Monthly Archives: June 2017

A New Theory on How Researchers Can Solve the Reproducibility Crisis: Do the Math – The Chronicle of Higher Education

Posted: June 29, 2017 at 10:46 am

Lionel Cironneau, AP Images

Jeanne Calment of France was believed to be the worlds longest lived person when she died in 1997 at age 122. A recent headline-grabbing study about the limits of the human life span has drawn rebuttals with implications for how universities and scientists might approach the reproducibility crisis in research.

From the beginning, it seemed like a difficult prediction.

In an article published last October in Nature, three researchers affiliated with the Albert Einstein College of Medicine in New York City said they had crunched the numbers and concluded that humans will never consistently live much beyond 115 years.

"From now on, this is it," one of the three authors, Jan Vijg, a professor of genetics at Albert Einstein, told The New York Times one of several major news outlets that helped promote the sobering news. "Humans will never get older than 115."

With more statistical expertise on research teams, one expert argues, scientists could think with more nuance about whether a research finding is significant.

But almost immediately, the conclusion was attacked by numerous critics citing various problems with the Albert Einstein teams statistical analysis. That criticism cascaded Wednesday when Nature published another five rebuttals.

Among the allegations: Mr. Vijg and his partners failed to properly consider what statisticians call the "null hypothesis." In this case, Bryan G. Hughes and Siegfried Hekimi of McGill University explained in one of the critiques, applying the null hypothesis means statistically including the possibility that the maximum human life span actually will continue to increase.

"There are strong statistical grounds to question the validity of their conclusions," wrote another team, comprising Maarten P. Rozing, Thomas B.L. Kirkwood, and Rudi G.J. Westendorp of the University of Copenhagen. "There might be a limit to human lifespan, but we believe that their results provide no evidence," wrote a third, Adam Lenart and James W. Vaupel of the University of Southern Denmark.

Mr. Vijg stands by his work. The "real problem," he said, "is that some people get hysterical when someone openly sheds doubt on the idea that we can live forever, or at least much longer than we do now."

As scientists across various fields move through a period of soul-searching over the disturbing number of studies that apparently cannot be reproduced, the leading suspects include industry bias, financial and career pressures, poor study design, and wide variations in research methodologies, equipment, and standards.

But the conversation over the study on aging points to another possibility: that too much research is hamstrung by a lack of pure statistical ability. Universities, scientists, and advocacy groups may have overlooked the seriousness of that problem as they hunt for more complex or nefarious causes of the reproducibility crisis.

Cory Fournier, an adjunct instructor in mathematics at the University of Massachusetts at Lowell, came to that conclusion earlier this year, after he cobbled together $1,000 in scarce union funds to journey to a big national conference on scientific reproducibility.

Mr. Fournier said he made the trip to the National Academy of Sciences headquarters in Washington, D.C., expecting to commune with fellow statisticians. After all, he reasoned, there are lots of ways that research errors can be tied to poor statistical analyses including haste-induced shortcuts, technical confusion, and outright manipulation.

Instead, upon arrival in the conference hall, he noticed a strange absence. "I dont believe that I met any other statisticians," he said.

At least one did speak at the three-day event Giovanni Parmigiani, a professor of biostatistics at Harvard University. And Mr. Parmigiani and other experts assembled by the National Academies did cite statistical rigor as one of the key areas needing improvement.

But Mr. Fournier sees an oversight at a more fundamental level. In all fields, he said, researchers need either to develop a working knowledge of statistics or to include someone with statistical expertise on their research teams.

And with that expertise, scientists should think with more statistical nuance about questions such as whether a research finding is statistically significant, Mr. Fournier said.

Many studies answer that question with a simple "yes" or "no," relying on a calculation called a p-value to do so. For a p-value of .05, as is typical, a studys finding will be deemed significant if researchers identify a 95-percent chance that it is genuine.

More useful, Mr. Fournier said, would be a practice in which yes-or-no declarations would be replaced in journal articles by more specific estimates of how likely it is that a particular research observation did not just randomly occur: such as 1 in 20, or 1 in 100, or 1 in 1,000.

That numerical specificity of estimates may already exist inside many articles, Mr. Fournier said. But highlighting it in words, he said, should help emphasize what statisticians know to be true science cannot make definitive yes-or-no declarations in most cases and perhaps also encourage the publication of studies now abandoned in the belief they failed to show a useful outcome. Better statistical expertise also could help scientists construct experiments that are more likely to be reliable in the first place, he said.

One of the conference organizers, Victoria Stodden of the University of Illinois at Urbana-Champaign, said she recognizes the ways that biases of various types financial conflicts of interest, academic promotion incentives, and the allure of fame can contribute to irreproducibility problems in science.

