Monthly Archives: August 2018

Cancer biology graduate student travels ‘ROCKy’ road toward a cure for post-radiation dry mouth

Source: medicalxpress.com
Author: staff, University of Arizona

The United States is in the midst of a head-and-neck cancer epidemic. Although survival rates are relatively high—after treatment with chemotherapy and radiation—survivors can suffer permanent loss of salivary function, potentially leading to decades of health problems and difficulties eating.

It is unknown why the salivary gland sometimes cannot heal after radiation damage, but Wen Yu “Amy” Wong, BS, a University of Arizona cancer biology graduate student, may have taken a step toward solving that riddle.

Radiation often comes with long-term or even permanent side effects. With a head-and-neck tumor in radiation’s crosshairs, the salivary gland might suffer collateral damage.

“When you get radiation therapy, you end up targeting your salivary glands as well,” Wong said. Losing the ability to salivate predisposes patients to oral complications and an overall decrease in their quality of life. “Salivary glands help you digest food, lubricate your mouth and fight against bacteria. After radiation, patients could choke on their food because they can’t swallow. They wake up in the middle of the night because their mouth is so dry. They often get cavities.”

Favorite foods may lose their flavor. “Saliva produces certain ions that help you taste,” she said. “Patients lose the ability to enjoy food. The best steak is very bland to them.”

The quest to restore salivary function in post-radiation head-and-neck cancer patients starts with learning why the salivary gland is unable to heal itself after radiation damage.

Wong’s study may have helped to unravel this mystery. Her team looked closely at two proteins, E-cadherin and β-catenin, which allow communication between cells. Normally, these proteins bind cells together, but after radiation damage, these connections are severed. “Think of them as telephone wires,” Wong said. “Radiation is like lightening hitting a telephone pole. That breaks the ability of one friend to talk to another on the other side of the city.”

Just as a maintenance crew can repair downed telephone poles after a storm, the body is able to heal itself after injury. Unfortunately, in post-radiation dry mouth, salivary glands’ ability to regenerate might be blocked.

In the lab, Wong was able to artificially force the regeneration of salivary glands, allowing her to learn where there are obstructions in the regeneration process. Wong particularly was interested in something called the ROCK pathway, which might go awry in the wake of radiation, blocking E-cadherin and β-catenin from reuniting.

“If I use an inhibitor to prevent this ROCK signaling pathway, these two proteins come back together,” Wong said.

The next step is to learn more about how a defective ROCK pathway blocks salivary glands’ natural ability to regenerate following radiation damage. Unlocking this secret could uncover novel ways to treat or cure post-radiation dry mouth.

Earlier this month, Wong and her co-authors were recognized by the American Physiological Society for their investigation, which was published in June by the American Journal of Physiology—Regulatory, Integrative and Comparative Physiology. Wong, along with Maricela Pier, BS, a research specialist with the UA College of Medicine—Tucson Department of Cellular and Molecular Medicine, and Kirsten Limesand, Ph.D., of the UA Cancer Center and professor of nutritional sciences with the UA College of Agriculture and Life Sciences, was selected for the APSselect award, given to the best articles in physiological research.

Wong selected Dr. Limesand’s lab as her “home base” throughout her graduate studies because “I wanted to connect with a woman in science who understands the difficulties. She was very easy to talk to, and the people in the lab provide a very nurturing environment. She is a great mentor.”

Dr. Limesand takes her role as a mentor seriously, and finds it deeply satisfying.

“Hands down, the most rewarding aspect of my career is training students,” Dr. Limesand said. “They’re our next generation of scientists, tackling the big questions that need to be solved.”

Dr. Limesand is a professor with the UA Cancer Biology Graduate Interdisciplinary Program, which emphasizes translational research to address significant problems relating to cancer development and treatment. Students are prepared for careers in cancer research through an interdisciplinary approach involving faculty members from a wide range of disciplines.

“I have students from cancer biology and physiological sciences, and I’ve been on committees of genetics students and immunobiology students,” said Dr. Limesand. “These diverse perspectives add to the research we’re doing.”

August, 2018|Oral Cancer News|

How early do the effects of smoking start? Earlier than you think

Source:
Author: Julia Mullaney

Smoking’s destructive nature has been known for quite a while. But many people think that a cigarette here and there is okay, or smoking is fine as long as you quit while you’re young. But what’s the truth? How much — and for how long — do you need to smoke before it does irreversible damage to your health? We broke down all the facts.

Put out the cigarette and prolong your life. BrianAJackson/Getty Images

Smoking’s negative effects start with the first puff
The moment you inhale a cigarette, there are instant effects — even if it’s only your first time. The tar in cigarette smoke instantly hits your teeth and starts damaging your enamel. It also hits the gums and starts to do damage. Over time, the gums turn black.

The smoke then hits the throat, where it damages the esophagus lining. In time, this is what leads to throat cancer. It also damages the cilia in your trachea, preventing them from being able to clean away the tar. The smoke then travels to the lungs, where the tar builds up and stays. The tar damages the lungs’ natural cleaning process, which hurts lungs’ ability to work and makes them more susceptible to serious infections.

