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Role of erbB2 in breast cancer chemosensitivity
1Department of Surgical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston 77030, USA. dyu@notes.mdacc.tmc.edu
Abstract:
The erbB2 gene, which encodes a transmembrane growth factor receptor, is overexpressed in approximately 30% of breast cancers. Overexpressing this gene makes breast cancers resistant to certain chemotherapeutic agents. In this article, we review what is known about ErbB2-mediated chemoresistance and the controversies surrounding it. We also examine the antiapoptotic function of erbB2 as one of the molecular mechanisms of ErbB2-mediated Taxol resistance and describe several emerging strategies for overcoming intrinsic ErbB2-mediated chemoresistance. Finally, we discuss future avenues for studies of chemosensitivity in ErbB2-overexpressing breast cancers that may lead to the development of effective biology-based treatment strategies.
Insights
Overexpression of the erbB2 gene in breast cancer causes chemoresistance. Understanding ErbB2
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The erbB2 gene encodes a transmembrane growth factor receptor.
- ErbB2 overexpression occurs in ~30% of breast cancers.
- This overexpression confers resistance to chemotherapy.
Purpose of the Study:
- Review ErbB2-mediated chemoresistance mechanisms and controversies.
- Examine ErbB2's antiapoptotic role in Taxol resistance.
- Discuss strategies to overcome ErbB2-mediated chemoresistance.
Main Methods:
- Literature review of ErbB2-mediated chemoresistance.
- Analysis of molecular mechanisms, including antiapoptotic function.
- Evaluation of emerging therapeutic strategies.
Main Results:
- ErbB2 overexpression is a key factor in breast cancer chemoresistance.
- ErbB2's antiapoptotic function contributes to Taxol resistance.
- Several strategies show promise for overcoming this resistance.
Conclusions:
- Further research into ErbB2-overexpressing breast cancers is crucial.
- Developing effective, biology-based treatment strategies is the goal.
- Targeting ErbB2 pathways may improve treatment outcomes.