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Drug Resist Updat. 2000 Dec;3(6):319-324.

Effects of HER-2/neu on chemosensitivity of tumor cells.

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Institute of Medical Technology, University of Tampere, Tampere University Hospital, Tampere, Finland


In solid tumors, such as breast and ovarian cancer, the predominant genetic mechanism for oncogene activation is through gene amplification. The HER-2 (also known as ErbB2/c-erbB2/HER-2 / neu) oncogene is the most frequently amplified oncogene in breast cancer and its overexpression is associated with poor clinical outcome. In addition to its role in tumor progression, HER-2 has been implicated in altering tumor cell chemosensitivity to cytotoxic chemotherapy, particularly to anthracyclines. However, sophisticated in vitro studies have recently indicated that HER-2 may not have anything to do with the sensitivity of the cancer cells to cytotoxic drugs. Topoisomerase IIalpha gene is a target gene for many cytotoxic drugs and is located just by the HER-2 at the 17q12-q21. TopoIIalpha amplification and deletion may account for both relative chemosensitivity and resistance to anthracycline-therapy depending on the specific genetic defect at the topoIIalpha locus. Whereas HER-2 is an oncogene that clearly can drive tumor induction and growth, its function as a marker for chemoselection may be due to associated genetic changes in the topoIIalpha gene.


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