Monthly Archives: September 2018

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|

OCF’s Tobacco Cessation Spokesperson and Bradley Cooper’s Stunt Double Rides in Pendleton

You won’t find Cody Kiser at this year’s NFR, but you will find him working as a stuntman in the 2014 blockerbuster hit “American Sniper” starring Bradley Cooper.

The biographical war drama was directed by Clint Eastwood, and told the story of U.S. Navy Seal Chris Kyle.

Kiser, who rode Saturn Rocket for a 75.5-point score Friday at the Pendleton Round-Up, stepped in for Bradley during the scene that shows Kyle riding broncs during his rodeo days before he joined the Navy.

“That was the coolest thing I have ever done,” Kiser said. “I got to hang out for a day with Clint Eastwood and Bradley Cooper. Clint told me I looked a lot like Bradley. They said they wished they had me for the whole movie.”

A friend of Kiser’s who does stunt work in California put Kiser in touch with the people from the movie.

“They needed a bareback rider who had a certain look,” he said. “They had me and a saddle bronc rider, but he couldn’t ride bareback very well, so the job was mine.”

Kiser, 27, said he was living in Texas near where Kyle was shot in 2013, and that he had a friend working at the Rough Creek Ranch-Lodge in Erath County, Texas, where Kyle was shot.

“It’s such a small world,” he said.

Kiser earned a nice paycheck for his work, but said playing Kyle, even in a stunt role, was an honor.

“To be a part of that was unreal,” he said.

September, 2018|OCF In The News|

New Book: Vaccines Have Always Had Haters

Date: 09/23/18
Source: National Public Radio
Author: Susan Brink

Vaccinations have saved millions, maybe billions, of lives, says Michael Kinch, associate vice chancellor and director of the Center for Research Innovation in Business at Washington University in St. Louis. Those routine shots every child is expected to get can fill parents with hope that they’re protecting their children from serious diseases.

But vaccines also inspire fear that something could go terribly wrong. That’s why Kinch’s new book is aptly named: Between Hope and Fear: A History of Vaccines and Human Immunity.

He wrote it, he says, to present the science behind vaccines and to highlight the fallacy of anti-vaccine movements. NPR talked with Kinch about vaccines. This interview has been edited for clarity and length.

The first attempts to control smallpox go back at least 1,000 years and didn’t involve vaccines. Can you describe those attempts?

Smallpox was probably killing a half a million people a year in Europe alone. The medical community had adopted a practice called nasal insufflation. You could take a little bit of the material from a smallpox scab, turn it into a powder and have a child snort it into the nose. Or you could intentionally scrape the skin and put material from a smallpox pustule under the skin of a healthy individual. That was called variolation. Those procedures caused smallpox, and people got sick. But far fewer of them died because most people would get a less virulent form of disease than if they were infected through exposure to a smallpox patient. Those who survived were then immune to smallpox.

How do you suppose people even thought of doing those disgusting things with scabs and pus?

You have to make assumptions. Maybe someone who was caring for a person with smallpox got a cut, and the cut got infected with pus from the patient. Then the caretaker noticed that afterward, they were immune to smallpox infection.

Variolation and nasal insufflation worked reasonably well, but they were not vaccines. What is a vaccine?

A vaccine is an intentional procedure using killed or weakened germs to trigger an immune response. The exposure to the virus or bacteria allows your body’s defenses to work, clearing the germs from the body. With the next exposure to those germs, the body is ready to fight off infection. Vaccines are generally delivered in an injection in the muscle, because the vaccine stays in place long enough for the immune system to detect and fight it.

The development of the smallpox vaccine was a breakthrough by Edward Jenner in 1796. What did science learn from the smallpox vaccine?

It took about a century for all the lessons to be learned. The smallpox vaccine made people understand that, once you identify a pathogen, you can kill or weaken it. Inoculating people with those weakened or killed forms alerts their immune systems but without causing disease, without causing harm. But first, pathogens had to be identified. A whole slew of discoveries happened from the 1880s through the early 20th century. People discovered anthrax bacteria, discovered measles, mumps, rubella viruses, discovered diphtheria, pertussis and tetanus. Then scientists could weaken or kill the germs and create vaccines.

