Gene Therapy - the impossible dream?
Gene Therapy - the impossible dream?

By: stockyard71

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Gene Therapy - the impossible dream? - Video

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The ProSavin treatment uses an inert virus to carry corrective genes directly into the striatum region of the brain that controls movement.

It is designed to convert ordinary nerve cells into factories for making dopamine, the signalling chemical that is lost in Parkinson's patients.

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Lack of dopamine activity leads to the common Parkinson's symptoms of tremor, slow movement and rigidity.

The trial tested the safety, tolerability and effectiveness of three different doses of ProSavin in 15 patients aged 48 to 65 with advanced Parkinson's disease who were not responding to conventional treatments.

A standard system of rating motor functions was used, covering speech, tremors, rigidity, finger taps, posture, gait, and slow movement. Lower scores indicated better muscle control and co-ordination.

Significant score improvements were seen after six months and a year in all patients not taking medication.

Reporting their findings in The Lancet medical journal, the researchers led by Professor Stephane Palfi, from Les Hopitaux Universitaires Henri-Mondor in Creteil, France, wrote: "ProSavin was safe and well tolerated in patients with advanced Parkinson's disease. Improvement in motor behaviour was observed in all patients."

They stressed that, while promising, the results at this stage were still limited and should be "interpreted with caution".

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Gene therapy for Parkinson's produces promising results in first patient trial

Recommendation and review posted by Bethany Smith

10/01/2014 - 07:15:45Back to World Home

A gene therapy for Parkinsons disease has produced promising results in its first patient trial, say researchers.

The ProSavin treatment uses an inert virus to carry corrective genes directly into the striatum region of the brain that controls movement.

It is designed to convert ordinary nerve cells into factories for making dopamine, the signalling chemical that is lost in Parkinsons patients.

Lack of dopamine activity leads to the common Parkinsons symptoms of tremor, slow movement and rigidity.

The trial tested the safety, tolerability and effectiveness of three different doses of ProSavin in 15 patients aged 48 to 65 with advanced Parkinsons disease who were not responding to conventional treatments.

A standard system of rating motor functions was used, covering speech, tremors, rigidity, finger taps, posture, gait, and slow movement. Lower scores indicated better muscle control and co-ordination.

Significant score improvements were seen after six months and a year in all patients not taking medication.

Reporting their findings in The Lancet medical journal, the researchers led by Professor Stephane Palfi, from Les Hopitaux Universitaires Henri-Mondor in Creteil, France, wrote: ProSavin was safe and well tolerated in patients with advanced Parkinsons disease. Improvement in motor behaviour was observed in all patients.

They stressed that, while promising, the results at this stage were still limited and should be interpreted with caution.

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Gene therapy provides hope for Parkinson's sufferers

Recommendation and review posted by Bethany Smith

PARIS: A closely-watched prototype therapy to inject corrective genes into the brain to treat Parkinson's disease has cleared an important safety hurdle, doctors said Friday.

Tested on 15 volunteers with an advanced form of the degenerative nerve disease, the technique proved safe and the results were encouraging, they said.

The experiment aims to reverse the lack of a brain chemical called dopamine, which is essential for motor skills.

It entails tucking three genes into a disabled horse virus of the family lentiviruses.

The modified virus is then injected directly into a specialised area of the brain, where it infiltrates cells. In doing so, it delivers corrective pieces of DNA, prompting defective brain cells to once again start producing dopamine.

Called ProSavin, the British-designed treatment was authorised for tests on humans after it was tried on lab monkeys.

It is being closely watched by specialists to see if it works better than conventional therapies -- the veteran drug levodopa or electrical stimulation of the brain -- or another experimental gene technique which uses a modified cold virus.

French neurosurgeon Stephane Palfi, who led the early-stage trial published in The Lancet, said 15 patients aged 48-65 were given the genes in one of three doses.

They developed better coordination and balance, had less muscle twitching and improved speech.

