Herceptin: Mechanisms of action and resistance

Rita Nahta; Francisco J. Esteva

doi:10.1016/j.canlet.2005.01.041

Herceptin: Mechanisms of action and resistance

Rita Nahta, Francisco J. Esteva

Breast Medical Oncology

Research output: Contribution to journal › Review article › peer-review

389 Scopus citations

Abstract

HER-2 is overexpressed in 20-25% of invasive breast cancers and is associated with an aggressive tumor phenotype and reduced survival rate. The HER-2 status of a tumor is the critical determinant of response to the HER-2-targeted antibody Herceptin. Thus, accurate assessment of HER-2 expression levels is essential for identifying breast cancer patients who will benefit from HER-2-targeted therapy. Herceptin combined with chemotherapy increases response rates, time to disease progression, and survival. However, the majority of cancers that initially respond to Herceptin begin to progress again within 1 year. This review describes mechanisms by which Herceptin inhibits cell growth in breast cancers that overexpress HER-2 and highlights possible mechanisms contributing to Herceptin resistance.

Original language	English (US)
Pages (from-to)	123-138
Number of pages	16
Journal	Cancer Letters
Volume	232
Issue number	2
DOIs	https://doi.org/10.1016/j.canlet.2005.01.041
State	Published - Feb 8 2006

Keywords

Breast
IGF-IR
Monoclonal antibodies
Trastuzumab
Tyrosine kinase receptor
p27

ASJC Scopus subject areas

Oncology
Cancer Research

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10.1016/j.canlet.2005.01.041

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title = "Herceptin: Mechanisms of action and resistance",

abstract = "HER-2 is overexpressed in 20-25% of invasive breast cancers and is associated with an aggressive tumor phenotype and reduced survival rate. The HER-2 status of a tumor is the critical determinant of response to the HER-2-targeted antibody Herceptin. Thus, accurate assessment of HER-2 expression levels is essential for identifying breast cancer patients who will benefit from HER-2-targeted therapy. Herceptin combined with chemotherapy increases response rates, time to disease progression, and survival. However, the majority of cancers that initially respond to Herceptin begin to progress again within 1 year. This review describes mechanisms by which Herceptin inhibits cell growth in breast cancers that overexpress HER-2 and highlights possible mechanisms contributing to Herceptin resistance.",

keywords = "Breast, IGF-IR, Monoclonal antibodies, Trastuzumab, Tyrosine kinase receptor, p27",

author = "Rita Nahta and Esteva, {Francisco J.}",

note = "Funding Information: The authors wish to acknowledge funding from the AACR-Amgen, Inc. Fellowship in Clinical/Translational Cancer Research (R. Nahta), the M.D. Anderson Cancer Center Odyssey Special Fellowship, and the Theodore N. Law Award for Scientific Achievement (R. Nahta). We thank the Nellie B. Connally Breast Cancer Research Fund for supporting the Breast Cancer Translational Research Laboratory at M.D. Anderson Cancer Center, and the NCI for the Cancer Center Core Grant (CA16672). The authors thank Michael Worley for editorial assistance.",

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doi = "10.1016/j.canlet.2005.01.041",

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AU - Esteva, Francisco J.

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N2 - HER-2 is overexpressed in 20-25% of invasive breast cancers and is associated with an aggressive tumor phenotype and reduced survival rate. The HER-2 status of a tumor is the critical determinant of response to the HER-2-targeted antibody Herceptin. Thus, accurate assessment of HER-2 expression levels is essential for identifying breast cancer patients who will benefit from HER-2-targeted therapy. Herceptin combined with chemotherapy increases response rates, time to disease progression, and survival. However, the majority of cancers that initially respond to Herceptin begin to progress again within 1 year. This review describes mechanisms by which Herceptin inhibits cell growth in breast cancers that overexpress HER-2 and highlights possible mechanisms contributing to Herceptin resistance.

AB - HER-2 is overexpressed in 20-25% of invasive breast cancers and is associated with an aggressive tumor phenotype and reduced survival rate. The HER-2 status of a tumor is the critical determinant of response to the HER-2-targeted antibody Herceptin. Thus, accurate assessment of HER-2 expression levels is essential for identifying breast cancer patients who will benefit from HER-2-targeted therapy. Herceptin combined with chemotherapy increases response rates, time to disease progression, and survival. However, the majority of cancers that initially respond to Herceptin begin to progress again within 1 year. This review describes mechanisms by which Herceptin inhibits cell growth in breast cancers that overexpress HER-2 and highlights possible mechanisms contributing to Herceptin resistance.

KW - Breast

KW - IGF-IR

KW - Monoclonal antibodies

KW - Trastuzumab

KW - Tyrosine kinase receptor

KW - p27

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Herceptin: Mechanisms of action and resistance

Abstract

Keywords

ASJC Scopus subject areas

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