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New cancer classification system might boost patient outcomes

Sun, Aug 10, 2014


Source: health.usnews.com
Author: Robert Preidt, HealthDay Reporter

Changes to the way cancers are classified could lead to more accurate diagnoses and perhaps more effective treatments in about one in 10 cancer patients, new research suggests.

Typically, cancers are categorized according to the tissue in which they originated, such as breast, bladder or kidney cancer. But tissues are composed of different types of cells.

In this study, researchers who analyzed more than 3,500 tumor samples of 12 different cancer types concluded that defining tumors by their cellular and molecular features, rather than by the tissues in which they originated, would improve diagnoses in about 10 percent of cancer cases.

“This genomic study not only challenges our existing system of classifying cancers based on tissue type, but also provides a massive new data resource for further exploration, as well as a comprehensive list of the molecular features distinguishing each of the newly described cancer classes,” study co-senior author Dr. Christopher Benz, professor at the Buck Institute for Research on Aging at the University of California, San Francisco, said in a university news release.

The study, published online Aug. 7 in the journal Cell, is part of The Cancer Genome Atlas initiative, which is led by the U.S. National Cancer Institute and U.S. National Human Genome Research Institute.

The researchers report particularly significant findings in bladder and breast cancers. They identified at least three different subtypes of bladder cancer, including one that was nearly identical to a form of non-small cell lung cancer called lung adenocarcinoma, and another most similar to squamous-cell cancers of the head and neck and of the lungs.

The findings may explain why bladder cancer patients “often respond very differently when treated with the same systemic therapy for their seemingly identical cancer type,” Benz said.

The researchers confirmed known differences between two forms of breast cancers called basal-like and luminal. But they also discovered that these differences are significant and that basal-like breast cancers — commonly referred to as triple-negative — are a distinct class of tumor.

“What’s amazing is that basal breast cancer is as different from luminal breast cancer as it is from, say, kidney cancer,” study co-lead author Denise Wolf, a research scientist based in UCSF’s Department of Laboratory Medicine, said in the news release.

Basal-like cancers are highly aggressive and more common among black and younger women.

“Even though these basal-like cancers arise in the breast, on the molecular level they have more in common with ovarian cancers and cancers of squamous-cell origin than with other subtypes of breast cancer,” explained study co-lead author Christina Yau, a staff scientist at the Buck Institute and assistant professor of surgery at UCSF.

“This is the first time ever you’ve been able to point to important molecular features shared by basal breast cancer, and by squamous head-and-neck cancer and lung cancer,” Wolf said.

“And the same is true of immune activation — we found that different cancer types have very similar immune signatures, a factor that may be relevant clinically with the rise of new immune therapies,” she added.

Further research could reveal that as many as 30 to 50 percent of cancers need to be reclassified, according to Benz.

“Although follow-up studies are needed to validate and refine this newly proposed cancer classification system, it will ultimately provide the biologic foundation for that era of personalized cancer treatment that patients and clinicians eagerly await,” Benz believes.

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Tumour Suppressor Mutations Alone Cannot Explain Deadly Cancer

Fri, Aug 8, 2014


Source: www.domain-b.com
Author: Staff

Although mutations in a gene dubbed ”the guardian of the genome” are widely recognized as being associated with more aggressive forms of cancer, researchers at the University of California, San Diego School of Medicine, have found evidence suggesting that the deleterious health effects of the mutated gene may in large part be due to other genetic abnormalities, at least in squamous cell head and neck cancers.

The study, published online 3 August in the journal Nature Genetics, shows that high mortality rates among head and neck cancer patients tend to occur only when mutations in the tumour suppressor gene coincide with missing segments of genetic material on the cancer genome’s third chromosome.

The link between the two had not been observed before because the mutations co-occur in about 70 per cent of head and neck tumours and because full genetic fingerprints of large numbers of cancer tumours have become available only recently.

