Department of Morphology, Surgery and Experimental Medicine, Section of Obstetrics and Gynecology, University of Ferrara, Ferrara, Italy.
Eur Rev Med Pharmacol Sci. 2018 Oct;22(19):6294-6299. doi: 10.26355/eurrev_201810_16038.
Endometrial cancer (EC) is a complex gynecological neoplasm with several clinical, histopathological and genetic features. Different hormonal, metabolic and biochemical axes are involved in pathogenesis. Obesity is a well-known risk factor for this disease and the role of local and systemic effects of adipose tissue, especially in the promotion of subclinical chronic inflammation, is an important issue. Indeed, inflammation is related to the pathogenesis of different tumors, including EC. This review aims to remark the role of obesity and inflammation in the pathogenesis of EC cancer through an exploration of the current literature.
We performed a comprehensive review of the literature through a PubMed search using key words and including English language papers looking at this topic.
Only few authors analyzed the role of inflammatory cytokines released by adipose tissue in visceral abdominal fat depots. Tumor Necrosis Factor-α, Interleukin-6, Interleukin-1 Receptor Antagonist, Nuclear Factor-kB, Leptin, Adiponectin and C Reactive Protein were studied for cancer risk prediction models, risk stratification or targeted therapies. Furthermore, genetic studies evaluated the effect of inflammatory cytokines secreted by visceral adipocytes in the modulation of angiogenesis and signaling pathways such as PI3K/AKT/mTOR, that result altered in the pathogenesis of EC.
The identification of inflammatory biomarkers released by adipose tissue, in the pathogenesis of EC, could be useful in improving diagnostic accuracy, identifying targets of therapy, suggesting useful lifestyle behaviors. A deeper knowledge of the genetic background of alterations in inflammatory pathway genes could better define the population exposed to a higher susceptibility to EC due to genetic polymorphisms. Future studies are needed to better understand this field.
子宫内膜癌（EC）是一种复杂的妇科肿瘤，具有多种临床、组织病理学和遗传学特征。不同的激素、代谢和生化轴参与其发病机制。肥胖是这种疾病的一个众所周知的危险因素，脂肪组织的局部和全身效应，尤其是在促进亚临床慢性炎症方面的作用，是一个重要问题。事实上，炎症与包括 EC 在内的不同肿瘤的发病机制有关。本综述旨在通过探讨当前文献，阐述肥胖和炎症在 EC 发病机制中的作用。
我们通过使用关键词在 PubMed 上进行全面的文献检索，并包括探讨这一主题的英文论文，对文献进行了综述。
只有少数作者分析了内脏腹部脂肪堆积中脂肪组织释放的炎性细胞因子在发病机制中的作用。肿瘤坏死因子-α、白细胞介素-6、白细胞介素-1 受体拮抗剂、核因子-kB、瘦素、脂联素和 C 反应蛋白被用于癌症风险预测模型、风险分层或靶向治疗的研究。此外，遗传研究评估了内脏脂肪细胞分泌的炎性细胞因子在调节血管生成和信号通路（如 PI3K/AKT/mTOR）中的作用，这些信号通路在 EC 的发病机制中发生改变。
鉴定脂肪组织在 EC 发病机制中释放的炎症生物标志物，可能有助于提高诊断准确性、确定治疗靶点、提出有益的生活方式行为。更深入地了解炎症通路基因改变的遗传背景，可以更好地定义由于遗传多态性而易患 EC 的人群。未来的研究需要更好地理解这一领域。
