Genetic fingerprints that reveal where a brain cell came from remain distinct even after the cell becomes a brain tumor, an international coalition of scientists will report in the February 1 issue of Cancer Research.
The finding adds a new layer of complexity to the quest to understand the causes of childhood brain cancers, according to senior author David H. Gutmann, M.D., Ph.D., the Donald O. Schnuck Family Professor of Neurology at Washington University School of Medicine in St. Louis and co-director of the neuro-oncology program at the Siteman Cancer Center.
"Our findings suggest that brain tumors arising in different regions may be genetically distinct as a consequence of their unique cellular origins," Gutmann says. "This is yet another factor we need to consider when trying to understand how pediatric brain tumors form."
Researchers use information about tumor origins to develop new tests and treatments for the tumors. Brain tumors are the leading cause of cancer-related death in children, and the most common childhood brain tumor is the pilocytic astrocytoma (PA). Approximately 15 percent of all PAs are linked to neurofibromatosis 1 (NF1), a genetic condition that causes childhood brain tumors and is a primary focus of Gutmann's research. However, the genetic basis for the majority of PAs is unexplained.
In the new study, Gutmann led six laboratories in the most detailed genetic analysis of PAs to date.
"We were hoping to identify genes that contribute to the formation of these tumors and find indicators that might help us predict which tumors will be relatively well-behaved and which will be more aggressive," Gutmann says. Previous studies have failed to produce any solid leads on the genetic alterations that predispose children to PAs.
"It should be recognized that the genetic alterations in this tumor may be very subtle," Gutmann notes. "When we looked at gene activity levels in the tumors as a function of b
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Contact: Michael C. Purdy
purdym@wustl.edu
314-286-0122
Washington University School of Medicine
1-Feb-2007