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Endometrial cancer is the most prevalent type of female genital tract malignancy in the developed countries. It represents nearly 50% of all new genital cancers in the Western world, surpassing the incidence of cervical cancer. Endometrial cancer is a disease of postmenopausal women (median age 63 years) and 90% of cases occur in patients over 50 years of age. Clinical risk factors include early onset of menstruation, obesity, sedentarism, nulliparity, infertility, late menopause, diabetes mellitus, hypertension, estrogen exposure and prolonged tamoxifen treatment. Some 5% of endometrial cancers are associated with hereditary non-polyposis colorectal carcinoma (Lynch syndrome type II). There are different subtypes of endometrial cancer but the most common is the endometrioid type (90% of cases). Other subtypes are papillary, serous, clear cell carcinoma and carcinosarcomas. Endometrioid cancer has a good prognosis, while the other subtypes are associated with a bad prognosis.

 

Abdominal obesity is a well-established risk factor for endometrial cancer, but mechanisms underlying the association are unclear. Luhn and colleagues [1] recently reported the influences of serum estradiol, adiponectin, leptin and visfatin on endometrial cancer risk in a nested case–control sample of postmenopausal women included in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. The studied population included 167 incident endometrial cancer cases and 327 matched controls with similar sociodemographic characteristics. Estradiol and adipokine (adiponectin, leptin and visfatin) levels were categorized into tertiles (T). Conditional logistic regression showed inverse association between adiponectin levels (T3 vs. T1) for the risk of endometrial cancer (odds ratio (OR) 0.48; 95% confidence interval (CI) 0.29–0.80), while high leptin levels had a positive association (OR 2.77; 95% CI 1.60–4.79). The associations were stronger when considering only women not using menopause hormone therapy. There were non-significant associations between serum visfatin levels and endometrial cancer risk.

Author(s)

  • Faustino R. Pérez-López
    Professor of Obstetrics and Gynecology, University of Zaragoza Faculty of Medicine & Lozano Blesa University Hospital, Zaragoza, Spain

Citations

  1. Luhn P, Dallal CM, Weiss JM, et al. Circulating adipokine levels and endometrial cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Cancer Epidemiol Biomarkers Prev 2013;22:1304-12.
    http://www.ncbi.nlm.nih.gov/pubmed/23696194
  2. Potischman N, Hoover RN, Brinton LA, et al. Case-control study of endogenous steroid hormones and endometrial cancer. J Natl Cancer Inst 1996;88:1127-35.
    http://www.ncbi.nlm.nih.gov/pubmed/8757192
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    http://www.ncbi.nlm.nih.gov/pubmed/18398032
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    http://www.ncbi.nlm.nih.gov/pubmed/23033315
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  8. Cust AE, Allen NE, Rinaldi S, et al. Serum levels of C-peptide, IGFBP-1 and IGFBP-2 and endometrial cancer risk; results from the European Prospective Investigation into Cancer and Nutrition. Int J Cancer 2007;120:2656-64.
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  9. Moon HS, Chamberland JP, Aronis K, Tseleni-Balafouta S, Mantzoros CS. Direct role of adiponectin and adiponectin receptors in endometrial cancer: in vitro and ex vivo studies in humans. Mol Cancer Ther 2011;10:2234-43.
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  10. Chedraui P, Pérez-López FR. Nutrition and health during mid-life: searching for solutions and meeting challenges for the aging population. Climacteric 2013; 16(Suppl 1):85-95.
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