The presence of HPV16 and HPV18 is believed to be responsible for the tumorigenesis of cervical cancer. As not all HPV-infected patients proceed consistently to carcinoma of the uterine cervix, it is important to clarify at the genetic level the mechanism of the disease progression following HPV infection. We recently investigated the loss of heterozygosity (LOH) in p53 gene, using the quantitative Southern hybridization-incorporated Imaging Plate method with a p53 cDNA probe. According to the detection of heterozygote in p53 allele, 11 (61.1%) out of 18 patients with cervical cancer, and 4 out of 11 heterozygotes cases (36.4%) exhibited a loss of heterozygosity in p53 allele. It could be suggested that the occurrence of LOH is produced through chromosomal alteration in the tumorigenesis of cervical cancer.