-
Views
-
Cite
Cite
Li Mao, Waun Ki Hong, How Does Human Papillomavirus Contribute to Head and Neck Cancer Development?, JNCI: Journal of the National Cancer Institute, Volume 96, Issue 13, 7 July 2004, Pages 978–980, https://doi.org/10.1093/jnci/djh209
Close - Share Icon Share
Extract
Human papillomavirus (HPV) is the major etiologic factor in the development of cervical cancer ( 1 ) and has been the target for detection and prevention of the disease ( 2 , 3 ). Results of recent molecular and epidemiologic studies suggest that HPV may also be an etiologic factor in a subset of head and neck squamous-cell carcinomas (HNSCCs), particularly those that develop at oropharyngeal sites ( 4 – 6 ).
In this issue of the Journal, Braakhuis et al. ( 7 ) report the striking finding that HNSCCs with active HPV type 16 DNA (i.e., HPV16 DNA that expressed the viral E6 and E7 genes) had substantially lower rates of loss of heterozygosity (LOH) at chromosomal regions 3p, 9p, and 17p than tumors that contained inactive HPV DNA (i.e., HPV DNA that did not express E6 and E7). This finding did not extend to LOH at chromosomes 13q, 18q, 8p, and 6q ( 7 ). Not surprisingly, Braakhuis et al. ( 7 ) also observed a negative association between active HPV DNA and mutations in TP53, the gene encoding the p53 tumor suppressor, as has been reported by other groups ( 5 , 8 ). Because the chromosomal regions analyzed in the Braakhuis et al. study contain tumor suppressor genes and are commonly deleted in HNSCC, it is believed that LOH at these regions plays a role in head and neck tumorigenesis. The striking finding, therefore, suggests that HPV16 may play a role similar to those of the tumor suppressor genes located at the three chromosomal regions.