Assessed at least 12 months after the injection, "motor symptoms remained improved in all the patients," Palfi said.

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Novel gene therapy for Parkinson's clears hurdle

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Restoring Sensorimotor Hand Function by Selectively Activating and Recording from Arm Nerves
Gregory A. Clark, Ph.D., University of Utah. Dr. Clark is a CDMRP-funded investigator supported by the DoD Spinal Cord Injury Research Program (SCIRP).

By: CDMRP

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Restoring Sensorimotor Hand Function by Selectively Activating and Recording from Arm Nerves - Video

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PUBLIC RELEASE DATE:

8-Jan-2014

Contact: David McKeon DMckeon@nyscf.org 212-365-7440 New York Stem Cell Foundation

NEW YORK, NY (January 8, 2014) Scientists at The New York Stem Cell Foundation (NYSCF) Research Institute in collaboration with scientists at the Icahn School of Medicine at Mount Sinai (ISMMS) successfully generated a stem cell model of familial Alzheimer's disease (FAD). Using this stem cell model, researchers identified fourteen genes that may be implicated in the disease and one gene in particular that shows the importance that inflammation may play in the brain of Alzheimer's patients.

In this study, published today in PLOS ONE, the team of scientists produced stem cells and neural precursor cells (NPCs), representing early neural progenitor cells that build the brain, from patients with severe early-onset AD with mutations in the Presenilin 1 (PSEN1) gene. These NPCs had elevated Abeta42/Abeta40 ratios, indicating elevation of the form of amyloid found in the brains of Alzheimer's patients. These levels were greater than those in adult cells that did not have the PSEN1mutation. This elevated ratio showed that these NPCs grown in the petri dish were accurately reflecting the cells in the brains of FAD patients.

"Our ability to accurately recapitulate the disease in the petri dish is an important advance for this disease. These genes provide us with new targets to help elucidate the cause of sporadic forms of the disease as well provide targets for the discovery of new drugs," said Susan L. Solomon, Chief Executive Officer of The New York Stem Cell Foundation.

"The gene expression profile from Noggle's familial Alzheimer's stem cells points to inflammation which is especially exciting because we would not usually associate inflammation with this particular Alzheimer's gene. The greatest breakthroughs come with 'unknown unknowns', that is, things that we don't know now and that we would never discover through standard logic," said Sam Gandy, MD, PhD, Professor of Neurology and Psychiatry and Director of the Center for Cognitive Health at the Icahn School of Medicine at Mount Sinai and a co-author on the study. Gandy is also Associate Director of the NIH-Designated Mount Sinai Alzheimer's Disease Research Center.

The researchers generated induced pluripotent stem (iPS) cells from affected and unaffected individuals from two families carrying PSEN1 mutations. After thorough characterization of the NPCs through gene expression profiling and other methods, they identified fourteen genes that behaved differently in PSEN1 NPCs relative to NPCs from individuals without the mutation. Five of these targets also showed differential expression in late onset Alzheimer's disease patients' brains. Therefore, in the PSEN1 iPS cell model, the researchers reconstituted an essential feature in the molecular development of familial Alzheimer's disease.

Although the majority of Alzheimer's disease cases are late onset and likely result from a mixture of genetic predisposition and environmental factors, there are genetic forms of the disease that affect patients at much earlier ages. PSEN1 mutations cause the most common form of inherited familial Alzheimer's disease and are one hundred percent penetrant, resulting in all individuals with this mutation getting the disease.

The identification of genes that behaved differently in patients with the mutation provides new targets to further study and better understand their effects on the development of Alzheimer's disease. One of these genes, NLRP2, is traditionally thought of as an inflammatory gene.

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Stem cell research identifies new gene targets in patients with Alzheimer's disease

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One North West family is desperately seeking a bone marrow donor for their 8-year-old son as he battles a life-threatening blood disorder.

