Oropharyngeal Cancer

P3, N=89, Completed, Incyte Corporation | Active, not recruiting --> Completed

A subset of cells also harbored HPV16 ecDNA derived from the intrachromosomal HPV- TP63 DNAs. These findings define previously unrecognized higher-order architecture of integrated HPV DNA and highlight the power of FISH for distinguishing intrachromosomal from extrachromosomal DNA structures.

P1/2, N=24, Recruiting, Gustave Roussy, Cancer Campus, Grand Paris | Trial primary completion date: Aug 2025 --> Nov 2025

P1, N=32, Active, not recruiting, Baylor College of Medicine | Trial primary completion date: Oct 2025 --> Jan 2026

P=N/A, N=100, Recruiting, Griffith University

The ROC analysis confirmed the diagnostic accuracy of salivary EBV DNA load. Our preliminary results indicate the usefulness of determining EBV DNA load in saliva as a non-invasive prognostic biomarker in EBV-positive oropharyngeal cancer, but confirmation in larger cohort studies is required.

These findings highlight NKT cell differentiation as a strong prognostic indicator in OPSCC and support further exploration of epigenetic-immunologic interactions as potential therapeutic targets.

Surprisingly, we find that human A3B is incapable of blocking the replication of a murine papillomavirus ( Mus musculus papillomavirus 1, MmuPV1) in relevant primary cells from these animals or in infected tissues in vivo . These findings highlight the complexity of teasing apart host-pathogen interactions and suggest that papillomaviruses may have a general mechanism for escaping restriction by antiviral enzymes such as A3B.

P2, N=44, Not yet recruiting, National Cancer Institute (NCI) | Trial completion date: May 2027 --> Nov 2027 | Trial primary completion date: May 2027 --> Nov 2027

A 264-gene signature from HPVon HMSC cells correlated with worse prognosis in HPV + OPSCC (p < 0.003), suggesting an alternate role for HPV. Further validation of the HPV-MYB association and gene signature may improve therapeutic strategies in HPV-related malignancies.

P3, N=242, Recruiting, Radboud University Medical Center | Trial completion date: Dec 2028 --> Dec 2029 | Trial primary completion date: Dec 2028 --> Dec 2029

We demonstrate this mechanism of DDR activation in multiple systems: keratinocytes expressing only E2, in foreskin keratinocytes immortalized by HPV16, in HPV16 positive keratinocytes derived from a cervical lesion, in pre-neoplastic lesions induced by mouse papillomavirus MmuPV1, in head and neck cancer cell lines that retain E2 expression, and in HPV16 positive oropharyngeal patient derived xenografts that retain E2 expression. ATM inhibition preferentially killed cells expressing E2, presenting a novel strategy for treating HPV early preneoplasia and a large subset of HPV+ oropharyngeal cancers retaining E2 expression and episomal genomes.