Bobby Gaspar: "Translational research in the ex vivo gene therapy of monogenic diseases"
Educational Day* at ESGCT Conference in Madrid. "Translational research in the ex vivo gene therapy of monogenic diseases". Bobby Gaspar, Professor of Paedi...

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Ruben Hernandez: "Recent developments in the gene therapy of solid tumours"
Educational Day* at ESGCT Conference in Madrid. Rubn Hernndez, PI in Cancer Gene Therapy at Universita de Nvarra (University of Navarra, Spain) gives a le...

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Odile Cohen: "Ethic issues in cell and gene therapy"
Dr Odile COHEN HAGUENAUER, MCU-PH at Hpital Saint-Louis and School of Medicine at Denis Diderot University (Paris 7), talks about "Ethical Issues in Cell an...

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Personalized Gene Therapy Reducing HIV In Some Patients
For the first-time ever, doctors at the University of Pennsylvania have successfully used personalized gene therapy in a dozen patients with HIV, knocking the virus down to the point where...

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Newswise UCLA stem cell researchers have pioneered a stem cell gene therapy cure for children born with adenosine deaminase (ADA)-deficient severe combined immunodeficiency (SCID), often called Bubble Baby disease, a life-threatening condition that if left untreated can be fatal within the first year of life.

The groundbreaking treatment was developed by renowned stem cell researcher and UCLA Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research member Dr. Donald Kohn, whose breakthrough was developed over three decades of research to create a gene therapy that safely restores immune systems in children with ADA-deficient SCID using the patients own cells with no side effects.

To date, 18 children with SCID have been cured of the disease after receiving the stem cell gene therapy in clinical trials at UCLA and the National Institutes of Health.

All of the children with SCID that I have treated in these stem cell clinical trials would have died in a year or less without this gene therapy, instead they are all thriving with fully functioning immune systems said Kohn, a professor of pediatrics and of microbiology, immunology and molecular genetics in Life Sciences.

To protect children born with SCID they are kept in isolation, in controlled environments because without an immune system they are extremely vulnerable to illness and infection that could be lethal.

Other current options for treating ADA-deficient SCID are not always optimal or feasible for many children, said Kohn. We can now, for the first time, offer these children and their families a cure, and the chance to live a full healthy life.

Defeating ADA-Deficient SCID: A Game-Changing Approach

Children born with SCID, an inherited immunodeficiency, are generally diagnosed at about six months. They are extremely vulnerable to infectious diseases, and in a child with ADA-deficient SCID even the common cold can prove fatal. The disease causes cells to not create an enzyme called ADA, which is critical for production of the healthy white blood cells that drive a normal, fully-functioning immune system. About 15 percent of all SCID patients are ADA-deficient.

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UCLA Stem Cell Researcher Pioneers Gene Therapy Cure for Children with "Bubble Baby" Disease

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LOS ANGELES (KABC) --

In bright daylight, 10-year-old Mark Devoe has no trouble seeing his friends. But inside or even in the shade, Mark's eyes sometimes don't work.

"I have trouble seeing like, trees, when the road ends, and when there's like a drop there," said Mark.

At age 6, Mark's doctors diagnosed him with the genetic condition choroideremia, which causes people to progressively lose vision until they are completely blind.

"I don't know what it's like to live in darkness, but I've seen it," said Susan Devoe, Mark's mother.

Susan is a carrier of the blindness gene. Mark's grandfather has the condition.

"Watching my father go blind was devastating," said Susan. "I was a little girl. You know, you count on daddy to do things, and daddy couldn't do them."

Dr. Jean Bennett is one of two U.S. researchers preparing to test a gene therapy for choroideremia in humans.

"I think gene therapy holds a huge promise for developing treatments for blinding diseases," said Bennett.

Researchers will use a virus carrying a small choroideremia gene and inject the virus just under the retina. The gene should begin to work in a few weeks.

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Gene treatment promising in fight against degenerative blindness

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The gene therapy that has seemingly cured a 2-year-old girl could be used to treat other diseases, like Sickle Cell Anemia.

