HPV

As HPV-related cancer rates climb, experts scrutinize barriers to HPV vaccination

Source: www.cancertherapyadvisor.com
Author: Bryant Furlow

Oropharyngeal squamous cell carcinomas (SCCs) are now the most commonly diagnosed human papillomavirus (HPV)-associated cancers in the United States, with 15,479 men and 3438 women diagnosed in 2015, according to an analysis by the Centers for Disease Control and Prevention (CDC).1

Between 1999 and 2015, cervical cancer and vaginal squamous cell carcinoma (SCC) rates declined, by 1.6% and 0.6% per year, respectively. But rates for vulvar SCC increased by 1.3% annually during the same period. Anal SCC rates also climbed by approximately 2% a year among men and 3% among women.1

Rates of oropharyngeal SCC — cancers of the throat and tongue — climbed as well, particularly among men (2.7% a year vs 0.8% in women).

All told, more than 43,000 Americans were newly diagnosed with HPV-related cancers in 2015, the analysis showed, up from 30,115 in 1999.1 Most people diagnosed with HPV-associated malignancies are older than 49 years.1 Most women diagnosed with cervical cancer are older than 30 years.1

“We don’t actually know what caused the increase in HPV infections but we know now that we have a safe and effective vaccine that can prevent infections,” said Lois Ramondetta, MD, professor of gynecologic oncology and reproductive medicine at the University of Texas MD Anderson Cancer Center, Houston.

“We’re seeing people who were infected decades ago developing these cancers,” Dr Ramondetta said. “We’ll see rates continue to rise over the coming years because the vaccine wasn’t available before 2006.”

HPV vaccination rates are improving, Dr Ramondetta noted.

Overall, approximately half of adolescents in the United States have completed the HPV vaccine dose-series — well shy of the 2020 herd immunity goal of 80%.

“That’s the overall up-to-date vaccination rates for adolescents aged 13 to 17,” Dr Ramondetta explained. “That’s definitely not where we want it to go but it is 5% higher than last year. If you look at the one-completed-dose vaccine initiation rate, that’s 65.5%.”

HPV vaccination rates are improving more rapidly among boys than girls.

“For some reason, safety is not as big a concern for boys and their parents,” Dr Ramondetta said. “It shouldn’t be a concern at all. This vaccine has been studied more than just about any other vaccine. But if you ask parents why girls are not vaccinating, safety seems to be a concern for some.”

There appears to be less stigma among parents about sons becoming sexually active than there is about the sexual activity of daughters, said Debbie Saslow, PhD, senior director of HPV-related and women’s cancers at the American Cancer Society in Atlanta, Georgia.

Vaccination rates vary geographically, both between countries and within the US. Only a handful of states require that public school students receive the HPV vaccine. Vast expanses of the rural US have few or no pediatricians and limited access to the vaccine.

Australia introduced HPV vaccines at the same time as the US, nearly a decade ago, but Australia achieved 80% vaccination rates in just a year, Dr Saslow said. That was largely because the Australian government paid for the vaccines and they were administered in schools. As a result, this year, Australia changed cervical cancer screening recommendations to reflect the reduced risk: at age 25, women start undergoing HPV testing (rather than pap tests) every 5 years.

That will eventually happen in the US as well, Dr Saslow predicted.

“It’s going to happen but the question is when,” she said. “What will happen is we’ll start screening later, at age 25 and maybe eventually 30, and screening will get away from Pap testing, because Pap tests are not as effective in vaccinated people: they’ll detect a bunch of cervical changes unrelated to cancer. It will all be false positives. We’ll need to go to strictly HPV-based testing” or potentially some new type of screening test, according to Dr Saslow.

In the US, there appear to be socioeconomic or class barriers at play regarding HPV vaccination. Completion rates tend to be higher among more affluent groups, meaning that those who get the first vaccine are more likely to complete the series.

But there’s also a “reverse disparity” in initiating HPV vaccination at all Dr Saslow noted. “Poor and minority kids have higher rates of [the] first dose. Providers might be doing their own risk-based recommendations to parents, which they should not be doing, saying these kids are at higher risk.”

In high-socioeconomic-status urban and suburban communities, vaccine hesitance and prevalent “anti-vax” conspiracy theories may be barriers to vaccination. In rural areas, religious conservativism about sex and sexually transmitted disease — as well as the political climate — are likely factors, Dr Ramondetta added. Rates of HPV vaccination are worse than those for, say, polio or measles, suggesting that hesitance is related to the sexual nature of HPV transmission.

“There’s still a stigma about HPV infection, which is crazy, since most people are exposed,” said Dr Ramondetta. “Normalizing HPV is important — it’s just an aspect of the human condition, like flu.”