But Ms. Stodden, an associate professor of information sciences, said she agrees that the ongoing misuse of statistics is a broader problem. While researchers may need to work harder to include statisticians on their teams, she said, statisticians also must to work harder to study how they could be more helpful to their interdisciplinary colleagues.

"Developing a research agenda within the statistical community to address issues surrounding reproducibility is imperative," she said.

For his part, Mr. Vijg isnt convinced his team failed basic statistical analysis. His paper used records from sources that included the International Database on Longevity and the Human Mortality Database. It then made calculations suggesting that, while average human life expectancy may continue to increase, the maximum of age of the oldest surviving humans will not substantially move beyond about 115 years.

"We went through a highly experienced and reputed statistician before submitting the work," Mr. Vijg said in a written exchange about the criticisms. At the same time, he argued that resolving differences in findings between competing labs is less a matter of procuring advanced statistical expertise and more a matter of the two groups getting together and identifying variations in their experimental conditions.

"Look, statistics is a tool, nothing more," he said. "It certainly is not the arbiter of scientific truth."

Look, statistics is a tool, nothing more. It certainly is not the arbiter of scientific truth.

An author of another of the five critiques published Wednesday by Nature, Nicholas J.L. Brown of the University of Groningen, said the case exhibits multiple problems seen across science including statistical errors and some researchers basic pursuit of fame.

The statistical errors, wrote Mr. Brown and his colleagues at Groningen, included a failure by Mr. Vijgs team to compare the fit of its model to alternatives, and the use of small sample sizes that failed to properly handle the case of a lone outlier, Jeanne Calment of France, who died in 1997 at the record age of 122.

Mr. Vijg said repeatedly that his Nature paper made no "definitive statement" about a maximum human age and that he felt "amazement" that anyone might think otherwise. But he acknowledged approving a news release about his study issued by Albert Einstein College with the headline: "Maximum human lifespan has already been reached, Einstein researchers conclude."

The scientific question at hand never even seemed to make much sense, said Mr. Brown, a doctoral student in health psychology at Groningen, because advances in average human lifespan are far more important than the future maximum age of a single person. "The whole article might as well have been designed to create clickbait headlines," he said.

That type of low-value scientific pursuit is only becoming more common with the advent of modern computer-processing capabilities, Mr. Brown said. Computers let people "explore a half-million alternative realities in 10 minutes," and then pick out something that seems interesting, without spending too much time on developing meaningful hypotheses, he said.

Without qualified statistical experts to guide them, researchers will continue to encounter big problems, Mr. Brown said. "Statistics is demanding in the same way as flying a plane, but many scientists only have the equivalent of a drivers license," he said. "As a result, theyre crashing into the side of a mountain on a rather regular basis."

Paul Basken covers university research and its intersection with government policy. He can be found on Twitter @pbasken, or reached by email at paul.basken@chronicle.com.

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A New Theory on How Researchers Can Solve the Reproducibility Crisis: Do the Math - The Chronicle of Higher Education

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Mum calls for 4 ‘miracle’ cream that cured her baby’s eczema to be … – The Independent

Posted: at 10:45 am

A mother has praised a 3.99 high street miracle cream that she says helped cure her daughter's painful eczema in just a week.

Paige Sweeney, 23, from Nottingham, spent more than two years taking her daughter Evie-Rose to dermatologists trying to find a cure for her skin condition, but nothing worked.

Instead, her baby girl was left with battling with painful patches on her hands, mouth and backs of knees that she would scratch until she bled.

As a last resort, the concerned mother decided to buy the 3.99 cream after she spotted it at a local Boots store.

And, to her amazement, baby Evies eczema had cleared up within a week.

However, the National Eczema Association points out that when it comes to treatments, not everyone will respond in the same way. "It's best to familiarise yourself with all of the options and talk to your doctor to find a treatment regimen that works for you."

Describing it as a miracle cream, the mother-of-one is now calling for Childs Farm baby moisturiserto be available on prescription and says that it could save the NHS a fortune.

I saw the moisturising cream on the shelf in Boots and decided to give it a go, Sweeney told the Daily Mail.

Evie-Rae also has a nut, soya and egg allergy, so we have to be careful with what we give her, but I could see the ingredients were all natural.

Paige Sweeney spent more than two years taking her daughter Evie-Rose to dermatologists trying to find a cure for her skin condition (Facebook: Paige Sweeney)

Within a matter of days I could see her skin starting to clear up. I couldn't believe it.

After suffering with eczema since she was born, Evie-Rae had to endure painful rashes all over her body which, despite being prescribed a range of antibiotics and steroid creams, could not be controlled.

Evie-Rae battled with painful patches on her hands, mouth and backs of knees that she would scratch until she bled (Image: Paige Sweeney)

Sweeney has since taken to Facebook to post Evie-Raes before and after images which have now been shared more than 30,000 times.

While some creams seem to bring incredible results to some children, they may not work on others.

