Monthly Archives: March 2013

Major study finds no link between vaccines and autism

By: Agence France-Presse
Date: Friday, March 29, 2013 
A girl receives polio vaccination drops from a medical volunteer on April 15, 2012 in India. (AFP)

A US study out Friday sought to dispel the fears of about one third of American parents that giving a series of vaccines to children may be linked to autism.

Even though children are receiving more vaccines today than they did in the 1990s, there is no link between “too many vaccines too soon” and autism, said the study in the Journal of Pediatrics.

About one in 10 US parents refuse or delay vaccinations for their children because they believe it is safer than following the schedule put out by the Centers for Disease Control and Prevention, according to previous research.

Prior studies have already shown there is no link between vaccines and autism, including a 2004 comprehensive review by the Institute of Medicine.

This time, researchers at the CDC decided to look children’s exposure to antigens, the substances in vaccines that cause the body to produce antibodies to fight infection and disease.

Researchers looked at data from 256 children with autism spectrum disorder across three separate managed care organizations in the United States.

They compared the cumulative exposure to antigens in those children to 752 children without autism.

“We found no evidence indicating an association between exposure to antibody-stimulating proteins and polysaccharides contained in vaccines during the first two years of life and the risk of acquiring autism spectrum disorder, autism disorder or autism spectrum disorder with regression,” said the study.

Nor were there any links between autism and cumulative exposure to antigens, either from birth to two years of age or within the course of a single day after receiving multiple vaccines at the doctor’s office, it said.

“These results indicate that parental concerns that their children are receiving too many vaccines in the first two years of life or too many vaccines at a single doctor visit are not supported in terms of an increased risk of autism,” it said.

Autism affects as many as one in 88 in the United States and about one in 100 in Britain. The brain disorder has no single known cause but experts believe it may be triggered by a combination of genetics and environment.


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



March, 2013|Oral Cancer News|

Professor studies plants, foods to prevent cancer

Author: Jennifer R. Lloyd, Staff Writer

Twigs, leaves and berries may sound like the diet of the destitute, but for molecular medicine professor Michael Wargovich, certain plants, like those in traditional medicines and food in developing countries could be gold mines in the fight against cancer.

In his newly outfitted lab at the University of Texas Health Science Center at San Antonio, Wargovich and his staff are testing the cancer-preventing properties of green tea. They’ll also soon start investigating the anti-inflammatory abilities of the neem tree, native to India, and which already is used in some toothpastes available in the United States. Wargovich, 60, cited World Health Organization statistics showing that the hot spots for cancer will move south of the equator by 2020 as the population swells and its residents, immunized from many infectious diseases, live longer and assume a more Western lifestyle.

“They’re giving up their traditional diets,” he said. “The things that we’ve found are protecting us against cancer are disappearing as everybody tries to be homogenized and Western and going to fast-food places.”

He said undetectable chronic inflammation sets people up for illnesses such as heart disease, cancer, obesity and diabetes. Yet foods with anti-inflammatory properties — fruits, vegetables, spices and herbs — are disappearing from the world’s plate.

As a side project, Wargovich and an executive chef are developing an anti-inflammatory diet to reintegrate beneficial foods into modern-day dining. In April, Wargovich will give a free public lecture about cancer-fighting foods. Visit the Cancer Therapy & Research Center’s website,, where details will be listed soon.

Back in his lab, he excitedly pops open plastic containers full of dried foliage, such as neem and the West African “headache plant,” Bridelia ferruginea, which he admits looks like debris he swept off his driveway. He said he met with healers in Guinea to learn about plants in traditional medicines. In the case of the “headache plant,” suffering clients boil it and inhale the steam.

“I’m just delighted to find that what we’re told as general advice from grandparents and people from other cultures had a grain of truth in it,” he said.

Keya Mukhopadhyay, 35, a fellow in Wargovich’s lab, said people in her native India called neem “the wonder tree” and use it for oral health and in body wash and soap to alleviate heat rash. She said the lab will begin testing its properties by inducing oral cancer in rats and treating them with neem extract.

Also interested in how plant compounds can reduce the side effects of current cancer therapies, Wargovich said he will start a clinical trial in South Carolina to test whether a neem mouthwash helps sooth painful mouth inflammation that occurs after patients with head and neck cancers begin therapy.

