Black raspberries reduce DNA damage in oral cancer survivors

Source: www.prweb.com
Author: press release

New research presented Wednesday, April 10, at the American Association for Cancer Research Annual Meeting 2013 in Washington, DC, suggests that a food-based cancer prevention study aimed at oral cancer survivors was effective at attenuating highly reactive oxygen molecules that can damage DNA and trigger cancer. In the study, a phase 1b clinical trial conducted at The Ohio State University, participants consumed 4 – 8 grams of black raspberries daily for six months. The berries were well tolerated by the participants and adherence to the regimen was good.

This study provides compelling data that indicate biochemical markers of cancer-causing DNA damage were reduced in participants who adhered to the food-based regimen and supports other evidence from a phase 2 human trial linking application of black raspberry gel to precancerous lesions to a reduced risk of developing oral cancer.

Black raspberries, not to be confused with blackberries, are almost exclusively grown in Oregon, on the west coast of the United States. They have been studied extensively because of their high concentration of certain phytonutrients and antioxidants. BerriProducts, an Oregon-based company, has been supplying black raspberry products to research universities across the country for the last four years.

Researchers document molecular tumor subtypes of head and neck cancer

Source: www.oncologynurseadvisor.com
Author: Kathy Boltz, PhD

Head and neck squamous cell carcinoma (HNSCC) is the seventh most common form of cancer in the United States. However, other than an association with the human papillomavirus (HPV), no validated molecular profile of the disease has been established. By analyzing data from DNA microarrays, a study has confirmed the presence of four molecular classes of the disease. Also, previous results have been extended by suggesting an underlying connection between the molecular classes and observed genomic events, some of which affect cancer genes. This study also demonstrated the clinical relevance of the classes and certain genomic events, paving the way for further studies and possible targeted therapies.

“Cancer is a disease caused by alteration in the DNA and RNA molecules of tumors. A cancer results when broken molecules initiate a cascade of abnormal signals that ultimately results in abnormal growth and spread of tissues that should be under tight control within the body,” said Neil Hayes, MD, MPH, of the University of North Carolina Lineberger Comprehensive Cancer Center and of The Cancer Genome Atlas.

“However, most common tumors, including head and neck cancer, have relatively little information in the public record as to how these signals coordinate to create different patterns of abnormalities. This study is among the largest ever published to document reproducible molecular tumor subtypes. Subtypes, such as those we describe, represent attractive models to understand and attack cancers for treatment and prognosis.”

The team analyzed a set of nearly 140 HNSCC samples. By searching for recurrent patterns known as gene expression signatures, they detected four gene expression subtypes. These subtypes are termed basal, mesenchymal, atypical, and classical, based on similarities to established gene expression subtypes in other tumor types and expression patterns of specific genes. For potential clinical use, these subtypes are complementary to classification by HPV status and the putative high-risk marker CCND1 copy number gain.

In spite of being the seventh most common form of cancer in the United States, HNSCC is relatively understudied in comparison to other tumor types (eg, breast and lung). By leveraging the similarities found in the gene expression subtypes, the results of this study provide a connection to a range of well-established findings and additional insight into the disease.

Source: This study was published in PLOS ONE (2013; doi:10.1371/journal.pone.0056823).

DNA adducts linked to oral cancer in smokers

Source: www.news-medical.net
Author: Sarah Guy, medwireNews Reporter

Having a high susceptibility to certain types of DNA damage caused by tobacco smoking could significantly increase the risk for oral cancer, show results of a Taiwanese study.

Levels of BaP 7,8-diol 9,10-epoxide (BPDE) – a metabolite of Benzo[a]pyrene, an important carcinogen found in cigarette smoke – correlated positively with smoking status in a cohort of individuals with oral cancer, report the researchers.

The findings also indicate a significantly increased risk for oral cancer among individuals with high DNA adduct levels compared with their peers with low levels.

“Based on our finding, we suggest that detected BPDE-like DNA adducts could be used as a biomarker for oral cancer risk,” write Huei Lee (Taipei Medical University) and colleagues in the Archives of Oral Biology.

