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Molecular Pathology of
Endometrial Cancer
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Region Incidence Overall Incidence Males Incidence Females Deaths Overall Deaths Males Deaths Females
USA 43470 0 43470 7950 0 7950

Affected Protein Pathway Sub-Type Ethnicity Stage Frequency (%) Gene Amplification Activating Mutation Inactivating Mutation Deletion Promoter Hypermethylation Comment  
FGFR-2 (k-sam) Receptor Tyrosine Kinase Signaling
primary uterine tumor endometrioid subtype 16%
p53 p53 Tumor Suppressor Pathway
high-grade endometrioid adenocarcinomas 17% rare in low-grade endometrioid adenocarcinomas
p53 p53 Tumor Suppressor Pathway
non-endometrioid adenocarcinomas 54 - 85% Immunohistochemical overexpression of p53
Pi3-kinase PI3-Kinase Signaling
endometrial carcinoma 30 - 36% frequent coexistence of PIK3CA and PTEN mutations in endometrial carcinomas
PTEN PI3-Kinase Signaling
endometrial carcinomas 30 - 54% more frequent in endometrioid adenocarcinomas than in non-endometrioid adenocarcinomas
PTEN PI3-Kinase Signaling
endometrial carcinomas 68% absence of protein expression
PTEN PI3-Kinase Signaling
endometrial carcinomas 19%

See Clinical Trials in in the TTC Database
CANCER.GOV PDQ® - Standard Treatments for Endometrial Cancer