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New cancer test isn’t ready for prime time

Author: H Gilbert Welch
Date: February 14, 2018
Source: http://www.cnn.com/2018/02/13/opinions/liquid-biopsy-opinion-welch/index.html

(CNN)- A simple blood test to detect cancer early. How great is that?

There has been enthusiasm about the so-called “liquid biopsy” for years. In mid-January, however, doctors learned more — both about this vision and its problems.

A widely reported study in the journal Science described a liquid biopsy test — CancerSEEK — which combined measuring eight tumor biomarkers with testing for pieces of DNA with cancer associated mutations in 16 genes.

It’s not one test; it’s a battery of tests. And while collecting the blood may be simple, the subsequent analysis is extraordinarily complex.

The task at hand is particularly challenging. We all have pieces of DNA in our blood. Distinguishing the tumor DNA from the background DNA requires finding the mutations specifically associated with cancer.

Adding to the complexity, healthy individuals can have mutations. To avoid labeling innocuous mutations as cancerous requires a bunch of statistical fine-tuning.

In other words, there are a lot of steps in a liquid biopsy and much potential for things to go awry.

To their credit, the CancerSEEK investigators were very forthright that the study conditions were ideal for the test to accurately detect cancer. The liquid biopsy simply had to discriminate between patients with known cancer (the majority of whom had symptoms) and healthy individuals. And the statistical fine-tuning was tailored to the study participants — with the knowledge of who had, and who did not have, cancer.

Although the test was able to detect most of the late-stage cancers, it detected less than half of the stage 1 cancers.

But doctors don’t screen to find advanced cancer, we screen to find early cancer. And we don’t screen people with symptoms of cancer, we screen people who don’t have symptoms of cancer.

There’s no doubt that there would be more detection errors in the less controlled environment of the real world.

Just how often was made clear in a recent JAMA-Oncology study. Forty patients with metastatic prostate cancer received liquid biopsies to tailor therapy in real time to the genetics of their spreading tumors. That’s the vision for precision medicine.

But the investigators added a little twist. They wanted to know whether it mattered which lab the liquid biopsies were sent to. So they sent each patient’s blood for two different commercial liquid biopsies: Guardant360 and PlasmaSELECT. Both tests were designed to detect mutations in the same genes.

Yet in over half of the 40 patients, the tests gave different answers about which mutations were present. Different liquid biopsy tests give different answers in a majority of patients? That’s not precision, that’s awful.

Sure, the analyses of liquid biopsies will improve. But if this much confusion exists about what mutations are present in the blood of patients with metastatic cancer (who have a lot of tumor DNA), imagine the uncertainty that will exist for asymptomatic individuals not known to have cancer — the very people who would be screened.

And then there is the question of what to do with a positive result. This is very different than detecting a concerning lung nodule on a screening chest CT scan or a concerning breast mass on a screening mammogram. In these cases, it’s clear what to do to get a definitive answer: surgically biopsy the nodule or the mass. But with a liquid biopsy, the anatomic location of a cancer can be a mystery. It may not even be clear what organ the cancer is in.

Imagine what this might mean for a patient: A doctor says, “It looks like you have cancer, but we are not sure where.”

Even if there is certainty that the cancer is in, say, the liver, doctors may not know where in the organ. What to do then? Randomly biopsy different parts of the liver?

This is doubly concerning when screening average-risk individuals, because most positive results are expected to be false alarms. We typically learn that a screening test is falsely positive because a surgical biopsy is normal. But absent the knowledge of where to biopsy, how can we ever be sure a positive liquid biopsy is wrong?

Doctors won’t know where to look, but we will keep looking. Liquid biopsies are a recipe for more health anxiety, more procedures, more complications and more overdiagnoses. Not to mention, more out-of-pocket costs for our patients.

Of course, we should continue to study liquid biopsies. The detection of circulating tumor DNA may ultimately prove useful in selected settings, such as tailoring therapy for aggressive cancers that are rapidly mutating. But the real enthusiasm is for screening average-risk individuals.

One reason is obvious: there is a lot of money to be made. A Goldman Sachs video estimated the potential liquid biopsy market to be $14 billion annually, adding “and we’re just at the beginning.” That kind of money doesn’t come from testing the few patients with aggressive cancer, that comes from screening millions of people.

And there is a less obvious reason: it is easier for a new test to pass regulatory muster than it is for a new drug. While the FDA has a longstanding mandate to protect us from snake oil treatments, this often doesn’t extend to snake oil testing.

The enthusiasm for finding things that might benefit people in the future ignores the fact that doing so can cause people to have problems now. In short, a bad test can do as much damage as a bad drug. Worrisome liquid biopsies will start a cascade of subsequent, not-so-simple tests and procedures. People will be hurt in the process.

February, 2018|Oral Cancer News|

CDHA Urges Hygienists to Remind Patients of Oral Cancer Screening

Author: Canadian Dental Hygienists Association
Date: January 29, 2018
Source: https://www.oralhealthgroup.com

World Cancer Day (February 4) is a perfect time for dental hygienists across Canada to remind the public of the importance of regular oral cancer screenings, not only during dental appointments, but also now at home.

The Canadian Cancer Society projected in 2017 that 4,700 Canadians would be diagnosed with oral cavity cancer, and that 1,250 Canadians would die.  In hopes of improving the long-term outcomes for people diagnosed with oral cancer, the Canadian Dental Hygienists Association (CDHA) has partnered with the Oral Cancer Foundation and the American Dental Hygienists Association on a “Check Your Mouth™” initiative to help individuals identify the early signs and symptoms of oral cavity cancers.  “Dental hygienists recognize that early detection has great potential to reduce the oral cancer burden in Canada,” states Sophia Baltzis, CDHA president. “Between dental visits, which usually include an oral cancer screening, our clients can and should examine their mouths for suspicious tissue changes.”

The Check Your Mouth™ campaign features an interactive website (www.checkyourmouth.org) that offers easy-to-use tools and tips for a quick visual and tactile examination of the oral cavity.  Individuals can learn to self-discover the early symptoms of disease and then seek further evaluation from a dental professional if necessary.  “Dental hygienists are your partners in prevention,” adds Baltzis. “We encourage all Canadians to maintain a healthy lifestyle, practice good oral hygiene habits, and spot the early signs of oral cancer. The Check Your Mouth™ website is a valuable resource that everyone should explore.”  By raising public awareness of oral cancer and its early signs and symptoms, dental hygienists are helping to meet the global challenge of saving lives. Together, we can make a difference!

Serving the profession since 1963, CDHA is the collective national voice of more than 28,495 registered dental hygienists working in Canada, directly representing 19,000 individual members including dental hygienists and students. Dental hygiene is the 6th largest registered health profession in Canada with professionals working in a variety of settings, including independent dental hygiene practice, with people of all ages, addressing issues related to oral health. For more information on oral health,

January, 2018|Oral Cancer News|

Study Identifies Potential Cause of Hearing Loss from Cisplatin

Author: NCI Staff
Date: January 26, 2018
Source: National Cancer Institute (https://www.cancer.gov/news-events)

Results from a new study may explain why many patients treated with the chemotherapy drug cisplatin develop lasting hearing loss.

Researchers found that, in both mice and humans, cisplatin can be found in the cochlea—the part of the inner ear that enables hearing—months and even years after treatment. By contrast, the drug is eliminated from most organs in the body within days to weeks after being administered.

The study, led by researchers from the National Institute on Deafness and other Communication Disorders (NIDCD), part of the National Institutes of Health, was published November 21 in Nature Communications.

Cisplatin, a platinum-based chemotherapy drug, is commonly used for the treatment of many cancers, including bladder, ovarian, and testicular cancers. But cisplatin and other similar platinum-containing drugs can damage the cochlea, leaving 40%–80% of adults, and at least 50% of children, with significant permanent hearing loss, a condition that can greatly affect quality of life.

