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Genetic variants are associated with susceptibility to mouth and throat cancer

Source: www.eurekalert.org
Author: news release

A number of genetic variants associated with susceptibility to oral cavity and pharyngeal cancer have been described in an international study published in the journal Nature Genetics.

The most noteworthy finding was an association between cancer of the oropharynx and certain polymorphisms (alternative versions of a given DNA sequence) found in the human leukocyte antigen (HLA) genomic region. HLAs, proteins found on the surface of most cells in the body, play an important role in recognizing potential threats and triggering the immune response to foreign substances.

According to Eloiza Helena Tajara, a professor at the São José do Rio Preto Medical School (FAMERP) in São Paulo State, Brazil, and co-author of the article, a specific group of variants in this region, located on chromosome 6, is associated with enhanced protection against oropharyngeal cancer caused by human papilloma virus (HPV).

“Previous research showed that these same variants confer protection against cancer of the uterine cervix, which is known to be associated with HPV,” Tajara said. “Our findings suggest that the genes that control the immune system play a key role in predisposition to HPV-related tumors. This discovery points to the possibility of clarifying the mechanisms whereby such tumors develop and of designing methods for monitoring risk groups.”

The study was coordinated by the International Agency for Research on Cancer (IARC) and involved 40 research groups in Europe, the United States, and South America. The Brazilian participants are members of the Head & Neck Genome Project (GENCAPO), a consortium of scientists affiliated with several institutions.

In a recent study, GENCAPO evaluated more than 7 million genetic variants in samples from 6,034 patients with head and neck cancer. The cases comprised 2,990 oral cavity tumors, 2,641 oropharyngeal tumors, 305 tumors in the hypopharynx (the bottom part of the pharynx near the esophagus), and 168 tumors in other regions or more than one region concurrently. The study population also included samples from 6,585 people without cancer as controls.

The researchers detected eight loci (genomic sites) associated with susceptibility to these types of tumor. Seven had not previously been linked to mouth or throat cancer.

According to Tajara, the IARC set out to focus on analyzing oral cavity and oropharynx tumors because there are no genome-wide association studies of these two tumor types. Although these cancers are predominantly caused by tobacco and alcohol use, the importance of HPV, particularly HPV16, as a cause of oropharyngeal cancer has become more evident in recent years.

“The throat is the most affected area among head and neck cancer subsites, likely because its tissue is more receptive to the virus,” Tajara said.

In the article, the researchers note that the proportion of HPV-related oropharyngeal cancer cases is estimated to be approximately 60% in the US and 30% in Europe but lower in South America.

“One finding that was expected to some extent was the absence of HLA associations with oropharyngeal cancer, which may be due to the fact that the frequency of HPV-positive oropharyngeal cancer is less than 10% in South America,” Tajara said. “The same factor appears to account for the weak association between the variants identified and HPV-positive oral cavity cancer, which is also far less frequent than HPV-negative oral cavity cancer.”

In her view, the strong rise in cases linked to HPV in the US could be partly due to a change in sexual habits, especially regarding the practice of oral sex. “It’s possible that Brazil is still in a transition stage and that the habits that favor infection are only starting to become more common. If so, the effects will appear in a few years’ time,” she said.

Previous studies have already shown that HPV-associated head and neck cancers affect younger people and develop rapidly. By contrast, cases associated with tobacco and alcohol use as well as poor oral hygiene are more prevalent in those over fifty years old and progress more slowly but are harder to treat.

In addition to DNA in tissue samples taken from participants of the study, data were also collected on environmental and clinical factors possibly associated with the development of this type of cancer, such as smoking, alcohol consumption, and age.

According to Tajara, thanks to the joint efforts of 40 research groups it was possible to obtain data on a significant number of patients, thus enhancing the impact and reliability of the results. The GENCAPO team contributed some 1,000 samples from tumors for analysis.

“Based on these results, we can try to understand from the molecular standpoint how the observed polymorphisms interfere with the response to HPV infection,” Tajara said. “This may give us clues as to how to protect people and how to reduce the incidence of this type of tumor.”

December, 2016|Oral Cancer News|

Predicting throat cancer recurrence with a blood test

Source: knowridge.com
Author: from University of Michigan Health System

A new study suggests the possibility of predicting at its earliest stages when a type of head and neck cancer will come back.

Oropharyngeal cancer — which occurs in the throat, tonsils and back of the tongue — is frequently linked to the human papilloma virus. That’s good news, in a way, as HPV-related cancers are generally more responsive to treatment.

But for about 15 to 20 percent of these patients, the treatment won’t work and their cancer will return. There are no known biomarkers to predict when treatments are likely to fail.

