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JCI online early table of contents: May 17, 2010
Date:5/10/2010

sion.

COMMD1 is known to inhibit two gene regulatory proteins linked to tumor growth, survival, and metastasis. The team, led by Ezra Burstein and Marc Vooijs, therefore set out to test the hypothesis that COMMD1 is inactivated or repressed in tumors. Their initial analysis indicated that COMMD1 expression is indeed decreased in a variety of cancers and that for both prostate cancer and endometrial cancer patients this is associated with increased tumor invasion and worse clinical outcomes. A substantial amount of additional data, including information generated in a chick xenograft model of tumor invasion and a mouse model of tumor spread, led the authors to their conclusion that COMMD1 has an important role in tumor invasion.

TITLE: COMMD1 disrupts HIF-1alpha/beta dimerization and inhibits human tumor cell invasion

AUTHOR CONTACT:
Ezra Burstein
University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Phone: 214.648.2008; Fax: 214.648.2019; E-mail: ezra.burstein@utsouthwestern.edu.

Marc Vooijs
University Medical Centre Maastricht, Maastricht, The Netherlands.
Phone: 31.0.43.388.2972; Fax: 31.0.43.388.4540; E-mail: marc.vooijs@maastro.unimaas.nl.

View this article at: http://www.jci.org/articles/view/40583?key=7ad73f0c4cf8f031dc76


ONCOLOGY: New way to inactivate a key tumor suppressor

A key step in the formation and progression of many tumors is inactivation of the protein PTEN. While this often occurs through mutation of the gene responsible for generating PTEN, it has been suggested that affects via negative regulators of PTEN might also be important, but it has been hard to identity these proteins. Now, Damu Tang and colleagues, at McMaster University, Hamilton,
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Contact: Karen Honey
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Journal of Clinical Investigation
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