human papillomavirus

Should kids be required to get the HPV vaccine?

Source: www.forbes.com
Author: Bruce Y. Lee

If a bill recently introduced in Florida passes, the human papillomavirus (HPV) vaccine would be mandatory for adolescents attending public school in the state. Currently, the vaccine is mandatory for boys and girls in Rhode Island and just girls in Virgina and Washington, DC. (AP Photo/John Amis, File)

Florida isn’t kidding about low human papillomavirus (HPV) vaccination rates. If you are a kid enrolled in a Florida public school, come July 1, 2018, you may be required to get the HPV vaccine. That is if you are old enough and if a bill now being debated in the Florida state legislature ends up passing.

If it gets through, Senate Bill 1558 would then become known as the “Women’s Cancer Prevention Act”, which is a much easier name to remember and also reflects some major benefits of the HPV vaccine. As the National Cancer Institute explains, HPV vaccine can help prevent not only cervical cancer but also many vaginal and vulvar cancers. In fact, two types of HPV (16 and 18) cause around 70% of cervical cancers. But just because you don’t have a vagina, cervix, and vulva doesn’t mean that you are in the clear. HPV is responsible for about 95% of anal cancers, 70% of oropharyngeal (the middle part of the throat) cancers, and 35% of penile cancers. Thus, the “Women’s Cancer Prevention Act” is really a “Cancer Prevention Act.”

Regardless, Florida State Senator José Javier Rodríguez (D-Miami) filed this bill on January 4 in an effort to boost Florida’s not so great HPV vaccination rates. According to the just-released Blue Cross Blue Shield Association (BCBSA) Health of America Report, only 29.0% of adolescents in Florida got the first dose of the HPV vaccine and only 7.3% got all doses in the series as of 2016. Those numbers are lower than the national average (34.4% got the first dose) but not the worst in the country.

New Jersey was the worst (not in general as a state but in terms of HPV vaccination rates). Based on the BCBSA report, as of 2016, only 20.6% of adolescents in New Jersey had gotten the HPV vaccine by age 13 and only 3.4% had completed the series. The Health of America report was the result of an analysis of medical claims data from 2010 through 2016 of over 1.3 million BCBSA commercially-insured adolescents across the country. The analysis considered vaccination to be on time if performed between the adolescent’s 10th and 13th birthdays, corresponding with the Centers for Disease Control and Prevention (CDC) recommendations of 11 to 12 year olds getting the vaccine.

Of course, the analysis did not include all adolescents in America. As BCBSA Chief Medical Officer Trent Haywood, MD, JD, explained, “the analysis represented the commercial population and didn’t include Medicaid populations. Also, to be included in the analysis, an adolescent had to be continuously enrolled with BCBS.” But studying such a large population is a pretty good shot at trying to figure what’s going on with shots and adolescents nationwide.

The report also showed that girls were better than boys (again, not in general, but in terms of HPV vaccination rates). In 2016, 37% of girls had received the first dose of the HPV vaccines by age 13 compared to 32%.

The best state of the bunch? Rhode Island with 57% of adolescents having received their first dose by age 13. Not coincidentally Rhode Island is the only state requiring HPV vaccine for both male and female students, starting with the first dose by 7th grade. Virginia and Washington, DC, have requirements just for females.

The good news is that nationwide vaccination rates steadily rose from 22% getting the first dose by age 13 in 2013 to 34% in 2016. But why are vaccination rates still well below 50% in most states? A BCBSA-commissioned survey of over 700 parents of adolescents aged 10-13 revealed the following top three reasons for parents not vaccinating their child against HPV:

  • Being concerned about adverse side effects (59.4%)
  • Not thinking their child is at risk (23.6%)
  • Not knowing their child needed an HPV vaccination (15.7%)

Is requiring the HPV vaccine the solution? One argument against making the HPV vaccine mandatory is that people should be allowed freedom of choice. When Rhode Island first introduced its requirement, protests resulted various groups such as parents, a 2,400-member plus Facebook group, and the American Civil Liberties Union.

However, the counter-argument is that freedom of choice does not always hold when in the words of Spock, “the needs of the many outweigh the needs of the few.” You aren’t free to run up and down the aisle of an airplane naked and screaming because the needs of other on the plane outweigh the needs of you. Similarly, the HPV vaccine could help slow and even stop the transmission of HPV throughout the population, which can result in cancers that not only affect the cancer victims but also society by adding to health care costs.

