Uterin Endometrioid Karsinomlar ve Seröz Karsinomlarda Moleküler Değişiklikler ve Sağkalım Analizlerinin Karşılaştırılması: İn Silico Çalışma

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YILMAZ Z. S.

Archives of current medical research (ACMR) (Online), cilt.7, sa.1, ss.244-254, 2026 (TRDizin)

Özet

Background: Endometrioid and serous endometrial carcinomas exhibit distinct molecular, epigenetic, and clinical charac- teristics. This study aimed to compare mutations, survival, and biological pathway analysis between these two subtypes using an in silico approach. Methods: Endometrioid (n=399) and serous (n=109) carcinomas from The Cancer Genome Atlas Uterine Corpus Endo- metrial Carcinoma (PanCancer Atlas) dataset were analyzed via cBioPortal. Genomic mutations, mRNA expression lev- els, MSI (microsatellite instability) sensor scores and overall survival were compared. Differentially mutated genes were identified. P< 0.0.5 and q< 0.05 were considered statistically significant. Pathway enrichment analyses were performed using g:Profiler and WebGestalt. Results: 662 genomic mutations and 10757 mRNA expression levels showed significant differences. In endometrioid car- cinomas, PTEN, ARID1A, CTNNB1, CTCF, KMT2B, KRAS, NEB, and RNF43 were the most significantly mutated genes; whereas in serous carcinomas, TP53 and PPP2R1A were the predominantly mutated genes (p<0.001 and q<0.001). The MSI-High rate was higher in endometrioid tumors (31.6% vs. 0.9%, p = 7.215e-3). The median survival was 102.83 months in endometrioid tumors and 63.91 months in serous tumors (p=5.28e-8). Pathway analyses revealed enrichments in pro- teasome, mismatch repair, DNA replication, spliceosome, base excision repair, as well as developmental and metabolic pathways. Conclusion: It was observed that endometrioid tumors develop through gradual genetic disruptions within the PI3K– PTEN–AKT–mTOR and WNT/β-catenin axes, whereas serous tumors develop through high genomic instability driven by TP53 mutations, and DNA repair pathway defects. This molecular distinction explains the more aggressive clinical be- havior and lower survival rates of serous carcinomas, emphasizing the importance of specific diagnostic and therapeutic strategies.