Akademik Veri Yönetim Sistemi
European Biotechnology Congress 2025, Tirane, Arnavutluk, 11 - 13 Eylül 2025, cilt.9, sa.13, ss.19-20, (Özet Bildiri)
Chronic alcohol consumption causes dysbiosis and disrupts microbial functions. However, the potential role of alcohol-related dysbiosis in cancer development remains largely unexplored. Here, the possible contributions of alcohol-related microbiota alterations to carcinogenesis were investigated by in silico analysis. Microbial taxa associated with alcoholism were extracted from the Disbiome database, and taxon set enrichment analysis was performed to identify the gene sets related to these taxa. Host-intrinsic factors were determined using MicrobiomeAnalyst. The identified genes were then compared with the DisGeNET database to assess their functional relevance in alcohol-related comorbidities. Additionally, the cancer-related functions of the genes were evaluated using GEPIA, which utilizes public data from the Cancer Genome Atlas. Thirteen genes (FBXO34, PCDHA2, PIWIL4, CPA2, CDH20, SLC45A4, NTNG2, CHRNA2, DAPL1, TELO2, MANBA, PLXNC1, KCNIP4) were determined to be associated with alcoholism-related microbial taxa. Metabolic syndrome was the most significantly associated disease related to a total of 20 taxa. CPA2, NTNG2, DAPL1 and PLXNC1 were differentially expressed in at least one cancer dataset; DAPL1 was most commonly altered across cancer types. Our findings provide in silico evidence linking alcoholism-related dysbiosis to alcohol-induced diseases, particularly cancer, and shed light on the importance of microbiome-based strategies for risk assessment and alcohol cessation interventions.