Which vaccines does the world most need now?

The two holy grails are an AIDS vaccine and a universal influenza vaccine. AIDS has proven particularly challenging because the virus mutates very rapidly, and AIDS has found really good ways to circumvent an immune response. And the influenza virus changes constantly. It kills 30,000 to 40,000 Americans a year, and every few generations, there’s a pandemic. Exactly 100 years ago, we had the Spanish flu that wiped out tens of millions of people.

There are others. The current scourge of the world is malaria. The organism that causes it can change and thus hide from a vaccine. New pathogens always arise, and with global warming they’re working their way north, where they haven’t been seen before.

The current anti-vaccination movement fears that vaccinations are linked to autism, though the original study suggesting the link has been roundly discredited. Were there always “anti-vaxers” throughout history?

The anti-vax movement is actually older than vaccines. There was a well-established anti-variolation movement when people were using scabs and pus to try to prevent smallpox. Lady Mary Wortley Montagu was the wife of the British ambassador to the Ottoman Empire and a progressive thinker. She strong-armed the embassy physician to perform variolation on her four-year-old son in 1715, but her husband was opposed to it and she had to do it behind his back.

For virtually any vaccine you can name, there was an anti-vax movement around it. An 1802 cartoon was titled “The Wonderful Effects of the New Inoculation.” It was a spoof, reflecting widespread fear and showing people sprouting cow’s heads and horns and tails after being vaccinated against smallpox. (Note: Smallpox vaccine was made with cowpox virus, which rendered people immune to both cowpox and smallpox.)

Have there been scientifically valid reasons for people to fear vaccines?

There have been mistakes. When Dr. Jonas Salk announced his polio vaccine in 1955, bells were rung around the country to celebrate. But as people started getting immunized, Cutter Laboratories, which manufactured the vaccine in California, didn’t properly prepare the vaccine. A lot of kids were unintentionally infected with polio, and the incident created a lot of fear. (According to the National Institutes of Health, 40,000 cases of polio were caused by 200,000 vaccinations from the bad batch; 10 children died and 40 were left with varying degrees of paralysis).

Vaccines aren’t perfect. But there’s no substance in the world, including water and oxygen, that is entirely safe.

Why did you write this book now?

I saw that things were getting worse. It’s becoming more expensive to develop vaccines and less profitable. We haven’t developed a novel vaccine in decades. Pharmaceutical companies are abandoning vaccines. The anti-vax movement, I would argue, is stronger than ever. They’re highly organized, highly motivated and well-funded.

September, 2018|Oral Cancer News|

Penn-led study raises hopes for vaccine to treat head and neck cancer

Date: 09/21/18
Source: The Inquire, philly.com
Author: Marie McCullough

The patient’s head and neck cancer came roaring back, spreading to his lymph nodes and skin, which developed bleeding tumors. Yet despite a grim prognosis, that man is alive and cancer-free more than two years later.

In a study led by the University of Pennsylvania and published Friday, researchers hypothesize that his remarkable remission is due to a promising combination: an experimental cancer vaccine that activated his disease-fighting T cells, plus Opdivo, one of the revolutionary “checkpoint inhibitor” drugs that cut a brake on the immune system.

“Of course, I’m biased,” said Charu Aggarwal, the Penn oncologist who led the study. “In my career, I haven’t seen a vaccine as impactful as this.”

However, the remission may have been due to Opdivo alone; the study lacks data to rule out that possibility.

Robert Ferris, director of the University of Pittsburgh Medical Center’s Hillman Cancer Center and head of the pivotal study leading to approval of Opdivo, called the Penn-led study “an important intermediate step exploring a strategy that we hope will work.”

Conventional vaccines prevent diseases by priming the immune system to recognize the distinctive “antigens” on invading microbes. Therapeutic cancer vaccines, like the one in this study, are intended to work after cancer develops by provoking a heightened immune response.

Despite decades of research, this approach remains experimental. The only approved product, the prostate cancer vaccine Provenge, was barely effective; the maker filed for bankruptcy in 2015.