To her amazement baby Evies eczema had cleared up within a week thanks to the 'miracle' cream (Image: Paige Sweeney)

A number of other specialist baby creams are on the market aimed at children, including Weleda White Mallow Body Lotion, MooGoo Irritable Skin Balm, and Green People Organic Babies soothing baby salve.

The NHS points out that there are a number of different possible treatments for people - including avoiding triggers, intensive moisturising, and using topical corticosteroids.

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A new innovative treatment for eczema could be on its way, researchers say – Netdoctor

Posted: at 10:45 am

Our skin is home to all sorts of different types of bacteria, viruses and fungi, and for decades scientists have hypothesised that these complex societies of microbes are at least partly to blame for common conditions such as acne and eczema.

However, it now seems that bacteria could also be part of the treatment, too. Dermatologists at the University of California in San Diego recently came up with a novel microbial treatment for eczema which is thought to affect one in five children and one in 20 adults in the UK the recipe for which is actually pretty straightforward.

What I now know about acne and stress

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Lead dermatologist Dr Richard Gallo and his team discovered that Staphylococcus hominis and Staphylococcus epidermidis two harmless bacteria of the human skin microbiome have the ability to kill off Staphylococcus aureus, which is known to play a role in eczema.

Having swabbed the first two types of bacteria from the skin of several volunteers who suffered with eczema. The team then grew them in a lab and later incorporated them into an easy-to-apply lotion. Upon using the cream on their forearms, the levels of helpful skin bacteria was drastically increased in the volunteers almost eliminating S. aureus entirely within 24 hours. The report reads:

"These findings show how commensal skin bacteria protect against pathogens and demonstrate how dysbiosis (a microbial imbalance) of the skin microbiome can lead to disease."

Getty Ross Whitaker

Speaking to the New York Times, Elizabeth Grice, a research dermatologist and microbiologist at the University of Pennsylvania who was not involved in the experiment, said:

"[This is] the first time anything like this has been shown What remains to be seen is whether this kind of treatment can reduce the severity of skin disease over the long term."

Despite this huge step forward in the treatment of skin conditions, scientists say there is still a lot to learn about what microbial ecosystems look like on healthy skin, how they change during illness, and how to safely interfere before we'll get to see any products on the market.

However, Dr Gallo's comment that "there are so many new potent medicines right under our nose" although specifically referring to the bacterial makeup of our skin isn't actually that far from the truth.

Earlier this week we reported that something as simple as heading out in the summer sun can help reduce eczema symptoms. It was found that UV light triggers a release of nitric oxide into the blood stream, dampening inflammation and therefore reducing symptoms such as itchiness and redness. Professor Richard Weller, senior lecturer in Dermatology at the University of Edinburgh, said:

"It is clear that the health benefits of sunlight stretch far beyond vitamin D and we are starting to fill in these blank spaces."

The first study was published in the journal Science Translational Medicine, and the latter in the Journal of Allergy and Clinical Immunology.

Simple ways to make older people feel safe in their home environment

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Global Psoriasis Treatment Market to Reach $12.8 Billion by 2025 … – Business Wire (press release)

Posted: at 10:45 am

DUBLIN--(BUSINESS WIRE)--Research and Markets has announced the addition of the "Global Psoriasis Treatment Market Size, Market Share, Application Analysis, Regional Outlook, Growth Trends, Key Players, Competitive Strategies and Forecasts, 2017 to 2025" report to their offering.

The Global Psoriasis Treatment Market was valued at US$ 7.9 Bn in 2016, and is expected to reach US$ 12.8 Bn by 2025, expanding at a CAGR of 5.4% from 2017 to 2025.

The psoriasis treatment market is rapidly growing due to factors such as growing prevalence in some countries, significant unmet needs, promising pipeline molecules would drive the growth of psoriasis market worldwide. For the purpose of study, global psoriasis treatment market is segmented on the basis of drug class such as TNF Inhibitors, Vitamin D analogues, interleukin blockers and other psoriasis medication. It is observed that, in the base year 2016, interleukin blockers was major revenue contributing segment due to its long-term safety with lower risk of infection and malignancy. Psoriasis treatment market is categorized on the basis of route of administration such as topical, oral and parenteral therapeutic drugs.

Currently, topical therapeutic drugs hold largest market share due to its safety, more effectiveness and targeted drug delivery. It is anticipated that parenteral therapeutic drugs would show significant growth during forecast period because newly approved biologics are generally preferred in moderate to severe psoriasis.

Companies Mentioned

Key Topics Covered:

Chapter 1 Preface

Chapter 2 Executive Summary

Chapter 3 Psoriasis Treatment Market Analysis

Chapter 4 Global Psoriasis Treatment Market, by Drug Class

Chapter 5 Global Psoriasis Treatment Market, by Route of Administration

Chapter 6 Global Psoriasis Treatment Market, by Geography

Chapter 7 Company Profiles

For more information about this report visit https://www.researchandmarkets.com/research/wnpcpw/global_psoriasis

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New colistin resistance gene identified in China – CIDRAP

Posted: at 10:44 am

Researchers in China have discovered another gene that confers resistance to the last-resort antibiotic colistin.

