Source: MedPage Today
Author: Crystal Phend

Rising rates of oropharyngeal squamous cell carcinoma may stem from a new epidemic of sexually-transmitted human papillomavirus (HPV), according to a review.

The incidence of oral cancer has been on the rise over recent decades in the U.S. and some northern European countries, noted Torbjörn Ramqvist, of the Karolinska Institute in Stockholm, and Tina Dalianis, of the Swedish Institute for Infectious Disease Control in Solna, Sweden.

The corresponding increase in the percentage of those tumors positive for HPV over the past 10 years isn’t simply because of more sensitive testing, they wrote in the November issue of Emerging Infectious Diseases.

For example, the Swedish Cancer Registry documented a 2.8-fold increase in tonsillar cancer around Stockholm from 1970 to 2002. Examination of all available tonsillar cancer samples indicated a rise in HPV-positive tumors over this period from 23% to 68%, with a further jump to 93% by 2007.

Similar patterns were seen for tumors at the base of the tongue, the second most common type of oropharyngeal squamous cell carcinoma.

“We suggest that this increase is caused by a slow epidemic of HPV infection–induced oropharyngeal squamous cell carcinoma,” Ramqvist and Dalianis wrote in the paper.

Changes in sexual patterns are likely to blame, “such as increased oral sex or increasing numbers of sex partners,” they added.

The HPV-positive rate is much higher — at 45% to 100% — in oropharyngeal squamous cell carcinomas than for other types of head and neck squamous cell carcinomas, in which HPV DNA has shown up in only about one-quarter of tumors over the past decades, the reviewers noted.

Studies have shown that HPV present in these tumors is integrated into the genome and actively involved in their development with gene expression similar to that seen in HPV-positive cervical and vulvar cancer.

The International Agency for Research against Cancer now recognizes HPV infection as a risk factor for oropharyngeal squamous cell carcinoma, particularly the high-risk HPV type 16 (which accounts for about 90% of HPV in these tumors).

Other known risk factors — smoking and drinking — are often absent in patients with HPV-positive oropharyngeal squamous cell carcinoma.

One study recently linked open-mouth kissing to development of oral HPV infection, which “could play a major role in timing of prophylactic vaccination of children,” according to the review.

Vaccines directed again HPV16 (Cervarix and Gardasil) are recommended for girls at age 11 or 12, before becoming sexually active, but can be given to girls as young as 9, depending on circumstances.

“Although it will likely take several decades before the effects of HPV vaccination on cancer incidence will be detected, it is crucial to monitor the effects of the present HPV vaccination, not only on the incidence of cervical cancer but also on the incidence of oropharyngeal squamous cell carcinoma,” the reviewers wrote.