Finally, inhaling that puff of smoke also means inhaling carbon monoxide, which gets absorbed in the blood stream instantly. You might feel tired and out of breath, and over time this leads to heart disease because it takes away the oxygen that is supposed to travel through your cells and replaces it with carbon monoxide. The nicotine in the cigarette also travels to your brain, which releases “feel good” dopamine and makes you want more. And so the smoking addiction begins.

Smoking’s lasting effects can begin as early as your teen years
In a 2018 study, it was found that teens who smoke and drink alcohol already showed signs of stiffening arteries — something that can lead to serious heart trouble down the road. If you begin smoking as a teen, you don’t even make it out of your teen years before the body starts to be seriously damaged. Smoking and drinking at a young age leads to the progression of atherosclerosis, which occurs when plaque forms on the inner walls of the arteries. Eventually, you might suffer a heart attack, heart disease, and heart failure.

If you start smoking before 25, your lungs will never fully develop
The lungs don’t fully develop until around age 25. If you start smoking as a teen, they never get the chance to reach full size because of the damage caused by cigarettes. Even if you quit, your lungs won’t magically get bigger. However, if you don’t begin smoking until your lungs are fully developed, you can at least reverse most of the damage done to the lungs — but that also depends at what age you quit. According to Thrillist, in order to cut your risk of smoking-related death by 90%, you need to stop smoking before you turn 40. However, the sooner the better.

Smoking for less than one week can inhibit your lungs’ performance
It doesn’t take long for smoking’s effects to damage the body. Actually, it only takes about five to seven days. Since a cigarette fills your lungs with dangerous chemicals, the lungs can’t make a full recovery. And if you keep smoking — say, a few times per day — the lungs never have a chance to get rid of the gunk that filled them. After just a little while, those chemicals will harbor in the lungs and cause lasting damage. Plus, they can lead to various cancers.

But quitting still outweighs not quitting, despite the lasting effects
While the lungs of a smoker will never as healthy as smokeless lungs, the benefits of quitting greatly outweigh not quitting. Your body does have the ability to bounce back. After being smoke-free for just six hours, the carbon monoxide levels in your body decline and the heart starts to function more normally. After a couple of months, your lung function can improve by up to 30%, and you won’t have the horrid cough you’ve had for years. After nine months, your heart is almost totally out of the danger zone (this does depend on age, though). Over time, the body rebuilds itself and heals the damage.

August, 2018|Oral Cancer News|

DCD: Oropharyngeal squamous cell carcinoma now and most common HPV associated with cancer

In 2015, oropharyngeal squamous cell carcinoma surpassed cervical cancer as the most common HPV-associated cancer in the U.S., with 15,479 cases among men and 3,438 cases among women, according to data from the CDC published in Morbidity and Mortality Weekly Report.

The report also showed that rates of HPV-related anal squamous cell carcinoma and vulvar cancer increased over the past 15 years, whereas rates of HPV-related cervical cancer and vaginal squamous cell carcinoma decreased.

“Although smoking is a risk factor for oropharyngeal cancers, smoking rates have been declining in the United States, and studies have indicated that the increase in oropharyngeal cancer is attributable to HPV,” Elizabeth A. Van Dyne, MD, epidemic intelligence services officer in division of cancer prevention and control at the National Center for Chronic Disease Prevention and Health Promotion of the CDC, and colleagues wrote.

“In contrast to cervical cancer, there currently is no U.S. Preventive Services Task Force recommended screening for other HPV-associated cancers,” they added.

The trends in HPV-related cancers report included data from 1999 to 2015 from cancer registries — CDC’s National Program of Cancer Registries and NCI’s SEER program — covering 97.8% of the U.S. population.

The CDC reported 30,115 new cases of HPV-associated cancers in 1999 compared with 43,371 new cases in 2015.

During the study period, researchers observed a 2.7% increase in rates of oropharyngeal squamous cell carcinoma among men and a 0.8% increase among women. Rates of anal squamous cell carcinoma increased by 2.1% among men and 2.9% among women.

Among women, researchers observed a 1.6% decrease in HPV-related cervical cancer and a 0.6% decrease in rates of HPV-related vaginal squamous cell carcinoma. Rates of vulvar squamous cell carcinoma increased by 1.3%.

Rates of penile squamous cell carcinoma remained stable from 1999 to 2015.

Overall, rates of HPV-related cancers varied by age and race/ethnicity.

Researchers observed a 4% increase in the rate of oropharyngeal squamous cell carcinoma among men aged 60 to 69 years compared with a 0.8% increase among men aged 40 to 49 years.

For anal squamous cell carcinoma, the largest increases occurred among women aged 50 to 69 years (4.6% to 4.8%) and men aged 50 to 59 years (4%).

Several factors contribute to the increased incidence of oropharyngeal and anal squamous cell carcinomas, including changes in sexual behavior.

