ArticleCancer discovery2025
Human Papillomavirus Integration Induces Oncogenic Host Gene Fusions in Oropharyngeal Cancers.
Article in Cancer discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The role of human papillomavirus in oral squamous cell and verrucous carcinomas: a systematic review with case series.Oncology reviews · 2026Pooled it
- Hybrid extrachromosomal DNA in HPV-driven cancers.Journal of virology · 2026Review
- FGFR3::TACC3 Fusion and NOTCH1 Loss-of-Function in a Case of HPV-Associated Sinonasal Squamous Cell Carcinoma: Diagnostic Challenge and Implications for Targeted Therapy.Head and neck pathology · 2026Article
- Clinical Significance of Biomarkers in Oropharyngeal Squamous Cell Carcinoma: Recurrence Prediction and Treatment Response.Cancer reports (Hoboken, N.J.) · 2026Review
- Therapeutic scheduling of WEE1 inhibition preserves T cell function and promotes immune control of HPVbioRxiv : the preprint server for biology · 2026Article
- Molecular heterogeneity of HPV-associated cancers and strategies to overcome treatment resistance.Cancer heterogeneity and plasticity · 2026Article
- Virus-mediated gene fusion: igniting and sustaining oncogenesis.Trends in cancer · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Human papillomavirus (HPV) integration disrupts host genomic structure and expression, but whether these alterations promote cancer development remains unclear. Multiple genomic analyses of oropharyngeal cancers identified several host fusion genes, including recurrent FGFR3-TACC3 fusions, expressed from rearranged genomic loci adjacent to HPV integration sites. Evolutionary modeling pointed to integration of virus concatemers into the host genome as a common initiating event in fusion formation. Coexpression of HPV16 E6/E7 and FGFR3-TACC3, but neither alone, was sufficient for tumor development in both xenograft and syngeneic mouse models and led to unique transcriptional programs implicated in carcinogenesis. FGFR3-TACC3 expression decreased the ubiquitination and degradation of E6 and E7, thereby increasing oncoprotein abundance. We conclude that expression of HPV16 oncoproteins and host-gene fusions generated from HPV integration sites can be sufficient for cancer development. SIGNIFICANCE: Fusion genes are frequently cancer drivers, but the molecular mechanisms underlying their formation have remained unclear. In this study, we identified HPV integration as the instigator of genomic rearrangements that lead to the formation of FGFR3-TACC3 and other fusion genes. FGFR3-TACC3 expression decreased the ubiquitination and degradation of HPV E6 and E7, furthering the oncogenesis of HPV.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.