“The state of the art in 2013 from the oncologist is to put ice chips in your mouth and suck it up or they bomb you on narcotics to lessen the pain,” Wargovich said, adding that combining a prevention chemical with therapy is “going to be the frontier for us.”
In another experiment, he said, they are applying the antioxidant found in green tea to cancer cells to figure out how the compound inhibits cancer cell growth.

Wargovich likens a cancer cell to a car without brakes.

“It doesn’t only break the brakes, it breaks the cables. It breaks the steering wheel. Anything that can put a regulation on a tumor cell is broken by a tumor cell,” he said. “Some of these natural products put the brakes back on.”

March, 2013|Oral Cancer News|

‘Immortal’ gene mutation may allow some cancerous cells to live forever

Author: Makini Brice

For years, it has remained a mystery how cancer cells are able to live forever, while typical cells die. Recent research performed by scientists at the Duke Cancer Institute have found that a single gene may be responsible for three of the most common types of brain tumors, in addition to liver cancer, tongue cancer and cancer of the urinary tract. In addition, the study involved research into the inner workings of 1,200 tumors and 60 different types of cancer. Researchers hope that, with this finding, doctors will soon be able to beat cancer at its own game.

The secret is in the telomere, which sticks to the end of the chromosome and prevents the ends from fraying or sticking together. When cells divide normally, the telomeres become shorter and shorter. When the telomere reaches a certain length, the cell can no longer divide and it dies. This process requires the use of an enzyme called telomerase.

Scientists have found that some cancerous cells have a gene mutation that affects the enzyme. Because the telomere does not become shorter and shorter, the cells become immortal and are able to divide forever. The researchers at Duke Cancer Institute found nine cancer types that are highly associated with this gene mutation. All of the cancerous cells arise in areas of the body where there is a low rate of cell renewal, so it seems that the cells needed such a mechanism to stay alive.

The cancer types include the following: melanomas; liposarcomas; hepatocellular carcinomas; transitional cell carcinomas of the urinary tract; squamous cell carcinomas of the tongue; medulloblastomas; as well as subtypes of gliomas, which includes 83 percent of primary glioblastomas, the most common brain tumor in adults, a devastating illness with a median survival of only 15 months.

“Now we see this,” Zachary J. Reitman, Ph.D., the co-lead author of the study, said in a statement. “This is a major discovery in brain tumors, because this single mutation can now distinguish one tumor from another – and these are tumors that are difficult to classify with a typical pathology test. For primary glioblastoma, the TERT mutation is remarkably common, while for astrocytomas, it is rare. Using both IDH1 and TERT, we can greatly improve diagnosis and prognosis.”

Spotting the mutation means that the biomarker could provide an early way of spotting liver and urinary tract cancer, improving prognoses of the disease. It could also serve as a new target for drugs against cancer. However, many cancer types, like breast and prostate cancers, did not have this mutation, which indicates that the cancerous cells in those region have developed another way to live forever.

Note: The study was published in the Proceedings of the National Academy of Science.

March, 2013|Oral Cancer News|

Bidi smoking causes cancer

Author: staff

The country’s (India) first such study, using cohort groups, has proven conclusively that smoking bidi (tobacco wrapped in the leaf of the tendu plant) increases the propensity for cancer. P. Jayalekshmi of the Regional Cancer Centre (RCC) here, who led the study on bidi-induced lung, oral, laryngeal and hypopharyngeal cancer, said lung cancer risk among former bidi smokers was higher than in those who never smoked bidis.

Separate studies on the impact of bidi smoking on lung and oral cancers, and cancers of larynx and hypopharynx in close to 70,000 men between the age group of 30-84 in Karunagappally in Kollam district shows that bidi is among the most harmful smoking products.

“The risk of cancer affecting the cheek (buccal) and lips (labial) showed a nearly four-fold increase in the cohort study covering 66,277 men.

“Excessive use of bidis significantly increased the risk associated with cancer of the gum and mouth,” Jayalekshmi said.

The mainstream smoke of bidi contains a much higher concentration of carcinogenic hydrocarbons. Bidi smokers also are found to be taking five puffs per minute, compared to two puffs by cigarette smokers in the same time, the study showed.