UCLA DR. DONALD KHON has perfected the treatment that has now affected the lives of over a dozen families, including the parents of Evangelina, who was born with the deadly SCID. The immune system disease is known by its common name, Bubble Baby disease, because the children have to live in bubbles, since their immune systems do not function. Most die within the first year of life, unless they can get and survive a bone marrow transplant.

Evangelina's twin sister, Annabella, was not a bone marrow transplant. So Dr Kohn included the sick twin in his study, transfering the patient's own bone marrow to the child. At two, her immune system is working well.

It's a difficult and time consuming process, but it seems to work. The same procedure could work with other blood diseases that are curable with bone marrow transfusions. That includes sickle cell anemia, which will be the focus of the next trial.

The implications are huge, as there are 30 or 40 diseases where the treatment could work.

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Bubble Baby: Gene Therapy Cured 2-year-old Girl Of Deadly SCID At UCLA

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Newswise UCLA stem cell researchers have pioneered a stem cell gene therapy cure for children born with adenosine deaminase (ADA)-deficient severe combined immunodeficiency (SCID), often called Bubble Baby disease, a life-threatening condition that if left untreated can be fatal within the first year of life.

The groundbreaking treatment was developed by renowned stem cell researcher and UCLA Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research member Dr. Donald Kohn, whose breakthrough was developed over three decades of research to create a gene therapy that safely restores immune systems in children with ADA-deficient SCID using the patients own cells with no side effects.

To date, 18 children with SCID have been cured of the disease after receiving the stem cell gene therapy in clinical trials at UCLA and the National Institutes of Health.

All of the children with SCID that I have treated in these stem cell clinical trials would have died in a year or less without this gene therapy, instead they are all thriving with fully functioning immune systems said Kohn, a professor of pediatrics and of microbiology, immunology and molecular genetics in Life Sciences.

To protect children born with SCID they are kept in isolation, in controlled environments because without an immune system they are extremely vulnerable to illness and infection that could be lethal.

Other current options for treating ADA-deficient SCID are not always optimal or feasible for many children, said Kohn. We can now, for the first time, offer these children and their families a cure, and the chance to live a full healthy life.

Defeating ADA-Deficient SCID: A Game-Changing Approach

Children born with SCID, an inherited immunodeficiency, are generally diagnosed at about six months. They are extremely vulnerable to infectious diseases, and in a child with ADA-deficient SCID even the common cold can prove fatal. The disease causes cells to not create an enzyme called ADA, which is critical for production of the healthy white blood cells that drive a normal, fully-functioning immune system. About 15 percent of all SCID patients are ADA-deficient.

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UCLA Stem Cell Researcher Pioneers Gene Therapy Cure for Children with "Bubble Baby" Disease

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NEW YORK (TheStreet) -- Shares ofNeoStem (NBS) plummeted 25.52% to $5.05 in late morning trading Tuesdayafter the biotech company announced poor results from a trial of its proprietary cardiac stem-cell therapy NBS10.

NBS10, which used to be called AMR-001, missed two primary endpoints in the study to test the therapy's efficacy.The stem-cell therapy comesfrom a patient's own bone marrow and is injected into patients after a heart attack. The stem cells are then supposed to help blood flow and build cardiac muscle.

NeoStem's trial used non-invasive imaging to monitor blood flow through the heart six months after a one dose of NBS10 or a placebo. The study showed no difference between NBS and placebo, NeoStem said.

Must Read:NeoStem's Stem Cell Therapy Fails Mid-Stage Heart Attack Study

Jim Cramer and Stephanie Link reveal their investment tactics while giving advanced notice before every trade.

Access the tool that DOMINATES the Russell 2000 and the S&P 500.

Jim Cramer's protg, David Peltier, uncovers low dollar stocks with extraordinary upside potential that are flying under Wall Street's radar.

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NeoStem (NBS) Stock Plummets Today on Disappointing Cardiac Stem-Cell Therapy Data

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WESTWOOD (CBSLA.com) Doctors say a groundbreaking stem cell therapy treatment out of UCLA may have cured Bubble Baby syndrome once and for all.

