The impact of poor metabolic health on aggressive breast cancer: adipose tissue and tumor metabolism

被引:4
|
作者
Sankofi, Barbara Mensah [1 ]
Valencia-Rincon, Estefania [1 ]
Sekhri, Malika [1 ]
Ponton-Almodovar, Adriana L. [2 ,3 ,4 ]
Bernard, Jamie J. [2 ,3 ,4 ]
Wellberg, Elizabeth A. [1 ]
机构
[1] Univ Oklahoma, Hlth Sci Ctr, Dept Pathol, Oklahoma City, OK 73104 USA
[2] Michigan State Univ, Dept Pharmacol & Toxicol, E Lansing, MI USA
[3] Michigan State Univ, Nicolas V Perricone Div Dermatol, E Lansing, MI USA
[4] Michigan State Univ, Dept Med, E Lansing, MI USA
来源
关键词
breast cancer; adipose; fibroblast growth factor; obesity; diabetes; BODY-MASS INDEX; GROWTH-FACTOR RECEPTOR; EPITHELIAL-MESENCHYMAL TRANSITION; SELECTIVE AROMATASE INHIBITOR; ESTROGEN-RECEPTOR; DIABETES-MELLITUS; ENDOCRINE THERAPY; MOLECULAR PORTRAITS; MEGESTROL-ACETATE; RISK-FACTOR;
D O I
10.3389/fendo.2023.1217875
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Obesity and type 2 diabetes are chronic metabolic diseases that impact tens to hundreds of millions of adults, especially in developed countries. Each condition is associated with an elevated risk of breast cancer and with a poor prognosis after treatment. The mechanisms connecting poor metabolic health to breast cancer are numerous and include hyperinsulinemia, inflammation, excess nutrient availability, and adipose tissue dysfunction. Here, we focus on adipose tissue, highlighting important roles for both adipocytes and fibroblasts in breast cancer progression. One potentially important mediator of adipose tissue effects on breast cancer is the fibroblast growth factor receptor (FGFR) signaling network. Among the many roles of FGFR signaling, we postulate that key mechanisms driving aggressive breast cancer include epithelial-to-mesenchymal transition and cellular metabolic reprogramming. We also pose existing questions that may help better understand breast cancer biology in people with obesity, type 2 diabetes, and poor metabolic health.
引用
收藏
页数:13
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