The team analyzed BPDE-DNA adduct levels in oral tissue samples from 158 oral cancer patients and 64 individuals without cancer (controls), using immunohistochemistry and enzyme-linked immunosorbent assay (ELISA).

The results of these assays significantly and positively correlated , so that immunohistochemistry-negative patients did not have detectable DNA adduct levels using ELISA and vice versa.

DNA adduct levels also positively correlated with smoking status among the cancer patients, note the researchers, with significantly higher adduct levels among smokers than nonsmokers, at 93.18 versus 0.04 adducts per 108 nucleotides.

Lee and co-workers also observed that cancer patients had significantly higher DNA adduct levels than controls, at a range of 0-358.00 versus 0-39.50 adducts per 108 nucleotides.

Indeed, DNA adduct level was an independent risk biomarker for oral cancer in multivariate analysis, which indicated a 9.94-fold increased risk for the disease among individuals with high levels, defined as more than two standard deviations above the mean adduct level in the low group – which equates to 34.03 adducts per 108 nucleotides.

“These results strongly suggest that a high susceptibility to DNA damage derived from exposure to cigarette carcinogens is associated with the high risk of oral cancer in Taiwanese oral cancer patients,” conclude Lee et al.

Source: medwireNews

DNA alone inadequate to identify HPV-related cancers

Source: www.oncologypractice.com
Author: Mary Ann Moon

Testing for the presence of human papillomavirus DNA alone, especially using polymerase chain reaction methods, is not adequate to identify which head and neck squamous cell carcinomas are caused by the virus, according to two studies published online Sept. 18 in Cancer Research.

Identifying HPV-driven malignancies is important because they respond better to treatment and have better outcomes than those unrelated to HPV infection. Indeed, treatment of head and neck squamous cell carcinoma (HNSCC) may soon be guided by the tumor’s HPV status, since trials are now underway to determine whether de-escalation of chemo- and radiotherapy is safe and effective in such patients.

At present, however, the biomarkers that are best suited to making this identification are unclear.

Case Series Assesses Biomarkers
In the first study, researchers assessed the usefulness of four biomarkers in determining which HNSCCs in a case series were driven by HPV. They began by examining fresh-frozen tumor biopsy samples from 199 German adults diagnosed as having oropharyngeal squamous cell cancer between 1990 and 2008.

The four biomarkers were HPV-16 viral load, viral oncogene RNA (E6 and E7), p16INK4a, and RNA patterns similar to those characteristic of cervical carcinomas (CxCa RNA), said Dr. Dana Holzinger of the German Cancer Research Center at Heidelberg (Germany) University and her associates.

The simple presence of HPV DNA in a tumor sample was found to be a poor indicator of prognosis, likely because it often signaled past HPV infections or recent oral exposure, rather than active HPV infection that progressed to malignancy, the investigators said (Cancer Res. 2012 Sept. 18).

Instead, “we showed that high viral load and a cancer-specific pattern of viral gene expression are most suited to identify patients with HPV-driven tumors among patients with oropharyngeal cancer. Viral expression pattern is a completely new marker in this field, and viral load has hardly been analyzed before,” Dr. Holzinger said in a press statement accompanying the publication of these findings.

“Once standardized assays for these markers, applicable in routine clinical laboratories, are established, they will allow precise identification” of cancers that are or are not HPV-driven, which will in turn influence prognosis and treatment, she added.

Results Back Combination Approach
In the second study, Dr. Caihua Liang of Brown University, Providence, R.I., and her associates examined 488 HNSCC samples as well as serum samples collected in a population-based study in the Boston area during 1999-2003.

As in the first study, these investigators found that the mere presence of HPV-16 DNA in these tumors, particularly when detected by PCR analysis, did not accurately predict overall survival or progression-free survival.

