Journal
EXPERIMENTAL AND MOLECULAR PATHOLOGY
Volume 87, Issue 1, Pages 1-11Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yexmp.2009.05.001
Keywords
HER2; Metastasis; Breast cancer; Cancer stem cell; Untransformed cell
Categories
Funding
- NCI NIH HHS [T32CA09140, R01 CA055306-14A1, CA055306, T32 CA009140, R01 CA055306] Funding Source: Medline
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The HER2 gene encodes the receptor tyrosine kinase HER2 and is often over-expressed or amplified in breast cancer. Up-regulation of HER2 contributes to tumor progression. Many aspects of tumor growth are favorably affected through activation of HER2 signaling. Indeed, HER2 plays a role in increasing proliferation and survival of the primary tumor and distant lesions which upon completion of full transformation cause metastases. P185(HER2/neu) receptors and signaling from them and associated molecules increase motility of both intravasating and extravasating cells, decrease apoptosis, enhance signaling interactions with the microenvironment, regulate adhesion, as well as a multitude of other functions. Recent experimental and clinical evidence supports the view that the spread of incompletely transformed cells occurs at a very early stage in tumor progression. This review concerns the identification and characterization of HER2, the evolution of the metastasis model, and the more recent cancer stem cell model. In particular, we review the evidence for an emerging mechanism of HER2+ breast cancer progression, whereby the untransformed HER2-expressing cell shows characteristics of stem/progenitor cell, metasta-sizes, and then completes its final transformation at the secondary site. (C) 2009 Elsevier Inc. All rights reserved.
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