Endometrial Cancer

Author(s):  
Marta Crous-Bou ◽  
Immaculata de Vivo ◽  
Pagona Lagiou

Lifestyle factors contribute appreciably to endometrial cancer risk, with obesity accounting for over one-third of incident cases in high-income societies. Unlike cervical cancer, which is a model of viral carcinogenesis, endometrial cancer is considered a model of hormonal carcinogenesis, as use of unopposed estrogens postmenopausally and obesity are the best-established risk factors. Endometrial cancer is also the only known malignancy for which cigarette smoking has been shown to confer protection. Risk reduction conferred by current smoking, past oral contraceptive use, childbearing, and physical activity is believed to be mediated by hormones. This may also apply to the increase in risk associated with obesity, which increases peripheral production of estrogens, and with diabetes mellitus. Hence, it should be possible to prevent a substantial fraction of endometrial cancers through lifestyle modification. Pathological classification of endometrial cancer is currently evolving and studies are revealing different molecular subtypes within the same histological groups.

2007 ◽  
Vol 17 (2) ◽  
pp. 441-446 ◽  
Author(s):  
V. M. Chia ◽  
P. A. Newcomb ◽  
A. Trentham-Dietz ◽  
J. M. Hampton

Endogenous and exogenous sources of estrogen and characteristics altering these hormone levels have been related to endometrial cancer risk; however, their relationship to survival following diagnosis is less clear. In a population-based study, we examined whether mortality after endometrial cancer diagnosis was affected by prediagnosis obesity, diabetes, smoking, oral contraceptive use, parity, or postmenopausal hormone (PMH) use. Eligible women, aged 40–79 years, diagnosed from 1991–1994 with incident invasive endometrial cancer and identified through the Wisconsin statewide mandatory cancer registry were invited to participate. Of 745 eligible cases, 166 women were deceased after 9.3 years of follow-up, with 43 attributable to endometrial cancer, based upon vital records linkage. Hazard rate ratios (HRR) and 95% confidence intervals were adjusted for age at diagnosis, menopausal status, stage of disease, and other exposures of interest. Obese women (body mass index [BMI] ≥30 kg/m2) prior to endometrial cancer diagnosis had an increased risk of both all-cause (HRR = 1.6, 95% CI 1.0–2.5) and endometrial cancer (HRR = 2.0, 95% CI 0.8–5.1) mortality, compared with nonoverweight women (BMI < 25 kg/m2). Endometrial cancer cases with diabetes also had an increased risk of all-cause mortality compared with nondiabetic women (HRR = 1.7, 95% CI 1.1–2.5), although there was no association with endometrial cancer mortality. There were no associations between PMH use, oral contraceptive use, parity, or smoking and mortality from any cause. The results suggest that history of obesity and diabetes may increase risk of mortality after endometrial cancer diagnosis; modification of these characteristics may improve survival after endometrial cancer diagnosis.


2010 ◽  
Vol 17 (4) ◽  
pp. 1007-1019 ◽  
Author(s):  
Laure Dossus ◽  
Sabina Rinaldi ◽  
Susen Becker ◽  
Annekatrin Lukanova ◽  
Anne Tjonneland ◽  
...  

Obesity, a major risk factor for endometrial cancer, is a low-grade inflammatory state characterized by elevated concentrations of cytokines and acute phase reactants. The current study had two aims: first to investigate the associations of C-reactive protein (CRP), interleukin 6 (IL6), and IL1 receptor antagonist (IL1Ra) with endometrial cancer risk and second to examine to which extent these markers can influence the association between obesity and endometrial cancer. We conducted a case–control study, nested within the European Prospective Investigation into Cancer and Nutrition, which comprised 305 incident cases of endometrial cancer and 574 matched controls. CRP, IL6, and IL1Ra were measured in prospectively collected blood specimens by immunoassays. Data were analyzed using conditional logistic regression. All statistical tests were two-sided, and P values <0.05 were considered statistically significant. We observed a significant increase in risk of endometrial cancer with elevated levels of CRP (odds ratio (OR) for top versus bottom quartile: 1.58, 95% confidence interval (CI): 1.03–2.41, Ptrend=0.02), IL6 (OR for top versus bottom quartile: 1.66, 95% CI: 1.08–2.54, Ptrend=0.008), and IL1Ra (OR for top versus bottom quartile: 1.82, 95% CI: 1.22–2.73, Ptrend=0.004). After adjustment for body mass index (BMI), the estimates were strongly reduced and became non-significant. The association between BMI and endometrial cancer was also substantially attenuated (∼10–20%) after adjustment for inflammatory markers, even when the effects of C-peptide or estrone had already been taken into account. We provided epidemiological evidence that chronic inflammation might mediate the association between obesity and endometrial cancer and that endometrial carcinogenesis could be promoted by an inflammatory milieu.


BMC Cancer ◽  
2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Noemie Body ◽  
Vincent Lavoué ◽  
Olivier De Kerdaniel ◽  
Fabrice Foucher ◽  
Sébastien Henno ◽  
...  

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