The odds of finding a donor for Rebaone are one in 100,000 (file photo)

In April 2013, 8-year-old Rebaone Nkuyagae from Klerksdorp was diagnosed with aplastic anaemia, a blood disorder in which a patients bone marrow does not produce enough new blood cells.

Unfortunately, there is no hospital that can treat Rebaone in Klerksdorp, so he and his family have to travel 170 km to the Donald Gordon Medical Centre in Johannesburg every second week for treatment.

Rebaone and his mother, Lerato, usually make the trip by bus with support from the non-profit Wings and Wishes, which provides financial support to transport critically-ill children between their homes and care facilities.

For Lerato, dealing with Rebaones illness means trying to keep him safe at home and on the playground. With a condition that makes it difficult for his body to stop the bleeding if he gets cut, Rebaone has had to stay off the sports field.

While it had been difficult, Lerato said she stays positive.

I have to ensure he does not play contact sports as he shouldnt get any cuts or be pinched, Lerato told OurHealth. Its hard for me, but I will always stay positive.

Rebaone is receiving platelets, which help blood clot, and blood transfusions regularly, but his doctors have informed Lerato that he will need a bone marrow transplant in the near future.

His family is desperately hoping to find a suitable donor but the odds of finding a match are one in 100,000. A donor is most likely to be found within a patients ethnic group, as the markers that are tested when searching for a match are genetically inherited

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Klerksdorp boy seeks bone marrow donor

Recommendation and review posted by Bethany Smith

Sugar Land orthopedic surgeon Dr. Mark Maffet of Houston Methodist Orthopedics & Sports Medicine is the first orthopedic surgeon in Fort Bend County who is using stem cells to help accelerate healing and recovery after surgery.

Stem cells hold a great deal of promise in orthopedics, Dr. Maffet said. Right now, their use is cutting edge but I believe they will ultimately play a huge role in making surgical repair more successful.

Stem cells are found in bone marrow, blood and various types of tissue. Because they can differentiate into specialized cells and continuously divide, stem cells act as a repair system for the body and can replenish damaged tissue.

Dr. Maffet used stem cells to surgically repair Amy Statlers ACL tear. ACL tears are a common sports injury that often requires reconstruction of the knee.Statleris an active woman who enjoys playing softball and exercising and wanted to get back to her active lifestyle quickly.

Dr. Maffet made me feel comfortable by explaining the process and answering all of my questions about the surgery;it was important for me to have a quick recovery,"Statlerexplained."I am currently in physical therapy and am expected to be back on the softball field for our first practice in February. I am so happy with my recovery thus far and I feel better every day.

During ACL reconstruction surgery, orthopedic surgeons take a tendon from the knee or hamstring (either a patient's own or from a donor) and use it to replace the damaged ACL ligament. Dr. Maffet has begun using stem cells to help the body accept the new tendon and to speed the healing process.

The new ACL graft is soaked in a concentrate full of stem cells and other growth factors prior to fixation, he explained. In other cases, we can simply suture the torn ligament and inject the stem cell concentrate into the affected area.

Dr. Maffet is also using stem cells in rotator cuff repairs of the shoulder. By creating vascular channels down into the bone at the repair site, his goal is to trigger the stem cells located there and improve tendon healing. Other physicians throughout Houston Methodist, including Dr. David Lintner in the Medical Center, are also offering this procedure.

In time, I believe we will be able to show that the use of stem cells in orthopedic applications is making a difference in the lives of our patients, he said. The potential to repair and regenerate damaged tissue or bone, using the patients own stem cells, will give us a fantastic new tool in treating sports injuries and other orthopedic issues. The ability to make our patients recoveries easier and more successful is exciting.

For more information about Houston Methodist Orthopedics & Sports Medicine located in Sugar Land, visit methodistorthopedics.com. For an appointment, call 281.690.4678 or emailmostappts@houstonmethodist.org.