“There is ample evidence of the efficacy, safety and durability of this vaccine,” Dr Ramondetta said. “We need to find new ways to educate the public. We can talk to one another all we want in journals but meanwhile, social media is filled with [misinformation] … We need to take a larger role in social media, flooding it with accurate information.”

“Most parents just need reassurance,” she added. “Their motivation is to keep their kids safe.”

Doctors should recommend HPV vaccination every time they see adolescent patients and their parents, Dr Saslow emphasized. And, oncologists need to reach out to family physicians and pediatricians, she said.

References
1. Van Dyne EA, Henley SJ, Saraiya M, Thomas CC, Markowitz LE, Benard VB. Trends in human papillomavirus-associated cancers — United States, 1999-2015. MMWR Morb Mortal Wkly Rep. 2018;67(33);918–924.

October, 2018|Oral Cancer News|

Oral treatment may not be far off for head and neck cancer patients

Source: app.secure.griffith.edu.au
Author: staff, Griffith University

A highly promising approach to treating HPV-driven head and neck cancer is on the way, and it could be in the shape of a simple oral medication. This is according to new breakthrough research led by Griffith University, which has conducted trials showing that the drug, Alisertib, tested in trials to treat other cancers such as lung and kidney, can also successfully destroy the cancer cells associated with head and neck cancer.

Human Papilloma Virus (HPV) is the main culprit in head, neck and oral cancers. The virus is thought to be the most common sexually transmitted infection (STI) in the world, and most people are infected with HPV at some time in their lives.

The latest trials – which have taken place over the past three years at Griffith’s Gold Coast campus – have shown a particular enzyme inhibitor in the drug, has the ability to prevent proliferation of HPV cancer cells in advanced head and neck cancers.

A 100 per cent success rate
Led by Professor Nigel McMillan, program director from Griffith’s Menzies Health Institute Queensland, the trials have shown a 100 per cent success rate in the drug eradicating the cancerous tumours in animals.

“Head and neck cancers can unfortunately be very difficult to treat, just by the very nature of where they are located in and around the throat, tongue and mouth,” says Professor McMillan.

“This part of the body contains some delicate areas such as the vocal chords and areas relating to speech, taste, smell, saliva etc, therefore there can be some significant side effects with the current treatment options.

“Quality of life is a major consideration in this patient group and therefore a simple oral treatment regimen will have massive benefit over other treatments in terms of reducing some quite drastic side effects.”

In Australia, there are over 5000 new cases of head and neck cancer each year. First line treatments include radiation and surgery (increasingly of the robotic type), followed by chemotherapy, however survival rates of around 70 per cent have remained unchanged for the past 35 years.

Half of all head and neck cancers are known to be caused by the HPV virus, with four times as many men (784) as women (250) estimated to have already died from the disease in Australia during 2018.

In the United States, there are now more cases of head and neck cancer than there are cervical cancer, a disease which is now set to become much more rare in Australia due to the introduction a decade ago of the world-leading national (HPV) vaccination program for schoolchildren.

Professor McMillan says the next step in the research is for the drug to be extended to human trials at the Gold Coast with patients for whom other treatments have so far proved unsuccessful.

October, 2018|Oral Cancer News|

FDA approves expanded use of Gardasil 9 to include individuals 27 through 45 years old

The U.S. Food and Drug Administration today approved a supplemental application for Gardasil 9 (Human Papillomavirus (HPV) 9-valent Vaccine, Recombinant) expanding the approved use of the vaccine to include women and men aged 27 through 45 years. Gardasil 9 prevents certain cancers and diseases caused by the nine HPV types covered by the vaccine.

“Today’s approval represents an important opportunity to help prevent HPV-related diseases and cancers in a broader age range,” said Peter Marks, M.D., Ph.D., director of the FDA’s Center for Biologics Evaluation and Research. ”The Centers for Disease Control and Prevention has stated that HPV vaccination prior to becoming infected with the HPV types covered by the vaccine has the potential to prevent more than 90 percent of these cancers, or 31,200 cases every year, from ever developing.”

According to the CDC, every year about 14 million Americans become infected with HPV; about 12,000 women are diagnosed with and about 4,000 women die from cervical cancer caused by certain HPV viruses. Additionally, HPV viruses are associated with several other forms of cancer affecting men and women.

Gardasil, a vaccine approved by the FDA in 2006 to prevent certain cancers and diseases caused by four HPV types, is no longer distributed in the U.S. In 2014, the FDA approved Gardasil 9, which covers the same four HPV types as Gardasil, as well as an additional five HPV types. Gardasil 9 was approved for use in males and females aged 9 through 26 years.

