由于医疗支出节俭，人们普遍放弃筛查，导致早期诊断率下降到15%，那么这意味着更多的患者将在癌症晚期才被确诊。这种晚期诊断比例的增加，将直接导致整体人群的胃癌五年生存率大幅下降，并增加治疗的复杂性和医疗费用。

  3. 不同癌症的筛查成本效益：

    • 虽然早期筛查需要一定的投入，但从长远来看，筛查的成本效益通常优于晚期治疗。例如，前列腺癌筛查在欧洲被证明可能具有成本效益 73。肺癌低剂量CT筛查也被认为具有成本效益，并能显著降低肺癌死亡率 7476。结直肠癌筛查（如粪便检测或肠镜）能显著减少CRC发病率和死亡率 72。这些研究表明，在早期筛查上的投入，能够有效避免晚期治疗的高昂费用和患者痛苦，提高生存率。
    • 此外，随着技术发展，新的生物标志物筛查方法（如基于血液或尿液的检测）的成本效益正在被评估，有望进一步降低筛查门槛，提高依从性 75。但如果民众因“节俭”而拒绝参与，这些技术的潜在益处将无法实现。

总而言之，节俭行为在医疗健康领域的表现，往往导致癌症诊断阶段的推迟。这种延迟不仅使得治疗方案更加复杂、痛苦和昂贵，更重要的是，极大地削弱了患者的生存机会。因此，在医疗健康方面进行适度的投入，是实现长期健康和避免更大损失的关键。

4. 节俭习惯的健康误区与科学替代方案

4.1 风险行为的科学甄别

在讨论“省出来的癌症”时，区分“真风险”与“伪节俭”至关重要。有些节俭行为确实蕴含健康风险，需要避免；而另一些行为则在合理操作下是安全的，甚至有助于可持续生活。识别这些差异，有助于我们在节约资源的同时，保障自身健康。

  1. “真风险”：高致癌性节俭行为

    • 食用轻微霉变食物（高风险）：任何肉眼可见的霉菌都意味着食物可能已被霉菌毒素（如黄曲霉毒素）污染。即使是轻微的霉变，也可能产生强致癌物质，这些毒素不易被烹饪破坏，长期摄入会显著增加肝癌等风险。例如，根据联合国粮食及农业组织（FAO）的一项研究，全球约有25%的粮食和饲料产品受到霉菌毒素污染 83。一些霉菌毒素具有遗传毒性/致癌性，重点在于低暴露条件下的危害评估 84。食用霉变食物是典型的“真风险”行为，应坚决避免。
    • 反复使用高度加热的食用油（高风险）：食用油在高温下反复使用会产生多种有害物质，如多环芳烃、醛类和极性化合物，这些物质具有细胞毒性和致癌性，并可促进慢性炎症。此类行为构成明确的健康风险。
    • 使用磨损、涂层脱落的厨具（高风险）：不粘锅涂层脱落后，可能释放全氟化合物（PFAS）进入食物；受损的陶瓷或金属餐具可能溶出重金属。这些都属于高风险行为，应及时更换。
    • 忽视早期症状和癌症筛查（高风险）：这是最危险的“节俭”之一，延迟就医往往导致癌症发现时已是晚期，错失最佳治疗时机。如前文所述，胰腺癌和口腔癌的延迟诊断与晚期分期显著相关。

  2. “伪节俭”：合理操作下安全的节俭行为

    • 合理储存剩菜（低风险）：剩菜并非“毒药”，关键在于储存方式。熟食在室温下存放不应超过2小时，应尽快冷藏，并在24小时内食用完。将剩菜分装在密封容器中，迅速冷却并冷藏（0-4°C），可有效抑制细菌生长和亚硝酸盐的产生。对于绿叶蔬菜，如果实在需要储存，建议焯水后快速冷却再冷藏，并尽快食用。美国膳食指南也强调了食品安全储存的重要性 85。因此，合理储存并及时食用的剩菜，其健康风险极低，属于可接受的节俭行为。
    • 重复使用安全的容器（安全）：并非所有重复使用的容器都存在风险。玻璃容器、陶瓷碗碟、不锈钢制品等在清洗干净后可以安全重复使用。对于塑料容器，应关注其材质标识（如PP聚丙烯、HDPE高密度聚乙烯通常较为安全），避免将其用于高温加热或盛放酸性、高油食物，尤其是标有“PC”或无标识的塑料容器。明确标示为食品级且耐热的塑料容器，在遵循其使用说明的前提下，也可以重复使用。
    • 健康搭配低成本食材（安全）：并非所有廉价食物都不健康。豆类、全谷物、当季蔬菜和水果等，既经济又营养丰富。通过合理的膳食搭配，可以实现低成本的营养均衡，例如“豆类+蔬菜”的组合能提供充足的蛋白质、膳食纤维和维生素。一项研究表明，基于菜单规划和杂货配送的“食物处方”试点项目，证明了低成本且营养全面的饮食方案是可行和可接受的，并能显著改善健康饮食指数 86。这表明，在有限预算下，通过科学规划，完全可以实现健康的饮食。
    • 延长部分物品使用寿命（安全）：一些物品，如衣物、家具等，只要功能完好、清洁卫生，延长其使用寿命是环保且经济的行为，不会对健康造成直接风险。这与重复使用不安全的厨具或塑料容器有本质区别。

因此，公众需要学习识别真正的健康风险，避免因盲目节俭而损害健康；同时，也要掌握科学的节俭方法，将可持续的生活方式与健康有效地结合起来。

4.2 低成本健康替代策略

在明确了“真风险”与“伪节俭”之后，关键在于如何找到既能节俭又能保障健康的替代方案。这些低成本健康策略旨在帮助个人和家庭在经济有限的情况下，依然能够采取健康的生活方式，降低癌症风险。

  1. 食物储存与处理：科学保鲜，减少浪费

    • 分餐冷藏：烹饪食物时，可预先将部分食物分装到小份保鲜盒中，待完全冷却后立即放入冰箱冷藏（0-4°C），并尽快在24小时内食用。对于易腐败的肉类、豆制品等，最好在24小时内吃完。冷藏可以有效抑制微生物生长，延长食物保鲜期 8788。
    • 使用安全保鲜盒：选择玻璃、陶瓷或食品级不锈钢材质的保鲜盒，这些材质稳定且不释放有害物质。若使用塑料保鲜盒，请选择底部标识为“5”（PP聚丙烯）的材质，此类塑料耐热性较好，避免用于高温加热或盛放高油脂食物。定期检查保鲜盒是否有划痕或老化，及时更换。
    • 合理利用冷冻技术：对于短期内无法食用的肉类、鱼类、部分蔬菜（如西兰花、豆角等）和主食（如米饭、馒头），可进行分装后冷冻。冷冻能最大限度地保留食物营养，并阻止微生物活动，大大延长储存时间。解冻时应在冰箱冷藏室进行，避免反复冻融。
    • 避免食用霉变食物：一旦发现食物霉变，即使是轻微的霉斑，也应立即丢弃。切勿认为切除霉变部分即可安全食用，因为霉菌毒素（特别是黄曲霉毒素）可能已扩散到食物其他看起来正常的部分。
    • 减少腌制和熏制食品摄入：可以通过新鲜蔬菜和香料来丰富口味，减少对高盐、腌制食品的依赖。例如，自制泡菜可以通过控制发酵过程和减少盐分来降低亚硝酸盐风险，但仍不建议大量摄入。
    • 健康用油习惯：烹饪用油应避免反复高温加热，特别是油炸用油。尽量选择小包装食用油，避免油品长期存放氧化。烹饪方式优先选择蒸、煮、炖、炒，减少煎、炸、烧烤。

  2. 饮食搭配：低成本高营养组合

    • 增加豆类摄入：豆类（如大豆、扁豆、鹰嘴豆）是优质植物蛋白的极佳来源，富含膳食纤维、维生素和矿物质，价格低廉且易于储存。可以将豆类作为肉类的部分替代品，或添加到汤、粥、沙拉中，增加饱腹感和营养价值。
    • 多样化蔬菜水果：选择当季、本地产的蔬菜水果，通常价格更优惠。例如，根茎类蔬菜（如胡萝卜、土豆）、十字花科蔬菜（如白菜、菜花）和一些叶类蔬菜都非常经济且营养丰富。每天保证足量的蔬菜水果摄入，提供抗氧化剂和膳食纤维。
    • 全谷物替代精制谷物：将部分精米白面替换为糙米、全麦面、玉米、燕麦等全谷物，增加膳食纤维和B族维生素摄入，有助于维持血糖稳定和肠道健康。
    • 自制健康餐：外卖和加工食品往往含有过多的盐、糖和不健康脂肪。自己动手做饭，能更好地控制食材选择和烹饪方式，既省钱又健康。

  3. 医疗支出：重视预防与早期发现

    • 利用公共医疗资源：了解并充分利用当地医保政策、免费体检项目以及社区提供的癌症筛查服务。例如，意大利的肺癌筛查项目RISP旨在为特定高危人群提供筛查 89，而其他地方的结直肠癌筛查干预措施也可能有助于提高筛查率 90。
    • 定期健康检查：即使经济条件有限，也应尽量进行基础的健康检查，特别是血压、血糖、血脂等常规指标。对于有家族史或其他高危因素的人群，应咨询医生，制定个性化的筛查计划。
    • 重视身体信号：学习识别癌症的早期预警信号（如不明原因的体重减轻、持续咳嗽、异常出血、淋巴结肿大等），一旦出现异常及时就医，避免因拖延导致病情恶化，增加后期治疗成本。

  4. 物品使用：选择安全耐用品，避免重复利用风险品

    • 选择安全材质厨具：投资购买高质量、耐用的不锈钢、铸铁或陶瓷厨具，避免使用涂层脱落的旧厨具 91。玻璃、陶瓷和不锈钢餐具是长期使用的安全选择。
    • 避免重复使用一次性塑料：一次性塑料水瓶、餐盒等不建议重复使用，特别是用于盛装热水或加热。选择可重复使用的水杯和餐具（如不锈钢保温杯、玻璃饭盒），既环保又健康。
    • 关注产品标识：购买食品接触材料时，留意产品上的材质标识和使用说明，避免将不适合加热或长期使用的容器用于不当用途。

通过采纳这些低成本的健康替代策略，人们可以在不额外增加经济负担的情况下，有效降低多种癌症的风险，实现真正的健康节俭。

5. 社会经济因素与公共卫生干预的作用

5.1 经济压力对节俭行为的驱动机制

经济压力是驱动个体和家庭采取高风险节俭行为的核心因素之一，尤其对低收入群体影响深远。这种压力并非简单的金钱匮乏，而是通过复杂的社会经济机制，间接影响健康行为选择，最终增加癌症风险。

  1. 食品选择的经济驱动：

    • 廉价食品的优先选择：在经济拮据的情况下，消费者往往被迫优先考虑食品的价格而非营养价值。加工食品、高盐、高糖、高脂肪的超加工食品通常价格低廉且易于储存，成为低收入家庭的常见选择 92。这些食品往往缺乏新鲜蔬菜、水果和优质蛋白质所提供的必需营养素，却富含潜在的致癌物质或促炎成分。例如，与新鲜蔬果相比，腌制食品和加工肉制品通常更为便宜，且保质期长，这使得它们在经济压力下成为更具吸引力的选项。
    • 新鲜蔬果摄入不足：新鲜的蔬菜和水果价格相对较高，且保质期短，对于经济有限的家庭来说，购买和储存都存在挑战。长期缺乏新鲜蔬果，意味着抗氧化剂、维生素和膳食纤维摄入不足，从而削弱身体的抗癌防御能力。有研究表明，收入水平越高的女性，其营养状况和生活方式越健康，BMI指数也越低，自我健康感知也更好 93。

  2. 医疗支出挤压与筛查率降低：

    • “金融毒性”的普遍存在：癌症治疗的经济负担（即“金融毒性”）是一个全球性问题。即使在高收入国家，超过30%的乳腺癌患者也会遭受金融毒性，而在中低收入国家，这一比例高达78.8% 94。这种巨大的经济压力使得许多人在尚未确诊癌症时，就会因担心医疗费用而延迟甚至放弃必要的检查和筛查。
    • 早期筛查的忽视：癌症筛查项目，如乳腺X光检查、结肠镜检查等，虽然在长期内具有成本效益，但在短期内仍需要一定的费用支出和时间投入。
    • 忽视早期症状：当身体出现一些早期、非特异性的癌症症状时，低收入人群可能选择忽视，寄希望于“自行好转”，而非立即就医。这种行为模式源于对医疗费用（包括挂号费、检查费、交通费、误工费等）的担忧。结直肠癌患者的纵向研究发现，较低的邻里社会经济地位与更高的金融毒性相关 95。新的医疗技术在诊断和治疗前列腺癌方面取得了显著进展，但这些新技术通常比传统方法更昂贵，可能加剧患者的经济负担 96。

  3. 生活方式选择受限：

    • 居住环境与健康风险：低收入群体往往居住在环境条件较差的地区，可能面临更高的环境污染暴露（如二手烟、工业污染物），而这些都增加了癌症风险。
    • 体力活动与健康教育缺乏：经济压力下，人们可能没有时间和金钱参与健身活动，或者缺乏获取健康知识的途径。此外，贫困也与久坐不动的生活方式和饮食习惯相关 93。
    • 心理压力与健康行为：长期的经济压力本身就是一种慢性应激源，可能导致心理健康问题，进一步影响健康行为的采纳，例如增加吸烟、饮酒等不良习惯。

综上所述，经济压力并非直接导致癌症，而是通过一系列复杂的社会经济和行为机制，驱动个体采纳看似“节俭”实则高风险的生活方式，包括不健康的饮食选择、对医疗服务的规避以及不利的生活环境，最终增加了癌症的发生率和死亡率。

5.2 公共卫生政策的干预路径

为了平衡经济压力与健康需求，降低节俭行为带来的致癌风险，公共卫生政策需要采取多方面的干预措施。这些措施应涵盖健康教育、经济补贴和社区支持等层面，形成一个综合性的干预体系。

  1. 健康教育：提升认知与行为改变

    • 普及癌症预防知识：通过多媒体平台（电视、广播、网络、社交媒体）和社区活动，普及癌症早期信号识别、健康饮食原则、食品安全储存等知识。例如，明确告知公众霉变食物、不当储存的剩菜、反复使用的食用油等潜在风险，纠正“省小钱”的错误观念。重点针对黄曲霉毒素的危害性、腌制食品与亚硝胺的关系，以及高温烹饪对食用油的影响进行科普。
    • 强调筛查重要性：解释各类癌症筛查（如宫颈癌TCT、乳腺X光、结肠镜等）的必要性和益处，降低对筛查的恐惧感和费用顾虑，提高公众对早期诊断的认知。例如，可以引用早期诊断率对五年生存率的巨大影响，鼓励民众参与筛查。
    • 推广低成本健康饮食方案：教育居民如何利用当地当季的廉价食材进行营养搭配，如推广豆类、全谷物、绿叶蔬菜等经济且营养丰富的食物组合。例如，西班牙提出的“食物政策力量”（PODER）就包括了对不健康食品和饮料广告的管制，以及推广健康食品供应的政策 97。

  2. 补贴政策：降低健康成本，减轻经济负担

    • 新鲜蔬果补贴：政府可以考虑对新鲜蔬菜和水果提供补贴，降低其市场价格，使其更容易被低收入群体负担。英国的研究表明，对不健康食品征税并将税收用于补贴水果和蔬菜，每年可以避免多达6400例心血管疾病和癌症死亡 98。
    • 癌症筛查免费或减免：将高风险人群的癌症早期筛查项目纳入基本医疗保险报销范围，或由政府提供免费筛查服务。例如，美国医疗补助计划（Medicaid）扩大覆盖范围，虽然在短期内对吸烟率降低影响不显著，但提供戒烟服务仍是其重要的组成部分 99。对于癌症筛查，免费或减免政策能显著提高参与率，有助于早期发现。
    • 贫困癌症患者救助机制：建立健全针对癌症患者的医疗救助体系，特别是对确诊后需要长期治疗的低收入患者，减轻其“金融毒性”的压力，避免因病致贫、因贫放弃治疗。例如，中国在结直肠癌患者健康相关生活质量的研究中发现，经济压力增加与患者生活质量下降密切相关 100，提示需要关注患者的经济困境。

  3. 社区支持：构建健康环境，促进行为改变

    • 社区健康导航员：在社区设立健康导航员，为居民提供一对一的健康咨询、筛查预约协助、营养指导等服务，特别关注边缘化和高风险人群。患者导航项目已被证明能有效改善患者的就医可及性，减少健康不平等 101。
    • 集体采购与共享菜园：鼓励社区组织居民进行集体采购，通过大宗购买降低新鲜农产品的成本；或推广社区菜园项目，让居民有机会自己种植健康蔬菜，同时增强社区凝聚力。
    • 改善食品环境：与零售商合作，增加社区内新鲜蔬果的可及性和供应量，减少高糖、高盐、高脂肪食品的推广。在教育、医疗和体育场所推广100%健康的商品供应 97。
    • 食品安全监管：加强对食品生产、流通和销售环节的监管，确保食品质量安全，特别是针对散装食品和农贸市场的食品，减少霉变、过期食品流入市场。

通过上述多层次、多维度的公共卫生干预，政府和社会可以共同努力，减轻经济压力对健康行为的负面影响，引导公众采取更健康的“节俭”方式，从而有效降低“省出来的癌症”的风险。

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参考文献

1Dietary patterns, BCMO1 polymorphisms, and primary lung cancer risk in a Han Chinese population: a case-control study in Southeast China.PubMed

Fei He, Ren-Dong Xiao, Tao Lin, et al.
BMC Cancer. 2018 Apr 19;18(1):445. doi: 10.1186/s12885-018-4361-2.
BACKGROUND: We investigated whether BCMO1 variants and dietary patterns are associated with lung cancer risk. METHODS: Case-control study including 1166 lung cancer cases and 1179 frequency matched controls was conducted for three BCMO1 variants (rs6564851, rs12934922, and rs7501331) and four dietary patterns were investigated. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). RESULTS: The rs6564851, rs12934922, and rs7501331 were not found to be associated with lung cancer risk (P > 0.05). In multivariable-adjusted models, compared to the lowest quartile of the score on the "fruits and vegetables" pattern, the highest quintile was associated with a 78.4% decreased risk (OR = 0.216; 95% CI, 0.164-0.284; P for trend < 0.001). Other patterns were not found the association. The "fruits and vegetables" pattern was associated with a reduced risk of lung cancer with all 3 SNPs irrespective of genotypes (all P for trend< 0.001). The association for the "Frugal" pattern was associated with increased risk of lung cancer among smokers (P for interaction = 0.005). The protective effects of the "cereals/wheat and meat" pattern was more evident for squamous cell carcinoma and other histological type. CONCLUSIONS: We did not observe associations of BCMO1 variants and lung cancer. Diets rich in fruits and vegetables may be protective against lung cancer.

2ESPEN guidelines on nutrition in cancer patients.PubMed

Jann Arends, Patrick Bachmann, Vickie Baracos, et al.
Clin Nutr. 2017 Feb;36(1):11-48. doi: 10.1016/j.clnu.2016.07.015. Epub 2016 Aug 6.
Cancers are among the leading causes of morbidity and mortality worldwide, and the number of new cases is expected to rise significantly over the next decades. At the same time, all types of cancer treatment, such as surgery, radiation therapy, and pharmacological therapies are improving in sophistication, precision and in the power to target specific characteristics of individual cancers. Thus, while many cancers may still not be cured they may be converted to chronic diseases. All of these treatments, however, are impeded or precluded by the frequent development of malnutrition and metabolic derangements in cancer patients, induced by the tumor or by its treatment. These evidence-based guidelines were developed to translate current best evidence and expert opinion into recommendations for multi-disciplinary teams responsible for identification, prevention, and treatment of reversible elements of malnutrition in adult cancer patients. The guidelines were commissioned and financially supported by ESPEN and by the European Partnership for Action Against Cancer (EPAAC), an EU level initiative. Members of the guideline group were selected by ESPEN to include a range of professions and fields of expertise. We searched for meta-analyses, systematic reviews and comparative studies based on clinical questions according to the PICO format. The evidence was evaluated and merged to develop clinical recommendations using the GRADE method. Due to the deficits in the available evidence, relevant still open questions were listed and should be addressed by future studies. Malnutrition and a loss of muscle mass are frequent in cancer patients and have a negative effect on clinical outcome. They may be driven by inadequate food intake, decreased physical activity and catabolic metabolic derangements. To screen for, prevent, assess in detail, monitor and treat malnutrition standard operating procedures, responsibilities and a quality control process should be established at each institution involved in treating cancer patients. All cancer patients should be screened regularly for the risk or the presence of malnutrition. In all patients - with the exception of end of life care - energy and substrate requirements should be met by offering in a step-wise manner nutritional interventions from counseling to parenteral nutrition. However, benefits and risks of nutritional interventions have to be balanced with special consideration in patients with advanced disease. Nutritional care should always be accompanied by exercise training. To counter malnutrition in patients with advanced cancer there are few pharmacological agents and pharmaconutrients with only limited effects. Cancer survivors should engage in regular physical activity and adopt a prudent diet.

3ESPEN expert group recommendations for action against cancer-related malnutrition.PubMed

J Arends, V Baracos, H Bertz, et al.
Clin Nutr. 2017 Oct;36(5):1187-1196. doi: 10.1016/j.clnu.2017.06.017. Epub 2017 Jun 23.
Patients with cancer are at particularly high risk for malnutrition because both the disease and its treatments threaten their nutritional status. Yet cancer-related nutritional risk is sometimes overlooked or under-treated by clinicians, patients, and their families. The European Society for Clinical Nutrition and Metabolism (ESPEN) recently published evidence-based guidelines for nutritional care in patients with cancer. In further support of these guidelines, an ESPEN oncology expert group met for a Cancer and Nutrition Workshop in Berlin on October 24 and 25, 2016. The group examined the causes and consequences of cancer-related malnutrition, reviewed treatment approaches currently available, and built the rationale and impetus for clinicians involved with care of patients with cancer to take actions that facilitate nutrition support in practice. The content of this position paper is based on presentations and discussions at the Berlin meeting. The expert group emphasized 3 key steps to update nutritional care for people with cancer: (1) screen all patients with cancer for nutritional risk early in the course of their care, regardless of body mass index and weight history; (2) expand nutrition-related assessment practices to include measures of anorexia, body composition, inflammatory biomarkers, resting energy expenditure, and physical function; (3) use multimodal nutritional interventions with individualized plans, including care focused on increasing nutritional intake, lessening inflammation and hypermetabolic stress, and increasing physical activity.