The cohort study on bidi and lung cancer, covering a total of 65,829 men, found that bidi smokers had a 3.9-fold increase in lung cancer incidence, when compared to those who never smoked bidis.

The study showed that tongue cancer risk increased significantly among men who smoked bidis for 30 years or longer, and among men who started bidi smoking at 18 years or younger.

Yet another cohort study conducted on 69,943 men, again in the 30-84 age group in Karunagappally, shows a significant relationship between bidi smoking and cancers affecting the larynx and hypopharynx.

The results show that those with a history of bidi smoking for more than 30 years have a higher risk of laryngeal cancers. Smokers who puff more than 15 bidis a day are at increased risk of hypopharyngeal cancer.

Figures with Regional Cancer Centre here show that 821 and 863 males registered as lung and oral cancer patients, respectively, during 2011-12 alone. Another 392 patients registered for care of hypopharyngeal and laryngeal cancers during the same period.

As many as 1.6 million males in Kerala smoke bidis and the Karunagappally studies have also reiterated the common knowledge that bidi smoking is more widespread among those with lower levels of education and family income.

Bidi smokers in Kerala spend nearly Rs.140 monthly on this habit.

The study, however, provides encouragement to those seeking to kick the bidi habit — the risk of lung cancer is lower in former smokers than current smokers, it showed. The lung cancer risk was found to decrease significantly among those who had stopped bidi smoking for 10 years or longer, when compared to current bidi smokers.

March, 2013|Oral Cancer News|

Noninvasive oral cancer test eases patient fears

Author: Donna Domino, Features Editor

A new, noninvasive cytology test for oral cancer, ClearPrep OC, is being offered free to dentists. The test, aimed at “watch and wait” lesions, is less expensive than biopsies and less frightening for patients, according to Resolution Biomedical, the company that is commercializing it.

The chairside oral cancer test — which can be ordered directly from the company — is designed to be a diagnostic option for assessing lesions when a biopsy is not warranted or the patient fears getting a biopsy, according to Donald Williams, MD, chief medical officer of Resolution Biomedical.

The test involves a cyto-brush sampling method that measures gross changes in the nuclear DNA content of oral epithelial cells, providing information about the precancerous or cancerous state of a lesion, the company explained. The samples are sent to medical testing labs, and the report is sent to the dentist within four to five days, the same time frame as biopsies. Dentists send the samples to the company, which prepares the slides and sends them to labs, which prepare a diagnostic report for the dentists.

“It’s a way to triage patients where something may be suspicious but the patient is balking about getting a biopsy,” Dr. Williams told “It could be leukoplakia lesions or thrush instead of an indication of a neoplasm. It rules out biopsies without an invasive process.”

When dentists refer patients to periodontists to get biopsies of suspicious lesions, many patients don’t follow through on the recommendation because they find it a daunting procedure, Dr. Williams noted.

“Some patients think, ‘I’ve had this for years and it hasn’t killed me, so I don’t want to be biopsied,’ ” he said. “It’s kind of frightening to say you’re going to have a piece of meat cut out of your mouth.”

The most logical application is for worrisome lesions that are likely benign, Dr. Williams said.

Ongoing clinical trial
Resolution Biomedical conducted about five validation studies of the ClearPrep OC test in general practices over six months, Dr. Williams said. It is now being tested with Southern California dentists.

In addition, the test is in the second phase of a trial study with cancer patients in the City of Hope cancer research hospital in Duarte, CA. ClearPrep OC and saliva samples will be taken, and p16 stains will be done on the biopsy specimens. All the modalities then will be combined before a blind match is done. The company plans to do a joint publication based on the results with the University of California, Los Angeles, Dr. Williams said. The test was primarily designed for gynecologic cytology pap tests, but Resolution Biomedical realized it also had potential to detect oral cancer.

The company does not plan on doing an official launch of the product, which has no marketing restrictions since nongynecologic cytology tests are an established medical practice, according to Dr. Williams. As a result, the test does not require U.S. Food and Drug Administration clearance or need to be Clinical Laboratory Improvement Amendments (CLIA)-certified, he said.

While the test is being provided for free to dentists, patients and labs pay $60 to $125 — much less than biopsies, which range from $400 to $500, according to Dr. Williams. It is usually covered by insurance, and dentists can charge a collection fee for the process, including interpreting the final report, according to Dr. Williams. Company revenues will be derived from the testing labs it uses for analysis.