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Sugar Land surgeon becomes first in Fort Bend to use stem cells in orthopedic surgery

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KYOTO A team of Japanese researchers has developed a new way to easily culture induced pluripotent stem cells that has a low risk of infection in transplant therapy, a British science journal reported.

The team, which includes Kyoto Universitys Center for iPS Cell Research and Application, can create a culture system that unlike the existing technique doesnt have to use animal ingredients, which are at risk of infection, the journal Scientific Reports said Wednesday.

The researchers said in the journal that the new culture system will be vital in speeding up efforts to apply iPS cells in regenerative medicine.

They found that using fragments of a protein called laminin-511, which can stick cells together, enables cells to be stable on culture dishes or plates. With the method, they have created a safer method for producing iPS cells using amino acids and vitamins instead of animal ingredients.

The conventional method for culturing iPS cells has been to graft them on cell culture dishes and used feeder cells or mouse cells and bovine serum-containing medium as nutrients.

But because there are risks to infections in using tissues and cells, which are created from iPS cells under the existing culture system, there is a need to conduct time-consuming safety tests, Scientific Reports said.

They discovered that human iPS cells developed based on this system can also transform into nerve cells that produce neurotransmitter dopamine, insulin-producing cells and blood cells.

The researchers hope the discovery will eventually lead to clinical applications for illnesses such as Parkinsons disease and diabetes.

The new culture system can also be applied to embryonic stem cells, the journal said.

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Team develops new way to culture iPS cells with reduced ...

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Newswise Imagine you are building a house. You would need a team of specialists, including an architect, a general contractor, carpenters, an electrician, a plumber and many others. Now picture yourself leading an effort to develop a new therapeutic drug or device. For that, youd need a very different kind of specialized team.

The National Eye Institute (NEI), part of the National Institutes of Health, has a research program designed to support this team-based approach. NEIs Translational Research Program (TRP) on Therapy for Visual Disorders provides a lead investigator with up to $1.75 million per year for up to five years in order to assemble a multidisciplinary team, and moveor translatepotential new therapies beyond the research lab and into clinical trials.

In addition to bringing together an expert research team, investigators can use funding from the TRP to recruit experts on navigating the drug and device approval process overseen by the Food and Drug Administration (FDA). They can also use TRP funds to seek help in patenting new therapies. These steps are no less essential than lab work for bringing new therapies to patients.

The program enables investigators to assemble multidisciplinary teams that can tackle scientific, technical, and regulatory issues that are beyond the capabilities of any single research group, said Neeraj Agarwal, Ph.D., who oversees programs in research training and workforce development at NEI. The TRP began in 2000, and has funded one or two projects each year since.

Eyeing new drugs for retinal diseases

Krzysztof Palczewski, Ph.D., professor and chair of the pharmacology department at Case Western Reserve University in Cleveland, received a grant (EY021126) through the TRP in 2010. His goal is to develop new drugs for diseases that damage the retina, the light-sensitive tissue at the back of the eye.

Vision begins with cells inside the retina called photoreceptors. Chemicals called retinoids, which are derived from vitamin A, play a key role inside these cells. One type of retinoid, when combined with a protein called opsin, acts as a light-sensitive switch, converting light into electrical signals that are ultimately sent from the photoreceptors to the brain.

Unfortunately, the supply of retinoids is limited and they need to be recycled. Moreover, the recycling process isnt 100 percent efficient. Dr. Palczewski has found that it can lead to the formation of a toxic byproduct called all-trans-retinal (atRAL), which may contribute to some diseases of the retina, such as age-related macular degeneration (AMD) and Stargardt disease. AMD is a leading cause of vision loss among people age 50 and older. Stargardt disease is a rare genetic disease that begins in childhood but has some similarities to AMD.