Here is a Today show segment on the HPV vaccine:

Also, when a child doesn’t get vaccinated, it is usually because of the parent’s choice and not the child’s. Could making the vaccine mandatory in fact be protecting the child?

Another argument used by some is that the HPV vaccine has adverse effects. There are websites claiming that HPV vaccine can cause “crippling side effects” and “death.” But many of these scarier claims are not supported by rigorous scientific evidence. (Note: there are also websites that say that the Earth is flat, Elvis was an alien, and the government controls the weather). While nothing is completely safe (e.g., even a chocolate chip cookie in the right situation could do some real damage) and all vaccines do have their risks, the risks of the HPV vaccine are comparatively very low and far outweighed by the potential benefits as indicated by the CDC.

As I wrote before for Forbes, some have argued that the HPV vaccine is a “gateway to sex” and thus making it mandatory would increase the number of teenagers having sex and encourage promiscuity. However, this goes counter to the recent trend of teenagers delaying when they first have sex and suggests that teenagers would not have sex if it weren’t for that darn HPV vaccine. A related argument is that the HPV vaccine would give teens a false sense of security that they are protected against all sexually transmitted infections, leading them to not practice safe sex. However, raising awareness of what the HPV vaccine actually does could help overcome this concern.

All of this does not necessarily mean that making HPV vaccination mandatory is the solution. However, what then is the solution to a majority of adolescents still not getting vaccinated (at least by age 13 and when sexual activity for some begin)? As Haywood described, this is a situation in which many are “not taking full advantage of preventive measures. A big issue is lack of awareness of the HPV vaccine and its benefits.” HPV vaccine awareness campaigns may help push up vaccination rates, but by how much?

The wonderfully straight-forward and transparent world of politics will help determine whether Senate Bill 1558 becomes a law in Florida. A similar bill failed to pass in 2011. But things have changed since 2011, in good ways and bad.

February, 2018|Oral Cancer News|

Should dentists ask their patients about their sexual health to fight cancer?

Source: www.ibtimes.co.uk
Author: Kashmira Gander

A visit to the dentist often involves a quick check-up, a spot of gum cleaning and, if you’re unlucky, a filling. But should dentists also ask their patients about their sex lives in order to prevent oral cancer caused by human papillomavirus (HPV)?

A recent report published in the Journal of the American Dental Association highlighted it was important for dentists to actively check their patients mouths for signs that HPV has caused cancer. The most common sexually transmitted infections (STI), HPV is transmitted through vaginal, anal, and oral sex.

The study involved four focus groups with a total of 33 dentists. It showed that many dentists did not know how to approach the subject of cancer caused by HPV.

Those with HPV can show no symptoms and most people with the virus do not suffer health problems, according to the US Centre for Disease Control. “Others may only find out once they’ve developed more serious problems from HPV, such as cancers,” the website warned.

Up to 93% of oral cancer cases are preventable, according to Cancer Research UK. Over 12,000 cases of head and neck cancer were dignosed according to the latest statistics from 2015, while over 2,300 people died that year.

Mouth cancer can occur anywhere in the head and neck area, including the tongue, lips, salivary glands and even the throat, Dr Eddie Coyle’s, clinical director at Bupa Dental Care, told IBTimes UK.

“There are a number of symptoms that patients should look out for, which include sores and swelling in or around your mouth that doesn’t heal or bleed; persistent mouth ulcers; persistent lumps in the lymph glands in the neck or in the mouth; tongue pain; changes in your voice or speech; unexplained weight loss: a sore throat and difficulty in chewing or swallowing.”

However, Dr Coyle stressed that while it was important to be aware of mouth cancer, similar symptoms are often a sign of less serious conditions. “Therefore, we would only recommend they visit a dentist or doctor only if these have lasted for longer than two weeks,” Dr Coyle added.

The study sparked headlines suggesting that dentists may ask patients about their sexual history.

However, lead author Ellen Daley of the University of South Florida, told Newsweek that a person aware they have HPV can cause unnecessary anxiety as it may never cause cancer. Clinicians should instead focus on prevention, including advising patients to get vaccinated against HPV.

