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Antioxidants May Cause More Harm Than Good in Cancer Patients

Mon, Jul 14, 2014

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Source: medscape.com
Author: Zosia Chustecka
 

While alternative health gurus often encourage increasing antioxidants in the diet and the taking of antioxidant nutritional supplements such as beta-carotene, vitamins A, C, and E, and selenium, new research findings suggest that antioxidants could do more harm than good, especially in cancer patients.

The idea is discussed in a perspective article on the promise and perils of antioxidants for cancer patients in the July 10 issue of the New England Journal of Medicine.

Coauthor David Tuveson, MD, PhD, professor and deputy director of the Cold Spring Harbor Laboratory Cancer Center in New York, explained in an interview with Medscape Medical News that the idea that antioxidants could be useful in cancer goes back to Linus Pauling, and is based on observations that oxidation within cells is needed for cell growth. “As cancer cells growth rapidly, a cancer cell would have more oxidation within it than a normal cell,” he added, and the hope was that antioxidants would interfere with these cellular oxidative processes and would suppress the growth.

“Although some early preclinical studies supported this concept,” the authors write, there have now been several clinical trials that have shown no effect of antioxidants on reducing the incidence of cancer, and there have even been suggestions of harm in persons who are at risk for cancer.

Dr. Tuveson noted a clinical trial from Scandinavia in the early 1990s, which found that high doses of antioxidants, particularly beta-carotene, were associated with more lung cancer rather than less as had been hoped for.

There was a similar finding from the Selenium and Vitamin E Cancer Prevention Trial (SELECT), which found that the antioxidants did not reduce the risk for prostate cancer, as had been hoped, and in fact increased the risk in some men.

Dose-dependent Harmful Effect

The perspectives article was prompted by new findings reported earlier this year, he said. An animal study carried out by Swedish researchers showed that the harm from antioxidants was dose-dependent (Sci Transl Med. 2014;6:221ra15). The study was conducted in a genetically engineered mouse model that mimics early human non-small-cell lung cancer. The researchers studied N-acetylcysteine (which is used in patients with chronic obstructive pulmonary disease) and also derivatives of vitamin E, and they found that these antioxidants “actually increased cancer burden and mortality in a dose-dependent manner.”

“The mice got lung cancer faster and they died more quickly of the disease,” Dr. Tuveson said.

In their perspective article, Dr. Tuveson and coauthor Navdeep Chandel, PhD, from Northwestern University in Chicago, address the question of why.

It turns out that all cells have not only oxidative mechanisms producing reactive oxygen species, they also have a mechanism by which they produce antioxidants, and so there is a balance between the 2 in each cell. “And cancer cells, because they make more oxidants, also make more antioxidants,” Dr. Tuveson explained.

“So when adding an antioxidant as a supplement, all you are doing is increasing a pool of what is already there,” he said. “But you are not actually stopping the oxidative mechanisms, and you are not stopping the production of oxidants in the first place, and the pathways that are fuelling cell growth,” he added.

“All you are doing is helping the cancer cell deal with the toxic effects of the oxidants, and by doing so you may be actually making the cancer cell even stronger,” Dr. Tuveson said.

“The antioxidants that we take as a supplement or in our diet don’t go after the root cause of how oxidants promote cancer cell biology,…and our suggestion is that we need to look much more carefully at these mechanisms if we are to truly develop strategies to prevent cancer,” he said.

In their article, the authors propose 2 strategies for further research — the development of antioxidants that target specific intracellular sites of oxidant production, and also a synthetic lethal strategy directed at antioxidants produced within the cell. Both of these strategies are currently at the research stage, with work focused on developing compounds that could be tested in humans.

As for the clinical implications of the research so far, Dr. Tuveson said: “We don’t firmly say that taking antioxidants is dangerous for cancer patients…but I do believe that our article will cause those discussions to begin.”

However, others have already warned cancer patients not to take antioxidants; for instance, prostate cancer patients have been warned against taking selenium, as previously reported by Medscape Medical News.

In addition, there is a question of whether antioxidants may interfere with common cancer treatments, such as chemotherapy and radiotherapy, as these work by increasing oxidation within cancer cells, Dr. Tuveson commented. This is an area that needs to be studied more, he said.

