Objective: In most laryngeal cancers, the function ofp53 gene is down regulated. To explore the potential use ofp53 in gene therapy of laryngeal cancer, by introducingwhd-type p53 into laryngeal cancer cell line via arecombinant adenoviral vecton Ad5CMV-p53 andanalyring its effects on cell and tumor growth. Methods: Ahuman laryngeal cancer cell line Hep-2 was used.Recombinant cytomegalovi rus - promoted adenovirusescontaining human wild-type p53 cDNA was transientlyintroduced into Hep-2 line. The growth suppression of theHep-2 cells and established s.c. squamous carcinoma modelwas examined. The p53 protein expression was detectedusing immunohistochemical analysis. Results: The transduction cfficiencies of Hep-2 cell line were 100% at amultiplicity of 100 or greater. The p53 protein expressionpeaked on day 2 after infection and lasted far 5 days. Invitro growth assays revealed cell death following Ad5CMVp53 infected. In vivo studies, Ad5CMV-p53 inhibited thetumorigenicity of Hep-2 cell, and in nude mice withestablished s.c. squamous carcinoma nodules showed thattumor volumes were significantly reduced in mice thatreceived peritumoral infiltration of Ad5CMV-p53. Conclusion: Adenovirus-mediated antitumor therapy carryingthe p53 gene is an efficient method to inhibit laryngealcancer growth. Transfection of laryngeal cancer cells withthe wild-type p53 gene via Ad5CMV-p53 is a potential novelapproach to the therapy of laryngeal cancer.