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Drug resistance is defined as the ability of an organism or cell to survive and proliferate despite the presence of a drug that would normally inhibit or kill it. It arises through various mechanisms including enzymatic drug modification, alteration of drug targets, increased efflux of drugs, reduced drug uptake, and other adaptive changes at the genetic or epigenetic level[1][3][7]. "Drug resistance" can be intrinsic (natural, always present) or acquired (develops through mutation or horizontal gene transfer)[3][7]. It is a major problem in the treatment of infectious diseases (such as bacterial infections) and cancer, leading to persistent disease and increased public health risk[9]. The underlying specific molecular determinants—such as beta-lactamases, efflux pumps, or mutation in target enzymes—are what serve as true drug targets for overcoming resistance. If your use case requires a "target" suitable for structured drug annotation, you should instead identify the specific molecular cause of resistance (e.g., "Beta-lactamase," "Multidrug resistance-associated protein 1 (MRP1)," "P-glycoprotein," "DNA gyrase (GyrA)," etc.), not the overarching phenomenon of "drug resistance."
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