”These two genetic malfunctions are not two separate stab wounds to the body,” says co-senior author Trey Ideker, PhD, chief of the division of genetics. ”One exposes the Achilles tendon and the other is a direct blow to it.”

To patients with these cancers, the study’s results mean that there may be therapeutic value in testing tumours for the two genetic identifiers, known as a TP53 mutation (short for tumour protein 53) and a 3p deletion (short for deletions of genetic information on the short arm ”p” of the third chromosome).

TP53 plays a key role in regulating cell growth, detecting and fixing DNA, and directing cell apoptosis (death) if the DNA damage is irreparable. Because of this, the TP53 protein is sometimes called the ”guardian of the genome.”

The study’s findings suggest that if both markers are present, treatment should be intensified. If only one mutation is present, treatment might be de-intensified because the TP53 mutation alone is less deadly than previously thought. The latter would have immediate benefits in reducing deaths caused by complications related to medical care.

”We are in the early stages of being able to personalize head and neck cancer treatments based on the tumor’s actual biology, the same as what’s done with breast cancers,” says co-senior author Quyen Nguyen, MD, PhD, associate professor of otolaryngology-head and neck surgery. ”In the past, treatments have been based largely on the size and location of the tumor. Now, we know that some large tumors may respond to less aggressive treatment while some small tumors may need intensified treatment. This will have a huge impact for patients.”

The study analysed the complete genomic signatures of 250 cases of squamous cell head and neck cancer extracted from The Cancer Genome Atlas, a repository of sequenced cancer genomes for more than 20 different types of human cancers maintained by the National Institutes of Cancer. All of the tumors were from patients younger than 85 years of age.

Of these, 179 had both mutations; 50 had one of the two mutations; and 22 had neither mutation. Comparisons with patient outcome data showed that half of patients with both mutations were likely to die of cancer within two years, while 66 per cent of patients with one or neither mutation would be expected to live five years or more. These survival statistics were independent of the patients’ clinical cancer stage.

Besides causing cervical cancer, the human papilloma virus (HPV) is implicated in the growing epidemic of head and neck cancers in otherwise healthy adults. It is believed that the virus can co-opt the activity of TP53, affecting cells in much the same way as a TP53 mutation but without causing a mutation. For this reason, the analysis examined HPV-positive and HPV-negative tumours separately.

One of the study’s more compelling discoveries is that among HPV-positive tumours, the most aggressive cancer cases were also highly linked to the presence of 3p deletions.

”Our findings raise fundamental questions about the role of TP53 in cancer and suggest that some of the deleterious health effects of TP53 mutations might actually be due to something else going on in the third chromosome,” said lead author Andrew Gross, a graduate student in the Bioinformatics and Systems Biology Program.

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

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Cowboy Cody Kiser Joins Anti-Tobacco Campaign to Help Educate Young Consumers

Fri, Aug 8, 2014


Source: parade.condenast.com
Author: Lindsay Lowe


The campaign to educate consumers about the dangers of tobacco has a new all-American hero: rodeo cowboy Cody Kiser, who’s partnering with the Oral Cancer Foundation (OCF) to educate parents and kids about the health risks associated with smokeless tobacco.

While chewing tobacco has long been popular among rodeo cowboys, Kiser, 23, says the drug never appealed to him, and says he hopes to serve as a positive example in an industry with traditionally strong sponsorship ties to the tobacco industry.

“My dad was a cowboy, so I know what it’s like looking up to cowboys as heroes for my whole life,” he said in a release. “Health and fitness have always been incredibly important to my family. My dad was a positive role model in my life growing up in that regard, and the idea of using spit tobacco never appealed to me.”

Tobacco and rodeo have a long intertwining history; the Professional Rodeo Cowboys Association was sponsored by the U.S. Smokeless Tobacco Company from 1986 to 2009, when the Cowboys Association decided to end its relationship with tobacco advertisers.

One can of spit tobacco has the equivalent nicotine of 40 cigarettes, and a “30-minute chew” is the equivalent of smoking three cigarettes, according to the OCF, meaning that an addiction to smokeless tobacco “can be one of the hardest to break.”

