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Background and Objectives:Although the role of c-myb in head and neck tumor has not been studied, aberant expresion of c-myb in various cancer has been demonstrated recently, suggesting that c-myb may play a role in tumorigenesis. Consequently, disrupting c-myb function might prove a possible stratergy for controlling cancer cell growth. The purpose of this study is to investigate the posibility of clinical application of adenovirus-mediated dominant negative c-myb (DN-myb) gene therapy in head and neck cancer. Materials and Method:neck tumors and were assayed the expresion of c-myb and bcl-2 in tumor and normal tissue by RT-PCR. We have generated a replication-deficient recombinant adenovirus encoding the dominant negative c-myb (Ad/DN-myb) or control adenovirus enco-ding no transgene (Ad/GFP) and infected adenovirus to SNU-1076, head and neck tumor cell line. We examined cell proliferation by 3H-thymidine assay, apoptosis by DNA fragmentation, bcl-2 expresion and Akt/PKB phosphorylation by Western imunob-IGF-II, VEGF mRNA expresion by RT-PCR. Results:c-myb expression of head and neck tumor tisues was significan-tly higher than that of normal tisue, indicating that these genes may play an important role in carcinogenesis of head and neck tumor. Ad/DN-myb infected SNU-1076 cells decreased cell proliferation, IGF-1I and VEGF expression, and remarkably increased their apoptosis through the down-regulation of bcl-2 expression and the inhibition of Akt/PKB pathway activation. Conclusion:myb induced apoptosis of head and neck tumor cells and the adenovirusmedia-ted DN-myb gene therapy may be a potential molecular therapy for the treatment of head and neck tumor. (Korean J Otolaryngol 2003 ;46 :677-85)