4The Cost-Effectiveness of Adjunctive Lifestyle Interventions for the Management of Cancer: A Systematic Review.PubMed

Andrew Gallagher, Violetta Shersher, Duncan Mortimer, et al.
Appl Health Econ Health Policy. 2023 Mar;21(2):225-242. doi: 10.1007/s40258-022-00759-4. Epub 2022 Sep 27.
OBJECTIVE: There is a paucity of papers synthesizing the cost-effectiveness (CE) of lifestyle interventions to support cancer patients, and the synthesis papers available have used analytic methods that do not permit easy comparison between studies. We therefore evaluated the CE of adjunctive lifestyle interventions compared with usual care. METHODS: A systematic literature search of Scopus, MEDLINE, EMBASE, PsycINFO, CINAHL and the Cochrane Library databases was conducted from database inception until June 2021. Eligible studies were economic evaluations from randomised controlled trials or modelled economic evaluations that recruited subjects with a confirmed diagnosis of cancer and were allocated to a lifestyle intervention as an adjunct or supportive treatment, or usual care. Studies were excluded if there was no cost-effectiveness analysis or if costs were identified but not related back to measures of effectiveness. CE of the included interventions was recalculated, adjusting for key differences (with respect to absolute resource costs and timing) between the broad range of study settings and a common 'target' setting. All CE data were converted into incremental net monetary benefit using a common cost-effectiveness threshold to facilitate comparison. The quality of the studies was evaluated for risk of bias using the ECOBIAS check list. RESULTS: Nine studies were included in our review. Seven studies investigated the benefits of physical exercise in combination with cancer treatment and two studies investigated the combination of exercise and psychosocial counselling alongside cancer treatment. Six studies with an exercise intervention reported larger quality-adjusted life year (QALY) gains compared with usual care and when cost per QALY gained was considered, three of the interventions were cost effective. One of the two interventions combining exercise with psychosocial counselling was cost effective. All studies were considered of good quality but all had some limitations. CONCLUSIONS: The evidence to support the cost effectiveness of lifestyle interventions in patients with cancer is mixed with four of the nine interventions found to be cost effective and two remaining cost effective when uncertainty was taken into account. Sensitivity analysis showed the influence of the CE threshold on the results, highlighting the importance of selecting a CE threshold that is appropriate to the setting. SYSTEMATIC REVIEW REGISTRATION: PROSPERO Registration Number: CRD42020185376.

5Sacral Agenesis: Late Presentation and the Psychological Impact of Delayed Diagnosis.PubMed

Jyoti Bhutani, Vinayak Rengan, Vishnu Pansari, et al.
Cureus. 2023 Oct 22;15(10):e47456. doi: 10.7759/cureus.47456. eCollection 2023 Oct.
Sacral agenesis (SA) is a rare condition characterized by the absence of one or more lower sacral vertebral bodies. In India, children with this condition often present late with symptoms primarily related to urinary and bowel dysfunction. Maternal diabetes is the only confirmed risk factor, significantly elevating the incidence rate. We discuss a case of a nine-year-old female who presented to the pediatric outpatient department (OPD) with chronic constipation and urinary retention, having experienced symptoms since infancy. Initial investigations at peripheral hospitals had yielded no clear diagnosis, leading to undue psychological distress to the child and family. The child had been born to a mother with diabetes mellitus during pregnancy. Physical examination revealed mild dehydration, anemia, and sacral dimpling. Further evaluation showed renal injury and SA confirmed by MRI, along with other associated findings. This case report highlights the importance of early diagnosis and intervention in pediatric SA, especially given the risk of renal disease progression. The treatment in this case included clean intermittent self-catheterization (CIC), dietary management, and counseling on renal health. Crucially, uncovering the root cause provided immense psychological relief to the child and her family. Pediatric SA remains a diagnostic challenge, often leading to psychological distress in affected individuals who present late. Early recognition and comprehensive management are crucial, especially in cases associated with maternal diabetes, to mitigate the risk of renal complications and improve the overall quality of life for affected children.

6Prostate cancer diagnostic pathway in men with lower urinary tract symptoms or performing opportunistic screening: The Italian Society of Urology (SIU) position paper.PubMed

Vincenzo Ficarra, Riccardo Bartoletti, Marco Borghesi, et al.
Minerva Urol Nephrol. 2024 Oct;76(5):530-535. doi: 10.23736/S2724-6051.24.06118-4.
BACKGROUND: Voluntary PCa screening frequently results in excessive use of unnecessary diagnostic tests and an increasing risk of detection of indolent PCa and unaffordable costs for the various national health systems. In this scenario, the Italian Society of Urology (Società Italiana di Urologia, SIU) proposes an organized flow chart guiding physicians to improve early diagnosis of significant PCa avoiding unnecessary diagnostic tests and prostate biopsy. METHODS: According to available evidence and international guidelines [i.e., European Association of Urology (EAU), American Association of Urology (AUA) and National Comprehensive Cancer Network (NCCN)] on PCa, a Panel of expert urologists selected by Italian Society of Urology (SIU, Società Italiana di Urologia) proposed some indications to develop a stepwise diagnostic pathway based on the diagnostic tests mainly used in the clinical practice. The final document was submitted to six expert urologists for external revision and approval. Moreover, the final document was shared with patient advocacy groups. RESULTS: In voluntary men and symptomatic patients with elevated PSA value (>3 ng/mL), the Panel strongly discourage the use of antibiotic agents in absence of urinary tract infection confirmed by urine culture. DRE remains a key part of the urologic physical examination helping urologists to correctly interpret PSA elevation and prioritizing the execution of multiparametric Magnetic Resonance Imaging (mpMRI) in presence of suspicious PCa. Men with negative mpMRI and low clinical suspicion of PSA (PSA density < 0.20 ng/mL/cc, negative DRE findings, no family history) can be further monitored. Men with negative mpMRI and a higher risk of PCa (familial history, suspicious DRE, PSAD>0.20 ng/mL/cc or PSA>20 ng/mL) should be considered for systematic prostate biopsy. While PI-RADS 4-5 lesions represent a strong indication for prostate biopsy, PI-RADS 3 lesions should be further stratified according to PSAD values and prostate biopsy performed when PSAD is higher than 0.20. Accreditation, certification, and quality audits of radiologists and centers performing prostatic mpMRI should be strongly considered. The accessibility and/or the waiting list for MRI examinations should be also evaluated in the diagnostic pathway. The panel suggests performing transperineal or transrectal targeted plus systematic biopsies as standard of care. CONCLUSIONS: Scientific societies must support the use of shared diagnostic pathway with the aim to increase the early detection of significant PCa reducing a delayed diagnosis of advanced PCa. Moreover, a shared diagnostic pathway can reduce the incorrect use of antibiotic, the number of unnecessary laboratory and radiologic examinations as well as of prostate biopsies.

7Nutritional Assessment in Cancer Patients.PubMed

Muhammad Naveed Sheas, Syeda Ramsha Ali, Waseem Safdar, et al.
Cancer Treat Res. 2023;185:285-310. doi: 10.1007/978-3-031-27156-4_14.
Malnutrition in cancer patients is highly prevalent. The metabolic and physiologic changes associated with the disease and the side effects of treatment regimens all combine together to produce a detrimental effect on the patient's nutritional status. A poor nutritional status significantly reduces the efficacy of treatment methods and the patient's overall chances of survival. Therefore, an individualized nutrition care plan is essential to counter malnutrition in cancer. Nutritional assessment is the first step of this process which sets the foundation for developing an effective intervention plan. Currently, there is no single standard method for nutritional assessment in cancer. Hence, to get a true picture of the patient's nutritional state, a comprehensive analysis of all aspects of the patient's nutritional status is the only reliable strategy. The assessment includes anthropometric measurements and evaluation of body protein status, body fat, inflammation markers, and immune markers. A thorough clinical examination which factors in the medical history and physical signs, along with the dietary intake patterns of the patient, is also important components of nutritional assessment of cancer patients. To facilitate with the process, various nutritional screening tools like patient-generated subjective global assessment (PGSGA), nutrition risk screening (NRS), and malnutrition screening tool (MST) have been developed. While these tools have their own benefits, they only give a glimpse of the nutritional problems and do not bypass the need for a complete assessment employing various methods. This chapter covers all four of the elements of nutritional assessment for cancer patients in detail.

8[Not Available].PubMed

Alexander Ströhle, Christian Löser, Isabel Behrendt, et al.
Rehabilitation (Stuttg). 2018 Feb;57(1):55-70. doi: 10.1055/s-0043-124048. Epub 2018 Feb 21.
Alternative diets (AD) differ from the current common mixed diet; AD are recommended as a permanent diet. These diets are based on ethical, philosophical and health promoting principles and lead to very different recommendations for food selection. Even within a particular AD there is usually a broad spectrum of versions, so that a general evaluation is only possible to a limited extent. This is also true for single AD. Vegetarian diets and partly paleo-diets have been investigated to a reasonable extent. Plant based diets are appropriate as permanent diets and offer health benefits as compared with currently practiced diets (risk reduction of cancers by 10-18% and of heart diseases by 30%; favorable effect on blood pressure and lipid profile; no risk reduction on cancer and total mortality). Vegan diets have to be critically assessed: they are linked to an increased risk of deficits for single nutrients (vitamin B, iodine and as the case may be. calcium and long chain omega-3 fatty acids), if suitable supplements or fortified foods are not consumed.

9Diet Changes and Underlying Motives in Cancer Patients.PubMed

Alexandra Schmid, Viktoria Mathies, Jens Buentzel, et al.
Nutr Cancer. 2022;74(6):2017-2028. doi: 10.1080/01635581.2021.1986553. Epub 2021 Oct 5.
With rising cancer incidence rates and numbers of long-term cancer survivors, diet increasingly comes into view of patients as well as healthcare providers. The aim was to analyze cancer patients' concepts of nutrition, changes in diet and reasons for these changes. This study is a cross-sectional single-center study. Data was collected 12/2017 - 01/2019 using a questionnaire. The study was set at an outpatient department at a German university hospital. 102 patients (male = 47, female = 54; age 34 to 86 years [mean = 62.3]) with cancer were included in the study. Statistical calculation was performed with Mann-Whitney-U-Test and Wilcoxon-signed-rank. < 0.05 was considered significant. Patients were more concerned with diet after their diagnosis than before ( < 0.01). Seventy-one (70%) patients reported that they changed their diet or planned to do so. Some changes included an increased intake of vegetables or fruits. Patients who changed their diet more often were convinced that there was a positive influence of diet on the course of cancer ( < 0.05). Diet is an important topic for many cancer patients. Some patients seem to have a lack of information regarding the effect of diet on health. Physicians and dietitians should provide more education on healthy and safe diets for cancer patients.

10Diet and nutrition in the etiology of oral cancer.PubMed

D M Winn
Am J Clin Nutr. 1995 Feb;61(2):437S-445S. doi: 10.1093/ajcn/61.2.437S.
Epidemiological studies worldwide have implicated dietary and nutritional factors in the development of oral and pharyngeal cancer. Dietary information in these case-control studies generally was collected through food-frequency questionnaires. Consistently, these studies observed a protective effect of a diet high in fruit intake, reflected in a 20-80% reduction in oral cancer risk. A high intake of foods considered to be dietary staples in particular cultural groups, possibly indicating a generally impoverished diet, has been linked to excess risk. Indigenous dietary practices that in single studies were found to increase risk include a high intake of chili powder and wood stove cooking. Supplementation with various vitamins has been protective in a few studies. Chemoprevention trials generally have found that chemopreventive agents reduce the size of oral leukoplakia lesions or the frequency of second primary oral cancers. The most consistent dietary findings across multiple cultural settings are a protective effect of high fruit consumption and the carcinogenic effect of high alcohol intake.

11Aflatoxins and disease.PubMed

R C Patten
Am J Trop Med Hyg. 1981 Mar;30(2):422-5. doi: 10.4269/ajtmh.1981.30.422.
These days it is widely believed by experts that most cancers are caused by environment factors. The epidemiology of most of these suspected factors is still equivocal. One such factor which has been widely studied is aflatoxin, a chemical produced by the fungus Aspergillus flavus. Because of the widespread distribution of this agent, its known toxicity, and its frequent ingestion by humans, aflatoxin may well be a significant cause of cancer worldwide. This paper attempts to summarize some of the historical and epidemiological evidence regarding aflatoxins and disease.

12Aflatoxins: biosynthesis, occurrence, toxicity, and remedies.PubMed

Muhammad Abrar, Faqir Muhammad Anjum, Masood Sadiq Butt, et al.
Crit Rev Food Sci Nutr. 2013;53(8):862-74. doi: 10.1080/10408398.2011.563154.
Food contagion with aflatoxins is the modern concern and has received a great awareness during the last few decades. The intermittent incidence of these toxins in agricultural commodities has negative role on the economy of the affected regions where harvest and postharvest techniques for the prevention of mold growth, are seldom practiced. Aflatoxins are difuranocoumarin derivatives produced by a polyketide pathway by the fungus Aspergillus flavus and Aspergillus parasiticus via polyketide pathway which are highly hepatotoxic, hepatocarcinogenic, teratogenic, and mutagenic in nature and contaminate a wide variety of important agricultural commodities before, during, and after harvest in various environmental conditions. The production of aflatoxins in innate substrates depends upon the various factors, that is, type of substrate, fungal species, moisture contents of the substrate, minerals, humidity, temperature, and physical damage of the kernels. These toxins cause several ailments such as cancer, hepatitis, mutation abnormalities, and reproduction disorders. Minimization and inactivation of aflatoxins contaminants through proper crop management at farm level and with physical, chemical, and biological techniques are the limelight of the article.

13Household dietary exposure to aflatoxins from maize and maize products in Kenya.PubMed

Robert M Kilonzo, Jasper K Imungi, William M Muiru, et al.
Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2014;31(12):2055-62. doi: 10.1080/19440049.2014.976595. Epub 2014 Nov 17.
Aflatoxicosis has repeatedly affected Kenyans, particularly in the eastern region, due to consumption of contaminated maize. However, save for the cases of acute toxicity, the levels of sub-lethal exposure have not been adequately assessed. It is believed that this type of exposure does exist even during the seasons when acute toxicity does not occur. This study, therefore, was designed to assess the exposure of households to aflatoxins through consumption of maize and maize products. Twenty samples each of maize kernels, muthokoi and maize meal were randomly sampled from households in Kibwezi District of Makueni County in Eastern Kenya and analysed for aflatoxin contamination. The samples were quantitatively analysed for aflatoxin contamination using HPLC. The uncertainty and variability in dietary exposure was quantitatively modelled in Ms Excel using Monte Carlo simulation in @Risk software. Aflatoxins were found in 45% of maize kernels at between 18 and 480 μg kg⁻¹, 20% of muthokoi at between 12 and 123 μg kg⁻¹, and 35% of maize meal at between 6 and 30 μg kg⁻¹. The mean dietary exposure to aflatoxin in maize kernels was 292 ± 1567 ng kg⁻¹ body weight day⁻¹, while the mean dietary exposure to aflatoxin in maize meal and muthokoi were 59 ± 62 and 27 ± 154 ng kg⁻¹ body weight day⁻¹ respectively. The results showed that the amount and frequency of consumption of the three foods is the more important contributing factor than the mean aflatoxin concentration levels, to the risk of dietary exposure to aflatoxins.

14Aflatoxins.PubMed

IARC Monogr Eval Carcinog Risks Hum. 1993;56:245-395.

15Chronic and Acute Toxicities of Aflatoxins: Mechanisms of Action.PubMed

Noreddine Benkerroum
Int J Environ Res Public Health. 2020 Jan 8;17(2):423. doi: 10.3390/ijerph17020423.
There are presently more than 18 known aflatoxins most of which have been insufficiently studied for their incidence, health-risk, and mechanisms of toxicity to allow effective intervention and control means that would significantly and sustainably reduce their incidence and adverse effects on health and economy. Among these, aflatoxin B1 (AFB1) has been by far the most studied; yet, many aspects of the range and mechanisms of the diseases it causes remain to be elucidated. Its mutagenicity, tumorigenicity, and carcinogenicity-which are the best known-still suffer from limitations regarding the relative contribution of the oxidative stress and the reactive epoxide derivative (Aflatoxin-exo 8,9-epoxide) in the induction of the diseases, as well as its metabolic and synthesis pathways. Additionally, despite the well-established additive effects for carcinogenicity between AFB1 and other risk factors, e.g., hepatitis viruses B and C, and the hepatotoxic algal microcystins, the mechanisms of this synergy remain unclear. This study reviews the most recent advances in the field of the mechanisms of toxicity of aflatoxins and the adverse health effects that they cause in humans and animals.

16[Nitrosamines. Review].PubMed

D Klein, B Poullain, G Debry
Ann Nutr Aliment. 1976;30(1):1-13.
Nitrosamines are an extremely carcinogenic class of compounds. The hasard, bound with the occurrence of this compounds in the food and the possibility to be formed in vivo, during the digestion, justifies the current works. The authors quoting numerous works on different laboratory's animals, remind the toxicity. and carcinogenicity of this compounds. The metabolism is also discussed. The N-nitroso, compounds may be formed in food from the presence of the precursors (nitrite or nitrate, amines and amino-acides). The synthesis takes place during the technological processes, the storage and the house cooking. Today, the marginal effect dose is estimated as 10 mug/kg of daily food. The carcinogenicity has not been demonstrated in human, but is strongly suspected. The amount of N-nitroso compounds in human food is generally low. Many factors can influence the reaction; it is inversely related to the basicity of secondary amine and optimum pH is around pH 4. A lot of compounds such as sodium ascorbate inhibit the synthesis in food. A number of recent reports using reliable methodology have identified nitrosamines at the lower part per billion level. Dimethyl-nitrosamines occurs, very sporadically in a number of cooked meat samples. The nitrosopyrrolidine appears frequently in fried but not in uncooked products. The nitrosopiperidine seems to be bind with the presence of pepper in food. Finally the presence of nitrosamides (nitrososarcosine) and nitrosoaminoacides (nitrosoproline, nitrosohydroxy-proline) is being quested. The N-nitroso compounds may be synthetized in vivo during the digestion at the acide medium of the stomach or by bacterial action during the transit in the gut...

17Nitrosamines and cancer.PubMed

Nutr Rev. 1975 Jan;33(1):19-20. doi: 10.1111/j.1753-4887.1975.tb07081.x.

18Nitrosamines and human cancer: introduction and overview.PubMed

P N Magee
Eur J Cancer Prev. 1996 Sep;5 Suppl 1:7-10. doi: 10.1097/00008469-199609001-00002.

19Metabolic reprogramming by tobacco-specific nitrosamines (TSNAs) in cancer.PubMed

Saharnaz Sarlak, Claude Lalou, Nivea Dias Amoedo, et al.
Semin Cell Dev Biol. 2020 Feb;98:154-166. doi: 10.1016/j.semcdb.2019.09.001. Epub 2019 Nov 4.
Metabolic reprogramming is a hallmark of cancer and the link between oncogenes activation, tumor supressors inactivation and bioenergetics modulation is well established. However, numerous carcinogenic environmental factors are responsible for early cancer initiation and their impact on metabolic reprogramming just starts to be deciphered. For instance, it was recently shown that UVB irradiation triggers metabolic reprogramming at the pre-cancer stage with implication for skin cancer detection and therapy. These observations foster the need to study the early changes in tissue metabolism following exposure to other carcinogenic events. According to the International Agency for Research on Cancer (IARC), tobacco smoke is a major class I-carcinogenic environmental factor that contains different carcinogens, but little is known on the impact of tobacco smoke on tissue metabolism and its participation to cancer initiation. In particular, tobacco-specific nitrosamines (TSNAs) play a central role in tobacco-smoke mediated cancer initiation. Here we describe the recent advances that have led to a new hypothesis regarding the link between nitrosamines signaling and metabolic reprogramming in cancer.

20Gut microbiota carcinogen metabolism causes distal tissue tumours.PubMed

Blanka Roje, Boyao Zhang, Eleonora Mastrorilli, et al.
Nature. 2024 Aug;632(8027):1137-1144. doi: 10.1038/s41586-024-07754-w. Epub 2024 Jul 31.
Exposure to environmental pollutants and human microbiome composition are important predisposition factors for tumour development. Similar to drug molecules, pollutants are typically metabolized in the body, which can change their carcinogenic potential and affect tissue distribution through altered toxicokinetics. Although recent studies demonstrated that human-associated microorganisms can chemically convert a wide range of xenobiotics and influence the profile and tissue exposure of resulting metabolites, the effect of microbial biotransformation on chemical-induced tumour development remains unclear. Here we show that the depletion of the gut microbiota affects the toxicokinetics of nitrosamines, which markedly reduces the development and severity of nitrosamine-induced urinary bladder cancer in mice. We causally linked this carcinogen biotransformation to specific gut bacterial isolates in vitro and in vivo using individualized bacterial culture collections and gnotobiotic mouse models, respectively. We tested gut communities from different human donors to demonstrate that microbial carcinogen metabolism varies between individuals and we showed that this metabolic activity applies to structurally related nitrosamine carcinogens. Altogether, these results indicate that gut microbiota carcinogen metabolism may be a contributing factor for chemical-induced carcinogenesis, which could open avenues to target the microbiome for improved predisposition risk assessment and prevention of cancer.

