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Anti-EGFR Therapy: Mechanism and Advances in Clinical Efficacy in Breast Cancer

This review will focus on recent advances in the application of antiepidermal growth factor receptor (anti-EGFR) for the treatment of breast cancer. The choice of EGFR, a member of the ErbB tyrosine kinase receptor family, stems from evidence pinpointing its role in various anti-EGFR therapies. Ther...

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Detalles Bibliográficos
Autores principales: Flynn, John F., Wong, Christina, Wu, Joseph M.
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2668926/
https://www.ncbi.nlm.nih.gov/pubmed/19390622
http://dx.doi.org/10.1155/2009/526963
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author Flynn, John F.
Wong, Christina
Wu, Joseph M.
author_facet Flynn, John F.
Wong, Christina
Wu, Joseph M.
author_sort Flynn, John F.
collection PubMed
description This review will focus on recent advances in the application of antiepidermal growth factor receptor (anti-EGFR) for the treatment of breast cancer. The choice of EGFR, a member of the ErbB tyrosine kinase receptor family, stems from evidence pinpointing its role in various anti-EGFR therapies. Therefore, an increase in our understanding of EGFR mechanism and signaling might reveal novel targets amenable to intervention in the clinic. This knowledge base might also improve existing medical treatment options and identify research gaps in the design of new therapeutic agents. While the approved use of drugs like the dual kinase inhibitor Lapatinib represents significant advances in the clinical management of breast cancer, confirmatory studies must be considered to foster the use of anti-EGFR therapies including safety, pharmacokinetics, and clinical efficacy.
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spelling pubmed-26689262009-04-23 Anti-EGFR Therapy: Mechanism and Advances in Clinical Efficacy in Breast Cancer Flynn, John F. Wong, Christina Wu, Joseph M. J Oncol Review Article This review will focus on recent advances in the application of antiepidermal growth factor receptor (anti-EGFR) for the treatment of breast cancer. The choice of EGFR, a member of the ErbB tyrosine kinase receptor family, stems from evidence pinpointing its role in various anti-EGFR therapies. Therefore, an increase in our understanding of EGFR mechanism and signaling might reveal novel targets amenable to intervention in the clinic. This knowledge base might also improve existing medical treatment options and identify research gaps in the design of new therapeutic agents. While the approved use of drugs like the dual kinase inhibitor Lapatinib represents significant advances in the clinical management of breast cancer, confirmatory studies must be considered to foster the use of anti-EGFR therapies including safety, pharmacokinetics, and clinical efficacy. Hindawi Publishing Corporation 2009 2009-04-14 /pmc/articles/PMC2668926/ /pubmed/19390622 http://dx.doi.org/10.1155/2009/526963 Text en Copyright © 2009 John F. Flynn et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Flynn, John F.
Wong, Christina
Wu, Joseph M.
Anti-EGFR Therapy: Mechanism and Advances in Clinical Efficacy in Breast Cancer
title Anti-EGFR Therapy: Mechanism and Advances in Clinical Efficacy in Breast Cancer
title_full Anti-EGFR Therapy: Mechanism and Advances in Clinical Efficacy in Breast Cancer
title_fullStr Anti-EGFR Therapy: Mechanism and Advances in Clinical Efficacy in Breast Cancer
title_full_unstemmed Anti-EGFR Therapy: Mechanism and Advances in Clinical Efficacy in Breast Cancer
title_short Anti-EGFR Therapy: Mechanism and Advances in Clinical Efficacy in Breast Cancer
title_sort anti-egfr therapy: mechanism and advances in clinical efficacy in breast cancer
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2668926/
https://www.ncbi.nlm.nih.gov/pubmed/19390622
http://dx.doi.org/10.1155/2009/526963
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