Table 1.
Comparison of the key characteristics of HPV+ and HPV– OPSCCs
| Characteristics | HPV+ OPSCC | HPV– OPSCC |
|---|---|---|
| Patient characteristics | ||
| Average age at diagnosis (years) | 59a | 60 (P < 0.001)38 |
| Sex | 86.9% male | 76.8% male (P < 0.001)38 |
| Ethnicity | 90% white | 75.9% white (P < 0.001)38 |
| Role of smoking | Rising incidence of HPV+ OPSCC in smokers, as well as in nonsmokers38 | |
| Role of alcohol | HPV− OPSCC associated with greater alcohol consumption7 | |
| Role of sexual history | High number of sexual partners a risk factor for HPV+ OPSCC7 | |
| Tumour characteristics | ||
| Incidence per 100,000 | 4.62 | 1.82 (ref.38) |
| Anatomical location | More prevalent in oropharynx (94.2% HNSCC); specifically the base of tongue and tonsils2 | Less prevalent in the oropharynx (72.8% HNSCC)38 |
| Stage (AJCC 7th edn) | Early stage (T1–2); frequently with nodal metastasis at presentation156 | All stages (T1–4)38 |
| Histopathological appearance | Immature, basal-like/basaloid, non-keratinizing156 | Frequently keratinizing SCC |
| Cancer-specific mortality | HPV+ OPSCC associated with a more favourable prognosis (aHR 0.40, P < 0.001)38 | |
| Biological characteristics | ||
| Genetic alterations | More frequent alterations in genes encoding DNA damage response proteins, FGF and JAK–STAT signalling proteins, as well as immune-related genes such as HLA-A/B; PIK3CA mutations more commonly observed95 | Aberration of TP53 and cell-cycle pathways (such as CDKN2A loss); oxidative stress regulation more frequently mutated95 |
| Other aberrations | p53 and Rb degradation by E6 and E7, respectively243 | NR |
aIncidence of human papillomavirus-positive oropharyngeal squamous cell carcinoma (HPV+ OPSCC) increasing in older men. AJCC, American Committee on Cancer; aHR, adjusted hazard ratio; HNSCC, head and neck squamous cell carcinoma; NR, not reported; OPSCC, oropharyngeal squamous cell carcinoma; SCC, squamous cell carcinoma.