CDKN2A and neuroblastoma: Genetic inactivation of p16 has been found in nearly 50% of all human cancers resulting in the bypass of this critical cell cycle control mechanism; on the other hand the overexpression of p16 at both mRNA and protein levels is associated with poor prognosis in several cancers including neuroblastoma, cervical, ovarian, breast, prostate and oral neoplasms [29] suggesting that p16 overexpression is a surrogate marker for rapid cell proliferation with failure to eliminate left-over p16 between mitoses [39].