“This study starts to explain why patients who receive the drug sustain hearing loss,” said Percy Ivy, M.D., associate chief of NCI’s Investigational Drug Branch, who was not involved in the study. “This is very important, because as we come to understand how cisplatin-related hearing loss occurs, over time we may figure out a way to block it, or at least diminish its effects.”

A New Approach to Researching Cisplatin-Induced Hearing Loss

The new study differs from previous research because it is a comprehensive look at the pharmacokinetics, or concentration, of the drug in the inner ear, explained study investigator Andrew Breglio, of NIDCD.

The research team primarily used a technique called inductively coupled plasma mass spectrometry (ICP-MS) to quantify the amount of platinum left in inner ear tissue following cisplatin treatment in mice.

Lisa Cunningham, Ph.D., of NIDCD, who led the research team, noted that instead of using one high dose of cisplatin with mice as other studies have, they developed a treatment protocol like those used in everyday care, in which the drug is given in cycles.

Testing done following each cisplatin cycle showed increasingly progressive hearing loss in the mice. The researchers also measured platinum levels in various organs throughout the drug cycles and found that, whereas other organs eliminated the drug relatively quickly, the cochlea retained the cisplatin, showing no significant loss of platinum 60 days after the last administration of the drug.

The researchers also conducted postmortem analysis of inner ear tissue of human patients who had received cisplatin, and found that platinum was retained in cochleae at least 18 months after the last treatment. In addition, they found that in the cochlea of one pediatric patient (the only one available for study), significantly more platinum was retained than in adult patients, consistent with the fact that children’s ears are known to be more susceptible to cisplatin-induced hearing loss.

In both the mouse model and in studies of human tissue, the researchers determined that the platinum accumulates in a part of the cochlea called the stria vascularis, which, Breglio explained, regulates the makeup of the fluid that bathes the sensory hair cells in the ear “and is critical to their proper function.”

This lengthy retention in the cochlea could explain why this drug is damaging the inner ear, Breglio said. Furthermore, these findings, demonstrating the accumulation of the drug and identifying where it is retained, mean that future studies need to “look beyond hair cells” to explain cisplatin-induced hearing loss, the researchers wrote.

Findings That Could Lead to Hearing Loss Treatment and Prevention

The finding that cisplatin is retained in the cochlea indefinitely is important for patient care, Dr. Ivy said.

Hearing loss from cisplatin “is not a static injury, it doesn’t stay the same. It can progress over time and it can occur late,” she added. “That suggests that a long-term survivor needs ongoing monitoring of their hearing.”

She said it will be up to practitioners to continue this monitoring and to rapidly intervene with devices that assist in hearing, such as hearing aids.

Hearing loss can have a particularly negative impact on children, she said.

“If adults develop hearing loss, they’re more acutely aware of it, and are more likely to seek assistance, whereas younger children who develop hearing loss might not notice it as much or be unable to explain the problem,” she explained. “Since they can’t hear very well, they may have trouble paying attention and that could be misconceived as a learning disability or a behavior problem. And yet, if they get the appropriate intervention, they perform at the same level they did prior to receiving platinum.”

This is why researchers on Dr. Cunningham’s team are trying to find ways to block cisplatin from entering the inner ear. They are looking at the cellular mechanism by which cisplatin is taken up by the cells of the stria vascularis to find ways to block uptake, as well as identify drugs that might “target cisplatin itself, and bind it or sequester it” before it can get into the inner ear, Breglio said.

“[Cisplatin] is one of the most widely used anticancer drugs on the planet, and it’s saving a lot of lives,” Dr. Cunningham said. But the hearing loss is permanent. “So these patients are surviving and they have this hearing loss for the rest of their lives. What we’d like to be able to do is develop a therapy that will allow patients to take the life-saving drug, but preserve their hearing.”

 

January, 2018|Oral Cancer News|

Anti-smoking plan may kill cigarettes–and save Big Tobacco

Date: January 19, 2018
Author: Matthew Perrone
Source: www.apnews.com

WASHINGTON (AP) — Imagine if cigarettes were no longer addictive and smoking itself became almost obsolete; only a tiny segment of Americans still lit up. That’s the goal of an unprecedented anti-smoking plan being carefully fashioned by U.S. health officials.

But the proposal from the Food and Drug Administration could have another unexpected effect: opening the door for companies to sell a new generation of alternative tobacco products, allowing the industry to survive — even thrive — for generations to come.

The plan puts the FDA at the center of a long-standing debate over so-called “reduced-risk” products, such as e-cigarettes, and whether they should have a role in anti-smoking efforts, which have long focused exclusively on getting smokers to quit.

“This is the single most controversial — and frankly, divisive — issue I’ve seen in my 40 years studying tobacco control policy,” said Kenneth Warner, professor emeritus at University of Michigan’s school of public health.

The FDA plan is two-fold: drastically cut nicotine levels in cigarettes so that they are essentially non-addictive. For those who can’t or won’t quit, allow lower-risk products that deliver nicotine without the deadly effects of traditional cigarettes.

 

US health officials are pushing ahead with an unprecedented plan to make cigarettes less addictive and provide lower-risk alternative products to US smokers. (Jan. 19)

This month the government effort is poised to take off. The FDA is expected to soon begin what will likely be a years-long process to control nicotine in cigarettes. And next week, the agency will hold a public meeting on a closely watched cigarette alternative from Philip Morris International, which, if granted FDA clearance, could launch as early as February.

The product, called iQOS (pronounced EYE-kose), is a penlike device that heats Marlboro-branded tobacco but stops short of burning it, an approach that Philip Morris says reduces exposure to tar and other toxic byproducts of burning cigarettes. This is different from e-cigarettes, which don’t use tobacco at all but instead vaporize liquid usually containing nicotine.

For anti-smoking activists these new products may mean surrendering hopes of a knockout blow to the industry. They say there is no safe tobacco product and the focus should be on getting people to quit. But others are more open to the idea of alternatives to get people away from cigarettes, the deadliest form of tobacco.

Tobacco companies have made claims about “safer” cigarettes since the 1950s, all later proven false. In some cases the introduction of these products, such as filtered and “low tar” cigarettes, propped up cigarette sales and kept millions of Americans smoking. Although the adult smoking rate has fallen to an all-time low of 15 percent, smoking remains the nation’s leading preventable cause of death and illness, responsible for about one in five U.S. deaths.

Anti-smoking groups also point to Big Tobacco’s history of manipulating public opinion and government efforts against smoking: In 2006, a federal judge ruled that Big Tobacco had lied and deceived the American public about the effects of smoking for more than 50 years. The industry defeated a 2010 proposal by the FDA to add graphic warning labels to cigarette packs. And FDA scrutiny of menthol-flavored cigarettes — used disproportionately by young people and minorities — has been bogged down since 2011, due to legal challenges.

“We’re not talking about an industry that is legitimately interested in saving lives here,” said Erika Sward of the American Lung Association.

But some industry observers say this time will be different.

“The environment has changed, the technology has changed, the companies have changed — that is the reality,” said Scott Ballin, a health policy consultant who previously worked for the American Heart Association.

Under a 2009 law, the FDA gained authority to regulate certain parts of the tobacco industry, including nicotine in cigarettes, though it cannot remove the ingredient completely. The same law allows the agency to scientifically review and permit sales of new tobacco products, including e-cigarettes. Little has happened so far. Last year, the agency said it would delay the deadline for manufacturers to submit their vapor-emitting products for review until 2022.

The FDA says it wants to continue to help people quit by supporting a variety of approaches, including new quit-smoking aids and opening opportunities for a variety of companies, including drugmakers, to help attack the problem. As part of this, the FDA sees an important role for alternative products — but in a world where cigarettes contain such a small amount of nicotine that they become unappealing even to lifelong smokers.

“We still have to provide an opportunity for adults who want to get access to satisfying levels of nicotine,” but without the hazards of burning tobacco, said FDA Commissioner Dr. Scott Gottlieb. He estimates the FDA plan could eventually prevent 8 million smoking-related deaths.

