GBM and Coxsackie B virus
Purpose of Study: Determine if there is a link between Glioblastoma Multiforme (GBM) and high blood titers for the Coxackie B virus (CBV) following surgical resection of the tumor.
Background: Glioblastoma multiforme is the most common and most deadly primary tumor found in the CNS. Treatment regimens for this tumor, and overall prognosis still remains poor when compared with other primary CNS tumors. Current treatment for this tumor is a combination of surgery, radiation and high dose chemotherapy, which only gives the patient a modest improvement in survival time, and most patients die from the disease within a year.
The link between viruses and primary CNS tumors has long been suspected and indeed some studies have shown a link between the two. For example, adenoviruses and SV40 are known to be particularly effective in inducing neoplasias in mice. Several RNA retroviruses also have been shown to induce tumor formation in experimental animals. It is known that there are genetic changes in tumor suppressor genes within astrocytic cells that lead to uncontrolled proliferation of these damaged cells. There has also been a link established between anaplastic astrocytomas in children and infection with the polio virus. Coxsackie B virus has been shown to be able to cause encephalitis in patients, and three patients with GBM were recently tested for CBV titers and were shown to have elevated titers, particularly CBV4 titers.
The supranormal Coxsackie blood titers may be due to a cause and effect response, however, multiple other possibilities exist. Glioblastomas may display surface antigens induced by related viruses or even factors simply sharing common antigen sites. Furthermore, it is possible that the Coxsackie virus may up-regulate tumor promoter genes or down-regulate tumor suppressor genes, each producing the common problem of Glioblastoma formation. By determining if there is sharing among surface antigens, additional markers may be identified in a blood test leading to improved diagnostics.