“Unprotected oral sex and receptive anal sex are risk factors for HPV infection,” the researchers wrote. “White men have the highest number of lifetime oral sex partners and report first performing oral sex at a younger age compared with other racial/ethnic groups; these risk factors could be contributing to a higher rate of oropharyngeal squamous cell carcinoma among white men than other racial/ethnic groups.”

Cervical cancer rates remained stable among women aged 35 to 39 years; however, younger and older woman demonstrated decreases ranging from 1.2% to 4.2%.

Cervical carcinoma rates decreased across all racial/ethnic groups, although decreases appeared more prominent among Hispanics than non-Hispanics (3.4% vs. 1.5%).

“The decline in cervical cancer from 1999 to 2015 represents a continued trend since the 1950s as a result of cancer screening,” the researchers wrote. “Rates of cervical carcinoma in this report decreased more among Hispanics, American Indian/Alaska Natives and blacks than other groups; however, incidence rates were still higher among Hispanics and blacks than among whites in 2015. These persistent disparities in incidence suggest that health care delivery needs of some groups are not fully met.”

The limitations of the report included the fact that the cancer registries do not routinely determine the HPV status of cancers and that race/ethnicity data was derived from medical records.

“Further research to understand the progression from HPV infection to oropharyngeal cancer would be beneficial,” the researchers wrote. “Continued surveillance through high-quality registries is important to monitor changes in HPV-associated cancer incidence.” – by Cassie Homer

August, 2018|Oral Cancer News|

E-cigarettes ‘could give you mouth cancer by damaging your DNA’

Source: metro.co.uk
Author: Zoe Drewett

Researchers say vaping could lead to an increased risk of developing mouth cancer. A study carried out by the American Chemical Society found evidence to suggest using e-cigarettes raises the level of DNA-damaging compounds in the mouth. If cells in the body are unable to repair the DNA damage after vaping, the risk of cancer can increase, the study claims.

The long-term effects of e-cigarettes are not yet known but researchers say they should be investigated further (Picture: PA)

The researchers admit the long-term health effects of using electronic cigarettes are still unknown. Researcher Dr Romel Dator said: ‘We want to characterize the chemicals that vapers are exposed to, as well as any DNA damage they may cause.’

Since they were introduced in 2004, e-cigarettes have been marketed as a safer alternative to smoking. But the team carrying out the study claim genetic material in the oral cells of people who vape could be altered by toxic chemicals. E-cigarettes work by heating a liquid – which usually contains nicotine – into an aerosol that the user inhales. It is often flavoured to taste like fruit, chocolate or bubblegum.

‘It’s clear that more carcinogens arise from the combustion of tobacco in regular cigarettes than from the vapor of e-cigarettes,’ Silvia Balbo, the project’s lead investigator said. ‘However, we don’t really know the impact of inhaling the combination of compounds produced by this device. ‘Just because the threats are different doesn’t mean that e-cigarettes are completely safe.’ The latest study, due to be presented at a meeting of the American Chemical Society this week, analysed the saliva and mouth cells of five e-cigarette users before and after a 15-minute vaping session.

Researchers found levels of the toxic chemicals formaldehyde, acrolein and methylglyoxal had increased after vaping. Now they plan to follow up on the preliminary study with a larger one involving more e-cigarette users. They also want to see how the level of toxic chemicals differs between e-cigarette users and regular cigarette smokers.

According to a 2016 report by the US Surgeon General, 13.5% of middle school students, 37.7% of high school students and 35.8% of 18 to 24-year-olds have used e-cigarettes, compared with 16.4% of adults aged 25 and over. Ms Balbo, a professor at the Masonic Cancer Center at the University of Minnesota, said:

‘Comparing e-cigarettes and tobacco cigarettes is really like comparing apples and oranges.  The exposures are completely different. ‘We still don’t know exactly what these e-cigarette devices are doing and what kinds of effects they may have on health, but our findings suggest that a closer look is warranted.’

 

August, 2018|Oral Cancer News|

Why a patient paid a $285 copay for a $40 drug

Source: pbs.org
Author: Megan Thompson

Two years ago Gretchen Liu, 78, had a transient ischemic attack — which experts sometimes call a “mini stroke” — while on a trip to China. After she recovered and returned home to San Francisco, her doctor prescribed a generic medication called telmisartan to help manage her blood pressure.

Liu and her husband Z. Ming Ma, a retired physicist, are insured through an Anthem Medicare plan. Ma ordered the telmisartan through Express Scripts, the company that manages pharmacy benefits for Anthem and also provides a mail-order service.

The copay for a 90-day supply was $285, which seemed high to Ma.

“I couldn’t understand it — it’s a generic,” said Ma. “But it was a serious situation, so I just got it.”

A month later, Ma and his wife were about to leave on another trip, and Ma needed to stock up on her medication. Because 90 days hadn’t yet passed, Anthem wouldn’t cover it. So during a trip to his local Costco, Ma asked the pharmacist how much it would cost if he got the prescription there and paid out of pocket.

The pharmacist told him it would cost about $40.

