Washington, Mar. 26 (ANI): Two kids, who were suffering from an aggressive form of childhood leukemia, had a complete remission after they were treated with a novel cell therapy that reprogrammed their immune cells to rapidly multiply and destroy malignant cells.

7-year-old Emily Whitehead, was featured in news stories in December 2012 after the experimental therapy led to her dramatic recovery after she relapsed following conventional treatment.

11 months after receiving bioengineered T cells that zeroed in on a target found in this type of leukemia, called acute lymphoblastic leukemia (ALL), Emily is now healthy and cancer-free.

The other patient, a 10-year-old girl, who also had a complete response to the same treatment, suffered a relapse two months later when other leukemia cells appeared that did not harbour the specific cell receptor targeted by the therapy.

"This study describes how these cells have a potent anticancer effect in children," said co-first author Stephan A. Grupp, M.D., Ph.D., of The Children's Hospital of Philadelphia, where both patients were treated in this clinical trial.

The current study builds on Grupp's ongoing collaboration with Penn Medicine scientists who originally developed the modified T cells as a treatment for B-cell leukemias.

The new study used a relatively new approach in cancer treatment: immunotherapy that manipulates immune system to increase its cancer-fighting capabilities. Here the researchers engineered T cells to selectively kill another type of immune cell called B cells, which become cancerous.

The researchers removed some of each patient's own T cells and modified them in the laboratory to create a type of CAR (chimeric antigen receptor) cell called a CTL019 cell. These cells are designed to attack a protein called CD19 that occurs only on the surface of certain B cells.

By creating an antibody that recognizes CD19 and then connecting that antibody to T cells, the researchers created in CTL019 cells a sort of guided missile that locks in on and kills B cells, thereby attacking B-cell leukemia.

The research has been published in The New England Journal of Medicine. (ANI)

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Novel T- cell therapy cures aggressive leukemia in 2 kids

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

Contact: Holly Auer holly.auer@uphs.upenn.edu 215-200-2313 University of Pennsylvania School of Medicine

Philadelphia, March 25, 2013 - Two children with an aggressive form of childhood leukemia had a complete remission of their disease-showing no evidence of cancer cells in their bodies-after treatment with a novel cell therapy that reprogrammed their immune cells to rapidly multiply and destroy leukemia cells. A research team from The Children's Hospital of Philadelphia and the University of Pennsylvania published the case report of two pediatric patients Online First today in The New England Journal of Medicine. It will appear in the April 18 print issue.

One of the patients, 7-year-old Emily Whitehead, was featured in news stories in December 2012 after the experimental therapy led to her dramatic recovery after she relapsed following conventional treatment. Emily remains healthy and cancer-free, 11 months after receiving bioengineered T cells that zeroed in on a target found in this type of leukemia, called acute lymphoblastic leukemia (ALL).

The other patient, a 10-year-old girl, who also had a complete response to the same treatment, suffered a relapse two months later when other leukemia cells appeared that did not harbor the specific cell receptor targeted by the therapy.

"This study describes how these cells have a potent anticancer effect in children," said co-first author Stephan A. Grupp, M.D., Ph.D., of The Children's Hospital of Philadelphia, where both patients were treated in this clinical trial. "However, we also learned that in some patients with ALL, we will need to further modify the treatment to target other molecules on the surface of leukemia cells."

Grupp is the director of Translational Research for the Center for Childhood Cancer Research at The Children's Hospital of Philadelphia, and a professor of Pediatrics at the Perelman School of Medicine at the University of Pennsylvania. Michael Kalos, Ph.D., an adjunct associate professor in the department of Pathology and Laboratory Medicine in the Perelman School of Medicine at Penn, is co-first author on the study.

The current study builds on Grupp's ongoing collaboration with Penn Medicine scientists who originally developed the modified T cells as a treatment for B-cell leukemias. The Penn team reported on early successful results of a trial using this cell therapy in three adult chronic lymphocytic leukemia (CLL) patients in August of 2011. Two of those patients remain in remission more than 2 years following their treatment, and as the Penn researchers reported in December 2012 at the annual meeting of the American Society of Hematology, seven out of ten adult patients treated at that point responded to the therapy. The team is led by the current study's senior author, Carl H. June, M.D., the Richard W. Vague Professor in Immunotherapy in the department of Pathology and Laboratory Medicine and the Perelman School of Medicine at the University of Pennsylvania and director of Translational Research in Penn's Abramson Cancer Center.

