| Literature DB >> 30851382 |
Priya Bhardwaj1, CheukMan C Au2, Alberto Benito-Martin2, Heta Ladumor3, Sofya Oshchepkova2, Ruth Moges2, Kristy A Brown4.
Abstract
Obesity is a risk factor for estrogen receptor-positive (ER+) breast cancer after menopause. The pro-proliferative effects of estrogens are well characterized and there is a growing body of evidence to also suggest an important role in tumorigenesis. Importantly, obesity not only increases the risk of breast cancer, but it also increases the risk of recurrence and cancer-associated death. Aromatase is the rate-limiting enzyme in estrogen biosynthesis and its expression in breast adipose stromal cells is hypothesized to drive the growth of breast tumors and confer resistance to endocrine therapy in obese postmenopausal women. The molecular regulation of aromatase has been characterized in response to many obesity-related molecules, including inflammatory mediators and adipokines. This review is aimed at providing an overview of our current knowledge in relation to the regulation of estrogens in adipose tissue and their role in driving breast tumor development, growth and progression.Entities:
Keywords: Aromatase; Breast cancer; Endocrine resistance; Endocrine therapy; Estrogen; Metastasis; Obesity; Tumorigenesis
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Year: 2019 PMID: 30851382 PMCID: PMC6502693 DOI: 10.1016/j.jsbmb.2019.03.002
Source DB: PubMed Journal: J Steroid Biochem Mol Biol ISSN: 0960-0760 Impact factor: 4.292