A major obstacle to treatment vaccines is the fact that cancer arises from the body’s own cells. Although cancer cells produce antigens as they mutate, using these telltale proteins as targets for the immune system has proved to be very difficult.

Even so, at least four pharmaceutical groups are developing therapeutic vaccines that target human papillomavirus, HPV, the sexually transmitted virus that causes cervical cancer, head and neck cancer, and some rare genital cancers.

These diseases can be warded off with the preventive HPV vaccine that is recommended for all adolescents, but it didn’t exist until 12 years ago. Much to the dismay of public health authorities, vaccination rates remain low. And while screening can detect and treat cervical precancers, there are no early detection methods for head and neck cancers; experts call the surging incidence of these malignancies an “epidemic.”

The vaccine in the new study, called MEDI0457, was originally developed by Inovio with technology pioneered at Penn. In 2015, MedImmune, which is part of AstraZeneca, acquired exclusive rights to the drug.

MEDI0457 contains a DNA ring called a plasmid that programs the patient’s cells to produce two HPV antigens. The vaccine is injected into the patient’s muscle and enters cells with the help of a small electrical pulse applied to the skin. When the cells make the antigens, this triggers the immune system to activate disease-fighting white blood cells, so-called “killer” T cells.

For the study, published Friday in Clinical Cancer Research, 22 patients with head and neck cancer received conventional treatment — either surgery or chemotherapy and radiation — that eliminated all signs of cancer. This was supplemented by four doses of the experimental vaccine, which caused no serious side effects.

Eighteen patients, or 80 percent, showed elevated T cell activity that lasted at least three months after the final vaccine dose. While that is an encouraging sign, the study was too preliminary to detect clinical effectiveness such as tumor shrinkage or improved survival.

In the one patient who relapsed, cancer recurred seven months after vaccine treatment and spread to his lymph nodes and skin. He was given Opdivo and, eight weeks later, the cancer was gone.

Aggarwal and her co-authors note that such remarkable remissions do occasionally occur with checkpoint inhibitors. But they speculate that the vaccine revved up the patient’s T cells, then Opdivo removed the immune brake, enabling the T cells to attack the cancer.

“The response suggests the vaccine may in some manner prime the immune system, potentially boosting the effects of subsequent [checkpoint inhibitor] therapy,” Aggarwal said.

Rajarsi Mandal, director of the head and neck cancer immunotherapy research program at Johns Hopkins University, took a more conservative view: “They demonstrated vaccine specific T cell proliferation very nicely. But there is not a lot of data to suggest the vaccine is inducing any clinical response in these patients. Overall, it’s very interesting, but future studies are needed to demonstrate definitive clinical responses to the vaccine.”

Still, the combination approach is sufficiently promising that MedImmune is now funding a Penn-led clinical trial of MEDI0457 and MedImmune’s own experimental checkpoint inhibitor.

Ferris, meanwhile, said he is part of a trial of a competing experimental vaccine for HPV-related cancers, plus the approved checkpoint inhibitor Keytruda.

“The preventive HPV vaccine works really well,” he said. “But if you’re too old to get it, there is hope that you can stimulate the immune system to fight the cancer. This [new study] suggests the next logical step.”

September, 2018|Oral Cancer News|

Youth vaping has soared in 2018, new data show

Source: www.wsj.com
Authors: Betsy McKay and Jennifer Maloney

Number of high schoolers who used e-cigarettes in the past 30 days has risen some 75% in 2018

Teen use of e-cigarettes has soared this year, according to new research conducted in 2018 that suggest fast-changing youth habits will pose a challenge for public-health officials, schools and parents.

The number of high-school students who used e-cigarettes in the past 30 days has risen roughly 75% since last year, according to a person who has seen new preliminary federal data.

That would equate to about three million, or about 20% of high-school students, up from 1.73 million, or 11.7% of high-school students in the most recently published federal numbers from 2017.

Nearly a third of 13-to-18-year-olds who responded to a separate survey conducted by The Wall Street Journal with research firm Mercury Analytics said they currently vape.