KNX 1070s Brian Ping reports Dr. Donald Kohn has perfected a gene therapy that has now cured 18 children born without an immune system, known as ADA-deficient severe combined immunodeficiency (SCID).

Only weeks after giving birth to fraternal twins in 2012, Alysia and Christian Padilla-Vaccaro found out their daughter Evangelinas immune system was so deficient that she could have no exposure to the outside world.

After enrolling their daughter in Dr. Donald Kohns revolutionary stem cell gene therapy treatment which was nearly three decades in the making doctors extracted stem cells from the bone marrow in Evangelinas hip, then used a modified mouse virus to correct her faulty gene before replacing the marrow.

You hear the words mouse virus and you want to run the other way, said mom Alysia. But they modify it so that its teaching it to do something that they want it to do, which is put something in there that was missing.

Evangelinas new immune system developed without side effects and she is now living a healthy normal life.

Her mother Alysia said while the process was difficult for any mom to go through, it was all worth it.

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UCLA Doctors Hail Potential Cure For Bubble Baby Syndrome

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Turning the Tide Against Cancer 2014 Welcome and Introductory Remarks
Edward Abrahams, Ph.D., President, Personalized Medicine Coalition, delivers opening remarks at the second Turning the Tide Against Cancer Through Sustained Medical Innovation national ...

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Piuma Nanoindenter in action
Microscope video of the Piuma Nanoindenter at work. For this example, it is indenting a glass slide in a 3x3 matrix. For each point, it finds the surface accurately, then indents with a fine...

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Surviving Lung Cancer Thanks to Personalized Medicine
Diagnosed with stage IV lung cancer in 2011, Deb Smith who has never smoked turned to clinical trials and personalized cancer medicine to control her dis...

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The Nancy and Stephen Grand Israel National Center for Personalized Medicine
Personalized medicine is about people, and in this video, people talk about personalized medicine specifically, the Weizmann Institute #39;s just-dedicated Nan...

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What Kind of Challenges Do Spinal Injury Patients Face?
There are different types of back injury that can cause devastating effects. Depending on what part of the spine is injured can affect the victim #39;s symptoms, possibly leading to breathing...

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What Money Damages Can a Spinal Cord Victim Recover?
How can a lawyer help someone with a spinal cord injury? If someone else played a role in the accident, then victims could receive compensation to cover medical bills, home modifications, wheelchai...

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Sue Walters only chance of survival from leukaemiawas a stem cell transplant No one in her family matched her tissue type Doctors searched the worldwide donor register They found Nicola Gerber, a student from Mechern, near the French border

By Chloe Lambert for the Daily Mail

Published: 20:21 EST, 17 November 2014 | Updated: 04:28 EST, 18 November 2014

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When Sue Walters was diagnosed with leukaemia, she hoped that the best of medical science would be used to cure it.

What she could never have anticipated was that her life would be saved by an 18-year-old boy from a remote German village.

Sues only chance of survival was a stem cell transplant previously known as a bone marrow transplant.

What Nicola has done is amazing it really is a gift of life. If I hadnt had the transplant, it was unlikely Id have lived beyond three months,' said Sue Walters of her donor Nicola Gerber

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Donor: The German teenager who saved my life

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By: Adam Feuerstein | 11/18/14 - 10:16 AM EST

Inject a cocktail of undifferentiated stem cellsinto a patient who has suffered a heart attack, and days or even weekslater, the stem cells transform into cardiac cells and rebuild the damaged heart muscle. Months later, the patient has a "new" healthy heart.It's a great story. But so far, the proof remains elusive though not for a lack of trying.

The latest company to fulfill this ambitious scenario is NeoStem (NBS) which presented disappointing (but not surprising) results from a small study of its proprietary cardiac stem-cell therapy NBS10 at the American Heart Association annual meeting Monday. NeoStem tried to put some positive spin on the bad news but shares are down 25% to $5.10.