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Translational Research Through Teamwork

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PUBLIC RELEASE DATE:

8-Jan-2014

Contact: Jim Newman jnewman@mdanderson.org 713-792-0662 University of Texas M. D. Anderson Cancer Center

HOUSTON, TX - Some surprising research findings from scientists at The University of Texas MD Anderson Cancer Center suggest it's possible a simple blood test could be developed to determine whether gene mutations associated with pancreatic cancer exist without the need of locating and testing tumor tissue. This appears possible following the discovery that tiny particles the size of viruses called 'exosomes,' which are shed by cancer cells into the blood, contain the entire genetic blueprint of cancer cells. By decoding this genomic data and looking for deletions and mutations associated with cancer, the research team believes this discovery could be translated into a test that helps physicians detect cancer and treat patients. The findings are based on research led by Raghu Kalluri, M.D., Ph.D., chairman and professor in MD Anderson's Department of Cancer Biology. The research results appear in the current online edition of the Journal of Biological Chemistry.

"At the present time, there is no single blood test that can screen for all cancer related DNA defects," said Kalluri. "In many cases, current protocols require a tumor sample to determine whether gene mutations and deletions exist and therefore determine whether the tumor itself is cancerous or benign. To procure tumor tissue, one needs to know that a tumor exists and if so, is it accessible for sample collection or removal? Finally, there are always risks and significant costs associated with surgical procedures to acquire tumor tissue."

Historically, researchers were aware these miniscule particles existed and that they carried nucleic acids and proteins. It was also believed that exosomes carried small portions of the person's DNA. However, upon further investigation, the MD Anderson research team was surprised to learn that the person's entire double-stranded genomic DNA spanning all chromosomes can be found in exosomes, including those mutated chromosomes that cause various cancers. Furthermore, Kalluri and colleagues discovered that DNA derived from exosomes carried the same cancer-related genetic mutations compared to the cancer cells taken from tumor.

"Because different forms of cancer are associated with different chromosomal mutations , we believe analysis of exosome DNA taken from blood samples may not only help determine the presence of a cancerous tumor somewhere in the body but also identify mutations without a need for tumor sample," added Kalluri. "We also believe this "fingerprint" will help lead us to the likely site of the tumor in the body. For instance, certain mutation spectrums would suggest pancreatic cancer or a brain-based tumor. While there is much more work to be conducted to develop such a test, having a tool such as this would increase our abilities to detect cancer in an earlier stage and therefore increase our chances of effective treatment."

"This seminal discovery paves the way for highly sensitive screening for driver mutations of cancer in the blood without the need for biopsy of tumor tissue and importantly, lays the foundation for a new method for the early detection of cancer when the chance for cure is greatest," said MD Anderson President Ronald A. DePinho, M.D.

###

The National Institutes of Health, Cancer Prevention and Research Institute of Texas and MD Anderson all provided funding to support this research.

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Research suggests a blood test to locate gene defects associated with cancer may not be far off

Recommendation and review posted by Bethany Smith

New York, NY (PRWEB) January 08, 2014

A stem cell model of familial Alzheimers disease (FAD) was successfully generated, allowing researchers to identify 14 genes potentially implicated in the disease. One gene in particular demonstrates the important role inflammation may play in the brain of Alzheimers patients. The study was completed by scientists at The New York Stem Cell Foundation (NYSCF) Research Institute in collaboration with scientists at the Icahn School of Medicine at Mount Sinai (ISMMS) and funded in part by the Cure Alzheimers Fund(CAF).

In the study published today in PLOS ONE, a team of scientists produced stem cells and neural precursor cells (NPCs), representing early neural progenitor cells that build the brain from patients with severe early-onset AD with mutations in the Presenilin 1 (PSEN1) gene. These NPCs had elevated Abeta42/Abeta40 ratios, indicating elevation of the form of amyloid found in the brains of Alzheimers patients. These levels were greater than those in adult cells that did not have the PSEN1 mutation. This elevated ratio shows that the NPCs grown in the petri dish accurately reflected the cells in the brains of FAD patients.

