We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
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 .
To save content items 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.
Resistance to chemotherapy invariably occurs in breast cancer patients being treated for metastatic disease. As with hormonal therapy, resistance may be either ‘intrinsic’, manifest as a failure to respond to initial therapy, or ‘acquired’, seen as progression after a variable length of time in patients who initially respond to cytotoxic therapy. In the adjuvant setting resistance to chemotherapy is inferred by rapid relapse following completion of therapy. In vitro models have established that cancer cells exhibit varying degrees of intrinsic drug-specific resistance, but may also acquire the same phenotype following long-term exposure to a given agent. Many of the established mechanisms of resistance are associated with genetic abnormalities such as activation of dominantly active oncogenes, or loss of tumour suppressor genes. Both patterns of intrinsic and acquired resistance are consistent with a model of cumulative genetic change during the development and progression of breast cancer.
Although many of the mechanisms involved in chemoresistance have been investigated extensively in vitro, other factors such as systemic drug metabolism and bioavailability may influence the likelihood of tumour response/resistance in vivo. Clinical studies have been used to verify whether a given genetic or biochemical change observed in experimental studies of drug resistance is relevant to clinical practice. There are several limitations in this approach when studying biological markers of resistance, not least the methodologic problems in analyzing clinical specimens (for example, protein vs. RNA analysis, type of antibody used, tissue fixation) and sampling errors due to heterogeneous expression within human tumours.
Recommend this
Email your librarian or administrator to recommend adding this to your organisation's collection.