NBS10, formerly known as AMR-001, is an autologous stem-cell therapy derived from a patient's own bone marrow. When injected back into patients following a heart attack, the stem cells are supposed torestore blood flow, rebuild damaged cardiac muscle and improve function.

Except in NeoStem's study, NBS10 fell short on two primary endpoints designed to assess the therapy's efficacy. The study used non-invasive imaging to assess blood flow through the heart, six months after a single infusion of NBS10 or a placebo. There was no difference between NBS and placebo, NeoStem said.

The study's other co-primary efficacy endpoint was a measurement of adverse cardiac "MACE" events --defined as cardiovascular death, a repeatheart attack, heart failure hospitalization and coronary revascularization. To date, 17% of patientstreated with NBS10 have suffered a MACE event compared to 19% of patients in the placebo arm -- a difference which was not statistically significant.

NeoStem said NBS10 therapy was safe relative to placebo and that no patients treated with the stem cells have died compared to three deaths in the placebo patients. But with only one year of follow up on a small number of patients, any claims about a mortality benefit are clinically meaningless.

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NeoStem's Stem Cell Therapy Fails Mid-Stage Heart Attack Study

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PUBLIC RELEASE DATE:

17-Nov-2014

Contact: Sally Stewart sally.stewart@cshs.org 310-248-6566 Cedars-Sinai Medical Center @cedarssinai

LOS ANGELES (NOV. 17, 2014) - Researchers at the Cedars-Sinai Heart Institute have found that injections of cardiac stem cells might help reverse heart damage caused by Duchenne muscular dystrophy, potentially resulting in a longer life expectancy for patients with the chronic muscle-wasting disease.

The study results were presented today at a Breaking Basic Science presentation during the American Heart Association Scientific Sessions in Chicago. After laboratory mice with Duchenne muscular dystrophy were infused with cardiac stem cells, the mice showed steady, marked improvement in heart function and increased exercise capacity.

Duchenne muscular dystrophy, which affects 1 in 3,600 boys, is a neuromuscular disease caused by a shortage of a protein called dystrophin, leading to progressive muscle weakness. Most Duchenne patients lose their ability to walk by age 12. Average life expectancy is about 25. The cause of death often is heart failure because the dystrophin deficiency leads to cardiomyopathy, a weakness of the heart muscle that makes the heart less able to pump blood and maintain a regular rhythm.

"Most research into treatments for Duchenne muscular dystrophy patients has focused on the skeletal muscle aspects of the disease, but more often than not, the cause of death has been the heart failure that affects Duchenne patients," said Eduardo Marbn, MD, PhD, director of the Cedars-Sinai Heart Institute and study leader. "Currently, there is no treatment to address the loss of functional heart muscle in these patients."

During the past five years, the Cedars-Sinai Heart Institute has become a world leader in studying the use of stem cells to regenerate heart muscle in patients who have had heart attacks. In 2009, Marbn and his team completed the world's first procedure in which a patient's own heart tissue was used to grow specialized heart stem cells. The specialized cells were then injected back into the patient's heart in an effort to repair and regrow healthy muscle in a heart that had been injured by a heart attack. Results, published in The Lancet in 2012, showed that one year after receiving the experimental stem cell treatment, heart attack patients demonstrated a significant reduction in the size of the scar left on the heart muscle.

Earlier this year, Heart Institute researchers began a new study, called ALLSTAR, in which heart attack patients are being infused with allogeneic stem cells, which are derived from donor-quality hearts.

Recently, the Heart Institute opened the nation's first Regenerative Medicine Clinic, designed to match heart and vascular disease patients with appropriate stem cell clinical trials being conducted at Cedars-Sinai and other institutions.

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Cardiac stem cell therapy may heal heart damage caused by Duchenne muscular dystrophy

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Using next generation gene sequencing techniques, cancer researchers at UT Southwestern Medical Center have identified more than 3,000 new mutations involved in certain kidney cancers, findings that help explain the diversity of cancer behaviors.

