Archive for the ‘Gene Therapy Research’ Category

Public release date: 26-Mar-2013 [ | E-mail | Share ]

Contact: Rosie Waldron r.waldron@ucl.ac.uk 020-767-99041 University College London

Previous research has shown that obesity runs in families, and twin studies suggest that this is largely due to genetic factors, with heritability estimates over 50%. 32 genes have been identified as risk factors for obesity but previous analyses suggest that these genes alone cannot fully explain the high level of heritability in childhood obesity, as together they explain only 2% of individual differences in childhood body weight. This has led to a problem of 'missing heritability'.

In this study, researchers used a new method called Genome-wide Complex Trait Analysis (GCTA), to investigate the molecular genetic heritability of body weight in children. GCTA takes advantage of the fact that some people are more genetically similar to one another than others, by chance; and looks to see whether individuals who just happen to be more genetically similar might also be more similar in weight. Using this approach, GCTA estimates the combined effects of all known common genes across the whole genome, associated with childhood body weight.

The study is based on data from a population-based cohort of 2,269 children aged between eight and eleven years old. Researchers looked at whether children who happen to be more genetically similar might also be more similar in body weight. Using the GCTA method, the researchers found that additive effects of multiple genes across the whole genome accounted for 30% of individual difference in childhood body weight.

Clare Llewellyn from UCL Health Behaviour Research Centre and lead author of the study, said: "These findings are important because they confirm that in children genes play a very important role in determining body weight. At present only a few genetic variants have been discovered, and these explain a very small amount of individual differences in body weight (~2%). These findings suggest there are hundreds of other genetic variants influencing body weight that are yet to be discovered".

This study underlines the importance of genetic effects in childhood obesity, supporting the current thinking that children of obese parents are most at risk of becoming obese.

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Notes for Editors

1. For more information or to speak to Clare Llewellyn, please contact Rosie Waldron in the UCL Media Relations Office on tel: 44-020-7679-9041, out of hours 44-07917-271-364, e-mail: r.waldron@ucl.ac.uk

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Study finds strong genetic component to childhood obesity

Mar. 25, 2013 A new analysis has found that genetic alterations in a particular cellular pathway are linked with bladder cancer risk, recurrence, disease progression, and patient survival. Published early online in CANCER, a peer- reviewed journal of the American Cancer Society, the findings could help improve bladder cancer screening and treatment.

Alterations in the regulators of G-protein signaling (RGS) pathway, which is important for various cellular processes, have been implicated in several cancers. Eugene Lee, MD, of the MD Anderson Cancer Center in Houston, and his colleagues sought to determine the role of RGS alterations in bladder cancer risk, recurrence, disease progression, and patient survival. Dr. Lee is currently a fellow of Dr. Ashish M. Kamat. The researchers worked together with Dr. Xifeng Wu's Epidemiology Lab. They studied 803 patients with non-muscle invasive or muscle invasive bladder cancer and 803 healthy individuals.

After evaluating 95 single nucleotide alterations or variants in 17 RGS genes, the investigators identified several that were linked with overall risk of bladder cancer. The strongest association was seen with the rs10759 variant on the RGS4 gene: it was linked with a 0.77-fold reduced risk of overall bladder cancer. The researchers also found that with an increasing number of unfavorable variants, the risk of bladder cancer increased. "Screening for bladder cancer has proven to be difficult on a population level, and our work may be a first step in identifying molecular markers for potential genetic-based screening tests. This will help recognize specific groups at increased risk beyond the existing known risk factors such as smoking and chemical exposure," said Dr. Lee.

Dr. Lee and his team also revealed that in patients with non-muscle invasive bladder cancer, 11 variants were linked with recurrence and 13 variants were linked with progression. Ten were associated with earlier death in patients with muscle invasive bladder cancer; rs2344673 was the most significant, with an average survival of 13.3 months in patients with the variant compared with 81.9 months in patients without it.

In the current era of personalized medicine, an individual's genetic information can provide valuable information on screening, treatment, and surveillance. "Our study provides an initial step in how we can use a patient's genetic makeup to identify those at risk for bladder cancer. Furthermore, we can identify patients who already have a diagnosis of bladder cancer that are at increased risk of worsening of disease or dying from their cancer," said Dr. Lee. "The goal is to find as many genetic alterations that confer risk and create a panel of markers that would aid in diagnosis, treatment, and follow- up."

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The medical and human drama of the T-cell therapy, developed at the University of Pennsylvania, is unfolding in ways the defy the staid traditions of scientific research. On Monday, the New England Journal of Medicine fast-tracked online publication of a paper about Children's first two pediatric patients. But those results - and more - have been out for months, released by the researchers at a conference, or by the families.

The first pediatric patient, Emily Whitehead, 7, of Phillipsburg, Pa., who remains in remission after almost dying, was the subject of worldwide headlines in December.

And last week, the larger story - the harnessing of the immune system to fight cancer after decades of trying - broadened beyond Penn and Children's.

Researchers at Memorial Sloan-Kettering Cancer Center in New York published results from five adult leukemia patients treated with an experimental T-cell therapy much like Penn's. Three of them have been in remission for up to two years; one went into remission but died of a blood clot; and one relapsed and died.

Penn's therapy has worked in adults, too, but those seven patients, who had complete or partial remissions, had a less aggressive form of the disease called chronic myelogenous leukemia.

Sloan-Kettering's results are very impressive, Penn researcher David Porter said.

