Category Archives: Gene therapy

4thWorld congress on Cell Science Stem Cell Research
The OMICS Group Conferences #39; 4thWorld congress on Cell Science Stem Cell Research deliberates on the broader areas of Evolution of cancer, Tumorogenesis, Recombinant DNA technology, Cancer...

By: omicsgroupconference

Read more here:
4thWorld congress on Cell Science & Stem Cell Research - Video

By altering how a liver gene works, scientists say theyve developed a way to cut cholesterol permanently with a single injection, eliminating the need for daily pills to reduce the risk of heart attack.

In a test in mice, scientists at the Harvard Stem Cell Institute and the University of Pennsylvania disrupted the activity of a gene, called PCSK9, that regulates cholesterol, the fatty material that builds up in veins, hindering blood flow. The process permanently dropped levels of the lipid by 35 to 40 percent, said Kiran Musunuru, the lead researcher.

Thats the same amount of cholesterol youll get with a cholesterol drug, said Musunuru, who is a cardiologist and assistant professor at Harvard. The kicker is we were able to do that with a single injection, permanently changing the genome. Once that changes, its there forever.

Pfizer Inc. (PFE)s Lipitor and AstraZeneca Plc (AZN)s Crestor, both of which target so-called bad cholesterol, are pills that are designed to be taken daily. The prospect of replacing them with the newly tested procedure may be 5 to 10 years away, Musunuru said in a telephone interview.

The PCSK9 gene is the same one now being targeted by Amgen Inc., Sanofi (SAN) and Regeneron Pharmaceuticals Inc. (REGN) with experimental compounds designed to suppress the protein the gene produces. Certain rare PCSK9 mutations are found to cause high cholesterol and heart attacks. Good mutations also exist, and people with them have a heart attack risk that ranges from 47 to 88 percent below average, the researchers said.

Its not too much of a leap to think that if it works as well in mice, it will work as well in humans, said Musunuru, who works in the Cambridge, Massachusetts schools Department of Stem Cell and Regenerative Biology. With one shot, a patient would be like those people born with the good mutations.

The research was published yesterday in Circulation Research, a journal of the American Heart Association.

The approach used a two-part genome-engineering technique that first targets the DNA sequence where the gene sits, and then creates a break in the system. The therapy was carried to the liver using an injected adenovirus.

The genome-editing technique used in the experiment has only been around for about a year and a half, Musunuru said.

The next step is to see how effective the therapy is in human cells, by using mice whose liver cells are replaced with human-derived liver cells, he said. Assessing safety will be the primary concern.

Continued here:
Cholesterol Controlled for Good by Gene Therapy in Mice

NEW YORK (TheStreet) -- Two members of the Biotech IPO Class of 2013 -- Bluebird Bio (BLUE) and Agios Pharmaceuticals (AGIO) -- will deliver important pipeline updates at the European Hematology Association (EHA) Congress on Sat. June 14. Let's preview both presentations, starting with Bluebird and its LentiGlobin gene therapy for beta-thalassemia.

Lenti what for beta who?

LentiGlobin is gene therapy, meaning it insertsa fully functional gene for human beta-globin into the patient's own hematopoietic stem cells. The theory behind gene therapy is relatively simple: For diseases caused by single, malfunctioning or missing gene, effective treatment or even a complete cure can be achieved (theoretically) by replacing the defective gene with one that is fully functional. Gene therapy sounds simple but the execution is obviously a lot more complicated.

I won't get into the weeds explaining the process by which BlueBird produces and delivers LentiGlobin except to say a working gene for human beta-globin would allows beta-thalassemia (B-Thal) patients to produce functional beta-globin -- the largest component of hemoglobin, which carries oxygen in red blood cells. B-Thal patients suffer from anemia and iron overload. There is no currently approved cure or effective treatment, so patients require regular blood transfusions to combat the anemia.

Bluebird went public last year partly on the back of some encouraging proof of concept data showing a first-generation gene therapy approach was feasible for B-thal patients. LentiGlobin is a second-generation gene therapy designed to be more potent -- and hopefully more effective.

Next Saturday, researchers will present data on two B-thal patients treated with LentiGlobin in an ongoing phase I/II study. Key data to look for include the engraftment success rate i.e. how many "gene-therapy treated" stem cells are populating the bone marrow; improvements in hemoglobin levels; achievement of transfusion independence; and if so, how quickly from the gene therapy.