“SMOKE-FREE FUTURE”

Philip Morris International and its U.S. partner Altria will try to navigate the first steps of the new regulatory path next week.

At a two-day meeting before the FDA, company scientists will try and convince government experts that iQOS is less-harmful than cigarettes. If successful, iQOS could be advertised by Altria to U.S. consumers as a “reduced-risk” tobacco product, the first ever sanctioned by the FDA.

Because iQOS works with real tobacco the company believes it will be more effective than e-cigarettes in getting smokers to switch.

Philip Morris already sells the product in about 30 countries, including Canada, Japan and the United Kingdom.

iQOS is part of an elaborate corporate makeover for Philip Morris, which last year rebranded its website with the slogan: “Designing a smoke-free future.” The cigarette giant says it has invested over $3 billion in iQOS and eventually plans to stop selling cigarettes worldwide — though it resists setting a deadline.

Philip Morris executives say they are offering millions of smokers a better, less-harmful product.

Matthew Myers of the Campaign for Tobacco-Free Kids still sees danger. He says FDA must strictly limit marketing of products like iQOS to adult smokers who are unable or unwilling to quit. Otherwise they may be used in combination with cigarettes or even picked up by nonsmokers or young people who might see the new devices as harmless enough to try.

“As a growing percentage of the world makes the decision that smoking is too dangerous and too risky, iQOS provides an alternative to quitting that keeps them in the market,” Myers says.

It’s unclear whether existing alternatives to cigarettes help smokers quit, a claim often made by e-cigarette supporters. Research from the Centers for Disease Control and Prevention suggests about 60 percent of adult e-cigarette users also smoke regular cigarettes.

THE CASE FOR LOWER NICOTINE

Experts who study nicotine addiction say the FDA plan is grounded in the latest science.

Several recent studies have shown that when smokers switch to very low-nicotine cigarettes they smoke less and are more likely to try quitting. But they also seek nicotine from other sources, underscoring the need for alternatives. Without new options, smokers would likely seek regular-strength cigarettes on the black market.

Crucial to the FDA proposal is a simple fact: nicotine is highly addictive, but not deadly. It’s the burning tobacco and other substances inhaled through smoking that cause cancer, heart disease and bronchitis.

“It’s hard to imagine that using nicotine and tobacco in a way that isn’t burned, in a non-combustible form, isn’t going to be much safer,” said Eric Donny, an addiction researcher at the University of Pittsburgh.

A study of 800 smokers by Donny and other researchers showed that when nicotine was limited to less than 1 milligram per gram of tobacco, users smoked fewer cigarettes. The study, funded by the FDA, was pivotal to showing that smokers won’t compensate by smoking more if nicotine intake is reduced enough. That was the case with “light” and “low-tar” cigarettes introduced in the 1960s and 1970s, when some smokers actually began smoking more cigarettes per day.

Still, many in the anti-smoking community say larger, longer studies are needed to predict how low-nicotine cigarettes would work in the real world.

LEGAL RISKS

Key to the FDA plan is the assumption that the two actions will happen at the same time: as regulators cut nicotine in conventional cigarettes, manufacturers will provide alternative products.

But that presumes that tobacco companies will willingly part with their flagship product, which remains enormously profitable.

Kenneth Warner, the public policy professor, said he would be “astonished” if industry cooperates on reducing nicotine levels.

“I don’t think they will. I think they will bring out all of their political guns against it and I’m quite certain they will sue to prevent it,” he said.

In that scenario, the FDA plan to make cigarettes less addictive could be stalled in court for years while companies begin launching FDA-sanctioned alternative products. Tobacco critics say that scenario would be the most profitable for industry.

“It’s like Coke, you can have regular Coke, Diet Coke, Coke Zero, we’ll sell you any Coke you like,” said Robin Koval, president of the Truth Initiative, which runs educational anti-tobacco campaigns.

But the FDA’s Gottlieb says the two parts of the plan must go together. “I’m not going to advance this in a piecemeal fashion,” he said.

When pressed about whether industry will sue FDA over mandatory nicotine reductions, tobacco executives for Altria and other companies instead emphasized the long, complicated nature of the regulatory process.

“I’m not going to speculate about what may happen at the end of a multiyear process,” said Jose Murillo, an Altria vice president. “It will be science and evidence-based and we will be engaged at every step of the way.”

 

January, 2018|Oral Cancer News|

HPV vaccine is safe, effective after 10 years: study

Author: AFP/RelaxNews
Date: November 30, 2017
Source: Globalnews.ca

New research looking into the long-term effects of the human papillomavirus (HPV) vaccine has found it to be both safe and effective in protecting against the most virulent strains of the virus.

Led by Dr. Daron G. Ferris, professor in the Department of Obstetrics and Gynecology at the Medical College of Georgia and at the Georgia Cancer Center at Augusta University, the study is the longest followup to date on the vaccine, looking at data from 1,661 male and female participants who were followed for just under 10 years.

Of these participants, around two-thirds received a three-dose regimen of the vaccine when they were ages nine to 15 and sexually inactive.

Initially about one-third received a placebo — not a vaccine — however, the placebo group also received the vaccine 30 months into the study, meaning that these individuals were followed a shorter period of time.

Ferris found that the vaccine was virtually 100 per cent effective in preventing the disease, although vaccinating earlier produced the most robust initial and long-term antibody response, the proteins found in the blood which help fight infection.

“We needed to answer questions like if we vaccinate earlier in life, will it last,” explained Ferris, “The answer is yes, this cancer prevention vaccine is working incredibly well 10 years later. A booster vaccine likely will not be needed by these young people. I think now we have come full circle.”

The new finding also supports previous research which suggests that a more widespread and earlier administration of the HPV vaccine, before teens and preteens are exposed to the infection, is the preferred option.

Although the disease can be cleared in around two-thirds of infected individuals, the virus can persist in the remaining one-third, potentially causing a wide range of further health problems.

The quadrivalent vaccine, which protects against HPV types 6, 11, 16 and 18, is designed to better arm the immune system to eliminate the virus.

According to the National Cancer Institute, HPV types 16 and 18 account for essentially all cervical cancer and for most other HPV-related cancers such as penile and anal cancers. Types 6 and 11 account for about 90 per cent of genital warts as well as non-cancerous tumour growths in the respiratory tract.

 

HPV is the most sexually transmitted infection in the U.S.A. Around 79 million Americans, most in their late teens and early 20s, are infected according to the Centers for Disease Control and Prevention (CDC). HPV is also the most common cause of cervical cancer.

The Food and Drug Administration approved the first quadrivalent vaccine, Gardasil, in June 2006, with the vaccine currently approved for patients ages nine to 26.

 

Although the CDC reports that around 43 per cent of U.S. teens are up to date on recommended doses of the HPV vaccine, Ferris added that, “Now we need to push for more young people to get vaccinated. We are doing miserably in the United States.”

The HPV researchers added that the vaccine can be given along with the meningococcal and tetanus, diphtheria and pertussis vaccines, to 11- and 12-year-olds.

The results can be found published online in the journal Pediatrics.

November, 2017|Oral Cancer News|

10 Facts Everyone Should Know About HPV

Author: Lindsay Holmes
Date: November 27, 2017
Source: Huffingtonpost.com

First thing: Don’t stress.

An HPV diagnosis from your doctor doesn’t have to be scary.

In the first season of HBO’s “Girls,” Lena Dunham’s character, Hannah, gets a startling wake-up call when she tests positive for the human papillomavirus. She gets upset and confronts her ex-boyfriend about it. Her best friend tells her “all adventurous women” have HPV, but she generally buys into the overblown idea that her life is over.
Diagnoses like HPV can be complicated, and also unfairly laden with stigma. Research shows that shame and fear surrounding sexual health issues can be a barrier to testing and management.
But it doesn’t have to be this way. Experts say that educating yourself can help take the scariness out of an HPV diagnosis and help you manage your health.

