Elvina Jeyakumar, Sathyavathi Sundararaju, Stephanie Annett, Mohamed A Elrayess
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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.
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).