"The gene expression profile from the familial Alzheimers stem cells points to inflammation, which is especially exciting because we would not usually associate inflammation with this particular Alzheimer's gene," said Sam Gandy, MD, PhD, Professor of Neurology and Psychiatry and Director of the Center for Cognitive Health at the Icahn School of Medicine at Mount Sinai and a co-author on the study. Gandy is also Associate Director of the NIH-Designated Mount Sinai Alzheimers Disease Research Center and leader of the Cure Alzheimers Fund Stem Cell Consortium.

"This is the kind of innovative science that will help us better understand the cause of Alzheimers and how to approach the disease with effective therapies," said Tim Armour, President and CEO of Cure Alzheimers Fund (CAF). "It also showcases how targeted investment of critical resources can make a difference in finding solutions to this debilitating disease."

The researchers generated induced pluripotent stem (iPS) cells from affected and unaffected individuals from two families carrying PSEN1 mutations. After thorough characterization of the NPCs through gene expression profiling and other methods, they identified 14 genes that behaved differently in PSEN1 NPCs relative to NPCs from individuals without the mutation. Five of these targets also showed differential expression in late onset Alzheimers disease patients brains. Therefore, in the PSEN1 iPS cell model, the researchers reconstituted an essential feature in the molecular development of familial Alzheimers disease.

The studys co-lead authors Sam Gandy, MD, PhD and Scott Noggle, PhD are both members of CAFs Stem Cell Consortium, which supported this research. The Stem Cell Consortium is an international group of scientists collaborating on innovative research that investigates, for the first time, the brain cells from individuals with the common form of Alzheimers disease. Other members of the Consortium include Kevin Eggan, PhD, of Harvard University, Marc Tessier-Lavigne, PhD, of Rockefeller University, Doo Kim, PhD, of Harvard Medical School, and Tamir Ben-Hur, MD, PhD, of Hadassah University.

Stem cells are the least mature cells in the body. This means they can be treated with a defined cocktail of factors that can cause maturation of cells along discrete cell types. With iPS cells, which are cells that can become any cell type in the body, it now is possible to take skin cells from adults and return them to an immature state. By redirecting skin cells from Alzheimers patients and turning them into nerve cells, investigators are able to study adult Alzheimers neurons (nerve cells) in the lab.

Although the majority of Alzheimers disease cases are late onset and likely result from a mixture of genetic predisposition and environmental factors, there are genetic forms of the disease that affect patients at much earlier ages. PSEN1 mutations cause the most common form of inherited familial Alzheimers disease and are one hundred percent penetrant, resulting in all individuals with this mutation getting the disease.

Identifying genes that behaved differently in patients with the mutation provides new targets to further study and better understand their effects on the development of Alzheimers disease. One of these genes, NLRP2, is traditionally thought of as an inflammatory gene.

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Breakthrough Research Provides Valuable Insight On Cause Of Alzheimer’s

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

8-Jan-2014

Contact: Darrell E. Ward Darrell.Ward@osumc.edu 614-293-3737 Ohio State University Wexner Medical Center

COLUMBUS, Ohio Currently, doctors use chromosome markers and gene mutations to determine the best treatment for patients with acute myeloid leukemia (AML). But a new study suggests that a score based on seven mutated genes and the epigenetic changes that the researchers discovered were also present might help guide treatment by identifying novel subsets of patients.

The findings, published in the Journal of Clinical Oncology, come from a study led by researchers at The Ohio State University Comprehensive Cancer Center Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC James).

The epigenetic change used in the study is DNA methylation. It involves the addition of methyl groups to DNA, which can reduce or silence a gene's activity, or expression. Abnormal DNA methylation alters normal gene expression and often plays an important role in cancer development.

Overall, the findings suggest that patients with a low score indicating that one or none of the seven genes is overexpressed in AML cells had the best outcomes, and that patients with high scores that is, with six or seven genes highly expressed had the poorest outcomes.

"To date, disease classification and prognostication for AML patients have been based largely on chromosomal and genetic markers," says principal investigator Clara D. Bloomfield, MD, Distinguished University Professor, Ohio State University Cancer Scholar and Senior Adviser.

"Epigenetic changes that affect gene expression have not been considered. Here we show that epigenetic changes in previously recognized and prognostically important mutated genes can identify novel patient subgroups, which might better help guide therapy," says Bloomfield, who is also the William Greenville Pace III Endowed Chair in Cancer Research at Ohio State.

The seven-gene panel was identified in 134 patients aged 60 and older with cytogenetically normal acute myeloid leukemia (CN-AML) who had been treated on Cancer and Leukemia Group B (CALGB)/Alliance clinical trials.

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AML score that combines genetic and epigenetic changes might help guide therapy

Recommendation and review posted by Bethany Smith

Jan. 8, 2014 Currently, doctors use chromosome markers and gene mutations to determine the best treatment for a patient with acute myeloid leukemia (AML). But a new study suggests that a score based on seven mutated genes and the epigenetic changes that the researchers discovered were present might help guide treatment by identifying novel subsets of patients.

The findings, published in the Journal of Clinical Oncology, come from a study led by researchers at The Ohio State University Comprehensive Cancer Center -- Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC -- James).

The epigenetic change used in the study is DNA methylation. It involves the addition of methyl groups to DNA, which can reduce or silence a gene's activity, or expression. Abnormal DNA methylation alters normal gene expression and often plays an important role in cancer development.

Overall, the findings suggest that patients with a low score -- indicating that one or none of the seven genes is overexpressed in AML cells -- had the best outcomes, and that patients with high scores -- that is, with six or seven genes highly expressed -- had the poorest outcomes.

"To date, disease classification and prognostication for AML patients have been based largely on chromosomal and genetic markers," says principal investigator Clara D. Bloomfield, MD, Distinguished University Professor, Ohio State University Cancer Scholar and Senior Adviser.

"Epigenetic changes that affect gene expression have not been considered. Here we show that epigenetic changes in previously recognized and prognostically important mutated genes can identify novel patient subgroups, which might better help guide therapy," says Bloomfield, who is also the William Greenville Pace III Endowed Chair in Cancer Research at Ohio State.

The seven-gene panel was identified in 134 patients aged 60 and older with cytogenetically normal acute myeloid leukemia (CN-AML) who had been treated on Cancer and Leukemia Group B (CALGB)/Alliance clinical trials.

The researchers computed a score based on the number of genes in the panel that were highly expressed in patients' AML cells, and retrospectively tested the score in two groups of older patients (age 60 and up) and two groups of younger patients (age 59 and under).

Patients with a low score -- indicating that one or none of the seven genes is overexpressed -- had the best outcomes. Patients with high scores -- that is, with six or seven genes highly expressed -- had the poorest outcomes.

"For this seven-gene panel, the fewer highly expressed genes, the better the outcome," says first author Guido Marcucci, MD, professor of medicine and the associate director for translational research at the OSUCCC -- James. "In both younger and older patients, those who had no highly expressed genes, or had one highly expressed gene had the best outcomes."

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AML score combining genetic, epigenetic changes might help guide therapy

Recommendation and review posted by Bethany Smith

Jan. 8, 2014 Some surprising research findings from scientists at The University of Texas MD Anderson Cancer Center suggest it's possible a simple blood test could be developed to determine whether gene mutations associated with pancreatic cancer exist without the need of locating and testing tumor tissue. This appears possible following the discovery that tiny particles the size of viruses called 'exosomes,' which are shed by cancer cells into the blood, contain the entire genetic blueprint of cancer cells. By decoding this genomic data and looking for deletions and mutations associated with cancer, the research team believes this discovery could be translated into a test that helps physicians detect cancer and treat patients.

