Book contents
- Frontmatter
- Contents
- Terms used in the book
- 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
3 - Molecular aspects of drug resistance
Published online by Cambridge University Press: 03 May 2010
- Frontmatter
- Contents
- Terms used in the book
- 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
Summary
Introduction
There are approximately 60 different chemical compounds generally available for the treatment of cancer (not including hormones or biological response modifiers). They are of diverse structure and from a variety of sources. They do not readily fit into a single classification system and are usually described partly on the basis of their chemical structure, partly on their primary source (fungi, plant, etc.) and partly on what is thought to be their general mechanism of action (antimetabolite, alkylating agent, etc.) (Table 3.1). We can generalize by stating that all of the drugs appear to exert their therapeutic effect by interfering with the processes involved in cell division. This interference results in the cell being physically disrupted or rendered permanently sterile. We can further say that cancer cells have the potential to become resistant to any of the drugs in our inventory and the cell can, moreover, express resistance to a great many agents simultaneously. Although we are not aware of the experiment actually having been done, it seems more than probable that an individual cancer cell could display resistance to all 60 available drugs concurrently. As we will see, this capacity to express resistance to many agents is, in part, related to the fact that there are a large number of mechanisms that once expressed by the cell will generate broad degrees of cellular resistance.
It would be well beyond the scope of this book to discuss in any detail the molecular changes that have been described for all of the various cytotoxic agents. However, we will mention the general processes involved in drug action and how these may be modified in the drug-resistant state.
- Type
- Chapter
- Information
- Drug Resistance in CancerMechanisms and Models, pp. 59 - 89Publisher: Cambridge University PressPrint publication year: 1998
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