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Kenyan malaria success strengthens call for free insecticide-treated nets for all

Experts have today called for international agencies to provide insecticide-treated bed nets for all children in Africa as the most equitable way of tackling malaria. Their call is supported by new research co-funded by the Wellcome Trust showing how successful a scheme run by the Kenyan government has been at distributing the nets.

Over a million children die from malaria in Africa each year. Scientists have known for over 15 years that sleeping under a mosquito net treated with insecticide can halve the number of episodes of malaria and save lives. However, successful and equitable distribution of the nets has been difficult – by the end of 2004, only 7% of children in rural Kenya were reported to sleeping under the nets and only 3% among the poorest sectors of these communities.

“Even when the price of a treated net is heavily subsidised and made more accessible through clinics, parents have to choose between school fees and food or a net,” explains Professor Bob Snow from the Kenya Medical Research Institute–Wellcome Trust (KEMRI-WT) Research Programme in Kenya, who led the research. “The result is that few children are protected. Those who can afford to protect their children tend to benefit most, but not those who can’t.”

In 2006 the Kenyan government initiated a programme to provide 3.4 million treated nets free to as many young children as possible in only two weeks. The nets were distributed at clinics, schools, vaccination points and by Ministry of Health staff walking from house-to-house . In this short period of time, coverage rose to two-thirds of all children sleeping under a treated net, with no difference between children from rich or poor homes. The results of the study to evaluate the initiative are published today in the open access journal PLoS Medicine.

However, despite the success of the Kenyan government’s programme, Dr Abdisalan Mohamed Noor, lead author of the study, warns against complacency.

“We’ve shown what can be achieved with the right strategy, but one in three children are still unprotected, and every year 1.5 million children are born in Kenya who require new treated nets,” says Dr Noor from KEMRI-WT and the University of Oxford. “The momentum started in 2006 must continue and not be seen as a one off success.”

The researchers believe that the findings should prompt international aid agencies to revisit their distribution policies to make the nets more widely accessible.

“For a decade now, we have been asking the international agencies to recognise the importance of treated nets in child survival programmes,” says Professor Snow. “We would never expect countries or African families to pay for measles vaccination. Why then ask them to pay for an intervention that saves more lives in Africa each year””

Contact: Craig Brierley
c.brierley@wellcome.ac.uk
44-207-611-7329
Wellcome Trust

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August 17, 2007 Posted by | Global Health Vision, Global News, Health, Malaria, RSS Feed, Washington DC City Feed, Wellcome Trust, World News | Leave a comment

Flip of genetic switch causes cancers in mice to self-destruct, Stanford researchers find

STANFORD, Calif. – Killing cancerous tumors isn’t easy, as anyone who has suffered through chemotherapy can attest. But a new study in mice shows that switching off a single malfunctioning gene can halt the limitless division of tumor cells and turn them back to the path of their own planned obsolescence.

The surprising possibility that a cell’s own natural mechanism for ensuring its mortality could be used to vanquish tumors opens the door to a new approach to developing drugs to treat cancer patients, according to Dean Felsher, MD, PhD, associate professor of medicine (oncology) and of pathology at the Stanford University School of Medicine. Felsher is the senior author of the study to be published July 30 in the advance online version of the Proceedings of the National Academy of Sciences.

“Our research implies that by shutting off a critical cancer gene, tumor cells can realize that they are broken and restore this physiologic fail-safe program,” said Felsher.

Cancer can be notoriously resistant to medical treatment. Not only do cancer cells proliferate uncontrollably, they somehow circumvent the mechanism that causes normal cells to die when they get old or malfunction. That makes cancer cells effectively immortal unless doctors manage to squelch them.

The gene Felsher’s team studied produces a protein called Myc (pronounced “mick”), which promotes cell division. A mutation of the gene causes cells to overproduce the protein, prompting perpetual cell division and tumor growth. By turning off the mutated gene, the researchers found that not only did uncontrolled cell division cease, but the cells also reactivated a normal physiological mechanism, called senescence, which makes it possible for a cell to eventually die.

“What was unexpected was just the fact that cancer cells had retained the ability to undergo senescence at all,” said Felsher. Cancer researchers had long thought the senescence process had to be irreversibly disrupted for a tumor to develop.

The researchers worked with a series of mice engineered to have Myc-triggered cancers of either the liver, blood or bones, along with a specially constructed version of the Myc gene that they could switch off by feeding the mice antibiotics. When the mice dined on doses of the drugs, invariably, the tumors ceased growing and then diminished, with some disappearing over the course of just a few days.