Instead, “our study strongly suggests that the combination of detection of HPV-16 DNA in HNSCC tumors [plus] p16 immunostaining with E6/E7 antibodies represents the most clinically valuable surrogate marker for the identification of patients . . . who have a better prognosis,” they said (Cancer Res. 2012 Sept. 28).

“Assessment of HPV DNA using polymerase chain reaction methods as a biomarker in individual head and neck cancers is a poor predictor of outcome, and is also poorly associated with antibody response indicative of exposure and/or infection by HPV,” senior author Dr. Karl T. Kelsey added in the press statement.

“We may not be diagnosing these tumors as accurately and precisely as we need to for adjusting treatments,” said Dr. Kelsey, a professor in the department of epidemiology and the department of pathology and laboratory medicine at Brown University.

Dr. Holzinger’s study was funded in part by the European Commission, BMBG/HGAF-Canceropole Grand-Est, and the German Research Foundation. Her associates reported ties to Qiagen and Roche. Dr. Liang’s study was supported by the National Institutes of Health and the Flight Attendant Medical Research Institute, and one associate reported ties to Bristol-Myers Squibb.

2012-09-24T13:36:21-07:00September, 2012|Oral Cancer News|

Predicting oral cancer

Source: www.dailyrx.com

Oral cancers can occur anywhere in the mouth. As with any cancer, the sooner it’s found, the better. A new tool helps doctors know when oral cancer may be in a patient’s future.

A recent study finds that a set of molecular markers can help judge which lesions in the mouth are most likely to turn into oral cancer.

The Oral Cancer Prediction Longitudinal Study was conducted in Canada at the Oral Cancer Prevention Program at the BC Cancer Agency in Vancouver.

“The results of our study should help to build awareness that not everyone with a low-grade oral premalignant lesion will progress to cancer,” said Program Director, Miriam Rosin, PhD. “However, they should also begin to give clinicians a better idea of which patients need closer follow-up.”

Every year, cancer shows up in the mouths of nearly 300,000 people around the globe. Some of these start as spots – or lesions – in the mouth that have not yet become cancerous.

It’s always been difficult to tell which of these pre-malignant lesions will progress to full blown cancer.

In an earlier study, Rosin’s team had analyzed the DNA of tissue that eventually turned into oral cancer. This research provided a method for grouping patients according to risk.

For this study, researchers examined pre-cancerous tissue from nearly 300 patients, who were followed over a period of years. These patients were placed into either low-, intermediate- or high-risk groups.

Two additional DNA markers were used to zero in on a patient’s oral cancer risk factors.

“Compared with the low-risk group, [the] intermediate-risk patients had an 11-fold increased risk for progression, and the high-risk group had a 52-fold increase in risk for progression,” Dr. Rosin said.

Only about 3 percent of the people in the low-risk group developed cancer within five years.For those in the intermediate-risk, just over 16 percent saw the disease progress to cancer, while about 63 percent of high-risk patients developed oral cancer within five years.

To translate, this means that two out of every three high-risk lesions are progressing toward cancer, Dr. Rosin says.

“Identifying which early lesions are more likely to progress may give clinicians a chance to intervene in high-risk cases, and may help to prevent unnecessary treatment in low-risk cases,” Dr. Rosin said.

This study was published August 21 in Cancer Prevention Research, a journal of the American Association for Cancer Research. No financial information was available.

2012-09-11T08:13:58-07:00September, 2012|Oral Cancer News|

Molecular markers help predict oral cancer progression

Source: DrBicuspid.com

August 21, 2012 — A group of molecular markers has been identified that can help clinicians determine which patients with low-grade oral premalignant lesions are at high risk for progression to oral cancer, according to data from the Oral Cancer Prediction Longitudinal Study published in Cancer Prevention Research (August 21, 2012).

“The results of our study should help to build awareness that not everyone with a low-grade oral premalignant lesion will progress to cancer,” said Miriam Rosin, PhD, director of the Oral Cancer Prevention Program at the British Columbia (BC) Cancer Agency, in a press release issued by the American Association of Cancer Research, which publishes the journal. “However, they should also begin to give clinicians a better idea of which patients need closer follow-up.”