In a study yesterday in mBio, the researchers report that the MCR-3 gene was discovered in a fecal sample obtained from an apparently healthy pig at a farm in Shangdong province during a routine surveillance study of antimicrobial resistant bacteria. The gene was located on a colistin-resistant Escherichia coli isolate, on a plasmid that contained 18 additional antibiotic resistance genes.

The authors of the study say they're concerned the gene may already be widely disseminated, and that scientists should be on the lookout for it. "Screening for the mcr-3 gene should be urgently included in the surveillance of colistin-resistant Gram-negative pathogens from animals, humans, and the environment," they write.

The discovery was made by several members of the research team that first reported the discovery of the mobile colistin resistance gene MCR-1 in E coli from pigs, pork products, and humans in China in November 2015. That finding raised international concern, given that colistin is an antibiotic of last resort for multidrug-resistant bacterial infections. The gene's location on plasmids, which are highly mobile pieces of DNA that can be shared within and between different bacterial species, means that resistance to colistin can quickly spread.

Since then, MCR-1 has been identified in bacteria from humans, animals, and the environment in more than 30 countries, including the United States, and studies have documented the spread of the gene to the clinical setting in China. Earlier this year, Chinese scientists reported an outbreak of MCR-1carrying Klebsiella pneumoniae among patients in a pediatric leukemia ward.

In addition, six different variants of the MCR-1 gene have been reported, along with a second mobile resistance gene, MCR-2.

In yesterday's study, the researchers report that MCR-3 was identified when molecular testing showed the colistin-resistant E coli isolate was negative for both MCR-1 and MCR-2, but contained an unknown colistin resistance gene that could be transferred to another E coli strain. Further analysis revealed that the gene was located on a plasmid similar to MCR-1carrying plasmids.

The investigators also found that the genomic sequence of MCR-3 closely resembled sequences found in Enterobacteriaceae and Aeromonas bacteria collected from both clinical infection and environmental samples in 12 countries on four continents, a finding that suggests the previously unidentified gene may already have spread. "Due to the ubiquitous profile of aeromonads in the environment and the potential transfer of mcr-3 between Enterobacteriaceae and Aeromonas species, the wide spread of mcr-3 may be largely underestimated," they write.

Up until recently, colistin was widely used in Chinese agriculture, and MCR-1 is thought to be a product of selection pressure caused by that use. China banned use of the drug in animal feed in 2016, based in part on the discovery of MCR-1.

Because of its toxicity, colistin was rarely used in human medicine until the late 1990s, when resistance to other last-resort drugs, including carbapenems, necessitated its use in serious multidrug-resistant infections. Colistin is on the World Health Organization's list of critical antimicrobials for human medicine.

One of the major concerns about MCR-1 and its offshoots is that it's often located on plasmids that contain other antibiotic resistance genes. That raises the possibility of bacterial infections that will not respond to any antibiotic. The authors say continuous monitoring for mobile resistance elements in colistin-resistant bacteria is "imperative for understanding and tackling the dissemination of mcr genes in both the agricultural and health care sectors."

Scientists with the SENTRY Antimicrobial Surveillance Program, which monitors worldwide pathogens and changes in antibiotic resistance patterns, have been tracking the global spread of MCR-1 since it was identified, while the Centers for Disease Control and Prevention has been hunting for the gene in the United States.

Patients Who Tested Positive For Genetic Mutations Fear Bias … – NPR – NPR

Posted: at 10:44 am

Patients who underwent genetic screenings now fear that documentation of the results in their medical records could lead to problems if a new health law is enacted. Sam Edwards/Caiaimage/Getty Images hide caption

Patients who underwent genetic screenings now fear that documentation of the results in their medical records could lead to problems if a new health law is enacted.

Two years ago, Cheasanee Huette, a 20-year-old college student in Northern California, decided to find out if she was a carrier of the genetic mutation that gave rise to a disease that killed her mother. She took comfort in knowing that whatever the result, she'd be protected by the Affordable Care Act's guarantees of insurance coverage for pre-existing conditions.

Her results came back positive. Like her mother, she's a carrier of one of the mutations known as Lynch syndrome. The term refers to a cluster of mutations that can boost the risk of a wide range of cancers, particularly colon and rectal.

As Republican lawmakers advance proposals to overhaul the ACA's consumer protections, Huette frets that her future health coverage and employment options will be defined by that test.

She even wonders if documentation of the mutation in her medical records and related screenings could rule out individual insurance plans. She's currently covered under her father's policy. "Once I move to my own health care plan, I'm concerned about who is going to be willing to cover me, and how much will that cost," she says.

