Mechanisms of drug resistance in neoplastic cells /

Bristol-Myers Cancer Symposia, Volume 9: Mechanisms of Drug Resistance in Neoplastic Cells provides information on both basic scientific and clinical studies on the causes and implications of tumor cell resistance to common antineoplastic agents. The book describes the colon cancer as a model for re...

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Bibliographic Details
Corporate Authors: Elsevier Science & Technology.; Bristol-Myers Symposium on Cancer Research Washington, D.C.)
Group Author: Woolley, Paul V., 1939-; Tew, Kenneth D
Published: Academic Press,
Publisher Address: San Diego :
Publication Dates: 1988.
Literature type: eBook
Language: English
Series: Bristol-Myers cancer symposia ; 9
Subjects:
Online Access: http://www.sciencedirect.com/science/book/9780127633626
Summary: Bristol-Myers Cancer Symposia, Volume 9: Mechanisms of Drug Resistance in Neoplastic Cells provides information on both basic scientific and clinical studies on the causes and implications of tumor cell resistance to common antineoplastic agents. The book describes the colon cancer as a model for resistance to antineoplastic drugs; mathematical modeling of drug resistance; and the mechanism of induced gene amplification in mammalian cells. The text also discusses the cellular concomitants of multidrug resistance; resistance to alkylating agents; and the phosphoprotein and protein kinase C chan.
Item Description: Proceedings of the Ninth Bristol-Myers Symposium on Cancer Research, held in Washington, D.C., on Oct. 15-16, 1986.
Carrier Form: 1 online resource (xxv, 390 pages) : illustrations.
Bibliography: Includes bibliographical references and index.
ISBN: 9781483220758
1483220753
Index Number: RC271
CLC: R730.53-532
Contents: Front Cover; Mechanisms of Drug Resistance in Neoplastic Cells; Copyright Page; Table of Contents; Contributors; Editor's Foreword; Foreword; Preface; PART 1: General Considerations of Drug Resistance; Chapter 1. Colon Cancer as a Model for Resistance to Antineoplastic Drugs; I. Introduction; II. Types of Resistance: Intrinsic and Acquired; III. Clinical Resistance of Colon Cancer; IV. Behavior of Colon Cancer Cells in the Human Tumor Stem-Cell Assay; V. Effects of Radiation and Oxygen Radicals on Colon Carcinoma Cells; VI. A Model of Colon Cancer Resistance; VII. Circumventing Resistance.
AcknowledgmentsReferences; Chapter 2. Mathematical Modeling of Drug Resistance; I. Introduction; II. A Model for the Appearance of a Single Resistant Phenotype; III. Implications of a Stem-Cell Model of Tumor Growth for the Acquisition of Drug Resistance; IV. Effect of Variability in the Mean Value of the Mutation Rate in the System; V. Effect of Treatment Sequencingand the Question of Dose intensity; VI. Partial Resistance; VII. Summary and Conclusions; References; Chapter 3. On the Mechanism of Induced Gene Amplification in Mammalian Cells; I. Introduction; II. Enhancement of the Frequ.
III. Overreplication of DNA following Inhibition of DNA SynthesisIV. On the Mechanism of Overreplication of DNA; V. Overreplication-Recombination and the Generation of Amplifications and Chromosomal Aberrations-Mutations; VI. Consequences for Tumor Progressionand Chemotherapy Resistance; Acknowledgments; References; Chapter 4. Cellular Concomitants of Multidrug Resistance; I. Introduction; II. Plasma Membrane Glycoprotein(gp150-180/P-Glycoprotein); III. Chromosomal Organizationof Amplified MDRA Genes; IV. Low-Molecular-Weight Cytosolic Protein (Sorcin/V19); V. EGF Receptor.
VI. Summary and OverviewAcknowledgments; References; Chapter 5. Resistance to Alkylating Agents:Basic Studies and Therapeutic Implications; I. Introduction; II. Development of Resistanceto Alkylating Agents; III. High-Dose Effect of Alkylating Agents-Experimental Model; IV. Cross-Resistance among Alkylating Agents; V. Resistance Mechanisms-Heterogeneity; VI. Other Studies of Resistance Mechanisms; VIII. Multilog Cell Kill for Alkylating Agents and Nonalkylating Agents against Sensitive Tumors; IX. Cross-Resistance among Alkylating Agents as Determined from Multilog Kill Analyses.