In line with this advice, the British Dental Association is leading calls for the UK government to extend its HPV vaccination programme for girls to boys.

“Dentists are on the front line in the battle against oral cancer, and are often the first to spot the tell-tale signs,” BDA Chair Mick Armstrong told IBTimes UK.

“HPV is fuelling this preventable disease, a killer that can have a 90% survival rate – but only if it’s spotted early.

“Men aren’t currently protected from HPV through jabs offered at school, so patients shouldn’t be surprised if they are asked about their sexual health,” he said.

“These questions would be redundant if the government finally bit the bullet and brought boys into the vaccination programme.”

MORE

February, 2018|Oral Cancer News|

HPV leads to increase In head and neck cancer In men

Source: www.nbcdfw.com
Author: Bianca Castro

The number of men diagnosed with head and neck cancer caused by human papillomavirus has skyrocketed. This report found that 11 million men and 3.2 million women in the United States are infected with some type of oral HPV and oncologists say it’s leading to more head and neck cancer in men.

“From the 1970’s to today, the prevalence of this HPV-related head and neck cancer has increased by three to five percent per year from then until now, and it is continuing that same rate,” said Oncologist Jerry Barker, Jr., M.D. at Texas Oncology.

“This is a silent epidemic. Most patients who are exposed to this virus, they don’t know it. They’ll never have symptoms from it, but some of those patients will move on to develop a cancer,” said Dr. Barker.

Jeff Busby, of Weatherford, is one of those patients. The aerospace engineer and owner of Busby Quarter Horses says he was diagnosed with throat cancer in February of 2016. His wife Andrea, who documented their journey here, says they were both shocked.

“We were just busy living life. You don’t ever think that shoe is going to drop,” said Andrea.

Jeff says the symptoms began as pain in his ear which lead to pain in his throat. Nine months later, he had a biopsy done on what was a mass in his neck.

“I had just been toughing it out and my partner said, ‘hey, you can’t just tough these kinds of things out. You’ve got to go get this checked out,'” said Jeff.

“It was the cancer putting pressure on and radiating nerve pain to the ear. There was nothing wrong with the ear whatsoever,” said Jeff.

A biopsy revealed Jeff had throat cancer caused by the human papillomavirus, the most common sexually transmitted infection.

Jeff was likely exposed in his teens or 20s, but now decades later, created a cancer with one of the most gruesome treatment protocols. He needed surgery to remove his bottom teeth and part of his jaw, 35 radiation treatments and six rounds of chemotherapy.

“I couldn’t let any of my energy go towards feeling sorry for myself because I had to have every amount of energy I had to beat this thing,” said Jeff.

Jeff had never heard of HPV before, while Andrea says she thought it was linked to only cervical cancer.

While pap smears screen for cervical cancer, there is no screening for hpv-related head and neck cancer and that may be part of the reason rates of hpv-related head and neck cancer has surpassed the rate of hpv-related cervical cancer.

There is way to stop the epidemic. The HPV vaccine is recommended for children as early as 11-years-old and young adults as old as 26 years of age. However, according to this study, in Texas, only 35 percent of children get the vaccine.

“Somewhere along the way, these vaccines developed the idea that they had to do with human sexuality and preventing a sexually transmitted disease, but in reality, they are designed to prevent cancer. These are cancer vaccines,” said Dr. Barker.

“If you could just see what some of our patients have to go through to cure one of these cancers, you would run to get the needle in the arm to prevent that from happening to one of your children.”

At 55, Jeff never had the chance to benefit from the vaccine, approved for use in 2006. He’s now cancer free and in some ways, he says, life is better than before cancer.

“I thank God for this challenge and I still wouldn’t change it today. I wouldn’t take it all away because I didn’t think I could be closer to the Lord or to my wife and I certainly have a much better relationship with both,” said Jeff.

He and Andrea are focused on raising vaccination rates and preventing the kind of cancer battle they fought from from happening to someone else.

“There are so many parents that even hear about but still choose not to do it. It’s beyond me. I can’t understand that,” said Jeff.

“Whether it gets a kid vaccinated or somebody sitting on their couch goes, ‘I have ear pain when I swallow. I should go to the doctor.’ That’s why we are doing this,” said Andrea.