"We're hopeful that our efforts to treat patients with these personalized cellular therapies will reduce or even replace the need for bone marrow transplants, which carry a high mortality risk and require long hospitalizations," June said. "In the long run, if the treatment is effective in these late-stage patients, we would like to explore using it up front, and perhaps arrive at a point where leukemia can be treated without chemotherapy."

The research team colleagues adapted the original CLL treatment to combat another B-cell leukemia: ALL, which is the most common childhood cancer. After decades of research, oncologists can currently cure 85 percent of children with ALL. Both children in the current study had a high-risk type of ALL that stubbornly resists conventional treatments.

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T- cell therapy eradicates an aggressive leukemia in 2 children

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PHILDELPHIA Two children with an aggressive form of childhood leukemia had a complete remission of their diseaseshowing no evidence of cancer cells in their bodiesafter treatment with a novel cell therapy that reprogrammed their immune cells to rapidly multiply and destroy leukemia cells. A research team from The Childrens Hospital of Philadelphia and the University of Pennsylvania published the case report of two pediatric patients Online First today in The New England Journal of Medicine. It will appear in the April 18 print issue.

The other patient, a 10-year-old girl, who also had a complete response to the same treatment, suffered a relapse two months later when other leukemia cells appeared that did not harbor the specific cell receptor targeted by the therapy.

This study describes how these cells have a potent anticancer effect in children, said co-first author Stephan A. Grupp, M.D., Ph.D., of The Childrens Hospital of Philadelphia, where both patients were treated in this clinical trial. However, we also learned that in some patients with ALL, we will need to further modify the treatment to target other molecules on the surface of leukemia cells.

Grupp is the director of Translational Research for the Center for Childhood Cancer Research at The Childrens Hospital of Philadelphia, and a professor of Pediatrics at the Perelman School of Medicine at the University of Pennsylvania. Michael Kalos, Ph.D., an adjunct associate professor in the department of Pathology and Laboratory Medicine and director of the Translational and Correlative Studies Laboratory in the Perelman School of Medicine at Penn, is co-first author on the study.

The current study builds on Grupps ongoing collaboration with Penn Medicine scientists who originally developed the modified T cells as a treatment for B-cell leukemias. The Penn team reported on early successful results of a trial using this cell therapy in three adult chronic lymphocytic leukemia (CLL) patients in August of 2011. Two of those patients remain in remission more than 2 years following their treatment, and as the Penn researchers reported in December 2012 at the annual meeting of the American Society of Hematology, seven out of ten adult patients treated at that point responded to the therapy. The team is led by the current studys senior author, Carl H. June, M.D., the Richard W. Vague Professor in Immunotherapy in the department of Pathology and Laboratory Medicine and the Perelman School of Medicine at the University of Pennsylvania and director of Translational Research in Penns Abramson Cancer Center.

Were hopeful that our efforts to treat patients with these personalized cellular therapies will reduce or even replace the need for bone marrow transplants, which carry a high mortality risk and require long hospitalizations, June said. In the long run, if the treatment is effective in these late-stage patients, we would like to explore using it up front, and perhaps arrive at a point where leukemia can be treated without chemotherapy.

The research team colleagues adapted the original CLL treatment to combat another B-cell leukemia: ALL, which is the most common childhood cancer. After decades of research, oncologists can currently cure 85 percent of children with ALL. Both children in the current study had a high-risk type of ALL that stubbornly resists conventional treatments.

The new study used a relatively new approach in cancer treatment: immunotherapy, which manipulates the immune system to increase its cancer-fighting capabilities. Here the researchers engineered T cells to selectively kill another type of immune cell called B cells, which had become cancerous.

T cells are the workhorses of the immune system, recognizing and attacking invading disease cells. However, cancer cells fly under the radar of immune surveillance, evading detection by T cells. The new approach custom-designs T cells to see and attack the cancer cells.

The researchers removed some of each patients own T cells and modified them in the laboratory to create a type of CAR (chimeric antigen receptor) cell called a CTL019 cell. These cells are designed to attack a protein called CD19 that occurs only on the surface of certain B cells.

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T- Cell Therapy Eradicates an Aggressive Leukemia in Two Children

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Mar. 22, 2013 A new mechanism for guiding the growth of nerves that involves cell-death machinery has been found by scientists at the University of Nevada, Reno that may bring advances in neurological medicine and research. The team obtained the evidence in studies of fruit flies and reported their discovery in an article published in the publication Cell Reports.

"Although the fly is a relatively simple organism, almost every gene identified in this species appears to be carrying out similar functions in humans," said Thomas Kidd, associate professor in the University's biology department in whose lab the work was performed.

