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JCI online early table of contents: Feb. 15, 2010
Date:2/15/2010

itro analysis of human neuroblastoma cell lines indicated that both decreasing NT-3 expression and culturing in the presence of an antibody that blocked NT-3 binding to TrkC triggered the cells to undergo apoptosis. More importantly, blocking the NT-3/TrkC interaction inhibited tumor growth and metastasis in both a chick and a mouse xenograft model of neuroblastoma. The authors therefore suggest that disrupting the NT-3/TrkC interaction might provide a new approach to treating neuroblastoma, a form of cancer for which treatment options are currently limited.

TITLE: Neurotrophin-3 production promotes human neuroblastoma cell survival by inhibiting TrkC-induced apoptosis

AUTHOR CONTACT:

Patrick Mehlen
CNRS UMR5238, Universit de Lyon, Lyon, France.
Phone: 33.4.78.78.28.70; Fax: 33.4.78.78.28.87; E-mail: mehlen@lyon.fnclcc.fr.

View this article at: http://www.jci.org/articles/view/41013?key=7f26b0d679e4415a781a

DEVELOPMENT: Deciphering the role of the protein RET in development

Several diseases and developmental defects, including Hirschsprung disease and congenital anomalies of kidneys or urinary tract (CAKUT) syndrome, are caused by mutations in the RET gene. It is not clear, however, how RET gene mutations lead to such a range of diseases, which can occur in isolation or combination. Insight into this issue has now been provided by Sanjay Jain and colleagues, at Washington University School of Medicine, St. Louis, through their analysis of ten strains of RET mutant mice. Specifically, it was determined that different RET-stimulated signaling pathways control the development of the genitourinary system and the enteric and autonomic nervous systems. This conclusion suggests that an individual's disease symptoms are determined by which signaling pathways are disrupted by the RET gene mutation
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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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