In 2000, Rosin and colleagues used samples of oral premalignant lesions in which progression to cancer was known to have subsequently occurred to develop a method for grouping patients into low- or high-risk categories based on differences in their DNA.

In their current population-based study, the researchers confirmed that this approach was able to correctly categorize patients as less or more likely to progress to cancer. They analyzed samples from 296 patients with mild or moderate oral dysplasia identified and followed over years by the BC Oral Biopsy Service, which receives biopsies from dentists and ear, nose, and throat surgeons across the province. Patients classified as high-risk had an almost 23-fold increased risk for progression.

Next, the researchers added two additional DNA molecular risk markers related to loss of heterozygosity to the analysis in an attempt to better differentiate patients’ risks. They used the disease samples from the prospective study and categorized patients into low-, intermediate-, and high-risk groups.

“Compared with the low-risk group, intermediate-risk patients had an 11-fold increased risk for progression and the high-risk group had a 52-fold increase in risk for progression,” Rosin said.

Of patients categorized as low-risk, only 3.1% had disease that progressed to cancer within five years. In contrast, intermediate-risk patients had a 16.3% five-year progression rate and high-risk patients had a 63.1% five-year progression rate.

“That means that two out of every three high-risk cases are progressing,” Rosin said. “Identifying which early lesions are more likely to progress may give clinicians a chance to intervene in high-risk cases and may help to prevent unnecessary treatment in low-risk cases.”

This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

2012-08-22T09:55:45-07:00August, 2012|Oral Cancer News|

Demystifying the immortality of cancer cells

Source: http://medicalxpress.com/
Author:

In cancer cells, normal mechanisms governing the cellular life cycle have gone haywire. Cancer cells continue to divide indefinitely, without ever dying off, thus creating rapidly growing tumors. Swiss scientists have discovered a protein complex involved this deregulated process, and hope to be able to exploit it to stop tumor formation in its tracks.

The telomeres can be seen as white dots on these chromosomes © National Institute of Health

All our cells come equipped with an automatic self-destruct mechanism; they are programmed to die after a certain number of divisions. This internal clock is of great interest to cancer researchers, because most forms of cancer exhibit a defect in this innate timing mechanism. Cancer cells continue to divide indefinitely, long past the moment at which a normal cell would self-destruct. A team of researchers from professor Joachim Lingner’s laboratory at EPFL has learned how this defect is regulated in a tumor. Post-doctoral researcher Liuh-Yow Chen led the team in publishing an article appearing in the journal Nature on the 4th of July 2012. Their hope is that the discovery will provide new targets for drug therapies to combat the deadly disease.

Cellular immortality, which is responsible for cancer formation, hearkens back to a critical function of the cells of the developing embryo. At the ends of every chromosome there is a special sequence of DNA known as a telomere, whose length is governed by the telomerase enzyme. This sequence represents the lifespan of the cell. Every time the cell divides, it is shortened, and when the telomere finally runs out, the cell dies. This reserve allows most cells to divide about 60 times – sufficient for the cell to play its given role in the organism, without succumbing to inevitable genetic mutation.

Cellular immortality, cancer’s common denominator
Normally, once the embryonic stage is completed, our cells stop producing telomerase – with the notable exception of somatic stem cells. But occasionally, a cell will mutate and reactivate production of the enzyme, so that when the cell divides, the telomere gets longer instead of shorter. This is what gives cancer cells their immortality.

“This mutation, on its own, is not enough to cause cancer,” explains Joachim Lingner, co-author and head of the lab. “But cellular immortality is a critical element in tumor formation in 90% of known cancers.” Researchers the world over hope to be able to stop the runaway growth of cancer cells by targeting this mechanism with drug therapy.

But interestingly enough, even in a cancer cell the telomere doesn’t grow indefinitely long. With each cell division it loses some 60 nucleotides, like most cells, but then the activated telomerase causes it to gain just as many back. The internal clock is reset to zero, and the cell becomes immortal. But there’s one interesting question here: What is stopping the telomere from getting indefinitely long?

