The tumor-suppressor gene p53 acts as "the guardian of the genome", sensing DNA 
damage and initiating protective responses. To examine the hypothesis that p53 
abnormality leads to increased genomic alterations in primary tumor cells, our 
study utilized 51 primary tumors of cervical carcinoma and 10 microsatellite 
markers. These markers were mapped to the short arms of chromosomes 3 and 5, 
covering the regions 3p13-25 and 5p15.1-15.3. Genomic deletion on 3p and 5p was 
correlated with genetic or epigenetic p53 inactivation pathways, including p53 
mutation, genetic deletion of p53 and cervical infection with human 
papillomavirus. The proportion of abnormal p53 was found to be significantly 
higher in the cases exhibiting loss of heterozygosity (LOH) on 5p (p < 0.001), 
supporting the hypothesis of the presence of a p53-dependent pathway to cervical 
tumorigenesis. In contrast, however, LOH on 3p was found to be independent of 
p53 inactivation. A common deletion region, 3p22-24, was identified in 44% of 
informative cases, and genomic loss at this specific region was correlated with 
early tumorigenic onset and poor grade of tumor differentiation. Diversity 
within the patterns of genomic alteration in the same form of cancer suggests 
different sets of risk/tumorigenic profiles, molecular pathogenesis, as well as 
prognosis and outcome.