Role of microsatellite instability in young patients with laryngeal carcinoma

To determine whether early development of carcinoma in young patients could be explained by an alternative pathway such as microsatellite instability or whether it follows the classical tumor suppressor pathway characterized by loss of heterozygosity.

Microsatellite instability, loss of heterozygosity, and multiple mismatch repair, p16, p53, and p63 protein expression were analyzed in a series of 18 young patients with laryngeal cancer.

Only 2 of the 18 cases showed low microsatellite instability, whereas 9 of 17 presented loss of heterozygosity in at least one of the markers tested. All cases retained multiple mismatch repair protein expression. The p53, p16, and p63 expression profiles were consistent with the classical tumor suppressor pathway.

Laryngeal carcinoma in young patients develops through the classical tumor suppressor pathway.