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. 2022 Mar 23;23(7):3483. doi: 10.3390/ijms23073483

Table 1.

Table summarizing the main clinicopathological and molecular differences distinguishing the HPV− and the HPV+ HNSCC [1,4,6,7].

HPV− Clinicopathological
Aspects		 HPV+
  • -

    Alcohol and tobacco

 Main risk factors
  • -

    Sexual behavior
  • -

    Mainly oral cavity and larynx

 Anatomical subsite
  • -

    Mainly oropharynx
  • -

    Higher

 Age of diagnosis
  • -

    Lower (within the 6th decade of life)
  • -

    Modestly to well differentiated.

  • -

    More keratinized

 Cellular differentiation
status
  • -

    Poorly differentiated.

  • -

    Less keratinized
  • -

    Lower

 Immune infiltration
  • -

    Higher
  • -

    Worse

 Response to conventional therapies
  • -

    Better
  • -

    Less favorable: ~55%

 Prognosis: 5-year survival rates
  • -

    More favorable: 75–80%
HPV− Molecular Features HPV+
  • -

    Frequently mutated

 p53
  • -

    Generally WT

  • -

    Degraded by the E6 hr-HPV oncoviral protein
  • -

    Low expressed

 p16Ink4a
  • -

    Highly expressed
  • -

    High

 Mutational burden
  • -

    Low
  • -

    Hypermutational status and chromosomal instability induced mainly by alcohol and tobacco carcinogens

 Factors mediating cellular transformation
  • -

    E6 and E7 hr-HPV oncoproteins

  • -

    Genomic rearrangements induced by viral genome integration
HPV− and HPV+ HNSCC are characterized by
different transcriptional and mutational profiles