In recent years, doctors have urged patients to be screened for a variety of diseases and predisposition to illness, confident it would not affect their future insurability. Being predisposed to an illness such as carrying the BRCA gene mutations associated with breast and ovarian cancer does not mean a patient will come down with the illness. But knowing they could be at risk may allow patients to take steps to prevent its development.

Under the current health law, many screening tests for widespread conditions such as prediabetes are covered in full by insurance. The Centers for Disease Control and Prevention and the American Medical Association have urged primary care doctors to test patients at risk for prediabetes. But doctors, genetic counselors and patient advocacy groups now worry that people will shy away from testing as the ACA's future becomes more uncertain.

Dr. Kenneth Lin, a family physician at Georgetown University School of Medicine in Washington, D.C., says if the changes proposed by the GOP become law, "you can bet that I'll be even more reluctant to test patients or record the diagnosis of prediabetes in their charts." He thinks such a notation could mean hundreds of dollars a month more in premiums for individuals in some states under the new bill.

Huette says she's sharing her story publicly since her genetic mutation is already on her medical record.

But elsewhere, there have been "panicked expressions of concern," says Lisa Schlager of the patient advocacy group Facing Our Risk of Cancer Empowered (FORCE). "Somebody who had cancer even saying, 'I don't want my daughter to test now.' Or 'I'm going to be dropped from my insurance because I have the BRCA mutation.' There's a lot of fear."

Those fears, which come in an era of accelerating genetics-driven medicine, rest upon whether a gap that was closed by the ACA will be reopened. That remains unclear.

A law passed in 2008, the Genetic Information Nondiscrimination Act, bans health insurance discrimination if someone tests positive for a mutation. But that protection stops once the mutation causes "manifest disease" essentially, a diagnosable health condition.

That means "when you become symptomatic," although it's not clear how severe the symptoms must be to constitute having the disease, says Mark Rothstein, an attorney and bioethicist at the University of Louisville School of Medicine in Kentucky, who has written extensively about GINA.

The ACA, passed two years after GINA, closed that gap by barring health insurance discrimination based on pre-existing conditions, Rothstein says.

On paper, the legislation unveiled by Senate Majority Leader Mitch McConnell last week wouldn't let insurers set higher rates for people with pre-existing conditions, but it could effectively exclude such patients from coverage by allowing states to offer insurance plans that don't cover certain maladies, health analysts say. Meanwhile, the bill that passed the House last month does have a provision that allows states to waive protections for people with pre-existing conditions, if they have a gap in coverage of 63 days or longer in the prior year.

When members of a Lynch Syndrome social media group were asked for their views on genetic testing amid the current health care debate, about two dozen men and women responded. Nearly all said they were delaying action for themselves or suggesting that family members, particularly children, hold off.

Huette was the only one who agreed to speak for attribution. She says before the ACA was enacted, she witnessed the impact that fears about insurance coverage had on patients. Her mother, a veterinarian, had wanted to run her own practice but instead took a federal government job for the guarantee of health insurance. She died at the age of 57 of pancreatic cancer, one of six malignancies she had been diagnosed with over the years.

Huette says she doesn't regret getting tested. Without the result, Huette points out, how would she have persuaded a doctor to give her a colonoscopy in her 20s?

"Ultimately, my health is more important than my bank account," she says.

Kaiser Health News, a nonprofit health newsroom whose stories appear in news outlets nationwide, is an editorially independent part of the Kaiser Family Foundation.

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The gene behind follicular lymphoma – Medical Xpress

Posted: at 10:44 am

June 28, 2017 Disruption of a region in chromosome 6 or epigenetic modifications of the DNA block Sestrin1 expression and these contribute to the development of follicular lymphoma. Credit: Elisa Oricchio/Natalya Katanayeva/EPFL

Follicular lymphoma is an incurable cancer that affects over 200,000 people worldwide every year. A form of non-Hodgkin lymphoma, follicular lymphoma develops when the body starts making abnormal B-cells, which are white blood cells that in normal conditions fight infections. This cancer is associated with several alterations of the cell's DNA, but it has been unclear which gene or genes are involved in its development. EPFL scientists have now analyzed the genomes of more than 200 patients with follicular lymphoma, and they discover that a gene, Sestrin1, is frequently missing or malfunctioning in FL patients. The discovery opens to new treatment options and it is now published in Science Translational Medicine.

One of the common features of follicular lymphoma is a genetic abnormality between two chromosomes (14 and 18). In an event known as "chromosomal translocation" the two chromosomes "swap" certain parts with each other. This triggers the activation of a gene that protects cells from dying, making cells virtually immortalthe hallmark of a tumor.

