肥胖和乳腺癌双重流行中的乳腺脂肪功能障碍。

IF 2.9 3区 医学 Q2 ONCOLOGY
Elvina Jeyakumar, Sathyavathi Sundararaju, Stephanie Annett, Mohamed A Elrayess
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引用次数: 0

摘要

乳腺癌是女性死亡的主要原因之一,肥胖是一个重要因素。肥胖的乳腺脂肪组织(MAT)功能障碍创造了一个支持肿瘤的环境,导致风险增加。在肥胖中,MAT发生显著变化,包括肥胖增加、慢性炎症、芳香化酶过表达、胰岛素抵抗和脂肪因子信号改变,共同形成促肿瘤微环境。脂肪细胞和癌细胞之间的相互作用通过代谢串扰和免疫逃避进一步加剧了乳腺癌的进展。这篇综述探讨了MAT功能障碍在乳腺癌发病率和进展以及肥胖中的作用。有趣的是,肥胖似乎对乳腺癌风险有矛盾的影响,对绝经前妇女有潜在的保护作用,但对绝经后妇女有增加的风险,主要是由于雌激素水平的差异。解决肥胖MAT的代谢、炎症和激素异常有助于开发精确的治疗方法,降低乳腺癌风险,改善肥胖患者的治疗效果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mammary Adipose Dysfunction in the Dual Epidemic of Obesity and Breast Cancer.

Breast cancer is one of the leading causes of death among women, with obesity being a significant factor. Mammary adipose tissue (MAT) dysfunction in obesity creates a tumor-supportive environment, leading to increased risk. In obesity, MAT undergoes significant changes, including increased adiposity, chronic inflammation, aromatase overexpression, insulin resistance, and altered adipokine signaling, collectively fostering a pro-tumorigenic microenvironment. The interaction between adipocytes and cancer cells further exacerbates breast cancer progression through metabolic crosstalk and immune evasion. This review examines the role of MAT dysfunction in breast cancer incidence and progression, in obesity. Interestingly, obesity appears have a paradoxical effect on breast cancer risk, offering a potentially protective role in premenopausal women, but increased risk in post-menopausal women, primarily due to differences in estrogen levels. Addressing the metabolic, inflammatory, and hormonal abnormalities in obese MAT can aid in enabling the development of precision therapies that reduce breast cancer risk and improve treatment outcomes in obese patients.

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来源期刊
Carcinogenesis
Carcinogenesis 医学-肿瘤学
CiteScore
9.20
自引率
2.10%
发文量
95
审稿时长
1 months
期刊介绍: Carcinogenesis: Integrative Cancer Research is a multi-disciplinary journal that brings together all the varied aspects of research that will ultimately lead to the prevention of cancer in man. The journal publishes papers that warrant prompt publication in the areas of Biology, Genetics and Epigenetics (including the processes of promotion, progression, signal transduction, apoptosis, genomic instability, growth factors, cell and molecular biology, mutation, DNA repair, genetics, etc.), Cancer Biomarkers and Molecular Epidemiology (including genetic predisposition to cancer, and epidemiology), Inflammation, Microenvironment and Prevention (including molecular dosimetry, chemoprevention, nutrition and cancer, etc.), and Carcinogenesis (including oncogenes and tumor suppressor genes in carcinogenesis, therapy resistance of solid tumors, cancer mouse models, apoptosis and senescence, novel therapeutic targets and cancer drugs).
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