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More throat, mouth cancers linked to HPV

by Jill Coley
Of The Post and Courier
About once a week, Boyd Gillespie, M.D., shocks a young nonsmoker with the diagnosis that he has cancer in the back of his mouth.
Most oral cancers are related to a lifetime of tobacco or alcohol abuse, but that profile is changing.
Gillespie, a head and neck cancer surgeon at MUSC’s Hollings Cancer Center, is seeing an increasing number of patients who are young, have little if any smoking history and have cancers predominantly of the tonsil and the back of the tongue.
The culprit is human papillomavirus, or HPV, the same sexually transmitted virus that causes cervical cancer. The oral cancer does not discriminate between sexes, striking men and women at equal rates, Gillespie said.
About 25 percent of the 40,000 head and neck cancers annually in the United States, or about 10,000 cases, might be attributable to HPV, Gillespie said. A decade ago, the number of mouth cancers related to the virus was nearly zero.
It’s a trend that other head and neck practitioners around the country also have witnessed, he said. Boyd and virologist Natalie Sutkowski, Ph.D., have studied and confirmed that factors such as age, smoking history and tumor location and appearance are highly predictive of which tumors are caused by HPV.
Risk factors are similar to those for cervical cancer: younger age of first sexual intercourse and multiple sexual partners. With throat and mouth cancers, oral sexual contact also is a factor.
“Oral sex is probably a bigger part of first sexual contact than maybe it was in the past,” Gillespie said. A 2005 national study reported that more than half of U.S. teenagers from 15 to 19 years of age had engaged in oral sex. That percentage jumped to 70 percent by ages 18 and 19.
But the complete story of the virus’s transmission is not known. “It’s unclear if it’s only passed through sexual contact,” Sutkowski said. “It would not be impossible in my mind that it could be passed through kissing.” A recent study in Nature Clinical Practice Oncology reported that “direct mouth-to-mouth contact or other means could not be excluded.”
Another factor contributing to the rise in HPV-related oral cancers could be that doctors 10 years ago didn’t necessarily look for the virus, Sutkowski said, and methods of testing have improved.
Also, more people smoked 10 years ago, so it was easier to blame tobacco.
But as more patients in their 20s and 30s appeared who didn’t smoke or abuse alcohol, the medical community took note.
Symptoms of HPV-related oral cancer include a visible growth or lesion on the tonsils or the base of the tongue that might affect speech or swallowing.
The ulcer might be sore, might bleed and could cause hoarseness. Gillespie recommends patients seek medical attention if they’ve had symptoms for a month or longer.
Some positive news is that HPV-related oral cancers have a good prognosis. But early intervention is key, Gillespie said, as survival rates fall from 90 percent to 50 percent when the cancer spreads to the lymph nodes.
To help people get medical attention early, the Hollings Cancer Center will open the Oral Lesion Clinic this month. The clinic will be staffed by a head and neck surgeon and an oral pathologist who will evaluate sores, ulcers and growths in the mouth or throat. A majority of patients will be referred by doctors or dentists.
The increased attention could lead to a push in boys receiving the HPV vaccine marketed as Gardasil by Merck.
There are more than 100 strains of HPV, about 13 of which are considered high-risk.
The vaccine protects against four types: HPV-16, which is responsible for half of cervical cancers and the majority of virus-related mouth and throat cancers, HPV-18, which is also responsible for cervical cancers; and strains 11 and 6, which are associated with genital warts.
Whether the vaccine protects against oral cancer remains to be seen but seems logical, Boyd said.
“Our hope is that by reducing the number of people incubating HPV-16 in the community, we will also see a dropoff of throat cancer,” he added

From virus to tumor
How a virus interacts with tissue and becomes a tumor is complicated. Sutkowski might have unlocked one process that contributes to human papillomavirus’s transformation to cancer.
Sutkowski has discovered an ancient viral conversation that takes place when HPV meets human DNA.

About 8 percent of human DNA is derived from virus particles that have worked their way into the human genome over millions of years, Sutkowski said.
Normally, these viral particles do nothing. But when HPV is introduced, the viral particles are activated and cause inflammation. The increased blood flow, in turn, nourishes tumors.
“It’s known that inflammation helps tumors grow,” Sutkowski said. “And these viral particles turn on inflammation. So maybe it’s just as simple as that— the inflammation may be helping tumors grow.”
Sutkowski is now turning her attention to searching for drugs to inhibit these ancient genes, stop the inflammation and interrupt the tumors’ growth.

Editor’s note: The article ran Jan. 14 in the Post and Courier and is reprinted with permission.


Friday, Jan. 25, 2008
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