“I was very shocked,” said Ma. “I had no idea if I asked to pay cash, they’d give me a different price.”

Ma’s experience of finding a copay higher than the cost of the drug wasn’t that unusual. Insurance copays are higher than the cost of the drug about 25 percent of the time, according to a study published in March by the University of Southern California’s Schaeffer Center for Health Policy and Economics.

USC researchers analyzed 9.5 million prescriptions filled during the first half of 2013. They compared the copay amount to what the pharmacy was reimbursed for the medication and found in the cases where the copay was higher, the overpayments averaged $7.69, totaling $135 million that year.

USC economist Karen Van Nuys, a lead author of the study, had her own story of overpayment. She discovered she could buy a one-year supply of her generic heart medication for $35 out of pocket instead of $120 using her health insurance.

Van Nuys said her experience, and media reports she had read about the practice, spurred her and her colleagues to conduct the study. She had also heard industry lobbyists refer to the practice as “outlier.”

“I wouldn’t call one in four an ‘outlier practice,’” Van Nuys said.

“You have insurance because your belief is, you’re paying premiums, so when you need care, a large fraction of that cost is going to be borne by your insurance company,” said Geoffrey Joyce, a USC economist who co-authored the study with Van Nuys. “The whole notion that you are paying more for the drug with insurance is just mind boggling, to think that they’re doing this and getting away with it.”

Joyce told PBS NewsHour Weekend the inflated copays could be explained by the role in the pharmaceutical supply chain played by pharmacy benefit managers, or PBMs. He explained that insurers outsource the management of prescription drug benefits to pharmacy benefit managers, which determine what drugs will be covered by a health insurance plan, and what the copay will be. “PBMs run the show,” said Joyce.

In the case of Express Scripts, the company manages pharmacy benefits for insurers and also provides a prescription mail-delivery service.

Express Scripts spokesperson Brian Henry confirmed to PBS NewsHour Weekend the $285 copay that Ma paid in 2016 for his wife’s telmisartan was correct, but didn’t provide an explanation as to why it was so much higher than the $40 Costco price. Henry said that big retailers like Costco sometimes offer deep discounts on drugs through low-cost generics programs.

USC’s Geoffrey Joyce said it is possible that Costco negotiated a better deal on telmisartan from the drug’s maker than Express Scripts did, and thus could sell it for cheaper. But, he said, the price difference, $285 versus $40, was too large for this to be the likely explanation.

Joyce said it is possible another set of behind-the-scenes negotiations between the pharmacy benefit managers and drug makers played a role. He explained that drug manufacturers will make payments to pharmacy benefit managers called “rebates.”

Rebates help determine where a drug will be placed on a health plan’s formulary. Formularies often have “tiers” that determine what the copay will be, with a “tier one” drug often being the cheapest, and the higher tiers more expensive.

Pharmacy benefit managers usually take a cut of the rebate and then pass them on to the insurer. Insurers say they use use the money to lower costs for patients.

Joy said a big rebate to a pharmacy benefit manager can mean placement on a low tier with a low copayment, which helps drives more patients to take that drug.

In the case of Ma’s telmisartan, Express Scripts confirmed to PBS NewsHour Weekend that the generic drug was designated a “nonpreferred brand,” which put it on the plan’s highest tier with the highest copay.

Joyce said sometimes pharmacy benefit managers try to push customers to take another medication for which it had negotiated a bigger rebate. “It’s financially in their benefit that you take the other drug,” said Joyce. “But that’s of little consolation to the person who just goes to the pharmacy with a prescription that their physician gave them.”

But Joyce said the pharmacy benefit managers also profit when collecting copays that are higher than the cost of the drug.

In recent years, the industry has taken a lot of heat from the media and elected officials over a controversial practice called “clawbacks.” This happens when a pharmacist collects a copay at the cash register that’s higher than the cost of the drug, and the pharmacy benefit manager takes most of the difference.

August, 2018|Oral Cancer News|

Smoking, cancer, heart disease, and the oral-systemic link: Where we are with research

Source: www.dentistryiq.com
Author: Richard H. Nagelberg, DDS

Dr. Richard Nagelberg examines the links between smoking, lung cancer, and heart disease, as well as the types of research and studies that established the strength of their credibility over time. Likewise, he considers where we are today with the link between oral health and overall health as he evaluates the current state of oral-systemic research.

Perhaps the most universally accepted facts in health care are the detrimental effects of tobacco, particularly cigarette smoking, for nearly every part of the body. It is safe to say that no one disputes the direct causal links between cigarette smoking, lung cancer, and heart disease. Listed below are only two statements regarding the state of this knowledge.

✔️The scientific evidence is incontrovertible: inhaling tobacco smoke, particularly from cigarettes, is deadly. Since the first Surgeon General’s Report in 1964, evidence has linked smoking to diseases of nearly all organs of the body. (surgeongeneral.gov. June 21, 2018)

✔️Smoking is by far the biggest preventable cause of cancer. Thanks to years of research, the links between smoking and cancer are now very clear. Smoking accounts for more than 1 in 4 UK cancer deaths, and 3 in 20 cancer cases. (cancerresearchuk.org)

There is a boatload of research supporting this link. However, there has never been one large-scale double-blinded interventional study demonstrating that smoking causes lung cancer and heart disease. The fact that this link exists is based on the cumulative results of numerous smaller studies over a long period of time.

