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Published on: December 26, 2016
Hyperresistinemia is associated with postmenopausal breast cancer
Maria Dalamaga1, Konstantinos Karmaniolas, Evangelia Papadavid
1Department of Clinical Biochemistry, University of Athens Medical School, Attikon General University Hospital, Chaidari, Athens, Greece. madalamaga@med.uoa.gr
Menopause (New York, N.Y.)
|March 14, 2013
Summary
Higher serum resistin levels are linked to postmenopausal breast cancer (PBC). This finding suggests resistin may play a role in PBC development or progression, potentially serving as a future biomarker.
Area of Science:
- Endocrinology
- Oncology
- Immunology
Background:
- Obesity, insulin resistance, and adipocytokines are associated with postmenopausal breast cancer (PBC) risk and prognosis.
- Altered resistin secretion may link obesity to PBC.
- This study investigates serum resistin's association with PBC, considering various risk factors.
Purpose of the Study:
- To explore the association between serum resistin levels and postmenopausal breast cancer.
- To evaluate resistin in relation to established risk factors including adipokines, metabolic, and inflammatory markers.
Main Methods:
- A case-control study involving 102 postmenopausal women with invasive breast cancer and 102 matched controls.
- Measurements included serum resistin, adiponectin, leptin, insulin resistance (HOMA-IR), inflammatory markers (TNF-α, IL-6, hs-CRP), and tumor markers (CEA, CA 15-3).
Main Results:
- Serum resistin levels were significantly higher in breast cancer cases than controls (P < 0.001).
- Multivariable analysis, adjusting for numerous factors, confirmed this association (OR, 1.17; 95% CI, 1.03-1.34; P = 0.02).
- In cases, resistin correlated with tumor markers and inflammatory parameters, but not metabolic or anthropometric variables.
Conclusions:
- Further research is needed to determine if hyperresistinemia causes PBC or reflects its progression, and if resistin can be a PBC biomarker.
- Targeting resistin inhibition may be a therapeutic strategy for breast cancer by modulating the inflammatory microenvironment.
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