Stopping the clock with three proteins
The EPFL team was able to provide an answer to this question; they identified three proteins that join together and then attach themselves to the telomere. A bit like a lid on a pot, this protein complex prevents telomerase from acting on the telomere. But in the cancer cell, their timing is off – their involvement takes place too late.

“If we could cause these proteins to act earlier, or if we could recreate a similar mechanism, the cancer cell would no longer be immortal,” explains Ligner. The cancer cells would die a normal death. Clinical applications are still a long way off, however, he insists. “Our discovery may allow us to identify potential targets – for example, a secondary protein to which these three proteins also attach. But right now our work is still in the basic research stages.”

Source: Cancer July 5, 2012

Genes May Link Disparate Diseases

Source: The Wall Street Journal

Diseases that strike different parts of the body—and that don’t seem to resemble each other at all—may actually have a lot in common.

Scientists have identified the genetic basis for many separate diseases. Now, some researchers are looking at how the genes interact with each other. They are finding that a genetic abnormality behind one illness may also cause other, seemingly unrelated disorders. Sometimes diseases are tangentially linked, having just one gene in common. But the greater the number of shared genetic underpinnings a group of diseases has, the greater the likelihood a patient with one of the illnesses will contract another.

Researchers have found evidence, for example, that there is a close genetic relationship between Crohn’s disease, a gastrointestinal condition, and Type 2 diabetes, despite the fact the two conditions affect the body in very distinct ways. Other illnesses with apparently close genetic links are rheumatoid arthritis and Type 1 diabetes, the form of the disease that usually starts in childhood, says Joseph Loscalzo, chairman of the department of medicine at Brigham and Women’s Hospital in Boston.

This network approach, known among scientists as systems biology, could change the way medical specialists view and treat disease, according to some researchers. Rather than only looking to repair the parts of the body that are directly affected by illness, “we should be looking at what the wiring diagram [inside of cells] looks like,” says Albert-László Barabási, a physicist at Northeastern University’s Center for Complex Network Research in Boston.

Research work in the field is being done by geneticists, biologists and physicists at several universities and drug makers. The aim is to map how genes and the proteins they produce interact within cells in order to gain a better understanding of what goes wrong in the body to cause disease.

The information could help better predict a person’s risk of developing diseases, researchers say. It also could aid drug development. By figuring out which proteins are most critical to the normal functioning of the body, pharmaceutical companies could target those key proteins to treat disease. In some cases, drug companies may want to avoid interfering with key proteins to avoid too many unintended side effects, says Marc Vidal, director of the Center for Cancer Systems Biology at Dana-Farber Cancer Institute in Boston.

Since all the DNA in the human body was first sequenced in 2000, some 4,000 diseases with a known genetic basis have been identified, according to the National Institutes of Health. But only about 250 of those diseases have treatments, leaving many genetic puzzles left to untangle.

Scientists have long known that proteins and other molecules in the body don’t act alone. In order for the body to operate efficiently, biological substances must bind to or pass chemical messages to each other to start and stop working. The system is complex: Each gene is thought to produce, on average, five separate substances, mostly proteins, and these products interact with each other. When a protein, or group of proteins, malfunctions, it appears to give rise to a variety of distinct illnesses.

Dr. Barabási and his colleagues set out to see which diseases shared genetic underpinnings. They used information from a vast database at Johns Hopkins University in Baltimore that pulled together research from around the world on diseases and genes they were linked to. The scientists then mapped out a network indicating which diseases were seemingly connected to each other through common genes.

Of the 1,284 diseases mapped, nearly 900 had genetic links to at least one other disease. And 516 of these formed a so-called disease cluster, in which illnesses, mainly cancers, were linked to each other through multiple genetic connections.

