Archive for the ‘Gene Therapy Research’ Category

Extraterrestes,camino hacia la Luz-Vol.038-Luz Genética.(2ª)Juan Marco
La genética produce diferentes informaciones para su manifestación en la vida, una parte, biológica, otra psicosomática, la más importante; como podemos apre...

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369| Protective Style Files, a New Journey! v.1
WATCH IN HD! Please check here for answers to your question. Thank you. I love you for watching. Visit my website! http://KinkyCurlyCoilyMe.com Hey loves! #39;v...

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369| Protective Style Files, a New Journey! v.1 - Video

Season 5 - Episode 49 Fabricators and Genes
Now that Xycraft is out, I get to show you guys Fabricators! Meanwhile, I #39;m working with Genetics.... Keep up with my thread here: http://www.minecraftforum....

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Season 5 - Episode 49 Fabricators and Genes - Video

La scienza narrata - Vicenza 7.02.2013 - Lezione prof. Edoardo Boncinelli
Lezione del Prof. Edoardo Boncinelli (genetista e docente universitario) Palazzo Cordellina 7.02.2013 Sono intervenuti i docenti: Dott. Giovanni Nucci e Prof...

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La scienza narrata - Vicenza 7.02.2013 - Lezione prof. Edoardo Boncinelli - Video

Qu #39;est-ce que l #39;agroécologie? Bernard Chevassus-au-Louis en parle à Gembloux Agro-Bio Tech (ULg)
"Quelques principes d #39;agroécologie", c #39;est le thème de la conférence donnée par Bernard Chevassus-au-Louis à Gembloux Agro-Bio Tech le 22 mars 2013. Bernard ...

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Qu'est-ce que l'agroécologie? Bernard Chevassus-au-Louis en parle à Gembloux Agro-Bio Tech (ULg) - Video

I #39;m a Gym Virgin, What Should I Do?
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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Newswise STONY BROOK, NY, March 26, 2013 The possible link between genetics and the development of autism will be the topic of the 17th Annual Swartz Foundation Mind/Brain Lecture at Stony Brook University on Monday, April 1, 2013 at 4:30 pm on the Main Stage of the Staller Center for the Arts. Guest lecturer Michael Wigler, Professor of Genetics at Cold Spring Harbor Laboratory and a trailblazer in the field of biomedical research, will present his findings on the connection.

The lecture, Considering the Genetics of Cognitive Function Through the Prism of Autism, is intended for a general audience and free and open to the public. The Mind/Brain Lecture Series is sponsored by Stony Brook University and its Department of Neurobiology and Behavior, and by The Swartz Foundation, which supports research at 11 centers for theoretical and computational neuroscience.

During the discussion, Professor Wigler will detail how genetics may be involved in the development of autism. The terms autism and autism spectrum disorders are used to describe a common developmental cognitive-behavioral disorder characterized by disabling defects in social response and communication, along with inappropriate repetitive behaviors. There is a strong male bias among those diagnosed, especially among the lesser affected. While the influence of the environment is a factor in causation, the involvement of genetics is clear.

The autism risk for a newborn is more than tenfold higher if a prior sibling has the disorder, and nearly 50 percent for a male newborn if two previous siblings have been affected. Professor Wigler will discuss the evidence that new mutations in the parental germline, especially the fathers, contributes to the disorder, and increases with parental age. He will present a unified model that seeks to explain sporadic and familial autism.

Professor Wiglers lab estimates from the mutation data that the number of target genes is on the order of hundreds, and they have identified several dozen likely gene targets, many of which may be linked to neuroplasticity, the process by which our brains adapt to change. Although a very significant advance, the genetics does not yet fully explain the observed incidence rate. Professor Wigler will discuss the reason why, what scientists may be missing and what his research may mean for future treatment of those with autism.

The Swartz Foundation is pleased to have Professor Wigler as the guest lecturer at the 2013 Mind/Brain Lecture, said Dr. Jerome Swartz, Chairman of The Swartz Foundation. Professor Wigler's work on autism, especially the effects of new mutations of the gene transfers on the newborn's neural systems, are an intriguing and potentially powerful insight into a growing and frightening disease epidemic. It is very likely that not only will this research provide important information on autism, but it may also give us further insights into the normal workings of our neurological structures.

Please arrive early as seating is limited. A reception with the speaker will immediately follow the talk. For more on the lecture and to watch a preview video of Professor Wigler discussing his genetic/autism research, visit http://www.stonybrook.edu/sb/mind.