21Oils and cancer.PubMed

P E Tolbert
Cancer Causes Control. 1997 May;8(3):386-405. doi: 10.1023/a:1018409422050.
Epidemiologic evidence on the relationship between mineral oil exposure and cancer is reviewed. The review is restricted to occupations involving substantial dermal and inhalational exposure and for which an epidemiologic literature exists: metal machining, print press operating, and cotton and jute spinning. Mineral oils are complex mixtures of aliphatic hydrocarbons, naphthenics, and aromatics, the relative distribution of which depends on the source of the oil and the method of refinement. End-use products contain a variety of additives, and contamination by other agents generally occurs during use. Suspect agents include polycyclic aromatic hydrocarbons (PAH) (particularly benz[a]pyrene), nitrosamines, chlorinated paraffins, long-chain aliphatics, sulfur, N-phenyl-2-naphthylamine, and formaldehyde. The heterogeneity of this exposure makes epidemiologic study difficult and meta-analysis inappropriate. Nonetheless, several associations emerge from the literature with varying degrees of support. There is clear evidence that early formulations of mineral oils used in cotton and jute spinning and in metal machining were carcinogenic to the skin. Associations of mineral oil exposure with laryngeal and rectal cancer have received some support in the literature, particularly with respect to straight oils. Evidence is suggestive that grinding operations (which can entail either mineral oil-based or ethanolamine-based fluids) are associated with excess risk of cancer of the esophagus, stomach, and pancreas. A number of bladder cancer case-control studies have noted an association with work as a machinist. There is limited evidence of an association with cancer of the colon, prostate, and sinonasal region. Several studies of printers have yielded positive findings for lung cancer, whereas studies in metal machinists have been generally negative. The PAH and nitrosamine content of current formulations is lower than in the past and the implications of these changes in composition to the carcinogenicity of the formulations are not yet known.

22Atmospheric polycyclic aromatic hydrocarbons in India: geographical distribution, sources and associated health risk-a review.PubMed

Bhupander Kumar, Virendra Kumar Verma, Sanjay Kumar
Environ Geochem Health. 2024 May 2;46(6):186. doi: 10.1007/s10653-024-01969-6.
Atmospheric distribution of polycyclic aromatic hydrocarbons and associated human health risks have been studied in India. However, a comprehensive overview is not available in India, this review highlights the possible sources, and associated cancer risks in people living in different zones of India. Different databases were searched for the scientific literature on polycyclic aromatic hydrocarbons in ambient air in India. Database searches have revealed a total of 55 studies conducted at 139 locations in India in the last 14 years between 1996 and 2018. Based on varying climatic conditions in India, the available data was analysed and distributed with four zone including north, east, west/central and south zones. Comparatively higher concentrations were reported for locations in north zone, than east, west/central and south zones. The average concentrations of ∑PAHs is lower in east zone, and concentrations in north, west/central and south zones are higher by 1.67, 1.47, and 1.12 folds respectively than those in east zone. Certain molecular diagnostic ratios and correlation receptor models were used for identification of possible sources, which aided to the conclusion that both pyrogenic and petrogenic activities are the mixed sources of PAH emissions to the Indian environment. Benzo(a)pyrene toxicity equivalency for different zones is estimated and presented. Estimated Chronic daily intake (CDI) due to inhalation of PAHs and subsequently, cancer risk (CR) is found to be ranging from extremely low to low in various geographical zones of India.

23Interactions between polycyclic aromatic hydrocarbons in complex mixtures and implications for cancer risk assessment.PubMed

Ian W H Jarvis, Kristian Dreij, Åse Mattsson, et al.
Toxicology. 2014 Jul 3;321:27-39. doi: 10.1016/j.tox.2014.03.012. Epub 2014 Apr 5.
In this review we discuss the effects of exposure to complex PAH mixtures in vitro and in vivo on mechanisms related to carcinogenesis. Of particular concern regarding exposure to complex PAH mixtures is how interactions between different constituents can affect the carcinogenic response and how these might be included in risk assessment. Overall the findings suggest that the responses resulting from exposure to complex PAH mixtures is varied and complicated. More- and less-than additive effects on bioactivation and DNA damage formation have been observed depending on the various mixtures studied, and equally dependent on the different test systems that are used. Furthermore, the findings show that the commonly used biological end-point of DNA damage formation is insufficient for studying mixture effects. At present the assessment of the risk of exposure to complex PAH mixtures involves comparison to individual compounds using either a surrogate or a component-based potency approach. We discuss how future risk assessment strategies for complex PAH mixtures should be based around whole mixture assessment in order to account for interaction effects. Inherent to this is the need to incorporate different experimental approaches using robust and sensitive biological endpoints. Furthermore, the emphasis on future research should be placed on studying real life mixtures that better represent the complex PAH mixtures that humans are exposed to.

24Polycyclic aromatic hydrocarbons and cancer in man.PubMed

G Mastrangelo, E Fadda, V Marzia
Environ Health Perspect. 1996 Nov;104(11):1166-70. doi: 10.1289/ehp.961041166.
Various substances and industrial processes, surrogates of exposure to polycyclic aromatic hydrocarbons (PAHs), are currently classified as human carcinogens. This paper reviews recent epidemiological studies reporting direct evidence of the carcinogenic effects of PAHs in occupationally exposed subjects. Risks of lung and bladder cancer were dose dependent when PAHs were measured quantitatively and truly nonexposed groups were chosen for comparison. These new findings suggest that the current threshold limit value of 0.2 mg/m3 of benzene soluble matter (which indicates PAH exposure) is unacceptable because, after 40 years of exposure, it involves a relative risk of 1.2-1.4 for lung cancer and 2.2 for bladder cancer.

25Smoking and lung cancer.PubMed

Tevfik Ozlü, Yilmaz Bülbül
Tuberk Toraks. 2005;53(2):200-9.
Nowadays, around one-third of adults are known to be smokers, and smoking rates are increasing among the female population. It is estimated that deaths attributable to tobacco use will rise to 10 million by 2025, and one-third of all adult deaths are expected to be related to cigarette smoking. The association between cigarettes and lung cancer has been proven by large cohort studies. Tobacco use has been reported to be the main cause of 90% of male and 79% of female lung cancers. 90% of deaths from lung cancer are estimated to be due to smoking. The risk of lung cancer development is 20-40 times higher in lifelong smokers compared to non-smokers. Environmental cigarette smoke exposure and different types of smoking have been shown to cause pulmonary carcinoma. DNA adducts, the metabolites of smoke carcinogens bound covalently with DNA, are regarded as an indicator of cancer risk in smokers. In recent decades, there has been a shift from squamous and small cell lung cancer types to adenocarcinoma, due to increasing rates of smoking among female population and rising light cigarette usage. After smoking cessation, the cumulative death risk from lung cancer decreases. Patients who continue smoking experience greater difficulties during cancer treatment. Stopping smoking may prolong survival in cancer patients, and also decreases the risk of recurrent pulmonary carcinoma. In order to save lives and prevent smoking related hazards, physicians should advise both healthy individuals and those with cancer of the benefits of stopping smoking.

26Adverse outcome pathways for ionizing radiation and breast cancer involve direct and indirect DNA damage, oxidative stress, inflammation, genomic instability, and interaction with hormonal regulation of the breast.PubMed

Jessica S Helm, Ruthann A Rudel
Arch Toxicol. 2020 May;94(5):1511-1549. doi: 10.1007/s00204-020-02752-z. Epub 2020 May 13.
Knowledge about established breast carcinogens can support improved and modernized toxicological testing methods by identifying key mechanistic events. Ionizing radiation (IR) increases the risk of breast cancer, especially for women and for exposure at younger ages, and evidence overall supports a linear dose-response relationship. We used the Adverse Outcome Pathway (AOP) framework to outline and evaluate the evidence linking ionizing radiation with breast cancer from molecular initiating events to the adverse outcome through intermediate key events, creating a qualitative AOP. We identified key events based on review articles, searched PubMed for recent literature on key events and IR, and identified additional papers using references. We manually curated publications and evaluated data quality. Ionizing radiation directly and indirectly causes DNA damage and increases production of reactive oxygen and nitrogen species (RONS). RONS lead to DNA damage and epigenetic changes leading to mutations and genomic instability (GI). Proliferation amplifies the effects of DNA damage and mutations leading to the AO of breast cancer. Separately, RONS and DNA damage also increase inflammation. Inflammation contributes to direct and indirect effects (effects in cells not directly reached by IR) via positive feedback to RONS and DNA damage, and separately increases proliferation and breast cancer through pro-carcinogenic effects on cells and tissue. For example, gene expression changes alter inflammatory mediators, resulting in improved survival and growth of cancer cells and a more hospitable tissue environment. All of these events overlap at multiple points with events characteristic of "background" induction of breast carcinogenesis, including hormone-responsive proliferation, oxidative activity, and DNA damage. These overlaps make the breast particularly susceptible to ionizing radiation and reinforce that these biological activities are important characteristics of carcinogens. Agents that increase these biological processes should be considered potential breast carcinogens, and predictive methods are needed to identify chemicals that increase these processes. Techniques are available to measure RONS, DNA damage and mutation, cell proliferation, and some inflammatory proteins or processes. Improved assays are needed to measure GI and chronic inflammation, as well as the interaction with hormonally driven development and proliferation. Several methods measure diverse epigenetic changes, but it is not clear which changes are relevant to breast cancer. In addition, most toxicological assays are not conducted in mammary tissue, and so it is a priority to evaluate if results from other tissues are generalizable to breast, or to conduct assays in breast tissue. Developing and applying these assays to identify exposures of concern will facilitate efforts to reduce subsequent breast cancer risk.

27DNA methylation and carcinogenesis.PubMed

A V Lichtenstein, N P Kisseljova
Biochemistry (Mosc). 2001 Mar;66(3):235-55. doi: 10.1023/a:1010249510906.
In the world of easy things truth is opposed to lie; in the world of complicated things one profound truth is opposed to another not less profound than the first. Neils Bohr The hypothesis of the exclusively genetic origin of cancer ("cancer is a disease of genes, a tumor without any damage to the genome does not exist") dominated in the oncology until recently. A considerable amount of data confirming this hypothesis was accumulated during the last quarter of the last century. It was demonstrated that the accumulation of damage of specific genes lies at the origin of a tumor and its following progression. The damage gives rise to structural changes in the respective proteins and, consequently, to inappropriate mitogenic stimulation of cells (activation of oncogenes) or to the inactivation of tumor suppressor genes that inhibit cell division, or to the combination of both (in most cases). According to an alternative (epigenetic) hypothesis that was extremely unpopular until recently, a tumor is caused not by a gene damage, but by an inappropriate function of genes ("cancer is a disease of gene regulation and differentiation"). However, recent studies led to the convergence of these hypotheses that initially seemed to be contradictory. It was established that both factors--genetic and epigenetic--lie at the origin of carcinogenesis. The relative contribution of each varies significantly in different human tumors. Suppressor genes and genes of repair are inactivated in tumors due to their damage or methylation of their promoters (in the latter case an "epimutation", an epigenetic equivalent of a mutation, occurs, producing the same functional consequences). It is becoming evident that not only the mutagens, but various factors influencing cell metabolism, notably methylation, should be considered as carcinogens.

28Mechanisms of cadmium induced genomic instability.PubMed

Metka Filipič
Mutat Res. 2012 May 1;733(1-2):69-77. doi: 10.1016/j.mrfmmm.2011.09.002. Epub 2011 Sep 17.
Cadmium is an ubiquitous environmental contaminant that represents hazard to humans and wildlife. It is found in the air, soil and water and, due to its extremely long half-life, accumulates in plants and animals. The main source of cadmium exposure for non-smoking human population is food. Cadmium is primarily toxic to the kidney, but has been also classified as carcinogenic to humans by several regulatory agencies. Current evidence suggests that exposure to cadmium induces genomic instability through complex and multifactorial mechanisms. Cadmium dose not induce direct DNA damage, however it induces increase in reactive oxygen species (ROS) formation, which in turn induce DNA damage and can also interfere with cell signalling. More important seems to be cadmium interaction with DNA repair mechanisms, cell cycle checkpoints and apoptosis as well as with epigenetic mechanisms of gene expression control. Cadmium mediated inhibition of DNA repair mechanisms and apoptosis leads to accumulation of cells with unrepaired DNA damage, which in turn increases the mutation rate and thus genomic instability. This increases the probability of developing not only cancer but also other diseases associated with genomic instability. In the in vitro experiments cadmium induced effects leading to genomic instability have been observed at low concentrations that were comparable to those observed in target organs and tissues of humans that were non-occupationally exposed to cadmium. Therefore, further studies aiming to clarify the relevance of these observations for human health risks due to cadmium exposure are needed.

29Reactive oxygen species: Janus-faced molecules in the era of modern cancer therapy.PubMed

Aine O'Reilly, Wenchao Zhao, Stina Wickström, et al.
J Immunother Cancer. 2024 Dec 7;12(12):e009409. doi: 10.1136/jitc-2024-009409.
Oxidative stress, that is, an unbalanced increase in reactive oxygen species (ROS), contributes to tumor-induced immune suppression and limits the efficacy of immunotherapy. Cancer cells have inherently increased ROS production, intracellularly through metabolic perturbations and extracellularly through activation of NADPH oxidases, which promotes cancer progression. Further increased ROS production or impaired antioxidant systems, induced, for example, by chemotherapy or radiotherapy, can preferentially kill cancer cells over healthy cells. Inflammatory cell-derived ROS mediate immunosuppressive effects of myeloid-derived suppressor cells and activated granulocytes, hampering antitumor effector cells such as T cells and natural killer (NK) cells. Cancer therapies modulating ROS levels in tumors may thus have entirely different consequences when targeting cancer cells versus immune cells. Here we discuss the possibility of developing more efficient cancer therapies based on reduction-oxidation modulation, as either monotherapies or in combination with immunotherapy. Short-term, systemic administration of antioxidants or drugs blocking ROS production can boost the immune system and act in synergy with immunotherapy. However, prolonged use of antioxidants can instead enhance tumor progression. Alternatives to systemic antioxidant administration are under development where gene-modified or activated T cells and NK cells are shielded ex vivo against the harmful effects of ROS before the infusion to patients with cancer.

30Zinc and human health: an update.PubMed

Christos T Chasapis, Ariadni C Loutsidou, Chara A Spiliopoulou, et al.
Arch Toxicol. 2012 Apr;86(4):521-34. doi: 10.1007/s00204-011-0775-1. Epub 2011 Nov 10.
The importance of micronutrients in health and nutrition is undisputable, and among them, zinc is an essential element whose significance to health is increasingly appreciated and whose deficiency may play an important role in the appearance of diseases. Zinc is one of the most important trace elements in the organism, with three major biological roles, as catalyst, structural, and regulatory ion. Zinc-binding motifs are found in many proteins encoded by the human genome physiologically, and free zinc is mainly regulated at the single-cell level. Zinc has critical effect in homeostasis, in immune function, in oxidative stress, in apoptosis, and in aging, and significant disorders of great public health interest are associated with zinc deficiency. In many chronic diseases, including atherosclerosis, several malignancies, neurological disorders, autoimmune diseases, aging, age-related degenerative diseases, and Wilson's disease, the concurrent zinc deficiency may complicate the clinical features, affect adversely immunological status, increase oxidative stress, and lead to the generation of inflammatory cytokines. In these diseases, oxidative stress and chronic inflammation may play important causative roles. It is therefore important that status of zinc is assessed in any case and zinc deficiency is corrected, since the unique properties of zinc may have significant therapeutic benefits in these diseases. In the present paper, we review the zinc as a multipurpose trace element, its biological role in homeostasis, proliferation and apoptosis and its role in immunity and in chronic diseases, such as cancer, diabetes, depression, Wilson's disease, Alzheimer's disease, and other age-related diseases.

31Discovery of human zinc deficiency: its impact on human health and disease.PubMed

Ananda S Prasad
Adv Nutr. 2013 Mar 1;4(2):176-90. doi: 10.3945/an.112.003210.
The essentiality of zinc in humans was established in 1963. During the past 50 y, tremendous advances in both clinical and basic sciences of zinc metabolism in humans have been observed. The major factor contributing to zinc deficiency is high phytate-containing cereal protein intake in the developing world, and nearly 2 billion subjects may be zinc deficient. Conditioned deficiency of zinc has been observed in patients with malabsorption syndrome, liver disease, chronic renal disease, sickle cell disease, and other chronic illnesses. Major clinical problems resulting from zinc deficiency in humans include growth retardation; cell-mediated immune dysfunction, and cognitive impairment. In the Middle East, zinc-deficient dwarfs did not live beyond the age of 25 y, and they died because of intercurrent infections. In 1963, we knew of only 3 enzymes that required zinc for their activities, but now we know of >300 enzymes and >1000 transcription factors that are known to require zinc for their activities. Zinc is a second messenger of immune cells, and intracellular free zinc in these cells participate in signaling events. Zinc has been very successfully used as a therapeutic modality for the management of acute diarrhea in children, Wilson's disease, the common cold and for the prevention of blindness in patients with age-related dry type of macular degeneration and is very effective in decreasing the incidence of infection in the elderly. Zinc not only modulates cell-mediated immunity but is also an antioxidant and anti-inflammatory agent.

32Zinc in cancer prevention.PubMed

Ananda S Prasad, Frances W J Beck, Diane C Snell, et al.
Nutr Cancer. 2009;61(6):879-87. doi: 10.1080/01635580903285122.
Essentiality of zinc for humans was discovered 45 yr ago. Deficiency of zinc is prevalent world wide in developing countries and may affect nearly 2 billion subjects. The major manifestations of zinc deficiency include growth retardation, hypogonadism in males, cell-mediated immune dysfunctions, and cognitive impairment. Zinc not only improves cell mediated immune functions but also functions as an antioxidant and anti-inflammatory agent. Oxidative stress and chronic inflammation have been implicated in development of many cancers. In patients with head and neck cancer, we have shown that nearly 65% of these patients were zinc deficient based on their cellular zinc concentrations. Natural killer (NK) cell activity and IL-2 generation were also affected adversely. Th2 cytokines were not affected. In our patients, zinc status was a better indicator of tumor burden and stage of disease in comparison to the overall nutritional status. Zinc status also correlated with number of hospital admissions and incidences of infections. NF-kappa B is constitutively activated in many cancer cells, and this results in activation of antiapoptotic genes, VEGF, cyclin DI, EGFR, MMP-9 and inflammatory cytokines. Zinc inhibits NF-kappa B via induction of A-20. Thus, zinc supplementation should have beneficial effects on cancer by decreasing angiogenesis and induction of inflammatory cytokines while increasing apoptosis in cancer cells. Based on the above, we recommend further studies and propose that zinc should be utilized in the management and chemoprevention of cancer.

33Zinc Deficiency as a General Feature of Cancer: a Review of the Literature.PubMed

Rie Sugimoto, Lingaku Lee, Yuki Tanaka, et al.
Biol Trace Elem Res. 2024 May;202(5):1937-1947. doi: 10.1007/s12011-023-03818-6. Epub 2023 Sep 2.
Trace elements are minerals that are present in very low concentrations in the human body and yet are crucial for a wide range of physiological functions. Zinc, the second most abundant trace element, is obtained primarily from the diet. After being taken up in the intestine, zinc is distributed to various target organs, where it plays key roles in processes such as immunity, protein folding, apoptosis, and antioxidant activity. Given the important role of zinc in a wide range of enzymatic reactions and physiological processes, zinc deficiency has been identified in a variety of diseases, notably cancer. In recent years, multiple meta-analyses and reviews looking at zinc levels in individual cancer types have been published, as have a plethora of primary studies demonstrating a link between low zinc levels and specific types of cancer. In this review, we summarize recent evidence implicating low zinc concentrations in serum or tissues as a characteristic in a wide range of cancers. We also discuss preliminary findings indicating that zinc level measurement could ultimately become a useful clinical tool for cancer diagnosis and predicting outcomes in patients with cancer. Finally, we suggest future directions for further elucidating the role of zinc deficiency in cancer development and progression.

34[Zinc Suppresses Colorectal Cancer Development through Cell-mediated Immunity].PubMed

Keigo Nishida, Naoya Nakagawa
Yakugaku Zasshi. 2024;144(5):475-481. doi: 10.1248/yakushi.23-00154-1.
Zinc is one of the essential trace elements, and is involved in various functions in the body. Zinc deficiency is known to cause immune abnormalities, but the mechanism is not fully understood. Therefore, we focused our research on tumor immunity to elucidate the effect of zinc on colorectal cancer and its mechanisms. Mice were treated with azoxymethane (AOM) and dextran sodium sulfate (DSS) to develop colorectal cancer, then the relationship between zinc content in the diet and the number and area of tumors in the colon was observed. The number of tumors in the colon was significantly higher in the no-zinc-added diet group compared to the normal zinc intake group, and about half the number in the high-zinc-intake group compared to the normal-zinc-intake group. In T-cell-deficient mice, the number of tumors in the high-zinc-intake group was similar to that in the normal-zinc-intake group, suggesting that the inhibitory effect of zinc was dependent on T cells. Furthermore, we found that the amount of granzyme B transcript released by cytotoxic T cells upon antigen stimulation was significantly increased by the addition of zinc. We also showed that granzyme B transcriptional activation by zinc addition was dependent on calcineurin activity. Collectively, we have shown that zinc exerts its tumor-suppressive effect by acting on cytotoxic T cells, the center of cellular immunity, and that it increases the transcription of granzyme B, one of the key molecules involved in tumor immunity. In this symposium, we would like to introduce our latest data on the relationship between zinc and tumor immunity.