In a new study in Clinical Cancer Research, researchers found that patients whose oropharyngeal cancer recurred had higher levels of antibodies for two proteins, E6 and E7, which are found in HPV-fueled cancers. The finding suggests a potential blood-based marker that could predict when cancer is likely to return.

For this study, researchers looked back at 52 patients with advanced oropharyngeal cancer who had enrolled in a prior study: 22 who had developed recurrence and 30 who had not. The two groups were similar in age, cancer classification and smoking status. All tumors were linked to the human papilloma virus.

On average, cancer recurred 13 months after a patient’s treatment ended. Serum was measured via a blood test at diagnosis or start of treatment, then repeated after treatment ended and about every three months after.

Initially, there was no difference in E6 and E7 antibody levels between those patients who recurred and those who didn’t. All patients showed a decline in their antibody levels three months after treatment.

That makes sense, says study author Matthew E. Spector, M.D., assistant professor of otolaryngology at the University of Michigan Health System. After three months, all or most of the cancer had been wiped out. Since oropharyngeal cancer almost never recurs three months after treatment, antibody levels declined in all the patients studied.

“Most patients recur within the first two years, so the window to catch it is two years after treatment. Everyone’s level goes down over time, but some start to go up a little — and those are the ones we have to focus on,” Spector says.

Finding answers in antibodies

When the researchers looked at E6 and E7 antibody levels over time, they found that in patients whose cancer recurred, the levels of E7 were not decreasing as quickly as patients who did not recur. And they could begin to detect that prior to the point when the recurrence was discovered.

“If we can monitor someone through blood markers, then instead of a patient coming for a clinic visit every two to three months, they could get blood drawn near home. If there’s evidence of high E7, we can tell the patient to come in for more evaluation,” Spector says.

The key is to look at the ratio of E7 antibodies. Every patient had a different baseline level, and the absolute level was not an indication.

“It’s very patient-specific,” Spector says. “Each patient will have different levels, but the question is what happens when you track it over time. If it rises, that suggests recurrence.”

Oropharyngeal cancer most commonly recurs in the throat, neck or lungs. If recurrence is caught early, surgery to remove the cancer in the throat or neck can eliminate the disease and is likely to be a cure. If the cancer spreads to the lungs, offering targeted therapies earlier might improve outcomes.

The test for E6 and E7 antibodies is a standard laboratory test that any cancer treatment facility could perform, so it would likely be inexpensive to implement.

More testing among a larger number of patients is needed. The U-M team has opened a phase II trial to assess the potential for E7 antibodies as a biomarker for recurrence. For information, call the U-M Cancer AnswerLine at 800-865-1125.

December, 2016|Oral Cancer News|

Blood-borne HPV antibodies indicate head, neck cancer prognosis

Source: medicalxpress.com
Author: provided by Brown University

People with head and neck cancers with evidence of human papillomavirus (HPV) infection generally have a better prognosis than people without evidence of infection. A new study in JAMA Oncology suggests that to produce a strong, reliable prognostic signal, all that’s needed is a blood serum test for two specific HPV antibodies, rather than lab work on a biopsy. Further, the researchers said, the study shows that this blood-based biomarker is predictive of outcome for all types of head and neck cancer.

bloodbornehp

The human papillomavirus causes not only cervical cancer but also cancers of the head and neck. Credit: National Cancer Institute

“What this adds is that it helps us know how best to measure clinically the HPV contribution to this disease,” said study senior author Karl Kelsey, a professor of epidemiology and of pathology and laboratory medicine at Brown University. Kelsey collaborated with lead author Heather Nelson of the University of Minnesota Masonic Cancer Center in making the findings.

Moreover, Nelson, Kelsey and their colleagues wrote, referring to the common HPV16 strain of the virus: “These data are among the first to demonstrate a convincing relationship between HPV16 and improved patient survival for tumors of the larynx and oral cavity.”

Appraising antibodies
The study examined blood serum samples and five-year survival rates among more than 1,000 Boston-area head and neck cancer patients diagnosed between 1999 and 2011. Overall, those who tested positive for antibodies to the oncogenic HPV proteins E6 or E7 were less likely to die during the five year follow-up period after diagnosis compared to those who tested negative for the antibodies. Based on the analysis, the researchers estimated that those with evidence of an immune response to HPV were 25% less likely to die during the course of follow-up compared to those with no immune response to HPV.

The study’s purpose was to determine whether the antibodies provide a reliable indication of prognosis. In ongoing trials, doctors are testing whether patients with HPV-associated cancers can be treated less aggressively—and hopefully with fewer negative side effects—than people with non-HPV-associated cancers, Kelsey said. If trials prove successful, then it will be particularly important to determine whether cancers are HPV-associated.

