title: Inflammatory events in endometrial adenocarcinoma.
abstract: Endometrial adenocarcinoma is the most common gynaecological malignancy in western countries. Many of the established risk factors for developing endometrial cancer are associated with excess exposure to oestrogen unopposed by progesterone. These include nulliparity, late onset of the menopause, post-menopausal hormone replacement therapy and obesity. However, a number of risk factors also promote inflammation, another feature proposed to influence cancer development. The human cycling endometrium undergoes regular and cyclical episodes of inflammation. Moreover, hormonal and genetic changes that occur early in the development of endometrial adenocarcinoma can exacerbate the local inflammatory environment. Via alterations in the expression of local mediators and immune cell function, these may contribute to the development of endometrial cancer. This review discusses the contribution of inflammation to the initiation and progression of endometrial adenocarcinoma. Manipulation of inflammatory pathways may therefore represent a therapeutic target in endometrial adenocarcinoma.
authors.affiliation: MRC Human Reproductive Sciences Unit, The Queen's Medical Research Institute, Centre for Reproductive Biology, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.
authors.forename: Alison E
authors.initials: AE
authors.lastname: Wallace
authors.forename: Douglas A
authors.initials: DA
authors.lastname: Gibson
authors.forename: Philippa T K
authors.initials: PT
authors.lastname: Saunders
authors.forename: Henry N
authors.initials: HN
authors.lastname: Jabbour
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D000728:Androgens / Q000378:metabolism; D018925:Chemokines / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D018450:Disease Progression; D016889:Endometrial Neoplasms / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D004967:Estrogens / Q000378:metabolism; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D005938:Glucocorticoids / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D007962:Leukocytes / Q000276:immunology; D008598:Menstruation / Q000276:immunology; D009154:Mutation; D016328:NF-kappa B / Q000378:metabolism; D051059:PTEN Phosphohydrolase / Q000235:genetics; D011374:Progesterone / Q000378:metabolism; D011453:Prostaglandins / Q000378:metabolism; D011518:Proto-Oncogene Proteins / Q000235:genetics; D016283:Proto-Oncogene Proteins p21(ras); D012307:Risk Factors; D015398:Signal Transduction; D014158:Transcription, Genetic; D015854:Up-Regulation; D018631:ras Proteins / Q000235:genetics
chemical_list: D000728:Androgens; D018925:Chemokines; D016207:Cytokines; D004967:Estrogens; D005938:Glucocorticoids; C117307:KRAS protein, human; D016328:NF-kappa B; D011453:Prostaglandins; D011518:Proto-Oncogene Proteins; D011374:Progesterone; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins