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Published by Humana, 2009
ISBN 10: 1607611775ISBN 13: 9781607611776
Seller: HPB-Red, Dallas, TX, U.S.A.
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hardcover. Condition: Good. Connecting readers with great books since 1972! Used textbooks may not include companion materials such as access codes, etc. May have some wear or writing/highlighting. We ship orders daily and Customer Service is our top priority!.
Published by Humana Press, 2009
ISBN 10: 1607611775ISBN 13: 9781607611776
Seller: booksXpress, Bayonne, NJ, U.S.A.
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Hardcover. Condition: new.
Published by Humana Press, Totowa, N.J., 2010
ISBN 10: 1607611775ISBN 13: 9781607611776
Seller: Research Ink, Takoma Park, MD, U.S.A.
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Hardback. Condition: Very Good. Dust Jacket Condition: jacketcondition. xiv + 273 pp. Cancer Drug Discovery and Development. Rubber-stamped on front free endpaper. book.
Published by Humana Press, 2009
ISBN 10: 1607611775ISBN 13: 9781607611776
Seller: Buchpark, Trebbin, Germany
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Condition: Sehr gut. Zustand: Sehr gut - Neubindung, Buchschnitt leicht verkürzt, Buchrücken und -ecken leicht angestoßen, Auflage 2010 | Seiten: 288 | Sprache: Englisch.
Published by SPRINGER NATURE, 2009
ISBN 10: 0387894446ISBN 13: 9780387894447
Seller: Buchpark, Trebbin, Germany
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Condition: Sehr gut. Zustand: Sehr gut - Neubindung, Buchecke leicht angestossen | Seiten: 363 | Sprache: Englisch.
Published by Humana Press, 2012
ISBN 10: 1617796352ISBN 13: 9781617796357
Seller: booksXpress, Bayonne, NJ, U.S.A.
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Published by Springer, 2010
ISBN 10: 1441927948ISBN 13: 9781441927941
Seller: Ria Christie Collections, Uxbridge, United Kingdom
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Published by Springer, 2010
ISBN 10: 1441927948ISBN 13: 9781441927941
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Published by Springer, 2009
ISBN 10: 0387894446ISBN 13: 9780387894447
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Published by Springer, 2009
ISBN 10: 0387894446ISBN 13: 9780387894447
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Published by Springer, 2009
ISBN 10: 0387894446ISBN 13: 9780387894447
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Published by Springer, 2009
ISBN 10: 0387894446ISBN 13: 9780387894447
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Published by Humana Press, 2009
ISBN 10: 1607611775ISBN 13: 9781607611776
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Published by Springer, 2010
ISBN 10: 1441927948ISBN 13: 9781441927941
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Published by Humana, 2012
ISBN 10: 1617796352ISBN 13: 9781617796357
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Published by Humana, 2012
ISBN 10: 1617796352ISBN 13: 9781617796357
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Published by Springer, 2009
ISBN 10: 0387894446ISBN 13: 9780387894447
Seller: Lucky's Textbooks, Dallas, TX, U.S.A.
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Condition: New.
Published by Humana, 2009
ISBN 10: 1607611775ISBN 13: 9781607611776
Seller: Lucky's Textbooks, Dallas, TX, U.S.A.
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Condition: New.
Published by Springer, 2009
ISBN 10: 0387894446ISBN 13: 9780387894447
Seller: GreatBookPricesUK, Castle Donington, DERBY, United Kingdom
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Published by Humana Press, 2012
ISBN 10: 1617796352ISBN 13: 9781617796357
Seller: Ria Christie Collections, Uxbridge, United Kingdom
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Condition: New. PRINT ON DEMAND Book; New; Fast Shipping from the UK. No. book.
Published by Humana, 2012
ISBN 10: 1617796352ISBN 13: 9781617796357
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Published by Humana Press Sep 2009, 2009
ISBN 10: 1607611775ISBN 13: 9781607611776
Seller: BuchWeltWeit Ludwig Meier e.K., Bergisch Gladbach, Germany
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Buch. Condition: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -Much work over the last two decades has firmly established that loss of cell cycle checkpoint regulation, and resultant unabated cellular proliferation, is an inherent characteristic of cancer. This loss may occur through aberration in any single component involved in signal transduction pathways that orchestrate checkpoint regulation, which may manifest through either a failure to activate the checkpoint or a failure to respond to the activated checkpoint. In normal cells, checkpoint pathways are activated when genetic or cellular homeostasis is compromised, and signals are then transduced to re-stabilize homeostasis, and, failing this, to activate the apoptotic machinery to induce a cellular suicidal response. This implies that both survival and cell death pathways are induced following checkpoint activation, and that the final decision is dependant on the net result of integrating the two sets of signals.It is intriguing that checkpoint pathways are also critical in cancer therapy to provide an apoptotic stimulus when cellular damage induced by the therapeutic agent is detected by the sensor system. Therefore, it is not surprising that failure in pro-survival checkpoint response will render tumor cells hypersensitive to cytotoxics and, conversely, failure in pro-apoptotic checkpoint response will induce genetic instability and/or therapeutic resistance. Understanding the intricacies of checkpoint response is, therefore, central to the design of therapeutic regimen that will enhance antitumor effects. Although early versions of this design entail combination of cytotoxic agents with cell cycle or checkpoint inhibitors, a greater understanding of the concepts could make such combinations clinically more effective. The contributions in this book will consolidate the current state of knowledge on checkpoint responses that may lay the foundation for hypothesis-driven rational approaches in advancing the management of cancer. The immediate attraction of the book to the scientific community is that it represents a timely opportunity to build upon existing concepts of checkpoints to expand our understanding of the inner workings of the critical checkpoint machinery. The present understanding has provided ample appreciation that response to checkpoint activation is manifested through coordinated inhibition of cyclin-dependent kinase (CDK) complexes in G1, S and/or the G2 phase in order to arrest the cell cycle. Kinase inhibition can occur through several mechanisms, including inhibitory phosphorylation of CDK, destruction of the cognate cyclins, and recruitment of CDK inhibitors from the INK and WAF1/CIP1 families. However, the wealth of information from recent discoveries needs to be examined critically to consolidate our conceptual knowledge of checkpoints. At the same time, there is acute awareness in the diversity of checkpoint response between cytotoxic agents, and this serves as a reminder of the magnitude of complexity that is inherent in checkpoint regulation. This volume is intended to bring the cancer research community closer toward an improved understanding of this regulation, how checkpoint abnormalities can impact negatively on cancer therapy, and emerging strategies to target checkpoint response as a therapeutic end-point. 288 pp. Englisch.
Published by SPRINGER NATURE Okt 2010, 2010
ISBN 10: 1441927948ISBN 13: 9781441927941
Seller: BuchWeltWeit Ludwig Meier e.K., Bergisch Gladbach, Germany
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Taschenbuch. Condition: Neu. This item is printed on demand - it takes 3-4 days longer - 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.
Published by Humana Press, 2009
ISBN 10: 1607611775ISBN 13: 9781607611776
Seller: moluna, Greven, Germany
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Gebunden. Condition: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Brings together experts, who are defining the field of checkpoints, and as such represents a unique collection of insightful contributions that will serve as an important resource for both the research community and the medical oncologistsSince ch.
Published by Humana Press, 2012
ISBN 10: 1617796352ISBN 13: 9781617796357
Seller: moluna, Greven, Germany
Book Print on Demand
Condition: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Brings together experts, who are defining the field of checkpoints, and as such represents a unique collection of insightful contributions that will serve as an important resource for both the research community and the medical oncologistsSince ch.
Published by Springer, 2009
ISBN 10: 0387894446ISBN 13: 9780387894447
Seller: GreatBookPricesUK, Castle Donington, DERBY, United Kingdom
Book
Condition: As New. Unread book in perfect condition.