Spit tobacco (which can refer to smokeless tobacco, dip, snuff, chew, and chewing tobacco) can cause gum disease, tooth decay, and “white patches and oral lesion that can lead to oral cancer.”

An alarming “15 percent of high school boys, and 9 percent of all high school students, are already using spit tobacco,” the foundation says, while 3.5 percent of adults use the drug. An estimated 43,000 people will be diagnosed with some form of oral cancer in 2014, and the “fastest-growing segment” of that group are “young non-smokers,” says the OCF.

Kiser says he hopes to serve as a role model for young people who idolize rodeo heroes and prevent them from becoming another oral cancer statistic.



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


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Study Finds a ‘Fat Burning Process’ Termed ‘Cachexia’ Kills about One Third Cancer Patients

Thu, Aug 7, 2014


Source: scicast.com
Author: Staff

Madrid, Spain (Scicasts) — Most cancer researchers are working on the biology of the tumour. However, Michele Petruzzelli, a member of Erwin Wagner’s group at the Spanish National Cancer Research Centre (CNIO), has been looking for ways to attack the disease indirectly. 

He focused on the effects of tumours on the rest of the body, and not on the tumour itself. His work on the body’s response to a tumour has uncovered that cachexia—the extreme thinness and weakness eventually being the real cause of death in one third of patients with cancer—is triggered by a process that is heavily studied not to fight cancer, but to fight obesity: the conversion of white fat tissue into brown fat tissue.

“It is the first time that this phenomenon we might call burning fat has been associated with a negative effect”, says Erwin Wagner, the Director of the BBVA Foundation-CNIO Cancer Cell Biology Programme. “What we observe is that the transformation of white fat into brown fat, currently one of the most researched subjects because of its potential effects on obesity and diabetes, has very severe consequences in the context of cancer”. The study is published in Cell Metabolism.

The researchers also argue that if it is possible to reduce the transformation of fat tissue, the symptoms of cachexia will improve, although they do not completely disappear. The authors demonstrate this by blocking mediators of inflammation, a process linked to cachexia, specifically, to the expression of the pro-inflammatory cytokine IL-6.

“Inhibiting the conversion of white fat into brown fat is therefore a promising way of improving cachexia for cancer patients”, the authors state in their article.

The CNIO has a large variety of animal (mouse) models for different types of cancer. The starting point for this study, says Petruzzelli, was to choose a dozen of these mouse models to investigate the changes that develop in their bodies as the tumour progresses. The researchers observed several changes in different organ systems, which varied depending on the animal model used as well as the tumour type. Nevertheless, a consistent white fat to brown fat transformation was observed in all organ systems very early, before any sign of cachexia became apparent.

‘Good’ Fat and ‘Bad’ Fat

There is a growing interest in this study because of its significance in two ways. It relates to the transformation of white fat into brown fat, which is beneficial to fight obesity and diabetes, but has a huge disadvantage in cancer-associated cachexia (CAC), which for different reasons has not been studied very much in the past. In recent years both approaches have become hot topics for researchers around the world.

The importance of the transformation process of white fat into brown fat in humans was only discovered a couple of years ago. Most fat in adult humans is white—white adipose tissue—and we know that its main function, but not its only function, is to store energy (those love handles). Brown fat, however, is burned to produce heat; baby fat and the fat of hibernating animals is like that. In the context of the current obesity epidemic, white fat has been labelled bad fat, while brown fat is the good one.

The discovery that adult humans can turn white/bad fat into brown/good fat via exercise or exposure to low temperatures has opened a new line of attack on obesity, and in fact the active search for pharmacological tools to induce the transformation of fat is well underway.

The work of Wagner’s group in the article in Cell Metabolism does not discuss the advantages or disadvantages of each type of fat, it rather highlights that a process that could be strengthened to fight obesity must be fought against in cancer patients.

