Antineoplastic resistance is the multidrug resistance of neoplastic (cancerous) cells, rather than drug resistance involving microorganisms such as bacteria, fungi and viruses. Cancer cells have the ability to become resistant to multiple drugs by many mechanisms:
- Increased efflux of drug (as by P-glycoprotein (ABCB1), multidrug resistance-associated protein (ABCC1), and breast cancer resistance protein (also known as mitoxantrone resistance associated protein, MXR, or ABCG2)
- Enzymatic deactivation (i.e., glutathione conjugation)
- Decreased permeability (drugs cannot enter the cell)
- Altered binding-sites
- Alternate metabolic pathways (the cancer compensates for the effect of the drug).
Because efflux is a significant contributor for multidrug resistance in cancer cells, current research is aimed at blocking specific efflux mechanisms. Treatment of cancer is complicated by the fact that there is such a variety of different DNA mutations that cause or contribute to tumor formation, as well as myriad mechanisms by which cells resist drugs.
Notable differences between antibiotic drugs and antineoplastic (anticancer) drugs that complicate their design are that cancer cells are altered human cells and thus more difficult to damage without damaging healthy cells.
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