Although Felsher’s lab had previously shown that mouse tumors diminished and disappeared when Myc was switched off, they hadn’t been sure how the process actually worked. Historically, most research involving genetic methods of battling cancer cells has focused on reactivating genes called tumor-suppressor genes, which are generally overcome by a proliferating cancer. No one had explored the idea that senescence might play a key role in diminishing tumors.

Felsher described senescence as acting like a fail-safe mechanism to stop cancer. When a cell detects a deleterious mutation, it launches the senescence process, resulting in the permanent loss of the cell’s ability to proliferate, thus halting any cancer.

“In order to become tumor cells, those cells have to overcome senescence,” said Chi-Hwa Wu, PhD, postdoctoral researcher in Felsher’s lab and first author of the study. Wu had the inspiration to explore whether the sudden diminishment they had observed in the tumors might be due to the reactivation of some latent remnant of the trigger for senescence.

Through a series of experiments looking at enzymes associated with the senescence process, as well as some molecular markers, Wu confirmed her suspicion. And not only was senescence occurring in cells that had been thought to be incapable of it, the process was reactivated in all the different tumors they studied.

Consider it a cell version of the Jekyll-and-Hyde transformation. “It’s sort of like Mr. Hyde realizing that there’s something wrong with him and then being able to put himself back into his normal state as Dr. Jekyll,” Felsher said.

In addition to the deepened understanding of how the process of senescence works, Felsher and Wu see a lot of potential for new approaches to treating cancer, beyond the traditional tactic of trying to kill cancer cells directly. “This work implies that maybe part of the strategy should involve figuring out how to get the cancer cells to just be allowed to do what they originally wanted to do anyway, which is to not be proliferating endlessly and growing uncontrolled,” said Felsher.

The next step for the team is to see how well the approach works in human cancer cells. “And we’re also trying to figure out what the mechanism is,” Felsher said. “What are the molecular mechanisms of this, so that we can figure out how to better treat cancer””

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Other authors on the research paper are Jan van Riggelen, PhD, postdoctoral researcher; Alper Yetil, graduate student in cancer biology; Alice Fan, MD, instructor in medicine (oncology), and medical student Pavan Bachireddy.

The study was funded by the National Cancer Institute, the National Institutes of Health, the Leukemia and Lymphoma Society, the Burroughs Wellcome Fund, the Damon Runyon Lilly Clinical Investigator Award, the Lymphoma Research Foundation and the Howard Hughes Medical Institute.

Stanford University Medical Center integrates research, medical education and patient care at its three institutions – Stanford University School of Medicine, Stanford Hospital & Clinics and Lucile Packard Children’s Hospital at Stanford. For more information, please visit the Web site of the medical center’s Office of Communication & Public Affairs at http://mednews.stanford.edu.

Contact: Lou Bergeron
louisb3@stanford.edu
650-723-3900
Stanford University Medical Center

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July 31, 2007 Posted by | acute lymphoblastic leukemia, Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Cancer, Cancer Biology, Cancer Biology and Therapy, Childhood Lukemia, France, Genes, Genetic, Genetic Link, Genetics, Genome, Genomic, Germany, Global, Global Health Vision, Global News, Health Canada, Howard Hughes Medical Institute, Human Genome, Italy, Japan, Leukemia, Medical Journals, Molecular Biology, National Cancer Institute, National Institutes of Health, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, NIH, non-Hodgkin's lymphoma, Nova Scotia, Nunavut, Osaka, Ottawa, Prince Edward Island, Public Health, Quebec, Research, RSS, RSS Feed, Toronto, UK, US, Virginia, Washington DC, Washington DC City Feed, Wellcome Trust, World News | Leave a comment

Largest ever study of genetics of common diseases published today

Contact: Craig Brierley
c.brierley@wellcome.ac.uk
44-207-611-7329
Wellcome Trust

The Wellcome Trust Case Control Consortium, the largest ever study of the genetics behind common diseases such as diabetes, rheumatoid arthritis and coronary heart disease, today publishes its results in the journals Nature and Nature Genetics.

The £9 million study is one of the UK’s largest and most successful academic collaborations to date. It has examined DNA samples from 17,000 people across the UK, bringing together 50 leading research groups and 200 scientists in the field of human genetics from dozens of UK institutions. Over two years, they have analysed almost 10 billion pieces of genetic information.