As for cachexia, it is a less-studied phenomenon despite that doctors have known for a long time that the treatment is difficult and the prognosis negative. Next to patients with cancer, it also affects patients in advanced phases of many illnesses, including infectious diseases, such as AIDS or tuberculosis, and chronic illnesses, such as multiple sclerosis.

It Is Not ‘Self-Cannibalism’

CAC has until recently been interpreted as a kind of self-cannibalism: the body ‘consumes’ itself while trying to supply the energy needs of the constantly growing tumour. Today we know that tumours of any size can cause cachexia, including very small ones, and even at very early stages of tumour development, which does not fit with the idea of self-cannibalism.

Researchers have observed that the process does not respond either to the body’s greater need to generate heat.

These new data, and the often ignored fact that it is the cachexia associated with the tumour—and not the tumour itself—that causes the death of one third of cancer patients, has encouraged the study of this syndrome in recent years. It is now known that this process is tightly associated with inflammation, a hallmark of many cancer types.

This is why in their study Wagner and his group explore the link between inflammation, cachexia and the process of transforming white fat tissue into brown fat tissue. Their results indicate that if the activity of one of the agents that promotes inflammation—cytokine IL-6—is blocked, the fat transformation process is substantially reduced and, as a consequence, the cachexia. The researchers do point out that it is not a cure: IL-6 is just one of several cytokines involved in the process and blocking it is not enough.

A Way To Prevent Cachexia

These novel results suggest that anti-inflammatory drugs could help fight cachexia, but there is a problem: the lack of knowledge about this syndrome is such that for now it is not possible to predict which cancer patient will develop cachexia. Furthermore, anti-inflammatory drugs have often side effects, and therefore these treatments cannot be used to prevent the appearance of cachexia in all cancer patients.

The current study in Cell Metabolism could open up a new way of discovering processes, e.g. the transformation of fat in the initial stages of cachexia. “It allows one to think of the possibility to identify biomarkers that would help to predict which patients are going to develop cachexia in a way we can treat them preventively”, says Petruzzelli.

*This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.
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Scientists Discover Genetic Mutations Linked to Salivary Gland Tumours

Wed, Aug 6, 2014


Source: scicasts.com
Author: Staff

Juniper, FL — Research conducted at the Florida campus of The Scripps Research Institute (TSRI) has discovered links between a set of genes known to promote tumour growth and mucoepidermoid carcinoma, an oral cancer that affects the salivary glands.

The discovery could help physicians develop new treatments that target the cancer’s underlying genetic causes.

The research, recently published online ahead of print by the Proceedings of the National Academy of Sciences, shows that a pair of proteins joined together by a genetic mutation—known as CRTC1/MAML2 (C1/M2)—work with MYC, a protein commonly associated with other cancers, to promote the oral cancer’s growth and spread.

“This research provides new insights into the molecular mechanisms of these malignances and points to a new direction for potential therapies,” says TSRI biologist Dr. Michael Conkright, who led the study.

The C1/M2 protein is created when the genes encoding CRTC1 and MAML2 mutate into a single gene through a process known as chromosomal translocation. Such mutant “chimera” genes are linked to the formation of several forms of cancer. The team discovered that the C1/M2 protein further activates genetic pathways regulated by MYC, in addition to CREB, to begin a series of cellular changes leading to the development of mucoepidermoid carcinoma.

“The identification of unique interactions between C1/M2 and MYC suggests that drugs capable of disrupting these interactions may have therapeutic potential in the treatment of mucoepidermoid carcinomas, ” said Dr. Antonio L. Amelio, first author of the study who is now assistant professor with the University of North Carolina (UNC) School of Dentistry and member of the UNC Lineberger Comprehensive Cancer Center.

Researchers have known about the role of C1/M2 and its interactions with another protein, CREB, in the development of mucoepidermoid carcinoma, and physicians screen patients for the presence of the C1/M2 protein when testing for this cancer. These new findings deepen the understanding of C1/M2’s role by revealing that it works with a family of cancer-associated genes known as the MYC family to drive the cellular changes necessary for a tumour to develop.

