We have been done the detailed deletion mapping of chromosome (chr.) 8p21.3- 23 to localize the candidate tumor suppressor gene(s) (TSGs) loci as well as studied the mechanism of activation of c myc gene, located at chr.8q24.1, by analyzing the amplification/rearrangement/HPV integration within approximately 580 kb of c myc locus in uterine cervical carcinoma (CaCx) of Indian patients. The association between the deletions in chr.8p21.3- 23 and alterations in the c myc locus has also been analyzed. The deletion mapping of chr.8p21.3- 23 was done by 15 microsatellite markers and the alterations in the c myc locus were analyzed by Southern hybridization using the pal- 1/c myc/mlvi- 4/HPV 16/18 probes in seven cervical intraepithelial neoplasia (CIN) and 55 primary uterine cervical carcinoma. The alterations in chr.8p/q have been correlated with the different clinicopathological parameters. Three discrete minimal deleted regions with high frequencies of loss of heterozygosity (LOH) (37- 43% ) were identified in the chr.8p23.1- 23.2 (D1), 8p23.1 (D2), and 8p 21.3- 22 (D3) regions within 0.41- 4.62 Mb. The deletion in the D1 region was significantly associated with the deletion in the D2 region (P = 0.03), whereas the deletion in D2 was marginally associated with the deletion in the D3 region (P = 0.07). The alterations in the c myc locus were seen in 43% of the samples. About 35% of the samples showed coalterations in both arms of chr.8. No significant association was observed with the alterations in chr.8p/q as well as with the different clinicopathological parameters. The deletions in chr.8p21.3- 23 and the alterations in the c myc locus are independently associated with the development of CaCx. The D1- D3 regions in chr.8p21.3- 23 could harbor candidate TSGs associated with the development of this tumor. The c myc gene was activated by amplification/rearrangement at the pal- 1/c myc/mlvi- 4 loci as well as HPV integration in the pal- 1 locus in this tumor. We have been done the detailed deletion mapping of chromosome (chr.) 8p21.3- 23 to localize the candidate tumor suppressor gene (s) (TSGs) loci as well as studied the mechanism of activation of c myc gene, located at chr. 8q24.1, by analyzing the amplification / rearrangement / HPV integration within about 580 kb of c myc locus in uterine cervical carcinoma (CaCx) of Indian patients. The association between the deletions in chr.8 p21.3- 23 and alterations in the c The deletion mapping of chr.8p21.3-23 was done by 15 microsatellite markers and the alterations in the c myc locus were analyzed by Southern hybridization using the pal-1 / c myc / mlvi-4 / HPV 16/18 probes in seven cervical intraepithelial neoplasia (CIN) and 55 primary uterine cervical carcinoma. The alterations in chr.8p / q have been correlated with the different clinicopathological parameters. Three discrete minimal deleted regions with high frequencies of loss of heterozygosity L (37-43%) were identified in the chr.8p23.1-23.2 (D1), 8p23.1 (D2), and 8p 21.3-22 (D3) regions within 0.41- 4.62 Mb. The deletion in the D1 The deletion was D2 was marginally associated with the deletion in the D3 region (P = 0.07). The alterations in the c myc locus were seen in 43% of the samples. About 35% of the samples showed coalterations in both arms of chr.8. No significant association was observed with the alterations in chr.8p / q as well as with the different clinicopathological parameters. The deletions in chr.8p21. The 23- 23 and the alterations in the c myc locus are independently associated with the development of CaCx. The D1- D3 regions in chr.8p21.3- 23 could harbor candidate TSGs associated with the development of this tumor. The c myc gene was activated by amplification / rearrangement at the pal-1 / c myc / mlvi-4 loci as well as HPV integration in the pal-1 locus in this tumor.