“The assessment of a patient’s HPV status likely will affect treatment,” he said. “That’s why there’s real interest in getting it right; for instance, how do you test?”

Better prognosis across the board
Prior studies have focused primarily on the role of HPV in the oropharynx—the area of the throat right behind the mouth. An important contribution of the current study, Nelson said, is demonstration that an immune response to HPV is important for all forms of head and neck cancer, although the benefit does show some variance based on the exact cancer location. Those patients with an HPV immune response with tumors located in the oropharynx and larynx had a similar risk of dying during the follow-up period, though the reduced risk was slightly attenuated for those patients with tumors located in the oral cavity.

The results didn’t depend significantly on whether people had high or low levels of the antibodies, so long as they had some, the researchers found, though testing positive for both E6 and E7 was better than for just one.

The reduced chance of dying by five years carried through for people who tested positive for the antibodies even if they consumed tobacco and alcohol. But the worst prognoses in the study were among smokers whose cancers could not be traced to HPV.

In all, the findings controlled for the statistical influences not only of tobacco and alcohol exposure, but also of age, race, gender, education and how far advanced the cancer was.

Relates to broader advances
Kelsey said the findings could help bring head and neck cancer treatment closer into line with two emerging practices of fighting the disease: personalized medicine and immunotherapy.

“To me, personalized medicine really reflects using all the information you can glean about an individual tumor to treat it appropriately,” Kelsey said. “Here HPV is an example of a causal factor that delineates the mechanism of the tumor suppressor genes that drive the tumor and that gives you insight into the differences in the tumor.”

Meanwhile, the study might help shed light on why immunotherapy—in which the body’s immune system is marshaled to attack cancer—appears to help for some head and neck cancers, Kelsey said. It may not be coincidence, for instance, that the prognosis is better among people whose cancers are associated with a virus that promotes a robust immune response, in the form of antibodies, than among people without a viral cause for their cancer.

If HPV-related cancers can indeed be treated differently, Kelsey said, then serum-based testing to determine the role of the virus could soon be available, too.

December, 2016|Oral Cancer News|

I get by with help from my friends: Maintaining immune cells in head and neck cancer

Source: www.eurekalert.org
Author: Medical University of South Carolina

In an article published September 22, 2016 in Frontiers in Immunology, researchers at the Medical University of South Carolina (MUSC) and the Ralph H. Johnson VA Medical Center report that inhibiting prostaglandin production slows the progression of premalignant lesions to head and neck squamous cell carcinoma (HNSCC). Preclinical studies showed that treatment of premalignant lesions with indomethacin, a nonsteroidal anti-inflammatory drug (NSAID) similar to aspirin, increased the presence of immune cells and lessened tumor burden.

Cancers of the head and neck begin with lesions in the oral cavity, including the larynx, pharynx, throat, lips, mouth, salivary glands, and nasal passages. Although the incidence of HNSCC has been on the decline over the past several decades, the National Cancer Institute reports that approximately 3% of all cancers in the U.S. result from HNSCC, with men being diagnosed twice as often as women. Treatment for HNSCC includes surgical removal and chemo-radiation treatment; however, these interventions often fail, and patients have a five-year survival rate of only 50%. It is critical to determine better treatment options for HNSCC patients.

One way researchers at MUSC are trying to improve the treatment of HNSCC is by enhancing the body’s own immune system to attack the tumor.

“There’s a lot of effort to stimulate immune reactivity using immunotherapy. The problem with that is cancer can protect itself against the immune defenses. Head and neck cancer is notorious for that,” said immunologist M. Rita Young, Ph.D., senior author for this study, who holds a dual appointment at MUSC and the Ralph H. Johnson VA Medical Center.

As an immunologist, Young has been working on addressing this problem by studying how the immune system affects tumor progression. Previous work from her laboratory has shown that the composition of immune cells within premalignant lesions differs from that within HNSCC. Significantly, as premalignant cells develop into HNSCC, the immune environment switches from stimulatory/inflammatory to immunosuppressive. This change in the tumor microenvironment prevents the immune system from combating the cancer. Prostaglandin may be an important mediator of this switch.

The current study used a novel mouse model of HNSCC to determine how inhibition of prostaglandin affects tumor progression. Mice with premalignant lesions were given indomethacin, an NSAID that inhibits the production of prostaglandin. Indomethacin treatment increased the presence of immune cells at the lesion site and led to a systemic activation of the immune system. Specifically, there was an increase in both Th1-associated cytokines (IL-2 and IFN-γ) as well as Th2-associated cytokines (IL-10). This activation of the immune system reduced the progression of premalignant lesions to HNSCC.