The Centers for Disease Control estimates that most Americans have some type of HPV strain but not all strains lead to cancer. Some of the symptoms are head and neck cancer include ear pain, difficulty swallowing and a painless lump on the side of the neck.

January, 2018|Oral Cancer News|

Young men should be required to get the HPV vaccine. It would have saved me from cancer.

Source: www.thedailybeast.com
Author: Michael Becker

In December 2015, at the age of 47, I was diagnosed with Stage IV oral squamous cell carcinoma.

More simply, I have advanced cancer of the head and neck. While initial treatment with grueling chemo-radiation appeared successful, the cancer returned one year later in both of my lungs. My prognosis shifted from potentially curable to terminal disease. The news was shocking and devastating—not just for me, but for my wife, two teenage daughters, and the rest of our family and friends.

Suddenly, my life revolved around regular appointments for chemotherapy, radiation therapy, imaging procedures, and frequent checkups. I made seemingly endless, unscheduled hospital emergency room visits—including one trip to the intensive care unit—to address some of the more severe toxicities from treatment.

All told, I suffered from more than a dozen side effects related to treatment and/or cancer progression. Some are temporary; others permanent. These include anxiety, depression, distorted sense of taste, clots forming in my blood vessels, dry mouth, weight loss, and many more.

My cancer started with a human papillomavirus (HPV) infection, a virus that is preventable with vaccines available for adolescent girls since 2006 and boys starting in 2011. The Food and Drug Administration (FDA) has approved three vaccines to prevent HPV infection: Gardasil®, Gardasil® 9, and Cervarix®. These vaccines provide strong protection against new HPV infections for young women through age 26, and young men through age 21, but they are not effective at treating established HPV infections. It was too late for me in 2011 when the HPV vaccine was made available to young men, and I was 43 years old.

According to the Centers for Disease Control and Prevention (CDC), more than 30,000 new cancers attributable to HPV are diagnosed each year. Unlike human immunodeficiency virus (HIV), which is spread by blood and semen, HPV is spread in the fluids of the mucosal membranes that line the mouth, throat, and genital tracts, and can be passed from one person to another simply via skin-to-skin contact.

While most HPV cases clear up on their own, infection with certain high-risk strains of HPV can cause changes in the body that lead to six different types of cancer, including cancers of the penis, cervix, vulva, vagina, anus, and head and neck (the last of which is what I have). Two of these, HPV strains 16 and 18, are responsible for most HPV-caused cancers.

Researchers believe that it can take between 10 and 30 years from the time of an initial HPV infection until a tumor forms. That’s why preventing HPV in the first place is so important and the HPV vaccine is so essential.

However, only 49.5 percent of girls and 37.5 percent of boys in the United States were up to date with this potentially lifesaving vaccination series, according to a 2017 CDC report. In sharp contrast, around 80 percent of adolescents receive two other recommended vaccines—a vaccine to prevent meningococcus (PDF), which causes bloodstream infections and meningitis, and the Tdap vaccine to prevent tetanus, diphtheria, and pertussis.

Even if you don’t think your child is at risk for HPV now, they almost certainly will be. HPV is extremely common. Nearly everyone gets it at some point; in fact, the CDC estimates that more than 90 percent and 80 percent of sexually active men and women, respectively, will be infected with at least one strain of HPV at some point in their lives. Around one-half of these infections are with a high-risk HPV strain.

As a cancer patient with a terminal prognosis, I find it infuriating that the HPV vaccine is tragically underutilized more than a decade since its introduction. Two simple shots administered in early adolescence can reduce a child’s risk of receiving a cancer diagnosis much later in life.

Parents who oppose the use of vaccines cite popular misconceptions that they are unsafe, ineffective, and that immunity is short-lived. Others argue that receiving the HPV vaccine may increase sexual promiscuity. Films like Vaxxed based on research that has been discredited, and directed by a researcher who fled the United Kingdom due to the misleading uproar he created, are still quoted as science.

Regardless, the fact remains that millions of adolescents aren’t getting a vaccine to prevent a virus known to cause cancer. We must counter untrue, exposed, and discredited research that keeps some parents from having their children vaccinated and put an end to the campaign of misinformation.