“Biopsies are invasive, expensive, and painful,” said company CEO Mike Friedl. “This is an intermediate way to rule out stuff while you’re still at the dentist rather than going to a specialist.”

The test is especially suitable if the condition is simply a treatable condition, such as a fungal change, and doesn’t require a trip to see a specialist, Friedl noted. Since the human papillomavirus (HPV) is now associated with many oral cancers, the company tests for it if the sample shows any degree of atypism.

Sol Silverman Jr., DDS, a professor of oral medicine in the University of California, San Francisco (UCSF) School of Dentistry and head of one of the oral medicine clinics at UCSF, called the ClearPrep test a good adjunctive diagnostic technique.

“Cytology has been around a long time, and it’s very high-quality,” Dr. Silverman told “Any technique that will accelerate the recognition of dysplasia is important. Early detection is still our best approach to good survival results.”

March, 2013|Oral Cancer News|

Spike in oral cancers puzzles experts

Author: Victoria Colliver/San Francisco Chronicle

Christine Schulz has never visited England, but she speaks with the clipped inflection of a vaguely British accent. It’s not an affectation but, rather, the mystifying after-effect of an 18-hour surgery she endured in 2009 to remove about half her tongue due to a cancerous growth that had spread to her lymph nodes.

Surgeons used skin from her wrist and upper leg to re-create the missing portions of her tongue. Through long term speech therapy, Schulz, 47, of Hollister, Calif., re-learned how to eat and talk with her reconstructed tongue. If she sounds as if she’s from a different country, Schulz isn’t complaining.

“At the moment I woke up from surgery, I realized exactly what a huge deal it was,” she said, describing how she had an incision in her throat to allow her to breathe and was prohibited to speak in her earliest days of healing.

Oral cancers, which include those of the mouth and tongue, are most common in men over 60 with a long history of smoking or chewing tobacco, often combined with heavy drinking. But in recent years, a spike in the incidence of oral cancers is being attributed to human papilloma virus or HPV.

But Schulz’s cancer was neither HPV– nor tobacco-related. That puts her in a camp of fewer than 7 percent of all oral cancers that have no identifiable cause, according to the Oral Cancer Foundation, an advocacy group based in Newport Beach, Calif.

“Surprisingly, a high percentage of tongue cancers — 45 percent — is not related to the virus. The cause, we don’t know,” said Dr. Steven Wang, a head and neck surgeon at the University of California San Francisco with expertise in microvascular reconstructive surgery.

Tongue cancer is relatively rare, diagnosed last year in about 13,000 U.S. patients — more than 9,000 men and 3,700 women. It leads to some 2,000 annual deaths, according to the National Cancer Institute. Overall, there were 42,000 diagnoses of the broader category of oral cancers, which include the mouth cavity, lips and the oropharynx, or the part of the throat at the back of the mouth. Oral cancers combined kill about 8,000 each year.

While statistics show many cancer types leveling off or even decreasing in recent years, the incidence of oral cancer has increased, due in large part to HPV. Between 1988 and 2004, the percentage of HPV-related oropharynx cancers skyrocketed by 225 percent, according to a 2011 study published in the Journal of Clinical Oncology. But that doesn’t explain the rise in oral cancers among patients with no known cause.

“It could be a genetic predisposition or it could be an outside source, a causal agent that hasn’t been discovered yet,” said Brian Hill, the Oral Cancer Foundation’s executive director.

Wang, who reconstructed Schulz’s tongue, said nonsmoking-related oral cancers tend to be less responsive to chemotherapy and radiation than HPV- and smoking-related tongue cancers. And often the symptoms are overlooked. His latest research, to be published in the journal Otolaryngology — Head and Neck Surgery, found that former or current smokers with a form or tongue cancer called squamous cell carcinoma had a better chance of surviving than patients with the same cancer who never smoked.

“People always notice the sore or the ulcer in the mouth, but they’re not thinking it’s cancer,” he said. “They’re thinking, ‘I’ve never smoked, I’m too young.’ And, unfortunately, their doctors are thinking the same thing.”