Published by Springer New York, 2009
ISBN 10: 0387894446ISBN 13: 9780387894447
Seller: moluna, Greven, Germany
Book Print on Demand
Condition: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Will serve as a single source for the current knowledge on genetic and epigenetic alterations that contribute to the development of drug resistance in cancer cells in form of comprehensive reviews by experts in the fieldIt was estimated that in 2.
Published by Springer New York, 2010
ISBN 10: 1441927948ISBN 13: 9781441927941
Seller: moluna, Greven, Germany
Book Print on Demand
Condition: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Will serve as a single source for the current knowledge on genetic and epigenetic alterations that contribute to the development of drug resistance in cancer cells in form of comprehensive reviews by experts in the fieldIt was estimated that in 2.
Published by Humana Press, 2009
ISBN 10: 1607611775ISBN 13: 9781607611776
Seller: AHA-BUCH GmbH, Einbeck, Germany
Book Print on Demand
Buch. Condition: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - Much work over the last two decades has firmly established that loss of cell cycle checkpoint regulation, and resultant unabated cellular proliferation, is an inherent characteristic of cancer. This loss may occur through aberration in any single component involved in signal transduction pathways that orchestrate checkpoint regulation, which may manifest through either a failure to activate the checkpoint or a failure to respond to the activated checkpoint. In normal cells, checkpoint pathways are activated when genetic or cellular homeostasis is compromised, and signals are then transduced to re-stabilize homeostasis, and, failing this, to activate the apoptotic machinery to induce a cellular suicidal response. This implies that both survival and cell death pathways are induced following checkpoint activation, and that the final decision is dependant on the net result of integrating the two sets of signals.It is intriguing that checkpoint pathways are also critical in cancer therapy to provide an apoptotic stimulus when cellular damage induced by the therapeutic agent is detected by the sensor system. Therefore, it is not surprising that failure in pro-survival checkpoint response will render tumor cells hypersensitive to cytotoxics and, conversely, failure in pro-apoptotic checkpoint response will induce genetic instability and/or therapeutic resistance. Understanding the intricacies of checkpoint response is, therefore, central to the design of therapeutic regimen that will enhance antitumor effects. Although early versions of this design entail combination of cytotoxic agents with cell cycle or checkpoint inhibitors, a greater understanding of the concepts could make such combinations clinically more effective. The contributions in this book will consolidate the current state of knowledge on checkpoint responses that may lay the foundation for hypothesis-driven rational approaches in advancing the management of cancer. The immediate attraction of the book to the scientific community is that it represents a timely opportunity to build upon existing concepts of checkpoints to expand our understanding of the inner workings of the critical checkpoint machinery. The present understanding has provided ample appreciation that response to checkpoint activation is manifested through coordinated inhibition of cyclin-dependent kinase (CDK) complexes in G1, S and/or the G2 phase in order to arrest the cell cycle. Kinase inhibition can occur through several mechanisms, including inhibitory phosphorylation of CDK, destruction of the cognate cyclins, and recruitment of CDK inhibitors from the INK and WAF1/CIP1 families. However, the wealth of information from recent discoveries needs to be examined critically to consolidate our conceptual knowledge of checkpoints. At the same time, there is acute awareness in the diversity of checkpoint response between cytotoxic agents, and this serves as a reminder of the magnitude of complexity that is inherent in checkpoint regulation. This volume is intended to bring the cancer research community closer toward an improved understanding of this regulation, how checkpoint abnormalities can impact negatively on cancer therapy, and emerging strategies to target checkpoint response as a therapeutic end-point.
Published by Springer New York, 2010
ISBN 10: 1441927948ISBN 13: 9781441927941
Seller: AHA-BUCH GmbH, Einbeck, Germany
Book
Taschenbuch. Condition: Neu. Druck auf Anfrage Neuware - Printed after ordering - 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 resistancereversalstrategiesthatwerecarriedoutinthe1990susingpumpinhib itors 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.