"These studies, which were performed in collaboration with Genentech Inc., identify novel therapeutic targets and suggest that predisposition to kidney cancer across species may be explained, at least in part, by the location of tumor suppressor genes with respect to one another in the genome," said Dr. James Brugarolas, Associate Professor of Internal Medicine and Developmental Biology, who leads UT Southwestern's Kidney Cancer Program at the Harold C. Simmons Cancer Center.

The scientists' findings are outlined in separate reports in the Proceedings of the National Academy of Sciences and Nature Genetics.

More than 250,000 individuals worldwide are diagnosed with kidney cancer every year, with lifetime risk of kidney cancer in the US estimated at 1.6 percent. Most kidney tumors are renal cell carcinomas, which when metastatic remain largely incurable.

Researchers with UT Southwestern's Kidney Cancer Program had previously identified a critical gene called BAP1 that is intimately tied to kidney cancer formation. Their latest research shows how BAP1 interacts with a second gene, VHL, to transform a normal kidney cell into a cancer cell, which in part appears to be based on the two gene's close proximity in humans, said Dr. Brugarolas, a Virginia Murchison Linthicum Endowed Scholar in Medical Research.

The newest findings suggest that the transformation begins with a mutation in one of the two copies of VHL, which is the most frequently mutated gene in the most common form of kidney cancer, clear cell type, which accounts for about 75 percent of kidney cancers. The VHL mutation is followed by a loss of the corresponding chromosome arm containing the second copy of VHL, as well as several other genes including PBRM1 and BAP1. This step eliminates the remaining copy of VHL and along with it, one of the two copies of PBRM1 and BAP1, two important genes that protect the kidney from cancer development. The subsequent mutation of the remaining copy of BAP1 leads to aggressive tumors, whereas mutation of the remaining copy of PBRM1 induces less aggressive tumors, said Dr. Payal Kapur, a key investigator of both studies who is an Associate Professor of Pathology and Urology, and the Pathology co-Leader of the Kidney Cancer Program.

This model also explains why humans born with a mutation in VHL have a high likelihood of developing kidney cancer during their life time. In these individuals, all kidney cells are already deficient for one VHL copy and a single deletion eliminates the second copy, along with a copy of BAP1 and PBRM1. In contrast, in other animals, these three genes are located on different chromosomes and thus more mutational events are required for their inactivation than in humans. Consistent with this notion, when UT Southwestern researchers mutated VHL and BAP1 together, kidney cancer resulted in animals.

In a second collaborative study with Genentech Inc., published in Nature Genetics, investigators implicated several genes for the first time in non-clear cell kidney cancer, a less common type that accounts for about 25 percent of kidney cancers. Researchers identified a gene signature that can help differentiate subtypes of non-clear cell tumors to better define their behavior. Specifically, the researchers characterized alterations from 167 human primary non-clear cell renal cell carcinomas, identifying 16 significantly mutated genes in non-clear cell kidney cancer that may pave the way for the development of novel therapies. The research team also identified a five-gene set that enabled molecular classifications of tumor subtypes, along with a potential therapeutic role for BIRC7 inhibitors for future study.

Story Source:

The above story is based on materials provided by UT Southwestern Medical Center. Note: Materials may be edited for content and length.

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Gene Mutations and Process for How Kidney Tumors Develop identified

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An international research consortium has discovered a new gene underlying progressive myoclonus epilepsy, one of the most devastating forms of epilepsy. The study showed that a single mutation in a potassium ion channel gene underlies a substantial proportion of unsolved cases. It is estimated that the mutation is carried by hundreds of patients worldwide. The study utilized modern DNA sequencing technologies, which have revolutionized genetic research of rare, severe diseases.

A study led by researchers at University of Helsinki, Finland and Universities of Melbourne and South Australia has identified a new gene for a progressive form of epilepsy. The findings of this international collaborative effort have been published today, 17 November 2014, in Nature Genetics.

Progressive myoclonus epilepsies (PME) are rare, inherited, and usually childhood-onset neurodegenerative diseases whose core symptoms are epileptic seizures and debilitating involuntary muscle twitching (myoclonus). The goal of the international collaborative study was to identify underlying genetic causes in 84 PME patients using DNA sequencing targeting the protein coding elements of the human genome.

