Drug Resistance in Cancer
Mechanisms and Models

An accessible and sophisticated account of the biological mechanisms of drug resistance in cancer and their mathematical modelling.

James H. Goldie (Author), Andrew J. Coldman (Author)

9780521111706, Cambridge University Press

Paperback, published 11 June 2009

256 pages, 22 b/w illus. 6 tables
22.9 x 15.2 x 1.5 cm, 0.38 kg

'… required reading for all trainees in oncology.' Paul P. Carbone, Oncology

Drug resistance in cancer, whereby a proportion of cancer cells evades chemotherapy, poses a profound and continuing challenge for the effective treatment of cancer. The principles underlying the biological mechanisms behind this phenomenon are clearly understood and explained in this volume. However, a deeper understanding of drug resistance requires a quantitative appreciation of the dynamic forces that shape tumour growth, including spontaneous mutation and selection processes. The authors seek to explain and to simplify these complex mechanisms, and to place them in a clinical context. Clearly explained mathematical models are used to illustrate the biological principles and provide an insight into tumour development and the effectiveness and limitations of drug treatment. It is suitable for those with a non-mathematical background and aims to enhance the effectiveness of cancer therapy.

Preface
1. The biological basis of cancer and the problem of drug resistance
2. Tumour growth, stem cells and experimental chemotherapy
3. Molecular aspects of drug resistance
4. Quantitative descriptions of the origins of drug resistance
5. Development and exploration of the random mutation model for drug resistance
6. Extensions of the random mutation model for drug resistance
7. Clinical predictions of the random mutation model
8. Directed versus random mutation and the problem of intrinsic resistance
9. Some final thoughts on the problem of drug resistance
Index.

Subject Areas: Human biology [PSX], Pharmacology [MMG], Oncology [MJCL], Pre-clinical medicine: basic sciences [MF]