This issue of antioxidants being harmful to cancer patients was raised last year by Nobel laureate James Watson, PhD, who is chancellor emeritus at the Cold Spring Harbor Laboratory. He described a new hypothesis on reactive oxygen species that he considers is “among my most important work since the double helix.”

Dr. Watson proposed that antioxidant levels within cancer cells are a problem and are responsible for resistance to treatment, and that the untreatability of late-stage cancer might be the result of “its possession of too many antioxidants.”

“The time has come to seriously ask whether antioxidant use more likely causes than prevents cancer,” Dr. Watson said. Nutritional intervention trials have shown no obvious effectiveness in preventing cancer or in lengthening mortality, and, “in fact, they seem to slightly shorten the lives of those who take them.”

Dr. Tuveson, who works at the same institution, commented at the end of the interview that “Dr. Watson is usually a few steps ahead of the rest of us.”

 

 *This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.
 
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Salivary gland cancers rare, but sometimes deadly

Sat, Jul 12, 2014

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Source: articles.baltimoresun.com
Author: Andrea K. Walker

Professional baseball great Tony Gwynn Sr., also known as Mr. Padre, died last month of salivary gland cancer, which he believed was caused by years of using smokeless chewing tobacco. The cancer is a rare form that begins in any of the salivary glands in the mouth, neck or throat. Two adults in 100,000 are diagnosed with salivary gland cancer each year. The chances of survival drop if the cancer has spread to other parts of the body. Dr. Patrick K. Ha, with Johns Hopkins Head and Neck Surgery at Greater Baltimore Medical Center, says new types of treatments and therapies are in the works to treat the disease.

What is salivary gland cancer and how common is it?
Salivary gland cancers are a diverse group of rare malignancies that can involve any of the major salivary glands (the parotid, submandibular and sublingual) or minor salivary glands, which are found within the lip, palate, tongue base, nasal cavity or sinuses. There are numerous different cancers that may arise from the salivary glands, and these may behave differently based on their cell of origin.

What causes it, and who is more likely to get it?
Little is known about the causes of salivary gland cancers. Unlike the more common head and neck cancers, which have a clear association with smoking, drinking or even the human papillomavirus (HPV), salivary gland cancers do not have such strong associations. There may be a link between significant radiation exposure (i.e., treatment level doses) in the development of salivary gland cancers, as well as with some environmental exposures such as nickel alloy, asbestos or woodworking materials. Tony Gwynn believed using chewing tobacco throughout his professional baseball career was the cause of his cancer, but salivary gland cancers aren’t as strongly linked to tobacco use as some other types of cancers. Nonetheless, we advise against smoking, using smokeless tobacco or even e-cigarettes. They are all addictive and tobacco products contain carcinogens relevant to other cancers.

We do know that men are more likely to get this type of cancer, with the average age of onset in the mid-60s.

What are the symptoms of salivary gland cancer?
Unfortunately, salivary gland cancers most often present as painless masses in the cheek, neck, or within the sinuses/tongue base. Because most of these masses are slow growing, the development of symptoms occurs relatively late. Depending on which gland is involved, the symptoms may include a visible lump, difficulty breathing, swallowing problems or pain. Late symptoms might include facial weakness/drooping, numbness or visual changes.

How is it diagnosed and is it hard to detect?
The ultimate diagnosis is made with a biopsy. A distinction can often be made between benign and cancerous masses with a small needle biopsy, but sometimes requires complete removal of the mass to make this determination. Imaging with a CT scan or MRI can be helpful, especially for operative planning. Depending on where the tumor is located, detection can be more difficult. For example, a mass on the outer surface of the parotid or submandibular gland will be more easily felt than a mass growing in the sinus.

How is it treated and what is the likelihood of survival?
Most salivary gland cancers are treated with surgery up front for complete removal, and possibly radiation afterwards, depending on how serious the disease appeared at the time of surgery and under the microscope. Chemotherapy is less well proven to be helpful in these cancers but could sometimes be considered as additional therapy along with radiation. While some forms of salivary gland cancer can be aggressive, most are relatively well treated, and the five-year survival rate can be upwards of 75 percent.