Overall, a genetic diagnosis was reached for almost one third of these hitherto unsolved patients. Findings of the study shed light on molecular genetic basis of progressive epilepsy, which aids in diagnostics and potential therapeutic interventions of the disease. The study also shows that modern DNA technologies are powerful in dissecting the underlying genetic causes of severe diseases.

The most important and surprising finding of the study was that a single mutation in a potassium channel encoding gene KCNC1 explains a significant proportion of unsolved PME cases. The mutation was found in a total of 13 patients and was not inherited from parents -- instead it has emerged in a germ cell of one of the parents or in the fertilized egg. Each individual has dozens of these new, "de novo", mutations but they are rarely disease causing. The researchers estimate that this mutation occurs in approximately 1 out of every 5.7 million conceptions, indicating that at least hundreds of patients could have this mutation globally.

"A fascinating aspect of this finding is that this single mutation can be found in several patients all over the world. The mutation site is an example of a 'mutation hotspot' of the genome -- a DNA nucleotide which is more prone for alterations," says Professor Anna-Elina Lehesjoki, the corresponding principal investigator of the study in University of Helsinki and Folkhlsan Research Center, Finland.

The new mutation identified in the study disrupts the function of a potassium channel, KV3.1, which has a central role in signal transmission in the brain. The likely consequence of the mutation is that inhibitory signals in certain parts of patient brain are reduced, which makes patients susceptible to epileptic seizures and myoclonus starting in childhood. In addition, the mutation causes degeneration of the cerebellum and subtle cognitive decline in some of the patients.

"The fact that the mutation occurs in a well-characterized ion channel gives hope to development of targeted therapy. There are anti-epileptic drugs in the market that target other similar ion channels and follow-up research aims to discover a way to rescue the function of the channel in PME patients," says Professor Lehesjoki.

The researchers of the project emphasize the importance of international collaboration for the study. "This study shows the power of combining sample collections and knowledge from different countries," says Professor Samuel Berkovic, University of Melbourne, who coordinated the patient sample collection spanning over 20 years and involving multiple epilepsy centers worldwide.

The central research institutes participating in the study were University of Helsinki, Institute for Molecular Medicine Finland FIMM and Folkhlsan Research Center (Finland), Universities of Melbourne and South Australia (Australia), Wellcome Trust Sanger Institute (UK), University of Tbingen (Germany) and several universities in Italy.

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A new genetic cause for a progressive form of epilepsy identified

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Genetic Engineering - Restriction Enzymes - Part 3 - Anytime Education
http://www.anytimeeducation.com for more awesome free biology lessons. http://www.twitter.com/James_Dundon http://www.facebook.com/anytimeeducation Restriction enzymes, also known as ...

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Wheat diseases caused by a host of viruses that might include wheat streak mosaic, triticum mosaic, soil-borne mosaic and barley yellow dwarf could cost producers 5 to 10 percent or more in yield reductions per crop, but a major advance in developing broad disease-resistant wheat is on the horizon.

John Fellers, molecular biologist for the U.S. Department of Agriculture's Agricultural Research Service, and Harold Trick, plant geneticist for Kansas State University, have led an effort to develop a patent-pending genetic engineering technology that builds resistance to certain viruses in the wheat plant itself. And although genetically engineered wheat is not an option in the market today, their research is building this resistance in non-genetically engineered wheat lines as well.

"(Wheat viruses) are a serious problem," Trick said. "Wheat streak mosaic virus is one of the most devastating viruses we have. It's prevalent this year. In addition to that, we have several other diseases, triticum mosaic virus and soil-borne mosaic virus, that are serious diseases."

Knowing how costly these diseases can be for producers, Fellers has worked on finding solutions for resistance throughout his career. As a doctoral student at the University of Kentucky, he used a technology in his research called pathogen-derived resistance, or RNA-mediated resistance -- a process that requires putting a piece of a virus into a plant to make it resistant to that particular virus. Most of the viruses that infect wheat are RNA viruses, he said.

