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SUMMARY OBJECTIVE: The objective of this study was to analyze the genetic alterations of tumors within the scope of the homologous recombination deficiency gene panel in patients diagnosed with synchronous endometrial ovarian cancer who have been followed for over 5 years using next-generation sequencing. METHODS: DNA was isolated from the patient’s formalin-fixed, paraffin-embedded tissue blocks. Next-generation sequencing was performed using the Illumina capture-based sequencing method. Samples were sequenced using the Sophia HR Solution DNA Kit. RESULTS: Seven patients were included in this study. The ratios of likely pathogenic (LP)/pathogenic (P) somatic mutations in ATM (serine/threonine kinase or Ataxia-telangiectasia mutated gene), BRCA2 (breast cancer type 2 susceptibility gene), BARD1 (BRCA1 associated RING domain 1), TP53 (tumor protein p53), BIRP1 (BRCA1-interacting helicase 1 gene), PALB2 (partner and localizer of BRCA2), and CHECK2 were 21 (48.8%), 8 (18.6%), 5 (11.6%), 3 (6.9%), 2 (4.6%), 2 (4.6%), and 2 (4.6%), respectively, in endometrium, and the ratios of somatic mutations in ATM, BRCA2, TP53, BARD1, RAD54L (DNA repair/recombination protein like), BIRP1, and RAD51D (RAD51 recombinase paralog D) were 24 (60%), 6 (15%), 5 (12.5%), 2 (5%), 2 (5%), 1 (2.5%), and 1 (2.5%), respectively, in ovary. In endometrioid-synchronous endometrial ovarian cancer cases, P/LP mutations were observed in ATM and CHECK2 genes in endometrium and ATM, BRCA2, and TP53 genes in ovary. In two non-endometrioid-synchronous endometrial ovarian cancer cases, CHEK2 (checkpoint kinase 2) mutations were observed in endometrium and ATM and TP53 mutations in ovary, whereas in one case, P/LP mutations in ATM and TP53 genes were common in both tissues. CONCLUSION: Pathogenic variations confirming the diagnosis of synchronous endometrial ovarian cancer with genetic alterations were identified in all but one case. ATM gene mutation emerged as the most common alteration and has a potential association with a favorable prognosis. OBJECTIVE nextgeneration next generation METHODS patient s formalinfixed, formalinfixed formalin fixed, fixed formalin-fixed paraffinembedded paraffin embedded blocks Nextgeneration Next capturebased capture based method Kit RESULTS LP/pathogenic LPpathogenic LP /pathogenic P (P serine/threonine serinethreonine serine threonine Ataxiatelangiectasia Ataxia telangiectasia gene, , gene) BRCA breast BARD BRCA1 (BRCA 1, 1) TP TP5 tumor p53, p53 p p53) BIRP BRCA1interacting BRCAinteracting interacting PALB partner BRCA2) CHECK 48.8%, 488 48.8% 48 (48.8%) 18.6%, 186 18.6% 18 (18.6%) 11.6%, 116 11.6% 11 (11.6%) 6.9%, 69 6.9% 9 (6.9%) 4.6%, 46 4.6% 4 (4.6%) respectively RADL RAD L repairrecombination repair like, like like) RADD D RAD51 (RAD5 60%, 60 60% (60%) 15%, 15 15% (15%) 12.5%, 125 12.5% 12 (12.5%) 5%, 5% (5%) 2.5%, 25 2.5% (2.5%) ovary endometrioidsynchronous endometrioid cases PLP nonendometrioidsynchronous non CHEK checkpoint case tissues CONCLUSION prognosis p5 48.8 (48.8% 18.6 (18.6% 11.6 (11.6% 6.9 (6.9% 4.6 (4.6% RAD5 (RAD (60% (15% 12.5 (12.5% (5% 2.5 (2.5% 48. (48.8 18. (18.6 11. (11.6 6. (6.9 4. (4.6 (60 (15 12. (12.5 (5 2. (2.5 (48. (18. (11. (6. (4. (6 (1 (12. ( (2. (48 (18 (11 (4 (12 (2