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JCI online early table of contents: March 14, 2011
Date:3/14/2011

he cancer are incompletely understood, and there is no animal model of the disease.

Recent work has suggested that activation of a particular cell signaling pathway may be required for PA formation, and mutations in one gene in that pathway, a kinase called BRAF, are found in more than half of all PA cases. In this paper, Peter Lichter and colleagues at the German Cancer Research Center, in Heidelberg, Germany investigated how BRAF protein contributes to PA formation. They found that expression of just part of the BRAF protein in mice was sufficient to induce the formation of brain tumors that closely resembled the human disease. They are hopeful that this new animal model helps define the molecular processes that lead to PA, and may be useful in the design and testing of new therapeutics.

TITLE: An activated mutant BRAF kinase domain is sufficient to induce pilocytic astrocytoma in mice

AUTHOR CONTACT:
Peter Lichter
German Cancer Research Center, Heidelberg, DEU
Phone: 49-6221424609; Fax: ; E-mail: peter.lichter@dkfz.de

View this article at: http://www.jci.org/articles/view/44656?key=6fc5f3671026c2e3de26


ONCOLOGY A new target to prevent lung cancer metastasis?

Lung cancer is the most common cause of cancer-related death in Western countries, and most often, lung cancer patients die due to metastasis. The ability of tumor cells to metastasize is thought to be related to their propensity to lose their cell-cell contacts and gain an ability to invade other tissues, a process called epithelial-to-mesenchymal transition (EMT). The factors that promote EMT are negatively regulated by a family of microRNAs called miR-200, and thus regulation of miR-200 may be a critical determinant of whether isolated tumors become metastatic cancer. In new research, Jonathan Kurie and his team, a
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Contact: Kathryn Claiborn
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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