More throat, mouth cancers linked to HPV
By Jill Coley
Many young nonsmokers get disease as result of contracting virus from oral sexual contact
About once a week, Dr. Boyd Gillespie 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 the Medical University of South Carolina’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 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 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.”
From virus to tumor
How a virus interacts with tissue and becomes a tumor is complicated. Virologist Natalie 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, working closely with head and neck cancer surgeon Boyd Gillespie, is now turning her attention to searching for drugs to inhibit these ancient genes, stop the inflammation and interrupt the tumors’ growth.
10 Percent of Women Infected with Human Papillomavirus by Age 16
A new study by the Health protection Agency estimates at least 10% of young women in England have been infected with one or more strains of the human papillomavirus (HPV) by the age of 16. The study will be discussed on the last day of the Health Protection Agency annual conference in Warwick.
The study, the first of its kind in England , investigated the proportion of women aged 10-29 years who had antibodies indicating they had been infected with HPV. Researchers tested blood samples from 1483 girls and women for types of HPV that can cause genital warts and cervical cancer. Results show that from the age of 14, the risk of HPV infection increases sharply.
Some HPV infections can cause cervical cancers in women and genital warts in both women and men, although most infections with HPV cause no symptoms and clear on their own.
Andrew Vyse, who is presenting the study to the conference said: “This study gives us vital information about how common HPV infection is in young women of different ages. However it does have some limitations and does not give a precise estimate of infection rates in young women in England therefore more work needs to be done.
“The study adds to what we already know about HPV, however we still need to learn more about the risks of infection and of the risks for persistent infection and progression to cancer.
Professor Pat Troop , Chief Executive of the Agency said: “This study is a valuable addition to our understanding of HPV infection in women in England and should contribute to effective policies to prevent genital warts and cervical cancer.
“With the Government’s recent announcement of the possible introduction of HPV vaccination, such research will help us and other public health experts to determine the impact of HPV vaccination.”
Basic facts on HPV
HPV (human papillomavirus) is the common wart virus. It is the cause of the various kinds of warts (genital warts, plantar warts, flat warts) as well as cervical dysplasia, vaginal dysplasia, and cervical cancer. HPV has been implicated as a cause of infertility, miscarriages, vaginosis, vaginitis, vulvar vestibulitis syndrome, prostate disease, and laryngeal papillomatosis.
Common misspellings for human papilloma virus include human papillomavirus, human papilloma virus, human papiloma virus, human papaloma virus, human papalloma virus, human pipiloma virus, human pipilloma virus, and many more.
It is impossible to determine how long someone has had an HPV infection. Neither men nor women are routinely tested for HPV. Women are “indirectly” tested for HPV by a Pap smear which shows “HPV characteristics” if the HPV has damaged some cells resulting in cervical dysplasia. If the cells are not damaged, the HPV goes undetected unless a Digene Hybrid Capture® HPV DNA Test is done.
Other test methods (specific blood tests) may show that there has been HPV infection in the past, but they cannot determine if HPV is currently present. HPV is usually diagnosed because the cervical or vaginal cells obtained by Pap smear or biopsy have the “characteristic appearance of HPV-infected cells” under the microscope.
HPV is not always transmitted sexually. However, the types that cause anogenital warts (also called condylomata acuminata, venereal warts, genital warts, vaginal warts, and penile warts) and cervical dysplasia are most commonly sexually transmitted, like low risk HPV types 6, 11, 42, 43, and 44. For this reason HPV is classified as an STD (sexually transmitted disease) and can be transmitted through sexual intercourse, oral sex, anal sex, or any skin-to-skin contact.
Some women develop genital warts, cervical/vaginal dysplasia, or both, while others become carriers with no signs or symptoms, or they become immune to certain HPV types. Men generally develop genital warts, become carriers, or develop immunity.
HPV is contagious even when warts and dysplasia are not present. Some HPV types have a greater association than others with cervical dysplasia and cancer like high risk HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 68. All of the HPV types are contagious.
HPV can lie dormant in humans for an unknown period of years. However, most individuals develop immunity, after which time they are no longer contagious.
It is impossible to prove that someone does NOT have any HPV types. It is relatively easy to prove when someone DOES have HPV, if (1) signs or symptoms are present, or (2) the Digene Hybrid Capture® HPV DNA Test is positive.
Some feel that HPV remains in a carrier state for years; however, this is probably uncommon. There are over 70 types of HPV. This may be the reason some believe that long carrier states are common. What may be viewed as a carrier state may simply be subsequent infections by different HPV types over the years. There are over 300 rhinoviruses (cold viruses), yet no one considers a cold virus to be in a perpetual carrier state that “flares up” periodically.
There is very little cross-immunity between the different HPV types. This means that if one has immunity to one HPV type, that specific immunity is not necessarily good against another HPV type.
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