The effectiveness of Gardasil is relevant to Gardasil 9 since the vaccines are manufactured similarly and cover four of the same HPV types. In a study in approximately 3,200 women 27 through 45 years of age, followed for an average of 3.5 years, Gardasil was 88 percent effective in the prevention of a combined endpoint of persistent infection, genital warts, vulvar and vaginal precancerous lesions, cervical precancerous lesions, and cervical cancer related to HPV types covered by the vaccine. The FDA’s approval of Gardasil 9 in women 27 through 45 years of age is based on these results and new data on long term follow-up from this study.

Effectiveness of Gardasil 9 in men 27 through 45 years of age is inferred from the data described above in women 27 through 45 years of age, as well as efficacy data from Gardasil in younger men (16 through 26 years of age) and immunogenicity data from a clinical trial in which 150 men, 27 through 45 years of age, received a 3-dose regimen of Gardasil over 6 months.

The safety of Gardasil 9 was evaluated in about a total of 13,000 males and females. The most commonly reported adverse reactions were injection site pain, swelling, redness and headaches.

The FDA granted the Gardasil 9 application priority review status. This program facilitates and expedites the review of medical products that address a serious or life-threatening condition.

The FDA granted approval of this supplement to the Gardasil 9 Biologics License Application to Merck, Sharp & Dohme Corp. a subsidiary of Merck & Co., Inc.

The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nation’s food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products.

October, 2018|Oral Cancer News|

HPV vaccine expanded for people ages 27 to 45

Source: www.nytimes.com
Authors: Denise Grady and Jan Hoffman

About 14 million women and men become infected with the human papillomavirus each year in the United States, according to the Centers for Disease Control and Prevention. CreditCreditKeith Bedford/The Boston Globe, via Getty Images

The HPV vaccine, which prevents cervical cancer and other malignancies, is now approved for men and women from 27 to 45-years-old, the Food and Drug Administration said on Friday.

The vaccine is Gardasil 9, made by Merck, and had been previously approved for minors and people up to age 26.

It works against the human papillomavirus, HPV, which can also cause genital warts and cancers of the vulva, anus, penis and parts of the throat. The virus has many strains. It is sexually transmitted, and most adults encounter at least one strain at some point in their lives. The vaccine protects against nine strains, including those most likely to cause cancers and genital warts.

“Today’s approval represents an important opportunity to help prevent HPV-related diseases and cancers in a broader age range,” Dr. Peter Marks, director of the F.D.A.’s Center for Biologics Evaluation and Research, said in a statement.

The approval was based on a study in women ages 27 to 45, showing that an earlier version of the vaccine was highly effective in preventing persistent HPV infection, genital warts, vulvar and vaginal precancers, cervical precancers and cervical cancers related to the virus types covered by the vaccine.

The vaccine’s effectiveness in men ages 27 to 45 is inferred from the data in women, from its efficacy in younger men and from evidence that it created immunity in a study of men 27 to 45-years-old.

The most common side effects of the vaccine include soreness at the injection site, swelling, redness and headaches.

If a person has already been exposed to a particular strain of HPV, the vaccine will not work against that strain. For that reason, vaccination has been strongly recommended for young people before they become sexually active.

But even someone who has already been exposed to a few strains — but not to all nine in the vaccine — can still gain protection against the strains they have not encountered.

“This is great,” Dr. Lois M. Ramondetta, a professor of gynecologic oncology at MD Anderson Cancer Center in Houston, said in an interview. “It’s a prevention vaccine. The best time to get it is before you turn 13 and have any intimate activity at all. But, that said, it protects against nine types of HPV, so if you have one of the types, you still can be protected from other HPV types.”

She added: “There is a whole generation of people we were missing who didn’t know about it. Doctors weren’t good at talking about it.”

She and Dr. William Schaffner, an infectious disease expert at Vanderbilt University, said people over 26 began asking doctors about the vaccine. Some were leaving marriages or monogamous relationships, expected to begin dating and realized they might be exposed to the virus.

“They want to feel protected to some extent,” Dr. Ramondetta said. “Now they have the opportunity.”

Younger people need two shots, but the older ones will need three, spaced a few months apart.

Dr. Ramondetta noted that tumors affecting part of the throat — called oropharyngeal cancers — caused by HPV are rising, particularly in men. The vaccine is believed to help prevent them.

Dr. Schaffner said a panel that advises the Centers for Disease Control and Prevention has already been discussing the data on using the vaccine in older people, and is expected to make a recommendation about it. The recommendation could be universal, meaning that everyone in that age range should receive it, or it could be “permissive,” meaning that the decision is up to doctors and patients.

Once that group, the Advisory Committee on Immunization Practices, recommends a vaccine, insurers generally cover it.

