Skip to main content Accessibility help
×
Hostname: page-component-5c6d5d7d68-ckgrl Total loading time: 0 Render date: 2024-08-18T06:19:51.160Z Has data issue: false hasContentIssue false

3 - Molecular aspects of drug resistance

Published online by Cambridge University Press:  03 May 2010

James H. Goldie
Affiliation:
University of British Columbia, Vancouver
Andrew J. Coldman
Affiliation:
University of British Columbia, Vancouver
Get access

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 Cancer
Mechanisms and Models
, pp. 59 - 89
Publisher: Cambridge University Press
Print publication year: 1998

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

Save book to Kindle

To save this book to your Kindle, first ensure coreplatform@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×