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JCI table of contents: June 20, 2008
Date:6/20/2008

teaga and Jeffrey Engelman, generated cancer cells resistant to the effects of gefitinib and found that these cells were constantly sending signals from a protein on their surface known as IGF1R. This meant that two proteins known as IRS-1 and PI3K were always associated. If this association was disrupted then the cells once again became susceptible to the effects of gefitinib. Further analysis showed that if mice with a human tumor were treated with gefitinib and a drug inhibiting IGF1R their tumors did not recur, whereas neither drug alone could prevent tumor recurrence. The authors therefore suggest that drug combinations that target both EGFR and IGF1R might be of benefit to individuals with cancers that are responsive to EGFR-targeted therapies.

TITLE: Acquired resistance to EGFR tyrosine kinase inhibitors in cancer cells is mediated by loss of IGF-binding proteins

AUTHOR CONTACT:
Carlos L. Arteaga
Vanderbilt University Medical Center, Nashville, Tennessee, USA
Phone: (615) 936-3524; Fax: (615) 936-1790; E-mail: carlos.arteaga@vanderbilt.edu.

Jeffrey A. Engelman
Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, Massachusetts, USA.
Phone: (617) 724-7298; Fax: (617) 724-9648; E-mail: jengelman@partners.org.

View the PDF of this article at: https://www.the-jci.org/article.php?id=34588

ACCOMPANYING COMMENTARY

TITLE: Mechanisms of resistance to ErbB-targeted cancer therapeutics

AUTHOR CONTACT:
Mark I. Greene
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: (215) 898-2870; Fax: (215) 898-2401; Email: greene@reo.med.upenn.edu.

View the PDF of this article at:

Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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