Related Experiment Video

Updated: Jan 29, 2026

Chromogenic In Situ Hybridization as a Tool for HPV-Related Head and Neck Cancer Diagnosis
06:57

Chromogenic In Situ Hybridization as a Tool for HPV-Related Head and Neck Cancer Diagnosis

Published on: June 14, 2019

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Genomic Enrichment and Functional Impact of TP53 and CYLD Alterations in Recurrent and Metastatic HPV-Associated Head

Manu Prasad1,2, Alex T Cheng1,2,3, Marcel Mayer1,2,4

  • 1Head and Neck Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|January 28, 2026
PubMed
Abstract

Insights

Recurrent, metastatic HPV-associated head and neck cancer is driven by TP53 mutations promoting metastasis and cisplatin resistance. CYLD loss in HPV+ tumors enhances radiation sensitivity and immune activation, suggesting biomarker potential.

Area of Science:

  • Oncology
  • Genetics
  • Cancer Biology

Background:

  • Recurrent and metastatic human papillomavirus-associated head and neck squamous cell carcinoma (R/M HPV+ HNSCC) presents a significant clinical challenge with limited curative options.
  • The underlying genetic drivers of R/M HPV+ HNSCC are not fully understood, hindering the development of targeted therapies.

Purpose of the Study:

  • To profile the genetic landscape of R/M HPV+ HNSCC.
  • To functionally characterize genetic alterations enriched in this cancer type.

Main Methods:

  • Comparative genomic profiling of 159 R/M HPV+ tumors against primary tumors.
  • Functional modeling of high-priority genetic alterations (TP53, CYLD) assessing cellular phenotypes, in vivo growth, metastasis, and therapy response.
  • Transcriptomic analysis to elucidate downstream molecular pathways and immune microenvironment.

Main Results:

  • TP53 mutations were significantly enriched in R/M HPV+ tumors compared to primary HPV+ tumors, correlating with poorer survival.
  • CYLD alterations were specific to HPV+ HNSCC, not observed in HPV- tumors.
  • TP53 gain-of-function mutants promoted metastatic potential and cisplatin resistance, while CYLD loss enhanced radiosensitivity and T-cell-inflamed microenvironment signatures.

Conclusions:

  • R/M HPV+ HNSCC progression is influenced by TP53 gain-of-function mutations and CYLD loss.
  • TP53 mutations confer metastatic phenotypes and cisplatin resistance.
  • CYLD loss identifies a subset of HPV+ HNSCC with increased radiosensitivity and immune activation, suggesting potential for combination therapies.

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