October, 2018|Oral Cancer News|

Oral sex and ‘deep kissing’ linked to increase in HPV-positive head and neck cancer

Source: www.sbs.com.au
Author: Amelia Dunn

Jake Simpson was 22 when he started to get painful toothaches. Trips back and forth to the dentist couldn’t seem to fix the growing lump at the back of his mouth It came as a total surprise to Jake, his partner Carly, and their newborn son Noah, when oncologists in Brisbane told him he had stage four head and neck cancer, and would need to start treatment immediately.

“We didn’t know what any of it meant. He was so young and healthy, we couldn’t believe it,” Carly said.

Despite rigorous treatment and surgery that removed more than two-thirds of his tongue, Jake’s cancer was too aggressive and spread to his lungs. He died within eight months of his diagnosis.

These cancers, known as oropharyngeal cancers in the back of the tongue and tonsils, are on the rise in young men, and are caused by the sexually transmitted disease HPV – human papillomavirus. While doctors believe it is most commonly passed on through oral sex, some argue it’s now as easy as ‘deep kissing’.

“Jake wasn’t tested for HPV because it was too aggressive from the day one, but that age bracket that he fell in, more than likely, the cause was HPV,” Carly said.

HPV has been dubbed the ‘common cold’ of STDs. Over 80 per cent of Australian adults will get HPV at one point in their lives, and most will clear it without even knowing.

But two particular strains, P16 and P18 are closely linked with cancer, not just in the cervix like widely known, but increasingly in the head and neck.

Two strains of HPV, P16 and P18 are closely linked with cancer, not just in the cervix like widely known, but increasingly in the head and neck.
Source: The Feed

Researchers across the US, UK and Australia say changing sexual practices over the last 50 years, and an increase in sexual partners has prompted the rising incidence rate of this cancer.

Oncologist Brett Hughes has witnessed the significant shift in the patient demographic, who says nearly 80 per cent of his patients now have HPV positive cancers.

“We now see an age group of people who generally live very healthy lifestyles; that don’t necessarily have to have drunk or smoke and the other risk factors that we’d normally associate with cancers in the mouth or throat.”

The cancer is also eight times more likely to present in men. Dr Hughes said oropharyngeal cancers are now the most common HPV related cancer in Australia, trumping cervical cancer, and are continuing to rise.

“It’s predicted for Australia and it may even be as late as in the 2030s that we might see the peak incidence which is a little bit scary considering how common this cancer is becoming.”

While this cancer is increasing, many take comfort in Australia’s strong vaccination program to fight HPV related cancers.

The Gardasil vaccine, developed by Australian of the year Professor Ian Frazer, was first administered to Australian girls in 2007, and then to boys in 2013 after it became clear HPV was affecting them as well. But Professor Frazer said people need to be given the vaccine before they’re sexually active.

“All the vaccines that we currently use are vaccines to prevent infection. A vaccine to cure an infection is a different beast all together,” he said.

Without a therapeutic vaccine, sexually active adults who missed out on the vaccine at school are still at risk of contracting persisting HPV, with Prof Frazer insisting “the big challenge now is to get something for oropharyngeal cancer.”

Right now, there is no vaccine for adults and no way of testing or preventing HPV positive oropharyngeal cancers. But there are people out there trying to change that.

After Jake Simpson passed away in 2016, he donated $20,000 for research into early intervention for these cancers.

His family chose a saliva research program currently underway at the Institute of Health and Biomedical Innovation in Brisbane lead by Professor Chamindie Punyadeera. The lab work is aimed at creating a simple and easy test everyone can do to monitor their HPV status at the dentist or GP.

“What we want to do is early intervention and detection,” she said.

“If you detect early, 80 per cent of patients survive. If you detect late, 20 per cent of them survive.”

But as the technology is still five years away from public use, and a therapeutic vaccine is perhaps even further away, Carly and Professor Punyadeera agree young people just need to be aware that this cancer exists, and is on the rise.

“Young boys think it’s a women’s cancer type. It’s not at all,” Prof Punyadeera said.

“It’s really sad and we all need to be aware of HPV associated head and neck cancers.”

October, 2018|Oral Cancer News|

Vaccine, anti-PD1 drug show promise against incurable HPV-related cancers

A tumor-specific vaccine combined with an immune checkpoint inhibitor shrank tumors in one third of patients with incurable cancer related to the human papilloma virus (HPV) in a phase II clinical trial led by investigators at The University of Texas MD Anderson Cancer Center and reported in JAMA Oncology.

“That encouraging response rate is about twice the rate produced by PD1 checkpoint inhibitors in previous clinical trials, so these results will lead to larger, randomized clinical trials of this combination,” said principal investigator Bonnie Glisson, M.D., professor of Thoracic/Head and Neck Medical Oncology and Abell-Hanger Foundation Distinguished Professor at MD Anderson.

Vaccines specific to HPV antigens found on tumors had previously sparked a strong immune response, but had not, by themselves, been active against established cancers, Glisson said.