The discovery of these new protein interactions may also reveal insights into the mechanisms behind other cancers that arise due to other genetic mutations involving the CREB and MYC pathways.

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

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Quick, low-cost blood test detects early signs of oral cancer

Sat, Aug 2, 2014


Source: www.drbicuspid.com
Author: DrBicuspid Staff

Australian researchers have developed a quick, low-cost blood test to detect the early signs of oral cancer. The diagnostic test examines the profile of small molecules called microRNA in the blood and can be done at the same time as other routine checks, such as for cholesterol.

At present, no routine screening tests for oral cancer are on the market. The researchers hope that a simple blood test could change that and, in doing so, help stem the global increase of various oral cancers.

About 300,000 new cases of oral cancer were reported globally in 2012, according to the researchers. The main barriers to treatment remain late detection and low disease awareness. Warning symptoms include pain, swelling, a hoarse voice, and difficulty swallowing — symptoms that are often dismissed or misdiagnosed as a common cold.

The test, called miLIFE, was developed by researchers Nham Tran, PhD, and doctoral candidate Samantha Khoury from the University of Technology, Sydney (UTS) Centre for Health Technologies. The blood-based test can be administered by healthcare providers to screen microRNA to reveal the oral cancer’s early warning signs. The turnaround time for the test is about 48 hours at present.

The levels of five specific microRNA molecules are detected with miLIFE and compared with those of healthy, noncancerous individuals. An overabundance or expression of these specific microRNAs would designate people at high risk for oral cancer. These patients would then be referred to a specialist for further examination.

“You don’t need a specialist to administer the test,” Khoury noted. “When you visit your GP [general practitioner] for routine checks of cholesterol, vitamin D, hemoglobin, and so on, the same blood sample can be used to check for the presence of microRNA biomarkers.”

The majority of oral cancer patients who go to the doctor have already developed an advanced lesion, but by then it is too late, Tran stated.

“At this stage, their diagnosis option is to undergo a tumor biopsy or a fine-needle aspiration, both highly invasive and painful procedures,” he noted. “We hope that through miLIFE we can provide early intervention to decrease the number who are diagnosed with oral cancer each year.”

The test is being filed under a UTS provisional patent, and Tran hopes it will be available within two to three years.

The technology, in development since 2006, has evolved via an ongoing collection of consenting cancer patient samples from surgeons based at several Sydney hospitals. The researchers collaborated with the Sydney Head and Neck Cancer Institute, the Cancer Council Australia, and Mount Sinai Hospital in New York.

Next the researchers plan to expand the project with the Vellore Christian Medical College Foundation in India. They targeted India because that country has the world’s highest rates of oral cancer, with 40,000 cases diagnosed annually.

“The introduction of a robust cancer screen will provide a platform for effective cancer management in low-resourced countries,” Tran noted.

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Blood test could predict oral cancer recurrence

Sat, Aug 2, 2014


Source: www.livescience.com
Author: Rachael Rettner, Senior Writer

A new blood and saliva test that looks for traces of the human papillomavirus (HPV) can predict whether some people with oral cancers will have their cancer come back, early research suggests.

It helps to know as soon as possible that cancer has returned, because tumors that are caught early are easier to treat.

In the study, the researchers analyzed blood and saliva samples from 93 people with head and neck cancers; about 80 percent of these patients had cancers that tested positive for HPV. All of their cancers had previously been treated with surgery, radiation or chemotherapy.

The researchers looked for fragments of DNA from HPV-16, a strain of the virus that is strongly linked with head and neck cancer. The virus may be found in cancer cells that linger in the body after treatment, the researchers said.

Among people with HPV-positive tumors, the new test identified 70 percent of those whose cancer returned within three years, the researchers said.

