Findings show that a monoclonal antibody detects HERV-K113 in glioblastoma, suggesting tumor progression impacts survival.
Glioblastoma (GBM) is the most frequent and lethal subtype of high-grade glioma, constituting about 48% of all malignant brain and central nervous system (CNS) tumors. The median survival is 12–15 months despite multimodal treatment plans, and an abysmal 5% five-year survival rate depends on the age at diagnosis, molecular characteristics, and clinical management. We have previously examined the possible role of viruses in the etiology and pathogenesis of GBM by assessing its metagenome. Our results verified the Human Cytomegalovirus’s (HCMV) absence and identified the Human Endogenous Retrovirus K133 (HERV-K113) in GBM samples. Furthermore, RT-PCR and sequencing analyses revealed a full-length open reading frame (ORF) of the HERV-K113 polymerase gene, suggesting that this sequence might be integrated into the GBM genome. Building on these findings, our current study establishes the clinical relevance of HERV-K113 in GBM. We developed a monoclonal antibody against the HERV-K113 polymerase, assessed its expression in a primary GBM cohort, and validated the results in an external treatment-naïve GBM cohort. High protein expression of HERV-K113 polymerase was significantly associated with reduced overall survival in our GBM cohort, an observation validated in the treatment-naïve GBM cohort. These results emphasize the potential prognostic utility of HERV-K113 and its role in GBM pathogenesis, providing new insights into the interplay between viral elements and tumor progression.
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Macamo et al. (2025) studied this question.
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