Among the findings: Deafness shared at least one of 41 genes with over 20 other diseases, suggesting that it sits centrally in a cluster of other diseases. These include cardiomyopathy, a condition in which the heart muscle deteriorates; and ectodermal dysplasia, an abnormal development of the skin, hair, nails or teeth. Colon cancer shared at least one of 34 genes with 50 other diseases. Also in the cancer cluster were squamous cell carcinoma, a type of skin cancer, and throat cancer, but these had fewer genetic links between them. The work was published in the Proceedings of the National Academy of Sciences in 2007.

Because the diseases in the cluster were linked at the level of the cellular network, “the breakdown of one gene can lead to many apparently unrelated diseases,” says Dr. Barabási.

Another study by Dr. Barabási’s team aimed to see if their database analysis of genetically linked diseases was borne out in real life. The researchers analyzed more than 32 million Medicare hospital claims.

When patients developed multiple conditions, they were more likely to get illnesses that had close genetic links to their original disease than they were to get other disorders.

The study, published in 2009 in one of the journals of the Public Library of Science, PLoS Computational Biology, also showed that patients who developed diseases that tend to coincide with many others were more likely to die sooner than people whose diseases were more tangentially connected.

Using the data, the researchers estimated people’s likelihood of getting a second disease. A patient with ischemic heart disease, for example, has a 60% greater risk of getting Type 2 diabetes than an average healthy person.

Other biological processes also link seemingly unrelated diseases. In work published in 2008 in the Proceedings of the National Academy of Sciences, Dr. Barabási’s team identified a cluster of diseases, including diabetes and anemia, or coronary heart disease and hypertension, that appear to share common metabolic pathways, such as how chemicals are broken down or used in the body.

Dr. Vidal is currently working with Dr. Barabási and other researchers to map out all the possible protein interactions within a human cell. Dr. Vidal says about 20% of the project is finished, making it already the most complete map of the human protein network. The researchers also are developing protein-network maps for other organisms, including a yeast cell and Caenorhabditis elegans, a tiny worm with some 19,000 genes, about the same number as humans.

To test the role played by key proteins, or hubs, the researchers selectively deleted proteins or genes in the organisms and observed what happened. In the yeast cell, they found only about a quarter of the genes and proteins appeared to be essential, in that they connected to large numbers of other proteins and substances. The organism died when these hubs were removed, Dr. Vidal says.

This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

HPV DNA, E6?I-mRNA expression and p16(INK4A) immunohistochemistry in head and neck cancer – how valid is p16(INK4A) as surrogate marker?

Source: HighWire- Stanford University

It has been proposed that p16(INK4A) qualifies as a surrogate marker for viral oncogene activity in head and neck cancer (HNSCC). By analyzing 78 HNSCC we sought to validate the accuracy of p16(INK4A) as a reliable marker of active HPV infections in HNSCC. To this end we determined HPV DNA (HPVD) and E6?I mRNA (HPVR) expression status and correlated these results with p16(INK4A) staining. In tonsillar SCC 12/20 were HPVD+ and 12/12 of these showed active HPV infections whereas in non-tonsillar SCC 10/58 were HPVD+ and 5/10 showed active HPV infections. Thus, we prove about 8% of non-tonsillar SCC to be also correlated with HPV-associated carcinogenesis. Strikingly, 3/14 (21.4%) of tonsillar and non-tonsillar HPVD+/HPVR+ cases did not show p16(INK4A) overexpression and these cases would have been missed when applying initial p16(INK4A) staining only. However, in 13 cases negative for HPV, DNA p16(INK4A) was overexpressed. In conclusion, our data confirm tonsillar SCC to be predominantly but not only associated with active HPV infections. Furthermore, our data show that p16(INK4A) overexpression is not evident in a subgroup of HNSCC with active HPV infection. Definitive HPV data should therefore be utilised in diagnostics and treatment modalities of HPV positive and HPV negative HNSCC patients, resulting in a paradigm shift regarding these obviously different tumour entities.

This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

Oral HPV infection affects 7% of the US population

Source: www.onclive.com
Author: Ben Leach

Approximately 7% of Americans are infected with oral human papillomavirus (HPV), and men are 3 times as likely to be infected as women, according to an analysis that helps define a leading factor in the rise of oropharyngeal cancer.

