The PIK3CA Gene as a Mutated Target for Cancer Therapy
- Authors: Sarah Croessmann, Justin Cidado, John P. Gustin, David Cosgrove, Ben Ho Park5,6
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View Affiliations Hide Affiliations5 The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA 6 The Johns Hopkins University, Department of Chemical and Biomolecular Engineering, Baltimore, MD 21218, USA
- Source: Advances in Cancer Drug Targets: Volume 1 , pp 3-21
- Publication Date: January 2013
- Language: English
The PIK3CA Gene as a Mutated Target for Cancer Therapy, Page 1 of 1
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The development of targeted therapies with true specificity for cancer relies upon exploiting differences between cancerous and normal cells. Genetic and genomic alterations including somatic mutations, translocations, and amplifications have served as recent examples of how such differences can be exploited as effective drug targets. Small molecule inhibitors and monoclonal antibodies directed against the protein products of these genetic anomalies have led to cancer therapies with high specificity and relatively low toxicity. Our group and others have demonstrated that somatic mutations in the PIK3CA gene occur at high frequency in breast and other cancers. Moreover, the majority of mutations occur at three hotspots, making these ideal targets for therapeutic development. Here we review the literature on PIK3CA mutations in cancer, as well as existing data on p110α inhibitors and inhibitors of downstream effectors for potential use as targeted cancer therapeutics.
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