The tumor suppressor gene - p16 INK4/CDKN2/MTS1 and its alternate splice product p14 (ARF), constitute the INK4a locus. We have examined the integrity of exon 1beta of p14(ARF) gene of oral squamous cell carcinomas (n=58) in untreated Indian patients. No mutations were detected in this region by PCR-SSCP analysis of the tumor DNA's. Further, PCR-based analysis revealed homozygous deletions of exon 1beta in 14 of the 58 tumors; these results were confirmed by hybridization of tumor DNAs with exon 1beta specific probe. The deletions were limited to the exon 1beta while the exons coding p16/INK4 were not affected. Except in two cases these deletions were mutually exclusive to the p53 inactivating mutations. These observations suggest an alternate mechanism of loss of p14(ARF) in the genesis of oral squamous cell carcinomas.