What new therapies are on the horizon for salivary gland cancers?
Currently, there are trials available to examine the role of chemotherapy in salivary gland cancer treatment. Additionally, work is being done to look into targeted therapy which can better treat the cancers without the significant side effects. Unfortunately, because these are rare cancers, we need to perform the basic research to understand how these cancers arise before we can really make significant advancements in their treatment.

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An effective and well-tolerated strategy in recurrent and/or metastatic head and neck cancer: successive lines of active chemotherapeutic agents

Sat, Jul 12, 2014

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Source: 7thspace.com
Author: staff

The combination platinum, 5-fluorouracil (5-FU) and cetuximab is the standard first-line regimen of recurrent and/or metastatic head and neck squamous cell carcinoma (HNSCC). Due to the toxicity of this treatment, alternative therapies are often offered to patients.

The aim of this study was to evaluate the overall survival obtained with a first line chemotherapy adapted to patients functional status and the administration of all active drugs within successive lines of chemotherapy.

Methods: This series included a total of 194 patients with recurrent and/or metastatic HNSCC treated from 2006 to 2011 in a single institution where the administration of successive lines of chemotherapies has been the standard clinical approach. Treatment was administered according to clinical practice guidelines.

Results: Most patients received at least two treatment lines.

Only 11 patients (6%) were treated with a combination of cisplatin, 5-FU and cetuximab in front line, but most patients received at least one platinum-based regimen (n = 154 patients, 78%); 162 (82%) received taxanes, 36 (18%) received 5-FU, 27 (14%) received capecitabine, 67 (34%) received methotrexate and 134 (68%) received cetuximab. The median overall survival was 9.8 months (95% CI: 8.1-11.4 months) and reached 13.1 months among the subgroup of 131 patients eligible for inclusion in a clinical trial.

Conclusion: The survival outcomes of patients treated in the first-line setting with chemotherapy regimens adapted to their functional status, followed by several subsequent regimens were comparable with published outcomes of patients treated by platinum, 5-FU and cetuximab.

Credits/Source: BMC Cancer 2014, 14:504

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ACS awards $1.7M to study racial disparities in HNC patients

Sat, Jul 12, 2014

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Source: http://www.drbicuspid.com/
Author: DrBicuspid Staff

The American Cancer Society (ACS) has awarded a $1.7 million grant to Philadelphia researchers to investigate factors that may contribute to the racial disparities seen among those diagnosed and treated for head and neck cancers (HNC) — specifically head and neck squamous cell carcinoma (HNSCC).

While head and neck cancers account for only 3% of all cancers in the U.S., a disproportionately high number of African Americans are affected. Recent research has shown that other biological factors, and tobacco and alcohol use, may have a role in the development of these cancers. Other studies suggest that low socioeconomic status and poor healthcare access are the main contributors to this disparity.

“Studies on genes involved in tobacco and drug metabolism and efflux suggest an association of genetic variants with head and neck cancer risk and survival in populations of European and Asian ancestries,” stated Camille Ragin, PhD, an associate professor at the Fox Chase Cancer Center and the study’s principal investigator, in a press release. “Genetic variants associated with the survival disparity of head and neck cancer in African-derived populations, however, is not yet clear.”

An accumulation of cancer-causing compounds occurs when products from tobacco smoke enter the body’s cells, in some cases enabled by alcohol, and are broken down by proteins. Variations in the genetic code that generate these proteins can lead to differences in their function and could affect the way disease may develop or respond to drug therapy. In many cases, the genetic makeup of these proteins differs according to race.

“Our group suggests that genetic factors and the environment work together to contribute to the observed racial disparities in HNSCC incidence and survival,” Ragin said. “With this grant we will be able to use novel techniques to look for variations in the genetic makeup in these genes that are unique to African Americans.”

These findings may help improve early detection and cancer prevention interventions by providing insight into the biology of the disease and factors that contribute to racial disparities.

