Cancer Drug Resistance (Cancer Drug Discovery and by Beverly A. Teicher

By Beverly A. Teicher

Major specialists summarize and synthesize the most recent discoveries in regards to the alterations that take place in tumor cells as they strengthen resistance to anticancer medicinal drugs, and recommend new ways to fighting and overcoming it. The authors evaluation physiological resistance established upon tumor structure, mobile resistance in line with drug shipping, epigenetic adjustments that neutralize or pass drug cytotoxicity, and genetic alterations that adjust drug objective molecules via lowering or putting off drug binding and efficacy. Highlights contain new insights into resistance to antiangiogenic treatments, oncogenes and tumor suppressor genes in healing resistance, melanoma stem cells, and the improvement of more desirable treatments. There also are new findings on tumor immune get away mechanisms, gene amplification in drug resistance, the molecular determinants of multidrug resistance, and resistance to taxanes and Herceptin.

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VEGF-VEGF receptor complexes as markers of tumor vascular endothelium. J Control Release 2001; 74:173–181. 30. Haroon ZA, Lai TS, Hettasch JM, Lindberg RA, Dewhirst MW, Greenberg CS. Tissue transglutaminase is expressed as a host response to tumor invasion and inhibits tumor growth. Lab Invest 1999; 79:1679–1686. 31. Hettasch JM, Bandarenko N, Burchette JL, et al. Tissue transglutaminase expression in human breast cancer. Lab Invest 1996; 75:637–645. 32. Iacobuzio-Donahue CA, Ashfaq R, Maitra A, et al.

2. At Elevated Temperatures Although the effect of methylmethane sulphonate (115), BCNU (115,131), methotrexate (137), bleomycin (115,131,134), and amphotericin B (4,115,131) were independent of the environmental pH at 37°C, their cytotoxicity increased in a low-pH environment if the cells were heated (see Table 2). Interestingly, the cytotoxicity of amphotericin B also increased when the environment was made alkaline at elevated temperatures (4,115). Hahn (138) suggested that heat may increase the cellular uptake of certain drugs or inhibit the repair of damage caused by drugs, and the acidic environment accentuates these processes.

6 medium, significant portions of cells were still in G2 arrest 72 h after irradiation (Fig. 6). Interestingly, the radiationinduced G2 arrest in acidic pH medium rapidly decayed as soon as the acidic pH medium was replaced with neutral pH medium (100). Importantly, the apoptosis and clonogenic cell death caused by irradiation were significantly less in acidic medium than in neutral pH medium (Fig. 7). It appeared that the increase in radioresistance in acidic pH environment resulted from an increased DNA damage repair during the prolonged G2 arrest.

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