35Nutrition Regulates Innate Immunity in Health and Disease.PubMed

Samuel Philip Nobs, Niv Zmora, Eran Elinav
Annu Rev Nutr. 2020 Sep 23;40:189-219. doi: 10.1146/annurev-nutr-120919-094440. Epub 2020 Jun 10.
Nutrient content and nutrient timing are considered key regulators of human health and a variety of diseases and involve complex interactions with the mucosal immune system. In particular, the innate immune system is emerging as an important signaling hub that modulates the response to nutritional signals, in part via signaling through the gut microbiota. In this review we elucidate emerging evidence that interactions between innate immunity and diet affect human metabolic health and disease, including cardiometabolic disorders, allergic diseases, autoimmune disorders, infections, and cancers. Furthermore, we discuss the potential modulatory effects of the gut microbiota on interactions between the immune system and nutrition in health and disease, namely how it relays nutritional signals to the innate immune system under specific physiological contexts. Finally, we identify key open questions and challenges to comprehensively understanding the intersection between nutrition and innate immunity and how potential nutritional, immune, and microbial therapeutics may be developed into promising future avenues of precision treatment.

36Single-cell RNA sequencing highlights the role of inflammatory cancer-associated fibroblasts in bladder urothelial carcinoma.PubMed

Zhaohui Chen, Lijie Zhou, Lilong Liu, et al.
Nat Commun. 2020 Oct 8;11(1):5077. doi: 10.1038/s41467-020-18916-5.
Although substantial progress has been made in cancer biology and treatment, clinical outcomes of bladder carcinoma (BC) patients are still not satisfactory. The tumor microenvironment (TME) is a potential target. Here, by single-cell RNA sequencing on 8 BC tumor samples and 3 para tumor samples, we identify 19 different cell types in the BC microenvironment, indicating high intra-tumoral heterogeneity. We find that tumor cells down regulated MHC-II molecules, suggesting that the downregulated immunogenicity of cancer cells may contribute to the formation of an immunosuppressive microenvironment. We also find that monocytes undergo M2 polarization in the tumor region and differentiate. Furthermore, the LAMP3 + DC subgroup may be able to recruit regulatory T cells, potentially taking part in the formation of an immunosuppressive TME. Through correlation analysis using public datasets containing over 3000 BC samples, we identify a role for inflammatory cancer-associated fibroblasts (iCAFs) in tumor progression, which is significantly related to poor prognosis. Additionally, we characterize a regulatory network depending on iCAFs. These results could help elucidate the protumor mechanisms of iCAFs. Our results provide deep insight into cancer immunology and provide an essential resource for drug discovery in the future.

37Single-cell transcriptomic analysis in a mouse model deciphers cell transition states in the multistep development of esophageal cancer.PubMed

Jiacheng Yao, Qionghua Cui, Wenyi Fan, et al.
Nat Commun. 2020 Jul 24;11(1):3715. doi: 10.1038/s41467-020-17492-y.
Esophageal squamous cell carcinoma (ESCC) is prevalent in some geographical regions of the world. ESCC development presents a multistep pathogenic process from inflammation to invasive cancer; however, what is critical in these processes and how they evolve is largely unknown, obstructing early diagnosis and effective treatment. Here, we create a mouse model mimicking human ESCC development and construct a single-cell ESCC developmental atlas. We identify a set of key transitional signatures associated with oncogenic evolution of epithelial cells and depict the landmark dynamic tumorigenic trajectories. An early downregulation of CD8 response against the initial tissue damage accompanied by the transition of immune response from type 1 to type 3 results in accumulation and activation of macrophages and neutrophils, which may create a chronic inflammatory environment that promotes carcinogen-transformed epithelial cell survival and proliferation. These findings shed light on how ESCC is initiated and developed.

38Impact of consumption of repeatedly heated cooking oils on the incidence of various cancers- A critical review.PubMed

Kumar Ganesan, Kumeshini Sukalingam, Baojun Xu
Crit Rev Food Sci Nutr. 2019;59(3):488-505. doi: 10.1080/10408398.2017.1379470. Epub 2017 Oct 20.
Repeated heating of vegetable oils at high temperatures during cooking is a very common cooking practice. Repeatedly heated cooking oils (RCO) can generate varieties of compounds, including polycyclic aromatic hydrocarbons (PAH), some of which have been reported as carcinogenic. RCO is one of the commonly consumed cooking and frying medium. These RCO consumption and inhalation of cooking fumes can pose a serious health hazard. Taking into account exploratory study, the present review aims to provide the consumption of RCO and its fumes cause the high incidence of genotoxic, mutagenic, tumorogenic and various cancers. The information on RCO and its fumes were collected through a library database and electronic search (ScienceDirect, PubMed, and Google Scholar). Remarkable studies demonstrated that the health adverse effects of RCO and its cooking fumes have been often attributed to their detrimental properties and ease to genotoxic, mutagenic and carcinogenic activities. RCO and its cooking fumes were found to enhance the incidence of aberrant cells, including breaks, fragments, exchanges and multiple chromosomal damages and micronuclei in a dose-dependent manner. Furthermore, the large consumption of RCO has been associated with a number of malignancies, including lung, colorectal, breast, and prostate cancers. The present review provides additional insights into the polluting features of PAHs produced various cancers via cooking activities in indoor environments.

39Analysis of oral cancer carcinogens in repeatedly heated cooking oils.PubMed

Vidhant Krishna Nambiar, Vidya Mudliar, Inosi Salababa
Heliyon. 2025 Jan 14;11(2):e41858. doi: 10.1016/j.heliyon.2025.e41858. eCollection 2025 Jan 30.
BACKGROUND: The consumption of fried food has assimilated itself as a part of food culture globally. Therefore, it is important to know the toxigenicity of cooking oils used when exposed to high temperatures. The incidence of oral cancer in recent years has been on the rise; ninety percent of the cancers present in the oral cavity are squamous cell carcinoma with multiple major contributing lifestyle factors such well as the presence of the human papilloma virus. Not all mechanisms of carcinogenesis are fully understood and are complex. Furthermore, most cooking oil manufacturers do not provide recommended cooking temperatures on their product labels. Instead, they typically advise storing oils away from direct sunlight and at room temperature, leaving consumers unaware of the safe usage lim-its during cooking. OBJECTIVE: This study was conducted to analyze repeated cooking oils available in Suva, Fiji for harmful levels of genotoxic carcinogens. : Six types of cooking oils (soya bean oil, olive oil, mustard oil, coconut oil, canola oil and sunflower oil) were analyzed for the presence of genotoxic carcinogens. The test group (T0-3) of oils were heated to 190 °C and tested for the presence of carcinogens using Gas chromatography Mass Spectroscopy after 1.5 h at recommended temperature (T0), reheated to 190 °C and tested after 1 h (T1), reheated to 190 °C and tested after 3 h (T2) and reheated to 190 °C and tested after 6 h (T3). The control group of oils were not heated and stored at recommended temperature before testing. RESULTS: The concentrations of Benzo[a]pyrene and Glycidol detected in the cooking oils tested were not significant, as they remained below 2 μg/kg. However, two measurable peaks in 3-monochloropropanediol (3-MCPD) were detected in olive oil (115.6 ng/ml) and Soya bean oil (117.2 ng/ml). CONCLUSION: Elevated 3-MCPD levels were found in Soya bean and olive reheated cooking oils exceeding tolerable daily intake levels and indicating potential health risks. Future research should evaluate the carcinogenic potential of cooking oils in real-world settings, such as fast-food establishments. This could inform public health policies on safer oil usage practices and raise consumer awareness about the risks of consuming foods cooked with overheated or reused oils.

40The science of fatty acids and inflammation.PubMed

Kevin L Fritsche
Adv Nutr. 2015 May 15;6(3):293S-301S. doi: 10.3945/an.114.006940. Print 2015 May.
Inflammation is believed to play a central role in many of the chronic diseases that characterize modern society. In the past decade, our understanding of how dietary fats affect our immune system and subsequently our inflammatory status has grown considerably. There are compelling data showing that high-fat meals promote endotoxin [e.g., lipopolysaccharide (LPS)] translocation into the bloodstream, stimulating innate immune cells and leading to a transient postprandial inflammatory response. The nature of this effect is influenced by the amount and type of fat consumed. The role of various dietary constituents, including fats, on gut microflora and subsequent health outcomes in the host is another exciting and novel area of inquiry. The impact of specific fatty acids on inflammation may be central to how dietary fats affect health. Three key fatty acid-inflammation interactions are briefly described. First, the evidence suggests that saturated fatty acids induce inflammation in part by mimicking the actions of LPS. Second, the often-repeated claim that dietary linoleic acid promotes inflammation was not supported in a recent systematic review of the evidence. Third, an explanation is offered for why omega-3 (n-3) polyunsaturated fatty acids are so much less anti-inflammatory in humans than in mice. The article closes with a cautionary tale from the genomic literature that illustrates why extrapolating the results from inflammation studies in mice to humans is problematic.

41The Importance of Food for Endotoxemia and an Inflammatory Response.PubMed

Charlotte Erlanson-Albertsson, Karin G Stenkula
Int J Mol Sci. 2021 Sep 3;22(17):9562. doi: 10.3390/ijms22179562.
Bacterial endotoxin is a potent inflammatory antigen abundant in the human intestine. Endotoxins circulate in the blood at low concentrations in all healthy individuals. Elevated levels of circulatory endotoxins may cause inflammation with the development of chronic disease, either affecting metabolism, neurological disease, or resistance to viral and bacterial infections. The most important endotoxin is LPS, being a superantigen. In this narrative review, the effect of various food components to postprandially elevate circulating LPS and inflammatory markers is described. There is evidence that the intake of food enriched in fat, in particular saturated fat, may elevate LPS and pro-inflammatory markers. This occurs in both normal-weight and obese subjects. In obese subjects, inflammatory markers are already elevated before meal consumption. The importance of food choice for endotoxemia and inflammatory response is discussed.

42Multivariate modelling analysis for prediction of glycidyl esters and 3-monochloropropane-1,2-diol (3-MCPD) formation in periodically heated palm oil.PubMed

Siti Nur Syahirah Nor Mahiran, Nurul Huda Abd Kadir, Maulidiani Maulidiani, et al.
Heliyon. 2023 Sep 24;9(10):e20413. doi: 10.1016/j.heliyon.2023.e20413. eCollection 2023 Oct.
Palm oil is a vegetable oil that is widely used for cooking and deep-frying because of its affordability. However, repeatedly heated palm oil is also prone to oxidation due to its significant content of unsaturated fatty acids and other chemical toxicants such as glycidyl esters and 3-monochloropropane-1,2-diol (3-MCPD). Initially, the physicochemical properties such as colour, viscosity, peroxide, anisidine and total oxidation (TOTOX) of periodically heated palm oil were investigated. Chemical profiling and fingerprinting of six different brands of palm cooking oil during heating cycles between 90 and 360 min were conducted using Fourier transform infrared (FTIR) and H Nuclear Magnetic Resonance (NMR) metabolomics. In addition, the multivariate analysis was employed to evaluate the H NMR spectroscopic pattern of repeatedly heated palm oil with the corresponding physicochemical properties. The FTIR metabolomics showed significant different of the chemical fingerprinting subjected to heating duration, which in agreement with the result of H NMR metabolomics. Partial least squares (PLS) model revealed that most of the physicochemical properties of periodically heated palm oil are positively correlated (R values of 0.98-0.99) to their spectroscopic pattern. Based on the findings, the color of the oils darkened with increased heating time. The peroxide value (PV), -anisidine value (-AnV), and total oxidation (TOTOX) values increased significantly due to degradation of unsaturated compounds and oxidation products formed. We identified targeted metabolites (probable carcinogens) such as 3-monochloropropane-1,2-diol (3-MCPD) and glycidyl ester (GE), indicating the conversion of 3-MCPD to GE in repeatedly heated oils based on PCA and OPLSDA models. Our correlation analysis of NMR and physicochemical properties has shown that the conversion of 3-MCPD to GE was significantly increased from 180 to 360 min cooking time. The combination spectroscopic techniques with physicochemical properties are a reliable and robust methods to evaluate the characteristics, stability and chemical's structure changes of periodically heated palm oil, which may contribute to probable carcinogens development. This study has proven that combination of NMR and physicochemical analysis may predict the formation of the probable carcinogens of heated cooking oil over time which emphasizing the need to avoid certain heating cycles to mitigate formation of probable carcinogens during cooking process.

43Genotoxic and carcinogenic risks associated with the dietary consumption of repeatedly heated coconut oil.PubMed

Smita Srivastava, Madhulika Singh, Jasmine George, et al.
Br J Nutr. 2010 Nov;104(9):1343-52. doi: 10.1017/S0007114510002229. Epub 2010 Aug 6.
Repeated heating of vegetable oils at high temperatures during cooking is a very common cooking practice. Repeated heating of edible oils can generate a number of compounds, including polycyclic aromatic hydrocarbons (PAH), some of which have been reported to have carcinogenic potential. Consumption of these repeatedly heated oils can pose a serious health hazard. The objectives of the present study were to evaluate the genotoxic and carcinogenic risks associated with the consumption of repeatedly heated coconut oil (RCO), which is one of the commonly consumed cooking and frying medium. The PAH were analysed using HPLC in fresh CO, single-heated CO (SCO) and RCO. Results revealed the presence of certain PAH, known to possess carcinogenic potential, in RCO when compared with SCO. Oral intake of RCO in Wistar rats resulted in a significant induction of aberrant cells (P<0·05) and micronuclei (P<0·05) in a dose-dependent manner. Oxidative stress analysis showed a significant (P<0·05) decrease in the levels of antioxidant enzymes such as superoxide dismutase and catalase with a concurrent increase in reactive oxygen species and lipid peroxidation in the liver. In addition, RCO given alone and along with diethylnitrosamine for 12 weeks induced altered hepatic foci as noticed by alteration in positive (γ-glutamyl transpeptidase and glutathione-S-transferase) and negative (adenosine triphosphatase, alkaline phosphatase and glucose-6-phosphatase) hepatospecific biomarkers. A significant decrease in the relative and absolute hepatic weight of RCO-supplemented rats was recorded (P<0·05). In conclusion, dietary consumption of RCO can cause a genotoxic and preneoplastic change in the liver.

44F4/80Ly6C Macrophages Lead to Cell Plasticity and Cancer Initiation in Colitis.PubMed

Alice E Shin, Yodit Tesfagiorgis, Frederikke Larsen, et al.
Gastroenterology. 2023 Apr;164(4):593-609.e13. doi: 10.1053/j.gastro.2023.01.002. Epub 2023 Jan 10.
BACKGROUND & AIMS: Colorectal cancer is a leading cause of cancer death, and a major risk factor is chronic inflammation. Despite the link between colitis and cancer, the mechanism by which inflammation leads to colorectal cancer is not well understood. METHODS: To investigate whether different forms of inflammation pose the same risk of cancer, we compared several murine models of colitis (dextran sodium sulfate [DSS], 2,4,6-trinitrobenzene sulfonic acid, 4-ethoxylmethylene-2-phenyloxazol-5-one, Citrobacter rodentium, Fusobacterium nucleatum, and doxorubicin) with respect to their ability to lead to colonic tumorigenesis. We attempted to correlate the severity of colitis and inflammatory profile with the risk of tumorigenesis in both azoxymethane-dependent and Dclk1/APC murine models of colitis-associated cancer. RESULTS: DSS colitis reproducibly led to colonic tumors in both mouse models of colitis-associated cancer. In contrast, all other forms of colitis did not lead to cancer. When compared with the colitis not associated with tumorigenesis, DSS colitis was characterized by significantly increased CD11bF4/80Ly6C macrophages and CD11bLy6G neutrophils. Interestingly, depletion of the CD11bF4/80Ly6C macrophages inhibited tumorigenesis, whereas depletion of CD11bLy6G neutrophils had no effect on tumorigenesis. Furthermore, the macrophage-derived cytokines interleukin-1β, tumor necrosis factor-α, and interleukin-6 were significantly increased in DSS colitis and promoted stemness of Dclk1 tuft cells that serve as the cellular origin of cancer. CONCLUSIONS: We have identified CD11bF4/80Ly6C macrophages as key mediators of cancer initiation in colitis-associated cancer. Development of new therapies that target these cells may provide an effective preventative strategy for colitis-associated cancer.

45Interleukin-22 promotes tumor angiogenesis.PubMed

Nicholas J Protopsaltis, Wei Liang, Eric Nudleman, et al.
Angiogenesis. 2019 May;22(2):311-323. doi: 10.1007/s10456-018-9658-x. Epub 2018 Dec 11.
T17 cells play important yet complex roles in cancer development and progression. We previously reported that T17 cells and IL-17 mediate resistance to anti-VEGF therapy by inducing recruitment of immunosuppressive and proangiogenic myeloid cells to the tumor microenvironment. Here, we demonstrate that IL-22, a key effector cytokine expressed by T17 cells, directly acts on endothelial cells to promote tumor angiogenesis. IL-22 induces endothelial cell proliferation, survival, and chemotaxis in vitro and neovascularization in an ex vivo mouse choroid explant model. Blockade of IL-22, with a neutralizing antibody, significantly inhibits tumor growth associated with reduced microvascular density. No synergistic effect of IL-22 with VEGF was observed. These results identify IL-22 as a potential therapeutic target for blocking tumor angiogenesis.

46Gut microbiota, inflammatory bowel disease and colorectal cancer.PubMed

Ana Elisa Valencise Quaglio, Thais Gagno Grillo, Ellen Cristina Souza De Oliveira, et al.
World J Gastroenterol. 2022 Aug 14;28(30):4053-4060. doi: 10.3748/wjg.v28.i30.4053.
The gut microbiota is a complex community of microorganisms that inhabit the digestive tracts of humans, living in symbiosis with the host. Dysbiosis, characterized by an imbalance between the beneficial and opportunistic gut microbiota, is associated with several gastrointestinal disorders, such as irritable bowel syndrome (IBS); inflammatory bowel disease (IBD), represented by ulcerative colitis and Crohn's disease; and colorectal cancer (CRC). Dysbiosis can disrupt the mucosal barrier, resulting in perpetuation of inflammation and carcinogenesis. The increase in some specific groups of harmful bacteria, such as () and enterotoxigenic (ETBF), has been associated with chronic tissue inflammation and the release of pro-inflammatory and carcinogenic mediators, increasing the chance of developing CRC, following the inflammation-dysplasia-cancer sequence in IBD patients. Therefore, the aim of the present review was to analyze the correlation between changes in the gut microbiota and the development and maintenance of IBD, CRC, and IBD-associated CRC. Patients with IBD and CRC have shown reduced bacterial diversity and abundance compared to healthy individuals, with enrichment of and . Specific bacteria are also associated with the onset and progression of CRC, such as , , , , and ETBF. Future research can evaluate the advantages of modulating the gut microbiota as preventive measures in CRC high-risk patients, directly affecting the prognosis of the disease and the quality of life of patients.

47A role for whey-derived lactoferrin and immunoglobulins in the attenuation of obesity-related inflammation and disease.PubMed

Rachel E Brimelow, Nicholas P West, Lauren T Williams, et al.
Crit Rev Food Sci Nutr. 2017 May 24;57(8):1593-1602. doi: 10.1080/10408398.2014.995264.
Obesity is a strong predictive factor in the development of chronic disease and has now superseded undernutrition as a major public health issue. Chronic inflammation is one mechanism thought to link excess body weight with disease. Increasingly, the gut and its extensive population of commensal microflora are recognized as playing an important role in the development of obesity-related chronic inflammation. Obesity and a high fat diet are associated with altered commensal microbial communities and increased intestinal permeability which contributes to systemic inflammation as a result of the translocation of lipopolysaccharide into the circulation and metabolic endotoxemia. Various milk proteins are showing promise in the prevention and treatment of obesity and chronic low-grade inflammation via reductions in visceral fat, neutralization of bacteria at the mucosa and reduced intestinal permeability. In this review, we focus on evidence supporting the potential antiobesogenic and anti-inflammatory effects of bovine whey-derived lactoferrin and immunoglobulins.

48Microbiome-Mediated Effects of the Mediterranean Diet on Inflammation.PubMed

Melisa A Bailey, Hannah D Holscher
Adv Nutr. 2018 May 1;9(3):193-206. doi: 10.1093/advances/nmy013.
The Mediterranean diet pattern is increasingly associated with improved metabolic health. Two mechanisms by which consuming a Mediterranean diet pattern may contribute to improved metabolic health are modulation of the gastrointestinal (GI) microbiota and reduction of metabolic endotoxemia. Metabolic endotoxemia, defined as a 2- to 3-fold increase in circulating levels of bacterial endotoxin, has been proposed as a cause of inflammation during metabolic dysfunction. As the largest source of endotoxins in the human body, the GI microbiota represents a crucial area for research on strategies for reducing endotoxemia. Diets high in saturated fat and low in fiber contribute to metabolic endotoxemia through several mechanisms, including changes in the GI microbiome and bacterial fermentation end products, intestinal physiology and barrier function, and enterohepatic circulation of bile acids. Thus, the Mediterranean diet pattern, rich in unsaturated fats and fiber, may be one dietary strategy to reduce metabolic endotoxemia. Preclinical studies have demonstrated the differential effects of dietary saturated and unsaturated fats on the microbiota and metabolic health, but human studies are lacking. The role of dietary fiber and the GI microbiome in metabolic endotoxemia is underinvestigated. Clinical research on the effects of different types of dietary fat and fiber on the GI microbiota and GI and systemic inflammation is necessary to determine efficacious dietary strategies for reducing metabolic endotoxemia, inflammation, and subsequent metabolic disease.