Below is a breakdown of the facts everyone ― yes, including men! ― should know about HPV:

  1. HPV IS INCREDIBLY COMMON.

Approximately 79 million Americans have HPV, according to the U.S. Centers for Disease Control and Prevention. Most of those infected are in their 20s.
“HPV is very common, and most people will be exposed to HPV at some time in their lives,” Dr. Grace Lau, an assistant professor in the Department of Obstetrics and Gynecology at NYU Langone Health, told HuffPost.

  1. HPV IS CONSIDERED A SEXUALLY TRANSMITTED INFECTION.

It’s the most common one, according to the CDC. It’s typically spread through vaginal or anal sex, and it can be passed on even if your partner isn’t showing any symptoms.

“It requires intimate skin to skin contact for transmission,” Lau said. “Condom usage decreases the risk of transmission, but doesn’t completely take away that risk.”

  1. MANY DOCTORS MAY NOT EVEN TEST FOR IT.

Physicians may not screen for HPV during routine Pap smears or other health testing because of how common it is, according to the American Cancer Society. They may wait until you show signs of an infection (like genital warts), or they may test for it if you’re a woman whose Pap smear comes back abnormal.

  1. MEN CAN GET HPV AND PASS IT TO THEIR PARTNERS.

If you think the virus is a women’s health issue, think again: Research published in 2014 found that 69 percent of men studied had HPV.

  1. BUT THERE ISN’T A REAL WAY TO TEST MEN.

Currently, there’s no real recommended HPV test for men, according to the CDC. Most tests are done on women through routine screenings for cervical cancer.

“Women should have regular visits with their gynecologist and get regularly screened with pap smears,” Lau said.

  1. IT MIGHT INCREASE YOUR RISK FOR CANCER OR OTHER HEALTH ISSUES.

HPV is most commonly associated with a risk for certain cancers, including cervical cancer or oral cancers. Some forms of the virus can also cause genital warts. However, as the CDC points out, there’s no need to panic, either:
Cancer often takes years, even decades, to develop after a person gets HPV. The types of HPV that can cause genital warts are not the same as the types of HPV that can cause cancers.
Regular check-ins with your doctor can help monitor your health so you stay on top of any potential issues, Lau said.

  1. HPV DOESN’T NECESSARILY STAY WITH YOU FOREVER.

“Patients commonly assume that HPV is a lifelong infection that will stay with them always,” Lau said. “But most HPV infections in most people can be cleared by the immune system within one to two years.”

That doesn’t necessarily give you a free pass to ignore it, though. Lau stresses that it’s important to monitor your heath with your physician.

“If you have been diagnosed, it’s important to follow up with your doctor to make sure it clears,” she said.

  1. THERE ARE HUNDREDS OF STRAINS OF THE VIRUS.

There are high-risk strains and low-risk strains of HPV. Two high-risk types, HPV 16 and 18, are most commonly associated with precancerous or cancerous cell growth.

“HPV is not just one virus, but a group of over 200 related viruses. Each virus is labeled with a number to distinguish it from the others, and different viruses can target different areas of the body and can cause different possible diseases in humans,” Lau said. “Some cause skin problems like warts and others can lead to cancers.”

The HPV vaccine targets those high-risk strains, along with the strains that cause 90 percent of genital warts.

  1. THE VACCINE CAN PROTECT YOU.

Lau says everyone who plans on being sexually active should be vaccinated. Doctors typically instruct preteens get the vaccine, but if that doesn’t happen, it’s OK: Lau says the vaccine can be recommended for women up through age 26 and men up through age 21.

“The HPV vaccine is indicated for people who haven’t had sex yet, because it protects them against the viruses they haven’t been exposed to yet. However, the vaccine may still be helpful in people who have been sexually active,” she added.

  1. IT’S NOTHING TO FEEL ASHAMED ABOUT.

Bottom line: There’s no reason to buy into any stigma surrounding HPV ― or any sexual health issue, for that matter. The best thing you can do is stay proactive and smart about your well-being.

“HPV is something to be aware of and to be informed about,” Lau said. That’s it.

November, 2017|Oral Cancer News|

Superseed? Apricot kernels, touted as cancer cure, linked to cyanide poisoning

Author: Catherine Solyom
Date: November 22, 2017
Source: flipboard.com

Brendan Brogan had just returned from a shopping trip on the Plateau laden with exotic snacks.

On a visit to Montreal from California, he stood in the doorway of his buddy Mike Guetta’s room, munching away on something as they discussed the absurdities of the day.

Then Guetta looked up.

“Those better not be almonds,” he said. “You know I’m allergic to those.”

“No, no,” Brogan replied, “I would never do that. These are apricot pits.”

“What?!? Don’t eat those! They’re poisonous!”

Brogan pooh-poohed the warning, arguing the kernels were organic and he’d bought them at the health food store.

“Look! It’s the superseed of the Hunza people, with Vitamin B17!”

Then he turned the bag over and read the fine print. His face went grey: “Caution: Do not consume more than 2-3 kernels per day. Keep out of the reach of children. Pregnant and nursing women should not consume apricot kernels. Health Canada warns that eating too many apricot kernels can lead to acute cyanide poisoning.”

After a quick call to poison control, Brogan rushed to the nearest emergency room. He had eaten a third of the bag.

Apricot kernels, like cherry pits and apple seeds, contain a product called amygdalin, also known as laetrile and marketed as Vitamin B17.

Bitter apricot kernels — the pits of the pits — are widely available in Montreal health food stores, including at Rachelle-Béry branches across the city, where Brogan bought some. They are gluten-free, pesticide-free, vegan and organic.

They are also potentially lethal, as Brogan found out.

The kernels, like cherry pits and apple seeds, contain a product called amygdalin, also known as laetrile and marketed as Vitamin B17, though it’s more like an anti-vitamin.

When the seeds are chewed and digested, the amygdalin is converted to cyanide in the stomach. Eat too much of them — more than three apricot kernels for an adult and just one kernel for a toddler — and cyanide poisoning can occur.

Cyanide cuts off oxygen supply. Symptoms include headache, dizziness, mental confusion, weakness, difficulty breathing, abdominal pain, nausea, vomiting, seizures, coma and, eventually, death.

That’s why Australia, for one, has banned the sale of apricot kernels. But that didn’t stop a Melbourne man from slowly poisoning himself by ingesting 17 mg of homemade apricot kernel extract per day, in the mistaken belief that it would cure his prostate cancer. When doctors performed routine surgery on him in September, they found cyanide levels in his blood that were 25 times the accepted level.

Germany and the United Kingdom have also restricted the sale of apricot kernels, after a number of cases of children hospitalized for cyanide poisoning. In 2011, for example, a 28-month old girl was rushed unconscious to hospital in Turkey. She died in hospital of acute cyanide poisoning 22 days later. She had eaten 10 kernels.

The U.S. Food and Drug Administration has prohibited the sale of apricot kernels if  “intended for use in the cure, mitigation, treatment, or prevention of disease.”

The Canadian Food Inspection Agency, for its part, issued a recall and health hazard alert for Our Father’s Farm brand of apricot kernels in 2009, after a reported case of cyanide poisoning.

Since then the agency has received two more complaints of illness.

Packaging must now carry Health Canada’s warning label. But other brands have filled the void left by Our Father’s Farm.

 

Brogan bought the Organic Traditions brand of the kernel. Manually harvested and imported from Uzbekistan, the kernels are perhaps the “prized superseed” of the Hunza people. It says so right there on the packaging, along with the following claims: “contains vitamin B17” and “used in Ancient Asian medicine for centuries.”

In texts dating back to the 1930s that are rehashed by consumer direct and alternative health websites, the Hunza or Burusho people of the Himalayan region of northern Pakistan are said to live to be 140 and never get sick.

