Endometrial Carcinoma MCQ — NEET PG Practice Question | NEETPGAI
Endometrial Carcinoma
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A 62-year-old postmenopausal woman presents with vaginal bleeding for 2 months. Transvaginal ultrasound shows an endometrial thickness of 8 mm with a polypoid mass. Histology confirms endometrial adenocarcinoma. The structure marked **B** in the diagram shows a polypoid endometrial mass with myometrial invasion. Which of the following molecular/genetic profiles is MOST COMMONLY associated with this type of endometrial carcinoma in this patient?
A. TP53 mutations with p53-aberrant immunohistochemistry and serous morphology (Type II non-endometrioid carcinoma)
B. Isolated BRCA1/BRCA2 mutations without TP53 involvement
C. POLE exonuclease domain mutations with ultramutated phenotype
D. PTEN, PIK3CA, KRAS, and ARID1A mutations with mismatch repair gene alterations (Type I endometrioid adenocarcinoma)
Explanation
Why option 1 is correct
The structure marked B represents endometrial adenocarcinoma with myometrial invasion. According to the TCGA molecular classification and Bokhman's dualistic model, Type I endometrioid adenocarcinoma (which accounts for 80–85% of endometrial cancers) is characterized by PTEN, PIK3CA, KRAS, ARID1A mutations and mismatch repair gene alterations (including Lynch syndrome-associated mutations). This type is estrogen-dependent, arises from endometrial hyperplasia with atypia (EIN), typically presents as a polypoid mass in postmenopausal women, and carries a relatively favorable prognosis compared to Type II. The patient's age (62), postmenopausal status, and polypoid morphology are classic for Type I endometrioid carcinoma. [FIGO Cancer Report 2023; TCGA Nature 2013; NCCN Uterine Neoplasms 2024]
Why each distractor is wrong
Option 2 (TP53 mutations, serous morphology): This describes Type II non-endometrioid carcinoma (serous, clear cell, carcinosarcoma), which accounts for only 10–15% of endometrial cancers, arises from atrophic endometrium, is estrogen-independent, and carries worse prognosis. It is NOT the most common molecular profile.
Option 3 (POLE mutations): While POLE-ultramutated endometrial cancers represent one of the four TCGA prognostic groups and carry the best prognosis, they account for a small minority (<5%) of endometrial cancers and are not the most common molecular profile.
Option 4 (BRCA1/BRCA2 without TP53): BRCA mutations are associated with ovarian and breast cancer predisposition, not the typical molecular signature of endometrial adenocarcinoma. This is a distractor unrelated to endometrial cancer pathogenesis.
High-YieldNEET PG
Type I endometrial adenocarcinoma (80–85% of cases) = estrogen-dependent + PTEN/PIK3CA/KRAS/ARID1A mutations + arises from EIN + good prognosis; Type II (10–15%) = estrogen-independent + TP53-mutant + serous morphology + poor prognosis.
