Zdravniški Vestnik (Dec 2002)
THE ROLE OF TUMOUR SUPPRESSOR GENES IN LARYNGEAL SQUAMOUS CELL CARCINOMA
Abstract
We offer a general overview on tumour suppressor gene alterations identified in laryngeal squamous cell carcinoma. Addressing the retinoblastoma susceptibility gene inactivation by molecular genetic methods is a hard task due to its enormous size. However, loss of immunohistochemical expression of retinoblastoma protein is an infrequent event that we have observed in only one out of 37 cases (3%). p53 can be inactivated by a number of mechanisms. p53 protein overexpression is detected in a half of the cases, but p53 mutations are detected in only 34% of cases. Thus, a number of cases with p53 protein overexpression occur in the absence of detectable gene mutation. The implication of HPV in the development of these tumours seems, at most, marginal. p21WAF1 is expressed with independence of the p53 gene status and is related to squamous cell differentiation. p16INK4a can be inactivated by mutation and allelic deletion or homozygous deletion (22% each), or promoter hypermethylation in less than 10% of cases.
