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JCI online early table of contents: Feb. 8, 2010
Date:2/8/2010

ht provide a new approach to treat Chuvash disease.

TITLE: The von Hippel-Lindau Chuvash mutation promotes pulmonary hypertension and fibrosis in mice

AUTHOR CONTACT:
M. Celeste Simon
University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Phone: 215.746.5532; Fax: 215.746.5511; E-mail: celeste2@mail.med.upenn.edu.

View this article at: http://www.jci.org/articles/view/36362?key=78a2f13d85364cc6f65c


ONCOLOGY: Rab25: a suppressor of tumor formation in intestines?

Colorectal adenocarcinoma accounts for the majority of cases of colorectal cancer. A series of genetic mutations in the cells lining the colon (intestinal epithelial cells) is thought to be the cause of colorectal adenocarcinoma. By studying mouse models of colon cancer and tissue from individuals with colorectal adenocarcinoma, James Goldenring and colleagues, at Vanderbilt University School of Medicine, Nashville, have now identified RAB25 as one gene that might be involved in the formation of colorectal adenocarcinomas.

Initial analysis indicated that expression of Rab25 was substantially decreased in human colon adenocarcinomas compared with normal colon and that lower Rab25 expression predicted shorter patient survival times. To follow up on these data, which suggested that Rab25 functions as a tumor suppressor (that is, a protein that when expressed at lower than normal levels due to mutation of the gene responsible for its generation fails to prevent tumors forming) in intestinal epithelial cells, the authors analyzed Rab25-deficient mice. Although these animals showed no gross abnormalities, when they were crossed with mice that model a hereditary syndrome that predisposes to colon cancer (ApcMin/+ mice), the Rab25-deficient ApcMin/+ mice developed increased numbers of int
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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