The reasons are the same for the lack of large-scale interventional studies investigating the link between smoking, lung cancer, and heart disease, among others, as well as that between the mouth and the body. These studies are too costly and full of variables that are difficult to control in a study spanning 20 years or more. It is the cumulative results of research that will demonstrate the strength of the link between oral health and overall health, rather than one definitive piece of research.

While the risks of smoking were being investigated, there were naysayers who doubted the emerging results. In fact, there was substantial skepticism within the medical community about whether the apparent increase in cancer deaths was real or the result of better diagnosis. The study that is credited with the beginning of the stop-smoking movement was published in 1954 by Hammond and Horn. Their paper ended with: “[we are of the opinion that the associations found between regular cigarette smoking and death rates from diseases of the coronary arteries and between regular cigarette smoking and death rates from lung cancer reflect cause and effect relationships.]” (1)

At present, we are in the middle of the oral-systemic research, waiting until a sufficient body of research provides incontrovertible evidence one way or the other.

Reference
1. Hammond EC, Horn D, The relationship between human smoking habits and death rates: a follow-up study of 187,766 men. J Am Med Assoc. 1954;155(15):1316-1328.

August, 2018|Oral Cancer News|

Study: Cetuximab, radiation inferior to standard HPV throat cancer treatment

Source: upi.com
Author: Allen Cone

Treating HPV-positive throat cancer with cetuximab and radiation had worse overall and progression-free survival results compared with the current method of treatment with radiation and cisplatin, the National Institutes of Health revealed Tuesday.

The trial, which was funded by the National Cancer Institute, was intended to test whether the combination would be less toxic than cisplatin but be just as effective for human papillomavirus-positive oropharyngeal cancer. The trial, which began in 2011, enrolled 849 patients at least 18 years old with the cancer to receive cetuximab or cisplatin with radiation. The trial is expected to finish in 2020.

Cetuximab, which is manufactured under the brand name Erbitux by Eli Lilly, and cisplatin, which as sold as Platinol by Pfizer, are used in chemotherapy.

The U.S. Food and Drug Administration had approved cetuximab with radiation for patients with head and neck cancer, including oropharyngeal cancer.

HPV, which is transmitted through intimate skin-to-skin contact, is the leading cause of oropharynx cancers, which are the throat at the back of the mouth, including the soft palate, the base of the tongue and the tonsils. Most people at risk are white, non-smoking males age 35 to 55 — including a 4-to-1 male ratio over females — according to The Oral Cancer Foundation.

The NIH released the trial results after an interim analysis showed that cetuximab with radiation wasn’t as effective.

In a median follow-up of 4.5 years, the test combination was found to be “significantly inferior” to the cisplatin method.

“Clinical trials designed to test less toxic treatment strategies for patients without compromising clinical benefit are a very important area of interest for NCI and the cancer research community,” said Dr. Shakun Malik, of NCI’s Division of Cancer Treatment and Diagnosis.

Toxic side effects were different, with adverse events of renal toxicity, hearing loss and bone marrow suppression more common in patients in the cisplatin group and body rash more frequent in the cetuximab method.

For patients who cannot tolerate cisplatin, cetuximab with radiation is an accepted standard of care.

“The goal of this trial was to find an alternative to cisplatin that would be as effective at controlling the cancer, but with fewer side effects,” lead investigator Dr. Andy Trotti, of the Moffitt Cancer Center in Tampa, Fla., said in a press release. “We were surprised by the loss of tumor control with cetuximab.”

August, 2018|Oral Cancer News|

Hundreds of Researchers From Harvard, Yale and Stanford Were Published in Fake Academic Journals

Source: motherboard.vice.com
Author: Daniel Oberhaus

In the so-called “post-truth era,” science seems like one of the last bastions of objective knowledge, but what if science itself were to succumb to fake news? Over the past year, German journalist Svea Eckert and a small team of journalists went undercover to investigate a massive underground network of fake science journals and conferences.

In the course of the investigation, which was chronicled in the documentary “Inside the Fake Science Factory,” the team analyzed over 175,000 articles published in predatory journals and found hundreds of papers from academics at leading institutions, as well as substantial amounts of research pushed by pharmaceutical corporations, tobacco companies, and others. Last year, one fake science institution run by a Turkish family was estimated to have earned over $4 million in revenue through conferences and journals.

The story begins with Chris Sumner, a co-founder of the nonprofit Online Privacy Foundation, who unwittingly attended a conference organized by the World Academy of Science, Engineering and Technology (WASET) last October. At first glance, WASET seems to be a legitimate organization. Its website lists thousands of conferences around the world in pretty much every conceivable academic discipline, with dates scheduled all the way out to 2031. It has also published over ten thousand papers in an “open science, peer reviewed, interdisciplinary, monthly and fully referred [sic] international research journal” that covers everything from aerospace engineering to nutrition. To any scientist familiar with the peer review process, however, WASET’s site has a number of red flags, such as spelling errors and the sheer scope of the disciplines it publishes.

