From endometrial hyperplasia to endometrial cancer

Insight into the biology and possible medical preventive measures

Melih C. Boruban, Kadri Altundag, Gokhan Kilic, Josef Blankstein

Research output: Contribution to journalArticle

52 Citations (Scopus)

Abstract

Controversies are still seen in the histological differential diagnosis of hyperplasia and well-differentiated endometrial carcinoma. Prediction of endometrial cancer in patients with hyperplasia with atypia, with the available markers has not been reliable yet. Hence these patients require more attention in the clinical management. Endometrial hyperplasia is proliferation of endometrial glands resulting in a higher gland : stroma ratio. Cytological atypia, which may progress to or co-exist with endometrial cancer and other pathological changes, result from estrogen stimulation unopposed by progesterone. Biomarkers whose expression is altered in cases of endometrial hyperplasia or cancer such as progesterone receptor, insulin-like growth factor I, retinaldehyde dehydrogenase type II, and secreted frizzled-related protein 4, seem to be promising to use as early-stage tumor markers. Mutation of PTEN is present in 83% of endometrial adenocarcinoma cases, making it the most frequent early molecular genetic alteration in type 1 endometrial tumors, which are generally associated with hyperplasia. p53 gene mutation is not found in endometrial hyperplasia, but researchers have detected this mutation in 20% of cases of endometrial carcinoma and 90% of cases of serous endometrial tumors. Cyclooxygenase-2 is important in tumorogenic transformation of hyperlasia. Expression of cyclooxygenase-2 decreases apoptosis, increases angiogenesis, and is related to invasiveness. Cyclooxygenase-2 expression increases significantly in cases of well-differentiated endometrial adenocarcinoma. Prostaglandin E2 is known to regulate aromatase gene expression and is the product of cyclooxygenase-2. The data about aromatase inhibitors are promising; in breast cancer patients, treatment with tamoxifen induces uterine abnormalities as early as 3 months after the initiation of therapy. In contrast, these abnormalities are not seen in patients who receive aromatase inhibitors and switched therapy after tamoxifen withdrawal may reverse tamoxifen-associated endometrial thickening.

Original languageEnglish (US)
Pages (from-to)133-138
Number of pages6
JournalEuropean Journal of Cancer Prevention
Volume17
Issue number2
DOIs
StatePublished - Apr 2008
Externally publishedYes

Fingerprint

Endometrial Hyperplasia
Endometrial Neoplasms
Cyclooxygenase 2
Tamoxifen
Hyperplasia
Aromatase Inhibitors
Mutation
Adenocarcinoma
Retinaldehyde
Aromatase
p53 Genes
Progesterone Receptors
Tumor Biomarkers
Insulin-Like Growth Factor I
Dinoprostone
Progesterone
Molecular Biology
Neoplasms
Oxidoreductases
Estrogens

Keywords

  • Biology
  • Endometrial cancer
  • Endometrial hyperplasia
  • Prevention

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

From endometrial hyperplasia to endometrial cancer : Insight into the biology and possible medical preventive measures. / Boruban, Melih C.; Altundag, Kadri; Kilic, Gokhan; Blankstein, Josef.

In: European Journal of Cancer Prevention, Vol. 17, No. 2, 04.2008, p. 133-138.

Research output: Contribution to journalArticle

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