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CMV Infection Accelerates Tumor Growth in Mouse Brain Cancer Model

By BiotechDaily International staff writers
Posted on 14 Jun 2013
Results of a recently published study suggested that Cytomegalovirus (CMV) might significantly accelerate the development and progression of glioblastoma, a deadly form of brain cancer.

Investigators at Ohio State University (Columbus, USA) worked with a genetic mouse model of glioblastoma (Mut3 mice) that harbored genetic mutations in the p53 and NF1 tumor suppressor genes in their brain cells that predisposed them to spontaneous formation of glioblastomas. Some of these animals were infected perinatally with murine CMV (MCMV).

Results published in in the June 1, 2013, issue of the journal Cancer Research revealed that Mut3 mice infected with MCMV had shorter survival times than non-MCMV-infected mice. Implanting human glioblastomas into the brains of MCMV-infected animals significantly shortened their survival compared with uninfected animals. MCMV infection increased levels of activated STAT3 in neural stem cells, the cells in which glioblastomas are thought to originate.

Stat3 (signal transducer and activator of transcription-3) is a member of the Stat protein family, which regulates many aspects of cell growth, survival, and differentiation. Malfunction of this signaling pathway is frequently observed in primary tumors and leads to increased angiogenesis and enhanced tumor survival. Knockout studies have provided evidence that Stat proteins are involved in the development and function of the immune system and play a role in maintaining immune tolerance and tumor surveillance. Constitutive Stat3 activation is associated with various human cancers and commonly suggests poor prognosis. It has antiapoptotic as well as proliferative effects.

Results of another series of experiments revealed that human CMV increased STAT3 activation and proliferation of patient-derived glioblastoma cells and that a STAT3 inhibitor reversed this effect in cell and animal models.

"CMV has been detected in many cancer types, suggesting that it might be reactivated when cancer occurs in the body," said senior author Dr. Chang-Hyuk Kwon, assistant professor of neurological surgery at Ohio State University. "Our data indicate that CMV contributes to glioblastoma when already-mutated cancer cells proliferate using the STAT3 signaling pathway. We believe that CMV's action occurs in the tumor's cells of origin early in tumor initiation."

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