49Ulcerative Colitis in Adults: A Review.PubMed

Beatriz Gros, Gilaad G Kaplan
JAMA. 2023 Sep 12;330(10):951-965. doi: 10.1001/jama.2023.15389.
IMPORTANCE: Ulcerative colitis (UC) is a chronic inflammatory condition of the colon, with a prevalence exceeding 400 per 100 000 in North America. Individuals with UC have a lower life expectancy and are at increased risk for colectomy and colorectal cancer. OBSERVATIONS: UC impairs quality of life secondary to inflammation of the colon causing chronic diarrhea and rectal bleeding. Extraintestinal manifestations, such as primary sclerosing cholangitis, occur in approximately 27% of patients with UC. People with UC require monitoring of symptoms and biomarkers of inflammation (eg, fecal calprotectin), and require colonoscopy at 8 years from diagnosis for surveillance of dysplasia. Risk stratification by disease location (eg, Montreal Classification) and disease activity (eg, Mayo Score) can guide management of UC. First-line therapy for induction and maintenance of remission of mild to moderate UC is 5-aminosalicylic acid. Moderate to severe UC may require oral corticosteroids for induction of remission as a bridge to medications that sustain remission (biologic monoclonal antibodies against tumor necrosis factor [eg, infliximab], α4β7 integrins [vedolizumab], and interleukin [IL] 12 and IL-23 [ustekinumab]) and oral small molecules that inhibit janus kinase (eg, tofacitinib) or modulate sphingosine-1-phosphate (ozanimod). Despite advances in medical therapies, the highest response to these treatments ranges from 30% to 60% in clinical trials. Within 5 years of diagnosis, approximately 20% of patients with UC are hospitalized and approximately 7% undergo colectomy. The risk of colorectal cancer after 20 years of disease duration is 4.5%, and people with UC have a 1.7-fold higher risk for colorectal cancer compared with the general population. Life expectancy in people with UC is approximately 80.5 years for females and 76.7 years for males, which is approximately 5 years shorter than people without UC. CONCLUSIONS AND RELEVANCE: UC affects approximately 400 of every 100 000 people in North America. An effective treatment for mild to moderate UC is 5-aminosalicylic acid, whereas moderate to severe UC can be treated with advanced therapies that target specific inflammation pathways, including monoclonal antibodies to tumor necrosis factor, α4β7 integrins, and IL-12 and IL-23 cytokines, as well as oral small molecule therapies targeting janus kinase or sphingosine-1-phosphate.

50Comprehensive single-cell analysis deciphered microenvironmental dynamics and immune regulator olfactomedin 4 in pathogenesis of gallbladder cancer.PubMed

Huisi He, Shuzhen Chen, Yong Yu, et al.
Gut. 2024 Aug 8;73(9):1529-1542. doi: 10.1136/gutjnl-2023-331773.
OBJECTIVE: Elucidating complex ecosystems and molecular features of gallbladder cancer (GBC) and benign gallbladder diseases is pivotal to proactive cancer prevention and optimal therapeutic intervention. DESIGN: We performed single-cell transcriptome analysis on 230 737 cells from 15 GBCs, 4 cholecystitis samples, 3 gallbladder polyps, 5 gallbladder adenomas and 16 adjacent normal tissues. Findings were validated through large-scale histological assays, digital spatial profiler multiplexed immunofluorescence (GeoMx), etc. Further molecular mechanism was demonstrated with and studies. RESULTS: The cell atlas unveiled an altered immune landscape across different pathological states of gallbladder diseases. GBC featured a more suppressive immune microenvironment with distinct T-cell proliferation patterns and macrophage attributions in different GBC subtypes. Notably, mutual exclusivity between stromal and immune cells was identified and remarkable stromal ecosystem (SC) heterogeneity during GBC progression was unveiled. Specifically, SC1 demonstrated active interaction between Fibro-iCAF and Endo-Tip cells, correlating with poor prognosis. Moreover, epithelium genetic variations within adenocarcinoma (AC) indicated an evolutionary similarity between adenoma and AC. Importantly, our study identified elevated olfactomedin 4 (OLFM4) in epithelial cells as a central player in GBC progression. OLFM4 was related to T-cell malfunction and tumour-associated macrophage infiltration, leading to a worse prognosis in GBC. Further investigations revealed that OLFM4 upregulated programmed death-ligand 1 (PD-L1) expression through the MAPK-AP1 axis, facilitating tumour cell immune evasion. CONCLUSION: These findings offer a valuable resource for understanding the pathogenesis of gallbladder diseases and indicate OLFM4 as a potential biomarker and therapeutic target for GBC.

51Global cancer statistics, 2012.PubMed

Lindsey A Torre, Freddie Bray, Rebecca L Siegel, et al.
CA Cancer J Clin. 2015 Mar;65(2):87-108. doi: 10.3322/caac.21262. Epub 2015 Feb 4.
Cancer constitutes an enormous burden on society in more and less economically developed countries alike. The occurrence of cancer is increasing because of the growth and aging of the population, as well as an increasing prevalence of established risk factors such as smoking, overweight, physical inactivity, and changing reproductive patterns associated with urbanization and economic development. Based on GLOBOCAN estimates, about 14.1 million new cancer cases and 8.2 million deaths occurred in 2012 worldwide. Over the years, the burden has shifted to less developed countries, which currently account for about 57% of cases and 65% of cancer deaths worldwide. Lung cancer is the leading cause of cancer death among males in both more and less developed countries, and has surpassed breast cancer as the leading cause of cancer death among females in more developed countries; breast cancer remains the leading cause of cancer death among females in less developed countries. Other leading causes of cancer death in more developed countries include colorectal cancer among males and females and prostate cancer among males. In less developed countries, liver and stomach cancer among males and cervical cancer among females are also leading causes of cancer death. Although incidence rates for all cancers combined are nearly twice as high in more developed than in less developed countries in both males and females, mortality rates are only 8% to 15% higher in more developed countries. This disparity reflects regional differences in the mix of cancers, which is affected by risk factors and detection practices, and/or the availability of treatment. Risk factors associated with the leading causes of cancer death include tobacco use (lung, colorectal, stomach, and liver cancer), overweight/obesity and physical inactivity (breast and colorectal cancer), and infection (liver, stomach, and cervical cancer). A substantial portion of cancer cases and deaths could be prevented by broadly applying effective prevention measures, such as tobacco control, vaccination, and the use of early detection tests.

52Gastric cancer actionable genomic alterations across diverse populations worldwide and pharmacogenomics strategies based on precision oncology.PubMed

Gabriela Echeverría-Garcés, María José Ramos-Medina, Rodrigo Vargas, et al.
Front Pharmacol. 2024 May 2;15:1373007. doi: 10.3389/fphar.2024.1373007. eCollection 2024.
Gastric cancer is one of the most prevalent types of cancer worldwide. The World Health Organization (WHO), the International Agency for Research on Cancer (IARC), and the Global Cancer Statistics (GLOBOCAN) reported an age standardized global incidence rate of 9.2 per 100,000 individuals for gastric cancer in 2022, with a mortality rate of 6.1. Despite considerable progress in precision oncology through the efforts of international consortia, understanding the genomic features and their influence on the effectiveness of anti-cancer treatments across diverse ethnic groups remains essential. Our study aimed to address this need by conducting integrated analyses to identify actionable genomic alterations in gastric cancer driver genes, assess their impact using deleteriousness scores, and determine allele frequencies across nine global populations: European Finnish, European non-Finnish, Latino, East Asian, South Asian, African, Middle Eastern, Ashkenazi Jewish, and Amish. Furthermore, our goal was to prioritize targeted therapeutic strategies based on pharmacogenomics clinical guidelines, drug prescriptions, and clinical trial data. Our comprehensive analysis examined 275,634 variants within 60 gastric cancer driver genes from 730,947 exome sequences and 76,215 whole-genome sequences from unrelated individuals, identifying 13,542 annotated and predicted oncogenic variants. We prioritized the most prevalent and deleterious oncogenic variants for subsequent pharmacogenomics testing. Additionally, we discovered actionable genomic alterations in the , and genes that could enhance the efficacy of anti-cancer therapies, as suggested by drug prescription analyses, reviews of current pharmacogenomics clinical guidelines, and evaluations of phase III and IV clinical trials targeting gastric cancer driver proteins. These findings underline the urgency of consolidating efforts to devise effective prevention measures, invest in genomic profiling for underrepresented populations, and ensure the inclusion of ethnic minorities in future clinical trials and cancer research in developed countries.

53Inequality in breast cancer: Global statistics from 2022 to 2050.PubMed

Ling Liao
Breast. 2025 Feb;79:103851. doi: 10.1016/j.breast.2024.103851. Epub 2024 Nov 22.
This study evaluates the global inequalities of breast cancer incidence and mortality from 2022 to 2050 with the latest GLOBOCAN estimates. It focuses on disparities across continents, age groups and Human Development Index (HDI) levels. In 2022, Africa shows the highest positive slope values of age-standardized rates (world) of mortality vs. incidence, both for those under 40 (0.346) and those 40 and older (0.335). These values contrast with those for Asia (0.085, 0.208), Europe (0.002, -0.014), Latin America and the Caribbean (0.17, 0.303), Northern America (-0.078, -0.188), and Oceania (0.166, -0.001). In both age groups, lower HDI levels are correlated with higher slope values and vice versa. Projections to 2050 indicate significant increases in the burden of breast cancer, with persistent yet varied disparities and differences. This highlights the need for differentiated strategies in breast cancer prevention, early-stage diagnosis, and treatment.

54Disparities in 36 cancers across 185 countries: secondary analysis of global cancer statistics.PubMed

Qianru Li, Changfa Xia, He Li, et al.
Front Med. 2024 Oct;18(5):911-920. doi: 10.1007/s11684-024-1058-6. Epub 2024 Aug 21.
Cancer is a major public health problem and represents substantial disparities worldwide. This study reported estimates for 36 cancers across 185 countries by incidence, mortality, 5-year prevalence, mortality-to-prevalence ratio (MPR), and mortality-to-incidence ratio (MIR) to examine its association with human development index (HDI) and gross national income (GNI). Data were collected from the GLOBOCAN 2020. MPR and MIR were calculated by sex, age group, country, and cancer type and then summarized into totals. Segi's population and global cancer spectrum were used to calculate age- and type-standardized ratios. Correlation analyses were conducted to assess associations. Results showed that breast cancer was the most diagnosed cancer globally. Low- and middle-income countries had high MPR and MIR. Cancers of esophagus, pancreas, and liver had the highest ratios. Males and the older population had the highest ratios. HDI and GNI were positively correlated with incidence and mortality but negatively correlated with MPR/MIR. Substantial disparities in cancer burden were observed among 36 cancer types across 185 countries. Socioeconomic development may contribute to narrowing these disparities, and tailored strategies are crucial for regional- and country-specific cancer control.

55Cervical cancer: the Indian perspective. FIGO 26th Annual Report on the Results of Treatment in Gynecological Cancer.PubMed

E Vallikad
Int J Gynaecol Obstet. 2006 Nov;95 Suppl 1:S215-33. doi: 10.1016/S0020-7292(06)60037-4.
Cancer of the uterine cervix is the commonest gynaecologic cancer in India, with most women presenting with disease extending beyond the cervix. The majority of women belong to the lower socioeconomic status, are rural, aged between 35 and 64 years and highly noncompliant for complete treatment and follow-up. Opportunistic screening with cytology, colposcopy and test for Human Papilloma Virus and appropriate treatment are available on payment at urban private medical centres but are not available at urban and rural government health centres that are accessed by women of the lower socioeconomic status. The Government's investment in health is 0.9% of the GDP. Thus cytology screening as a government health measure is not feasible. The 'social vaccine' of health empowerment along with visual inspection and appropriate referral by the rural and urban health personnel (Department of Health and Family Welfare); with an additional input of health awareness and motivation by Anganwadi Workers (Department of Women and Child Development), elected women representatives in the Panchayats (Department of Rural Development and Panchayati Raj) and non-governmental development agencies could be a collaborative effort towards "downstaging" cervical cancer. This could lay the foundation for the introduction of cytology screening when resources are available.

56Incidence of dysplasia and carcinoma of the uterine cervix in an Appalachian population.PubMed

G H Friedell, T C Tucker, E McManmon, et al.
J Natl Cancer Inst. 1992 Jul 1;84(13):1030-2. doi: 10.1093/jnci/84.13.1030.
BACKGROUND: Cervical cancer mortality rates in the Appalachian population of southeastern Kentucky have been shown to be unusually high. To better understand the high cervical cancer death rate in this area, we developed a population-based cervical disease registry. PURPOSE: This study describes the incidence of cervical dysplasia, carcinoma in situ, and invasive cervical cancer in 1986 and 1987 among White women in a 36-county area of Appalachian Kentucky based on histologic diagnoses. METHODS: We compared average annual age-adjusted incidence rates for carcinoma in situ and invasive cervical cancer in the study area with those for women in the Surveillance, Epidemiology, and End Results (SEER) Program. RESULTS: The incidence rate of invasive cervical cancer for women in the study area (14.9 per 100,000) was nearly twice that for White women in the SEER population (7.8 per 100,000), but it was similar to that for Black women in the SEER population (15.3 per 100,000). The incidence of carcinoma in situ for women in the study population (38.2 per 100,000) was 21% higher than that for White women (31.5 per 100,000) or for Black women (31.2 per 100,000) in the SEER population. The average annual age-adjusted incidence rate for all grades of dysplasia among women in the study population was 194.6 per 100,000. No comparable population-based incidence rates for dysplasia could be identified. CONCLUSIONS: Cervical cancer incidence rates are higher in Appalachian Kentucky than in the SEER population. Poverty appears to be a factor associated with these rates. IMPLICATIONS: Low-density populations such as those in rural Appalachia deserve greater attention in cancer control research. The population-based cervical dysplasia rates reported here may be useful for comparisons in future investigations.

57Disparities in Breast Cancer.PubMed

Victoria F Grabinski, Otis W Brawley
Obstet Gynecol Clin North Am. 2022 Mar;49(1):149-165. doi: 10.1016/j.ogc.2021.11.010.
In the western world, breast cancer is the most common lethal cancer in women and the second leading cause of cancer death behind lung cancer. When assessing registry data, incidence and mortalty vary significantly by race or ethnicity and by socioeconomic status. There are a number of established risk factors, that effect risk of not just risk of breast cancer overall but the risk of certain molecular subtypes of breast cancer. Other factors in the disparity in outcomes include certain populations experiencing lower quality of care; prevention, screening, diagnosis and treatment.

58The Persistent Poverty Initiative's Framework to Address Social and Economic Determinants of Cancer.PubMed

Robert A Hiatt, Amy E Kennedy, Alexandra K Adams, et al.
Cancer Epidemiol Biomarkers Prev. 2025 Aug 1;34(8):1235-1239. doi: 10.1158/1055-9965.EPI-24-1812.
Social determinants of health are known drivers of a broad range of cancer outcomes. These determinants influence factors at the structural and institutional levels of society, which disproportionately affects those living in persistent poverty. Americans living in persistent poverty areas experience higher cancer incidence, delayed cancer diagnosis and treatment, and greater cancer morbidity and mortality. This report describes the aims of the NCI's Persistent Poverty Initiative, a novel research program developed to study the association of structural and institutional factors that affect cancer outcomes in persistent poverty areas. The goals of the five funded centers located across the country are described. A detailed multilevel conceptual framework was developed to incorporate the perspectives of the five centers. The framework serves as a model for other researchers studying the complex social factors and pathways that contribute to cancer outcomes. Future research can build upon this work to integrate multilevel intervention models that can examine the association of upstream social determinants of health factors and cancer outcomes. The Persistent Poverty Initiative can serve as a model for addressing cancer outcomes at the structural and institutional levels, which will hopefully lead to improved local, state, and national strategies in an effort to achieve optimal health for all.

59Cancer statistics, 2019.PubMed

Rebecca L Siegel, Kimberly D Miller, Ahmedin Jemal
CA Cancer J Clin. 2019 Jan;69(1):7-34. doi: 10.3322/caac.21551. Epub 2019 Jan 8.
Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths that will occur in the United States and compiles the most recent data on cancer incidence, mortality, and survival. Incidence data, available through 2015, were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data, available through 2016, were collected by the National Center for Health Statistics. In 2019, 1,762,450 new cancer cases and 606,880 cancer deaths are projected to occur in the United States. Over the past decade of data, the cancer incidence rate (2006-2015) was stable in women and declined by approximately 2% per year in men, whereas the cancer death rate (2007-2016) declined annually by 1.4% and 1.8%, respectively. The overall cancer death rate dropped continuously from 1991 to 2016 by a total of 27%, translating into approximately 2,629,200 fewer cancer deaths than would have been expected if death rates had remained at their peak. Although the racial gap in cancer mortality is slowly narrowing, socioeconomic inequalities are widening, with the most notable gaps for the most preventable cancers. For example, compared with the most affluent counties, mortality rates in the poorest counties were 2-fold higher for cervical cancer and 40% higher for male lung and liver cancers during 2012-2016. Some states are home to both the wealthiest and the poorest counties, suggesting the opportunity for more equitable dissemination of effective cancer prevention, early detection, and treatment strategies. A broader application of existing cancer control knowledge with an emphasis on disadvantaged groups would undoubtedly accelerate progress against cancer.

60Making the Case for Investment in Rural Cancer Control: An Analysis of Rural Cancer Incidence, Mortality, and Funding Trends.PubMed

Kelly D Blake, Jennifer L Moss, Anna Gaysynsky, et al.
Cancer Epidemiol Biomarkers Prev. 2017 Jul;26(7):992-997. doi: 10.1158/1055-9965.EPI-17-0092. Epub 2017 Jun 9.
UNLABELLED: Estimates of those living in rural counties vary from 46.2 to 59 million, or 14% to 19% of the U.S. POPULATION: Rural communities face disadvantages compared with urban areas, including higher poverty, lower educational attainment, and lack of access to health services. We aimed to demonstrate rural-urban disparities in cancer and to examine NCI-funded cancer control grants focused on rural populations. Estimates of 5-year cancer incidence and mortality from 2009 to 2013 were generated for counties at each level of the rural-urban continuum and for metropolitan versus nonmetropolitan counties, for all cancers combined and several individual cancer types. We also examined the number and foci of rural cancer control grants funded by NCI from 2011 to 2016. Cancer incidence was 447 cases per 100,000 in metropolitan counties and 460 per 100,000 in nonmetropolitan counties ( < 0.001). Cancer mortality rates were 166 per 100,000 in metropolitan counties and 182 per 100,000 in nonmetropolitan counties ( < 0.001). Higher incidence and mortality in rural areas were observed for cervical, colorectal, kidney, lung, melanoma, and oropharyngeal cancers. There were 48 R- and 3 P-mechanism rural-focused grants funded from 2011 to 2016 (3% of 1,655). Further investment is needed to disentangle the effects of individual-level SES and area-level factors to understand observed effects of rurality on cancer. .

61Risk factors associated with gastric cancer in Mexico: education, breakfast and chili.PubMed

Alejandro Trujillo Rivera, Clara Luz Sampieri, Jaime Morales Romero, et al.
Rev Esp Enferm Dig. 2018 Jun;110(6):372-379. doi: 10.17235/reed.2018.5042/2017.
BACKGROUND AND AIM: the aim of the study was to use a validated questionnaire to identify factors associated with the development of gastric cancer (GC) in the Mexican population. METHODS: the study included cases and controls that were paired by sex and ± 10 years of age at diagnosis. In relation to cases, 46 patients with a confirmed histopathological diagnosis of adenocarcinoma-type GC, as reported in the hospital records, were selected, and 46 blood bank donors from the same hospital were included as controls. The previously validated Questionnaire to Find Factors Associated with Gastric Cancer (QUFA-GC©) was used to collect data. Odds ratio (OR) and 95% confidence interval (IC) were estimated via univariate analysis (paired OR). Multivariate analysis was performed by logistic regression. A decision tree was constructed using the J48 algorithm. RESULTS: an association was found by univariate analysis between GC risk and a lack of formal education, having smoked for ≥ 10 years, eating rapidly, consuming very hot food and drinks, a non-suitable breakfast within two hours of waking, pickled food and capsaicin. In contrast, a protective association against GC was found with taking recreational exercise and consuming fresh fruit and vegetables. No association was found between the development of GC and having an income that reflected poverty, using a refrigerator, perception of the omission of breakfast and time period of alcoholism. In the final multivariate analysis model, having no formal education (OR = 17.47, 95% CI = 5.17-76.69), consuming a non-suitable breakfast within two hours of waking (OR = 8.99, 95% CI = 2.85-35.50) and the consumption of capsaicin ˃ 29.9 mg capsaicin per day (OR = 3.77, 95% CI = 1.21-13.11) were factors associated with GC. CONCLUSIONS: an association was found by multivariate analysis between the presence of GC and education, type of breakfast and the consumption of capsaicin. These variables are susceptible to intervention and can be identified via the QUFA-GC

62Factors affecting occurrence of gastric varioliform lesions: A case-control study.PubMed

Tian-Hui Zou, Ru-Hua Zheng, Qin-Yan Gao, et al.
World J Gastroenterol. 2016 Jun 14;22(22):5228-36. doi: 10.3748/wjg.v22.i22.5228.
AIM: To investigate the factors influencing the occurrence of gastric varioliform lesions (GVLs) and their possible link with gastric cancer. METHODS: A 1:1 matched case-control study was performed to retrospectively analyze data from 1638 chronic gastritis patients who had undergone gastroscopy at one of two Chinese hospitals between 2009 and 2014. Patients with GVLs (cases) were compared to those without such lesions (controls). Endoscopic and pathological findings were recorded, along with interview information on Helicobacter pylori (H. pylori) infection, medical, drug and family histories, lifestyle and eating habits. The association between each factor and the occurrence of GVLs was estimated, and then multivariate conditional logistic regression was used to evaluate the independent factors. RESULTS: The frequency and severity of glandular atrophy, intestinal metaplasia (IM) and low-grade intraepithelial neoplasia were significantly increased in the GVL group (P < 0.01). Overall analysis showed that H. pylori infection [3.051 (2.157, 4.317), P <0.001], allergic respiratory diseases [3.636 (2.183, 6.055), P < 0.001], work-related stress [2.019 (1.568, 2.600), P < 0.001], irregular meals [2.300 (1.462, 3.619), P < 0.001], high intake of spicy food [1.754 (1.227, 2.507), P = 0.002] and high intake of fresh fruit [0.231 (0.101, 0.529), P = 0.001] were significantly correlated with the occurrence of GVLs (positively, except for the latter). Stratified analyses indicated that pickled food consumption in patients over 50 years old [7.224 (2.360, 22.115), P = 0.001] and excessive smoking in men [2.013 (1.282, 3.163), P = 0.002] were also positively correlated, and that, for antral GVLs, vegetable consumption [0.491 (0.311, 0.776), P = 0.002] was negatively correlated. CONCLUSION: Seven risk factors and two protective factors are determined for GVLs, which were found to be associated with premalignant abnormalities.