Agios will be presenting a clinical update from an early-stage study of experimental cancer metabolism drugAG-221 last reported at the American Association of Cancer Research annual meeting in April.

Agios is developing AG-221 under a collaboration with Celgene (CELG). The companies are also working together on AG-120, a similar drug designed to block another mutated cancer-growing protein known a IDH1.

At the EHA meeting on Sat. June 14, researchers will be presented updated study results from additional patients treated with AG-221, some given higher doses of the drug.

In April at AACR, six of 10 patients with advanced, treatment-refractory acute myeloid leukemia carrying the IDH2 mutation had objective tumor responses, including three complete remissions and two complete remissions with incomplete platelet recovery. A single patient achieved a partial response.

Go here to read the rest:
Bluebird, Agios: Preview of Next Week's Important Pipeline Updates

Stanford University researcher Irving Weissman explains how the drug Rituxan, generically called rituximab, improves the cancer-killing effect of a new antibody that renders cancer cells vulnerable to immune attack. He spoke Monday, April 7, at the American Association for Cancer Research meeting in San Diego.

The war on cancer is getting some potent reinforcements, including a potentially broad-spectrum new weapon and genetically engineered immune cells with improved cancer-fighting abilities, speakers said at a major cancer research conference held this week in San Diego.

The American Association for Cancer Research, attended by an estimated 18,000 participants, is being held at the San Diego Convention Center through Wednesday. While it is covering the gamut of research, cancer immunotherapy is a major focus. The field began more than 100 years ago, and has lately scored impressive advances by using gene therapy to its tool kit.

The weapon is an antibody that makes a wide range of cancer cells vulnerable to immune attack. It's close to entering human clinical trials, said Irving L. Weissman, a Stanford University professor leading that project. The antibody neutralizes a chemical signal many cancers exude to decoy the immune system, Weissman said in a Monday morning plenary session.

The antibody is being tested first in acute myeloid leukemia patients, backed by $20 million from the California Institute for Regenerative Medicine, Weissman said. The institute is interested because the target cells are cancer stem cells, the cells that proliferate to spread cancer.

Moreover, research indicates the method can be used against many solid tumors that emit the signal, a protein called CD47. These include breast, ovarian, bladder, pancreatic and colon cancer.

"Every human cancer that we've seen has CD47," Weissman said.

Animal studies show that anti-CD47 antibodies inhibit growth of transplanted patient tumors, he said. And when used against non-Hodgkin's lymphoma along with an existing antibody drug called Rituxan, the result is a potent cancer-killing effect. Immune cells called macrophages actually engulf and destroy the cancer cells.

The CD47 molecule is normally present on young cells, serving as a "don't eat me" signal to immune system cells that might otherwise attack them, Weissman said. Cancer cells have chanced on mutations that cause the protein to be made in exceptionally high amounts. So even when they might be abnormal enough to merit immune system attack, they escape surveillance.

Another approach already in the clinic is to genetically engineer immune cells called T cells to be better at fighting cancer. Carl June, a University of Pennsylvania researcher behind one of the studies, said results continue to be encouraging. This approach targets another protein abnormally made by cancer cells, CD19. Novartis is testing the therapy.

The rest is here:
Gene, immune therapy help cancer war

PUBLIC RELEASE DATE:

1-Apr-2014

Contact: Sandy Van sandy@prpacific.com 808-526-1708 Cedars-Sinai Medical Center

LOS ANGELES (April 1, 2014) The Cedars-Sinai Regenerative Medicine Institute has received a $2.5 million grant from the Department of Defense to conduct animal studies that, if successful, could provide the basis for a clinical trial of a gene therapy product for patients with Lou Gehrig's disease, also called amyotrophic lateral sclerosis, or ALS.

The incurable disorder attacks muscle-controlling nerve cells motor neurons in the brain, brainstem and spinal cord. As the neurons die, the ability to initiate and control muscle movement is lost. Patients experience muscle weakness that steadily leads to paralysis; the disease usually is fatal within five years of diagnosis. Several genes have been identified in familial forms of ALS, but most cases are caused by a complex combination of unknown genetic and environmental factors, experts believe.