###

About the Speaker Michael Wigler has been a trailblazer in the field of biomedical research, including human genetic disorders, population genetics and cancer genomics, and his contributions to the field of mammalian genetics have led to breakthroughs in the treatment of strokes, heart disease and cancer. Wiglers work on mammalian cell gene transfer is nothing short of groundbreaking with several major scientific discoveries occurring behind the walls of Cold Spring Harbor Laboratory, where he has been since 1979. Wigler remains on the forefront of molecular cancer research, unraveling the mysteries of the genetic mutations driving the evolution of cancer cells and those that underlie genetic diseases, such as autism, and discovering new disease-causing genes.

About The Swartz Foundation The Swartz Foundation was established by Jerry Swartz in 1994 to explore the application of mathematical physics, computer science and engineering principles to neurobiology, as a path to better understand the brain/mind relationship. The Foundation supports post-doc research in computational neuroscience at 11 universities and scientific institutions, through centers at Harvard University, Princeton University, Yale University, Columbia University, Cold Spring Harbor Laboratory, and UC San Diego, and in partnership with the Sloan Foundation at their five Centers for Theoretical Neurobiology at Salk Institute, Cal Tech, UC San Francisco, NYU/Courant and Brandeis University. Learn more at http://www.TheSwartzFoundation.org.

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Stony Brook University Mind/Brain Lecture: The Connection Between Genetics and Autism

SALT LAKE CITY, March 26, 2013 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) today announced that it has signed an agreement with PharmaMar, a leader in the development of marine-derived drugs. Under the terms of the agreement, Myriad will conduct homologous recombination deficiency (HRD) testing on patients enrolled in PharmaMar's Phase II clinical study of PM1183, a novel drug candidate which induces double-stranded DNA breaks to cause cell death. This partnership represents Myriad Genetics' first publicly announced commercial collaboration with its new HRD test.

"We are very pleased to collaborate with PharmaMar on their PM1183 development program with our new HRD test," said Peter Meldrum, President and Chief Executive Officer of Myriad Genetics, Inc. "We believe HRD status is the most effective mechanism for assessing patient response to DNA-damaging drugs and look forward to working closely with PharmaMar on this exciting new companion diagnostic program."

Myriad's HRD test is able to detect when a tumor has lost the ability to repair DNA damage and would therefore be more susceptible to the DNA-damaging classes of drugs. The test directly measures the end result of the loss of the DNA repair function regardless of the genomic causation. The HRD test is effective at detecting the loss of function irrespective of whether the defects in the genes involved in the DNA repair mechanism were caused by hereditary germ line mutations or somatic mutations accumulated during the patient's life.

Myriad's HRD test has been shown to accurately predict drug response in both ovarian cancer patients and triple negative breast cancer patients. It is estimated that 490,000 Americans are diagnosed with cancers each year that are eligible for treatment with DNA damaging classes of drugs. This represents a one to two billion dollar market opportunity for the HRD test in the United States alone.

Under the terms of the agreement, Myriad will assess HRD status in patients who have been treated with PM1183 in PharmaMar's Phase II clinical study. Utilizing this information, Myriad and PharmaMar will hope to garner more information surrounding the role of HRD status in PM1183 response.

About PharmaMar

PharmaMar is a biopharmaceutical subsidiary of Grupo Zeltia; it is a world leader in discovering, developing and selling marine-based drugs to treat cancer. Yondelis(R) is Spain's first antitumour drug. Yondelis(R) is currently approved for soft tissue sarcoma (STS) in 42 countries outside the EEA, and for platinum-sensitive relapsed ovarian cancer (ROC) in 31 of those countries plus Brazil. Yondelis(R) is approved for STS and platinum-sensitive ROC in all 30 countries of the EEA. Yondelis(R) is also undergoing Phase II trials on breast and paediatric cancers. PharmaMar has four other compounds in clinical development: Aplidin(R), PM01183, Zalypsis(R) and PM060184. PharmaMar also has a rich pipeline of pre-clinical candidates and a major R&D program. For more information, please visit the Company's website: http://www.pharmamar.com

About Myriad Genetics

Myriad Genetics is a leading molecular diagnostic company dedicated to making a difference in patients' lives through the discovery and commercialization of transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess risk of disease progression and recurrence. Myriad's portfolio of molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a commitment to improving an individual's decision making process for monitoring and treating disease. Myriad is focused on strategic directives to introduce new products, including companion diagnostics, as well as expanding internationally. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

Myriad, the Myriad logo, BART, BRACAnalysis, Colaris, Colaris AP, Melaris, TheraGuide, Prezeon, OnDose, Panexia and Prolaris are trademarks or registered trademarks of Myriad Genetics, Inc. in the United States and foreign countries. MYGN-G

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Myriad and PharmaMar Announce First Commercial Partnership With Myriad's New HRD Test

Mar. 27, 2013 Researchers have identified genetic risk factors that may accelerate a teen's progression to becoming a lifelong heavy smoker.

