Molecular and genetic profile of head and neck squamous cell carcinoma

Abstract

To determine the molecular pathways of head and neck squamous cell carcinoma (HNSCC) tumorogenesis there are held a great amount of investigations. New therapeutic models for HNSCC are discussed considering genetic and biochemical specifications and taking in account significant scientific strategies. Dividing HNSCC into 2 large groups in accordance to human papilloma virus (HPV) association with different survival rates is a great achievement of the last decades in carcinogenesis researching and treatment of HNSCC. It is well known that chemical carcinogens are the main cause of HPV-negative tumors development. HPV-positive HNSCC is associated with E6 and E7 HPV proteins. The results of whole exome sequencing of HNSCC are of the great interest. Molecular expression profile of Rb-E2F/p53 were diff erent in HPV-positive and HPV-negative tumors. The phosphorylated pRb and p16 proteins analysis showed low pRb and high p16 levels in HPV-positive tumors in contrast to HPV-negative samples due to the HPV E7 ability to degrade Rb. P16 expression was higher in HPV-positive tumors, so it is immunohystochemical marker of HPV-positive status. The p53 expression pattern is determined also to identify its mechanism of degradation in HPV-positive tumors. Due to carcinogenic HPV ability by inactivation of cell cycle regulators р53 and pRb with the help of E6 and E7 oncoproteins, mutations of TP 53 shouldn’t play leading role in HPV-induced tomorogenity. Nevertheless, there are controversial data concerning HPV-positive tumors that part of them gain p53-mutations at the same time having integrated HPV-genome. The p53 expression in HPV-positive samples was the same as if in the absence of HPV.