Abstract
Copyright: © 2015 Yiannakopoulou EC. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Trastuzumab (HerceptinTM) is a humanized anti-ErbB2 monoclonal antibody that has been approved for the treatment in the adjuvant and the metastatic setting of breast cancer patients that either overexpress ErbB2, or demonstrate ErbB2 gene amplification [1]. An important serious adverse event associated with trastuzumab is the reduction of left heart ejection fraction resulting to congestive heart failure. The role of pharmacogenomics in breast cancer targeted treatment has been well recognized [2]. However, data on the role of pharmacogenomics on the efficacy and safety of trastuzumab are still scarce.
Highlights
Trastuzumab (HerceptinTM) is a humanized anti-ErbB2 monoclonal antibody that has been approved for the treatment in the adjuvant and the metastatic setting of breast cancer patients that either overexpress ErbB2, or demonstrate ErbB2 gene amplification [1]
A non-synonymous coding Single-nucleotide polymorphisms (SNP) rs4252633 has been identified in the extracellular domain of HER2 that is targeted by trastuzumab
Antibody-dependent cell-mediated cytotoxicity via interactions with Fcγ receptors (FcγR) on leukocytes may contribute to the antitumor toxicity of trastuzumab
Summary
Trastuzumab (HerceptinTM) is a humanized anti-ErbB2 monoclonal antibody that has been approved for the treatment in the adjuvant and the metastatic setting of breast cancer patients that either overexpress ErbB2, or demonstrate ErbB2 gene amplification [1]. Could Pharmacogenomics Improve Efficacy and Safety of Trastuzumab? Eugenia Ch Yiannakopoulou* Department of Medical Laboratories Faculty of Health and Caring Professions Technological Educational Institute of Athens, Athens, Greece An important serious adverse event associated with trastuzumab is the reduction of left heart ejection fraction resulting to congestive heart failure.
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