The new numbers offer a rare look at evolving teen vaping habits. Sales of e-cigarettes are expected nearly to double this year over 2017, and researchers have wondered how much of that increase is because of teen use. But there can be a long lag time between the collection of data and public reports.

Most of the teens who vape said they are doing it for reasons other than to quit smoking, according to the Journal’s survey conducted in 49 states in May. More than half said they do it because they like the flavors that e-cigarette liquids come in and they think vaping is fun. More than two-thirds said they believe vaping can be part of a “healthy life.”

U.S. Food and Drug Commissioner Scott Gottlieb said last week that teen use “has reached an epidemic proportion.” He announced new measures to curb teen vaping and warned he is considering banning flavored products.

The preliminary federal numbers from 2018 are from the government’s latest National Youth Tobacco Survey, according to the person familiar with the data. The survey was conducted in the spring.

The number of high-school users of combustible, or traditional, cigarettes increased slightly from the 2017 survey, this person said.

Monitoring the Future, a long-running youth survey conducted by the University of Michigan, found in 2017 that 16.6% of 12th-graders and 13.1% of 10th-graders had vaped nicotine, marijuana or flavoring in the previous 30 days. Richard Miech, the survey’s principal investigator, said he believes there has been a “considerable jump” in adolescent vaping this year.

This year’s sales growth has been driven largely by the Juul, a slim device that resembles a flash drive and has become a status symbol among teens, who often vape sweet-flavored liquids like mango. Juul has a 72.8% dollar share of the estimated $2.5 billion market in channels measured by market-research firm Nielsen, according to a Wells Fargo analysis.

Health officials are concerned that the high levels of nicotine in some liquids can alter the chemistry of developing brains, making them more sensitive to addiction.

Juul Labs Inc. says its device is intended to help adult smokers quit. “We cannot be more emphatic on this point: No minor or non-nicotine user should ever try JUUL,” a spokeswoman said. “Our packaging includes a prominent nicotine label and clearly states for adult smokers.”

Parents and educators say they are trying to do more to combat vaping with children back to school. “There is a lot more that needs to be done because at this point there are so many thousands of kids who are addicted to nicotine,” said Meredith Berkman, a founder of Parents Against Vaping E-Cigarettes, which advocates for action to restrict e-cigarette access.

Trinity School in New York City, for example, plans this year to incorporate more material on e-cigarettes into its health-education program for students, said John Allman, head of school. “Parents are letting us know about this,” he said of teen use.

The Journal survey was conducted online with 1,722 participants initially, and most of the survey questions focused on 1,007 participants who said they either vape, used to vape, or know someone who vapes. Nearly three-quarters of the 1,007 participants were 17 or 18 years old; 62% were white, 21% were African-American and 18% were Hispanic. Rates of e-cigarette use are higher in older than younger teens.

A total of 501 participants said they vape: 153 regularly, and 348 occasionally. Their most common reasons for vaping were for the flavors, and because they think it’s cool. “I just enjoy the flavor and blowing really big clouds,” one participant wrote.

“It made me feel good the first time I tried it, and I got hooked,” wrote another.

When asked what they were inhaling, 71% said flavors, and 61% said nicotine.

More than two-thirds of the current vapers said they believe vaping can be part of a healthy life, though they believe there are some risks. More than half said their views of vaping had been influenced by posts on social media, an issue that has public-health experts concerned.

The percentage of respondents who said they vape is unusually high, and should be interpreted with caution, said David Abrams, a professor in the College of Global Public Health at New York University. “We can’t make too much of it,” he said, because the survey was conducted online, and the questions weren’t all asked the way they are asked on large academic or government surveys.

Measures taken by the FDA, Juul, schools and parents to limit underage access to vaping devices since this spring may also be having an effect, some experts say. “It’s possible that prevalence and use may decline over time,” said Jidong Huang, an associate professor of health management and policy at Georgia State University who studies e-cigarette use.

September, 2018|Oral Cancer News|

RJR Slapped with $6.5M verdict over musician’s mouth cancer

Source: blog.cvn.com
Author: Arlin Crisco

R.J. Reynolds was hit with a $6.5 million verdict Tuesday for the part jurors found the company played in the mouth cancer a Florida musician developed after years of smoking. Harewood v. R.J. Reynolds, 2007-CA-46331.

