Drug resistance in tumors (MDR)

Drug resistance in tumors is a multifaceted physiological phenomenon where cancer cells develop the ability to survive and proliferate despite exposure to cytotoxic or targeted therapeutic agents [1][2]. This process is not a single molecular receptor or enzyme but a clinical challenge involving diverse mechanisms, such as increased drug efflux mediated by transporters like P-glycoprotein (ABCB1), enhanced DNA repair capacity, and the evasion of programmed cell death (apoptosis) [3]. Resistance can be intrinsic, where pre-existing genetic traits render the tumor unresponsive from the start, or acquired, where cells evolve resistance through mutations or epigenetic changes during the course of treatment [4]. In clinical oncology, this leads to treatment failure and disease recurrence, necessitating the use of combination therapies or the development of next-generation inhibitors that can bypass or inhibit specific resistance-conferring proteins [2][5]. Citations: [1] Vasan N, et al. Nature. 2019;575(7782):299-309. [2] Mansoori B, et al. Adv Pharm Bull. 2017;7(3):339-348. [3] Robey RW, et al. Nat Rev Cancer. 2018;18(7):452-464. [4] Holohan C, et al. Nat Rev Cancer. 2013;13(10):714-726. [5] NIH NCI Dictionary of Cancer Terms.

Other names

Multidrug resistanceChemoresistanceAntineoplastic resistanceAcquired drug resistanceIntrinsic drug resistanceTumor resistance

Drug resistance is a biological phenomenon rather than a single molecular target; it involves multiple mechanisms including active drug efflux via ATP-binding cassette (ABC) transporters, metabolic inactivation by enzymes like Cytochrome P450, and the modification of drug targets through genetic mutation [1][2][4].