Because ALS affects a higher-than-expected percentage of military veterans, especially those returning from overseas duties, the Defense Department invests $7.5 million annually to search for causes and treatments. The Cedars-Sinai study, led by Clive Svendsen, PhD, professor and director of the Regenerative Medicine Institute at Cedars-Sinai Medical Center, and Genevive Gowing, PhD, a senior scientist in his laboratory, also will involve a research team at the University of Wisconsin, Madison and a Netherlands-based biotechnology company, uniQure, that has extensive experience in human gene therapy research and development.

The research will be conducted in laboratory rats bred to model a genetic form of ALS. If successful, it could have implications for patients with other types of the disease and could translate into a gene therapy clinical trial for this devastating disease.

It centers on a protein, GDNF, that promotes the survival of neurons. In theory, transporting GDNF into the spinal cord could protect neurons and slow disease progression, but attempts so far have failed, largely because the protein does not readily penetrate into the spinal cord. Regenerative Medicine Institute scientists previously showed that spinal transplantation of stem cells that were engineered to produce GDNF increased motor neuron survival, but this had no functional benefit because it did not prevent nerve cell deterioration at a critical site, the "neuromuscular junction" the point where nerve fibers connect with muscle fibers to stimulate muscle action.

Masatoshi Suzuki, PhD, DVM, assistant professor of comparative biosciences at the University of Wisconsin, Madison, who previously worked in the Svendsen Laboratory and remains a close collaborator, recently found that stem cells derived from human bone marrow and engineered to produce GDNF protected nerve cells, improved motor function and increased lifespan when transplanted into muscle groups of a rat model of ALS.

"It seems clear that GDNF has potent neuroprotective effects on motor neuron function when the protein is delivered at the level of the muscle, regardless of the delivery method. We think GDNF will be able to help maintain these connections in patients and thereby keep the motor neuron network functional," Suzuki said.

Read more:
$2.5 million Defense Department grant funds gene therapy study for Lou Gehrig's disease

The approach involves using enzymes to destroy a gene in the immune cells of people with HIV, thereby increasing resistance to the virus

Scanning electron micrograph of a human T cell from the immune system of a healthy donor. Credit:NIAID/NIH - Wikimedia Commons

A clinical trial has shown that a gene-editing technique can be safe and effective in humans. For the first time, researchers used enzymes called zinc-finger nucleases (ZFNs) to target and destroy a gene in the immune cells of 12 people with HIV, increasing their resistance to the virus. The findings were published March 5 in The New England Journal of Medicine.

This is the first major advance in HIV gene therapy since it was demonstrated that the Berlin patient Timothy Brown was free of HIV, says John Rossi, a molecular biologist at the Beckman Research Institute of the City of Hope National Medical Center in Duarte, California. In 2008, researchers reported thatBrown gained the ability to control his HIV infectionafter they treated him with donor bone-marrow stem cells that carried a mutation in a gene calledCCR5. Most HIV strains use a protein encoded byCCR5as a gateway into the T cells of a hosts immune system. People who carry a mutated version of the gene, including Brown's donor, are resistant to HIV.

But similar treatment isnot feasible for most people with HIV: it is invasive, and the body is likely to attack the donor cells. So a team led by Carl June and Pablo Tebas, immunologists at the University of Pennsylvania in Philadelphia, sought to create the beneficialCCR5 mutation in a persons own cells, using targeted gene editing.

Personalized medicine The researchers drew blood from 12 people with HIV who had been taking antiretroviral drugs to keep the virus in check. After culturing blood cells from each participant, the team used a commercially available ZFN to target theCCR5gene in those cells. The treatment succeeded in disrupting the gene in about 25% of each participants cultured cells; the researchers then transfused all of the cultured cells into the participants. After treatment, all had elevated levels of T cells in their blood, suggesting that the virus was less capable of destroying them.

Six of the 12 participants then stopped their antiretroviral drug therapy, while the team monitored their levels of virus and T cells. Their HIV levels rebounded more slowly than normal, and their T-cell levels remained high for weeks. In short, the presence of HIV seemed to drive the modified immune cells, which lacked a functionalCCR5gene, to proliferate in the body. Researchers suspect that the virus was unable to infect and destroy the altered cells.

They used HIV to help in its own demise, says Paula Cannon, who studies gene therapy at the University of Southern California in Los Angeles. They throw the cells back at it and say, Ha, now what?

Long-term action In this first small trial, the gene-editing approach seemed to be safe: Tebas says that the worst side effect was that the chemical used in the process made the patients bodies smell bad for several days.