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Oscar Award winning composer Ryuichi Sakamoto is diagnosed with Throat Cancer

Fri, Jul 11, 2014

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Author: Jun Hongo
Source: blogs.wsj.com/japanrealtime
 

World-renowned Japanese musician and composer Ryuichi Sakamoto says he has throat cancer and has canceled his scheduled shows and activities.

The Oscar-winning composer and anti-nuclear activist said Thursday that he was diagnosed with oropharyngeal cancer at the end of June.

“After much thought and consideration, I have decided to take time off of work in order to concentrate on treating it,” the 62-year-old said in a statement. “I promise to return after a full recovery.”

According to his management agency Avex Music Creative Inc., Mr. Sakamoto will step down as one of the directors of the Sapporo International Art Festival 2014, scheduled to start next week. He will also cancel live shows including a performance at Park Hyatt Tokyo on July 30.

Avex Music Creative said there is no time frame set for Mr. Sakamoto’s return, and that the artist will “dedicate all his time to treatment.” The agency declined to offer details on the current stage of Mr. Sakamoto’s cancer.

The pioneering musician debuted as a member of Yellow Magic Orchestra in 1978, playing a role in the emergence of electro pop and providing inspiration for a generation of electronic music and hip-hop producers. His creativity and prowess as a keyboard player, producer and composer extends to a large swath of genres and styles from pop rock to bossa nova. He won an Academy Award for composing the score music for Bernardo Bertolucci’s 1987 film “The Last Emperor,” a movie he also appeared in as an actor.

Among international honors bestowed on Mr. Sakamoto, he was named an Officier of the Ordre des Arts et des Lettres from the French government in 2009.

In addition to his work in music, producing and acting, Mr. Sakamoto has been one of the most vocal activists against nuclear power following the Great East Japan Earthquake in 2011.

He has also been a leading figure in recent moves to prevent outdated legislation being used to stop people dancing at nightclubs in Japan.

*This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.
 
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Jamie Dimon, CEO of JPChase Morgan, is diagnosed with throat cancer

Wed, Jul 2, 2014

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Author: Jessica Silver-Greenberg
Source: nytimes.com

 

Jamie Dimon the chief executive of JPMorgan Chase, has throat cancer and will begin treatment shortly at Memorial Sloan Kettering Cancer Center, he said in a note to the bank’s employees and shareholders late Tuesday.

Doctors discovered the cancer at an early stage, Mr. Dimon, 58, said, noting that his condition was “curable.”

After a series of tests, he said the doctors confirmed that the cancer had not spread beyond the “original site” and the adjacent lymph nodes on the right side of his neck.

Mr. Dimon assured employees at JPMorgan, the nation’s largest bank, that the prognosis from the doctors was “excellent.”

Mr. Dimon, who has held the dual roles of chief executive and chairman at the bank since 2006, has been atop JPMorgan longer than any other bank chief.

The announcement of his diagnosis came on Mr. Dimon’s 10-year anniversary at JPMorgan. That tenure, which began when JPMorgan acquired Bank One, has been marked by triumph — the bank emerged from the financial crisis in better shape than its rivals — and by tumult.

The bank has worked to mend its frayed relationships with regulators — a painful reconciliation that cost it roughly $20 billion. In November, JPMorgan reached a record $13 billion settlement with a range of government authorities over its sale of questionable mortgage-backed securities in the lead-up to the financial crisis. The bank also reached a $2 billion settlement over accusations that it failed to sound alarms about Bernard L. Madoff’s Ponzi scheme.

JPMorgan has also been buffeted by the departure of several top executives. In the last two years alone, at least 10 senior executives have left JPMorgan.

Most recently, Michael J. Cavanagh, once considered an heir to Mr. Dimon, left the bank to join the Carlyle Group, a private equity firm.

And like its rivals, JPMorgan, which will report second-quarter earnings on July 15, is grappling with a slowdown in its trading business.

It has been a particularly grueling stretch for trading units across Wall Street. The sluggish trading revenue traces, in part, to a spate of rules passed in the aftermath of the financial crisis.

In the past, banks made some of their riskiest wagers — bets that sometimes translated into rich profits — through trading complex derivatives, bonds and commodities. In the new banking landscape, where interest rates remain persistently low, the role of those businesses has been diminished.