“Many of the most common diseases are very complex, part ‘nature’ and ‘nurture’, with genes interacting with our environment and lifestyles,” says Professor Peter Donnelly, Chair of the Consortium, who is based at the University of Oxford. “By identifying the genes underlying these conditions, our study should enable scientists to understand better how disease occurs, which people are most at risk and, in time, to produce more effective, more personalised treatments.”

The study has substantially increased the number of genes known to play a role in the development of some of our most common diseases. Many of these genes that have been found are in areas of the genome not previously thought to have been related to the diseases.

“Just a few years ago it would have been thought wildly optimistic that it would be possible in the near future to study a thousand genetic variants in each of a thousand people,” says Dr Mark Walport, Director of the Wellcome Trust, the UK’s largest medical research charity, which funded the study. “What has been achieved in this research is the analysis of half a million genetic variants in each of seventeen thousand individuals, with the discovery of more than ten genes that predispose to common diseases.

“This research shows that it is possible to analyse human variation in health and disease on an enormous scale. It shows the importance of studies such as the UK Biobank, which is seeking half a million volunteers aged between 40 and 69, with the aim of understanding the links between health, the environment and genetic variation. New preventive strategies and new treatments depend on a detailed understanding of the genetic, behavioural and environmental factors that conspire to cause disease.”

Amongst the most significant new findings are four chromosome regions containing genes that can predispose to type 1 diabetes and three new genes for Crohn’s disease (a type of inflammatory bowel disease). For the first time, the researchers have found a gene linking these two autoimmune diseases, known as PTPN2.

The study has also confirmed the importance of a process known as autophagy in the development of Crohn’s disease. Autophagy, or “self eating”, is responsible for clearing unwanted material, such as bacteria, from within cells. The may be key to the interaction of gut bacteria in health and in inflammatory bowel disease and could have clinical significance in the future.

“The link between type 1 diabetes and Crohn’s disease is one of the most exciting findings to come out of the Consortium,” says Professor John Todd from the University of Cambridge, who led the study into type 1 diabetes. “It is a promising avenue for us to understand how the two diseases occur. The pathways that lead to Crohn’s disease are increasingly well understood and we hope that progress in treating Crohn’s disease may give us clues on how to treat type 1 diabetes in the future.”

Research from the Consortium has already played a major part in identifying the clearest genetic link yet to obesity and three new genes linked to type 2 diabetes, published in April in advance of the main study. It has found independently a major gene region on chromosome 9 identified by independent studies on coronary heart disease.

Researchers analysed DNA samples taken from people in the UK – 2,000 patients for each disease and 3,000 control samples – to identify common genetic variations for seven major diseases. These are bipolar disorder, Crohn’s disease, coronary heart disease, hypertension, rheumatoid arthritis and type 1 and type 2 diabetes. For each disease, the researchers will study larger population samples to confirm their results.

Although the human genome is made up of more than three billion sub-units of DNA, called nucleotides (or bases), most of these show little in the way of differences between individuals. A substantial part of the variation in DNA sequence between individuals is due to single-nucleotide polymorphisms (differences), also known as SNPs. There are approximately 8 million common SNPs in European populations. Fortunately, because SNPs that lie close together on chromosomes often tell quite similar stories, researchers in the Consortium were able to explore this variation through analysing a subset of these SNPs (in fact approximately 500,000).

“Human genetics has a chequered history of irreproducible results, but this landmark collaboration of scientists in Britain has shown conclusively that the new approach of analysing a large subset of genetic variants in large samples of patients and healthy individuals works,” says Professor Donnelly. “We are now able to effectively scan most of the common variation in the human genome to look for variants associated with diseases. This approach will undoubtedly herald major advances in how we understand and tackle disease in the future.”

Further analysis as part of the Consortium will be looking at tuberculosis (TB), breast cancer, autoimmune thyroid disease, multiple sclerosis and ankylosing spondylitis. The results are expected later this year.

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The Wellcome Trust Case Control Consortium, the largest ever study of the genetics behind common diseases such as diabetes, rheumatoid arthritis and coronary heart disease publishes its results in the journals Nature and Nature Genetics.

The £9 million study is one of the UK’s largest and most successful academic collaborations to date. It has examined DNA samples from 17,000 people across the UK, bringing together 50 leading research groups and 200 scientists in the field of human genetics from dozens of UK institutions. Over two years, they have analysed almost 10 billion pieces of genetic information.

Researchers have uncovered genetic variations for seven major diseases: bipolar disorder, Crohn’s disease, coronary heart disease, hypertension, rheumatoid arthritis and type 1 and type 2 diabetes.