Because treatment is frequently delayed, Wang said nonsmokers with tongue cancer are more likely to have the disease treated aggressively. Surgeons are able to reconstruct the tongue, but they have yet to find a way to re-create its function.

For Schulz, what started as a bump in the back of her tongue that wouldn’t go away turned into a life-altering experience. Her marathon surgery and reconstruction was followed by chemotherapy, radiation and a year and a half of speech therapy.

Most extremely sweet foods do not register on what’s left of her taste buds, although she loves chocolate more than ever. She avoids bread and crackers because those kinds of foods turn to cement in her mouth, and she finds salads just too much work.

“Putting food in my mouth still feels foreign,” she said, adding that it takes her a long time to eat. “I have to chew it. I have to have a thought about where it is inside my mouth and make sure it stays there, chew enough so I know I have to swallow and then I have to have water.”

Here are some signs and symptoms of the disease:

– Patches inside your mouth or on your lips
– A sore on your lip or in your mouth that doesn’t heal
– Bleeding in your mouth
– Loose teeth
– Difficulty or pain when swallowing
– Difficulty wearing dentures
– A lump in your neck
– An earache that doesn’t go away
– Numbness of lower lip and chin

Sources: National Cancer Institute; Oral Cancer Foundation

March, 2013|Oral Cancer News|

Science: Beef Good, Bacon Not So Bad

By: Stephanie Mencimer
Date: March 18, 2013


Note from OCF: While this story is not directly about oral cancer, we included it in our feed to show how studies often do not produce results that are useful or even accurate, as they may contain a great deal if bias in the study design. Poorly designed studies are plentiful even in reputable journals, from institutions with good reputations.


A new European study claims an increase in processed-meat consumption raises the risk of early death. But the real news? Red meat won’t kill you.

Earlier this month, researchers announced the results of a big new nutritional study in Europe that seemed to yield more evidence that processed meats like bacon and sausage can lead to an early grave. The media responded with the usual “Death by Salami” headlines. What news outlets downplayed about the study, though, is that despite their best efforts, the EU researchers couldn’t find any evidence that red meat will kill you. In fact, the study shows that not eating red meat is a risk factor for an early demise.

After correcting some measurement errors, the researchers in Europe had to conclude that not only was red meat intake “no longer associated with mortality” but “all-cause mortality was higher among participants with very low or no red meat consumption.”

The government, public health advocates, and the American Heart Association have long warned Americans that overconsumption of red meat can lead to heart disease and other ailments. Yet the scientific evidence supporting this hypothesis has always been weak. And in fact, this month’s study isn’t the first to fly in the face of these assumptions. A large study in Japan also found no increase in heart disease deaths from moderate meat consumption as well.

And last year, Harvard researchers published another similar large study. The media reporting on the study declared that researchers had found that “adding an extra portion of unprocessed red meat to someone’s daily diet would increase the risk of death by 13%. The figures for processed meat were higher, 20% for overall mortality.” But the Harvard data also showed that meat consumption had a protective effect for a lot of people. Up to a certain point, people who ate more of it fared better than those who ate little or none. The source of some of this confusion is simple: People who eat junk food are unhealthy in myriad ways that make it nearly impossible to zero in on a single food item as the source of their health woes.

To see what I mean, let’s take a closer look at the EU study. Known as the European Prospective Investigation in Cancer and Nutrition (EPIC), it included more than half a million people from 10 European countries who were queried on a host of different factors, from how much and what they ate to their levels of education, their age, their weight, and whether they’d ever smoked. The study indicated that people who eat a lot of processed meats are also more likely to smoke, eat few fruits and vegetables, and have lower levels of education. They’re much fatter and exercise less than the rest of the sample. And men in this category are also serious boozers. Oh, and the heavy meat eaters were older, too—so many of them were well into their 70s by the time they suffered the consequences of too many sausage rolls.

And the people who ate the most processed meat—which the study qualifies as more than 160 grams per day (about six sausage links’ worth)—didn’t only die of cardiovascular diseases and cancer, the things we associate with a bad diet; they also died of lots of “other causes,” a category that includes car crashes, accidental injuries, and other non-food-related causes. (The study’s big chicken eaters, on the other hand, were the Girl Scouts of the data pool: They don’t smoke much, they eat lots of vegetables, exercise, go to college, and no doubt brush their teeth, wear seatbelts, and get regular checkups.)