Moreover, approximately 30% of follicular lymphoma patients lose also a portion of chromosome 6, affecting multiple genes involved in suppressing the emergence of a tumor. These patients typically have poor prognosis. Another 20 % of patients have alterations causing chromosomal disorganization and the consequent malfunctioning of several genes and proteins. The bottom line is that for both group of patients it is very difficult to pinpoint which of all the affected genes are actually causing the disease.

The lab of Elisa Oricchio at EPFL, with colleagues from the US and Canada, analyzed the genomes of over 200 follicular lymphoma patients. Their analyses revealed that a specific gene, Sestrin1, can be harmed by both loss of chromosome 6 and silenced in patients.

Sestrin1 helps the cell defending itself against DNA damagefor example after exposure to radiationand oxidative stress. In fact, Sestrin1 is part of the cell's anti-tumor mechanism that stops potentially cancerous cells from growing.

Disruption of a region in chromosome 6 or epigenetic modifications of the DNA block Sestrin1 expression and these contribute to the development of Follicular Lymphoma.

Beyond identifying the Sestrin1 gene as frequently altered in FL patients, the scientists demonstrated that Sestrin1 is able to suppress tumors in vivo. They showed that Sestrin1 exerts its anti-tumor effects by blocking the activity of a protein complex called mTORC1, which is well known for controlling protein synthesis as well as acting as a sensor for nutrient or energy changes in the cell.

Finally, the identification of loss of Sestrin1 as a key event behind the development of follicular lymphoma is particular important because it helps identifying patients that will benefit from new therapies. Indeed, this study shows that the therapeutic efficacy of a new drug that is currently in clinical trial depends on Sestrin1. Importantly, this dependency can be extended beyond follicular lymphoma to other tumor types.

Explore further: Combination therapy may help patients with follicular lymphoma

More information: E. Oricchio el al., "Genetic and epigenetic inactivation of SESTRIN1 controls mTORC1 and response to EZH2 inhibition in follicular lymphoma," Science Translational Medicine (2017). stm.sciencemag.org/lookup/doi/10.1126/scitranslmed.aak9969

A new study in The Journal of Experimental Medicine reveals that a high-risk group of patients with follicular lymphoma could benefit from a novel drug combination.

Mutations present in a blood cancer known as follicular lymphoma have revealed new molecular targets for potential treatments, according to researchers at Queen Mary University of London (QMUL) together with collaborators ...

Immune cellular therapy is a promising new area of cancer treatment. Anti-cancer therapeutics, such as chimeric antigen receptor (CAR) modified T cells, can be engineered to target tumor-associated antigens to attack and ...

Follicular lymphoma (FL), the second most common form of non-Hodgkin lymphoma, is a largely incurable disease of B cells, yet in many cases, because of its indolent nature, survival can extend to well beyond 10 years following ...

The goal for many cancer patients is to reach the five-year, disease-free mark, but new research from UR Medicine's Wilmot Cancer Institute suggests that two years might be a more practical survival goal for people with follicular ...

(HealthDay)An initial watch-and-wait strategy does not have a detrimental effect on the freedom from treatment failure (FFTF) or overall survival rate in selected patients with low-tumor burden follicular lymphoma compared ...

While mutations in protein-coding genes have held the limelight in cancer genomics, those in the noncoding genome (home to the regulatory elements that control gene activity) may also have powerful roles in driving tumor ...

Cancerous tumors are formidable enemies, recruiting blood vessels to aid their voracious growth, damaging nearby tissues, and deploying numerous strategies to evade the body's defense systems. But even more malicious are ...

Leukemia researchers led by Dr. John Dick have traced the origins of relapse in acute myeloid leukemia (AML) to rare therapy-resistant leukemia stem cells that are already present at diagnosis and before chemotherapy begins.

Adding an investigational antibody to the chemotherapy rituximab appears to restore its cancer-killing properties in certain leukemia patients with a natural resistance to the drug, according to a small, proof-of-concept ...

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Researchers propose new approach to identify genetic mutations in men with prostate cancer – Medical Xpress

Posted: at 10:44 am

June 29, 2017 Micrograph showing prostatic acinar adenocarcinoma (the most common form of prostate cancer) Credit: Wikipedia

Scientists have had limited success at identifying specific inherited genes associated with prostate cancer, despite the fact that it is one of the most common non-skin cancers among men. Researchers at University of Utah Health studied prostate cancer patients with multiple cancer diagnoses, many who would not be recommended for genetic tests following current guidelines, to identify genetic mutations that may influence cancer treatment and cancer risk assessment for family members. Their findings are reported in the June issue of the journal Cancer.

"We commonly use a combination of a patient's personal and family cancer histories to identify those individuals who may have a mutation in a gene that predisposes that individual to developing cancers," said Patrick Pili, M.D., medical oncology fellow at the University of Texas MD Anderson Cancer Center. "Testing for hereditary cancers impacts not only the patient with cancer but also potentially the cancer screening and health outcomes of their entire family, but many prostate cancer patients do not meet the current guidelines to test for genetic cancer heritability."

