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饮食在前列腺癌风险和进展中的作用变化。

The evolving role of diet in prostate cancer risk and progression.

机构信息

Department of Radiation Oncology.

Department of Surgery, Division of Urology.

出版信息

Curr Opin Oncol. 2019 May;31(3):222-229. doi: 10.1097/CCO.0000000000000519.

Abstract

PURPOSE OF REVIEW

This overview examines the rationale for dietary interventions for prostate cancer by summarizing the current evidence base and biological mechanisms for the involvement of diet in disease incidence and progression.

RECENT FINDINGS

Recent data have further solidified the association between insulin resistance and prostate cancer with the homeostatic model assessment of insulin resistance. Data also show that periprostatic adipocytes promote extracapsular extension of prostate cancer through chemokines, thereby providing a mechanistic explanation for the association observed between obesity and high-grade cancer. Regarding therapeutics, hyperinsulinemia may be the cause of resistance to phosphatidylinositol-3 kinase inhibitors in the treatment of prostate cancer, leading to new investigations combining these drugs with ketogenic diets.

SUMMARY

Given the recently available data regarding insulin resistance and adipokine influence on prostate cancer, dietary strategies targeting metabolic syndrome, diabetes, and obesity should be further explored. In macronutrient-focused therapies, low carbohydrate/ketogenic diets should be favored in such interventions because of their superior impact on weight loss and metabolic parameters and encouraging clinical data. Micronutrients, including the carotenoid lycopene which is found in highest concentrations in tomatoes, may also play a role in prostate cancer prevention and prognosis through complementary metabolic mechanisms. The interplay between genetics, diet, and prostate cancer is an area of emerging focus that might help optimize therapeutic dietary response in the future through personalization.

摘要

目的综述

通过总结饮食在疾病发生和发展中的作用的现有证据基础和生物学机制,本文概述了饮食干预前列腺癌的基本原理。

最近发现

最近的数据进一步证实了胰岛素抵抗与前列腺癌之间的关联,胰岛素抵抗的稳态模型评估。数据还表明,前列腺周围的脂肪细胞通过趋化因子促进前列腺癌的包膜外扩展,从而为观察到的肥胖与高级别癌症之间的关联提供了一种机制解释。关于治疗学,高胰岛素血症可能是前列腺癌治疗中对磷脂酰肌醇-3 激酶抑制剂产生耐药性的原因,导致新的研究将这些药物与生酮饮食相结合。

总结

鉴于最近有关胰岛素抵抗和脂肪因子对前列腺癌影响的数据,应进一步探索针对代谢综合征、糖尿病和肥胖的饮食策略。在以宏量营养素为重点的治疗中,由于低碳水化合物/生酮饮食对体重减轻和代谢参数的影响更大,并且有令人鼓舞的临床数据,因此应优先考虑此类干预措施。类胡萝卜素番茄红素等微量营养素也可能通过互补的代谢机制在前列腺癌的预防和预后中发挥作用。遗传、饮食和前列腺癌之间的相互作用是一个新的关注领域,通过个性化,未来可能有助于优化治疗性饮食反应。

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