Human papillomavirus (HPV) infection is suspected of causing laryngeal carcinoma. The relationship of HPV-16 and 18 genotypes to apoptosis and p53 protein expression in Egyptian laryngeal carcinoma patients was studied. Biopsy specimens from 82 patients with laryngeal carcinoma and 28 with minimal pathological lesions serving as a control group were examined. In all specimens, HPV-16 and-18 were examined using PCR, p53 expression was studied by immunohistochemistry and DNA fragmentation to assess apoptosis was assayed using a biochemical method and gel electrophoresis. HPV-16 was detected in 51.2% of laryngeal carcinoma patients versus 14.3% of the control group (p=0.001). The surrounding areas of positive tumors were negative in 52.4% of them. HPV-16 was significantly higher in tumors with higher expression of p53 (p=0.026). An inverse significant relationship was found between HPV-16 and DNA fragmentation in the laryngeal carcinoma group (p=0.022). HPV-18 was detected in only 2.4% of laryngeal carcinoma patients. p53 protein was expressed in 76.8% of the malignant group with significant increasing positivity with increasing stage of the disease (p=0.025). Non of the control group was p53-positive. Our results suggest that highly oncogenic types of HPV may play a role in the pathogenesis of laryngeal carcinoma through inactivation of wild-type p53 with subsequent decrease in apoptosis and by induction of p53 mutation, which itself can induce malignant transformation. |