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Obesity‐induced Inflammation in Human Mammary Tissues: a Microenvironment Favorable for the Development of Postmenopausal Breast Cancer
Author(s) -
Roubert Agathe,
Lyu Lin,
Pfalzer Anna,
Gauger Kelly,
Choi Woojung,
Schneider Sallie,
Liu Zhenhua
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.405.6
Subject(s) - breast cancer , medicine , overweight , inflammation , obesity , wnt signaling pathway , cancer , mammary gland , cytokine , endocrinology , tumor necrosis factor alpha , oncology , signal transduction , biology , biochemistry
Epidemiological studies have convincingly suggested that overweight and obesity are a critical risk factor for postmenopausal breast cancer with a 12% increase in risk for every 5 kg/m 2 increase in BMI. Our laboratory has previously demonstrated that obesity is associated with increased colonic TNF‐α in parallel with elevated expression of tumorigenic Wnt‐signaling pathway target genes in a murine model. We hypothesized that the low‐grade inflammatory state associated with obesity also exists in human mammary tissue. Thirty‐one breast tissue samples were collected from women undergoing elective breast reduction surgery. Inflammatory cytokines (IFN‐γ, IL‐1β, IL‐2, IL‐6, IL‐8 and TNF‐α) were measured using a high‐performance, chemiluminescence immunoassay. A Pearson correlation was performed to determine the relationship between the expressions of those inflammatory cytokines and BMI. Among the 6 cytokines examined, the levels of IL‐1β, IL‐6 and TNF‐α, were positively associated with BMI (p‐values are 0.029, <0.001, and 0.032, respectively). This study demonstrated that overweight and obesity produced an inflammatory microenvironment in human breast tissue, which may promote the development of postmenopausal breast cancer. Further insights into how these cytokines mediate tumorigenic signaling pathways are needed.