J Ricardo McFaline-Figueroa1,2, Patrick Y Wen3. 1. Department of Neurology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA, 02115, USA. jmcfalinefigueroa@partners.org. 2. Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA. jmcfalinefigueroa@partners.org. 3. Harvard Medical School; Center for Neuro-Oncology, Dana-Farber/Brigham and Women's Cancer Institute, 450 Brookline Avenue, Boston, MA, 02215, USA.
Abstract
PURPOSE OF REVIEW: The high incidence of and mortality from glioblastoma are matched by a lack of effective therapies. Previous research suggests an association between viral infection and glioma formation. In this manuscript, we review the available evidence for this association and the efficacy of treatment strategies targeted against viral infection. RECENT FINDINGS: We find that while a wide array of viruses can drive glioma tumor formation in vitro and in xenograft models, the most convincing association is with the human Cytomegalovirus (HCMV). Detection of HCMV in glioblastoma resected from living patients suggests it may either drive gliomagenesis, support tumor growth, or reactivate silently in these tumors. However, there is conflicting evidence on its ubiquity and its role in tumor formation. Valganciclovir may extend survival in glioblastoma patients, though adequate data on its efficacy and mechanism of action are lacking. Immunotherapy provides the opportunity to specifically target the virus and possibly, glioblastoma, though there are no large, randomized trials testing its efficacy to date. Overall, despite mounting evidence for an association between HCMV and glioblastoma, its role as an oncogenic factor and a therapeutic target remains controversial.
PURPOSE OF REVIEW: The high incidence of and mortality from glioblastoma are matched by a lack of effective therapies. Previous research suggests an association between viral infection and glioma formation. In this manuscript, we review the available evidence for this association and the efficacy of treatment strategies targeted against viral infection. RECENT FINDINGS: We find that while a wide array of viruses can drive glioma tumor formation in vitro and in xenograft models, the most convincing association is with the human Cytomegalovirus (HCMV). Detection of HCMV in glioblastoma resected from living patients suggests it may either drive gliomagenesis, support tumor growth, or reactivate silently in these tumors. However, there is conflicting evidence on its ubiquity and its role in tumor formation. Valganciclovir may extend survival in glioblastomapatients, though adequate data on its efficacy and mechanism of action are lacking. Immunotherapy provides the opportunity to specifically target the virus and possibly, glioblastoma, though there are no large, randomized trials testing its efficacy to date. Overall, despite mounting evidence for an association between HCMV and glioblastoma, its role as an oncogenic factor and a therapeutic target remains controversial.
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