Inflammatory events in endometrial adenocarcinoma

J Endocrinol. 2010 Aug;206(2):141-57. doi: 10.1677/JOE-10-0072. Epub 2010 Apr 20.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adenocarcinoma / metabolism
  • Adenocarcinoma / pathology*
  • Adenocarcinoma / physiopathology
  • Androgens / metabolism
  • Chemokines / immunology
  • Cytokines / immunology
  • Disease Progression
  • Endometrial Neoplasms / metabolism
  • Endometrial Neoplasms / pathology*
  • Endometrial Neoplasms / physiopathology
  • Estrogens / metabolism
  • Female
  • Gene Expression Regulation, Neoplastic
  • Glucocorticoids / metabolism
  • Humans
  • Inflammation* / genetics
  • Inflammation* / immunology
  • Inflammation* / metabolism
  • Leukocytes / immunology
  • Menstruation / immunology
  • Mutation
  • NF-kappa B / metabolism
  • PTEN Phosphohydrolase / genetics
  • Progesterone / metabolism
  • Prostaglandins / metabolism
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins p21(ras)
  • Risk Factors
  • Signal Transduction
  • Transcription, Genetic
  • Up-Regulation
  • ras Proteins / genetics

Substances

  • Androgens
  • Chemokines
  • Cytokines
  • Estrogens
  • Glucocorticoids
  • KRAS protein, human
  • NF-kappa B
  • Prostaglandins
  • Proto-Oncogene Proteins
  • Progesterone
  • PTEN Phosphohydrolase
  • PTEN protein, human
  • Proto-Oncogene Proteins p21(ras)
  • ras Proteins