Sumner attended the WASET conference to get feedback on his research, but after attending it became obvious that the conference was a scam. After digging into WASET’s background, Sumner partnered with Eckert and her colleague Till Krause, who adopted fictitious academic personas and began submitting papers to WASET’s journal. The first paper to get accepted was titled “Highly-Available, Collaborative, Trainable Communication-a policy neutral approach,” which claims to be about a type of cryptoanalysis based on “unified scalable theory.” The paper was accepted by the WASET journal with minimal notes and praise for the authors’ contribution to this field of research.

There was just one problem: The paper was pure nonsense that had been written by a joke software program designed by some MIT students to algorithmically generate computer science papers. It was, in a word, total bullshit.

As detailed in a talk this year at Def Con, last year Eckert and Krause attended a conference organized by WASET in London to present their bullshit paper. The two journalists went in disguise as the fictitious academics Dr. Cindy Poppins and Dr. Edgar Munchhausen. When they arrived, they discovered the two-hour “conference” was actually just a half-dozen people in a room with a projector, all of whom had paid hundreds of dollars for the privilege. When Eckert and Krause approached Bora Ardil, the conference organizer, to learn more about WASET, they said he was cagey and declined to give straight answers about his affiliation with the conference. According to Eckert, he claimed he was just a doctoral student working with WASET.

After this initial foray into the world of predatory publishing, Eckert and Munchhausen partnered with Sumner to dig deeper into WASET. By analyzing 83 domain names affiliated with WASET and its conferences, Eckert and her colleagues discovered that the predatory journal network was a family con run by Cemal Ardil, his daughter Ebru and son Bora. Based on the WASET website, the Ardils have been running this con since 2007.

According to Eckert and her colleagues, WASET is just a single predatory publishing platform,but it hosts over 5,000 events around the world annually and publishes hundreds of papers in its online “journals.” WASET charges hundreds of dollars to publish in its journals and attend its conferences, which netted the Ardils an estimated $4.1 million in 2017 alone.

Yet WASET doesn’t hold a candle to OMICS Publishing Group, which is likely the largest predatory publisher in the world. In 2016, the Federal Trade Commission filed a suit against OMICS for “deceiving academics and researchers about the nature of its publications and hiding publication fees ranging from hundreds to thousands of dollars.” Last November, the FTC granted a preliminary injunction against OMICS that prohibits the company from “falsely representing that their journals engage in peer review, that their journals are included in any academic journal indexing service, or any measurement of the extent to which their journals are cited.”

By scraping the OMICS and WASET websites, Eckert and her colleagues discovered tens of thousand of abstracts for fake scientific papers. India accounted for nearly 15,000 of these abstracts alone, but researchers from the United States accounted for the second highest submission rate—approximately 10,000 American papers were submitted to OMICS journals and another 3,000 to WASET journals.

So who are the people submitting to these conferences? According to Eckert, these range from academics trying to boost their publishing profile to scientists affiliated with companies who want to boost their scientific cred by having some publications under their belt. A distressing number of these academics come from elite American universities, as well. Eckert and her colleagues discovered 162 papers submitted to WASET and OMICS journals from Stanford, 153 papers from Yale, 96 from Columbia, and 94 from Harvard in the last decade. Yet according to Krause, “this goes way beyond academia.”

“It’s one thing for professors to try to polish their publication list and get more money or reputation, but it can be used for many other purposes,” Krause said last weekend during a talk at Def Con. “We as a society have this feeling that if something is scientifically proven and published, it has value. Usually science does just that, but in the case of the predatory journals it is quite different.”

The danger of these journals is that they can be used by companies to provide scientific justification for unproven treatments. One notable example of this is the case of the company First Immune, which had published dozens of “scientific” papers in these predatory journals lauding the effectiveness of an unproven cancer treatment called GcMAF. GcMAF is a protein that was marketed First Immune starting in 2010, but came under investigation shortly thereafter for running an unlicensed medical facility. The CEO of First Immune, David Noakes, will stand trial in the UK later this year for conspiracy to manufacture a medical product without a license.

The problem is that these predatory journals gave First Immune an air of legitimacy for desperate patients with cancer. This predicament is illustrated in the autobiography of a famous German media personality Miriam Pielhau, who died of breast cancer in 2016. In Dr. Hope, Pielhau describes her battle with cancer and how she settled on GcMAF as a last resort and cited medical studies published in predatory journals as the basis of her decision.

The ease with which people can be duped into taking false medical advice was driven home by Eckert and co, who submitted a research paper to the WASET Journal of Integrative Oncology that claimed that bees wax was a more effective cancer treatment than chemotherapy. The paper was accepted and published in the journal with minimal revisions.

