Download Cancer Drug Resistance by Mark W. Dewhirst DVM, PhD, Yiting Cao MD, PhD, Benjamin PDF
By Mark W. Dewhirst DVM, PhD, Yiting Cao MD, PhD, Benjamin Moeller PhD, Chuan-Yuan Li PhD (auth.), Beverly A. Teicher PhD (eds.)
As genomic recommendations progressively exhibit the facility of malignant cells to reply to chemical and organic insults with extraordinary flexibility of phenotype, it turns into transparent that a lot is still performed to regulate and do away with such cells. In melanoma Drug Resistance, major scientists from the simplest educational associations and business laboratories summarize and synthesize the newest discoveries about the alterations that happen in tumor cells as they strengthen resistance to a large choice of anticancer therapeutics, in addition to recommend new techniques to the biology of drug resistance which could find the money for new healing possibilities. The authors evaluation physiological resistance dependent tumor structure, mobile resistance in accordance with drug shipping, epigenetic adjustments that neutralize or skip drug cytotoxicity, and genetic adjustments that adjust drug goal molecules via reducing or getting rid of drug binding and efficacy. Highlights comprise new insights into resistance to antiangiogenic cures, oncogenes and tumor suppressor genes in healing resistance, melanoma stem cells, and the improvement of more suitable cures. 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®.
Authoritative and insightful, melanoma Drug Resistance bargains easy and scientific investigators a state of the art synthesis of the numerous faceted learn now to be had at the biology and genetics of tumor resistance, in addition to intriguing new methods to its prevention and eradication.
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Haroon ZA, Raleigh JA, Greenberg CS, Dewhirst MW. Early wound healing exhibits cytokine surge without evidence of hypoxia. Ann Surg 2000; 231:137–147. 61. Graeber TG, Osmanian C, Jacks T, et al. Hypoxia-mediated selection of cells with diminished apoptotic potential in solid tumours. Nature 1996; 379:88–91. 62. Dvorak HF. Tumors: wounds that do not heal. Similarities between tumor stroma generation and wound healing. N Engl J Med 1986; 315:1650–1659. 63. Teicher BA, Sotomayor EA, Huang ZD. Antiangiogenic agents potentiate cytotoxic cancer therapies against primary and metastatic disease.
HIF-1 has been demonstrated to activate transcription of as many as 70 genes including glucose transporters and glycolytic enzymes, which may account for the increased anaerobic glycolysis and resultant acidification of tumors under a hypoxic environment (26–28). Like hypoxia, acidosis also upregulates transcription factors and activates a number of genes (77–79). We have observed that exposure of tumor cells to a low pH medium elevates significantly p53 expression and p21 expression (77). When the low pH medium was replaced with neutral pH medium, the expression of p53 and p21 promptly returned to normal level.
It has been reported that one of the mechanisms to maintain the cytosolic pH at physiological level is sequestration of cytosolic protons into acidic cellular vesicles such as endoplasmic reticulum, endosomes, and lysosomes. Interestingly, the ATPase-linked H+ pump has been identified in a number of intracellular organelles, indicating that the ATPase-linked H+ pump plays an important role in regulating pH in the vesicles and cytosol. The other two mechanisms are a H+-translocating 28 Song, Griffin, and Park Table 1 Genes Activated by Low pH AP-1 NFκB p53 p21 MTIIA GRPs Bax VEGF bFGF PDECGF IL-8 Cyclines HSPs NQO1 ATPase and a K+/H+ exchange ATPase, which can be suppressed by nigericin.