The findings of the HPV prevalence study were presented at the Multidisciplinary Head and Neck Symposium in Phoenix, Arizona, in January and concurrently published in the Journal of the American Medical Association.1

The cross-sectional study was based on samples taken from 5579 men and women between the ages of 14 to 69 years that were obtained at mobile examination centers as part of the National Health And Nutrition Examination Survey (NHANES) 2009-2010. The samples were obtained through an oral rinse and gargle, with subsequent DNA samples used to determine HPV type. Demographic data were obtained using standardized interviews.

Human Papillomavirus (HPV)

HPV prevalence in the overall study population was 6.9% (95% confidence interval [CI], 5.7%-8.3%). HPV type 16, which accounts for 90% of HPVpositive oropharyngeal squamous cell carcinomas, was the most common form, affecting 1.0% of the study population (95% CI, 0.7%-1.3%).

Prevalence of HPV was significantly higher in men versus women (10.1% [95% CI, 8.3%- 12.3%] for men compared with 3.6% [95% CI, 2.6%- 5.0%] for women; P < .001]). Sexual contact was identified as a major factor in the rate of infection, with 7.5% of those who had experienced any form of sexual contact (95% CI, 6.1%-9.1%) infected, compared with 0.9% (95% CI, 0.4%-1.8%; P < .001) of those without a history of any form of sexual contact.

“This study of oral HPV infection is the critical first step toward developing potential oropharyngeal cancer prevention strategies,” Maura Gillison, MD, PhD, lead author of the study, said during a press conference at the symposium. “This is clearly important because HPV-positive oropharyngeal cancer is poised to overtake cervical cancer as the leading type of HPV-caused cancers in the US. We currently do not have another means to prevent or detect these cancers early.”

Prevalence of HPV Infection
in the US Population, 2009-20101

Characteristic Number in Study
(With Infection)
HPV Prevalence
(%)
Sex
Male 2748 (295) 10.1
Female 2753 (113) 3.6
Age
14-17 656 (16) 1.7
18-24 792 (45) 5.6
25-29 463 (32) 7.1
30-34 436 (39) 7.3
35-39 461 (31) 5.4
40-44 495 (30) 6.3
45-49 482 (37) 7.3
50-54 474 (50) 8.3
55-59 381 (47) 11.2
60-64 498 (55) 11.4
65-69 363 (26) 4.2

Further analysis identified risk factors for infection: HPV prevalence in men and women who had more than 20 sexual partners in their lifetime was 20.5% (95% CI, 17.4%-23.9%); among those who smoked more than 20 cigarettes a day, HPV prevalence was 20.7% (95% CI, 12.6%-32.0%).

Although cigarette and alcohol use have classically been associated with the disease, Gillison said that this study suggests that oral HPV is predominantly sexually transmitted. As to why men had a higher overall rate of HPV prevalence than women, the study authors suggested factors such as sexual behavior (ie, does a higher probability of transmitting HPV through oral sex on women compared to men exist?) and hormonal differences affecting the duration of infection.

Overall, the incidence of HPV-positive oropharyngeal cancers increased by 225% between 1988 and 2004, according to National Cancer Institute research. There were an estimated 6700 cases of HPV-positive oropharyngeal cancers in 2010, up from 4000 to 4500 in 2004.

Gillison said that the study was not necessarily designed to be used to advocate for vaccinating boys and girls before they become sexually active. However, Gillison said that large, prospective studies on the effectiveness of HPV vaccinations should be the next step in determining whether the vaccinations should be made mandatory at a national or global level.

“It’s difficult to make public policy recommendations based on a hope or a speculation,” Gillison said.

Notes:
1. Gillison ML, Broutian T, Pickard RK, et al. Prevalence of oral HPV infection in the United States, 2009-2010. JAMA. 2012; 307(7):published online ahead of print January 26, 2012. doi:10.1001/jama.2012.101

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