“Vaccines are revving up the immune system, but the immunosuppressive tumor microenvironment probably prevents them from working,” Glisson said. “Our thinking was that inhibition of PD-1 would address one mechanism of immunosuppression, empowering the vaccine-activated T lymphocytes to attack the cancer.”

The team combined the vaccine ISA101, which targets important peptides produced by the strongly cancer-promoting HPV16 genotype of the virus, along with nivolumab, a checkpoint inhibitor that blocks activation of PD-1 on T cells.

Of the 24 patients with recurrent HPV16-related cancers, 22 had oropharyngeal (back of the throat) cancer, one had cervical cancer and one had anal cancer.

  • Eight (33 percent) had a tumor response, two were complete. All eight had oropharyngeal cancer. Median duration of response was 10.3 months.
  • Overall median survival was 17.5 months, progression-free survival was 2.7 months and 70 percent of patients survived to 12 months.
  • Five of the eight responders remain in response.

“The median survival of 17.5 months for these patients is promising and provides further support for randomized trials testing the contribution of ISA101 to PD-1 inhibition,” Glisson said.

HPV causes nearly all cervical cancers, and most oropharyngeal, anal, penile, vulvar and vaginal cancers. HPV16 and HPV18 are the leading viral genotypes that increase cancer risk. Given the viral cause of these cancers, immunotherapy has been considered a strong potential approach. The researchers note that three previous clinical trials of PD1 inhibitors alone for recurrent HPV-related cancers yielded response rates ranging from 16 to 22 percent.

Two patients had grade 3 or 4 side effects—elevated enzyme levels—that required them to discontinue nivolumab. Glisson said the team observed side effects expected from the two treatments separately, but the researchers were encouraged to see no sign of synergistic side effects caused by the combination.

“That’s important as we develop rational combination immunotherapy,” Glisson said. This clinical trial was among the first to combine vaccination with PD1 inhibition.

Randomized clinical trials of the vaccine and anti-PD1 combination for cervical and oropharyngeal cancer are being organized.

The single-arm trial was an investigator-initiated effort originated at MD Anderson, Glisson noted.

September, 2018|Oral Cancer News|

HPV-related cancer rates outpace vaccinations

Source: www.ctpost.com
Author: Cara Rosner, Conn. Health

Cancers linked to the human papillomavirus, commonly called HPV, rose dramatically in a 15-year period, even as the rates of young people being vaccinated climbed, the Centers for Disease Control and Prevention reported.

The 43,371 new cases of HPV-associated cancers reported nationwide in 2015 marked a 44 percent jump from the 30,115 cases reported in 1999, according to a CDC analysis. HPV vaccination rates have improved over the years, but not fast enough to stem the rise in cancers, the CDC said.

Oropharyngeal, or throat, cancer was the most common HPV-associated cancer in 2015, accounting for 15,479 cases among males and 3,438 among females. HPV infects about 14 million people each year. Between 1999 and 2015 rates of throat and vulvar cancer increased, vaginal and cervical cancer rates declined, and penile cancer rates were stable, according to the CDC.

“The (overall rise) seems to be mostly driven by oropharyngeal cancers,” said Dr. Sangini Sheth, assistant professor of obstetrics, gynecology and reproductive sciences at Yale School of Medicine.

“Vaccination is key to preventing those cancers,” said Sheth, who also is an associate medical director and director of colposcopy and cervical dysplasia at Yale New Haven Hospital’s Women’s Center. “Oropharyngeal cancer is most common in men, and HPV vaccination rates, while they are rising in the U.S. and Connecticut, became routine for boys later (than girls). And the rate of vaccinations among boys has definitely lagged that of girls. Hopefully, we will see vaccinating our boys have an impact on oropharyngeal cancer, but that’s going to take time.”

The push to vaccinate adolescents against HPV is a relatively recent development. The vaccination was included in the routine immunization program for females in 2006 and for males in 2011, according to the CDC.

At one time, the HPV-vaccine was viewed largely to prevent sexually transmitted diseases, and some parents “resented” it and thought it was unnecessary for their children, according to Dr. Richard Brauer, section head of otolaryngology at Greenwich Hospital. Now it’s marketed as a cancer vaccine and parents have become more receptive, said Brauer, who also has a private practice, Associates of Otolaryngology, in Greenwich.

In 2017, 65.5 percent of adolescents aged 13 to 17 nationwide had at least one dose of the HPV vaccine, up 5.1 percentage points from 2016, according to CDC data released in August.

In Connecticut, 75.4 percent of girls aged 13 to 17 had one dose of the vaccine, 67.1 percent had two doses and 58.4 received three doses. Among males, 67.3 percent received one dose, 58.8 percent got two and 37.8 percent got three, the 2017 data show. But even amid overall gains, hurdles remain. Gender disparity persists, and many teens received the first vaccine dose but failed to get necessary subsequent doses.