In his annual letter to shareholders in April, Mr. Dimon stressed that despite the “constant and intense pressure,” he was proud of the bank’s resiliency and its resolve. Last year, JPMorgan earned $17.9 billion in profit despite the legal costs.

Mr. Dimon reiterated his faith in the leadership of the bank on Tuesday. He did not outline any plans to cede the reins of the bank while he has treatment — a process that he said should last about eight weeks.

In his note, Mr. Dimon emphasized that the company would “continue to deliver first-class results for our customers.”

The illness of any chief executive naturally prompts questions about who is prepared to take over, at least for a little while. But Mr. Dimon emphasized in his note that he would remain immersed in the day-to-day operations of the bank.

JPMorgan’s board has remained firmly behind Mr. Dimon, redoubling support for him. The board awarded Mr. Dimon $20 million in annual compensation for his work in 2013. The raise came one year after the board had cut his compensation to $11.5 million.

Even before Mr. Dimon’s diagnosis the board agreed on various succession plans.

“The board had already established a short-term, medium-term and longer-term succession plan,” said a JPMorgan spokesman, Joseph Evangelisti.

Among the potential successors, people briefed on the matter said, are Gordon Smith, the head of JPMorgan’s consumer bank, and Mary Erdoes, who runs the asset management business.

The inclusion of Mr. Smith and Ms. Erdoes reflected the changing fortunes of banking. JPMorgan’s consumer business, for example, has taken on more prominence as the bank shifts its focus to credit cards and auto loans and away from intricate deal-making and trades that once were the hallmark of Wall Street.
 
 
* This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.
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Tony Gwynn makes statement regarding spit tobacco use weeks before death

Mon, Jun 30, 2014

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Author: Michael Chen
Source: 10news.com
 

SAN DIEGO – One of Tony Gwynn’s last acts was issuing a simple message about the habit he blamed for his cancer.

About two and half months ago, Gwynn received a request from the Professional Baseball Athletic Trainers Society – known as PBATS – to do a taped interview on the dangers of spit tobacco to be shown to players.

“It came back that Tony was entirely sick to do that,” said Neil Romano, adviser to the PBATS.

Romano says Gwynn’s agent then called, saying Gwynn felt bad for not taking part.

Gwynn blamed his decades-long use of chew tobacco for his mouth cancer.

On May 28, less than three weeks before Gwynn’s death, the group got final confirmation through his agent that they could use an emailed statement.

Gwynn’s message: “My advice to anyone would be if they aren’t using spit tobacco, please don’t start. And if you are using, try to quit, if not for yourself then do it for the people you love.”

“The fact that this was one of his last acts goes to his class, his character as a person, and frankly, his love for the game and the players,” said Romano.

When Gwynn was first diagnosed, Major League Baseball banned players from putting tins in pockets and using during interviews, but usage during games is still allowed.

Mark Grudzielanek retired in 2010 after a 15-year career. He never used but said when he started, it was readily available through clubhouse staff.

“Whatever we needed, they went and got it,” said Grudzielanek.

Romano says more than a decade ago, MLB started cracking down on that practice. Chew was also banned in the minors.

About a third of major league players still dip. Critics say that is a prime reason why a federal study found that 20 percent of high school boys chew.

Grudzielanek hopes Gwynn’s final message will make a difference. The five-minute film, which also commemorates Gwynn, was completed on June 13.

A few days ago, Gwynn protégé and pitcher Stephen Strasburg said he is quitting chew for his daughter.

“It’s taken lives and let’s hope this is the last life, and we can control this and get these guys to understand how bad it is for you,” said Grudzielanek. “To stop kids from doing it, it has to stop from the top.”

In recent days, some have called for a spit tobacco ban to be looked at with a new MLB player labor agreement in 2016.

 
*This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.
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Selective apoptotic cell death effects of oral cancer cells treated with destruxin B

Sun, Jun 29, 2014

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Source: 7thspace.com
Author: press release

Recent studies have revealed that destruxins (Dtx) have potent cytotoxic activities on individual cancer cells, however, data on oral cancer cells especial human are absent.

