A research study suggests that a type of herpes virus known as cytomegalovirus (CMV) may accelerate development and progression of glioblastoma, a deadly form of brain cancer. The virus may influence tumor development when two genes called p53 and Nf1 are mutated in tumor cells. Under normal conditions, these tumor suppressor genes cause cells to die before they become malignant. However, cancer-related changes can silence these genes, thereby allowing malignant cells to survive and form tumors.
Moreover, CMV was found to stimulate tumor-cell proliferation by activating a biochemical cell pathway called STAT3. This pathway plays an important role in controlling cell proliferation.
The researchers studied mouse models infected with murine CMV. They found that mice infected with murine CMV and harbored genetic p53 and NF1 mutations in their brain cells, which predisposed them to spontaneous glioblastoma, had shorter survival than non-infected mice with the same genetic mutations. Also, murine CMV infection increased levels of activated STAT3 in neural stem cells, where glioblastoma is thought to originate. Moreover, human CMV increased STAT3 activation and proliferation of patient-derived glioblastoma cells.
“Anti-viral therapy against CMV might now be justified for human cancers, and immune responses to such cancer-modulating viruses should be carefully studied,” said Antonio Chiocca, MD, PhD, BWH Department of Neurosurgery chairman, and co-corresponding study author.
The study was published June 1, 2013 in Cancer Research.