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Cancer epidemiology, biomarkers & prevention, 2005-12, Vol.14 (12), p.2840-2847
Ort / Verlag
Philadelphia, PA: American Association for Cancer Research
Erscheinungsjahr
2005
Quelle
MEDLINE
Beschreibungen/Notizen
Endometrial cancer is the most common gynecologic malignancy in the United States. Substantial epidemiologic data implicate
an imbalance of estrogens and progestogens in the etiology of this disease. We propose that inflammation also plays a role
in endometrial cancer development. Emerging laboratory data suggest that elevated levels of prostaglandin E 2 may underlie the transformation of normal endometrium to neoplastic tissue and that in vitro nonsteroidal anti-inflammatory drugs may inhibit endometrial cancer cell growth. In this review, we suggest that the risk
factors for endometrial cancer—unopposed estrogens, anovulation, polycystic ovary syndrome, excessive menstruation, early
menarche, and late menopause—may be viewed as factors increasing the exposure of the endometrium to inflammation, whereas
pregnancy and smoking, two likely protective factors, have the opposite effect. Chronic inflammation can induce rapid cell
division, increasing the possibility for replication error, ineffective DNA repair, and subsequent mutations. A proinflammatory
milieu can also directly increase estrogen production. Hence, inflammation may work in conjunction with or in addition to
estrogen exposure in the development of endometrial cancer. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2840–7)