HPV

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|

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|

Immokalee health clinic earns national award for vaccination rate

Source: www.naplesnews.com
Author: Liz Freeman

The public health department in Immokalee set a goal for getting children vaccinated against cancer and brought home a U.S. Centers for Disease Control and Prevention award for its high success rate.

The Florida Department of Health in Collier County, specifically the Immokalee location, was named the regional winner of the 2017 HPV Vaccine Award because of its 76.2 percent vaccine series completion rate among 13 to 15 year olds.

A point-in-time survey in August found 560 children aged 13 to 15 in Immokalee had been vaccinated against HPV, according to a health department spokeswoman.

In the last four years, the Immokalee clinic took on an ambitious campaign in the farmworker community to boost HPV vaccination rates, starting with ensuring that all staff members who have contact with clients are knowledgeable about the virus and the vaccine. The virus is common and can cause certain cancer of the genitals, head and neck. There are about 31,000 new cases of cancer a year caused by the virus, according to the CDC.

Controversy is attached to the HPV vaccine by some groups who argue that getting kids vaccinated may promote early sexual interaction with others. State governments that have authority over school vaccination requirements have faced debate over requiring it and over the cost

State Surgeon General and DOH Secretary Dr. Celeste Philip said she was proud of the Immokalee clinic and its success rate for the vaccinating young people against the virus.

“Their commitment to preventing cancers caused by HPV infection and ensuring that every child and parent that visits the clinic are educated about the benefits of the HPV vaccine has a positive impact on the health of their county and our state,” she said in a news release.

The CDC award criteria stipulates that candidates must achieve a vaccination series rate of at least 70 percent of the patient population aged 13 to 15, both girls and boys, seen in the last two years.

Stephanie Vick, administrator of the Collier health department, said the Immokalee team identified a public health challenge and set out to achieve results.

“Their efforts reflect their professionalism and dedication to tackling what for some groups can be a taboo subject and placed the focus upon a universally accepted prevention subject,” Vick said.

People get HPV from another person during sexual contact, and both men and women can get it. A person can get it even if the partner has no sign or symptoms. About 79 million Americans are infected with some type of HPV, and 14 million people become newly infected each year. Most infections go away by themselves within two years, but sometimes it can take longer and can cause cancer of the genitals, in the back of the throat and the tongue.

Since 2006, the CDC has recommended the HPV vaccine, initially in a three-dose series over six months, and then it changed its recommendation to two doses for people before the 15th birthday. The second does should be given six to 12 months after the first dose.

November, 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|

Oral sex increases men’s risk of cancer, new study finds

Source: www.deccanchronicle.com
Author: staff

An alarming new study found men who have performed oral sex on five or more partners are at risk of head and neck cancer related to HPV, according to a report by the Daily Mail.

Johns Hopkins researchers warn men may not be aware of this risk, particularly if they smoke. “Among men who did not smoke, cancer-causing oral HPV was rare among everyone who had less than five oral sex partners, although the chances of having oral HPV infection did increase with number of oral sexual partners, and with smoking,” lead author Dr Amber D’Souza, associate professor at the Johns Hopkins Bloomberg School of Public Health told the Daily Mail.

For the study, data was analysed of 13,089 people part of the National Health and Nutrition Examination Survey (NHANES) and tested for oral HPV. That information was compared to data with federal figures on oropharyngeal cancer diagnoses. The results indicated that men had a higher risk of developing the disease compared to women.

The new study’s findings suggest it is crucial for boys to get the HPV vaccine.

While there are 100 different kinds of HPV, only few cause cancer. HPV strains 16 and 18 trigger most cervical cancer. HPV16 also causes oropharyngeal cancer.

Identifying who is at risk is will help curb the disease. “For these reasons, it would be useful to be able to identify healthy people who are most at risk of developing oropharyngeal cancer in order to inform potential screening strategies, if effective screening tests could be developed,” Dr D’Souza told the Daily Mail.

Further research to explore oral HPV infection in young healthy men is currently being conducted.

The study was originally published in the journal Annals of Oncology.

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|

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|

B.C. to begin providing free HPV vaccines for Grade 6 boys

Source: ctvnews.ca
Author: Darcy Matheson
Date: September 26, 2017

For the first time in British Columbia, boys in Grade 6 will be receiving free vaccinations for the Human Papillomavirus.

HPV is one of the most commonly sexually transmitted infections and B.C. health authorities say three out of four sexually active people will get it at some point in their lives.

Often showing no physical symptoms, HPV can lead to cervical, vaginal, and vulvar cancers in women and penile cancer in men – and can also cause anal and throat cancer in both men and women.

Up until now, the vaccine to protect against HPV was only provided free to girls in Grade 6, with the assumption that boys would be indirectly protected through “herd immunity.”

Vancouver Coastal Health will soon be sending out letters to parents and caregivers through children’s schools regarding upcoming clinics for both girls and boys.

People can also be immunized through health-care providers, family doctors and local public health units.

Dr. Meena Dawar, medical health officer for Vancouver Coastal Health, said that immunizations are key because the symptom-less virus is often passed onto others without knowing it.

“Most often an HPV infection will clear on its own but sometimes HPV won’t go away and cells infected with the virus can become cancerous,” Dawar said in a statement.

Cancer survivor Sandy Yun had her 14-year-old daughter immunized as part of the B.C. program. She was going to pay for her 11-year-old son to get the vaccine but now she will be getting it for free.

“I wouldn’t want my kids, or anyone else, to go through what I went through,” the mom said in a statement.

“We have an easy way to protect our children from cancer, parents: this is a no-brainer.”

Each year in B.C. 200 women will get cervical cancer, and 50 will die from the disease.

B.C. joins Saskatchewan, Newfoundland and Labrador and New Brunswick in offering the vaccine for free to boys starting this month.

A study published this summer by the Canadian Medical Association Journal said the number of HPV-caused oral cancers has risen sharply in Canada — about 50 per cent between 2000 and 2012.

The majority of the cases featured in the CMAJ study – about 85 per cent – were men.

Researcher and co-author Sophie Huang, a research radiation therapist at Princess Margaret Cancer Centre in Toronto, said men have a weaker immune response to HPV than females, which may explain the higher incidence of oral cancers linked to the virus in men.

 

September, 2017|Oral Cancer News|