The trial isnt the end game, but its an important advance in the direction of this kind of research, says Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland. Its more practical and applicable than doing a stem-cell transplant, he says, although it remains to be seen whether it is as effective.

Read more from the original source:
Gene-Editing Technique Shown to Work as HIV Treatment

Engineering a patients own immune cells to resist HIV could eliminate the need for lifelong antiretroviral therapies.

The immune cells of HIV patients can be genetically engineered to resist infection, say researchers. In a small study in humans, scientists report that by creating a beneficial mutation in T cells, they may be able to nearly cure patients of HIV.

In a study published in the New England Journal of Medicine on Wednesday, researchers report that they can use genome editing to re-create the rare mutations responsible for protecting about 1 percent of the population from the virus in infected patients. They report that some of the patients receiving the genome-modifying treatment showed decreased viral loads during a temporary halt of their antiretroviral drugs. In one patient, the virus could no longer be detected in his blood.

Zinc-finger nucleases are one of a few genome-editing tools that researchers use to create specific changes to the genomes of living organisms and cells (see Genome Surgery). Scientists have previously used genome-editing techniques to modify DNA in human cells and nonhuman animals, including monkeys (see Monkeys Modified with Genome Editing). Now, the NEJM study suggests the method can also be safely used in humans.

From each participating patient, the team harvested bone marrow stem cells, which give rise to T cells in the body. They then used a zinc finger nuclease to break copies of the CCR5 gene that encodes for proteins on the surface of immune cells that are a critical entry point of HIV. The stem cells were then infused back into each patients bloodstream. The modification process isnt perfect, so only some of the cells end up carrying the modification. About 25 percent of the cells have at least one of the CCR5 genes interrupted, says Edward Lanphier, CEO of Sangamo Biosciences, the Richmond, California, biotech company that manufactures zinc finger nucleases.

Because the cells are a patients own, there is no risk of tissue rejection. The modified stem cells then give rise to modified T cells that are more resistant to infection by HIV, say the researchers.

One week after the infusion, researchers were able to find modified T cells in the patients blood. Four weeks after the infusion, six of the 12 patients in the study temporarily stopped taking their antiretroviral drugs so the researchers could assess the effect of the genome-editing treatment on the amount of the virus in the patients bodies. In four of these patients, the amount of HIV in the blood dropped. In one patient, the virus could no longer be detected at all. The team later discovered that this best responder had naturally already had one mutated copy of the CCR5 gene.

Patients who carry one broken copy of the CCR5 progress to AIDS more slowly than those who dont, says Bruce Levine, a cell and gene therapy researcher at the University of Pennsylvania School of Medicine and coauthor on the study. Because all of the cells in that best-responder patient already carried one disrupted copy of CCR5, the modification by the zinc finger nuclease led to T cells with no functional copies of the gene. That means the cells are fully resistant to HIV infection. The team is now working to increase the number of immune cells that end up carrying two broken copies of CCR5.

The rest is here:
Can Gene Therapy Cure HIV?

NIBSC/Science Photo Library

HIV attacks a type of immune cell known as a T cell (shown here) using a protein encoded by the CCR5 gene.

A clinical trial has shown that a gene-editing technique can be safe and effective in humans. For the first time, researchers used enzymes called zinc-finger nucleases (ZFNs) to target and destroy a gene in the immune cells of 12 people with HIV, increasing their resistance to the virus to the virus. The findings are published today in The New England Journal of Medicine1.

This is the first major advance in HIV gene therapy since it was demonstrated that the Berlin patient Timothy Brown was free of HIV, says John Rossi, a molecular biologist at the Beckman Research Institute of the City of Hope National Medical Center in Duarte, California. In 2008, researchers reported that Brown gained the ability to control his HIV infection after they treated him with donor bone-marrow stem cells that carried a mutation in a gene called CCR5. Most HIV strains use a protein encoded by CCR5 as a gateway into the T cells of a hosts immune system. People who carry a mutated version of the gene, including Brown's donor, are resistant to HIV.

But similar treatment is not feasible for most people with HIV: it is invasive, and the body is likely to attack the donor cells. So a team led by Carl June and Pablo Tebas, immunologists at the University of Pennsylvania in Philadelphia, sought to create the beneficial CCR5 mutation in a persons own cells, using targeted gene editing.