Methods: Destruxin B (DB) was isolated and used to evaluate the selective cytotoxicity with human oral cancer cell lines, GNM (Neck metastasis of gingival carcinoma) and TSCCa (Tongue squamous cell carcinoma) cells, and normal gingival fibroblasts (GF) were also included as controls. Cells were tested with different concentrations of DB for 24, 48, and 72 h by MTT assay.

Moreover, the mechanism of cytotoxicity was investigated using caspase-3 Immunofluorescence, annexin V/PI staining, and the expression of caspase-3, Bax, and Bcl-2 by western blotting after treated with different concentrations of DB for 72 h as parameters for apoptosis analyses.

Results: The results show that DB exhibited significant (p <0.01) and selective time- and dose-dependent inhibitory effects on GNM and TSCCa cells viability but not on GF cells. The data suggested that DB is capable to induce tumor specific growth inhibition in oral GNM and TSCCa cancer cells via Bax/Bcl-2-mediated intrinsic mitochondrial apoptotic pathway in time- and dose-dependent manners.

Conclusions: This is the first report on the anti-proliferation effect of DB in oral cancer cells.

The results reported here may offer further evidences to the development of DB as a potential complementary chemotherapeutic target for oral cancer complications.

Author: Rosa Huang Liu, Shih-Pin Chen, Tsong-Ming Lu, Wei-Yu Tsai, Chung-Hung Tsai, Chi-Chiang Yang, Yew-Min Tzeng
Source: BMC Complementary and Alternative Medicine 2014, 14:207

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Researchers find way to diagnose aggressiveness of oral cancer

Sun, Jun 29, 2014

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Source: www.news-medical.net
Author: staff

Studying mouth cancer in mice, researchers have found a way to predict the aggressiveness of similar tumors in people, an early step toward a diagnostic test that could guide treatment, according to researchers at Washington University School of Medicine in St. Louis.

“All patients with advanced head and neck cancer get similar treatments,” said Ravindra Uppaluri, MD, PhD, associate professor of otolaryngology. “We have patients who do well on standard combinations of surgery, radiation and chemotherapy, and patients who don’t do so well. We’re interested in finding out why.”

Reporting in Clinical Cancer ResearchK/em>, the investigators found a consistent pattern of gene expression associated with tumor spreading in mice. Analyzing genetic data from human oral cancer samples, they also found this gene signature in people with aggressive metastatic tumors.

“We didn’t automatically assume this mouse model would be relevant to human oral cancer,” said Uppaluri, who performs head and neck surgeries at Barnes-Jewish Hospital. “But it turns out to be highly reflective of the disease in people.”

Rather than use genetic methods to induce tumors in the mice, the research team repeatedly applied a known carcinogen, in much the same way humans develop cancer of the mouth.

“Patients often have a history of tobacco and alcohol use, which drive the development of these tumors,” Uppaluri said. “We felt that exposing the mice to a carcinogen would be more likely to produce similar kinds of tumors.”

The researchers, including first author Michael D. Onken, PhD, research assistant professor of cell biology and physiology, showed that this exposure sometimes produced tumors in the mice that did not spread, but other times resulted in aggressive metastatic tumors, similar to the variety of tumors seen in people. Uppaluri’s team then collaborated with Elaine Mardis, PhD, co-director of The Genome Institute at Washington University, to find out whether the mouse and human tumors also were genetically similar. They compared their mouse sequences to human data sets from The Cancer Genome Atlas (TCGA).

“When we sequenced these tumors, we found that a lot of the genetic mutations present in the mouse tumors also were found in human head and neck cancers,” Uppaluri said.

Further analysis identified a common signature in the expression of about 120 genes that was associated with the more aggressive tumors, whether in mice or people. The researchers confirmed this signature using data collected from 324 human patients. Subsequently, using oral cancer samples from patients treated at Washington University, they developed a proof of concept test from their signature that identified the aggressive tumors with about 93 percent accuracy.

Working with the Washington University Office of Technology Management, Uppaluri has a patent pending on this technology and recently received funding from the Siteman Cancer Frontier Fund to develop a laboratory test that predicts aggressive disease and would be easily available for any patient diagnosed with head and neck cancer.