Viruses that are preventable, such as HPV, should be eradicated just like previous success with polio and smallpox. Cancers that are preventable through HPV vaccination should be prevented. The safety and efficacy of these vaccines are no longer subject to serious debate (PDF). Research has shown that vaccinations work; they keep children healthy, save lives, and protect future generations of Americans—but only when they are utilized.

The lesson: Don’t wait. Talk to your pediatrician about vaccinating your 11-year-old boys and girls against HPV today to eradicate this cancer-causing virus.

I only wish my parents had that opportunity when I was young, as it could have prevented the cancer that’s killing me.

December, 2017|Oral Cancer News|

Know what’s worse than the risks of getting the HPV vaccine? Getting an HPV-related cancer. Trust me

Source: www.statnews.com
Author: Michael D. Becker

In an era of $500,000 cancer treatments, you’d expect a vaccine series that costs about $300 and helps prevent several types of cancer to be popular with physicians, insurers, and consumers. It’s not, and, as a result, people are dying. I should know — I’m one of them.

The human papillomavirus (HPV) can cause changes in the body that lead to six cancers: cervical, vaginal, and vulvar cancer in women; penile cancer in men; and anal cancer in both women and men. It can also cause oropharyngeal cancer — cancer in the back of the throat, including the base of the tongue and tonsils — in both sexes. In the U.S., approximately 30,000 new cancers attributable to HPV are diagnosed each year.

In 2006, the first vaccine became available to protect against HPV infection. I was 38 years old at the time, well above the upper age limit of 26 the Centers for Disease Control and Prevention recommends for getting the vaccine. Ideally it should be given before the teen years, but can be given up to age 26.

Uptake of the HPV vaccine in the U.S. is abysmal, with just 49 percent of girls and 37 percent of boys having received the recommended HPV vaccination series.

Individuals who oppose the use of vaccines argue that safety concerns should preclude the use of the HPV vaccine. I disagree. The safety and effectiveness of this vaccine to protect against cancer-causing strains of the HPV virus have been unquestionably proven. Others point to side effects of the HPV vaccine as a reason not to vaccinate young Americans. These may include pain, swelling, redness, itching, bruising, bleeding, or a lump at the injection site as well as headache, fever, nausea, dizziness, tiredness, diarrhea, abdominal pain, and sore throat. Most people who get the vaccine experience no side effects from it other than the pain that accompanies most shots.

Missing from the discussion are the risks of not getting the vaccine. As someone with HPV-related oropharyngeal cancer, I can describe a few of them. And I can say with certainty I would gladly have experienced any of the vaccine-related side effects rather than the dozen or so “side effects” of the cancer and its treatment that I’m living with. I’ve illustrated them on the image below.

Some of these side effects, like hair loss, aren’t hazardous. Others are. I’ve spent time in an intensive care unit for my rapid heart rate, and have had to go to the emergency department several times for my pleural effusion and other issues. All of these pale beside the biggest “side effect” — a terminal disease that will eventually take my life.

I urge all parents to talk to your child’s doctor about the HPV vaccine. I wish my parents had that opportunity when I was young, as it could have prevented the cancer that’s killing me.

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|

Should women older than 18 get the HPV vaccine?

Source: www.washingtonpost.com
Author: Erin Blakemore

About half of American teenagers have been vaccinated against the human papillomavirus (HPV), the most common sexually transmitted infection in the United States. Should adult women follow suit?

Yes, says Lauri Markowitz, a Centers for Disease Control and Prevention medical epidemiologist who has worked with the advisory committee that makes national vaccination recommendations. “Women 18 to 26 should be vaccinated.”

There’s good reason to follow that recommendation. According to the American Cancer Society, about 12,820 new cases of cervical cancer will be diagnosed in U.S. women this year and more than 4,000 will die of the disease. HPV is thought to be responsible for more than 90 percent of all cervical and anal cancers in men and women. The virus also causes vaginal, vulvar and throat cancers and genital warts.

Although the majority of HPV infections do not cause cancer — most people with an infection never show any symptoms, and infections usually go away on their own — some strains are particularly dangerous. Gardasil 9, the newest HPV vaccine approved by the Food and Drug Administration, protects against nine such strains and, researchers say, may be able to prevent up to 90 percent of cervical cancers. (Older vaccines protect against fewer strains of HPV.)

