İntaş, AdarMuslubaş, BerkeYılmazer Aktar, BerinAysan, ArzuAksu, Soner2026-09-202026-09-202026İntaş, A., Muslubaş, B., Yılmazer Aktar, B., Aysan, A., & Aksu, S. (2026, 17-19 Eylül). Investigation of the relationship between cancer and the homologous recombination repair (HRR) mechanism. [Poster]. 10th International Congress of the Molecular Biology Association of Türkiye, İstanbul, Türkiye.https://hdl.handle.net/20.500.13055/1657Background/Aim: A strong correlation exists between Double-strand breaks (DSBs), genomic instability, and cancer development. Homologous Recombination Repair (HRR) is the primary repair mechanism for highly accurate DSB repair. This study aimed to investigate the relationship between cancer and selected 12 genes involved in the HRR mechanism. Materials and Methods: Using the RT-qPCR analysis differences in the expression levels of the Ataxia Telangiectasia Mutated (ATM), BRCA1 Interacting Protein C-Terminal Helicase 1 (BRIP1), Fanconi Anemia Complementation Group D2 (FANCD2), Tumor Protein p53 Binding Protein 1 (TP53BP1), DNA Polymerase Theta (POLQ), RAD54 Like (RAD54L), AT-Rich Interaction Domain 1A (ARID1A), RAD52 DNA Repair Protein (RAD52), Bloom Syndrome Protein (BLM), SWI/SNF-Related Matrix-Associated Actin-Dependent Regulator of Chromatin Subfamily A Containing DEAD/H Box 1 (SMARCAD1), Werner Syndrome ATPDependent, Helicase (WRN) and RecQ Like Helicase 4 (RECQL4) genes between cancer and normal cell lines were investigated. Frequently used 10 cancer and 2 normal cell lines were used in this study. Results: It was determined that RAD52 was significantly up-regulated only in colon cancer cell lines. ARID1A was significantly down-regulated, particularly in breast and lung cancer. BLM, WRN, TP53BP1, ATM and RAD54L were down-regulated in all cancer types. RECQL4 was down-regulated in breast and lung cancer, but up-regulated in liver and brain cancer. BRIP1 was down-regulated in breast, brain, and lung cancer, but up-regulated in liver and colon cancer cell lines. FANCD2 was up-regulated only in lung cancer, and significantly down-regulated in all other cancer types. POLQ was significantly down regulated especially in lung cancer. Conclusion: This study has provided preliminary results suggesting that the expression differences observed in the interested genes could be used as a molecular indicator for the carcinogenesis. Meaningful results have also been obtained indicating that diagnostic panels based on gene expression levels can be developed for monitoring cancer progression.eninfo:eu-repo/semantics/closedAccessDouble-Strand BreaksHomologous Recombination RepairCancer Cell LinesGene ExpressionRT-qPCRConference Object