TP53 and retinoblastoma: For example, data suggest that loss of function mutations in p53 [5,6,7], retinoblastoma tumor suppressor [8,9] p16 [5] and activation of p63 (all constituents of the p53 pathway) [10,11,12] are known to be frequent mutations in HNSCC, with up to 80% of patients with HNSCC experiencing loss of function mutation in p53 [6,7].