The Kidd lab is part of a $10 million Center for Biomedical Research Excellence Project in Cell Biology of Signaling at the University, which is funded by the National Institute of Health's Institute of General Medical Sciences. The project is also funded by the National Science Foundation.

"Flies are useful because the neural mechanisms we are studying are similar to those in mammals," said Gunnar Newquist, lead author of the Cell Reports article and a post-doctoral neuroscience researcher in Kidd's lab. "We've found something no one has seen before, that blocking the cell-death pathway can make nerves deprived of guidance cues figure out the right way to connect with other neurons. This was completely unexpected and novel, but really exciting because it changes the way we look at nerve growth.

"Neurons have a natural ability to die, if they fail to make the right connections they usually die. Neurons, like most other cell types, have the capacity to commit suicide and many do so during the formation of the nervous system."

The wiring of nervous systems is composed of axons, specialized extensions of neurons that transmit electrical impulses. During development axons navigate long distances to their targets by using signals in their environment. Netrin-B is one of those signals. Kidd, Newquist and colleagues have shown that Netrin-B also keeps neurons alive.

"Take away the Netrin-B and growth and cell death goes haywire," Newquist said.

This led them to the discovery that the cell-death machinery is active in growing nerves, and appears to be an integral part of the navigation mechanism.

"We use fruit fly genetics to study how these axons navigate these long distances correctly when developing," Kidd said. "Understanding the mechanisms they use to navigate is of great interest, not only for understanding how our brains form, but also as a starting point to devise ways to stimulate the re-growth of axons after injury, especially spinal cord injuries.

"Our work suggests that therapeutics designed to keep neurons alive after injury may be able to stimulate neurons to start re-growing or sprouting new connections."

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Nerve regeneration research and therapy may get boost from new discovery

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

Contact: Press Office press.office@admin.ox.ac.uk 44-018-652-80530 University of Oxford

The first multi-gene DNA sequencing test that can help predict cancer patients' responses to treatment has been launched in the National Health Service (NHS), thanks to a partnership between scientists at the University of Oxford and Oxford University Hospitals NHS Trust.

The test uses the latest DNA sequencing techniques to detect mutations across 46 genes that may be driving cancer growth in patients with solid tumours. The presence of a mutation in a gene can potentially determine which treatment a patient should receive.

The researchers say the number of genes tested marks a step change in introducing next-generation DNA sequencing technology into the NHS, and heralds the arrival of genomic medicine with whole genome sequencing of patients just around the corner.

The many-gene sequencing test has been launched through the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre (BRC), a collaboration between Oxford University Hospitals NHS Trust and Oxford University to accelerate healthcare innovation, and which has part-funded this initiative.

The BRC Molecular Diagnostics Centre carries out the test. The lab, based at Oxford University Hospitals, covers all cancer patients in the Thames Valley area. But the scientists are looking to scale this up into a truly national NHS service through the course of this year.

The new 300 test could save significantly more in drug costs by getting patients on to the right treatments straightaway, reducing harm from side effects as well as the time lost before arriving at an effective treatment.

'We are the first to introduce a multi-gene diagnostic test for tumour profiling on the NHS using the latest DNA sequencing technology,' says Dr Jenny Taylor of the Wellcome Trust Centre for Human Genetics at Oxford University, who is programme director for Genomic Medicine at the NIHR Oxford BRC and was involved in the work. 'It's a significant step change in the way we do things. This new 46 gene test moves us away from conventional methods for sequencing of single genes, and marks a huge step towards more comprehensive genome sequencing in both infrastructure and in handling the data produced.'

Dr Anna Schuh, who heads the BRC Molecular Diagnostics Centre and is a consultant haematologist at Oxford University Hospitals, adds: 'Patients like the idea of a test that can predict and say up front whether they will respond to an otherwise toxic treatment. What the patient sees is no different from present. A biopsy is taken from the patient's tumour for genetic testing with a consultant talking through the results a few days later. It is part of the normal diagnostic process.'

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46 gene sequencing test for cancer patients on the NHS

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Mar. 25, 2013 The first multi-gene DNA sequencing test that can help predict cancer patients' responses to treatment has been launched in the National Health Service (NHS), thanks to a partnership between scientists at the University of Oxford and Oxford University Hospitals NHS Trust.

The test uses the latest DNA sequencing techniques to detect mutations across 46 genes that may be driving cancer growth in patients with solid tumours. The presence of a mutation in a gene can potentially determine which treatment a patient should receive.

The researchers say the number of genes tested marks a step change in introducing next-generation DNA sequencing technology into the NHS, and heralds the arrival of genomic medicine with whole genome sequencing of patients just around the corner.

