human papillomavirus infection, p53 overexpression and histopathologic characteristics in colorectal cancer

background there is evidence of a possible etiological role of human papillomaviruses (hpvs) in the development of colorectal cancer. loss of p53 tumor suppressor gene function has been found in many malignancies and it can occur in a variety of ways, including gene mutation and interaction with the e6 protein of oncogenic hpvs. the objective of this study was to determine the prevalence of hpv infection and p53 overexprssion in colorectal cancer (crc) tissue samples and its association with tumor histopathologic characteristics. materials and methods 60 tissue sections from patients with crc were investigated by immunocytochemistry techniques for aberrant expression of p53 using the streptavidin-biotin-peroxidase method with monoclonal antibodies. the hpv status was also analyzed using type-specific primers for hpv16/18 by polymerase chain reaction (pcr). results overall, 21 (35%) of 60 patients were found positive for hpv dna; hpv 18 was detected in 19 (32%) and hpv16 in 11 (18%) of 60 samples. an abnormal expression of tumor-suppressor protein p53 was observed in 29 (48%) samples. p53 overexpression was observed in 15 (71%) of 21 hpv-positive and in 14 (36%) of 39 hpv-negative patients (p=0.009). similar significant difference was found in p53 overexpression in hpv18-positive patients (p=0.007) but not in those positive for hpv 16 (p=0.261). hpv dna presentation was not significantly associated with histopathologic characteristics including tumor stage (p=0.509), grade (p=0.668), peri-neural invasion (p=0.265) and lympho-vascular invasion (p=0.275). conclusions p53 inactivation caused by hpv infection may play a role in the pathogenesis of colorectal cancer. there is no association between hpv infection and histopathologic characteristics.