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Abstract
The incidence of human papillomavirus (HPV)-related head and neck squamous cell carcinoma continues to increase. Accurate diagnosis of the HPV status of a tumor is vital, as HPV+ versus HPV– tumors represent two unique biological and clinical entities with different treatment strategies. High-risk HPV subtypes encode oncoproteins E6 and E7 that disrupt cellular senescence and ultimately drive tumorigenesis. Current methods for detection of HPV take advantage of this established oncogenic pathway and detect HPV at various biological stages. This review article provides an overview of the existing technologies employed for the detection of HPV and their current or potential future role in management and prognostication.
Highlights
The incidence of human papillomavirus (HPV)-related head and neck squamous cell carcinomas (HNSCCs) has been increasing in recent decades [1,2]
Buonocore et al recently suggested that the variation in the optimal cut-off for fine-needle aspiration biopsy (FNAB) specimens reported in the literature could be due to differences in fixation and preparation methods utilized, as FNAB specimen processing is not standardized across institutions [39]
The gold standard for HPV detection and the definition of p16 positivity in FNABs vary across studies, DNA in situ hybridization (ISH) and p16 IHC performed on FNAB samples have high concordance rates [38,40,41]
Summary
The incidence of human papillomavirus (HPV)-related head and neck squamous cell carcinomas (HNSCCs) has been increasing in recent decades [1,2]. The E7 viral oncoprotein binds to retinoblastoma protein (Rb), disrupting the cell cycle and, initiating the transcription of S-phase genes. E2F–pRb complex bycomplex displacing and binding to pRb. The to pRb. The subsequent release of E2F into its active state drives the expression of downstream gene subsequent release of E2F into its active state drives the expression of downstream gene products, products, allowing the cell to transition from the G1 to S phase. In a regulatory feedback attempt to inhibit inhibit further cell proliferation, p16 is upregulated, and can be a surrogate for HPV+ tumors. The simplest methodology for the detection of HPV takes advantage of this distinct oncogenic pathway and uses the upregulation of p16 expression as a surrogate for high-risk HPV [12].
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