Children who are 11 or 12 years old should get two shots of HPV vaccine six to 12 months apart, according to the CDC. Adolescents who get their shots less than five months apart need a third dose of the vaccine, as do all children older than 14. Three doses also are recommended for people ages nine to 26 who have certain immunocompromised conditions.

“It falls on the parent” whether children get vaccinated, said Dr. Bradford Whitcomb, chief of gynecologic oncology at UConn Health. “People associate HPV with female stuff. It needs to be pushed that we’re not just preventing female cancers.”

While it’s encouraging that vaccination rates are climbing, “we just may not see the benefit of that for years to come,” Whitcomb said. “It’s going to take a longer time, especially with the development of cancer, to see the effect. After the HPV infection, it can take years for a cancer to develop.”

Many people exposed to HPV will never get cancer, doctors said. The most common HPV-associated cancer among women is cervical cancer. Data show rates of that cancer are falling, but there are racial disparities.

Between 2011 and 2015, Hispanic women had the highest incidence rates of cervical cancer at 8.9 percent, according to an analysis by the Kaiser Family Foundation. That compares with 8.4 percent among black women, 7.4 percent among white women and 6.1 percent among Asian and Pacific Islander women.

Cervical cancer mortality rates also showed racial disparities during that time. Black women had the highest mortality rate at 3.7 percent, compared with 2.6 percent among Hispanics, 2.2 percent among whites and 1.8 percent among Asians and Pacific Islanders, data show.

It is crucial for doctors to talk to young patients and their parents about the HPV vaccine, even if it spurs conversations parents may feel awkward having, Sheth said.

“Clinicians need to feel comfortable normalizing the HPV vaccine and really present the HPV vaccine as a cancer prevention tool,” she said.

Note:
This story was reported under a partnership with the Connecticut Health I-Team, a nonprofit news organization dedicated to health reporting. (c-hit.org)

September, 2018|Oral Cancer News|

Men with more than two oral sex partners are more likely to contract HPV

Source: www.nzherald.co.nz
Author: Rebecca Sullivan

Men who have had more than two oral sex partners are “significantly” more likely to contract HPV, a viral infection that can develop into oesophageal cancer, a new study has found.

HPV, or the human papillomavirus, causes about 20-25 per cent of oesophageal cancer cases, said Professor Shan Rajendra from UNSW’s Ingham Institute.

Men are three times more likely than women to contract HPV through oral sex. Smoking and drinking are also big risk factors causing oesophageal cancer, reports news.com.au.

Actor Michael Douglas, who smoked and drank excessively, famously went public about the cause of his own oesophageal cancer after being diagnosed in August 2010.

“This particular cancer is caused by HPV [human papillomavirus], which actually comes about from cunnilingus.” Douglas, the husband of Catherine Zeta Jones, told The Guardian in 2013. “It’s a sexually transmitted disease that causes cancer.”

The study was presented at the Gastroenterological Society’s annual Australian Gastroenterology Week last weekend and was also published in the academic journal Diseases of the Oesophagus.

“What we found was that if you had more than two oral sex partners in your lifetime, then you increase your risk of HPV-associated esophageal cancer significantly,” Professor Rajendra said.

“It’s sexually transmitted. You swallow the virus and it gets absorbed by the body and gets into the lining of the oesophagus. In some people it doesn’t get cleared by the immune system. In most people it gets cleared but if it doesn’t get cleared it can cause cancers of the head and neck,” he said.

Straight men who perform cunnilingus are three times more likely than women to contract the virus, because vaginal fluid has a higher viral load and men’s bodies are less able to clear the virus, Prof Rajendra said.

Australia was the first country in the world to offer a vaccine for HPV. Introduced in 2008, it was a compulsory vaccine for teenage girls in years 11 and 12.

But the good news is the treatment success rates of oesophageal cancer are actually higher among those who contracted the disease via HPV. The prognosis is not as good for people whose throat cancer is caused by poor lifestyle choices such as smoking and drinking.

Professor Shan Rajendra’s study of 142 patients with esophageal cancer found those who were “virus positive” — meaning they developed the disease through having HPV — had the earliest stage cancers and responded best to treatment.

“They were responding to surgery or endoscopic treatments so much better than those who were virus negative. They also responded better to chemotherapy and radiotherapy,” he said.

“People with the virus live longer because their cancer proteins knock off the normal conventional pathway to cancer. That gives a favourable prognosis.”

September, 2018|Oral Cancer News|

Scientists map interactions between head and neck cancer and HPV virus

Source: medicalxpress.com
Author: staff, Gladstone Institutes

Human papillomavirus (HPV) is widely known to cause nearly all cases of cervical cancer. However, you might not know that HPV also causes 70 percent of oropharyngeal cancer, a subset of head and neck cancers that affect the mouth, tongue, and tonsils. Although vaccines that protect against HPV infection are now available, they are not yet widespread, especially in men, nor do they address the large number of currently infected cancer patients.