The many-gene sequencing test has been launched through the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre (BRC), a collaboration between Oxford University Hospitals NHS Trust and Oxford University to accelerate healthcare innovation, and which has part-funded this initiative.

The BRC Molecular Diagnostics Centre carries out the test. The lab, based at Oxford University Hospitals, covers all cancer patients in the Thames Valley area. But the scientists are looking to scale this up into a truly national NHS service through the course of this year.

The new 300 test could save significantly more in drug costs by getting patients on to the right treatments straightaway, reducing harm from side effects as well as the time lost before arriving at an effective treatment.

'We are the first to introduce a multi-gene diagnostic test for tumour profiling on the NHS using the latest DNA sequencing technology,' says Dr Jenny Taylor of the Wellcome Trust Centre for Human Genetics at Oxford University, who is programme director for Genomic Medicine at the NIHR Oxford BRC and was involved in the work. 'It's a significant step change in the way we do things. This new 46 gene test moves us away from conventional methods for sequencing of single genes, and marks a huge step towards more comprehensive genome sequencing in both infrastructure and in handling the data produced.'

Dr Anna Schuh, who heads the BRC Molecular Diagnostics Centre and is a consultant haematologist at Oxford University Hospitals, adds: 'Patients like the idea of a test that can predict and say up front whether they will respond to an otherwise toxic treatment. What the patient sees is no different from present. A biopsy is taken from the patient's tumour for genetic testing with a consultant talking through the results a few days later. It is part of the normal diagnostic process.'

Cancer is often described as a genetic disease, since the transition a cell goes through in becoming cancerous tends to be driven by changes to the cell's DNA. And increasingly, new cancer drugs depend on knowing whether a mutation in a single gene is present in a patient's cancer cells.

For example, a lung cancer patient may have a biopsy taken to check for changes in the EGFR gene. If there is a mutation, the patient may then be treated with a drug that works as an EGFR inhibitor. If there is no mutation, such drugs won't work and the patient would get a different drug that would be more effective for them. Knowing the presence or absence of mutations in a certain gene can choose the treatment path for that patient.

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Forty-six gene sequencing test for cancer patients in UK

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Black Ops 2: Genetic Engineering
What #39;s up guys?! If you enjoyed the video please give it a like! If you haven #39;t already, please subscribe!!

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World #39;s Greatest

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Synthetic biology has made such strides in recent years that the notion of reviving extinct species is no longer crazy talk. Researchers gathered recently in Washington, D.C. to discuss the prospects of bringing back a whole menagerie of fascinating creatures, including the passenger pigeon, once the most numerous bird in North America.

At least one scientist is busy devising a strategy to teach that genetic replica how to live like its flocking, migrating natural ancestors did. But other scientists arent convinced you could ever call this bird a true passenger pigeon.

Everything we know about species and individuals tells us that were a lot more than our genes, said David Blockstein of the National Council for Science and the Environment.

For one thing, an animals genes are influenced by its environment though chemical changes to DNA that affect how genes switch on and off. Those epigenetic changes may be a crucial part of what gives a species its unique characteristics, but the epigenetic profile of a bird created in a lab would never be the same as that of a bird raised in a flock by its natural parents, Blockstein says.

Conservation biologist David Ehrenfeld of Rutgers University is skeptical too.Lets say we could create a passenger pigeon with the same DNA and the same epigenetic marks, he said. That doesnt make it a passenger pigeon.

Ehrenfeld and others say passenger pigeons were perhaps the most social birds that have ever existed, living in flocks of hundreds of thousands. They needed enormous populations to nest properly and repel predators, Ehrenfeld said. Their behavior, as much as their DNA, defined the species.

This concept isnt lost on the people behind the plan to revive the passenger pigeon.

In my opinion you have to recreate the social structure, said Ben Novak, a young scientist who is heading the project, supported by a group called Revive & Restore. Novak outlined his plan at the meeting in Washington, and he described it in more detail in an interview with Wired last week.

The first passenger pigeons would be raised in captivity, with surrogate parents of a related species. Novak plans to cosmetically alter the surrogates with dyes to give them the reddish bellies and grey wings of passenger pigeons. These indoor aviaries would be adorned with tree branches and decorated to be as forest-like as possible. Ideally, birds would even have to forage for their own food, Novak says. After a few years of captive breeding to build up the population, the birds would gradually be transferred to outdoor aviaries.

As the captive flock continues to grow, Novak plans to train homing pigeons as guides to teach the passenger pigeons to migrate along the flyways of their extinct ancestors. The idea would be to dye the homing pigeons so they look like passenger pigeons, allow young passenger pigeons to imprint on them, and then release them all and hope that the passenger pigeons follow their homing-pigeon guides.

