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Updated: Jan 2, 2026
Chromogenic In Situ Hybridization as a Tool for HPV-Related Head and Neck Cancer Diagnosis
Published on: June 14, 2019
HPV33+ HNSCC is associated with poor prognosis and has unique genomic and immunologic landscapes
Kate Chatfield-Reed1, Shanying Gui1, Wendi Q O'Neill1
1Seidman Cancer Center, University Hospitals, Cleveland, OH 44106, United States; Department of Otolaryngology-Head and Neck Surgery, University Hospitals Cleveland Medical Center, Case Western Reserve University, School of Medicine, Cleveland, OH 44106, United States.
Objective:
To determine the influence of high-risk HPV genotype on outcomes in HNSCC patients.
Materials And Methods:
This is a retrospective analysis of The Cancer Genome Atlas HNSCC cohort.
Results:
Using multivariate Cox regression analysis, we revealed that HPV33+ HNSCC patients have inferior overall survival compared to HPV16+ HNSCC patients independent of anatomical site (HR 3.59, 95% CI 1.58-8.12; p = 0.002). A host anti-viral immune response, apolipoprotein B mRNA editing enzyme, and catalytic polypeptide-like mutational signature, was under represented and, aneuploidy and 3p loss were more frequent in HPV33+ tumors. A deconvolution RNA-Seq algorithm to infer immune cell fractions revealed that CD8+ cytotoxic T-cell infiltration was reduced in HPV33+ compared to HPV16+ tumors (1.3% vs. 2.7%, p = 0.007). TGFB1, a negative modulator of T-cell infiltration and function, showed expression and pathway enrichment in HPV33+ tumors.
Conclusions:
Our work reveals that HPV genotype, in particular HPV33, has a powerful impact on HNSCC patient survival. We argue that p16 immunohistochemistry as a surrogate biomarker for HPV+ status will lead to sub-optimal risk stratification and advocate HPV genotype testing as standard of care.
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