Patients with head and neck cancer caused by HPV respond very differently to treatments than those whose cancer is associated with the consumption of tobacco products. The first group generally has better outcomes, with almost 80 percent of patients surviving longer than 5 years after diagnosis, compared to only 45-50 percent for patients with tobacco-related cancers.

To better understand what might cause these differences, a team of scientists led by Nevan J. Krogan, Ph.D., senior investigator at the Gladstone Institutes, is taking a unique approach by focusing on the cancer-causing virus. They recently mapped the interactions between all HPV proteins and human proteins for the first time. Their findings are published today in the journal Cancer Discovery.

“With our study, we identified several new protein interactions that were previously not known to cause cancer, expanding our knowledge of the oncogenic roles of the HPV virus” said Krogan, who is also a professor of cellular and molecular pharmacology at UC San Francisco (UCSF) and the director of the Quantitative Biosciences Institute (QBI) at UCSF. “The human proteins we found interacting with HPV are involved in both virus- and tobacco-related cancers, which means they could be potential targets for the development of new drugs or therapies.”

A Complete Picture of Virus-Cancer Connections
Krogan and Manon Eckhardt, Ph.D., a postdoctoral scholar in his laboratory at Gladstone, developed an integrated strategy to identify all the interactions between HPV proteins and human proteins. First, using a method called mass spectrometry, they discovered a total of 137 interactions between HPV and human proteins.

Then, in collaboration with computational biologist Wei Zhang, Ph.D., in the laboratory of Trey Ideker, Ph.D., at UC San Diego School of Medicine, they looked at entire networks of each protein—rather than only individual proteins—to detect the most important players. They also compared their list of proteins with data from HPV-associated cancer samples published by The Cancer Genome Atlas project. This large consortium catalogued genetic mutations in tumors of various cancers.

“We integrated together these two sets of data to get a comprehensive look at potential cancer-causing interactions between HPV and head and neck cancers,” said Krogan, who is co-director of the Cancer Cell Map Initiative. “This combined proteomic and genetic approach provided us with a systematic way to study the cellular mechanisms hijacked by virally induced cancers.”

Common Pathways in HPV-Induced and Smoking-Related Cancers
By overlaying the protein interaction and genomics data, the scientists discovered that the HPV virus targets the same human proteins that are frequently mutated in smoking-related cancers. Interestingly, those proteins are not mutated in HPV-positive cancers.

For example, their findings reconfirmed a well-established interaction between the human protein p53 and an HPV protein called E6. In HPV-negative cancers (those related to smoking), p53 is mutated in nearly all cases. However, the same protein is rarely ever mutated in HPV-positive cancer patients.

“In both cases, when p53 is inactivated, it leads to cancer,” explained Eckhardt, one of the first authors of the paper. “The difference is that the HPV virus finds a different way of attacking the same protein.”

In smoking-related cancers, p53 is mutated, which causes the cancer. Instead, in HPV-positive cancers, the viral protein E6 interacts with p53 and inactivates it, resulting in the same cancer, but without the mutation. This suggests the establishment of the viral infection and the development of tumors share common pathways.

“We thought there must be more proteins that can cause cancer either by being mutated or hijacked by HPV, so we developed a new method to detect them,” added Eckhardt. “Our study highlighted two interesting instances where the interaction of HPV and human proteins play a role in the development or invasiveness of the cancer.”

Eckhardt showed that the HPV protein E1 interacts with the human protein KEAP1, which is often mutated in smoking-related cancers. In HPV-positive cancers, KEAP1 is not mutated. But, through its interaction with the protein E1, KEAP1 is inactivated, which helps cancer cells survive.

The researchers also found that the HPV protein L2, which is part of the virus’s packaging, interacts with two human proteins called RNF20 and RNF40. They demonstrated that in HPV-positive cancers, this protein interaction increases the tumor’s ability to spread and invade new parts of the body.

These results confirm that the HPV virus causes head and neck cancer by targeting the same proteins that go awry in response to smoking-induced mutations.

Connecting Cancer and Infectious Diseases
Krogan and his collaborators have shown that integrating HPV-human interaction with tumor genome data, and focusing on genes that are mutated in HPV-negative but not HPV-positive tumors, constitutes a powerful approach to identify proteins that serve as both viral targets and genetic drivers of cancer.

The scientists’ work should lay the groundwork to find better therapeutic options for both HPV-negative and HPV-positive head and neck cancers. In addition, Krogan’s long-term goal is to define a pipeline that will enable the study of many other virally induced cancers, including those linked to Hepatitis B and C, Epstein-Barr virus, and adenoviruses.

