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Abstract
Prostate cancer remains a significant global health issue, ranking as a leading cause of cancer-related mortality in men, with rising incidence rates. Docetaxel (DOC) is a primary chemotherapeutic agent for treating this cancer. However, the practical implementation of personalized pharmacogenetic-guided DOC therapy in clinical settings is still in progress. This study aims to explore pharmacogenomic approaches in analyzing the impact of genetic variations in key genes involved in drug metabolism, including cytochrome P450 enzymes (CYP3A4, CYP3A5, CYP1B1), ATP-binding cassette transporters (ABCB1, ABCC2, ABCG2), and solute carrier family members (SLCO1B1/OATP1B1, SLCO1B3/OATP1B3), on the efficacy of DOC in prostate cancer treatment. A narrative review was conducted (2004–2024) on genetic variations affecting docetaxel (DOC) metabolism in prostate cancer, using searches in PubMed, Google Scholar, Scopus, and ScienceDirect. Focused on clinical and genetic studies, highlighting personalized treatment strategies. The review highlights the influence of genetic variations in drug metabolism pathways, particularly in genes such as CYP3A4, ABCB1, and SLCO1B1, on DOC efficacy, toxicity, and overall survival. Additional genes like GSTP1, MDR1, CHST3, and KDM5D also play crucial roles. Furthermore, this study underscores the importance of localized pharmacogenomic research in Indonesia to identify region-specific genetic variations that could refine treatment strategies. Personalized prostate cancer treatment based on pharmacogenomic insights can enhance therapeutic outcomes and reduce side effects. Localized research in Indonesia is essential to optimize DOC-based therapy and improve patient care.





