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. Author manuscript; available in PMC: 2010 Feb 1.
Published in final edited form as: Nat Rev Cancer. 2009 Jun;9(6):415. doi: 10.1038/nrc2644
Type Histology Precursor Molecular features
I Low-grade serous carcinoma Cystadenoma–borderline tumour–carcinoma sequence Mutations in KRAS and/or BRAF (≥ 60%)
I Low-grade endometrioid carcinoma Endometriosis and endometrial cell-like hyperplasia* Mutations in CTNNB1, PTEN and PIK3CA with microsatellite instability
I Mucinous carcinoma Cystadenoma–borderline tumour–carcinoma sequence; metastases from bowel Mutations in KRAS; TP53 mutation associated with transition from borderline tumour to carcinoma
I Clear cell carcinoma Endometriosis PTEN mutation or loss of heterozygosity; PIK3CA mutation
II High-grade serous carcinoma De novo in epithelial inclusion cysts; fallopian tube TP53 mutation (up to 80%) and BRCA1 dysfunction
II High-grade
endometrioid carcinoma
Epithelial inclusion glands or cysts TP53 mutation and BRCA1 dysfunction; PIK3CA mutation
*

Endometriosis and adjacent low-grade endometrioid carcinoma share common genetic events such as loss of heterozygosity at the same loci involving the same allele (for example, PTEN). By contrast, high-grade and poorly differentiated endometrioid carcinomas are similar to high-grade serous carcinomas.

PIK3CA at 3q26 encodes the p110α catalytic subunit of PI3K19.