“Until now, there has been no reliable biological way to identify which patients are at higher risk for recurrence, so these tests should greatly help [to] do so,” study researcher Dr. Joseph Califano, professor of otolaryngology at Johns Hopkins School of Medicine, said in a statement.

Patients with head and neck cancer typically visit the doctor every one to three months during the first year after their diagnoses to check for cancer recurrence. But new tumors in the tonsils, throat and base of the tongue can be difficult to spot, and are often not detected early, the researchers said.

Still, more research is needed to confirm the findings, Califano said. Because HPV infection is common, the test may identify HPV infections that are not related to the cancer. “We can’t be sure our test results are cancer-specific, and not due to other forms of HPV infection or exposure,” Califano said.

The researchers are now looking for additional genetic markers that would increase the accuracy of their test.

The study is published today in the journal JAMA Otolaryngology–Head & Neck Surgery.

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University of Michigan researchers find protein that fuels repair of treatment-resistant cancer cells

Sat, Aug 2, 2014


Source: http://www.dentistryiq.com/
Author: DentistryIQ Editors

Imagine that you’re fighting for your life, but no matter how hard you hit, your opponent won’t go down.

The same can be said of highly treatment-resistant cancers, such as head and neck cancer. During radiation and chemotherapy, some cancer cells repair themselves to survive and thrive. Head and neck cancer is the sixth most common cancer in the world, but the late detection and treatment resistance result in a high mortality rate.

Now, University of Michigan researchers have found that a particular protein – TRIP13 – encourages those cancer cells to repair themselves, and they have identified an existing chemical that blocks this mechanism for cell repair.


Left: Untreated head and neck cancer cells are tagged fluorescent green. Right: Shows cells treated with the chemical inhibitor that blocks TRIP13, which results in a dramatically smaller tumor.

“This is a very significant advance because identifying the function of the protein that fuels the repair of cancer cells and having an existing chemical that blocks the process could speed the process of moving to clinical trials,” said principal investigator Nisha D’Silva, University of Michigan professor of dentistry and associate professor of pathology.

Typically, if scientists discover a promising drug therapy target, it takes years to develop drug compounds from scratch and move these into clinical trials.


Top: Cancer cells with TRIP13, the protein that encourages cancer cells to repair themselves. Bottom: Cancer cells in which researchers have removed or decreased TRIP13, which results in fewer cells due to cell death.

If cell DNA is damaged, and the cell cannot repair the damage, the cell dies. In head and neck cancers, D’Silva and colleagues showed how cancer cells that overexpress TRIP13 were able to repair their DNA enough to survive and continue to grow as cancer.

“Targeting this repair mechanism with specific drugs could increase effectiveness of treatment and improve survival of cancer patients,” D’Silva said. “And given the overexpression of TRIP13 in several treatment-resistant cancers, this strategy will likely be important for multiple cancers.”

Rajat Banerjee of the University of Michigan School of Dentistry is the first author of the study, “TRIP13 promotes error-prone nonhomologous end joining and induces chemoresistance in head and neck cancer,” which appeared online on July 31 in Nature Communications.

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Anti-vaccine fears aren’t only for vaccines anymore

Wed, Jul 30, 2014


Source: http://m.dailykos.com
Author: Staff member – Hunter

The anti-vaccination forces are gaining new victims:

In May, the Tennessean reported on a truly shocking medical problem. Seven infants, aged between seven and 20 weeks old, had arrived at Vanderbilt University’s Monroe Carell Jr. Children’s Hospital over the past eight months with a condition called “vitamin K deficiency bleeding,” or VKDB. This rare disorder occurs because human infants do not have enough vitamin K, a blood coagulant, in their systems. Infants who develop VKDB can bleed in various parts of their bodies, including bleeding into the brain. This can cause brain damage or even death.

Which is why newborns usually get a vitamin K shot immediately after birth, just in case. It’s not a vaccine, it’s a vitamin, and odds are good that many of the same people objecting to the this vitamin pop vitamin pills regularly. The problem is that yes, it’s an injection, and so parents are assuming (with the help of anti-vaccine groups, not-at-all-coincidentally) there must be something devious about that.