However, confusion about the way HPV vaccines protect against infection can deter some women. Gardasil 9 is approved for women up to age 26. Like other vaccines, it spurs the body’s immune system to defend itself against a virus. The FDA and CDC say the HPV vaccines are safe and extremely effective: HPV rates in women ages 14 to 19 years fell 64 percent within six years of the vaccine’s introduction in the United States in the mid-2000s and 34 percent in women ages 20 to 24.

The vaccines are most effective if administered before a woman becomes sexually active. The longer a woman has been sexually active and the more partners she has had, the more opportunities she has had to become infected with an HPV strain that overlaps with the vaccine. If she is vaccinated at an older age, the vaccine may be less effective in lowering her cancer risk, Markowitz says. The vaccine can’t clear any HPV that has taken hold; it can only prevent future infection. So essentially if you already have been exposed to one of the strains it protects against, it will be useless against that strain.

That doesn’t mean it’s useless to get vaccinated if you’re older than the recommended age of 11 or 12, Markowitz says. “Your chances of being protected are decreasing, but you will still have some protection,” she says. Although the likelihood that a sexually active woman has been infected with one of the strains the vaccine protects against increases as a woman has more partners, those who didn’t receive the vaccine at the recommended age are still urged to get vaccinated to increase the odds of protection.

Some insurance does not cover the vaccine for those older than 18 — the shots can be costly, though the manufacturer may provide assistance — but it really varies across the board.

October, 2017|Oral Cancer News|

Penn surgeons become world’s first to test glowing dye for cancerous lymph nodes

Source: www.phillyvoice.com
Author: Michael Tanenbaum, PhillyVoice Staff

Surgeons at the University of Pennsylvania have achieved a global first with the use of a fluorescent dye that identifies cancerous cells in lymph nodes during head and neck cancer procedures.

The study, led by otorhinolaryngologist Jason G. Newman, seeks to test the effectiveness of intraoperative molecular imaging (IMI), a technique that illuminates tumors to provide real-time surgical guidance.

More than 65,000 Americans will be diagnosed with head and neck cancers in 2017, accounting for approximately 4 percent of all cancers in the United States, according to the National Cancer Institute. About 75 percent of these cancers are caused by tobacco and alcohol use, followed by human papillomavirus (HPV) as a growing source for their development.

Common areas affected by these cancers include the mouth, throat, voice box, sinuses and salivary glands, with typical treatments including a combination of surgery, radiation and chemotherapy.

Lymph nodes, which act as filters for the immune system, are often among the first organs affected by head and neck cancers as they spread or resurface. Initial surgeries may leave microscopic cancerous cells undetected in the lymphoid tissue, heightening the risk that a patient’s condition will return after the procedure.

“By using a dye that makes cancerous cells glow, we get real-time information about which lymph nodes are potentially dangerous and which ones we can leave alone,” Newman said. “That not only helps us remove more cancer from our patients during surgery, it also improves our ability to spare healthy tissue.”

With the aid of a fluorescent dye, surgeons are able to key in on suspicious tissue without removing or damaging otherwise healthy areas. Previously adopted for other disease sites in the lungs and brain, the practice now allows Newman’s team to experiment with indocyanine green (ICG), an FDA-approved contrast agent that responds to blood flow.

Newman explained that since tumor cells retain the dye longer than most other tissues, administering the dye prior to surgery singles out the areas where cancer cells are present.

The current trial at Penn will enable researchers to determine whether ICG is the most suitable dye for head and neck cancers and provide oncologists with a deeper understanding of how cancer spreads in the lymph nodes.

October, 2017|Oral Cancer News|

Blood test for HPV may help predict risk in cancer patients

Source: www.newswise.com
Author: University of North Carolina Health Care System

A blood test for the human papillomavirus, or HPV, may help researchers forecast whether patients with throat cancer linked to the sexually transmitted virus will respond to treatment, according to preliminary findings from the University of North Carolina Lineberger Comprehensive Cancer Center.

HPV can cause oropharyngeal cancer, which is a cancer of the throat behind the mouth, including the base of the tongue and tonsils. Studies have shown that patients with HPV-positive oropharyngeal cancer have better outcomes than patients whose cancer is not linked to the virus.