Future studies in this area will be focused on maintaining a strong immune presence in pre-malignant lesions for patients. If studies in humans bear out these preclinical findings, further research using more specific prostaglandin inhibitors in combination with other immunomodulatory compounds could provide a better treatment regimen to prevent the formation of HNSCC.

“Immunotherapy should be considered as a treatment strategy for premalignant lesions before they progress to cancer. We can detect them. Why not treat them?” said Young. Furthermore, these intervention strategies may be able to help prevent smaller, as yet undetectable lesions from progressing to HNSCC.

This work provides strong evidence that treatment of premalignant lesions with indomethacin reduces the tumorigenicity of HNSCC. A better understanding of the mechanisms by which the immune system combats early-stage cancer could lead to improved clinical outcomes in HNSCC, and potentially, other types of cancer as well.

“If we can be more persistent and focused on finding premalignant lesions before they become malignant, simple therapies might be beneficial,” said Sara Johnson, Ph.D., a postdoctoral fellow at MUSC and a co-author on the article.

December, 2016|Oral Cancer News|

Bioscientists help throat cancer patients speak again

Source: medicalxpress.com
Author: staff, provided by the University of Kent

bioscientist

Voice Prosthesis Biofilm. Credit: Dr Campbell W. Gourlay, University of Kent

Through the work of the School of Biosciences team, in collaboration with East Kent Hospitals University NHS Foundation Trust, Kent has developed a new method of care for patients who have to have their larynx removed.

The Biosciences team found that the replacement voice boxes would last much longer if they dealt with the fungal infection Candida albicans that was causing the silicone versions to fail. For the first time, scientists were able to extend the life of the replacement voicebox by dealing with the fungal infection.

The team has developed clinical care for patients that has now been taken up by many NHS Trusts in the UK and which is anticipated could be used worldwide for throat cancer patients.

It means patients may be able to carry on using silicone voice prosthesis for much longer, enabling them to still speak and reducing the risk of dangerous secondary chest infections.

Dr Campbell Gourlay, Senior Lecturer in Cell Biology at Kent, said the University’s work, funded by the NHS and Kent Cancer Trust, will enable people who lose their larynx to maintain speech and enjoy a better quality of life.

December, 2016|Oral Cancer News|

Mouth cancer rates soar over 20 years

Source: www.sciencedaily.com
Author: staff

A new Cancer Research UK analysis reveals that rates of mouth (oral) cancer have jumped by 68 per cent1 in the UK over the last 20 years. The figures — released during Mouth Cancer Action Month — reveal the cancer is on the rise for men and women, young and old, climbing from eight to 13 cases per 100,000 people over the last two decades.

For men under 50, the rate has jumped by 67 per cent in the last 20 years2 — going up from around 340 cases to around 640 cases each year. For men aged 50 and over, rates have increased by 59 per cent climbing from around 2,100 cases to around 4,400 cases annually.

Oral cancer is more common in men, but there have been similar increases women3.

In women under 50, oral cancer rates have risen by 71 per cent in the last 20 years, with annual cases climbing from around 160 to around 300. Rates for women over 50 have also gone up by 71 per cent, with cases increasing from around 1,100 to around 2,200.

Around nine in 10 cases are linked to lifestyle and other risk factors. Smoking is the biggest avoidable risk factor, linked to an estimated 65 per cent of cases. Other risk factors include alcohol, diets low in fruit and vegetables, and infections with the Human Papilloma Virus (HPV).

Oral cancers include cancer of the lips, tongue, mouth (gums and palate), tonsils and the middle part of the throat (oropharynx)4.

Cancer Research UK — working with the British Dental Association — has developed an oral cancer toolkit5 to help GPs, dentists, nurses and hygienists spot the disease and refer suspected cases sooner.

Jessica Kirby, Cancer Research UK’s senior health information manager, said: “It’s worrying that oral cancer has become more common. It’s important to get to know your body and what’s normal for you, to help spot the disease as early as possible. An ulcer or sore in your mouth or tongue that won’t go away, a lump on your lip or in your mouth, a red or red and white patch in your mouth or an unexplained lump in your neck are all things to look out for. Speak to your GP or dentist about any changes that are unusual or don’t go away.

“Healthy lifestyles can help reduce the risk of developing the disease in the first place. Not smoking, drinking less alcohol and eating plenty of fruit and vegetables can all help to cut our risk of mouth cancer. HPV vaccination could help protect against oral HPV infections, and it can prevent a range of cancers associated with the HPV virus, so it’s a good idea to get the vaccine if you are offered it.”

