HPV is known to cause most cases of cervical cancer. Some studies have suggested that the virus may also play a role in the development of HNSCCs, and HPV DNA has been detected in the tumors of 10% to 20% of HNSCC patients. In addition, active HPV DNA can be found in the tumors of HNSCC patients who do not drink or smoke--factors that have been associated with an increased risk of HNSCC. It is believed that HPV infection is an independent risk factor, but an interaction with exposure to tobacco smoke can not be excluded. The mechanism by which HPV might cause HNSCC is not known.
To find a possible mechanism of HPV carcinogenesis, Boudewijn J. M. Braakhuis, Ph.D., of the VU University Medical Center in Amsterdam, Netherlands, and colleagues looked at HPV DNA and RNA and genetic alterations in the tumors of 143 patients with HNSCC.
HNSCCs that had transcriptionally active HPV DNA (i.e., specific viral genes were expressed in the tumor cells) had a distinct genetic pattern in which there was little chromosomal loss. HNSCCs that lacked transcriptionally active HPV DNA had a genetic pattern in which whole or large parts of chromosomal arms were lost early in tumor development. The observed patterns support the idea that HNSCCs can be subdivided into two genetically distinct categories and that HPV infection is involved in the early development of some HNSCCs, according to the authors.
"Our results are consistent with the hypothesis that HNSCCs develop by two different etiologies: one driven by exposure to environmental carcinogens (i
Contact: Sarah L. Zielinski
Journal of the National Cancer Institute