“Science can be siloed, and through these unbiased, holistic approaches we can start to find common pathways between different systems,” said Krogan, who also leads the Host Pathogen Map Initiative, which aims to compare protein and genetic interactions across many pathogens and identify similarities. “Our work is helping connect the dots between cancer and infectious diseases in ways that have never been considered.”

September, 2018|Oral Cancer News|

Why I tell Everyone I have HPV

Source: bustle.com
Author: Emma McGowen

I have HPV. Or, to be more accurate, I was diagnosed with HPV when I was 19 and found a little bump on my vulva in an area where there was no chance it could be an ingrown hair. The nurse at the health clinic at my college put acid on it, watched while it turned white, and told me it was definitely a wart. That was the one and only “outbreak” I’ve ever had, but it was enough for me to say, sure, I have HPV. And I’m not shy about telling people that.

But I wasn’t always this chill about it. When I was diagnosed, I basically lost it. I fell right down the slut-shaming hole. I told myself that was “what I get” for sleeping around, and cycled through the usual you can never have sex again/HPV doesn’t go away/your vagina is going to be covered in hideous warts/YOU’RE A TERRIBLE PERSON thoughts that so many of us go through when we get an STI diagnosis. Mid-freak out, I called a close friend. “Oh yeah, I have it, too,” she said. I got the same response from a female family member. And that’s when I calmed down and realized — HPV isn’t a big deal.

Or, at least, the type of HPV I have isn’t a big deal. What I didn’t know at the time of diagnosis — but learned with a little Googling and had reinforced since, in my training as a sex educator — is that the strains of HPV that cause warts don’t have any other negative health effects. Specifically, if you have a strain of HPV that causes warts, it won’t cause cancer. And the strains that cause cancer don’t cause warts. So while the kind that I was diagnosed with has a visible component, it’s really no more annoying than the occasional pimple. And I’ve had way more pimples since I was 19 than I’ve had warts.

The other thing I’ve realized about HPV is that it’s ridiculously common. Because HPV is a skin-to-skin STI, there’s no way to protect 100 percent against it, other than never touching another human being again. Also, most people with penises carry the virus, but don’t show any symptoms — and can still spread it. So there’s no way for them to know if they have it and no way for the people who are sleeping with them to know, either. As a result of all of these factors, the CDC estimates that anyone not vaccinated against HPV will have it at some point in their lives.

Did you catch that? I’m going to repeat it, really loudly, just in case: the CDC says that anyone who is not vaccinated against HPV will have it at some points in their lives.

And here’s another fun fact: Contrary to the popular belief that HPV “never goes away,” many people actually clear the virus. That’s especially true for young people — which is the group in which the virus shows up most frequently — who get it. It’s also why the CDC doesn’t say “everyone has HPV” but that everyone who isn’t vaccinated “will get HPV at some time in their life.” So even though I was diagnosedwith HPV when I was 19, I don’t necessarily have it now, at 31. Does that mean I for sure don’t? Nope. Does that mean I for sure don’t carry other strains of the virus, including the cancer-causing ones? Nope. And that’s why I go regularly for Pap tests, which are a great method of early detection of irregular cells caused by HPV that can morph into cervical cancer. And also another reason why I honestly DGAF about my HPV status.

So if everyone will get it at some point or another, why do we still freak out about it? The answer is simultaneously really simple and really complicated: STI stigma. STI stigma is the overblown fear and shame so many of us carry about STIs. It’s the idea that getting an STI somehow means a person is “dirty” or “immoral” or a “slut.” It’s the idea that an STI is somehow worse than any other illness that one human picks up from another human. And you know why so many of us believe that? Because our culture teaches us that sex — especially for pleasure or outside of heterosexual marriage — is wrong.

With that in mind, my challenge to you is this. Ask yourself: Do I think sex outside of heterosexual marriage is wrong? Do I think sex for pleasure is wrong? Do I think people who have that kind of sex are bad? If the answer is yes, then you will probably continue thinking that people with STIs are dirty or immoral. And while I disagree with you, that’s your choice.

But if the answer is no, then I ask you: What makes an STI so much more morally wrong than any other illness? Nothing. And when you think about it that way, STI stigma and freaking out about an STI diagnosis — the way I did when I was 19 — just doesn’t make any logical sense. I don’t beat myself up when I get a cold, so why would I beat myself up for getting HPV? In both cases, there are things I could have done to be “safer” and protect myself against the virus but, hey, life happens.

So, yeah, I tell everyone I have HPV. Because, ultimately, it’s not a big deal, and because talking about it can help to eliminate some of that stigma. I also carry many forms of the common cold virus. Want to talk about that, too?

September, 2018|Oral Cancer News|