By Beverly A. Teicher
Best specialists summarize and synthesize the most recent discoveries about the alterations that happen in tumor cells as they enhance resistance to anticancer medicines, and recommend new techniques to fighting and overcoming it. The authors assessment physiological resistance dependent upon tumor structure, mobile resistance in response to drug delivery, epigenetic adjustments that neutralize or skip drug cytotoxicity, and genetic alterations that adjust drug aim molecules by means of reducing or disposing of drug binding and efficacy. Highlights contain new insights into resistance to antiangiogenic remedies, oncogenes and tumor suppressor genes in healing resistance, melanoma stem cells, and the improvement of better cures. There also are new findings on tumor immune break out mechanisms, gene amplification in drug resistance, the molecular determinants of multidrug resistance, and resistance to taxanes and Herceptin.
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Additional info for Cancer Drug Resistance (Cancer Drug Discovery and Development)
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The Na+-coupled CI–/HCO3– exchange is also inhibited by depletion of ATP, and the Na+-independent Cl–/HCO3– exchange is inactivated by a low-pH environment (62,70). The relative importance in maintaining pHi at neutral range of the different mechanisms mentioned varies markedly in different cell types and under different conditions. The lactate /H+ symport, which is inhibited by the bioflavionoids quercetin and others, is one of the most active exchange in the regulation of pHi in tumor cells (71,72).
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Cancer Drug Resistance (Cancer Drug Discovery and Development) by Beverly A. Teicher