63[Relationship between genetic polymorphism of ERCC1 and susceptibility to liver cancer].PubMed

Zhi-Jian Hu, Jin-Fa Xue, Xiao-Yang Zhang, et al.
Zhonghua Liu Xing Bing Xue Za Zhi. 2010 Nov;31(11):1288-91.
OBJECTIVE: To investigate the association between genetic polymorphisms of ERCC1-C8092A and susceptibility to liver cancer, as well as the gene-environmental interaction on the etiology of liver cancer in Fuzhou. METHODS: A case-control study was conducted to collect the information on environmental exposure while genetic polymorphism of ERCC1 was analyzed by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. General relative risk regression models were further applied to fit the interaction between genetic polymorphisms of ERCC1-C8092A and the environmental factors of liver cancer. RESULTS: ERCC1-C8092A variant genotypes were associated with significant increasing risk of liver cancer adjusted odds ratio (OR = 3.789, 95%CI: 2.792 - 5.142), compared to the wild-type homozygote. Data from the analysis of interaction showed that genetic polymorphism of ERCC1-8092A appeared super-additive interaction with drinking pond-ditch or with hepatitis B, and super-multiplicative interaction with eating moldy food. CONCLUSION: The point mutation in ERCC1-8092A was possibly susceptible to liver cancer, and related synergistically with other risk factors in hepatocelluar carcinogenesis in Fuzhou.

64Dietary nitrate and nitrite intake and risk of colorectal cancer in the Shanghai Women's Health Study.PubMed

Curt T Dellavalle, Qian Xiao, Gong Yang, et al.
Int J Cancer. 2014 Jun 15;134(12):2917-26. doi: 10.1002/ijc.28612. Epub 2013 Nov 29.
Nitrate and nitrite are precursors of endogenously formed N-nitroso compounds (NOC), known animal carcinogens. Nitrosation reactions forming NOCs can be inhibited by vitamin C and other antioxidants. We prospectively investigated the association between dietary nitrate and nitrite intake and risk of colorectal cancer in the Shanghai Women's Health Study, a cohort of 73,118 women ages 40-70 residing in Shanghai. We evaluated effect modification by factors that affect endogenous formation of NOCs: vitamin C (at or above/below median) and red meat intake (at or above/below median). Nitrate, nitrite and other dietary intakes were estimated from a 77-item food frequency questionnaire administered at baseline. Over a mean of 11 years of follow-up, we identified 619 colorectal cancer cases (n = 383, colon; n = 236, rectum). Hazard ratios (HR) and 95% confidence intervals (CI) were estimated using Cox proportional hazard regression. Overall, nitrate intake was not associated with colorectal cancer risk (HR = 1.08; 95% CI: 0.73-1.59). However, among women with vitamin C intake below the median (83.9 mg day(-1) ) and hence higher potential exposure to NOCs, risk of colorectal cancer increased with increasing quintiles of nitrate intake (highest vs. lowest quintile HR = 2.45; 95% CI: 1.15-5.18; p trend = 0.02). There was no association among women with higher vitamin C intake. We found no association between nitrite intake and risk of colorectal cancer overall or by intake level of vitamin C. Our findings suggest that high dietary nitrate intake among subgroups expected to have higher exposure to endogenously formed NOCs increases risk of colorectal cancer.

65Source-specific nitrate and nitrite intake and association with colorectal cancer in the Danish Diet, Cancer and Health Cohort.PubMed

Dorit W Erichsen, Nicola P Bondonno, Pratik Pokharel, et al.
Environ Int. 2025 Aug;202:109658. doi: 10.1016/j.envint.2025.109658. Epub 2025 Jul 3.
INTRODUCTION: Nitrate and nitrite, present in food and drinking water, may contribute to colorectal cancer (CRC) through the formation of carcinogenic N-nitroso compounds (NOCs). This study examined source-specific associations with CRC and subtypes, considering potential dietary and lifestyle factors that influence NOC formation. METHODS: In the Danish Diet, Cancer, and Health Cohort (N=54,610), nitrate/nitrite intake was estimated from comprehensive databases and national monitoring data. Over 27 years, 2245 CRC cases (1508 colon and 737 rectal) were identified via the Danish Cancer Registry. Cox proportional hazards models adjusted for sociodemographic, diet, and lifestyle factors were used to examine associations, with stratified analyses by sex and factors influencing NOC formation. RESULTS: No associations were found between nitrate/nitrite intakes from plant, naturally-occurring animal sources, or additive-permitted meat sources and CRC. However, higher nitrate intake from tap water (mg/d) was associated with a higher rate of distal colon cancer [HR (95% CI); 1.48 (1.11, 1.97)], though not CRC overall. A nitrate concentration in tap water ≥9.25 mg/L was linked to a higher colon cancer rate [HR 1.52 (1.11, 2.07)] compared to <1.27 mg/L. This association appeared stronger in individuals with risk-promoting factors (smoking and high red meat intake) and weaker among those with a high intake of NOC inhibiting factors (vitamin C, vitamin E, folate, and flavonoids). CONCLUSION: Nitrate/nitrite intakes from food sources were not associated with rate of CRC in the cohort, but tap water nitrate, at higher intake levels and at concentrations over ≥9.25 mg/L were linked to higher rates of distal colon and colon cancer, respectively.

66Adherence to a Mediterranean diet and survival in a Greek population.PubMed

Antonia Trichopoulou, Tina Costacou, Christina Bamia, et al.
N Engl J Med. 2003 Jun 26;348(26):2599-608. doi: 10.1056/NEJMoa025039.
BACKGROUND: Adherence to a Mediterranean diet may improve longevity, but relevant data are limited. METHODS: We conducted a population-based, prospective investigation involving 22,043 adults in Greece who completed an extensive, validated, food-frequency questionnaire at base line. Adherence to the traditional Mediterranean diet was assessed by a 10-point Mediterranean-diet scale that incorporated the salient characteristics of this diet (range of scores, 0 to 9, with higher scores indicating greater adherence). We used proportional-hazards regression to assess the relation between adherence to the Mediterranean diet and total mortality, as well as mortality due to coronary heart disease and mortality due to cancer, with adjustment for age, sex, body-mass index, physical-activity level, and other potential confounders. RESULTS: During a median of 44 months of follow-up, there were 275 deaths. A higher degree of adherence to the Mediterranean diet was associated with a reduction in total mortality (adjusted hazard ratio for death associated with a two-point increment in the Mediterranean-diet score, 0.75 [95 percent confidence interval, 0.64 to 0.87]). An inverse association with greater adherence to this diet was evident for both death due to coronary heart disease (adjusted hazard ratio, 0.67 [95 percent confidence interval, 0.47 to 0.94]) and death due to cancer (adjusted hazard ratio, 0.76 [95 percent confidence interval, 0.59 to 0.98]). Associations between individual food groups contributing to the Mediterranean-diet score and total mortality were generally not significant. CONCLUSIONS: Greater adherence to the traditional Mediterranean diet is associated with a significant reduction in total mortality.

67Adherence to the MIND Diet and Risk of Breast Cancer: A Case-control Study.PubMed

Vajiheh Aghamohammadi, Asma Salari-Moghaddam, Sanaz Benisi-Kohansal, et al.
Clin Breast Cancer. 2021 Jun;21(3):e158-e164. doi: 10.1016/j.clbc.2020.09.009. Epub 2020 Sep 24.
INTRODUCTION: No data are available on the association between adherence to the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet and breast cancer. MATERIALS AND METHODS: This population-based case-control study was conducted among women aged ≥ 30 years, who were residing in Isfahan, Iran. The study included 350 patients with newly diagnosed stage I to IV breast cancer, for whom in situ or invasive status of breast cancer was confirmed by physical examination, mammography, and pathologic verification. Controls were 700 age-matched apparently healthy individuals who were randomly selected from the general population. Dietary data were collected using a validated 106-item Willett-format, semi-quantitative dish-based food frequency questionnaire. RESULTS: After adjustment for age and energy intake, women in the top tertile of the MIND diet score had 60% lower odds of breast cancer than women in the bottom tertile (odds ratio [OR], 0.40; 95% confidence interval [CI], 0.29-0.55). In the fully adjusted model including body mass index, those with the greatest MIND diet scores had 50% lower chance of breast cancer (OR, 0.50; 95% CI, 0.34-0.72) than those with the lowest adherence to the MIND diet. Postmenopausal women with the greatest adherence to the MIND diet were less likely to have breast cancer than those in the bottom tertile (OR, 0.45; 95% CI, 0.30-0.66). In addition, we found a significant inverse association between adherence to the MIND diet and odds of breast cancer among normal-weight women (OR, 0.39; 95% CI, 0.25-0.60). CONCLUSION: Adherence to the MIND diet was associated with a reduced chance of breast cancer in this case-control study.

68The association between plant-based dietary patterns and risk of breast cancer: a case-control study.PubMed

Somaye Rigi, Seyed Mohammad Mousavi, Sanaz Benisi-Kohansal, et al.
Sci Rep. 2021 Feb 9;11(1):3391. doi: 10.1038/s41598-021-82659-6.
Limited data are available, linking the plant-based diets to breast cancer (BC). We examined the association of overall plant-based diet index (PDI), hypothesized healthful (hPDI) and unhealthful versions of a plant-based diet index (uPDI) with BC in Iranian women. This population-based case-control study included 350 cases with newly diagnosed BC and 700 age-matched apparently healthy controls. We collected dietary data using a validated, Willett-format semi-quantitative food frequency questionnaire. Using these data, we generated a PDI by dedicating positive scores to plant foods, and reverse scores to animal foods, hPDI by assigning positive scores to healthy plant foods and reverse scores to less healthy plant foods and animal foods, and finally uPDI in which positive scores were assigned to less healthy plant foods and reverse scores to healthy plant foods and animal foods. After controlling for potential confounders, individuals in the highest quartile of PDI had 67% lower odds of BC than those in the lowest quartile (OR 0.33; 95% CI 0.22-0.50). Individuals with the greatest adherence to hPDI were 36% less likely to have BC than those with the lowest adherence, in the fully adjusted model (OR 0.64; 95% CI 0.43-0.94). In terms of uPDI, women in the top quartile had a 2.23 times greater chance of BC than those in the bottom quartile (OR 2.23; 95% CI 1.48-3.36). Greater adherence to PDI and hPDI was inversely associated with the risk of BC, whereas uPDI was associated with an increased risk.

69Rising incidence of early-onset colorectal cancer - a call to action.PubMed

Naohiko Akimoto, Tomotaka Ugai, Rong Zhong, et al.
Nat Rev Clin Oncol. 2021 Apr;18(4):230-243. doi: 10.1038/s41571-020-00445-1. Epub 2020 Nov 20.
The incidence of early-onset colorectal cancer (CRC), which occurs in individuals <50 years of age, has been increasing worldwide and particularly in high-income countries. The reasons for this increase remain unknown but plausible hypotheses include greater exposure to potential risk factors, such as a Western-style diet, obesity, physical inactivity and antibiotic use, especially during the early prenatal to adolescent periods of life. These exposures can not only cause genetic and epigenetic alterations in colorectal epithelial cells but also affect the gut microbiota and host immunity. Early-onset CRCs have differential clinical, pathological and molecular features compared with later-onset CRCs. Certain existing resources can be utilized to elucidate the aetiology of early-onset CRC and inform the development of effective prevention, early detection and therapeutic strategies; however, additional life-course cohort studies spanning childhood and young adulthood, integrated with prospective biospecimen collections, omics biomarker analyses and a molecular pathological epidemiology approach, are needed to better understand and manage this disease entity. In this Perspective, we summarize our current understanding of early-onset CRC and discuss how we should strategize future research to improve its prevention and clinical management.

70Early-onset colorectal cancer: initial clues and current views.PubMed

Lorne J Hofseth, James R Hebert, Anindya Chanda, et al.
Nat Rev Gastroenterol Hepatol. 2020 Jun;17(6):352-364. doi: 10.1038/s41575-019-0253-4. Epub 2020 Feb 21.
Over the past several decades, the incidence of early-onset colorectal cancer (EOCRC; in patients <50 years old) has increased at an alarming rate. Although robust and scientifically rigorous epidemiological studies have sifted out environmental elements linked to EOCRC, our knowledge of the causes and mechanisms of this disease is far from complete. Here, we highlight potential risk factors and putative mechanisms that drive EOCRC and suggest likely areas for fruitful research. In addition, we identify inconsistencies in the evidence implicating a strong effect of increased adiposity and suggest that certain behaviours (such as diet and stress) might place nonobese and otherwise healthy people at risk of this disease. Key risk factors are reviewed, including the global westernization of diets (usually involving a high intake of red and processed meats, high-fructose corn syrup and unhealthy cooking methods), stress, antibiotics, synthetic food dyes, monosodium glutamate, titanium dioxide, and physical inactivity and/or sedentary behaviour. The gut microbiota is probably at the crossroads of these risk factors and EOCRC. The time course of the disease and the fact that relevant exposures probably occur in childhood raise important methodological issues that are also discussed.

71Are dietary factors involved in the association of methylation and breast cancer risk?PubMed

Nannan Zhang, Liangliang Li, Zhiping Long, et al.
Br J Nutr. 2022 Jun 28;127(12):1868-1877. doi: 10.1017/S0007114521002804. Epub 2021 Jul 26.
DNA methylation is one of the most important epigenetic modifications in breast cancer (BC) development, and long-term dietary habits can alter DNA methylation. Cadherin-4 (, a member of the cadherin family) encodes Ca-dependent cell-cell adhesion glycoproteins. We conducted a case-control study (380 newly diagnosed BC and 439 cancer-free controls) to explore the relationship of methylation in peripheral blood leukocyte DNA (PBL DNA), as well as its combined and interactive effects with dietary factors on BC risk. A case-only study (335 newly diagnosed BC) was conducted to analyse the association between methylation in breast tissue DNA and dietary factors. methylation was detected using quantitative methylation-specific PCR. Unconditional logistic regressions were used to analyse the association of methylation in PBL DNA and BC risk. Cross-over analysis and unconditional logistic regression were used to calculate the combined and interactive effects between methylation in PBL DNA and dietary factors in BC. hypermethylation was significantly associated with increased BC risk in PBL DNA (OR (OR) = 2·70, (95 % CI 1·90, 3·83), < 0·001). hypermethylation also showed significant combined effects with the consumption of vegetables (OR = 4·33, (95 % CI 2·63, 7·10)), allium vegetables (OR = 7·00, (95 % CI 4·17, 11·77)), fish (OR = 7·92, (95 % CI 3·79, 16·53)), milk (OR = 6·30, (95 % CI 3·41, 11·66)), overnight food (OR = 4·63, (95 % CI 2·69, 7·99)), pork (OR = 5·59, (95 % CI 2·94, 10·62)) and physical activity (OR = 4·72, (95 % CI 2·87, 7·76)). Moreover, consuming milk was significantly related with decreased risk of methylation (OR = 0·61, (95 % CI 0·38, 0·99)) in breast tissue. Our findings may provide direct guidance on the dietary intake for specific methylated carriers to decrease their risk for developing BC.

72Comparative Effectiveness and Cost-Effectiveness of Colorectal Cancer Screening With Blood-Based Biomarkers (Liquid Biopsy) vs Fecal Tests or Colonoscopy.PubMed

Uri Ladabaum, Ajitha Mannalithara, Yingjie Weng, et al.
Gastroenterology. 2024 Jul;167(2):378-391. doi: 10.1053/j.gastro.2024.03.011. Epub 2024 Mar 26.
BACKGROUND & AIMS: Colorectal cancer (CRC) screening is highly effective but underused. Blood-based biomarkers (liquid biopsy) could improve screening participation. METHODS: Using our established Markov model, screening every 3 years with a blood-based test that meets minimum Centers for Medicare & Medicaid Services' thresholds (CMS) (CRC sensitivity 74%, specificity 90%) was compared with established alternatives. Test attributes were varied in sensitivity analyses. RESULTS: CMS reduced CRC incidence by 40% and CRC mortality by 52% vs no screening. These reductions were less profound than the 68%-79% and 73%-81%, respectively, achieved with multi-target stool DNA (Cologuard; Exact Sciences) every 3 years, annual fecal immunochemical testing (FIT), or colonoscopy every 10 years. Assuming the same cost as multi-target stool DNA, CMS cost $28,500/quality-adjusted life-year gained vs no screening, but FIT, colonoscopy, and multi-target stool DNA were less costly and more effective. CMS would match FIT's clinical outcomes if it achieved 1.4- to 1.8-fold FIT's participation rate. Advanced precancerous lesion (APL) sensitivity was a key determinant of a test's effectiveness. A paradigm-changing blood-based test (sensitivity >90% for CRC and 80% for APL; 90% specificity; cost ≤$120-$140) would be cost-effective vs FIT at comparable participation. CONCLUSIONS: CMS could contribute to CRC control by achieving screening in those who will not use established methods. Substituting blood-based testing for established effective CRC screening methods will require higher CRC and APL sensitivities that deliver programmatic benefits matching those of FIT. High APL sensitivity, which can result in CRC prevention, should be a top priority for screening test developers. APL detection should not be penalized by a definition of test specificity that focuses on CRC only.

73Systematic Review on the Cost Effectiveness of Prostate Cancer Screening in Europe.PubMed

Pieter Vynckier, Lieven Annemans, Sarah Raes, et al.
Eur Urol. 2024 Nov;86(5):400-408. doi: 10.1016/j.eururo.2024.04.036. Epub 2024 May 23.
BACKGROUND AND OBJECTIVE: In Europe, prostate cancer (PCa) is the most common cancer in men. Screening may therefore be crucial to lower health care costs, morbidity, and mortality. This systematic review aimed to provide a contemporary overview of the costs and benefits of PCa screening programmes. METHODS: A peer-reviewed literature search was conducted, using the PICO method. A detailed search strategy was developed in four databases based on the following key search terms: "PCa", "screening", and "cost effectiveness". Any type of economic evaluation was included. The search strategy was restricted to European countries, but no restrictions were set on the year of publication. KEY FINDINGS AND LIMITATIONS: A total of 7484 studies were identified initially. Of these, 19 studies described the cost effectiveness of PCa screening in Europe. Among the studies using an initially healthy study population, most focussed on risk- and/or age- and/or magnetic resonance imaging (MRI)-based screening in addition to prostate-specific antigen (PSA) testing and compared this with no screening. Incremental cost ratios (ICERs) varied from €5872 per quality-adjusted life year (QALY) to €372 948/QALY, with a median of €56 487/QALY. Risk-based screening followed by MRI testing seemed to be a more cost-effective strategy than no screening. CONCLUSIONS AND CLINICAL IMPLICATIONS: This systematic review indicates that screening programmes incorporating a risk-based approach and MRI have the potential to be cost effective. PATIENT SUMMARY: In this review, we looked at the cost effectiveness of prostate cancer screening in Europe. We found that a risk-based approach and incorporation of magnetic resonance imaging has the potential to be cost effective. However, there remains a knowledge gap regarding cost effectiveness of prostate cancer screening. Therefore, determinants of cost effectiveness require further investigation.

74Risk Model-Based Lung Cancer Screening : A Cost-Effectiveness Analysis.PubMed

Iakovos Toumazis, Pianpian Cao, Koen de Nijs, et al.
Ann Intern Med. 2023 Mar;176(3):320-332. doi: 10.7326/M22-2216. Epub 2023 Feb 7.
BACKGROUND: In their 2021 lung cancer screening recommendation update, the U.S. Preventive Services Task Force (USPSTF) evaluated strategies that select people based on their personal lung cancer risk (risk model-based strategies), highlighting the need for further research on the benefits and harms of risk model-based screening. OBJECTIVE: To evaluate and compare the cost-effectiveness of risk model-based lung cancer screening strategies versus the USPSTF recommendation and to explore optimal risk thresholds. DESIGN: Comparative modeling analysis. DATA SOURCES: National Lung Screening Trial; Surveillance, Epidemiology, and End Results program; U.S. Smoking History Generator. TARGET POPULATION: 1960 U.S. birth cohort. TIME HORIZON: 45 years. PERSPECTIVE: U.S. health care sector. INTERVENTION: Annual low-dose computed tomography in risk model-based strategies that start screening at age 50 or 55 years, stop screening at age 80 years, with 6-year risk thresholds between 0.5% and 2.2% using the PLCOm2012 model. OUTCOME MEASURES: Incremental cost-effectiveness ratio (ICER) and cost-effectiveness efficiency frontier connecting strategies with the highest health benefit at a given cost. RESULTS OF BASE-CASE ANALYSIS: Risk model-based screening strategies were more cost-effective than the USPSTF recommendation and exclusively comprised the cost-effectiveness efficiency frontier. Among the strategies on the efficiency frontier, those with a 6-year risk threshold of 1.2% or greater were cost-effective with an ICER less than $100 000 per quality-adjusted life-year (QALY). Specifically, the strategy with a 1.2% risk threshold had an ICER of $94 659 (model range, $72 639 to $156 774), yielding more QALYs for less cost than the USPSTF recommendation, while having a similar level of screening coverage (person ever-screened 21.7% vs. USPSTF's 22.6%). RESULTS OF SENSITIVITY ANALYSES: Risk model-based strategies were robustly more cost-effective than the 2021 USPSTF recommendation under varying modeling assumptions. LIMITATION: Risk models were restricted to age, sex, and smoking-related risk predictors. CONCLUSION: Risk model-based screening is more cost-effective than the USPSTF recommendation, thus warranting further consideration. PRIMARY FUNDING SOURCE: National Cancer Institute (NCI).

