Endometrial adenocarcinoma type II (serous endometrial carcinoma) has distinct molecular features compared to type I (endometrioid). Which molecular alteration is characteristic of serous endometrial carcinoma?

• A PTEN deletion, microsatellite instability, and KRAS mutations; estrogen-driven
• B CDH1 (E-cadherin) mutation causing dedifferentiation
• C CTNNB1 (beta-catenin) mutation with nuclear accumulation
• D TP53 mutation and HER2 amplification; non-estrogen-dependent, arises in atrophic endometrium ✓

Explanation

Type II serous endometrial carcinoma is characterized by TP53 mutations (~90%), frequent HER2 amplification (~30%), and absence of estrogen receptor expression. It arises in atrophic endometrium via endometrial intraepithelial carcinoma (EIC, the in-situ precursor), is not estrogen-driven, is high grade, and has aggressive behavior with early peritoneal spread. Type I endometrioid carcinoma is characterized by PTEN loss (~80%), microsatellite instability (~20-30%), KRAS mutations, and CTNNB1 mutations — arising in a background of endometrial hyperplasia driven by unopposed estrogen.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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