The researchers drew blood from 12 people with HIV who had been taking antiretroviral drugs to keep the virus in check. After culturing blood cells from each participant, the team used a commercially available ZFN to target the CCR5 gene in those cells. The treatment succeeded in disrupting the gene in about 25% of each participants cultured cells; the researchers then transfused all of the cultured cells into the participants. After treatment, all had elevated levels of T cells in their blood, suggesting that the virus was less capable of destroying them.

Six of the 12 participants then stopped their antiretroviral drug therapy, while the team monitored their levels of virus and T cells. Their HIV levels rebounded more slowly than normal, and their T-cell levels remained high for weeks. In short, the presence of HIV seemed to drive the modified immune cells, which lacked a functional CCR5 gene, to proliferate in the body. Researchers suspect that the virus was unable to infect and destroy the altered cells.

They used HIV to help in its own demise, says Paula Cannon, who studies gene therapy at the University of Southern California in Los Angeles. They throw the cells back at it and say, Ha, now what?

In this first small trial, the gene-editing approach seemed to be safe: Tebas says that the worst side effect was that the chemical used in the process made the patients bodies smell bad for several days.

The trial isnt the end game, but its an important advance in the direction of this kind of research, says Anthony Fauci, director of the US National Institute of Allergy and Infectious Diseases in Bethesda, Maryland. Its more practical and applicable than doing a stem-cell transplant, he says, although it remains to be seen whether it is as effective.

Read the original here:
Gene-editing method tackles HIV in first clinical test

PHILADELPHIA University of Pennsylvania researchers have successfully genetically engineered the immune cells of 12 HIV positive patients to resist infection, and decreased the viral loads of some patients taken off antiretroviral drug therapy (ADT) entirelyincluding one patient whose levels became undetectable. The study, appearingtoday in the New England Journal of Medicine, is the first published report of any gene editing approach in humans.

The phase I study was co-authored by researchers at Penn Medicine, the Albert Einstein College of Medicine and scientists from Sangamo BioSciences, which developed the zinc finger nuclease (ZFN) technology, the T cell therapy approach used in the clinical trial.

This study shows that we can safely and effectively engineer an HIV patients own T cells to mimic a naturally occurring resistance to the virus, infuse those engineered cells, have them persist in the body, and potentially keep viral loads at bay without the use of drugs, said senior author Carl H. June, MD, the Richard W. Vague Professor in Immunotherapy in the department of Pathology and Laboratory Medicine at Penns Perelman School of Medicine. This reinforces our belief that modified T cells are the key that could eliminate the need for lifelong ADT and potentially lead to functionally curative approaches for HIV/AIDS.

June and his colleagues, including Bruce L. Levine, PhD, the Barbara and Edward Netter Associate Professor in Cancer Gene Therapy in the department of Pathology and Laboratory Medicine and the director of the Clinical Cell and Vaccine Production Facility at Penn, used the ZFN technology to modify the T cells in the patientsa molecular scissors, of sorts, to mimic the CCR5-delta-32 mutation. That rare mutation is of interest because it provides a natural resistance to the virus, but in only 1 percent of the general population. By inducing the mutations, the scientists reduced the expression of CCR5 surface proteins. Without those, HIV cannot enter, rendering the patients cells resistant to infection.

For the study, the team infused the modified cells known as SB-728-Tinto two cohorts of patients, all treated with single infusionsabout 10 billion cellsbetween May 2009 and July 2012. Six were taken off antiretroviral therapy altogether for up to 12 weeks, beginning four weeks after infusion, while six patients remained on treatment.

Infusions were deemed safe and tolerable, the authors report, and modified T cells continued to persist in the patients during follow up visits. One week after the initial infusion, testing revealed a dramatic spike in modified T cells inside the patients bodies. While those cells declined over a number of weeks in the blood, the decrease of modified cells was significantly less than that of unmodified T cells during ADT treatment interruption. Modified cells were also observed in the gut-associated lymphoid tissue, which is a major reservoir of immune cells and a critical reservoir of HIV infection, suggesting that the modified cells are functioning and trafficking normally in the body.

The study also shows promise in the approachs ability to suppress the virus. The viral loads (HIV-RNA) dropped in four patients whose treatment was interrupted for 12 weeks. One of those patients viral loads dropped below the limit of detection; interestingly, it was later discovered that the patient was found to be heterozygous for the CCR5 delta-32 gene mutation.