75Cost-effectiveness of serum, urine, and tissue-based prostate cancer biomarkers.PubMed

Veerain K Gupta, Brian D Cortese, Ruchika Talwar
Curr Opin Urol. 2025 Jul 1;35(4):412-417. doi: 10.1097/MOU.0000000000001293. Epub 2025 Apr 25.
PURPOSE OF REVIEW: Prostate cancer remains a leading malignancy among men in the United States. While prostate-specific antigen (PSA) screening improves early detection, it also leads to over-diagnosis and over-treatment. Biomarkers offer a promising solution for risk stratification and guiding treatment decisions. This review examines the cost-effectiveness of serum, urine, and tissue-based biomarkers to assess their impact on healthcare expenditures and clinical decision-making. RECENT FINDINGS: Serum-based biomarkers like 4Kscore and PHI reduce unnecessary biopsies and healthcare costs. Urine-based biomarkers, including SelectMDx and ExoDx Prostate IntelliScore (EPI), have shown potential to optimize prostate cancer detection while being more cost-effective than some serum-based alternatives. Tissue-based biomarkers, such as OncotypeDx and Decipher, help in treatment selection, though their economic impact varies. Economic analyses suggest that biomarkers can enhance clinical decision-making while reducing healthcare expenditures, but real-world validation remains limited. SUMMARY: Prostate cancer biomarkers improve risk stratification and may lower healthcare costs. However, variations in cost-effectiveness, reimbursement policies, and guideline recommendations limit widespread adoption. Prospective studies are needed to validate real-world cost savings and refine biomarker integration into clinical practice. Addressing financial and policy challenges is essential to ensure equitable access and maximize their impact on prostate cancer management.

76The UK Lung Cancer Screening Trial: a pilot randomised controlled trial of low-dose computed tomography screening for the early detection of lung cancer.PubMed

John K Field, Stephen W Duffy, David R Baldwin, et al.
Health Technol Assess. 2016 May;20(40):1-146. doi: 10.3310/hta20400.
BACKGROUND: Lung cancer kills more people than any other cancer in the UK (5-year survival < 13%). Early diagnosis can save lives. The USA-based National Lung Cancer Screening Trial reported a 20% relative reduction in lung cancer mortality and 6.7% all-cause mortality in low-dose computed tomography (LDCT)-screened subjects. OBJECTIVES: To (1) analyse LDCT lung cancer screening in a high-risk UK population, determine optimum recruitment, screening, reading and care pathway strategies; and (2) assess the psychological consequences and the health-economic implications of screening. DESIGN: A pilot randomised controlled trial comparing intervention with usual care. A population-based risk questionnaire identified individuals who were at high risk of developing lung cancer (≥ 5% over 5 years). SETTING: Thoracic centres with expertise in lung cancer imaging, respiratory medicine, pathology and surgery: Liverpool Heart & Chest Hospital, Merseyside, and Papworth Hospital, Cambridgeshire. PARTICIPANTS: Individuals aged 50-75 years, at high risk of lung cancer, in the primary care trusts adjacent to the centres. INTERVENTIONS: A thoracic LDCT scan. Follow-up computed tomography (CT) scans as per protocol. Referral to multidisciplinary team clinics was determined by nodule size criteria. MAIN OUTCOME MEASURES: Population-based recruitment based on risk stratification; management of the trial through web-based database; optimal characteristics of CT scan readers (radiologists vs. radiographers); characterisation of CT-detected nodules utilising volumetric analysis; prevalence of lung cancer at baseline; sociodemographic factors affecting participation; psychosocial measures (cancer distress, anxiety, depression, decision satisfaction); and cost-effectiveness modelling. RESULTS: A total of 247,354 individuals were approached to take part in the trial; 30.7% responded positively to the screening invitation. Recruitment of participants resulted in 2028 in the CT arm and 2027 in the control arm. A total of 1994 participants underwent CT scanning: 42 participants (2.1%) were diagnosed with lung cancer; 36 out of 42 (85.7%) of the screen-detected cancers were identified as stage 1 or 2, and 35 (83.3%) underwent surgical resection as their primary treatment. Lung cancer was more common in the lowest socioeconomic group. Short-term adverse psychosocial consequences were observed in participants who were randomised to the intervention arm and in those who had a major lung abnormality detected, but these differences were modest and temporary. Rollout of screening as a service or design of a full trial would need to address issues of outreach. The health-economic analysis suggests that the intervention could be cost-effective but this needs to be confirmed using data on actual lung cancer mortality. CONCLUSIONS: The UK Lung Cancer Screening (UKLS) pilot was successfully undertaken with 4055 randomised individuals. The data from the UKLS provide evidence that adds to existing data to suggest that lung cancer screening in the UK could potentially be implemented in the 60-75 years age group, selected via the Liverpool Lung Project risk model version 2 and using CT volumetry-based management protocols. FUTURE WORK: The UKLS data will be pooled with the NELSON (Nederlands Leuvens Longkanker Screenings Onderzoek: Dutch-Belgian Randomised Lung Cancer Screening Trial) and other European Union trials in 2017 which will provide European mortality and cost-effectiveness data. For now, there is a clear need for mortality results from other trials and further research to identify optimal methods of implementation and delivery. Strategies for increasing uptake and providing support for underserved groups will be key to implementation. TRIAL REGISTRATION: Current Controlled Trials ISRCTN78513845. FUNDING: This project was funded by the National Institute for Health Research (NIHR) Health Technology Assessment programme and will be published in full in Health Technology Assessment; Vol. 20, No. 40. See the NIHR Journals Library website for further project information.

77Sociodemographic Factors in Pituitary Adenomas.PubMed

Adriana G Ioachimescu
Endocrinol Metab Clin North Am. 2023 Dec;52(4):705-717. doi: 10.1016/j.ecl.2023.05.008. Epub 2023 Jun 7.
Pituitary adenomas have been increasingly detected in recent years, especially in the older population. Black patients have a higher incidence than other racial groups. In patients with functioning tumors, presentation and comorbidities are influenced by age and sex, whereas the impact of ethnoracial background is unclear. Active surveillance recommendation and surgery refusal disproportionally affect Black and older patients. The likelihood of surgery at high-volume centers is lower for patients of Black or Hispanic background, uninsured or with lower socioeconomic status. Multicentric studies are necessary to delineate the influence of sociodemographic factors according to the adenoma type and to address the causes of health care disparities.

78Editorial: Social Inequality in Cancer Screening.PubMed

Guido Van Hal, Hajo Zeeb, Harry J de Koning
Front Public Health. 2022 Apr 28;10:854659. doi: 10.3389/fpubh.2022.854659. eCollection 2022.

79Understanding breast cancer as a global health concern.PubMed

Louise Wilkinson, Toral Gathani
Br J Radiol. 2022 Feb 1;95(1130):20211033. doi: 10.1259/bjr.20211033. Epub 2021 Dec 14.
Breast cancer is now the most commonly diagnosed cancer in the world. The most recent global cancer burden figures estimate that there were 2.26 million incident breast cancer cases in 2020 and the disease is the leading cause of cancer mortality in women worldwide. The incidence is strongly correlated with human development, with a large rise in cases anticipated in regions of the world that are currently undergoing economic transformation. Survival, however, is far less favourable in less developed regions. There are a multitude of factors behind disparities in the global survival rates, including delays in diagnosis and lack of access to effective treatment. The World Health Organization's new Global Breast Cancer Initiative was launched this year to address this urgent global health challenge. It aims to improve survival across the world through three pillars: health promotion, timely diagnosis, and comprehensive treatment and supportive care. In this article, we discuss the key challenges of breast cancer care and control in a global context.

80Diagnostic delay at diagnosis and time-to-treatment influence overall survival of pancreatic cancer patients.PubMed

Ruggero Ponz de Leon Pisani, Livia Archibugi, Pilar Lazzano, et al.
Dig Liver Dis. 2025 Jun;57(6):1308-1314. doi: 10.1016/j.dld.2025.03.009. Epub 2025 Apr 2.
BACKGROUND: Pancreatic adenocarcinoma (PDAC) presents with nonspecific symptoms, leading to long diagnostic delays and time-to-treatment. Data on the effects of diagnostic delay and time-to-treatment on the prognosis of PDAC patients are limited, dated and heterogeneous. AIMS: To investigate whether diagnostic delay, time-to-treatment, or diagnostic delay + time-to-treatment (overall delay) impact overall survival (OS) and whether they differ in patients followed up at a tertiary referral center compared to community hospitals. METHODS: This was a single-center prospective cohort of consecutive patients with PDAC, recording demographics, presenting symptoms, stage, treatments, and survival. RESULTS: A total of 282 patients were included. Diagnostic delay>49 days was significantly associated with a higher risk of death in univariate (HR 1.627; 95 % CI 1.15-2.28; p = 0.005) but not in multivariate analysis, whereas overall delay>104 days was significantly associated with a higher risk of death in both univariate (HR 1.83; 95 %CI 1.29-2.61; p = 0.0008) and multivariate (HR, 1.63; 95 % CI, 1.13-2.34; p = 0.008) analyses. Patients who were entirely cared for in tertiary center presented a significantly shorter median time-to-treatment (49 vs. 56 days; p = 0.048) than those in community hospitals. CONCLUSION: Prolonged diagnostic and overall delays seem to impair the survival of patients with PDAC. While diagnostic delay might be reduced with higher awareness of specific warning symptoms, the overall delay can be reduced through specific and faster dedicated therapeutic pathways in referral centers.

81Impact of delay in diagnosis and treatment-initiation on disease stage and survival in oral cavity cancer: a systematic review.PubMed

Benedicte Bitsch Lauritzen, Jakob Schmidt Jensen, Christian Grønhøj, et al.
Acta Oncol. 2021 Sep;60(9):1083-1090. doi: 10.1080/0284186X.2021.1931712. Epub 2021 May 27.
AIM/OBJECTIVES: This study aimed to systematically review the literature on the impact of delay in diagnosis and treatment of oral cavity cancer. METHODS: PubMed and Embase were systematically searched for articles reporting impact of delay in diagnosis and treatment on cancer-stage and survival of oral cavity cancer. Studies comprising at least ten patients, and published since the year 2000, were included. RESULTS: Sixteen studies ( = 45,001, range: 62-18,677 per study, 83% men), from Australia, Asia, Europe, North America and South America, met the inclusion criteria. Eleven studies ( = 1,460) examined , while five studies ( = 43,541) reported delay in treatment. Eight of the eleven studies, examining delay in diagnosis ( = 1,220), analyzed the correlation between delay in diagnosis and tumor stage at diagnosis. Three studies found a significant correlation between patient delay and advanced stage at diagnosis ( < 0.05), whereas three other studies did not. The studies reporting a significant correlation were from Asian countries, whereas the three studies that did not find a correlation were from other continents. Studies reporting on professional delay and total diagnostic delay, generally, did not find a significant correlation with advanced cancer at diagnosis. Time to treatment (TTI), defined as time from diagnosis to treatment, was found significantly correlated with survival in three studies ( < 0.01, < 0.001, < 0.05), and nonsignificant in two studies. CONCLUSION: A significant correlation between patient delay and advanced stage cancer was reported in Asian studies only, while professional delay and total diagnostic delay were generally found to be non-correlated with advanced stage cancer at diagnosis. TTI was in some studies reported to be correlated with poorer outcome, while other studies did not report a correlation. One study presented that there was no clear advantage in overall survival (OS) for patients treated within 30 days, compared to patients treated between 30 and 44 days.

82Hepatocellular carcinoma surveillance: An evidence-based approach.PubMed

Patrick S Harris, Ross M Hansen, Meagan E Gray, et al.
World J Gastroenterol. 2019 Apr 7;25(13):1550-1559. doi: 10.3748/wjg.v25.i13.1550.
Hepatocellular carcinoma (HCC) makes up 75%-85% of all primary liver cancers and is the fourth most common cause of cancer related death worldwide. Chronic liver disease is the most significant risk factor for HCC with 80%-90% of new cases occurring in the background of cirrhosis. Studies have shown that early diagnosis of HCC through surveillance programs improve prognosis and availability of curative therapies. All patients with cirrhosis and high-risk hepatitis B patients are at risk for HCC and should undergo surveillance. The recommended surveillance modality is abdominal ultrasound (US) given that it is cost effective and noninvasive with good sensitivity. However, US is limited in obese patients and those with non-alcoholic fatty liver disease (NAFLD). With the current obesity epidemic and rise in the prevalence of NAFLD, abdominal computed tomography or magnetic resonance imaging may be indicated as the primary screening modality in these patients. The addition of alpha-fetoprotein to a surveillance regimen is thought to improve the sensitivity of HCC detection. Further investigation of serum biomarkers is needed. Semiannual screening is the suggested surveillance interval. Surveillance for HCC is underutilized and low adherence disproportionately affects certain demographics such as non-Caucasian race and low socioeconomic status.

83Mycotoxins: An Underhand Food Problem.PubMed

Antonio Moretti, Antonio F Logrieco, Antonia Susca
Methods Mol Biol. 2017;1542:3-12. doi: 10.1007/978-1-4939-6707-0_1.
Among the food safety issues, the occurrence of fungal species able to produce toxic metabolites on the agro-food products has acquired a general attention. These compounds, the mycotoxins, generally provided of low molecular weight, are the result of the secondary metabolism of the toxigenic fungi. They may have toxic activity toward the plants, but mostly represent a serious risk for human and animal health worldwide, since they can be accumulated on many final crop products and they have a broad range of toxic biological activities. In particular, mainly cereals are the most sensitive crops to the colonization of toxigenic fungal species which accumulate in the grains the related mycotoxins both in the field, until the harvest stage, and in the storage. According to a Food and Agriculture Organization study, approximately 25 % of the global food and feed output is contaminated by mycotoxins. Therefore, since a large proportion of the world's population consumes, as a staple food, the cereals, the consumption of mycotoxin-contaminated cereals is a main issue for health risk worldwide. Furthermore, mycotoxin contamination can have a huge economic and social impact, especially when mycotoxin occurrence on the food commodities is over the regulation limits established by different national and transnational institutions, implying that contaminated products must be discarded. Finally, the climate change due to the global warming can alter stages and rates of toxigenic fungi development and modify host-resistance and host-pathogen interactions, influencing deeply also the conditions for mycotoxin production that vary for each individual pathogen. New combinations of mycotoxins/host plants/geographical areas are arising to the attention of the scientific community and require new diagnostic tools and deeper knowledge of both biology and genetics of toxigenic fungi. Moreover, to spread awareness and knowledge at international level on both the hazard that mycotoxins represent for consumers and costs for stakeholders is of key importance for developing all possible measures aimed to control such dangerous contaminants worldwide.

84Hazard characterisation for significant mycotoxins in food.PubMed

Frantisek Malir, Darina Pickova, Jakub Toman, et al.
Mycotoxin Res. 2023 May;39(2):81-93. doi: 10.1007/s12550-023-00478-2. Epub 2023 Mar 17.
This review updates the current status of activities related to hazard characterisation for mycotoxins, with special reference to regulatory work accomplished within the European Union. Because the relevant information on these topics is widely scattered in the scientific literature, this review intends to provide a condensed overview on the most pertinent aspects. Human health risk assessment is a procedure to estimate the nature and potential for harmful effects of mycotoxins on human health due to exposure to them via contaminated food. This assessment involves hazard identification, hazard characterisation, exposure assessment, and risk characterisation. Mycotoxins covered in this review are aflatoxins, ochratoxin A, cyclopiazonic acid, citrinin, trichothecenes (deoxynivalenol, nivalenol, T-2, and HT-2 toxins), fumonisins, zearalenone, patulin, and ergot alkaloids. For mycotoxins with clear genotoxic/carcinogenic properties, the focus is on the margin of exposure approach. One of its goals is to document predictive characterisation of the human hazard, based on studies in animals using conditions of low exposure. For the other, non-genotoxic toxins, individual 'no adverse effect levels' have been established, but structural analogues or modified forms may still complicate assessment. During the process of hazard characterisation, each identified effect is assessed for human relevance. The estimation of a 'safe dose' is the hazard characterisation endpoint. The final aim of all of these activities is to establish a system, which is able to minimise and control the risk for the consumer from mycotoxins in food. Ongoing research on mycotoxins constantly comes up with new findings, which may have to be implemented into this system.

85The History and Future of Dietary Guidance in America.PubMed

Lisa Jahns, Wendy Davis-Shaw, Alice H Lichtenstein, et al.
Adv Nutr. 2018 Mar 1;9(2):136-147. doi: 10.1093/advances/nmx025.
Evidence-based dietary guidance in the United States has progressed substantially since its inception >100 y ago. This review describes the historical development and significance of dietary guidance in the United States, including the Dietary Guidelines for Americans (DGAs), and emphasizes the foundations upon which they were developed, the process in the formation of past and current guidelines, and present and future applications. Dietary guidance during the first half of the 20th century was focused primarily on food groups in a healthy diet, food safety, safe food storage, and the role of some minerals and vitamins in the prevention of disease. This was punctuated by World War II messaging to reduce food waste and increase food storage. In 1980, the first DGA report was released, and later, the USDA and the Department of Health and Human Services (HHS) were given a mandate for reissuance and reassessment every 5 y. An ad hoc advisory committee made up of nongovernmental experts was established for each edition to review the scientific evidence and provide content recommendations to the Secretaries of the USDA and the HHS. Wording was changed from negative (avoid) to positive (choose) and emphasis was increasingly placed on reducing the prevalence of overweight and obesity and prevention of chronic diseases. Today, the DGAs guide all federally funded feeding and educational programs, including food policies, food assistance programs, and consumer education programs, as well as these programs at the regional, state, and local levels. Additional users include dietitians and other health professionals, food service personnel, food and beverage manufacturers, schools, and day care facilities. Currently, the DGAs are intended for individuals aged ≥2 y. Future editions of the DGAs will include guidance for infants and children <2 y, as well as pregnant women.

86Food prescription pilots: feasibility, acceptability and affordability of improving diet through menu planning and grocery delivery.PubMed

Deborah A Cohen, Erika L Estrada, Monica Montes, et al.
J Hum Nutr Diet. 2023 Aug;36(4):1556-1563. doi: 10.1111/jhn.13142. Epub 2023 Feb 2.
BACKGROUND: Lack of adherence is a primary reason people fail to maintain a healthy diet or lose weight. Multiple environmental factors, including aggressive marketing and convenience of nutrient-poor food, undermine people's best intentions. The aim was to assess the feasibility, acceptability and impact of food prescriptions in which participants' exposure to commercial food outlets is reduced, because the groceries are delivered with weekly menu plans and recipes. METHODS: This is a series of pre-post pilot proof-of-concept studies. We recruited 37 members of Kaiser Permanente interested in improving their diet or losing weight. Weekly meal plans meeting more than 90% of recommended dietary allowances were designed to be low cost, in line with Supplemental Nutrition Assistance Program (SNAP) allowances. Five separate pilots targeted different populations. Participants were required to provide 24-h dietary recalls (ASA24) before and during the interventions. Weight management pilot participants had height, weight and blood pressure measured before and after 4-week pilots and followed sustainability guidelines, limiting meat and dairy. RESULTS: Across pilots, the healthy eating index improved (+21.1 points; 95% CI [confidence interval] 15.9, 26.3). For the weight management pilots, most participants lost weight (average 10.3 lbs for men, 5.7 lbs for women; 95% CI -10.2, -5.4). The majority of participants liked the programme and considered it the easiest weight loss programme they ever tried. CONCLUSIONS: These pilots suggest that meal planning and grocery delivery can be affordable and acceptable and could ultimately have a major impact on diet-related chronic diseases. Longer-term studies are needed to confirm how long compliance will endure.

87Food preservation techniques and nanotechnology for increased shelf life of fruits, vegetables, beverages and spices: a review.PubMed

Adithya Sridhar, Muthamilselvi Ponnuchamy, Ponnusamy Senthil Kumar, et al.
Environ Chem Lett. 2021;19(2):1715-1735. doi: 10.1007/s10311-020-01126-2. Epub 2020 Nov 9.
Food wastage is a major issue impacting public health, the environment and the economy in the context of rising population and decreasing natural resources. Wastage occurs at all stages from harvesting to the consumer, calling for advanced techniques of food preservation. Wastage is mainly due to presence of moisture and microbial organisms present in food. Microbes can be killed or deactivated, and cross-contamination by microbes such as the coronavirus disease 2019 (COVID-19) should be avoided. Moisture removal may not be feasible in all cases. Preservation methods include thermal, electrical, chemical and radiation techniques. Here, we review the advanced food preservation techniques, with focus on fruits, vegetables, beverages and spices. We emphasize electrothermal, freezing and pulse electric field methods because they allow both pathogen reduction and improvement of nutritional and physicochemical properties. Ultrasound technology and ozone treatment are suitable to preserve heat sensitive foods. Finally, nanotechnology in food preservation is discussed.

88Recent developments in ultrasound approach for preservation of animal origin foods.PubMed

Akshay Rajendrabhai Bariya, Nikheel Bhojraj Rathod, Ajay Sureshbhai Patel, et al.
Ultrason Sonochem. 2023 Dec;101:106676. doi: 10.1016/j.ultsonch.2023.106676. Epub 2023 Nov 2.
Ultrasound is a contemporary non-thermal technology that is currently being extensively evaluated for its potential to preserve highly perishable foods, while also contributing positively to the economy and environment. There has been a rise in the demand for food products that have undergone minimal processing or have been subjected to non-thermal techniques. Livestock-derived food products, such as meat, milk, eggs, and seafood, are widely recognized for their high nutritional value. These products are notably rich in proteins and quality fats, rendering them particularly vulnerable to oxidative and microbial spoilage. Ultrasound has exhibited significant antimicrobial properties, as well as the ability to deactivate enzymes and enhance mass transfer. The present review centers on the production and classification of ultrasound, as well as its recent implementation in the context of livestock-derived food products. The commercial applications, advantages, and limitations of the subject matter are also subject to scrutiny. The review indicated that ultrasound technology can be effectively utilized in food products derived from livestock, leading to favorable outcomes in terms of prolonging the shelf life of food while preserving its nutritional, functional, and sensory attributes. It is recommended that additional research be conducted to investigate the effects of ultrasound processing on nutrient bioavailability and extraction. The implementation of hurdle technology can effectively identify and mitigate the lower inactivation of certain microorganisms or vegetative cells.