As detailed by Eckert and her colleagues, similar tactics are used to publish studies and host conferences funded by major corporations as well, including the tobacco company Philip Morris, the pharmaceutical company AstraZeneca, and the nuclear safety company Framatone. When the predatory journals publish these companies’ research, they can claim it is “peer reviewed” and thereby grant it an air of legitimacy.

Taken together, the predatory publishers investigated by Eckert and her colleagues only represent about 5 percent of the total research published every year. While this doesn’t pose an existential threat to science as a truth-seeking process, it does work to erode public trust in legitimate research.

Eckert, Krause, and Sumner argue that that the rise of predatory journals makes it imperative that the general public, researchers, and academics stay on their guard to combat the proliferation of bogus research. Science, like democratic politics, has been responsible for some of the greatest advances in the wellbeing of humanity, but that doesn’t mean it’s immune to being undermined by a small group of persistent bad faith actors.

August, 2018|Oral Cancer News|

How ablation destroys cancer to prolong lives

Source: The Guardian
Author: David Cox

Seven years ago, when Heather Hall was informed by her oncologist that her kidney cancer had spread to the liver, she initially assumed she had just months to live. “I’d been on chemotherapy for a while, but they’d done a CT scan and found three new tumours,” she says. “But they then said that, because the tumours were relatively small, they could try to lengthen my prognosis by removing them with ablation.”

Hall underwent a course of microwave ablation, a minimally invasive treatment where surgeons use hollow needles to deliver intense, focused doses of radiation to heat each tumour until it is destroyed. While ablation technologies – they also commonly include radiofrequency ablation and cryoablation, which destroys tumours using intense cold – are not tackling the underlying cause of the disease, their impact can be enormous as they relieve pain and often prolong survival for many years, all at a low cost.

Studies based on data gathered over the past 10 years show an increasing number of cases of terminally ill patients who have lived for well over a decade after being treated with repeated ablations. Hall’s treatment was successful, but two years later, another two tumours had appeared in her liver, in different locations. Once again they were removed with microwave ablation. Over the past seven years, she has had four separate treatments. “There’s some pain in the immediate aftermath and I’ve felt quite ill for a week afterwards,” she says. “But it seems to have slowed down the progression of the disease, and I still have full function of my liver. With surgery, they would have had to cut a section of it away.”

While there have been many breakthroughs in cancer treatment heralded by the media in recent years – most notably the advances in immunotherapy and combination therapies – the considerable advances in ablation technology and resulting impact on patient survival, have consistently slipped beneath the radar. Not so long ago, the only option for patients such as Hall would have been full or partial removal of an organ, greatly reducing quality of life. But now, with increasingly powerful and efficient devices, surgeons are able to destroy drug-resistant tumours in a growing number of diseases ranging from sarcomas to prostate cancer.

“When we were first using ablation we could only treat the simplest tumours – for example, the ones in the middle of the liver, away from the blood vessels, because the devices were less powerful and predictable,” says Matthew Callstrom, a professor of radiology at the Mayo Clinic, Minnesota. “But now, for example, with microwave ablation – which works by radiating an energy field out of the tip of the needle into the tumour, heating the water within the cancer cells until they are destroyed – you can tune the shape and diameter of that field to prescribe exactly how deep it goes into the tissue. This means we can safely go after more and more complex tumours.”

Major studies published in the past couple of years have confirmed the survival benefits. Last year, the results of the Clocc trial – a five-year study of 119 patients across 22 centres in Europe – showed that patients with colorectal cancer that had metastasised to the liver and who received ablation in addition to drug treatment lived significantly longer on average than those who received drugs alone.

“We work closely with oncologists to determine who is most likely to benefit from this and who isn’t,” says Andreas Adam, professor of interventional radiology at King’s College London. “But it can have huge benefits. For example, I had a patient with breast cancer that had spread to the liver. I ablated the tumours, destroyed them completely and every few months or years, another tumour would develop and I’d ablate again. She went on to live for almost 10 years.”

With ablation treatment allowing many patients to live for far longer, it has the potential to change the perspective on some diagnoses. Patients with metastatic disease who go on to live for another decade or more in relatively little discomfort, often come to view their condition as more like a chronic illness. “It’s a strange feeling because you are still living with an illness which is likely to be terminal sooner rather than later,” Hall says. “But it’s no longer in the forefront of your mind. I’ve even been able to return to work part-time.”

However, not every patient with metastatic disease is a suitable candidate for ablation. Surgeons typically only use the technique on patients with 10 tumours or fewer. Any more, and the only viable options are treatments such as chemotherapy or immunotherapy. “You wouldn’t dream of ablating 50 tumours, because if someone has 50 visible tumours, it’s likely that they have another 100 developing that are not yet visible, and so they need drug treatment to treat the disseminated disease,” Adam says.

But in the coming years, ablation is likely to become available to more and more patients, allowing surgeons to tackle cancers in ever more complex locations.