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Say We Really Do Bring the Passenger Pigeon Back From Extinction — Then What?

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Mar. 24, 2013 Research conducted in fruit flies at the University of North Carolina School of Medicine has pinpointed a specific DNA sequence that both triggers the formation of the "histone locus body" and turns on all the histone genes in the entire block.

Every time a cell divides it makes a carbon copy of crucial ingredients, including the histone proteins that are responsible for spooling yards of DNA into tight little coils. When these spool-like proteins aren't made correctly, it can result in the genomic instability characteristic of most birth defects and cancers.

Seven years ago, Dr. Joe Gall of the Carnegie Institute in Baltimore, Md. and coworkers noticed an aggregation of molecules along a a block of genome that codes for the critical histones, but they had no idea how this aggregate or "histone locus body" was formed.

Now, research conducted in fruit flies at the University of North Carolina School of Medicine has pinpointed a specific DNA sequence that both triggers the formation of this "histone locus body" and turns on all the histone genes in the entire block.

The finding, published March 25, 2013 in the journal Developmental Cell, provides a model for the coordinated synthesis of histones needed for assembly into chromatin, a process critical to keeping chromosomes intact and passing genetic information from generation to generation.

"Our study has uncovered a new relationship between nuclear architecture and gene activity," said senior study author Bob Duronio, PhD, professor of biology and genetics at UNC. "In order to make chromosomes properly, you need to make these histone building blocks at the right time and in the right amount. We found that the cell has evolved this complex architecture to do that properly, and that involves an interface between the assembly of various components and the turning on of a number of genes."

In the fruit fly, as in the human, the five different histone genes exist in one long chunk of the genome. The "histone locus" in flies contains 100 copies of each of the five genes, encompassing approximately 500,000 nucleotides of A's, C's, T's and G's. The proteins required for making the histone message -- a process that must happen every time a new strand of DNA is copied -- come together at this "histone locus" to form the "histone locus body."

Duronio and co-senior study author William Marzluff, PhD, Kenan Distinguished Professor of Biochemistry and Biophysics, wanted to figure out how these factors knew to meet at the histone locus.

They inserted different combinations of the five histone genes into another site of the genome, and looked to see which combinations recruited a new histone locus body. The researchers found that combinations that contained a specific 300 nucleotide sequence -- the region between the H3 and H4 histone genes -- formed a histone locus body. In contrast, combinations of genes that lacked this sequence did not form the body. They went on to show that this sequence turned on not only the H3 and H4 genes in its direct vicinity, but also other histone genes in the block.

Though the research was conducted entirely in fruit flies, it may lend insight into mechanisms that keep the genome from becoming unstable -- and causing early death or illness -- in higher organisms.

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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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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.

###

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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Genetics Mod Sneek Peek [Sonic Extractor Item]
Just a sneak peek of my new my Genetics Mod 😉 enjoy -------------------------------------------------------------------------------------------------------...

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IMPROVEMENT IN THE HEALTH OF INDIVIDUALS WITH ADHD: WHAT IS THE ROLE OF THE ASSOCIATIONS IN EUROPE?
Speakers: Andrea Bilbow - ADDISS - UK.

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GNDU jashan 2013 giddha by social science dept.

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Richard McGee, M.D.
Dr. Richard McGee is a medical oncologist and hematologist at the Swedish Cancer Institute. His special interests are in cancer research, advances in cancer ...

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Runescape 2007 | B0aty - First PK Trip !
2000 for my return to RuneScape PKing? ;D I #39;m absolutely so happy with this 🙂 Possibly the best first video i could of uploaded, unfortunately i #39;m not that...

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More Mobs Minecraft Ep 6- DNA!
There was a bit of a problem with this world and the update to 1.5. I am working on fixing the problem but I have a feeling I might have to wait for the mods...

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Losing Fat on Lower Abs Stomach
Thanks for the support! Please LIKE and COMMENT if you enjoy! #9675; Top 5 Bodybuilding Snacks: http://youtu.be/s0CLtvWk3dc #9675; Six Pack Abs Workout: http://youtu.b...

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YOU CAN #39;T BEAT ME! (The Hidden)
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Can I Get Rid of "Gyno"?
Sign up Grow Stronger Newsletter: http://hulsestrength.com/go/youtube Elliott #39;s Other Channel: http://www.youtube.com/user/elliottsaidwhat Elliott #39;s Facebook...

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MIND GAMES (The Hidden)
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Carbing Up Before Bed?
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