With smoking being the biggest preventable cause of oral cancer, Cancer Research UK is also calling on the public and local councillors to help protect vital Stop Smoking Services. These specialist services are the most successful way for people to quit smoking.

Andrea Fearon, 47 from Newbury, was diagnosed in 2013 with mouth cancer after a routine checkup by her dentist.

Andrea said: “I had thought that most people with mouth cancer are heavy smokers over the age of 50, so I completely shocked when I was diagnosed with the disease. I’m proof that this type of cancer isn’t limited to a particular age or sex. I thought seeing the dentist was about looking after your teeth — but it can save your life. It’s thanks to my dentist that the mouth cancer was caught early — that’s why I feel so lucky to be alive.”

Notes:
1. Based on oral cancer incidence rates for all ages, persons, from 8 cases per 100,000 people between 1993-1995 to 13 cases per 100,000 people between 2012-2014.

2. Based on oral cancer incidence rates, for males aged 0-49, the rise is from two cases per 100,000 males between 1993-1995 to three cases per 100,000 males between 2012-2014. For men aged 50 and over, this rise is from 26 cases per 100,000 between 1993-1995 to 41 cases per 100,000 men between 2012-2014.

3. Based on oral cancer incidence rates, for females aged 0-49 years, the rise is from one case per 100,000 females between 1993-1995 to two cases per 100,000 females between 2012-2014.

For women aged 50 and over, the rise is from 11 cases per 100,000 women between 1993-1995 to 18 cases per 100,000 women between 2012-2014.

Cases are based on the number of new diagnoses between 1993-1995 and between 2012-2014.

4. Oral cancer includes ICD-10 C00-C06, C09-C10 and C12-C14 (which include the lip, tongue, mouth, oropharynx, piriform sinus, hypopharynx and other and ill-defined sites of the lip, oral cavity and pharynx).

For the latest oral cancer statistics visit the Cancer Research UK statistics webpage http://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/oral-cancer

5. The toolkit covers the signs to look out for, how to respond, as well as possible risk factors for oral cancer. The toolkit also features a detailed image library, a referral guide, case studies, examination videos and a CPD accredited quiz.

Story Source:
Materials provided by Cancer Research UK. Note: Content may be edited for style and length.

November, 2016|Oral Cancer News|

For this cancer, ‘stage 4’ isn’t as bad as it sounds

Source: www.omaha.com
Author: Steve Hendrix – The Washington Post

Hearing the word “cancer” in a doctor’s office is bad enough. Hearing “stage 4” invokes even more dread. When I learned I had stage 4 HPV-related oral cancer, I didn’t know exactly what it meant, but I knew there wasn’t a stage 5.

Doctors use the standardized staging system to describe the location, size and extent of a cancer and its spread throughout the body. Using data on the treatment and survivability of each particular kind of cancer, clinicians combine these factors to produce a number from stage 1 (a small tumor confined to one spot) to stage 4 (a cancer that has spread, either to a single adjacent lymph node or to distant organs).

My cancer was stage 4A, a small tumor at the base of my tongue that had spread to a single lymph node in my neck.

My doctor immediately tried to soften the blow. There were problems with the staging rules as they applied to this kind of cancer, he said. HPV oropharyngeal cancers, while potentially fatal, were far more treatable than other oral cancers, particularly the ones related to tobacco and alcohol use that were used to define the staging standards.

He was right. A study published in the Lancet early this year found that the current guidelines lead to needless panic for the newly diagnosed. “At the present time, most patients with HPV+ oropharyngeal cancer are told they have (stage 4) disease, but the reality is that their outlook is similar to that of patients with the most curable malignant diseases,” the study authors wrote.

This month, the American Joint Committee on Cancer is releasing new guidelines for HPV-positive oropharyngeal cancer staging that will ease patient fears and make it easier for doctors to offer less-invasive treatment options.

“It’s remarkable,” said my own physician, Arjun Joshi of George Washington University. “Under the new system, you would only be a stage 1.”

November, 2016|Oral Cancer News|

E-cigarettes ‘just as harmful as tobacco’ for oral health

Source: www.medicalnewstoday.com
Author: Honor Whiteman

Electronic cigarettes are often marketed as a safer alternative to conventional cigarettes. When it comes to oral health, however, new research suggests vaping may be just as harmful as smoking.

a-woman-using-an-ecigarette

Researchers suggest vaping may be equally – if not more – harmful for oral health than smoking.

In a study published in the journal Oncotarget, researchers found that the chemicals present in electronic cigarette (e-cigarette) vapor were equally as damaging – in some cases, more damaging – to mouth cells as tobacco smoke.