Pili was part of a research team led by Kathleen Cooney, M.D., chair of the Department of Internal Medicine at U of U Health and a Huntsman Cancer Institute investigator, who proposed a strategy to identify germline mutations in men selected for the study based on their clinical history not their family history.

The study was highly selective, including 102 patients who had been diagnosed with prostate cancer and at least one additional primary cancer, like melanoma, pancreatic cancer, testicular cancer, or Hodgkin lymphoma.

The researchers examined the frequency of harmful germline mutations in this group of men. These mutations originate on either the egg or sperm and become incorporated into the DNA of every cell in the body of the resulting offspring.

Using next generation sequencing, the researchers found that 11 percent of the patients had a disease-causing mutation in at least one cancer-predisposing gene, which suggests these genetic variations contributed to their prostate cancer. Cooney found no difference in cancer aggressiveness or age of diagnosis compared to patients without these mutations.

In addition, a certified genetic counselor and co-investigator Elena Stoffel, M.D., University of Michigan Comprehensive Cancer Center, reviewed personal and family histories from each patient to determine whether they would meet clinical genetic testing guidelines. The majority of the men in the study, 64 percent, did not meet current criteria to test for hereditary cancer based on personal and/or family history.

The findings suggest that there are men with heritable prostate cancer-predisposing mutations that are not eligible for genetic screening under current guidelines.

"This is the first paper in which we can show the potential of using a clinical history of multiple cancers, including prostate cancer, in a single individual to identify inherited germline mutations," Cooney said.

The majority of harmful mutations identified were in genes involved in DNA repair.

"These mutations prevent the DNA from healing itself, which can lead to a predisposition for cancer," Cooney said.

This result is also beneficial because drugs like PARP [poly ADP ribose polymerase] inhibitors have a better success rate in treating cancers with the underlying gene mutation associated with DNA repair.

Cooney cautions that this is a small pilot study rather than a broader epidemiological survey, and it consists of a highly specific subset of patients.

"We cannot generalize these findings to the broader population, because we used highly selective criteria to tip us off to patients that may have mutations outside typical hereditary genetic patterns," she said.

The 102 patients included in the study were identified from the University of Michigan's Prostate Cancer Genetics Project, which registers patients who are diagnosed with prostate cancer before age 55 or who have a first- or second-degree relative with prostate cancer. In addition, the research team identified patients from the University of Michigan's Cancer Genetics Registry, which includes individuals with personal or family history suggestive of a hereditary risk of cancer.

"Our findings are in line with those of other studies, suggesting that approximately 1 in 10 men with advanced prostate cancer harbors a genetic variant associated with increased cancer risk," said Stoffel. "While family history is an important tool, there may be better ways to identify patients with genetic risk."

Future studies with larger sample sizes will include sequencing of tumors that will allow investigators to more carefully explore the different features associated with tumors that arise in individuals with germline mutations.

"This approach will help us identify patients at greater risk for aggressive prostate cancer so they can seek earlier screening while pre-symptomatic," Cooney said.

Explore further: Are men with a family history of prostate cancer eligible for active surveillance?

More information: Patrick G. Pili et al. Germline genetic variants in men with prostate cancer and one or more additional cancers, Cancer (2017). DOI: 10.1002/cncr.30817

Journal reference: Cancer

Provided by: University of Utah

Active surveillancecareful monitoring to determine if or when a cancer warrants treatmentis an increasingly prevalent choice for prostate cancer, but it's unclear if the strategy is appropriate for men with a family ...

Inherited mutations in genes that function to repair DNA may contribute to metastatic prostate cancer more than previously recognized, according to a study out today in the New England Journal of Medicine. Though infrequent ...

African-American men develop prostate cancer more often than other men, and it tends to be more deadly for this population. Some of the differences seem to be due to socioeconomic factors, but scientists wondered whether ...

(HealthDay)A man's risk of aggressive and fatal prostate cancer may be heavily influenced by gene mutations previously linked to breast and ovarian cancer in women, a trio of new studies suggests. Findings from the studies ...

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Researchers propose new approach to identify genetic mutations in men with prostate cancer - Medical Xpress

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Lynchings Wrong, Selective Outrage Equally Cringe Worthy – News18

Posted: at 10:44 am

Let us be clear that lynch narratives in India are never secular they are impassioned and lopsided either one way or the other. This is why the discussion on Jantar Mantar protests cannot be done in isolation as a purely people's movement - for it may have begun as one but it is not anymore.

The problem with the world we inhabit today is polarisation. The issue is either pro or anti. Black or white. National or anti national. Secular or Communal.

