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JCI online early table of contents: Feb. 7, 2011
Date:2/7/2011

ulation of double negative T cells partially compensate for CD4+ T cell function in these animals. The authors therefore suggest that it will be important to assess double negative T cells in HIV-infected patients, particularly to determine whether these cells are preserved and functional in those who do not progress to AIDS.

TITLE: Lack of clinical AIDS in SIV-infected sooty mangabeys with significant CD4+ T cell loss is associated with double-negative T cells

AUTHOR CONTACT:
Donald L. Sodora
Seattle Biomedical Research Institute, Seattle, Washington, USA.
Phone: 206.256.7413; Fax: 206.256.7229; E-mail: donald.sodora@seattlebiomed.org.

View this article at: http://www.jci.org/articles/view/44876?key=2e00f65a5f8ab42990eb


ONCOLOGY: New promoter of tumor development

Recent human data suggest that the protein CSN6 might have a role in regulating tumor development. Now, a team of researchers, led by Mong-Hong Lee, at the University of Texas M.D. Anderson Cancer Center, Houston, has identified a molecular mechanism by which CSN6 promotes tumorigenesis in mice and generated data that indicate that the gene that templates CSN6 is an oncogene.

Initial analysis indicated that levels of the CSN6 protein are upregulated in human breast and thyroid tumors and that expression of CSN6 positively correlated with expression of the protein MDM2, a potent negative regulator of the tumor suppressor p53. Further analysis confirmed this mechanism in mice and demonstrated that mice lacking one Csn6 gene were less susceptible than mice with both Csn6 genes intact to radiation-induced tumor development. The authors therefore suggest that CSN6 should be investigated as a prognostic marker and therapeutic target in cancers that involve dysregulated MDM2/p53 activity.

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Contact: Ushma Neill
press_releases@the-jci.org
734-546-5241
Journal of Clinical Investigation
Source:Eurekalert

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