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Viral proteins may be associated with human brain tumors, according to findings by Temple researchers

PHILADELPHIA -- An association between a common virus and brain tumors has been established by a group of researchers from Temple University, suggesting a possible role for it in the development of the most frequent type of malignant brain tumor in children.

Their study, Expression of human polyomavirus JCV late gene product agnoprotein in human medulloblastoma, appears in the Feb. 20 issue of the Journal of the National Cancer Institute.

Luis Del Valle, M.D., and Kamel Khalili, Ph.D., of Temples Center for Neurovirology and Cancer Biology, and their co-investigators found the viral genome and viral proteins T antigen and agnoprotein in samples of pediatric brain tumors, which may play a role in the development of these tumors.

There is a virus, the JC Virus (JCV), which infects greater than 70 percent of the human population worldwide during early childhood, says Khalili, director and professor of Temples Center for Neurovirology and Cancer Biology and one of the studys lead researchers.

What we have shown in this study is that medulloblastoma tumors that we see in pediatrics, have in some portions, the genome of the JC Virus, says Khalili. This genome expresses the viral proteins T antigen, which has oncogenic potential, and an agnoprotein, whose function is unknown.

T antigen may cause brain tumors in part by blocking tumor suppressor proteins such as p53 and pRb. The role of agnoprotein in the development of brain tumors is unknown. Recent studies suggest, however, that the interaction of T antigen with agnoprotein may affect T antigen's ability to control cell growth.

We know that the agnoprotein has the capacity to associate with the T antigen, adds Khalili. So it seems that the communication between these two viral proteins may impact the ability of the virus to induce brain tumors.

In the current study, the authors found the gene that produces agnoprotein in 69 percent of 16 medulloblastoma samples, and the gene
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Contact: Preston M. Moretz
pmoretz@temple.edu
215-204-7476
Temple University
19-Feb-2002


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