“This is like doing a survey about alcoholism and mortality and making the top group so small that it includes Billie Holiday and George Best and making headlines on this basis.”

The researchers did try to adjust for the booze and smoking, education, and even sugar consumption, but they couldn’t completely factor those things out or there would be very few people left in the study. Out of 127,000 or so male participants, a mere 619 were heavy processed-meat eaters who’d never smoked. And as it turns out, the scientists couldn’t find a significant association between heavy processed-meat consumers and nonsmokers, only former or current smokers—a finding they acknowledge is “compatible with residual confounding by smoking.” Which begs the question: Is it the bacon or is the cigarettes that’s killing these people? Concluding that it’s only the bacon that’s the culprit here seems like a stretch.

What’s more, not even 1 percent of of the people who died during the 12 years of the study were among those who ate the most processed meat. Zoe Harcombe, a British obesity researcher (and a participant in the EPIC study), points out that the researchers had to group the participants in an unusual way, so that the number of people in the high-processed-meat consumption category was very small. (There were so few women in this category that the association with processed meats and mortality wasn’t statistically significant for them.) She writes, “This is like doing a survey about alcoholism and mortality and making the top group so small that it includes Billie Holiday and George Best and making headlines on this basis.”

Of course there are plenty of good health reasons to avoid processed meats—think pink slime or listeria—not to mention environmental ones like factory farming and climate change. The EU researchers also point to salt, extra fat, and carcinogens like nitrite that are found in processed food as potential culprits that should make any health nut wary. But not all processed meat is created equal, either. The difference between some nice Italian prosciutto and that Spam-like stuff in Lunchables is vast (and perhaps one reason why Italians have a longer life expectancy than Americans).

In the final equation, eating some bacon for breakfast now and then probably isn’t going to kill you, and eating a nice (grass-fed) steak once in a while might even extend your life.


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

March, 2013|Oral Cancer News|

Decoding the oral leukoplakia/oral cancer link

Author: DrBicuspid Staff

Is there a direct relationship between oral leukoplakia and tobacco and alcohol consumption? Do all oral leukoplakias lead to oral squamous cell carcinoma (OSCC)? Is it possible to detect premalignant oral leukoplakia?

These are some of the questions a recent literature review in Oral Diseases attempted to answer (January 11, 2013).

A team of researchers from Italy, Spain, the U.K., and the U.S. did a literary search of Medline/PubMed, Embase, and Best Evidence from January 1966 to June 2012. Search terms included leukoplakia, oral leukoplakia, preneoplastic oral, precancerous oral, oral precancerous, oral dysplasia, oral mucosal lesion, proliferative verrucous leukoplakia, multifocal leukoplakias, tobacco, and alcohol.

The searches were designed to help the study authors address four key questions:
1.Do tobacco and alcohol cause oral leukoplakias?
2.What percentage of oral leukoplakias evolve into OSCC?
3.Can practitioners distinguish between premalignant and innocent oral leukoplakias?
4.Is proliferative verrucous leukoplakia (PVL) a specific entity or just a form of multifocal leukoplakia?

For the purposes of this study, the term oral leukoplakia was used to recognize “predominantly white plaques of questionable risk, having excluded (other) known diseases or disorders that carry no increased risk of cancer.”

Tobacco, alcohol, and oral leukoplakia
Although oral leukoplakia is generally considered one of the primary clinical precursors of OSCC, “the role of alcohol and smoking in this disorder has never been thoroughly assessed,” the researchers wrote. “Existing evidence suggests that tobacco and alcohol could be associated with at least a subset of [oral leukoplakia].”

It is important to recognize that, during the last few decades, the definition of oral leukoplakia has changed and new variations have emerged, suggesting potential misdiagnoses in older studies, they noted.

While an association between oral leukoplakia, smoking, and alcohol “could be reasonable and plausible,” the researchers wrote, “there is a lack of well-designed studies to examine the precise causal association,” and there are currently no systematic reviews demonstrating such a relationship.

“Current evidence indicates that tobacco consumption appears to be more likely to contribute to epithelial dysplasia than alcohol use,” they concluded.

