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打破肥胖与癌症关联的机制靶点和植物化学策略。

Mechanistic targets and phytochemical strategies for breaking the obesity-cancer link.

机构信息

Department of Nutritional Sciences, University of Texas , Austin, TX , USA.

出版信息

Front Oncol. 2013 Aug 19;3:209. doi: 10.3389/fonc.2013.00209. eCollection 2013.

Abstract

The prevalence of obesity, an established risk and progression factor for many cancers, has increased dramatically in many countries over the past three decades. Worldwide, an estimated 600 million adults are currently obese. Thus, a better understanding of the mechanistic links between obesity and cancer is urgently needed to identify intervention targets and strategies to offset the procancer effects of obesity. This review synthesizes the evidence on key biological mechanisms underlying the obesity-cancer association, with particular emphasis on obesity-associated enhancements in growth factor signaling, inflammation, and perturbations in the tumor microenvironment. These interrelated pathways and processes that are aberrantly regulated in obese individuals represent mechanism-based targets for disrupting the obesity-cancer link using phytochemicals.

摘要

在过去的三十年中,肥胖症的流行率——许多癌症的既定风险和进展因素——在许多国家急剧上升。在全球范围内,目前估计有 6 亿成年人肥胖。因此,迫切需要更好地了解肥胖症和癌症之间的机制联系,以确定干预目标和策略来抵消肥胖症的致癌作用。本综述综合了肥胖症与癌症相关性的关键生物学机制的证据,特别强调了与肥胖相关的生长因子信号、炎症和肿瘤微环境紊乱的增强。这些在肥胖个体中异常调节的相互关联的途径和过程代表了使用植物化学物质破坏肥胖与癌症联系的基于机制的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23fe/3746736/48680076522e/fonc-03-00209-g001.jpg

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