Such damage can lead to an array of oral health problems, including gum disease, tooth loss, and mouth cancer.

E-cigarettes are battery-operated devices containing a heating device and a cartridge that holds a liquid solution. The heating device vaporizes the liquid – usually when the user “puffs” on the device – and the resulting vapor is inhaled.

While e-cigarette liquids do not contain tobacco – a highly harmful component of conventional cigarettes – they do contain nicotine and other chemicals, including flavoring agents.

According to the Centers for Disease Control and Prevention (CDC), the use of e-cigarettes has increased in recent years, particularly among young people. In 2015, 16 percent of high-school students reported using the devices, compared with just 1.5 percent in 2011.

E-cigarettes are considered by many to be safer than conventional smoking, but because the devices are relatively new to the market, little is known about the long-term effects of vaping on health.

In particular, study leader Irfan Rahman, Ph.D., professor of environmental medicine at the University of Rochester School of Medicine and Dentistry in New York, and colleagues note that there has been limited data on how e-cigarette vapor affects oral health.

Flavored vapor worsens damage to gum tissue cells
To address this gap in research, the team exposed the gum tissue of nonsmokers to either tobacco- or menthol-flavored e-cigarette vapor.

The tobacco-flavored vapor contained 16 milligrams of nicotine, while the menthol flavor contained 13-16 milligrams of nicotine or no nicotine.

The researchers found that all e-cigarette vapor caused damage to gum tissue cells comparable to that caused by exposure to tobacco smoke.

“We showed that when the vapors from an e-cigarette are burned, it causes cells to release inflammatory proteins, which in turn aggravate stress within cells, resulting in damage that could lead to various oral diseases.” said Irfan Rahman, Ph.D.

The researchers note that nicotine is a known contributor to gum disease, but e-cigarette flavoring appeared to exacerbate the cell damage caused by e-cigarette vapor, with menthol-flavored vapor posing the most harm.

While further research is needed to investigate the long-term effects of e-cigarette use, Rahman and team believe their findings indicate that the devices may have negative implications for oral health.

“Overall, our data suggest the pathogenic role of [e-cigarette] aerosol to cells and tissues of the oral cavity, leading to compromised periodontal health,” they conclude.

E-cigarette vapor damaged, killed 53 percent of mouth cells in 3 days
Another study recently published in the Journal of Cellular Physiology builds on the findings from Rahman and colleagues, after finding a high rate of mouth cell death with exposure to e-cigarette vapor over just a few days.

To reach their findings, Dr. Mahmoud Rouabhia, of the Faculty of Dental Medicine at Université Laval in Canada, and colleagues placed epithelial cells from the mouth in a chamber that contained a liquid similar to saliva.

To simulate vaping, the researchers pumped e-cigarette vapor into the chamber at a rate of two 5-second puffs every 60 seconds for 15 minutes a day. This was performed over 1, 2, or 3 days.

On analyzing the vapor-exposed epithelial cells under a microscope, the researchers identified a significant increase in the rate of cell damage and death.

The rate of damage or death in unexposed cells is around 2 percent, the researchers note. However, they found that with exposure to e-cigarette vapor, the number of dead or dying cells rose to 18 percent, 40 percent, and 53 percent over 1, 2, and 3 days, respectively.

While the cumulative effects of the cell damage caused by e-cigarette are unclear, the researchers believe their findings are a cause for concern.

“Damage to the defensive barrier in the mouth can increase the risk of infection, inflammation, and gum disease. Over the longer term, it may also increase the risk of cancer. This is what we will be investigating in the future.” said Dr. Mahmoud Rouabhia

November, 2016|Oral Cancer News|

Curbing oral cancer

Source:.businessmirror.com.ph
Author: Henrylito D. Tacio

“Cancer is the third leading cause of death in the country today. Most of it can be prevented since its risk factors are lifestyle and environmentally related. Early detection of cancer is a crucial key to the survival and recovery of its victims. The earlier you detect the malignancy the higher the survival rate of the patient.”
—Dr. Vic Fileto Chua of Movement for Early Detection of Cancer

What’s the leading cause of oral cancer? Is it smoking or heavy drinking? Although smoking and drinking may cause oral cancer, the leading cause is oral sex, a sexual act that involves the stimulation of the genitalia using the mouth.