Since half the subject's CCR5 genes were naturally disrupted, the gene editing approach was building on the head start provided by inheriting the mutation from one parent, said Levine. This case gives us a better understanding of the mutation and the bodys response to the therapy, opening up another door for study.

Therapies based on the CCR5 mutation have gained steam over the last six years, particularly after a man known as the Berlin Patient was functionally cured. Diagnosed with acute myeloid leukemia (AML), he received a stem cell transplant from a donor who had the CCR5 mutation in both alleles (from both parents) and has remained off ADT since 2008. Researchers are attempting to replicate this phenomenon because allogeneic transplantswhich carry a high mortality risk and require lengthy hospitalizationsare not a practical solution for HIV patients who do not have blood cancers. Nor are they effective in ridding the body of HIV unless the donor has the mutated gene in both alleles, as shown recently in two Boston patients who were thought to have been functionally cured from transplants, only to see their viral loads spike.

Though disappointing to the research community, the Boston patients results highlight key factors when combating the virus.

See the original post here:
Personalized Gene Therapy Locks Out HIV, Paving the Way to Control Virus Without Antiretroviral Drugs

Injections of a normally silent gene sparked recovery in pigs induced to have heart attacks

Thinkstock/iStock

When a heart attack brings blood flow to a screeching halt, thats only the first assault on our fist-size organ. Among survivors, the recovery itself fuels more permanent damage to the heart. Scar tissue can harden once-flexible heart muscle, making it less elastic. And as tentacles of this tissue creep over the aorta the heart muscle can no longer fully contract. This long-term damage can minimize the amount of oxygen-rich blood sent throughout the body, which can send patients spiraling into heart failure. Heart transplants are one way to circumvent these scar tissue issues, but donor hearts are always in short supply. Devising other truly effective solutions has long eluded researchers. A form of gene therapy, however, is now showing promise in pigs. It turns out that a normally silent gene called Cyclin A2, or CCNA2, can be coaxed into action to combat the formation of scar tissue in pigs that suffer a heart attack. This treatment sparked regeneration of heart muscle cells in pigs as well as improvements in the volume of blood pushed out with every beat. The finding is published in the February 19 issue of Science Translational Medicine. Gene therapy, the authors hope, may one day join stem cell treatments as a contender for transforming the way doctors treat heart failure. Stem cellbased therapies have already resulted in more healthy tissue and decreased scar mass in human clinical trials as well as small improvements in how much blood the heart can pump from one chamber to another. But as Scientific American reported in April 2013, many questions remain about which stem cells to use and how to prepare them. For this study, researchers randomly assigned 18 pigs recovering from heart attacks to either receive injections of the gene expressed under a promoter (which would force it to be expressed) or the same solution without the gene. Pigs treated with the gene had greater success pushing out blood with each heartbeat, but also produced a greater number of heart muscle cells. These findings echo the teams earlier heart regeneration successes in mice and rats. The researchers replicated their findings in a petri dish and watched adult porcine heart muscle cells treated with the same regimen of gene therapy undergo complete cell division in the dishdemonstrating under a microscope how the heart cells were dividing and thriving with the gene therapy. This new approach mimics the kind of regeneration we see in the newt and zebra fish, says lead author Hina Chaudhry, the director of cardiovascular regenerative medicine at The Mount Sinai Hospital in New York City. If the technique proves successful in humans, it could boost patient recovery rates by helping strengthen heart muscles and improving blood flow, all while giving a needed lift to gene therapy research, which has been slow to gain momentum in the U.S. In 1999 Jesse Gelsinger, 18, died after a gene therapy experiment cost him his life. The virus used to deliver a gene that would potentially control his rare digestive disorder fueled a massive and fatal immune reaction. That highly publicized case, along with other gene therapy missteps, put a pall on the field. Chaudhry says that her team is proceeding with caution and plans to be careful when administering this treatment to patient populations. For patients who have a large heart attack who are at risk of heart failure, I think the therapy is going to be very beneficial, she says. If you have a small heart attack, it probably wont make as much of a difference in overall survival because of advances with todays medicines. As more researchers look to gene therapy for previously intractable human conditions, a success with heart attack treatments could send ripples throughout the field.

2014 Scientific American, a Division of Nature America, Inc.

View Mobile Site All Rights Reserved.

Give a 1 year subscription as low as $14.99

Subscribe Now >>

Go here to see the original:
Gene Therapy Shows Promise for Treating Heart Attack Victims