"The plant has its own biological defense system," Fellers said. "We were just triggering that with this technology."

Now Fellers, with the help of Trick, his wheat transformation facility and K-State graduate students, have developed transgenic wheat lines that contain small pieces of wheat streak mosaic virus and triticum mosaic virus RNA.

"It's kind of like forming a hairpin of RNA," Fellers said. "What happens is the plant recognizes this RNA isn't right, so it clips a piece of it and chops it up, but then it keeps a copy for itself. Then we have a resistance element."

Fellers compared the process to the old days of viewing most wanted posters on the post office wall. The piece of foreign RNA from the virus, which is a parasite, is one of those most wanted posters. Because the virus is a parasite, it has to seize or hijack part of the plant system to make proteins that it needs to replicate.

When the virus comes into the plant, the plant holds up that poster from the post office wall, recognizes the virus, and doesn't allow the virus to replicate and go through its lifecycle.

A broad resistance goal

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Helping wheat defend itself against damaging viruses

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worldhealth.net

SOUTH BEND, Ind.--- In 1990 the Human Genome Project started.

It was a massive scientific undertaking that aimed to identify and map out the body's complete set of DNA.

This research has paved the way for new genetic discoveries, and one of those has allowed scientists to study how to fix bad chromosomes.

Case Western Reserve University scientist, Anthony Wynshaw-Boris, is studying how to repair damaged chromosomes.

Our bodies contain 23 pairs of chromosomes, 46 in total, but if chromosomes are damaged, they can cause birth defects, disabilities, growth problems and even death.

Wynshaw-Boris is taking skin cells and reprogramming them to work like embryonic stem cells, which can grow into different cell types.

"We are taking an adults, or a child's, skin cells, said Wynshaw-Boris. We are not causing any loss of an embryo, and you're taking those skin cells to make a stem cell."

Scientists studied patients with a specific defective chromosome that was shaped like a ring. They took the patients' skin cells and reprogrammed them into embryonic-like cells in the lab.

They found this process caused the damaged "ring" chromosomes to be replaced by normal chromosomes.

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New DNA discovery could lead to chromosome therapies in the future

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November 18, 2014

Provided by Michael McCarthy, University of Washington Health Sciences/UW Medicine

Genetic analysis unveils airway and lung responses to pandemic flu and cystic fibrosis

In what is likely to be a major step forward in the study of influenza, cystic fibrosis and other human diseases, an international research effort has sequenced the ferret genome. The sequence was then used to analyze how the flu and cystic fibrosis affect respiratory tissues at the cellular level.

The National Institute of Allergy and Infectious Diseases, of the National Institutes of Health, funded the project, which was coordinated by Michael Katze and Xinxia Peng at the University of Washington in Seattle and Federica Di Palma and Jessica Alfoldi at the Broad Institute of MIT and Harvard.

The sequencing of the ferret genome is a big deal, said Michael Katze, UW professor of microbiology, who led the research effort. Every time you sequence a genome, it allows you to answer a wide range of questions you couldnt before. Having the genome changes a field forever.

Ferrets have long been considered the best animal model for studying a number of human diseases, particularly influenza, because the strains that infect humans also infect ferrets, These infections spread from ferret to ferret much as they do from human to human.

In the study, scientists at Di Palma and Alfoldi of the Broad Institute first sequenced and annotated the genome of a domestic sable ferret (Mustela putorius furo). They then collaborated with the Katze group on the subsequent analysis. A technique called transcriptome analysis identifies all the RNA that is being produced, or transcribed, from areas of the genome that are activated at any moment. This makes it possible to see how the ferret cells are responding when challenged by influenza and cystic fibrosis.

By creating a high quality genome and transcriptome resource for the ferret, we have demonstrated how studies in non-conventional model organisms can facilitate essential bioscience research underpinning health, said Di Palma, director of Science in Vertebrate & Health Genomics at The Genome Analysis Centre.

> Continue reading for more information

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Ferret Genome Sequenced, Holds Clues To Respiratory Diseases

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