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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:〔Resistance to cancer chemotherapy: failure in drug response from ADME to P-gp. http://www.cancerci.com/content/15/1/71〕 *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, research has been aimed at blocking specific efflux mechanisms. Treatment of cancer is complicated by the fact that there is 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. ==See also== *Antineoplastic drugs *Drug resistance 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Antineoplastic resistance」の詳細全文を読む スポンサード リンク
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