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JCI online early table of contents: Sept. 12, 2011
Date:9/12/2011

t British Columbia Cancer Agency Research Centre, Vancouver, has now identified an increase in the number of copies of the TRAF6 gene as a genetic change that can contribute to the development of human lung cancers. The team suggests that its data indicating that amplification of the TRAF6 gene is a common event in human lung cancers could explain why the signaling molecule NF-kappa-B is constitutively active in the majority of lung cancers.

TITLE: TRAF6 is an amplified oncogene bridging the RAS and NF-kappa-B pathways in human lung cancer

AUTHOR CONTACT:
Aly Karsan
British Columbia Cancer Agency Research Centre, Vancouver, British Columbia, Canada.
Phone: 604.675.8033; Fax: 604.675.8049; E-mail: akarsan@bccrc.ca.

View this article at: http://www.jci.org/articles/view/58818?key=f98695e6b1517c4b6a58


TUMOR IMMUNOLOGY: Understanding failure: why some anticancer therapies benefit only a few patients

For many years researchers sought to develop approaches to enhance the natural immune response to tumors in the hope that this would be clinically beneficial. As such, there are now several different ways to effectively direct immune responses toward tumor cells. However, surprisingly few patients have benefitted clinically from these approaches. A team of researchers, led by Dmitry Gabrilovich, at the H. Lee Moffitt Cancer Center, Tampa, has now identified one possible explanation as to why therapeutic approaches that induce responses mediated by immune cells known as cytotoxic T lymphocytes (CTLs) are not effective.

For CTLs to kill a cancer cell they must recognize on the cell's surface a protein complex known as an MHC molecule bound to a fragment of a cancer cellspecific protein. In the study, Gabrilovitch and colleagues found that in a mouse model of cancer, cells in
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Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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