89[Not Available].PubMed

Lorella Salce, Simona Barbato, Francesco Bianchini, et al.
Recenti Prog Med. 2024 Nov;115(11):568-569. doi: 10.1701/4365.43606.
IFO'S communication campaign for the Italian Lung Screening Network (RISP) study, used multiple online and offline channels to engage not only smokers but a diverse audience. Out-reach activities and lifelong learning helped to promote healthy lifestyles, research findings and precision medicine. The campaign has increased the enrollment in the screening program, which in IFO, two years after 'start-up, is 3300. The pilot study targets smokers and former smokers aged 55 to 75, for prevention and early detection of lung cancer. Funded by the Ministry of Health, it involves 19 Italian centers to enroll 10,000 people. The ultimate goal is the inclusion of lung screening in the Essential Levels of Care (LEA) that is, the services that the National Health Service is required to provide to all citizens, free of charge. Subjects involved perform multilayer low-dose CT scan of the chest and blood sampling with liquid biopsy. The success of the campaign rewards the communication strategy, multidisciplinary collaboration, and activities always in synergy with the mission of the IFOs committed to: "spreading" clinical excellence; promoting citizen empowerment; considering correct information an institutional duty because it is part of treatment and prevention.

90Promoting colorectal cancer screening: A scoping review of screening interventions and resources.PubMed

Kelsey M Leach, Marni E Granzow, Madyson L Popalis, et al.
Prev Med. 2021 Jun;147:106517. doi: 10.1016/j.ypmed.2021.106517. Epub 2021 Mar 9.
BACKGROUND: Early detection through screening can reduce colorectal cancer (CRC) mortality, but approximately 33% of adults aged 50-75 are not getting screened as recommended. Many interventions to increase CRC screening have been tested, but clinical and community organizations may be challenged in identifying the optimum programs and program materials to increase screening and ultimately reduce CRC mortality. METHODS: We conducted a scoping review to characterize existing, US-based interventions to improve CRC screening and to identify gaps in the literature. We used t-tests and correlations to analyze the relationship between project features and intervention effect sizes. RESULTS: The overall effect sizes were + 16% for changes in screening by any modality. The average effect sizes were greater for projects with more components, used patient navigation, and provided free/low-cost testing. CONCLUSION: Interventions varied greatly in terms of follow-up time, test modality, and data sources. Organizations seeking to implement a program aimed at increasing CRC screening should consider both intervention components and relevant program materials.

91Determination of toxic metal release from metallic kitchen utensils and their health risks.PubMed

Ye Ji Koo, Eun Chul Pack, Ye Jin Lee, et al.
Food Chem Toxicol. 2020 Nov;145:111651. doi: 10.1016/j.fct.2020.111651. Epub 2020 Aug 5.
The effect of simulants, repeated use, washing, and oiling on the release of toxic metals from metallic kitchen utensils was investigated. The release of As, Cd, Cr, Ni, and Pb from kitchen utensils composed of stainless steel, aluminum, copper alloy, and cast iron into food simulants was quantified using inductively coupled plasma-mass spectrometry. The results show that this release of toxic metals was highly dependent on pH. Generally, the release of toxic metals tended to decrease with repeated use, and the release of Cr and Ni from stainless steel samples was significantly higher in the first test, compared to the third test. The washing conditions affected the release of As and Cr, whose release levels were higher when washing only with water and with a steel wool pad, respectively. Furthermore, oiling cast iron cookware reduced the release of As, Cd, Cr, and Ni into acidic simulants by 66%, 83%, 71%, and 15%, respectively. The margin of exposure (MOE) was calculated for each toxic metal; the calculated MOE values indicated that it is improbable that the current level of exposure from metallic kitchen utensils would pose a health risk in Korea.

92Ultraprocessed Foods and Cancer in Low-Middle-Income Countries.PubMed

Aparna Gangopadhyay
Nutr Cancer. 2023;75(10):1863-1873. doi: 10.1080/01635581.2023.2272814. Epub 2023 Nov 30.
Low middle income countries (LMICs) are the predominant contributors to global cancer-related mortality and are projected to bear the greater share of the global cancer burden in the next few decades. Among other factors, lifestyle changes have been linked to the rising incidence of cancer in these countries. As one of the keys to a healthy lifestyle, a balanced diet plays a major role in the preservation of health. Globalization and rapid urbanization have prompted a paradigm shift in various aspects of daily life in LMICs; the influence on dietary choices has been particularly noticeable. Studies show a concerning rise in the sale and consumption of ultraprocessed foods in these countries. In addition to hyperpalatability, this trend has been attributed to various other factors including convenience, availability, economic considerations, and marketing strategies. Although several studies from LMICs recognize and recommend the need for effective public health measures to reduce the consumption of these foods, findings from certain studies suggest that established public health strategies occasionally fail in the real-world scenario. Barriers to effective policymaking also contribute to the prevailing dietary trends. This review of studies from the LMIC setting demonstrates the current problem, limitations of established public health measures, and the complexities associated with effective policymaking. In view of the threat posed to cancer risk, there is an urgent need to curb the consumption of ultraprocessed foods in LMICs. National policymakers therefore need to circumnavigate the challenges effectively to ensure timely achievement of the United Nations sustainable development goals.

93The Influence of Socio-Economic Factors on Diet and Active Lifestyle in the Spanish Female Population.PubMed

Elena Sandri, Eva Cantín Larumbe, Germán Cerdá Olmedo
Nutrients. 2023 Jul 26;15(15):3319. doi: 10.3390/nu15153319.
A balanced diet and healthy social habits are two pillars on which the health of the population is based. Therefore, the efforts of the health system should be aimed at prevention. To this end, it is important to know the prevalence of these habits in different population groups and how they vary according to socioeconomic variables. This is an observational, descriptive, cross-sectional study using surveys. A questionnaire was designed to explore a set of variables related to diet and an active lifestyle and was validated through a pilot study and a nominal group. Dissemination was carried out online through social networks by means of non-probabilistic snowball sampling, obtaining a sample of 14.784 women aged between 18 and 45 years. Bivariate comparative analyses were performed using the Mann-Whitney method and the principal component analysis (PCA) method of dimensionality reduction was used to study the relationships between ordinal numerical variables. Results indicate that nutrition was influenced by the age of the sample; adult women have better nutrition than younger women, although they are more sedentary and do less sport. Women with higher education and a medium-high income have better nutrition and healthier lifestyles and a lower BMI and higher self-perceived health status than women with basic education and a lower income. It was concluded that a higher level of income and a higher level of education generally lead to a healthier lifestyle. Spanish women aged 18-45 years need to make changes in their nutrition and lead a more active life.

94Financial Toxicity Among Patients With Breast Cancer Worldwide: A Systematic Review and Meta-analysis.PubMed

Anam N Ehsan, Catherine A Wu, Alexandra Minasian, et al.
JAMA Netw Open. 2023 Feb 1;6(2):e2255388. doi: 10.1001/jamanetworkopen.2022.55388.
IMPORTANCE: Financial toxicity (FT) is the negative impact of cost of care on financial well-being. Patients with breast cancer are at risk for incurring high out-of-pocket costs given the long-term need for multidisciplinary care and expensive treatments. OBJECTIVE: To quantify the FT rate of patients with breast cancer and identify particularly vulnerable patient populations nationally and internationally. DATA SOURCES: A systematic review and meta-analysis were conducted. Four databases-Embase, PubMed, Global Index Medicus, and Global Health (EBSCO)-were queried from inception to February 2021. Data analysis was performed from March to December 2022. STUDY SELECTION: A comprehensive database search was performed for full-text, English-language articles reporting FT among patients with breast cancer. Two independent reviewers conducted study screening and selection; 462 articles underwent full-text review. DATA EXTRACTION AND SYNTHESIS: A standardized data extraction tool was developed and validated by 2 independent authors; study quality was also assessed. Variables assessed included race, income, insurance status, education status, employment, urban or rural status, and cancer stage and treatment. Pooled estimates of FT rates and their 95% CIs were obtained using the random-effects model. MAIN OUTCOMES AND MEASURES: FT was the primary outcome and was evaluated using quantitative FT measures, including rate of patients experiencing FT, and qualitative FT measures, including patient-reported outcome measures or patient-reported severity and interviews. The rates of patients in high-income, middle-income, and low-income countries who incurred FT according to out-of-pocket cost, income, or patient-reported impact of expenditures during breast cancer diagnosis and treatment were reported as a meta-analysis. RESULTS: Of the 11 086 articles retrieved, 34 were included in the study. Most studies were from high-income countries (24 studies), and the rest were from low- and middle-income countries (10 studies). The sample size of included studies ranged from 5 to 2445 people. There was significant heterogeneity in the definition of FT. FT rate was pooled from 18 articles. The pooled FT rate was 35.3% (95% CI, 27.3%-44.4%) in high-income countries and 78.8% (95% CI, 60.4%-90.0%) in low- and middle-income countries. CONCLUSIONS AND RELEVANCE: Substantial FT is associated with breast cancer treatment worldwide. Although the FT rate was higher in low- and middle-income countries, more than 30% of patients in high-income countries also incurred FT. Policies designed to offset the burden of direct medical and nonmedical costs are required to improve the financial health of vulnerable patients with breast cancer.

95Patient-Reported Financial Burden of Treatment for Colon or Rectal Cancer.PubMed

Sheetal Kircher, Fenghai Duan, Na An, et al.
JAMA Netw Open. 2024 Jan 2;7(1):e2350844. doi: 10.1001/jamanetworkopen.2023.50844.
IMPORTANCE: The longitudinal experience of patients is critical to the development of interventions to identify and reduce financial hardship. OBJECTIVE: To evaluate financial hardship over 12 months in patients with newly diagnosed colorectal cancer (CRC) undergoing curative-intent therapy. DESIGN, SETTING, AND PARTICIPANTS: This prospective, longitudinal cohort study was conducted between May 2018 and July 2020, with time points over 12 months. Participants included patients at National Cance Institute Community Oncology Research Program sites. Eligibility criteria included age at least 18 years, newly diagnosed stage I to III CRC, not started chemotherapy and/or radiation, treated with curative intent, and able to speak English. Data were analyzed from December 2022 through April 2023. MAIN OUTCOMES AND MEASURES: The primary end point was financial hardship, measured using the Comprehensive Score for Financial Toxicity (COST), which assesses the psychological domain of financial hardship (range, 0-44; higher score indicates better financial well-being). Participants completed 30-minute surveys (online or paper) at baseline and 3, 6, and 12 months. RESULTS: A total of 450 participants (mean [SD] age, 61.0 [12.0] years; 240 [53.3%] male) completed the baseline survey; 33 participants (7.3%) were Black and 379 participants (84.2%) were White, and 14 participants (3.1%) identified as Hispanic or Latino and 424 participants (94.2%) identified as neither Hispanic nor Latino. There were 192 participants (42.7%) with an annual household income of $60 000 or greater. There was an improvement in financial hardship from diagnosis to 12 months of 0.3 (95% CI, 0.2 to 0.3) points per month (P < .001). Patients with better quality of life and greater self-efficacy had less financial toxicity. Each 1-unit increase in Functional Assessment of Cancer Therapy-General (rapid version) score was associated with an increase of 0.7 (95% CI, 0.5 to 0.9) points in COST score (P < .001); each 1-unit increase in self-efficacy associated with an increase of 0.6 (95% CI, 0.2 to 1.0) points in COST score (P = .006). Patients who lived in areas with lower neighborhood socioeconomic status had greater financial toxicity. Neighborhood deprivation index was associated with a decrease of 0.3 (95% CI, -0.5 to -0.1) points in COST score (P = .009). CONCLUSIONS AND RELEVANCE: These findings suggest that interventions for financial toxicity in cancer care should focus on counseling to improve self-efficacy and mitigate financial worry and screening for these interventions should include patients at higher risk of financial burden.

96New technology in prostate cancer and financial toxicity.PubMed

Avinash Maganty, Brent K Hollenbeck
Urol Oncol. 2023 Sep;41(9):376-379. doi: 10.1016/j.urolonc.2023.04.014. Epub 2023 May 10.
The management of prostate cancer has significantly evolved over the last few decades with the emergence of new diagnostic and treatment technologies, which are typically more expensive than the previous alternatives. However, decision-making regarding which diagnostics and treatment to pursue is often influenced by perceived benefits, adverse effects, and physician recommendations, without considering the financial liability borne by patients. New technologies may exacerbate financial toxicity by replacing less costly alternatives, promoting unrealistic expectations, and expanding treatment to those who would have previously gone untreated. More judicious use of technologies with an understanding of the contexts in which they are most beneficial may help prevent avoidable financial toxicity to patients.

97[Food policies to prevent obesity and the main non-transmissible diseases in Spain: where there's a will there's a way].PubMed

Miguel Ángel Royo-Bordonada, Fernando Rodríguez-Artalejo, Maira Bes-Rastrollo, et al.
Gac Sanit. 2019 Nov-Dec;33(6):584-592. doi: 10.1016/j.gaceta.2019.05.009. Epub 2019 Oct 1.
INTRODUCTION: In Spain, one third of all children and two-thirds of adults suffer from excess weight, a condition that generates a direct excess medical cost of 2000 million Euros. Obesogenic food environments cause obesity by promoting the consumption of sugar-sweetened beverages and ultra-processed foods. Accordingly, we propose five priority policies capable of reversing the epidemic of obesity and related non-communicable diseases through the creation of healthy food environments. THE POWER (PODER IN SPANISH) OF FOOD POLICIES: Advertising (Publicidad): regulation of unhealthy food and drink advertisements carried by all media and targeted at children, and prohibition of sponsorships of congresses, conferences or sports events and endorsements by scientific associations or health professionals. Supply (Oferta): promotion of a 100% healthy supply of goods on sale in vending machines sited at educational, health and sports centres. Demand (Demanda): levying a tax of at least 20% on sugar-sweetened beverages, accompanied by subsidies or reduced taxes on healthy foods and availability of drinking water free of charge at all public venues and areas. Labelling (Etiquetado): effective application of the Nutri-Score through the use of incentives, regulation and public-tender mechanisms. Reformulation (Reformulación): revising and redrawing reformulation agreements with the industry, setting more ambitious goals and mandatory compliance. A FINAL THOUGHT: These five proposed interventions, all of which have been successfully applied in other countries, will serve to raise population awareness and have a positive impact on health and the economy, through reducing the health care costs of obesity and enhancing work productivity. These measures should form part of a wide-ranging transformation of the food system, with agri-food policies that foster the sustainable production of healthy foods.

98Modelling income group differences in the health and economic impacts of targeted food taxes and subsidies.PubMed

Kelechi E Nnoaham, Gary Sacks, Mike Rayner, et al.
Int J Epidemiol. 2009 Oct;38(5):1324-33. doi: 10.1093/ije/dyp214. Epub 2009 May 29.
OBJECTIVE: To examine the effects, by income group, of targeted food taxes and subsidies on nutrition, health and expenditure in the UK. METHODS: A model based on consumption data and demand elasticity was constructed to predict the effects of four food taxation-subsidy regimens. Resulting changes in demand, expenditure, nutrition, cardiovascular disease (CVD) and cancer mortality were estimated. Data Expenditure data were taken from the Expenditure and Food Survey; estimates of price elasticities of demand for food were taken from a report based on the National Food Survey 1988-2000. Estimates of effect on CVD and cancer mortality of changing fat, salt, fruit and vegetable intake were taken from previous meta-analyses. RESULTS: (i) Taxing principal sources of dietary saturated fat is unlikely to reduce cardiovascular disease (CVD) or cancer mortality. (ii) Taxing 'less healthy' foods (defined by the WXYfm nutrient profiling model) could increase CVD and cancer deaths by 35-1300 yearly. (iii) Taxing 'less healthy' foods and subsidising fruits and vegetables by 17.5% could avert up to 2900 CVD and cancer deaths yearly. (iv) Taxing 'less healthy' foods and using all tax revenue to subsidize fruits and vegetables could avert up to 6400 CVD and cancer deaths yearly. Few obesity-related CVD deaths are averted by any of the regimens. All four regimens would be economically regressive and positive health effects will not necessarily be greater in lower-income groups where the need for dietary improvement is higher. CONCLUSIONS: A targeted food tax combined with the appropriate subsidy on fruits and vegetables could reduce deaths from CVD and cancer.

99Impact of Medicaid expansion on smoking prevalence and quit attempts among those newly eligible, 2011-2019.PubMed

Katy Ellis Hilts, Justin Blackburn, P Joseph Gibson, et al.
Tob Prev Cessat. 2021 Aug 5;7:16. doi: 10.18332/tpc/139812. eCollection 2021.
INTRODUCTION: Low-income populations have higher rates of smoking and are disproportionately affected by smoking-related illnesses. This study assessed the long-term impact of increased coverage for tobacco cessation through Medicaid expansion on past-year quit attempts and prevalence of cigarette smoking. METHODS: Using data from CDC's annual Behavioral Risk Factor Surveillance System 2011-2019, we conducted difference-in-difference regression analyses to compare changes in smoking prevalence and past-year quit attempts in expansion states versus non-expansion states. Our sample included non-pregnant adults (18-64 years old) without dependent children with incomes at or below 100% of the Federal Poverty Level (FPL). RESULTS: Regression analyses indicate that Medicaid expansion was associated with reduced smoking prevalence in the first two years post-expansion (β=-0.019, p=0.04), but that this effect was not maintained at longer follow-up periods (β=-0.006, p=0.49). Results of regression analyses also suggest that Medicaid expansion does not significantly impact quit attempts in the short-term (β=-0.013, p=0.52) or at longer term follow-up (β=-0.026, p=0.08). CONCLUSIONS: Expanded coverage for tobacco cessation services through Medicaid alone may not be enough to increase quit-attempts or sustain a reduction in overall prevalence of smoking in newly eligible populations over time. Medicaid programs should consider additional strategies, such as public education campaigns and removal of barriers, to support cessation among enrollees.

100Perceived economic pressure and health-related quality of life of patients with colorectal cancer after surgery: Evidence from China.PubMed

Yi Yang, Ziwei Wu, Junfang Xu, et al.
J Family Med Prim Care. 2025 Jun;14(6):2131-2137. doi: 10.4103/jfmpc.jfmpc_1344_24. Epub 2025 Jun 30.
BACKGROUND: Perceived economic burden and health-related quality of life (HRQOL) of patients with colorectal cancer after surgery are limited, which is benefit for understanding the health status of colorectal cancer patients, providing evidence for developing intervention measures, improving prognosis, and enhancing quality of life of patients. METHODS: A questionnaire-based online investigation was used to collect data from patients with colorectal cancer after surgery between November 2023 and March 2024. The severity of colorectal cancer was categorized to phases 1, 2, 3, and 4 based on the Chinese Society of Clinical Oncology Colorectal Cancer Diagnosis and Treatment Guidelines 2022 Edition. HRQOL was measured using EQ-5D-5L Chinese version. We obtained the health utility value through the integral conversion system, which assigns weights to different levels of the five health dimensions in the EQ-5D-5L scale. Univariate and multivariate logistic regressions were used to analyze the associated factors of utility and VAS score. RESULTS: 227 patients were investigated and incorporated to the data analysis. The mean age of the patients was 63.55 ± 11.71 years old with the average personal annual income of 60000 RMB. As the cancer progresses, different dimensions of HRQOL showed a trend of deterioration. More patients had slight problems in the dimension of pain/discomfort, followed by anxiety/depression, usual activities, self-care and mobility. The EQ-VAS score among colorectal cancer was 87.99, 90.85, 77.04 and 78.28 in phases 1, 2, 3 and 4, respectively ( = 0.000, X = 63.036). The utility score among colorectal cancer was 0.9443, 0.9632, 0.8759 and 0.8494 in phases 1, 2, 3 and 4, respectively ( = 0.000, X = 44.668). Compared to the phase 1, phases 3 and 4 were significantly related to the lower utility and VAS score. Having commercial health insurance was statistically with higher VAS score ( = 0.029). Having a certain amount of pressure was statistically with lower VAS score ( = 0.033). CONCLUSIONS: We found that postoperative colorectal cancer patients have a relatively high HRQOL but have poorer levels of anxiety/depression and pain/discomfort. Moreover, as the disease progresses and perceived economic pressure increases, the HRQOL of colorectal cancer patients shows a downward trend. Therefore, in daily clinical work, primary health physicians should pay attention to patient health management and economic toxicity, to improve patients' quality of life and reduce their economic pressure.

101Implementing patient navigation programs: Considerations and lessons learned from the Alliance to Advance Patient-Centered Cancer Care.PubMed

Elizabeth S Ver Hoeve, Melissa A Simon, Sankirtana M Danner, et al.
Cancer. 2022 Jul 15;128(14):2806-2816. doi: 10.1002/cncr.34251. Epub 2022 May 17.
BACKGROUND: Six multidisciplinary cancer centers were selected and funded by the Merck Foundation (2017-2021) to collaborate in the Alliance to Advance Patient-Centered Cancer Care ("Alliance"), an initiative to improve patient access, minimize health disparities, and enhance the quality of patient-centered cancer care. These sites share their insights on implementation and expansion of their patient navigation efforts. METHODS: Patient navigation represents an evidence-based health care intervention designed to enhance patient-centered care and care coordination. Investigators at 6 National Cancer Institute-designated cancer centers outline their approaches to reducing health care disparities and synthesize their efforts to ensure sustainability and successful transferability in the management of patients with cancer and their families in real-world health care settings. RESULTS: Insights are outlined within the context of patient navigation program effectiveness and supported by examples from Alliance cancer center sites: 1) understand the patient populations, particularly underserved and high-risk patients; 2) capitalize on the existing infrastructure and institutional commitment to support and sustain patient navigation; and 3) build capacity by mobilizing community support outside of the cancer center. CONCLUSIONS: This process-level article reflects the importance of collaboration and the usefulness of partnering with other cancer centers to share interdisciplinary insights while undergoing intervention development, implementation, and expansion. These collective insights may be useful to staff at other cancer centers that look to implement, enhance, or evaluate the effectiveness of their patient navigation interventions.