Penn's team, led by Carl June, will soon collaborate with Sloan-Kettering to see which version of the T-cell therapy works better, Porter said.

The two groups use slightly different viral "vectors" to deliver a therapeutic gene into the T cells. That gene programs the T cells to recognize and kill B cells, the blood component that turns malignant in the leukemias.

"One of the issues is how much does the vector contribute to the patient's response," Porter said. "So we'll trade vectors, then give patients T cells made from both vectors."

Penn is also adapting its T-cell therapy to treat solid tumors such as ovarian cancer. Meanwhile, the early success - although in a small number of patients - is stimulating the field of immunotherapy.

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Parents and Children's Hospital researchers await results on an experimental leukemia gene therapy

WITHIN just eight days of starting a novel gene therapy, David Aponte's "incurable" leukaemia had vanished. For four other patients, the same happened within eight weeks, although one later died from a blood clot unrelated to the treatment, and another after relapsing.

The cured trio, who were all previously diagnosed with usually fatal relapses of acute lymphoblastic leukaemia, have now been in remission for between 5 months and 2 years. Michel Sadelain of the Memorial Sloan-Kettering Cancer Center in New York, co-leader of the group that designed the trial, says that a second trial of 50 patients is being readied, and the team is looking into using the technique to treat other cancers.

The key to the new therapy is identifying a molecule unique to the surface of cancer cells, then genetically engineering a patient's immune cells to attack it.

In acute lymphoblastic leukaemia, immune cells called B-cells become malignant. The team were able to target a surface molecule known as CD19 that is only present on B-cells. Doctors extracted other immune cells called T-cells from the patients. These were treated with a harmless virus, which installed a new gene redirecting them to attack all cells bearing CD19. When the engineered T-cells were reinfused into the patients, they rapidly killed all B-cells, cancerous or otherwise.

"The stunning finding was that in all five patients, tumours were undetectable after the treatment," says Sadelain.

He reckons that the body should replenish the immune system with regular T-cells and healthy B-cells after a couple of months. However, the patients received donated bone marrow to ensure they could regrow a healthy immune system (Science Translational Medicine, doi.org/kwz).

The treatment is not the first to re-engineer T-cells to attack a form of leukaemia. Last year, an international company called Adaptimmune used the approach to treat 13 people with multiple myeloma it left 10 in remission.

"Although it's early days for these trials, the approach of modifying a patient's T-cells to attack their cancer is looking increasingly like one that will, in time, have a place alongside more traditional treatments," says Paul Moss of Cancer Research UK.

Sadelain's team is now investigating the scope for attacking other cancers. Where no single surface molecule is unique to a cancer, he is seeking to target pairs of molecules that only occur together on cancer cells. In January, he demonstrated this approach by wiping out human prostate tumours implanted in mice, using T-cells engineered to target two surface molecules (Nature Biotechnology, doi.org/kw2).

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Gene therapy cures leukaemia in eight days

Public release date: 25-Mar-2013 [ | E-mail | Share ]

Contact: Clare LaFond clareh@uw.edu 206-685-1323 University of Washington - Health Sciences/UW News, Community Relations & Marketing

In an animal study, researchers at the University of Washington show that it was possible to use gene therapy to boost heart muscle function. The finding suggests that it might be possible to use this approach to treat patients whose hearts have been weakened by heart attacks and other heart conditions.

Led by University of Washington (UW) Professor and Vice Chair of Bioengineering Michael Regnier and Dr. Chuck Murry, director of the Center for Cardiovascular Biology and co-director of the Institute for Stem Cell and Regenerative Medicine at UW, the study appears online today in the journal Proceedings of the National Academy of Sciences (PNAS).

Normally, muscle contraction is powered by a molecule, the nucleotide called Adenosine-5'-triphosphate (ATP). Other naturally occurring nucleotides can also power muscle contraction, but, in most cases, they have proven to be less effective than ATP.

In an earlier study of isolated muscle, however, Regnier, Murry and colleagues had found that one naturally occurring molecule, called 2 deoxy-ATP (dATP), was actually more effective than ATP in powering muscle contraction, increasing both the speed and force of the contraction, at least over the short-term.

In the new PNAS study, the researchers wanted to see whether this effect could be sustained. To do this, they used genetic engineering to create a strain of mice whose cells produced higher-than-normal levels of an enzyme called Ribonucleotide Reductase, which converts the precursor of ATP, adenosine-5'-diphosphate or ADP, to dADP, which, in turn, is rapidly converted to dATP.

"This fundamental discovery, that dATP can act as a 'super-fuel' for the contractile machinery of the heart, or myofilaments, opens up the possibility to treat a variety of heart failure conditions," Regnier said. "An exciting aspect of this study and our ongoing work is that a relatively small increase in dATP in the heart cells has a big effect on heart performance."

The researchers found that increased production of the enzyme Ribonucleotide Reductase increased the concentration of dATP within heart cells approximately tenfold, and even though this level was still less than one to two percent of the cell's total pool of ATP, the increase led to a sustained improvement in heart muscle function, with the genetically engineered hearts contracting more quickly and with greater force.

"It looks as though we may have stumbled on an important pathway that nature uses to regulate heart contractility," Murry added. "The same pathway that heart cells use to make the building blocks for DNA during embryonic growth makes dATP to supercharge contraction when the adult heart is mechanically stressed."

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Gene therapy may aid failing hearts