Speakers:

Dr Mark Walport – Director, Wellcome Trust

Professor Peter Donnelly (University of Oxford) – Chair, Wellcome Trust Case Control Consortium

Professor John Todd (University of Cambridge) – Type 1 diabetes

Dr Miles Parkes (Addenbrooke’s Hospital and University of Cambridge) – Crohn’s disease

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June 6, 2007 Posted by | Alberta, Arthritis, Calgary, Diabetes, Genetics, Global Health Vision, Global News, Heart Disease, Virginia, Washington DC, Wellcome Trust, World News | 2 Comments

Vitamin D supplements may offer cheap and effective immune system boost against TB

Contact: Craig Brierley
c.brierley@wellcome.ac.uk
44-207-611-7329
Wellcome Trust

Scientists have shown that a single 2.5mg dose of vitamin D may be enough to boost the immune system to fight against tuberculosis (TB) and similar bacteria for at least 6 weeks. Their findings came from a study that identified an extraordinarily high incidence of vitamin D deficiency amongst those communities in London most at risk from the disease, which kills around two million people each year.

The research, funded by the Wellcome Trust, the Department of Environmental Health at Newham Council and Newham University Hospital NHS Trust Respiratory Research Fund, is published online in the American Journal of Respiratory and Critical Care Medicine.

Whilst a diet of oily fish can provide some vitamin D, the main source of the body’s vitamin D comes from exposing the skin to sunlight. In Britain, however, the amount of sunlight is usually insufficient to make vitamin D in the skin between October and April, and much of the population becomes deficient during the winter and spring.

Researchers from Queen Mary’s School of Medicine and Dentistry, London, and the Wellcome Trust Centre for Research in Clinical Tropical Medicine, Imperial College London, studied patients at Newham University Hospital and Northwick Park Hospital in London who had been exposed to TB. They found that over 90% of such patients had a vitamin D deficiency.

Vitamin D was used to treat TB in the pre-antibiotic era, when special sanatoria were built in sunny locations, such as the Swiss Alps. But until now, no study has evaluated the effect of vitamin D supplementation on immunity to mycobacteria, the family of bacteria that cause TB.

The researchers performed a randomised control trial on a group of volunteers who were given either a 2.5mg supplement or a placebo. Samples of the volunteers’ blood were then tested in Dr Robert Wilkinson’s Wellcome Trust-funded laboratory at Imperial College, to see whether the supplement affected the immune system’s ability to withstand infection by mycobacteria.

“We found that a single large dose of vitamin D was sufficient to enhance a person’s immunity to the bacteria,” says Dr Adrian Martineau from Imperial College London, who co-ordinated the study. “This is very significant given the high levels of vitamin D deficiency in people at the highest risk of TB infection, and shows that a simple, cheap supplement could make a significant impact on the health of people most at risk from the disease.”

According to the Health Protection Agency, the incidence of TB in the UK is increasing, with around 8,000 new cases a year. Cases in the UK are predominantly confined to the major cities and about 40 per cent of all cases are in London. TB is also a major global problem: an estimated one-third of the world’s population – nearly two billion people – are infected. Nine million people a year develop the active disease worldwide, which kills two million each year.

“Most cases of TB in London arise from people who have already become infected with the bacteria but in whom it lies latent,” says Professor Chris Griffiths from Queen Mary’s School of Medicine and Dentistry. “Our results indicate that vitamin D supplementation may prevent reactivation of latent TB. Identifying people with latent TB and providing supplements could be an important strategy for tackling the disease.”

Treatment is both very cheap – about 60p per dose or 10p per week – and safe. Vitamin D supplements could be prescribed for patients with or at risk of latent TB through GP surgeries.

Dr Martineau points out: “Our work adds to the growing evidence that vitamin D may have a wide range of important health benefits, including preventing falls and fractures and reducing risk of cancer and diabetes, as well as boosting the immune system against infection. Population-wide supplementation needs to be considered by public health planners.”

“Milk and orange juice could be fortified with vitamin D, as in the US and Canada,” he says. “At present only margarine is supplemented in the UK, and recent studies show that this is not an effective way to prevent vitamin D deficiency.”

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May 15, 2007 Posted by | Alberta, Baltimore, Calgary, Global, Global Health Vision, Global News, News, News Australia, News Canada, News UK, News US, Preventive Medicine, TB, Tuberculosis, Washington DC, Wellcome Trust, World News | Leave a comment