Epidermal Growth Factor Receptor (EGFR) Mutations in Rare Histological Subtypes of Ovarian Cancer

BackgroundOvarian cancer comprises a heterogeneous group of malignancies with distinct molecular profiles across histological subtypes.While the molecular landscape of high-grade serous ovarian carcinoma (HGSOC) has been extensively investigated, data regarding rare epithelial and non-epithelial ovarian tumors remain limited.The clinical relevance of epidermal growth factor receptor (EGFR) alterations in ovarian cancer is still uncertain, particularly in uncommon histological subtypes.This study aimed to investigate the presence of clinically relevant EGFR mutations in rare ovarian cancer subtypes. MethodsA retrospective molecular analysis was performed on 24 formalin-fixed paraffin-embedded ovarian tumor tissue samples collected between 2010 and 2022.The cohort included five mucinous ovarian carcinomas, five clear cell ovarian carcinomas, five non-epithelial ovarian tumors, and nine low-grade serous ovarian carcinomas (LGSOCs).DNA was extracted from tumor tissue containing at least 25% tumor cellularity.EGFR mutation analysis was performed using the Cobas® EGFR Mutation Test v2 (Roche Molecular Systems Inc., Branchburg, New Jersey, USA), a real-time PCR-based assay capable of detecting 42 predefined mutations across exons 18-21. ResultsAll 24 samples yielded valid molecular results, with no assay failures or quality-control abnormalities.No EGFR mutations were detected in any of the analyzed specimens.Specifically, no alterations were identified in exons 18, 19, 20, or 21, including G719X, exon 19 deletions, S768I, T790M, exon 20 insertions, L858R, or L861Q.EGFR mutation status was uniformly negative across all investigated histological subtypes, including mucinous, clear cell, non-epithelial, and low-grade serous ovarian tumors.Results were concordant across independent analytical runs. ConclusionIn this cohort of rare ovarian cancer histological subtypes, no activating EGFR mutations were identified.These findings support the limited role of EGFR mutations in the molecular pathogenesis of these ovarian tumors and suggest that routine EGFR mutation testing is unlikely to provide substantial therapeutic benefit.Larger studies incorporating broader genomic profiling are warranted to identify alternative molecular alterations with potential prognostic or therapeutic relevance.