“These kinds of tests are available for other types of cancer, most notably breast cancer,” he said. “They are transformative genetic tests that can alter the clinical management of patients, tailoring therapies especially for them. It’s our goal to develop something like that for head and neck cancer.”

Source:
Washington University School of Medicine

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In one study, lower dose treatment for HPV oropharyngeal cancers is successful

Wed, Jun 25, 2014

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Author: Anthony Cmelak, M.D.
Source: medicalnewstoday.com
 

A new study suggests that lowering the dose of radiation therapy for some head and neck cancer patients may improve outcomes and cause fewer long-term side effects.

The research was presented by lead author Anthony Cmelak, M.D., professor of Radiation Oncology at Vanderbilt-Ingram Cancer Center (VICC), during the 50th annual meeting of the American Society of Clinical Oncology (ASCO), held recently in Chicago.

The study focused on patients with newly-diagnosed oropharyngeal cancers related to the human papilloma virus (HPV). More than two-thirds of new head and neck cancer patients have HPV-positive tumors and the number of these patients is on the rise. Cmelak’s prior cooperative group study found that patients with HPV-positive oropharyngeal cancer have significantly longer survival rates than patients whose tumors are HPV negative.

For the new study, 80 HPV-positive patients with stage III, or IVa,b squamous cell cancer of the oropharynx received inductionchemotherapy, including paclitaxel, cisplatin and cetuximab.

After chemotherapy, 62 of the patients showed no sign of cancer and were assigned to receive a 25 percent lower dose of intensity-modulated radiation therapy – an advanced technology that targets the radiation beam more accurately to treat the tumor without harming surrounding tissue. The rest of the patients received a standard IMRT dose. The drug cetuximab was also given to both groups of patients along with the IMRT treatment.

Two years after treatment, the survival for the low-dose IMRT patients was 93 percent. Those who did not have complete resolution of cancer following induction and went on to get full-dose radiation had an 87 percent two-year survival. Eighty percent of the low-dose patients and 65 percent of standard IMRT patients also showed no evidence of tumor recurrence. Ninety-six percent of those who had minimal or no smoking history had no evidence of tumor recurrence after two years following treatment, and long-term side effects were minimal.

The investigators concluded that patients with HPV-positive cancer who had excellent responses to induction chemotherapy followed by a reduced dose IMRT and cetuximab experienced high rates of tumor control and very low side effects particularly for those with a minimal smoking history.

Treating tumors in the delicate head and neck region often causes side effects that can be troublesome and long-lasting, including difficulty swallowing, speech impairment, dry mouth, problems with taste and thyroid issues, so any therapy option that reduces these side effects can have an impact on patient quality of life.

“Treatment for head and neck cancer can be quite grueling, so it’s very encouraging to see we can safely dial back treatment for patients with less aggressive disease and an overall good prognosis, particularly for young patients who have many years to deal with long-term side effects,” said Cmelak.

He noted that lower-dose IMRT is not recommended for patients with HPV-negative cancer or larger tumors.

The authors note that further studies of reduced-dose IMRT in HPV-positive patients are warranted.

Other investigators include Jill Gilbert, M.D., VICC; Shuli Li, Ph.D., Dana Farber Cancer Institute, Boston, Massachusetts; Shanthi Marur, M.D., William Westra, M.D., Christine Chung, M.D., The Johns Hopkins University School of Medicine, Baltimore, Maryland; Weiqiang Zhao, M.D., Ph.D., Maura Gillison, M.D., Ph.D., The Ohio State University, Columbus, Ohio; Julie Bauman, M.D., Robert Ferris, M.D., University of Pittsburgh Cancer Institute; Lynne Wagner, Ph.D., Feinberg School of Medicine, Northwestern University, Chicago, Illinois; David Trevarthen, M.D., Colorado Cancer Research Program, Denver; A. Demetrios Colevas, M.D., Stanford University, California; Balkrishna Jahagirdar, M.D., HealthPartners and Regions Cancer Care Center, St. Paul, Minnesota; Barbara Burtness, M.D., Fox Chase Cancer Center, Philadelphia, Pennsylvania.

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