Molecular pathology of endometrial carcinoma

Molecular pathology of endometrial carcinoma

This review paper discusses the main molecular alterations of endometrial carcinoma, the most common cancer of the female genital tract. Two clinicopathological variants are recognized: the oestrogen‐related (type I, endometrioid carcinoma) and the non‐oestrogen‐related (type II, non‐endometrioid ca...

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Veröffentlicht in:Histopathology 2013-01, Vol.62 (1), p.111-123
Hauptverfasser: Matias-Guiu, Xavier, Prat, Jaime
Format: Artikel
Sprache:eng
Schlagworte:
apoptosis
beta Catenin
Biomarkers, Tumor - genetics
Carcinoma, Endometrioid - genetics
Carcinoma, Endometrioid - pathology
Chromosomal Instability
Class I Phosphatidylinositol 3-Kinases
DNA, Neoplasm - analysis
E-cadherin
endometrial carcinoma
Endometrial Neoplasms - genetics
Endometrial Neoplasms - pathology
Female
Gene Expression
Genes, ras - genetics
Humans
K-RAS
Microsatellite Instability
molecular genetics
Pathology
Phosphatidylinositol 3-Kinases - genetics
PIK3CA
PTEN
PTEN Phosphohydrolase - genetics
Reproductive system
TP53
Tumor Suppressor Protein p53 - genetics
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Zusammenfassung:This review paper discusses the main molecular alterations of endometrial carcinoma, the most common cancer of the female genital tract. Two clinicopathological variants are recognized: the oestrogen‐related (type I, endometrioid carcinoma) and the non‐oestrogen‐related (type II, non‐endometrioid carcinoma). Whereas type I shows microsatellite instability and mutations in PTEN, PIK3CA, K‐RAS and CTNNB1 (beta‐catenin), type II exhibits TP53 mutations and chromosomal instability. Recent investigations regarding the role of non‐coding RNA have provided important information regarding tumour progression. Understanding pathogenesis at the molecular level is essential for identifying biomarkers of potential use in targeted therapies.
ISSN:0309-0167
1365-2559
DOI:10.1111/his.12053