You cannot talk logic and debate in a sustained fashion today, for the fear of uttering or writing something which is 'politically incorrect' - a term ideologically defined and defended by a group of elites in this country. Unfortunately, it has become imperative to wear an ideological cloak even while discussing moral questions, either because you have to defend selective secularism or because you have to expose the selective ideological amnesia and dementia. In the process, one may want to be as balanced as a weighing scale projecting two sides of the arguments, but one has to often choose 'touchy', 'politically incorrect', 'untouchable' issues for articulation. Balance can come only when there is equal and equitable, responsible and balanced articulation of reasons for and condemnation of all cases of human rights' violation, violence, rapes and riots.

There is of course no doubt that lynchings are inhuman, unfit as a marker of any human civilisation. And because all lynchings are wrong, the reportage of Muslims being killed by Hindus and Hindus being killed by 'some' people, in case the killers are Muslims, is as communal and targeted as lynchings themselves. For far too long narratives of organised hatred against the majority by the elite intellectuals and English media editors' guild in India have been defining a skewed and dangerous idea of secularism in this country.

Not everyone in this nation has the luxury of such incisive and piercing verbal articulation against violence or selective outrage. But their inability to capacitate the building of a verbose written or spoken narrative cannot be an impediment in a socialist democracy to dismiss their actions by a group of an entitled and intellectually elite mob.

A reaction can be and must be pulled out and called out for its socially debilitating ramifications. But a silence to even address the action which facilitated the reaction is as much a part of the lynch mob herd mentality. Unless we accept this reality, the facade of looking for solutions is optimistic hypocrisy.

I was expecting the 'organic' outburst of 'collective' anger at Jantar Mantar to protest against the recent humiliation of a Meghalayan woman by a part of this same English speaking colonial and feudal elite that has no qualms in calling a PM candidate unfit for his tea selling background.

I was expecting a protest against the murder of two males in the household of Kerala CM's home village and the pattern of lynch mob in Kerala. I was expecting a strong protest against Muslim lynch mobs who have brutally raped and murdered women in Hojai and Marghareita in Assam.

But I was expecting too much from the media perhaps who focused on Jantar Mantar and gave prime time slots to articulate what some elite groups comprising of some same faces who have made protests their way of overstaying their interests in Delhi.

Having said what I have said, I reiterate, all lynchings are wrong, abhorrent, a blot on humanity. And similarly cringe worthy is selective outrage. More pathetic is Congress-Communists clandestine combine that spills over its jugalbandi in such opportunistic free loading in protests like these.

(The author is assistant editor, India Foundation Journal, and project head, northeast operations. Views expressed are personal)

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Lynchings Wrong, Selective Outrage Equally Cringe Worthy - News18

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GUVNL vets proposals to take over imported-coal power plants – Moneycontrol.com

Posted: at 10:44 am

State-run Gujarat Urja Vikas Nigam Ltd (GUVNL) is evaluating proposals to take over majority stake in the imported coal-based power plants of Tata Power, Adani Power and Essar Power.

The three companies running imported coal-based plants in Mundra and Salaya were suffering losses due to disallowance of compensatory tariff to insulate these firms from higher coal prices in Indonesia due to change in regulation.

In a desperate measure, these companies had even offered GUVNL to take over majority stake in these power plants at a token consideration of Re 1 only.

There was a buzz that the Gujarat government had shown disinterest to take over these plants for a token consideration as it would be politically incorrect step in view of forthcoming assembly election in the state this year.

"These proposals are still under evaluation," a source in the GUVNL said.

Earlier on the issue, Power Minister Piyush Goyal said here was a lot of discussions about "what would happen to these plants and to the availability of low-cost power to some other states. Nothing has come out as yet".

"I had suggested that these imported coal-based plants may also look at technical solutions to try to use more domestic coal because under SHAKTI scheme we would soon come out with a policy which will allow imported coal-based plant to bid for domestic coal," he added.

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GUVNL vets proposals to take over imported-coal power plants - Moneycontrol.com

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Monthly Archives: June 2017

A New Theory on How Researchers Can Solve the Reproducibility Crisis: Do the Math – The Chronicle of Higher Education

Mum calls for 4 ‘miracle’ cream that cured her baby’s eczema to be … – The Independent

A new innovative treatment for eczema could be on its way, researchers say – Netdoctor

Global Psoriasis Treatment Market to Reach $12.8 Billion by 2025 … – Business Wire (press release)

New colistin resistance gene identified in China – CIDRAP

Patients Who Tested Positive For Genetic Mutations Fear Bias … – NPR – NPR

The gene behind follicular lymphoma – Medical Xpress

Researchers propose new approach to identify genetic mutations in men with prostate cancer – Medical Xpress

Lynchings Wrong, Selective Outrage Equally Cringe Worthy – News18

GUVNL vets proposals to take over imported-coal power plants – Moneycontrol.com

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