It must be because of the kernels, the story goes.

For example, a Facebook site liked by  997,744 people — titled “The truth about cancer” — says the Hunzas enjoyed near-perfect health.

“Some lived to be over 135 years old and no one in their clan had any of the conditions so common in the modern world, such as diabetes, obesity, heart attack, and cancer.” The website continues in bold lettering, noting that “they ate massive quantities of apricot seed kernels.”

Numerous other websites also claim that apricot kernels can prevent or cure cancer. The kernels are said to treat arthritis, boost your immune system and even serve as an aphrodisiac.

The truth about apricot seeds — and the Hunza people — is less rosy, however. A New York Times reporter who travelled to this Shangri-La in 1996 discovered a beautiful place indeed. But the elderly men who looked to be 140 were probably more like 70.

“The great Hunza secret to old age turned out to be its absence of birth records,” John Tierney wrote.

By  modern accounts, Hunza life expectancy is similar to other people in remote mountain regions who go through cycles of food scarcity — 50 to 60 years old.

On the seeds themselves, the science has been conclusive. Numerous studies show that amygdalin does kill cancer cells — and all other cells too.

Joe Schwarcz, the director of McGill University’s Office for Science and Society, said the initial idea — generating small amounts of cyanide to kill fast-multiplying cancer cells — was not a bad one. But it just doesn’t work, he said.

The sale of apricot seeds “clearly should not be allowed,” he said, surprised at how readily they are found on store shelves in Montreal.

Schwarcz says Health Canada is overwhelmed and useless at stopping the sale of bogus health remedies.

“With dietary supplements, they tend to say well, it’s not really dangerous, and let them be,” Schwarcz said, vowing to confront Health Canada about the sale of the seeds as a vitamin. “But this one is not in that category. You don’t need a lot of these kernels to do a lot of harm.”

A spokesperson for Health Canada said it is powerless to stop the sale of a product if its distributor does not claim any health benefits. It referred the Montreal Gazette to the Canadian Food Inspection Agency.

The CFIA said it merely enforces Health Canada directives.

Neither agency would comment on why apricot seeds are sold in Canada at all — as vitamins or snacks — given their known toxicity.

 

Upon arrival at Hôtel-Dieu Hospital, Brogan was given a tall Styrofoam cup of charcoal then placed on a gurney in the hallway to monitor his condition.

No one, from the person who answered the phone at poison control to the triage nurse to the doctor on duty, could believe that apricot seeds were being sold in Montreal.

Eight hours later, Brogan was released from hospital with a $1,125 bill. He had no health insurance, he explained.

“Those seeds were the most expensive snack I’ve ever eaten.”

Guetta went back to Rachelle-Béry to alert them of the danger. The store manager seemed alarmed and immediately took all the remaining packages off the shelves.

But when Guetta returned a few weeks later, there they were again. The superseed of the Hunza people.

 

 

 

 

 

November, 2017|Oral Cancer News|

The Unforgiving Math That Stops Epidemics

Author: Tara C. Smith
Source: www.quantamagazine.org
Date: October 26, 2017

As the annual flu season approaches, medical professionals are again encouraging people to get flu shots. Perhaps you are among those who rationalize skipping the shot on the grounds that “I never get the flu” or “if I get sick, I get sick” or “I’m healthy, so I’ll get over it.” What you might not realize is that these vaccination campaigns for flu and other diseases are about much more than your health. They’re about achieving a collective resistance to disease that goes beyond individual well-being — and that is governed by mathematical principles unforgiving of unwise individual choices.

When talking about vaccination and disease control, health authorities often invoke “herd immunity.” This term refers to the level of immunity in a population that’s needed to prevent an outbreak from happening. Low levels of herd immunity are often associated with epidemics, such as the measles outbreak in 2014-2015 that was traced to exposures at Disneyland in California. A study investigating cases from that outbreak demonstrated that measles vaccination rates in the exposed population may have been as low as 50 percent. This number was far below the threshold needed for herd immunity to measles, and it put the population at risk of disease.

The necessary level of immunity in the population isn’t the same for every disease. For measles, a very high level of immunity needs to be maintained to prevent its transmission because the measles virus is possibly the most contagious known organism. If people infected with measles enter a population with no existing immunity to it, they will on average each infect 12 to 18 others. Each of those infections will in turn cause 12 to 18 more, and so on until the number of individuals who are susceptible to the virus but haven’t caught it yet is down to almost zero. The number of people infected by each contagious individual is known as the “basic reproduction number” of a particular microbe (abbreviated R0), and it varies widely among germs. The calculated R0 of the West African Ebola outbreak was found to be around 2 in a 2014 publication, similar to the R0 computed for the 1918 influenza pandemic based on historical data.

Quantized Columns

If the Ebola virus’s R0 sounds surprisingly low to you, that’s probably because you have been misled by the often hysterical reporting about the disease. The reality is that the virus is highly infectious only in the late stages of the disease, when people are extremely ill with it. The ones most likely to be infected by an Ebola patient are caregivers, doctors, nurses and burial workers — because they are the ones most likely to be present when the patients are “hottest” and most likely to transmit the disease. The scenario of an infectious Ebola patient boarding an aircraft and passing on the disease to other passengers is extremely unlikely because an infectious patient would be too sick to fly. In fact, we know of cases of travelers who were incubating Ebola virus while flying, and they produced no secondary cases during those flights.

Note that the R0 isn’t related to how severe an infection is, but to how efficiently it spreads. Ebola killed about 40 percent of those infected in West Africa, while the 1918 influenza epidemic had a case-fatality rate of about 2.5 percent. In contrast, polio and smallpox historically spread to about 5 to 7 people each, which puts them in the same range as the modern-day HIV virus and pertussis (the bacterium that causes whooping cough).

Determining the R0 of a particular microbe is a matter of more than academic interest. If you know how many secondary cases to expect from each infected person, you can figure out the level of herd immunity needed in the population to keep the microbe from spreading. This is calculated by taking the reciprocal of R0 and subtracting it from 1. For measles, with an R0 of 12 to 18, you need somewhere between 92 percent (1 – 1/12) and 95 percent (1 – 1/18) of the population to have effective immunity to keep the virus from spreading. For flu, it’s much lower — only around 50 percent. And yet we rarely attain even that level of immunity with vaccination.

Once we understand the concept of R0, so much about patterns of infectious disease makes sense. It explains, for example, why there are childhood diseases — infections that people usually encounter when young, and against which they often acquire lifelong immunity after the infections resolve. These infections include measles, mumps, rubella and (prior to its eradication) smallpox — all of which periodically swept through urban populations in the centuries prior to vaccination, usually affecting children.

Do these viruses have some unusual affinity for children? Before vaccination, did they just go away after each outbreak and only return to cities at approximately five- to 10-year intervals? Not usually. After a large outbreak, viruses linger in the population, but the level of herd immunity is high because most susceptible individuals have been infected and (if they survived) developed immunity. Consequently, the viruses spread slowly: In practice, their R0 is just slightly above 1. This is known as the “effective reproduction number” — the rate at which the microbe is actually transmitted in a population that includes both susceptible and non-susceptible individuals (in other words, a population where some immunity already exists). Meanwhile, new susceptible children are born into the population. Within a few years, the population of young children who have never been exposed to the disease dilutes the herd immunity in the population to a level below what’s needed to keep outbreaks from occurring. The virus can then spread more rapidly, resulting in another epidemic.

An understanding of the basic reproduction number also explains why diseases spread so rapidly in new populations: Because those hosts lack any immunity to the infection, the microbe can achieve its maximum R0. This is why diseases from invading Europeans spread so rapidly and widely among indigenous populations in the Americas and Hawaii during their first encounters. Having never been exposed to these microbes before, the non-European populations had no immunity to slow their spread.

