Oct. 15, 2007 -- Scientists have shown how developing brain tumors can turn an encounter with a signaling molecule from a fatal experience for the tumor cells into a cue for their own growth and multiplication.
Researchers at Washington University School of Medicine in St. Louis found the transformation relies on at least two other molecules that can be modified with existing drugs, opening the possibility that they may be able to use the established drugs to treat brain tumors.
The study, reported in Cancer Research, was conducted in a mouse model of neurofibromatosis type 1 (NF1), a genetic condition that leads to the development of benign and malignant tumors.
"In addition to opening up several new, exciting possibilities for brain tumor treatment both in NF1 and generally, this research is leading to what could be a very important set of insights into fundamental mechanisms of tumor formation," says the paper's senior author, Joshua Rubin, M.D., Ph.D., assistant professor of pediatrics, neurology and of neurobiology.
Rubin studies general pediatric brain tumor development. His colleague and co-author David H. Gutmann, M.D., Ph.D., the Donald O. Schnuck Family Professor of Neurology, specializes in NF1 research and directs the University's Neurofibromatosis Center, where the research took place.
The signaling molecule that scientists studied, CXCL12, binds to a receptor called CXCR4 on the surfaces of brain cells. Other researchers first identified CXCR4 while searching for receptors targeted by HIV during infection. Initially, they assumed that CXCR4's primary responsibility was controlling the movement of immune system cells. However, when they genetically disabled the receptor in mice, it had catastrophic effects on organ systems throughout the body. Further study showed the receptor was associated not only with cell movement but also with cell survival and replication.
"All of those things are also changed in cancers: canc
|Contact: Michael C. Purdy|
Washington University in St. Louis