The over-activation of oncogenes is a critical genetic event in the development and progression of solid malignancies. Gene amplification and specific mutations represent the prominent mechanisms that convert proto-oncogenes into their active, oncogenic forms. C-myc oncogene (gene locus: 8q24.21) regulates crucial cell and tissue functions, whereas its deregulation is implicated in carcinogenesis. Our research aimed to investigate the impact C-myc numerical imbalances on a series of laryngeal squamous cell carcinomas (LSCCs) characterized by different clinic-pathological features.

We analyzed 55 LSCC archival tissue sections by implementing a dual-color gene/chromosome fluorescent in situ hybridization assay (C-myc/Chr 8 FISH).

According to the extracted C-myc gene/Chr 8 signal ratios, we identified 18 cases with numerical imbalances. The majority of them were gene amplifications (pure n=15, amplification and polysomy n=1), whereas the last two (n=2) cases presented multiple gene copies as a result of Chr 8 polysomy. C-myc amplification was correlated with advanced stage. Stage III/IV cases demonstrated the highest levels of gene amplification (p=0.024).

C-myc amplification, combined or not with Chr 8 polysomy, is a relatively frequent event in LSCC. This numerical imbalance is associated with an aggressive phenotype, and it seems to be a significant key element among other oncogenes and suppressor genes that form specific genomic signatures in the corresponding patients with LSCC.