If we further understand what constellation of factors contributes to an infection’s R0, we can begin to develop interventions to interrupt the transmission. One aspect of the R0 is the average number and frequency of contacts that an infected individual has with others susceptible to the infection. Outbreaks happen more frequently in large urban areas because individuals living in crowded cities have more opportunities to spread the infection: They are simply in contact with more people and have a higher likelihood of encountering someone who lacks immunity. To break this chain of transmission during an epidemic, health authorities can use interventions such as isolation (keeping infected individuals away from others) or even quarantine (keeping individuals who have been exposed to infectious individuals — but are not yet sick themselves — away from others).

Other factors that can affect the R0 involve both the host and the microbe. When an infected person has contact with someone who is susceptible, what is the likelihood that the microbe will be transmitted? Frequently, hosts can reduce the probability of transmission through their behaviors: by covering coughs or sneezes for diseases transmitted through the air, by washing their contaminated hands frequently, and by using condoms to contain the spread of sexually transmitted diseases.

These behavioral changes are important, but we know they’re far from perfect and not particularly efficient in the overall scheme of things. Take hand-washing, for example. We’ve known of its importance in preventing the spread of disease for 150 years. Yet studies have shown that hand-washing compliance even by health care professionals is astoundingly low — less than half of doctors and nurses wash their hands when they’re supposed to while caring for patients. It’s exceedingly difficult to get people to change their behavior, which is why public health campaigns built around convincing people to behave differently can sometimes be less effective than vaccination campaigns.

How long a person can actively spread the infection is another factor in the R0. Most infections can be transmitted for only a few days or weeks. Adults with influenza can spread the virus for about a week, for example. Some microbes can linger in the body and be transmitted for months or years. HIV is most infectious in the early stages when concentrations of the virus in the blood are very high, but even after those levels subside, the virus can be transmitted to new partners for many years. Interventions such as drug treatments can decrease the transmissibility of some of these organisms.

The microbes’ properties are also important. While hosts can purposely protect themselves, microbes don’t choose their traits. But over time, evolution can shape them in a manner that increases their chances of transmission, such as by enabling measles to linger longer in the air and allowing smallpox to survive longer in the environment.

By bringing together all these variables (size and dynamics of the host population, levels of immunity in the population, presence of interventions, microbial properties, and more), we can map and predict the spread of infections in a population using mathematical models. Sometimes these models can overestimate the spread of infection, as was the case with the models for the Ebola outbreak in 2014. One model predicted up to 1.4 million cases of Ebola by January 2015; in reality, the outbreak ended in 2016 with only 28,616 cases. On the other hand, models used to predict the transmission of cholera during an outbreak in Yemen have been more accurate.

The difference between the two? By the time the Ebola model was published, interventions to help control the outbreak were already under way. Campaigns had begun to raise awareness of how the virus was transmitted, and international aid had arrived, bringing in money, personnel and supplies to contain the epidemic. These interventions decreased the Ebola virus R0 primarily by isolating the infected and instituting safe burial practices, which reduced the number of susceptible contacts each case had. Shipments of gowns, gloves and soap that health care workers could use to protect themselves while treating patients reduced the chance that the virus would be transmitted. Eventually, those changes meant that the effective R0 fell below 1 — and the epidemic ended. (Unfortunately, comparable levels of aid and interventions to stop cholera in Yemen have not been forthcoming.)

Catch-up vaccinations and the use of isolation and quarantine also likely helped to end the Disneyland measles epidemic, as well as a slightly earlier measles epidemic in Ohio. Knowing the factors that contribute to these outbreaks can aid us in stopping epidemics in their early stages. But to prevent them from happening in the first place, a population with a high level of immunity is, mathematically, our best bet for keeping disease at bay.

November, 2017|Oral Cancer News|

FDA Cracks Down on Marijuana Cancer Treatment Claims

Author: Anna Edney; Jennifer Kaplan
Source: www.bloomberg.com
Date: November 1, 2017

U.S. officials sent a warning to the marijuana industry, alerting online sellers they cannot market their products as a treatment for cancer.

The Food and Drug Administration sent letters to four companies on Tuesday, warning them about unsubstantiated claims that their marijuana-derived products can combat tumors and kill cancer cells. The firms sell products including oils and capsules made from cannabidiol, also known as CBD, a component of the marijuana plant that doesn’t cause the mind-altering effects of the other main component, tetrahydrocannabinol, or THC.

The agency told the companies they cannot make claims to treat or cure a disease when a product has never been studied as a treatment. Curbing the sale of CBD products with health claims could put a damper on the medical-marijuana market. Producers that are required to nix references to medical ailments may move toward the recreational side of the legal cannabis industry.

Eight states and Washington, D.C., have legalized pot for recreational use. Twenty-one additional states have legalized for medical purposes.

“We don’t let companies market products that deliberately prey on sick people with baseless claims that their substance can shrink or cure cancer and we’re not going to look the other way on enforcing these principles when it comes to marijuana-containing products,” FDA Commissioner Scott Gottlieb said in a statement.

The crackdown could also have a wider impact on the pharmaceutical industry. CBD is being researched in labs as potential treatment for certain diseases. Biotech company GW Pharmaceuticals Plc, for instance, is testing the component to treat certain forms of epilepsy.

Gottlieb hinted almost a month ago at a congressional hearing that the FDA may get tough on unproven marijuana claims. The companies that received warning letters are: Greenroads Health, Natural Alchemist, That’s Natural! and Stanley Brothers Social Enterprises. The companies have 15 working days to tell the FDA what corrective steps they will take.

Stanley Brothers runs the company CW Hemp, which said in an emailed statement it takes “regulatory compliance very seriously” and will work with the FDA to better monitor the information on its website. The other companies didn’t return requests for comment.

 

November, 2017|Oral Cancer News|

Understanding personal risk of oropharyngeal cancer: risk-groups for oncogenic oral HPV infection and oropharyngeal cancer

Author: G D’Souza, T S McNeel, C Fakhry
Date: October 19, 2017
Source: Academic.oup.com

Abstract

Background

Incidence of human papillomavirus (HPV)-related oropharyngeal cancer is increasing. There is interest in identifying healthy individuals most at risk for development of oropharyngeal cancer to inform screening strategies.

Patients and methods

All data are from 2009 to 2014, including 13 089 people ages 20–69 in the National Health and Nutrition Examination Survey (NHANES), oropharyngeal cancer cases from the Surveillance, Epidemiology, and End Results (SEER 18) registries (representing ∼28% of the US population), and oropharyngeal cancer mortality from National Center for Health Statistics (NCHS). Primary study outcomes are (i) prevalence of oncogenic HPV DNA in an oral rinse and gargle sample, and (ii) incident oropharyngeal squamous cell cancer.

Results

Oncogenic oral HPV DNA is detected in 3.5% of all adults age 20–69 years; however, the lifetime risk of oropharyngeal cancer is low (37 per 10 000). Among men 50–59 years old, 8.1% have an oncogenic oral HPV infection, 2.1% have an oral HPV16 infection, yet only 0.7% will ‘ever’ develop oropharyngeal cancer in their lifetime. Oncogenic oral HPV prevalence was higher in men than women, and increased with number of lifetime oral sexual partners and tobacco use. Men who currently smoked and had ≥5 lifetime oral sexual partners had ‘elevated risk’ (prevalence = 14.9%). Men with only one of these risk factors (i.e. either smoked and had 2–4 partners or did not smoke and had ≥5 partners) had ‘medium risk’ (7.3%). Regardless of what other risk factors participants had, oncogenic oral HPV prevalence was ‘low’ among those with only ≤1 lifetime oral sexual partner (women = 0.7% and men = 1.7%).

Conclusions

Screening based upon oncogenic oral HPV detection would be challenging. Most groups have low oncogenic oral HPV prevalence. In addition to the large numbers of individuals who would need to be screened to identify prevalent oncogenic oral HPV, the lifetime risk of developing oropharyngeal caner among those with infection remains low.

