Skip to main content
. 2015 Sep 28;19(4):313–322. doi: 10.5114/wo.2015.54389

Table 2.

HPV-positive and HPV-negative HNSCC molecular profiles

Molecular change HPV-positive HPV-negative
Viral DNA integration into host DNA yes no
DNA lesions (carcinogen adducts, breaks) background level frequently detected
Mutations in crucial genes e.g. TP53 infrequent, no frequent
Failure of TP53 suppressor function binding of cellular proteins by viral proteins: E6 (p53) and E7 (Rb) dysfunction protein produced by mutated gene
TP16 expression overexpression common low expression following gene methylation
Loss of heterozygosity uncommon frequent
Chromosome instability induction of centrosome instability increased general instability
Chromosome aberrations occasional chromosome loss gross deletions
Oncogenic pathway disrupting p53 and pRb molecular pathways carcinogen exposure → DNA lesion → mutation → mutator phenotype → cancer