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JCI early table of contents for March 19, 2012
Date:3/19/2012

oorly understood mechanism. The research team identified a sodium channel that is targeted by PKCε in sensory neurons called nociceptors. Further, they showed depleting these specific sodium channels from nociceptors in a mouse model system blocked the development of hyperalgesia. These results provide new evidence for the molecular causes of hyperalgesia and suggest that targeting this pathway may be an effective strategy for designing new therapeutics to treat hyperalgesia.

TITLE:

PKC epsilon phosphorylation of NaV1.8 increases sodium channel function and produces mechanical hyperalgesia in mice

AUTHOR CONTACT:

Robert Messing

Univ. of Calif. San Francisco, Emeryville, CA, USA

Phone: 510-985-3950; Fax: 510-985-3101; E-mail: romes@gallo.ucsf.edu

View this article at: http://www.jci.org/articles/view/61934?key=df6009bb3364cd6c8a9b

ONCOLOGY

Learning from mistakes: why a promising therapy for follicular lymphoma failed | Back to top

Follicular lymphoma is a cancer characterized by abnormal proliferation of immune cells called B cells. One therapeutic strategy, Interleukin (IL) -12 therapy, was predicted to increase the clearing of malignant B cells by activating natural killer (NK) cells and T cells, components of the immune system. Unfortunately, this strategy had very limited efficacy in a previously conducted clinical trial of follicular lymphoma patients. Dr. Stephen Ansell and colleagues at the Mayo Clinic in Rochester, MN wanted to understand why IL-12 therapy had failed. They found that activation of the IL-12 pathway exhausted T cell populations through a previously unknown mechanism, rather than stimulating clearance of tumor cells. When the therapy was designed, it was hoped that IL-12 would promote T cell responsiveness through the pro
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Contact: Sarah Jackson
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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