Drug Resistance in Cancer Cells

Kapil Mehta

Verlag: Springer-Verlag Gmbh Mai 2009, 2009
ISBN 10: 0387894446 / ISBN 13: 9780387894447
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Neuware - It was estimated that in 2008, 1,437,180 patients would receive a new cancer diagnosisand 565,650individualswould die of cancer (Jemal et al. 2008).Since the vast majority of patients dying of cancer will have had anticancer therapy, both c- ventional chemotherapy and novel targeted therapy, it can be concluded that these patients are dying with drug resistant cancer. The term multidrug resistance is also apt - in that these patients die after having undergone multiple rounds of different and structurally unrelated cancer therapies. However, for some, the concept of m- tidrug resistance is a worn out idea, stemming from disappointment with the drug resistancereversalstrategiesthatwerecarriedoutinthe1990susingpumpinhibitors to block drug resistance mediated by P-glycoprotein, product of the MDR-1 gene. However, if one takes the larger de nition - multidrug resistance as simultaneous resistance to multiple structurally unrelated anticancer therapies - its existence c- not be denied. The purpose of this book is to explore new concepts related to drug resistance in cancer, including resistance to the new molecularly targeted agents. Perhaps new terminology is needed for resistance that occurs following therapy with the targeted agents: Novel Targeted Agent Resistance (NTR). Alternatively, we can return to the original de nition of multidrug resistance as simply the res- tance to multipleagents that occurs in the course of normalcancer progression.This resistance is likely to be mediated by many factors. 363 pp. Englisch. Buchnummer des Verkäufers 9780387894447

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Reseña del editor: It was estimated that in 2008, 1,437,180 patients would receive a new cancer diagnosisand 565,650individualswould die of cancer (Jemal et al. 2008).Since the vast majority of patients dying of cancer will have had anticancer therapy, both c- ventional chemotherapy and novel targeted therapy, it can be concluded that these patients are dying with drug resistant cancer. The term multidrug resistance is also apt – in that these patients die after having undergone multiple rounds of different and structurally unrelated cancer therapies. However, for some, the concept of m- tidrug resistance is a worn out idea, stemming from disappointment with the drug resistancereversalstrategiesthatwerecarriedoutinthe1990susingpumpinhibitors to block drug resistance mediated by P-glycoprotein, product of the MDR-1 gene. However, if one takes the larger de?nition – multidrug resistance as simultaneous resistance to multiple structurally unrelated anticancer therapies – its existence c- not be denied. The purpose of this book is to explore new concepts related to drug resistance in cancer, including resistance to the new molecularly targeted agents. Perhaps new terminology is needed for resistance that occurs following therapy with the targeted agents: Novel Targeted Agent Resistance (NTR). Alternatively, we can return to the original de?nition of multidrug resistance as simply the res- tance to multipleagents that occurs in the course of normalcancer progression.This resistance is likely to be mediated by many factors.

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Titel: Drug Resistance in Cancer Cells
Verlag: Springer-Verlag Gmbh Mai 2009
Erscheinungsdatum: 2009
Einband: Buch
Zustand: Neu

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Woolley, Paul V. und Kenneth D. Tew:
Verlag: San Diego - New York - Berkeley - Boston - London - Sydney - Tokyo, Academic Press, (1988)
ISBN 10: 0127633626 ISBN 13: 9780127633626
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Buchbeschreibung San Diego - New York - Berkeley - Boston - London - Sydney - Tokyo, Academic Press, 1988. hard cover. Zustand: Gut. 390 pp., illustrations library marking ISBN 0127633626 Sprache: Deutsch. Artikel-Nr. 52594

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Aanchal Sharma
Verlag: SPS Feb 2018 (2018)
ISBN 10: 620230457X ISBN 13: 9786202304573
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Buchbeschreibung SPS Feb 2018, 2018. Taschenbuch. Zustand: Neu. Neuware - Due to substantial technical improvements, clinical application of heat as a co-adjuvant in cancer treatment is acquiring new interest. The effect of hyperthermia on hepatoma cell lines Hep3B (p53 defective) and HepG2 (p53 wild type) when investigated led to an interesting observation that Hep3B cells are more susceptible to heat stress than HepG2 cells. In addition, heat-induced carboplatin resistance was observed in HepG2 cells only. To investigate the reasons, heat shock response was explored and it was observed that heat stress augmented heat shock protein 70 (Hsp70) expression levels in HepG2 and not in Hep3B cells. Furthermore, in HepG2 cells, induced Hsp70 is regulated by both p53 and heat shock transcription factor 1 (HSF1) wherein HSF1 levels are modulated by p53. The data implies that Hep3B are more susceptible to death upon heat stress than HepG2 cells because of non-induction of Hsp70. In addition, it was observed that inhibition of heat-induced p53 / HSF1 diminishes Hsp70 levels, thereby restoring the sensitivity of heat-stressed HepG2 cells to carboplatin-triggered cell death. 88 pp. Englisch. Artikel-Nr. 9786202304573

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