The team of scientists from the U.S., the U.K. and New Zealand examined earlier studies by other research teams to develop a genetic risk profile for heavy smoking. Then they looked at their own long-term study of 1,000 New Zealanders from birth to age 38 to identify whether individuals at high genetic risk got hooked on cigarettes more quickly as teens and whether, as adults, they had a harder time quitting.

Study participants who had the high-risk genetic profile were found to be more likely to convert to daily smoking as teenagers and then progress more rapidly to heavy smoking (a pack a day or more). When assessed at age 38, the higher-risk individuals had smoked heavily for more years, had more often developed nicotine dependence and were more likely to have failed in attempts to quit smoking.

"Genetic risk accelerated the development of smoking behavior," said Daniel Belsky, a post-doctoral research fellow at Duke University's Center for the Study of Aging and Human Development and the Duke Institute for Genome Sciences & Policy. "Teens at a high genetic risk transitioned quickly from trying cigarettes to becoming regular, heavy smokers."

A person's genetic risk profile did not predict whether he or she would try cigarettes. But for those who did try cigarettes, having a high-risk genetic profile predicted increased likelihood of heavy smoking and nicotine dependence.

The findings appear March 27 in JAMA Psychiatry. They were supported by multiple grants from the U.S. National Institutes of Health, as well as the U.K. Medical Research Council and the New Zealand Health Research Council.

The Duke researchers developed a new "genetic risk score" for the study by examining prior genome-wide associations (GWAS) of adult smokers. These studies scanned the entire genomes of tens of thousands of smokers to identify variants that were more common in the heaviest smokers. The variants they identified were located in and around genes that affect how the brain responds to nicotine and how nicotine is metabolized, but it is not yet known how the specific variants affect gene function.

It makes sense that the genes on which the group based their risk score are involved in nicotine metabolism and sensitivity, said Jed Rose, a Duke nicotine addiction researcher who was not involved in this study. "Addictions are a learned behavior and it requires reinforcement through neural pathways."

In their first step, the researchers found the genetic risk score they developed was able to predict heavy smoking among individuals in two large databases created by other researchers.

Then they turned to their New Zealand sample of 880 individuals of European descent to see whether the genetic risk score predicted who initiated smoking, who progressed to heavy smoking, and who developed nicotine dependence and experienced relapse after quitting.

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Genetics might determine which smokers get hooked

Gene Therapy infomercial
A Gene therapy infomercial.

By: Nicholas Totah

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Gene Therapy infomercial - Video

Washington, Mar. 27 (ANI): Researchers have shown that it is possible to use gene therapy to treat patients whose hearts have been weakened by cardiac arrests and other heart conditions.

The research group was 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.

Normally, muscle contraction is powered by a molecule, the nucleotide called Adenosine-5'-triphosphate (ATP).

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

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

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.

"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," Murry said.

Importantly, the elevated dATP effect was achieved without imposing additional metabolic demands on the cells, suggesting the modification would not harm the cell's functioning over the long-term.

The findings suggest that treatments that elevate dATP levels in heart cells may prove to be an effective treatment for heart failure.

The study has been published in the journal Proceedings of the National Academy of Sciences (PNAS). (ANI)

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Gene therapy may help restore heart function after attack

Stem Cell Therapy for Pets - Guiness Before After
Amazing before and after footage of Guiness, an 11 year old dog who received stem cell therapy for his arthritis and got an unexpected side benefit. For more...

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Stem Cell Therapy for Pets - Guiness Before

Stem Cell Therapy for Pets - Laleigh Before After
Amazing before and after footage of Laleigh, a 10 year old dog who received stem cell therapy for arthritis. For more information about stem cell therapy for...

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Stem Cell Therapy for Pets - Laleigh Before

Stem Cell Therapy for Pets - Sammy Before After
Amazing before and after footage of Sammy, a yellow lab who received stem cell therapy for his arthritic joints. For more information about stem cell therapy...

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Stem Cell Therapy for Pets - Sammy Before

Watch Stem Cell Therapy Cures Paralyzed Vet Video

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Watch Stem Cell Therapy Cures Paralyzed Vet Video - Video

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

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

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

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

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

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

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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Black Ops 2: Genetic Engineering - Video

World #39;s Greatest

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World's Greatest - Video

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?

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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Genetic sequence that helps to coordinate synthesis of DNA-packaging proteins identified