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Bypassing cellular EGF receptor dependence through epithelial-to-mesenchymal-like transitions

Over 90% of all cancers are carcinomas, malignancies derived from cells of epithelial origin. As carcinomas progress, these tumors may lose epithelial morphology and acquire mesenchymal characteristics which contribute to metastatic potential. An epithelial-to-mesenchymal transition (EMT) similar to...

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Autores principales: Barr, Sharon, Thomson, Stuart, Buck, Elizabeth, Russo, Suzanne, Petti, Filippo, Sujka-Kwok, Izabela, Eyzaguirre, Alexandra, Rosenfeld-Franklin, Maryland, Gibson, Neil W., Miglarese, Mark, Epstein, David, Iwata, Kenneth K., Haley, John D.
Formato: Texto
Lenguaje:English
Publicado: Springer Netherlands 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2471394/
https://www.ncbi.nlm.nih.gov/pubmed/18236164
http://dx.doi.org/10.1007/s10585-007-9121-7
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author Barr, Sharon
Thomson, Stuart
Buck, Elizabeth
Russo, Suzanne
Petti, Filippo
Sujka-Kwok, Izabela
Eyzaguirre, Alexandra
Rosenfeld-Franklin, Maryland
Gibson, Neil W.
Miglarese, Mark
Epstein, David
Iwata, Kenneth K.
Haley, John D.
author_facet Barr, Sharon
Thomson, Stuart
Buck, Elizabeth
Russo, Suzanne
Petti, Filippo
Sujka-Kwok, Izabela
Eyzaguirre, Alexandra
Rosenfeld-Franklin, Maryland
Gibson, Neil W.
Miglarese, Mark
Epstein, David
Iwata, Kenneth K.
Haley, John D.
author_sort Barr, Sharon
collection PubMed
description Over 90% of all cancers are carcinomas, malignancies derived from cells of epithelial origin. As carcinomas progress, these tumors may lose epithelial morphology and acquire mesenchymal characteristics which contribute to metastatic potential. An epithelial-to-mesenchymal transition (EMT) similar to the process critical for embryonic development is thought to be an important mechanism for promoting cancer invasion and metastasis. Epithelial-to-mesenchymal transitions have been induced in vitro by transient or unregulated activation of receptor tyrosine kinase signaling pathways, oncogene signaling and disruption of homotypic cell adhesion. These cellular models attempt to mimic the complexity of human carcinomas which respond to autocrine and paracrine signals from both the tumor and its microenvironment. Activation of the epidermal growth factor receptor (EGFR) has been implicated in the neoplastic transformation of solid tumors and overexpression of EGFR has been shown to correlate with poor survival. Notably, epithelial tumor cells have been shown to be significantly more sensitive to EGFR inhibitors than tumor cells which have undergone an EMT-like transition and acquired mesenchymal characteristics, including non-small cell lung (NSCLC), head and neck (HN), bladder, colorectal, pancreas and breast carcinomas. EGFR blockade has also been shown to inhibit cellular migration, suggesting a role for EGFR inhibitors in the control of metastasis. The interaction between EGFR and the multiple signaling nodes which regulate EMT suggest that the combination of an EGFR inhibitor and other molecular targeted agents may offer a novel approach to controlling metastasis.
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spelling pubmed-24713942008-07-16 Bypassing cellular EGF receptor dependence through epithelial-to-mesenchymal-like transitions Barr, Sharon Thomson, Stuart Buck, Elizabeth Russo, Suzanne Petti, Filippo Sujka-Kwok, Izabela Eyzaguirre, Alexandra Rosenfeld-Franklin, Maryland Gibson, Neil W. Miglarese, Mark Epstein, David Iwata, Kenneth K. Haley, John D. Clin Exp Metastasis Original Article Over 90% of all cancers are carcinomas, malignancies derived from cells of epithelial origin. As carcinomas progress, these tumors may lose epithelial morphology and acquire mesenchymal characteristics which contribute to metastatic potential. An epithelial-to-mesenchymal transition (EMT) similar to the process critical for embryonic development is thought to be an important mechanism for promoting cancer invasion and metastasis. Epithelial-to-mesenchymal transitions have been induced in vitro by transient or unregulated activation of receptor tyrosine kinase signaling pathways, oncogene signaling and disruption of homotypic cell adhesion. These cellular models attempt to mimic the complexity of human carcinomas which respond to autocrine and paracrine signals from both the tumor and its microenvironment. Activation of the epidermal growth factor receptor (EGFR) has been implicated in the neoplastic transformation of solid tumors and overexpression of EGFR has been shown to correlate with poor survival. Notably, epithelial tumor cells have been shown to be significantly more sensitive to EGFR inhibitors than tumor cells which have undergone an EMT-like transition and acquired mesenchymal characteristics, including non-small cell lung (NSCLC), head and neck (HN), bladder, colorectal, pancreas and breast carcinomas. EGFR blockade has also been shown to inhibit cellular migration, suggesting a role for EGFR inhibitors in the control of metastasis. The interaction between EGFR and the multiple signaling nodes which regulate EMT suggest that the combination of an EGFR inhibitor and other molecular targeted agents may offer a novel approach to controlling metastasis. Springer Netherlands 2008-01-31 2008 /pmc/articles/PMC2471394/ /pubmed/18236164 http://dx.doi.org/10.1007/s10585-007-9121-7 Text en © The Author(s) 2008 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Original Article
Barr, Sharon
Thomson, Stuart
Buck, Elizabeth
Russo, Suzanne
Petti, Filippo
Sujka-Kwok, Izabela
Eyzaguirre, Alexandra
Rosenfeld-Franklin, Maryland
Gibson, Neil W.
Miglarese, Mark
Epstein, David
Iwata, Kenneth K.
Haley, John D.
Bypassing cellular EGF receptor dependence through epithelial-to-mesenchymal-like transitions
title Bypassing cellular EGF receptor dependence through epithelial-to-mesenchymal-like transitions
title_full Bypassing cellular EGF receptor dependence through epithelial-to-mesenchymal-like transitions
title_fullStr Bypassing cellular EGF receptor dependence through epithelial-to-mesenchymal-like transitions
title_full_unstemmed Bypassing cellular EGF receptor dependence through epithelial-to-mesenchymal-like transitions
title_short Bypassing cellular EGF receptor dependence through epithelial-to-mesenchymal-like transitions
title_sort bypassing cellular egf receptor dependence through epithelial-to-mesenchymal-like transitions
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2471394/
https://www.ncbi.nlm.nih.gov/pubmed/18236164
http://dx.doi.org/10.1007/s10585-007-9121-7
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