Preliminary findings presented at this year’s American Society for Radiation Oncology Annual Meeting suggest a genetic test for HPV16 in the blood could be useful to help assess risk for patients, and could help identify patients suitable for lower treatment doses.

“Our work on this blood test is ongoing, but we are optimistic that ‘liquid biopsy’ tests such as ours may be useful in the personalization of therapy for many patients with HPV-associated oropharyngeal cancer,” said the study’s senior author Gaorav P. Gupta, MD, PhD, UNC Lineberger member and assistant professor in the UNC School of Medicine Department of Radiation Oncology.

To avoid over-treating patients and to spare them from toxic treatment side effects, UNC Lineberger’s Bhisham Chera, MD, an associate professor in the radiation oncology department, led studies testing whether favorable-risk patients with HPV-positive oropharyngeal cancer can be treated successfully with lower doses of radiation and chemotherapy. A phase II clinical trial using this de-intensified regimen have shown “excellent” cancer control, Chera said.

The researchers used a number of selection criteria to identify patients who can benefit from lower-doses: patients had to be positive for HPV, and they had to have smoked fewer than 10 pack years. Chera said this system is not perfect, however. The researchers have seen cancer recur in non-smoking patients as well as “excellent” cancer control in longtime smokers.

“This has led us to question whether we can get better prognostication with other biomarkers,” Chera said.

They developed a test that can detect HPV16 circulating in the blood, and found that circulating HPV16 DNA was detectable using the test in the majority of a group of 47 favorable-risk oropharyngeal cancer patients.

In a finding that seems counterintuitive, they discovered that very low or undetectable HPV16 pretreatment levels in their blood actually had higher risk of persistent or recurrent disease for chemotherapy and radiation treatment. In contrast, patients with high pretreatment levels of HPV16 in their blood had 100 percent disease control.

They hypothesized that, potentially, the patients with undetectable/low pre-treatment HPV16 levels in the blood may have different, more radiation/chemotherapy resistant cancers.

“Our current theory is that these patients with low or undetectable levels of HPV16 have a different genetic makeup—one that is perhaps less driven purely by HPV, and thus potentially less sensitive to chemotherapy and radiation,” Gupta said. “We are performing next generation sequencing on these patients to search for additional genetic markers that may give us a clue regarding why they have a worse prognosis.”

They also identified a subset of patients who rapidly cleared the HPV16 from their blood. Researchers hypothesize that they could use their findings to further stratify patients who may be eligible for lower intensity treatment.

“A tantalizing – and yet currently untested – hypothesis is whether this subset of ultra-low risk patients may be treated with even lower doses of chemoradiotherapy,” Gupta said.

October, 2017|Oral Cancer News|

HPV and cancer: Key mechanism may suggest treatment

Source: www.medicalnewstoday.com
Author: Maria Cohut

New research from Georgetown University in Washington, D.C., investigates how the human papillomavirus promotes cancer. The findings might point to a potential new and improved strategy for targeted treatment.
The human papillomavirus (HPV) refers to a group of viruses transmitted through sexual contact. Some types of HPV cause various kinds of cancer, including mouth, anus, and cervical cancer.

According to data from the Centres for Disease Control and Prevention (CDC), around 1 in 4 people in the United States are infected with HPV.

Although treatments for HPV-related conditions do exist, they either target non-cancerous outcomes (such as genital warts) or they focus on the prevention of cancer through screening of abnormal cell activity.

Treatments for cancers caused by HPV include surgical interventions and chemotherapy, but at present, none of the options specifically address the viral source.

Researchers from Georgetown University Medical Center in Washington, D.C., have now identified the mechanism that promotes the survival of cancerous cells due to HPV. The study, which was led by Dr. Xuefeng Liu, describes a molecular apparatus that renders cancer cells “immortal.” Understanding how this apparatus works may lead to better targeted treatments in the future, the researcher suggests.

“There is no targeted treatment now for these cancers since German virologist Harald zur Hausen, Ph.D., discovered in 1983 that HPV can cause cervical cancer,” says Dr. Liu.

“Recently,” he adds, “the numbers of HPV-linked head and neck cancers have increased in the U.S. Now we have a chance to develop and test a very specific, potentially less toxic way to stop these cancers.”

The researchers’ findings are published in the journal Oncotarget.

October, 2017|Oral Cancer News|