Introduction

Human papillomavirus (HPV) is the most commonly sexually transmitted infection in the United States. HPV now causes ∼70% of all oropharyngeal squamous cell cancer (OPC) in the United States [1] and the incidence of HPV-related OPC (HPV-OPC) among men has more than doubled over the past 20 years [2]. Indeed, OPC is projected to be more common than cervical cancer in the United States by 2020 [3]. Given the ‘epidemic’ of HPV-OPC, there is interest in identifying specific groups that could benefit from screening, if effective tests were developed.

Sexual behaviors responsible for exposure to oral HPV infection are common (80% of the US population reports ever performing oral sex) [4]. Given the ubiquitous exposure to HPV infection and resulting anxiety [5], there is interest in identifying healthy individuals most at risk for development of OPC. As oncogenic oral HPV infection is the precursor to malignancy, identification of individuals with oncogenic oral HPV infection may point to individuals with premalignant disease. Such risk triage could both inform screening approaches and assist the public in understanding personal risk. This analysis therefore aims to understand how common HPV16, oncogenic HPV and HPV-OPC are in groups of people with different risk factor profiles.

Methods

Study population

This study included 13 089 people ages 20–69 years old who participated in National Health and Nutrition Examination Survey (NHANES) between 2009 and 2014 and had oral HPV DNA testing. Analyses involving number of oral sex partners were limited to ages 20–59, with data for number of oral sex partners, resulting in a sample size of 9425. Incidence and incidence-based mortality data from SEER 18 registries between 2009 and 2014 [6] were used with NCHS mortality data for projections of OPC risk.

HPV measurement

As previously described [7, 8] oral HPV DNA was tested in exfoliated cells collected from an oral rinse and gargle sample using PCR amplification using PGMY 09/11 consensus primers and line blot for the detection of 37 specific HPV types. Oncogenic oral HPV was defined as detection of any of the following 12 types: HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59 [9].

Analytic methods

Analyses of NHANES oral HPV data were weighted by Mobile Examination Center (MEC) exam sampling weights, and conducted using SUDAAN software (release 11.0.1, Research Triangle Institute) to account for survey sample design. Projected OPC risk was calculated using DevCan software [10].

To better understand subgroup risk, prevalence of oncogenic HPV and HPV16 were explored stratifying by multiple factors including sex, sexual behavior, age, and current smoking. Groups with similar prevalence were combined to create parsimonious risk stratification of people with similar prevalence.

Results

Oncogenic oral HPV and oral HPV16 infection are rare in the general US population. As expected, prevalence of infection is higher among men than women of every age group (oncogenic HPV; 6.0% versus 1.1%, P < 0.001; Table 1). Prevalence of oncogenic oral HPV is contrasted with risk of OPC in Table 1 by sex and age groups. While oncogenic oral HPV is detected in 3.5% of all adults age 20–69, the lifetime risk of OPC is low (37 per 10 000). For example, among men 50–59 years old, 8.1% have an oncogenic oral HPV infection, 2.1% have an oral HPV16 infection, yet 0.7% will ‘ever’ develop OPC in their lifetime; and risk of developing OPC in the next 10 (0.2%) or 20 (0.4%) years is even lower (Table 1).

Table 1.

Oral HPV prevalence by sex and age, compared with the risk of developing oropharyngeal cancer (OPC) in each group

    Risk spectrum: infection to cancer

 

NHANESa (prevalence)

 

SEERb (OPC risk: cases/100 people) 

 

Sex  Age  Oncogenic Oral HPV (%)  Oral HPV16 (%)  Lifetime (%)  Next 20 years (%)  Next 10 years (%) 
Men
20–29 4.8 1.1 0.7 0.01 <0.01
30–39 4.7 1.5 0.7 0.07 0.01
40–49 6.2 2.3 0.7 0.3 0.06
50–59 8.1 2.1 0.7 0.4 0.2
60–69 6.1 2.4 0.5 0.4 0.3
Total 6.0 1.9 0.7
Women
20–29 1.4 0.3 0.2 <0.01 <0.01
30–39 1.0 0.3 0.2 0.01 <0.01
40–49 0.8 0.1 0.2 0.05 0.01
50–59 1.6 0.5 0.2 0.08 0.03
60–69 0.7 0.1 0.1 0.10 0.05
Total 1.1 0.3 0.2
Men and women All 3.5 1.1 0.4

a- Weighted prevalence accounting for NHANES study design weights to reflect the general US population.

b- Estimates of OPC risk combine data on cancer occurrence from SEER with population data. OPC is shown as risk per 100 people to contrast with HPV prevalence. For reference in interpretation, 0.6% risk represent that 0.6 people out of the 100 (or 6 out of 1000, or 600 out of 100 000) would develop OPC.

While prevalence of oncogenic oral HPV infection is low, the distribution of infections is not representative of the population (supplementary Table S1, available at Annals of Oncologyonline). Indeed 84% of oncogenic oral HPV infections in 20- to 69-year olds were among men. To elucidate why oncogenic oral HPV was more concentrated among certain groups, behavioral characteristics were considered. Performing oral sex and smoking are each strongly associated with detection of oncogenic oral HPV (Table 2) and HPV16 (supplementary Table S2, available at Annals of Oncology online). Oncogenic oral HPV prevalence is low (<2.5%) among both men and women who never performed oral sex. Prevalence of oncogenic oral HPV increased with number of lifetime oral sexual partners, up to 14.4% in men age 20–59 years old with ≥10 lifetime oral sexual partners (Table 2).

 

Table 2.

Oncogenic oral HPV prevalence by participant characteristics and behaviors

    Oncogenic oral HPV prevalencea(%)

 

 
Men  Women  All 
Characteristics (among those 20–69 years old)  No. of people  N = 6420  N = 6669  N = 13 089  P-valueb 
Sex
Women 6669 1.1 1.1 <0.0001
Men 6420 6.0 6.0
Currently smoke
No 10 041 4.5 0.9 2.6 <0.0001
Yes 3044 10.5 2.1 6.7
Age, in years
 20–29 2738 4.8 1.4 3.1 0.13
 30–39 2668 4.7 1.0 2.8
 40–49 2699 6.2 0.8 3.4
 50–59 2494 8.1 1.6 4.8
 60–69 2490 6.1 0.7 3.3
Race/ethnicity
 White non-Hispanic 5135 6.3 1.1 3.7 0.008
 Black non-Hispanic 2931 7.5 1.4 4.2
 Any race Hispanic 3347 4.5 1.3 2.9
 Other 1676 3.7 0.7 2.1
Ever oral sex (or man or woman)
 No 2453 2.3 0.2 1.1 <0.0001
 Yes 9272 6.5 1.4 4.0
Ever oral sex on a woman
 No 6660 3.6 1.0 1.4 <0.0001
 Yes 5095 6.4 3.5 6.2
Ever oral sex on a man
 No 7054 5.8 0.2 4.9 <0.0001
 Yes 4693 10.2 1.4 1.8
Number of partners performed oral sex on in lifetimec
 0 1661 2.4 0.2 1.2 <0.0001
 1 1877 1.2 1.0 1.1
 2–4 3165 4.8 0.7 2.5
 5–9 1363 3.9 2.5 3.3
 10+ 1359 14.4 3.0 11.1

a- Weighted prevalence accounting for NHANES study design weights to reflect the civilian non-institutionalized US population.

b-Wald F test (based on transforming the Wald χ2) for independence of row variable and oral HPV16, not accounting for sex (except where sex is the row variable).

C- Data on number of lifetime oral sex partners was not collected consistently in those 60 and older so is only presented among those 20–59 years old.

