HPV-associated oropharyngeal cancer: in search of surrogate biomarkers for early lesions

The incidence of oropharyngeal cancer (OPSCC) has escalated in the past few decades; this has largely been triggered by high-risk human papillomavirus (HPV). Early cancer screening is needed for timely clinical intervention and may reduce mortality and morbidity, but the lack of knowledge about prem...

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Bibliographic Details
Published in:Oncogene 2024-02, Vol.43 (8), p.543-554
Main Authors: Lim, Yvonne X., D’Silva, Nisha J.
Format: Article
Language:English
Subjects:
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Apoptosis
Biomarkers
Cancer
Cancer screening
Carcinoma, Squamous Cell
Cell Biology
Human Genetics
Human papillomavirus
Humans
Internal Medicine
Lesions
Medical screening
Medicine
Medicine & Public Health
Morbidity
Oncology
Oropharyngeal cancer
Oropharyngeal Neoplasms - genetics
Oropharynx
Papillomaviridae - genetics
Papillomavirus Infections - complications
Review
Review Article
Throat cancer
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Summary:The incidence of oropharyngeal cancer (OPSCC) has escalated in the past few decades; this has largely been triggered by high-risk human papillomavirus (HPV). Early cancer screening is needed for timely clinical intervention and may reduce mortality and morbidity, but the lack of knowledge about premalignant lesions for OPSCC poses a significant challenge to early detection. Biomarkers that identify individuals at high risk for OPSCC may act as surrogate markers for precancer but these are limited as only a few studies decipher the multistep progression from HPV infection to OPSCC development. Here, we summarize the current literature describing the multistep progression from oral HPV infection, persistence, and tumor development in the oropharynx. We also examine key challenges that hinder the identification of premalignant lesions in the oropharynx and discuss potential biomarkers for oropharyngeal precancer. Finally, we evaluate novel strategies to improve investigations of the biological process that drives oral HPV persistence and OPSCC, highlighting new developments in the establishment of a genetic progression model for HPV + OPSCC and in vivo models that mimic HPV + OPSCC pathogenesis.
ISSN:0950-9232
1476-5594
1476-5594
DOI:10.1038/s41388-023-02927-9