Among the most promising methods is a technology called irreversible electroporation, which involves electrodes being inserted through the skin into a tumour, allowing a high voltage to be generated across the cancer cell membranes, causing them to self-destruct. This is only offered by a small handful of specialised centres in the world, but is expected to become more widespread over the next decade. “It’s a non-thermal approach, so you can go into more sensitive areas such as the pancreas, or ablate tumours which are in the centre of the liver,” Callstrom says.

One day, surgeons may even be able to ablate the most difficult cancers of all – deep brain tumours. The Israeli company Insightec is developing a device that can use focused ultrasound to destroy brain lesions. Because these tiny pulses of energy can be detected on MRI scanners, surgeons can calibrate them to the exact millimetre. “Each pulse generates a single ablation the size of a grain of rice,” Callstrom says. “Because it’s so tiny this allows you to basically tattoo the tumour and so avoid the boundary to any blood vessels or neurons.”

So for the many patients who have cancer that doesn’t respond to any form of drug treatment, there is now often a way of managing and prolonging their lives, which wasn’t possible before.

“The results of these studies have completely changed the thinking regarding some cancers,” Callstrom says. “With patients with metastatic sarcomas, for instance, people used to think that if the drugs failed, that was that. But now we can monitor them. And every time new tumours pop up, we ablate them.”

August, 2018|OCF In The News|

The surge in throat cancer, especially in men

Source: newswise.com
Author: UC Davis Comprehensive Cancer Center

Humanpapilloma virus (HPV) is now the leading cause of certain types of throat cancer. Dr. Michael Moore, director of head and neck surgery at UC Davis and an HPV-related cancer expert, answers some tough questions about the trend and what can be done about it.

Q: What is HPV and how is it related to head and neck cancers?

A: There are about 150 different types of HPV, but HPV 16 is the one that most frequently causes cancers that affect the tissue in the oropharynx, which includes back of the throat, soft palate, tonsils and the back or base of the tongue. You can get non-cancerous lesions from other types of HPV that look like warts in the nose, mouth or throat, called papillomas. Some can develop in childhood just from exposure early in life. Some develop later in life and only occasionally turn into cancer.

Q: How do you get HPV?

A: HPV can spread from mother to her baby around the time of delivery. It also spreads through unprotected vaginal, anal or oral sex, and even open-mouth kissing. Some people have been found to be infected without an obvious cause.

Q: How does HPV cause cancer?

A: Most people who are infected clear the virus on their own. In a small group of people it hangs around and causes a persistent infection. Around 1% of US adults have a persistent HPV 16 infection, and in a small subset of these individuals the DNA of the virus incorporates itself into the DNA of the person infected and can start to make proteins that then predispose that person to developing cancer.

Q: How prevalent are HPV-related throat cancers?

A: Traditionally, the risk factors for head and neck cancers were tobacco and alcohol use, but over the last 20 or 30 years we found the rates of those cancers going down because smoking rates have gone down. Meanwhile, the incidence of head and neck cancers related to HPV has gone up more than 200 percent over this time period. This increase has been so dramatic that HPV-related throat cancer has recently surpassed cervical cancer as the most common HPV-related cancer in the United States.

Q: Why are the rates going up?

A: Unlike with cervical cancer, in which the PAP smear is highly effective at finding potentially cancerous or pre-cancerous cells, there is no good screening test for these head and neck cancers. Currently, the use of swab tests for HPV is effective in finding out if you have an HPV infection, but not in determining if the infection will be persistent or if you will ever develop cancer. As a result, such tests are not endorsed as a way to screen for these tumors.

Q: Do both men and women get thee cancers?

A: Men are four times more likely to be diagnosed with an HPV-related head and neck cancer. Researchers don’t yet know why. It may have to do with sexual practices or related to the types of exposure they receive. The local or systemic immune system may also play a role.

Q: Can HPV-related head and neck cancers be prevented?

A: We have a very effective vaccine against HPV, and we know the vaccine can prevent oral HPV infections. In fact, studies have shown that the vaccine is 93 percent effective in preventing the oral infections that cause head and neck cancers. We recommend two injections for adolescents under age 15 and three for those over 15. The vaccine is recommended for children age 10-11, but vaccination can start in children as young as age 9, and in boys as late as age 21 and in girls as late as 26. It is also important to maintain safe sexual practices and avoid other potentially cancer-causing exposures such as tobacco, alcohol and marijuana.

Q: What are the main barriers to vaccination?

A: Studies have shown that the biggest reason kids don’t get it is lack of physician endorsement or recommendation. The American Cancer Society is trying to change that, asking physicians to introduce it to parents when they discuss other adolescent vaccines. There has also been concern that parents aren’t comfortable talking about sexuality with their children, and some have worried that if the child gets the vaccine they are more likely to be sexually active. That theory has been debunked in scientific studies.

Q: How safe and effective is the HPV vaccine?

A: It has a very safe track record and is continually undergoing evaluation to look for potential side effects. While there are some risks with any vaccine, one of the most common side effects is that patients may feel light headed after being vaccinated, and it is recommended they are observed for 15 minutes afterward.

August, 2018|Oral Cancer News|