 

 

Oncogenic oral HPV prevalence was explored by sex, sexual behavior, and tobacco use to better understand groups that have higher and lower prevalence (Figure 1). Regardless of what other risk factors participants had, oncogenic oral HPV prevalence was low among those with only ≤1 lifetime oral sexual partner (women = 0.7% and men = 1.7%). Oncogenic oral HPV prevalence doubled among women with ≥2 versus 0–1 lifetime oral sexual partners (1.5% versus 0.7%, P = 0.02), but remained low among women with higher number lifetime oral sexual partners (Table 2). Oncogenic oral HPV prevalence was highest among men who currently smoked and had ≥5 lifetime oral sexual partners (14.9%, 95% CI = 11.4–19.1). Men with only one of these risk factors (i.e. either smoked and had two to four partners or did not smoke and had ≥5 partners) had ‘medium risk’, with 7.3% (95% CI = 5.8–9.1) oncogenic oral HPV prevalence (Figure 1). Findings were similar when considering oral HPV16 infection specifically.

 

What is my risk of oral HPV? Prevalence of oral HPV16 and any oncogenic oral HPV infection by risk group. In the ‘very low-risk’ group (among women with 0–1 lifetime oral sexual partners), oncogenic oral HPV was similar among smokers and nonsmokers (1.8% versus 0.5%, P = 0.26). In the ‘low-risk’ group of women, oncogenic oral HPV prevalence was 1.5% among women with two or more lifetime oral sexual partners. In the ‘low-risk’ group of men, oncogenic oral HPV prevalence was 1.7% among men with 0–1 lifetime oral sexual partners and was higher among men who did not smoke and had 2–4 lifetime oral sexual partners (4.1%, P = 0.0042). In the ‘medium risk’ group, oral HPV16 prevalence was 7.1% among men who smoke and had 2–4 partners and 7.4% among men who do not smoke and had 5+ partners (P = 0.87).

 

Discussion

This analysis highlights that the yield of oncologic oral HPV screening would be limited in most groups in the United States. With the increasing incidence of OPC, there is a need to understand how to identify individuals at risk of OPC. Oncogenic oral HPV detection is attractive as it samples the relevant epithelium in a non-invasive method, has relatively low cost and serves as a biomarker for HPV-OPC. However, for screening to succeed, a high prevalence population is needed to limit false positives, and balance the psychologic and physical harms of screening with the benefits.

From this analysis, it is clear that screening based upon oncogenic oral HPV detection would be challenging. Women across all categories have low prevalence of infection and low risk of OPC and therefore benefits of screening are unlikely to outweigh harms in this group. The higher prevalence of oncogenic oral HPV in men than women is thought be due to both a higher per partner risk of acquisition when performing oral sex [11, 12], and decreased clearance among men than women [11, 13]. While there are specific risk groups of men enriched for oncogenic oral HPV, most men have low prevalence of infection. Even among the elevated risk group, the majority of men do not have a prevalent oncogenic oral HPV. In addition to the large numbers of individuals who would need to be screened to identify prevalent oncogenic oral HPV, the lifetime risk of developing OPC among those with infection remains low [11, 14].

These characteristics suggest that other tests will need to be combined or supplant present methods to accurately identify those with the greatest risk of OPC in the population. Serum HPV oncoprotein antibody tests are specific [15], but are even rarer than oral HPV16 infection [16], so may be impractical to use in most groups. An additional challenge for screening is that precursor lesions for HPV-OPC have not been found and the ability to detect lesions early in an ‘elevated-risk’ group is unknown.

With growing appreciation of the relationship between oral sex, infection, and cancer, some individuals have questions about their risk of having oncogenic oral HPV infection. To address concerns about infection among individuals with high number of oral sex partners or others concerned about their cancer risk, the infographic can be used to reassure that oncogenic oral HPV prevalence is low among most groups. This analysis has several imitations. Data on oral HPV infection were cross-sectional, with no information linking HPV and SEER data used for cancer risk. Comparing oncogenic oral HPV prevalence and OPC risk in this way informs potential future screening studies, and personal risk assessment. In summary, this analysis shows that screening based upon oncogenic oral HPV infection will not be useful and presents data to communicate to the layperson the low risk of infection and cancer.

Acknowledgements

The authors acknowledge Maura Gillison who led the testing for oral HPV in NHANES provided in the publicly available dataset. This dataset has provided investigators the opportunity to better understand the epidemiology of oral HPV infection in the United States. We also acknowledge the contributions of the Oral Cancer Foundation.

Funding

National Institute of Dental and Craniofacial Research (NIDCR) (R35 DE026631).

Disclosure

The authors have declared no conflicts of interest.

 

References

1 Saraiya M, Unger ER, Thompson TD et al. US assessment of HPV types in cancers: implications for current and 9-calent HPV vaccines. J Natl Cancer Inst 2015; 107(6): djv086

 

2 Jemel A, Simard EP, Dorell C et al. Annual Report to the Nation on the Status of Cancer, 1975-2009, featuring the burden and trends in human papillomavirus(HPV)-associated cancers and HPV vaccination coverage levels. J Natl Cancer Inst 2013; 105(3): 175-201.

 

3 Chaturvedi AK, Engels EA, Pfeiffer RM et al. Human papillomavirus and rising oropharyngeal cancer incidence in the United States. J Clin Oncol 2011;29(32): 4294-4301

 

4 D’Souza G, Cullen K, Bowie J et al. Differnece in oral sexual behaviors by gender, age, and race explain observed difference in prevalence or oral human papillomavirus infection. PLoS One 2014; 9(1): e86023

 

5 D’Souza G, Zhang Y, Merritt S et al. Patient experience and anxiety during and after treatment for and HPV-related oropharyngeal cancer. Oral Oncol 2016; 60: 90-95.

 

6 SEER Incidence and Incidence-Based Mortality Date, SEER 18 Regs (Excl Lousiana) 1973-2014; http://seer.cancer.gov/date/ (8 May 2017, date last accessed).

 

7 Gillison ML, Broutain T, Pickard RKL et al. Prevalence of oral HPV infection in the United States, 2009-2010. JAMA 2012;307(7): 693-703.

 

8 NHANES 2013-2014: Human Papillomavirus (HPV)- Oral Rinse Data Documentation, Codebook, and Frequencies:

https://wwwn.cdc.gov/Nchs/Nhanes/2013-2014/ORHPV_H.htm (2 May 2017, date last accessed).

 

9 IARC. Human Papillomavirus; http://monographs.iarc.fr/ENG/Monographs/vol100B/mono100B-11.pdf (23 May 2017, date last accessed)

 

10 Devcan: Probability of Developing or Dying of Cancer- Surveillance Research Program; https://surveillance.cancer.gov/devcan/ (8 May 2017, date last accessed).

 

11 D’Souza G, Wentz A, Kluz N et al.   Sex differnces in risk factors and natural history of oral human papillomavirus (HPV) infection. J Infect Dis 2016;213(12):1893-1896.

 

12 Chaturvedi AK, Graubard Bl, Broutian T et al. NHANES 2009-2012 findings: association of sexual behaviors with higher prevalence of oral oncogenic human papillomavirus infections in U.S. men. Cancer Res 2015; 75(12): 2468-2477.

 

13 Beachler DC, Sugar EA, Margolick JB et al. Risk Factors acquisition and clearance or oral human papillomavisur infection among HIV-infected and HIV-uninfected adults. Am J Epidemiol 2015; 181(1): 40-53.

 

14 Pierce Campbell CM, Kreimer AR, Lin H-Y et al. Long-term persistence of oral human papillomavirus type 16: the HPV infection in men (HIM) Study. Cancer Pres Res Phila Pa 2015; 8(3): 190-196.

 

15 Holzinger D, Wichmann G, Baboci L et al. Sensitivity and specificity of antibodies against HPV16 E6 and other early proteins for the detection of HPV16-driven oropharyngeal squamous cell carcinoma. Int J Cancer 2017; 140(12):2748-2757.

 

16 Beachler DC, Waterboer T, Pierce Campbell CM et al. HPV16 E6 seropositivity among cancer-free men with oral, anal or genital HPV16 infection. Papillomavirus res 2016; 2: 141-144.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

October, 2017|Oral Cancer News|