Studies have shown that 64 percent of cancers of the oral cavity, head, and neck in the United States are caused by human papillomavirus (HPV), which is commonly spread via oral sex. The more oral sex you have – and the more oral sex partners you have – the greater the risk of developing these potentially deadly cancers.

oral_cancer

“An individual who has six or more lifetime partners—on whom they’ve performed oral sex—has an eightfold increase in risk compared to someone who has never performed oral sex,” explained Dr. Maura Gillison, an oncologist at Ohio State University. Gillison headed a team of researchers who examined 271 throat-tumor samples collected over 20 years ending in 2004. They found that the percentage of oral cancer linked to HPV surged to 72 percent from about 16 percent.

The study, which was published in the Journal of Clinical Oncology, said that by 2020, the virus-linked throat tumors—which mostly affected men—will more common than HPV-caused cervical cancer.

“The burden of cancer caused by HPV is going to shift from women to men in this decade,” observed Gillison. “What we believe is happening is that the number of sexual partners and exposure to HPV has risen over that same time period.”

In his weekly column in Philippine Daily Inquirer, Dr. Rafael D. Castillo noted: “Previously, it was well established that smoking (three-fold increase) and drinking alcohol (2.5 times) increased the risk for oral cancer, but even if you combine them, the risk is no match compared to that seen in those who frequently engage in oral sex.”

The government doesn’t have any data on the prevalence of oral cancer in the country but what alarms Castillo is that oral cancer might be rampant among young people. A study done by the University of the Philippines Population Institute showed that more than four million teenagers and young Filipinos are already engaged in sexual practices.

The findings of the third Young Adult Fertility Survey revealed that a total of 4.32 million Filipinos aged 15 to 24 are already sexually active. Another finding is that oral sex has become a common practice “among most sexually adventurous teens.”

“Doing simple math, if the expected prevalence of oral cancer in the general population is 1.5 percent, and with a nine-fold increase in risk, that means that we have approximately 583,000 young Filipinos aged 15 to 24 who are likely candidates to develop oral cancer,” Dr. Castillo surmised.

“Today’s teens consider oral sex to be casual, socially acceptable, inconsequential, and significantly less risky to their health than ‘real’ sex,” said Gillison. Teens simply think oral sex is “not that a big a deal,” added Dr. Bonnie Halpern-Felsher, professor of pediatrics at the University of California, San Francisco. “Parents and health educators are not talking to teens about oral sex. Period.”

Members of the Philippine Medical Association (PMA) and the Philippine Dental Association (PDA) also noted that the practice of oral sex can lead to infections of the oral cavity, which may result to cancer of the tonsils, tongue or throat.

“Any lesion in the mouth should be seriously considered,” said Dr. Anne Camus, PDA’s Manila dental chapter president. “Not all can develop to cancer but malignancy must always be taken as an imminent possibility.”

A regular check-up with a dentist would help detect malignancies in the mouth. “The dentists are usually the first to see lesions in the mouth of our patients,” Camus said. “At this early point, if the lesion turns out to be malignant, then chances are it is still curable.”

Oral cancer, or cancer of the mouth, most commonly involves the lips or the tongue. It may also occur on the: cheek lining, floor of the mouth, gums, and roof of the mouth (palate). Most oral cancers are a type called squamous cell carcinomas, which tend to spread quickly.

Aside from oral sex, smoking, and drinking, other factors that add to the risk of oral cancer include repeated irritation from the sharp edges of broken teeth, fillings, or dental prostheses (dentures). “The research regarding their involvement is uncertain. It is likely that there is a complex interaction of many external and internal factors that play a role in the development of oral cancer,” points out the Oral Cancer Foundation in the United States.

“Oral cancers are usually painless for a considerable length of time but eventually do cause pain,” notes “The Merck Manual of Medical Information.” “Pain usually starts when the cancer erodes into nearby nerves. When pain from cancer of the tongue or roof of the mouth begins, it usually occurs with swallowing as with a sore throat.”

The early growth of salivary gland tumors may or may not be painful. “When these tumors do become painful, the pain may be worsened by food, which stimulates the secretion of saliva,” the Merck manual informs. “Cancer of the jawbone often causes pain and a numb or pins-and-needles sensation, somewhat like the feeling of a dental anesthetic wearing off. Cancer of the lip or check may first become painful when the enlarged tissue is inadvertently bitten.”

Discolored areas on the gums, tongue, or lining of the mouth may be signs of cancer. “An area in the mouth that has recently become brown or darkly discolored may be a melanoma (malignant tumor),” the Merck manual states. “Sometimes, a brown, flat, freckle-like area (smoker’s patch) develops at the site where a cigarette or pipe is habitually held in the lips.”

“Keep in mind that your mouth is one of your body’s most important early warning systems,” reminds the Oral Cancer Foundation. “Don’t ignore any suspicious lumps or sores. Should you discover something, make an appointment for a prompt examination. Early treatment may well be the key to complete recovery.”