The award followed the Florida 11th Circuit Court jury’s conclusion that nicotine addiction and cigarettes caused the oral cancer doctors diagnosed Glenn Simmons with in 1995. Simmons, a bassist in bands throughout much of his life, began smoking as a teenager and smoked about a pack a day for decades. He died in 2003, at age 48, from complications related to cancer-related radiation therapy. Monday’s verdict found Reynolds liable on fraud and conspiracy claims related to a sweeping scheme to hide the dangers of cigarettes. However, while jurors awarded Simmons’ daughter, Hanifah Harewood $6.5 million in compensatory damages, they rejected a claim for punitives in the case.

The case is one of thousands of Florida’s Engle progeny lawsuits against the nation’s tobacco companies. They stem from a 2006 Florida Supreme Court decision decertifying Engle v. Liggett Group Inc., a class-action tobacco suit originally filed in 1994. Although the state’s supreme court ruled that Engle progeny cases must be tried individually, it found plaintiffs could rely on certain jury findings in the original case, including the determination that tobacco companies had placed a dangerous, addictive product on the market and had conspired to hide the dangers of smoking through much of the 20th century.

In order to be entitled to those findings, however, each Engle progeny plaintiff must prove the smoker at the heart of their case suffered from nicotine addiction that legally caused a specific smoking-related disease.

Key to the seven-day Simmons trial was the link between his smoking and his mouth cancer. During Monday’s closings, Reynolds’ attorney, King & Spalding’s Randall Bassett, argued the cancer’s location and Simmons’ relatively young age at diagnosis were inconsistent with smoking-related oral cancer. Bassett noted that defense expert Dr. Samir El-Mofty, an oral pathologist from Washington University, concluded Simmons’ cancer stemmed from an infection related to a tooth extraction. “Not a cancer caused by smoking, but a cancer caused by a virus that sometime along the way Mr. Simmons had been exposed to,” Bassett said.

But Harewood’s attorney, Koch, Parafinczuk, Wolf & Susen’s Austin Carr reminded jurors that Simmons’ treating physician, Dr. Francisco Civantos, a South Florida otolaryngologist, believed cigarettes caused Simmons’ cancer. “Dr. Civantos is the more credible, experienced, the more competent physician and surgeon,” Carr said during Monday’s closings. “He is the doctor that you should believe over [the defense] witness.”

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|

FDA to review application to modify health warning on Altria subsidiary’s smokeless tobacco product

Source: www.richmond.com
Author: staff

The U.S. Food and Drug Administration will review a request from an Altria Group Inc. subsidiary that wants to make the claim that a smokeless tobacco product is less dangerous than cigarettes. U.S. Smokeless Tobacco Co. said Friday that the FDA has agreed to do a substantive review of its “modified risk” application for Copenhagen Snuff Fine Cut. The company submitted the request for review earlier this year.

The snuff company wants to be able to use the claim “If you smoke consider this: Switching completely to this product from cigarettes reduces risk of lung cancer.”

The FDA requires smokeless tobacco products to carry statements that warn about the risk of mouth cancer, gum disease, tooth loss and addiction and that the product is not a safe alternative to cigarettes. The warnings are to be randomly rotated on packaging.

“We filed this application because we think adult smokers looking for potential reduced risk alternatives to cigarettes should have accurate information about the relative risks of Copenhagen Snuff,” Joe Murillo, Altria Client Services senior vice president for regulatory affairs, said in a statement.

The FDA defines modified risk tobacco products as tobacco products that are sold or distributed for use to reduce harm or the risk of tobacco-related disease associated with commercially marketed tobacco products.
In the review process, the FDA’s Tobacco Products Scientific Advisory Committee vets the scientific claims and makes a recommendation.

The FDA has reviewed more than 30 modified risk applications from tobacco companies since 2011, but none has been approved. Some remain under review, while others were denied by the agency or withdrawn by the companies that submitted them.

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|