Occurrence of p53 gene deletions and human papilloma virus infection in human head and neck cancer.

摘要: Abstract Little is known regarding the molecular genetic events in head and neck carcinoma. Epidemiological evidence suggests that both alcohol tobacco use are related to development of these neoplasms, viral infections have also been postulated play a role some tumors. Loss p53 tumor suppressor gene function has found many malignancies can occur through either mutation or by interaction with E6 protein oncogenic human papilloma viruses (HPV). Because mucosal surfaces exposed mutagens HPVs, we studied DNA derived from 30 stage I–IV squamous cell carcinomas (9 primary tumors 21 early passage lines) for mutations as well presence HPV DNA. Exons 2 11 were examined using single strand conformation polymorphism analysis followed direct genomic sequencing all variants. detection was done polymerase chain reaction amplification region type specific primers L1 degenerate (“consensus”) primers; determined restriction fragment length amplified Southern blotting Sixteen (53%) had detected 3 (10%) tumors, none which mutations. The mutational spectrum observed characterized equal frequencies transversions (6 16), transitions (5 deletions 16). This distribution differs reported esophageal (P = 0.05) lung 0.02) cancers, two other associated neoplasms. A previously undescribed clustering at codon 205 observed. trend toward shorter time recurrence after treatment noted those patients exhibiting mutations, no relationship between node status noted. Alteration appears common cancer, may reflect different mutagenic processes than responsible