According to the US National Cancer Institute, oral cancer treatments may include surgery, radiation therapy or chemotherapy. Some patients have a combination of these treatments.

November, 2016|Oral Cancer News|

HPV and mouth cancer

Source: www.hippocraticpost.com
Author: Thea Jourdan

hpv

Mouth cancer kills nearly 2000 people in the UK each year. The Human Papilloma Virus (HPV) of which there are over 100 different types, is more commonly associated with cervical cancer and genital warts, but it can also cause oral cancer, particularly of the back of the tongue and tonsils. The virus incorporates itself into the cell’s DNA and causes the cell to multiply out of control, leading to cancer.

In Britain, the number of mouth and throat cancers have increased by 40 per cent in just a decade, to 6,200 cases a year. According to Cancer Research UK, the HPV virus, which is transmitted to the mouth region from the genitals during oral sex, may be key to the ‘rapid rise’. Statistics also show that the more sexual partners you have the greater your chance of acquiring mouth cancer.

“There is now scientific evidence that a proportion of mouth and throat cancers are linked to HPV infection,” says Hazel Nunn, head of health information at Cancer Research UK. “We know that HPV is found in the mouth but we do not yet know how it gets there – whether through oral sex or otherwise. HPV virus has been found on the fingers and elsewhere on the body. It is possible that oral sex is having an impact but more research needs to be done into the kinds of behaviour that leads to this infection.”

“HPV has been causing mouth cancer for decades but the link is only now becoming clear. HPV is a hardy virus that likes sitting in lymphoid tissue wherever it is in the body,” explains Professor Mark McGurk, a senior consultant ENT surgeon based at London Bridge Hospital in London. That means it thrives in the lymphoid tissue in the mouth, including that of the tonsils and at the base of the tongue. For the same reason, it settles in the cervix, the vulva and around the anus.

For many people, HPV won’t cause any problems at all. “In fact, we know that 80 per cent of women and men will have the HPV infection at some time in their lives and clear it themselves without any symptoms,” explains Mr Mike Bowen, a consultant obstetrician and gynacologist based at St John and St Elizabeth Hospital in London. “But for a few it can cause cellular changes that lead to cancer.”

Professor McGurk says that over the last 30 years, he has seen a rise in oropharyngeal cancer, which typically affects sexually active men in their 50s and 60s. “They may have been infected with the virus for some time and ,” he explains. The cancer reveals itself as growths on the tonsils and back of the tongue.

Many patients are only diagnosed at the late stage of their disease. Michael Douglas, the actor, already had stage 4 cancer when his cancer was recognized. Fortunately, oral cancer caused by HPV is very treatable, even when it is very advanced, using radiotherapy. “We used to do surgery on these cases, but we don’t need to anymore. In many cases, the cancer simply melts away with radiotherapy,” explains Professor McGurk. Patients with stage 1 and 2 Oral cancer caused by HPV have an 85 per cent chance of surviving for 5 years after treatment, and patients with stage 4 disease have a 60 per cent chance of surviving five years – impressive compared to the survival rates for other types of oral cancer where overall survival is 50 per cent over 5 years. [Cancer Research UK]

Cancer research UK is pushing for all mouth tumors to be tested to see if they are HPV positive, to assist with effective treatment of patients. “At the moment, it varies massively depending on what hospital you are in. We think it should be standard,” says Hazel Nunn.

Professor McGurk believes there is a simple explanation why men are more likely to have HPV in their mouths than women. “Women harbor the virus in their genitalia which provides a hospitable environment while the male penile area is a relatively hostile area for the virus to settle.”

One way to try and turn the tide would be to introduce a HPV vaccination for boys and girls before they become sexually active. Girls from the age of 12 in the UK have been offered vaccinations since 2008 against the two most common strains of HPV -16 and 18- which are linked to cervical cancer.

Boys are not offered the vaccine, but this should change, according to Professor Margaret Stanley, a virologist based at Cambridge University who believes that boys must be given the vaccine for HPV too from the age of 12 or 13.

‘Obviously cervical cancer is the big one but the other cancers – cancers of the anus and increasingly the tonsil and tongue – there is no screening for them and no way of detecting them until they are proper cancers and they are more common in men than in women.’

Hazel Nunn of Cancer Research UK points out that there is no evidence that vaccinating boys will help protect them from oral cancer. “It is theoretically possible but there have been no trials that had this as an end point. There is a danger that we get too far ahead of ourselves without evidence-based medicine.”

She insists that although HPV is a worrying factor, by far the most significant risks associated with mouth and throat cancers of all types are smoking and alcohol. “

November, 2016|Oral Cancer News|