A quick Google search returns a number of dire warnings about vitamin K shots circulating on the Internet. One of the top results is an article at TheHealthyHomeEconomist.com, which urges readers to “Skip that Newborn Vitamin K Shot,” before going on to list an array of “dangerous ingredients in the injection cocktail.” (The site also calls vaccines “scientific fraud.”) [...]And then there’s physician Joseph Mercola (whose popular website calls vaccinations “very neurotoxic” and suggests they are associated with a list of conditions, including autism).

I can only presume that somebody’s keeping track of the body count on these things. Being an informed medical consumer is one thing, risking your child’s health based on paranoid/fringe internet theories is something entirely different.


*This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.
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Diabetes may increase risk for head and neck cancer

Sat, Jul 26, 2014


Source: www.medscape.com
Author: Larry Hand

The risk for head and neck cancer (HNC) was almost 50% higher in patients with diabetes than in individuals without diabetes, according to an article published online July 24 in JAMA Otolaryngology. The estimated risk is higher for people 40 to 65 years old.

Kuo-Shu Tseng, PhD, from Tainan University of Technology in Taiwan, and colleagues conducted a retrospective cohort study comparing the records of 89,089 patients newly diagnosed with diabetes with those of control patients matched by age, sex, and comorbidities. They obtained the data from Taiwan’s Longitudinal Health Insurance Research Database, which has claims information on 23.3 million beneficiaries between 1996 and December 31, 2011.

The researchers compared differences in estimated risk for head and neck cancer between groups by sex, age, and number of follow-up years after the first diabetes diagnosis date (index year) for patients. The incidence of head and neck cancer was 1.47 times higher for the diabetes group compared with for controls (P < .001)

The mean age among the diabetes group for cancer diagnosis was 55.52 years, and the mean interval between the index date and cancer diagnosis was 4.48 years.

Individuals aged 40 to 65 years in the diabetes cohort had significantly higher risk of developing head and neck cancer (incident risk ratio, 1.57; P < .001), and men had higher risk than women (incident risk ratio, 1.48; P < .001 for men).

The researchers computed hazard ratios for head and neck cancer, using Cox proportional hazards regression analysis, adjusting for age, sex, comorbidities, geographic distribution, and monthly income. The comorbidities were obesity, hypertension, coronary artery disease, chronic kidney disease, and chronic obstructive pulmonary disease.

The diabetes group had almost a 50% higher risk (adjusted hazard ratio [AHR], 1.48; 95% confidence interval [CI], 1.31 – 1.67) than the control group.

The most prevalent site of head and neck cancer was the oral cavity (57.1%) in the diabetes group (AHR, 1.74; 95% CI, 1.47 – 2.06). The next most prevalent cancer site was the nasopharynx (15.3%; AHR, 1.40; 95% CI, 1.03 – 1.89).

Overall survival of patients without head and neck cancer was significantly higher among the control patients (P < .001). Although the researchers found no significant effect on overall survival for the people in the diabetes group who developed cancer, follow-up periods for all patients with head and neck cancer are limited.

Possible Mechanisms
The researchers write that possible mechanisms for the link between diabetes and head and neck cancer include:

  • shared genetic risk factors;
  • epigenetic modifications of inherited or acquired genetic mutations;
  • long-term exposure to hyperinsulinemia, which leads to breast cancer;
  • exposure to high levels of insulin and insulin-like growth factor, which can increase cellular proliferation; and
  • metabolic dysfunctions parallel to diabetes.

A limitation of the study is that several suspected risk factors for head and neck cancer, such as patients’ histories of using alcohol, smoking tobacco, and physical activity, were not available in the database.

1. This research was supported by the Taipei Medical University and Chi Mei Medical Center Research Fund. The authors have disclosed no relevant financial relationships.
2. JAMA Otolaryngol. Published online July 24, 2014

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