Oral leukoplakia and OSCC
While the majority of oral leukoplakias are localized and benign, “small subsets of these lesions … acquire progressive dysplastic cellular changes and ultimately develop OSCC,” the researchers wrote (Clinical Cancer Research, June 2001, Vol. 7:6, pp. 1702-1710).

At present, there is no single marker or set of markers that can reliably predict malignant transformation of oral leukoplakia into OSCC, they noted, and the malignant transformation rate for all types of oral leukoplakias varies “enormously” from site to site in the mouth, population to population, and study to study.

However, “it is generally accepted that the detection of epithelial dysplasia is the most important predictor of malignant transformation of oral leukoplakia” (Oral Diseases, March 2007, Vol. 13:2, pp. 126-133), and it has been shown that precancerous lesions are more likely to develop into cancer in the presence of multiple genetic alterations, the researchers found.

While a number of biomolecular targets have been investigated in an attempt to identify markers that can predict the greatest risk of malignant progression, none of these has been “validated as a predictive factor for malignant transformations of oral leukoplakia,” the study authors wrote.

“Further efforts to identify the submicroscopic genetic, molecular, and/or epigenetic alterations are needed to advance this field,” they concluded.

Proliferative verrucous leukoplakia
PVL is generally described as “an uncommon form of progressive multifocal leukoplakia with a high rate of malignant transformation to either OSCC or verrucous carcinoma and a high probability of recurrence.”

The term was first introduced 35 years ago, but its diagnosis and clinical criteria remain “unresolved,” according to the study authors. It is essentially a clinical diagnosis that requires histological evaluation in order to exclude other conditions and confirm malignant development.

Based upon their literature review, “the distinction between early oral premalignant lesions of both multifocal leukoplakias and PVL is impossible,” the researchers wrote. “The diagnosis and early detection of PVL remain a difficult and challenging task due to the lack of pathologic and diagnostic predictors.”

Consecutive biopsies of the temporal progression of PVL and comparative analysis with conventional multifocal leukoplakias must be carried out to validate the various markers that have been previously suggested, they concluded.

March, 2013|Oral Cancer News|

Researchers document molecular tumor subtypes of head and neck cancer

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).

March, 2013|Oral Cancer News|

Are combination therapies effective for advanced SCCHN?

Author: DrBicuspid Staff

In a recent study, researchers from the University of North Carolina (UNC) Lineberger Comprehensive Cancer Center examined whether the addition of multiple drugs to radiation therapy is superior to the current standard of care therapy with one drug and radiation for locally advanced squamous cell carcinoma of the head and neck (SCCHN).

Their data, published in the Journal of Clinical Oncology, suggests that it does not (March 4, 2013). Standard therapy for SCCHN is a combination of the drug cisplatin and radiotherapy.

This clinical trial compared this combination to the combination with the addition of a small-molecule inhibitor of the epidermal growth factor receptor (EGFR) erlotinib. For the study, 204 patients with locally advanced SCCHN were recruited between December 2006 and October 2011. Participants were assigned to receive either cisplatin and radiotherapy or the same chemoradiotherapy with erlotinab.

EGFR is a therapeutic target for this type of cancer, and at least one other EGFR is approved for multiple uses in treating head and neck cancer, including in combination with radiation. To date, no data have been published on the use of EGFR inhibitors in combination with chemotherapy and radiation.

The goal of the current study was to determine if adding EGRF inhibition improved efficacy when combined with standard of care radiation. Unfortunately, the researchers found that the addition of EGRF did not improve clinical response rate or progression-free survival.

“There has been great enthusiasm and some confusion about the combinations of chemotherapy and biologic therapy such as EGFR inhibitors in conjunction with radiation in the treatment of squamous cell carcinomas of the head and neck,” stated lead author Neil Hayes, MD, MPH, from UNC Lineberger Comprehensive Cancer Center, in a press release. “For the moment, the data are clearly showing no added benefit.”

Future investigations will rely more on patients selected by the molecular tumor characteristics, he added.

Other institutions participating in the study were the University of Washington, Fred Hutchinson Cancer Research Center, Multicare Health Systems, University of New Mexico, Medical University of South Carolina, University of Miami, Coastal Carolina Radiation Oncology, and the University of Tennessee. Funding for the study was provided to the University of Washington by Genentech and Astellas Pharma Global Development.

March, 2013|Oral Cancer News|