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Deoxyribonucleoside metabolism refers to the network of biochemical pathways by which cells generate, salvage, and regulate deoxyribonucleosides and deoxyribonucleotides—the building blocks of DNA—through de novo biosynthesis, salvage pathways, and catabolic processes. These interconnected reactions are essential for maintaining adequate dNTP pools required for DNA synthesis and repair. Dysregulation has implications in cancer (where rapid DNA synthesis makes these pathways therapeutic targets) and in inherited metabolic diseases. The pathway involves numerous enzymes (e.g., ribonucleotide reductase, thymidylate synthase, dihydrofolate reductase, deoxycytidine kinase), many of which are individually druggable and serve as established cancer targets. However, "deoxyribonucleoside metabolism" as a term is not itself a discrete molecular target but rather a functional grouping of many targets. Key context: Individual enzymes within deoxyribonucleoside metabolism (such as ribonucleotide reductase or thymidylate synthase) are validated drug targets, especially in oncology, where their inhibition blocks DNA replication and cell proliferation. Drugs impacting this pathway include antimetabolites (e.g., hydroxyurea, 5-fluorouracil, methotrexate), which target specific enzymes, not the pathway as a whole. Pathway-level disruption can result in toxicities such as myelosuppression. Enzyme activity and dNTP pool balance can serve as biomarkers for some cancer therapies. Because "deoxyribonucleoside metabolism" refers to an entire process and not a defined molecular target, it should not be listed as a canonical drug target. For structured information, individual enzymes or molecular targets within this pathway should be specified instead.
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