The findings are based on research led by Raghu Kalluri, M.D., Ph.D., chairman and professor in MD Anderson's Department of Cancer Biology. The research results appear in the current online edition of the Journal of Biological Chemistry.

"At the present time, there is no single blood test that can screen for all cancer related DNA defects," said Kalluri. "In many cases, current protocols require a tumor sample to determine whether gene mutations and deletions exist and therefore determine whether the tumor itself is cancerous or benign. To procure tumor tissue, one needs to know that a tumor exists and if so, is it accessible for sample collection or removal? Finally, there are always risks and significant costs associated with surgical procedures to acquire tumor tissue."

Historically, researchers were aware these miniscule particles existed and that they carried nucleic acids and proteins. It was also believed that exosomes carried small portions of the person's DNA. However, upon further investigation, the MD Anderson research team was surprised to learn that the person's entire double-stranded genomic DNA spanning all chromosomes can be found in exosomes, including those mutated chromosomes that cause various cancers. Furthermore, Kalluri and colleagues discovered that DNA derived from exosomes carried the same cancer-related genetic mutations compared to the cancer cells taken from tumor.

"Because different forms of cancer are associated with different chromosomal mutations , we believe analysis of exosome DNA taken from blood samples may not only help determine the presence of a cancerous tumor somewhere in the body but also identify mutations without a need for tumor sample," added Kalluri. "We also believe this "fingerprint" will help lead us to the likely site of the tumor in the body. For instance, certain mutation spectrums would suggest pancreatic cancer or a brain-based tumor. While there is much more work to be conducted to develop such a test, having a tool such as this would increase our abilities to detect cancer in an earlier stage and therefore increase our chances of effective treatment."

"This seminal discovery paves the way for highly sensitive screening for driver mutations of cancer in the blood without the need for biopsy of tumor tissue and importantly, lays the foundation for a new method for the early detection of cancer when the chance for cure is greatest," said MD Anderson President Ronald A. DePinho, M.D.

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Blood test to locate gene defects associated with cancer may not be far off

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

8-Jan-2014

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, January 7, 2014Packaging replacement genes in viruses is an effective method to deliver them to target tissues, but the human body mounts an immune response against the virus. The systemic and local immune reactions induced by an adeno-associated virus (AAV)-based gene therapy to treat lipoprotein lipase deficiency, approved for use in Europe, does not affect the safety of gene therapy or expression of the replacement gene for at least one year after delivery, according to a study published in Human Gene Therapy, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available on the Human Gene Therapy website.

Valeria Ferreira and coauthors, uniQure BV and Academic Medical Center, Amsterdam, the Netherlands, and University of Montreal and Chicoutimi Hospital, Quebec, Canada, evaluated measures of inflammation and adverse clinical events and the expression of a replacement lipoprotein lipase (LPL) gene that was injected intramuscularly into patients with LPL deficiency. The gene was packaged in an AAV vector, as described in the article "Immune responses to intramuscular administration of alipogene tiparvovec (AAV1-LPLS447X) in a phase II clinical trial of Lipoprotein Lipase deficiency (LPLD) gene therapy."

"The clinical data published in this paper were critical to the approval of Glybera," says James Wilson, MD, PhD, Editor-in-Chief of Human Gene Therapy and Director of the Gene Therapy Program, Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia. "Furthermore, they provide context for laboratory measurements of immune responses which apparently did not impact product performance."

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About the Journal

Human Gene Therapy, the official journal of the European Society of Gene and Cell Therapy, British Society for Gene and Cell Therapy, French Society of Cell and Gene Therapy, German Society of Gene Therapy, and five other gene therapy societies, is an authoritative peer-reviewed journal published monthly in print and online. Human Gene Therapy presents reports on the transfer and expression of genes in mammals, including humans. Related topics include improvements in vector development, delivery systems, and animal models, particularly in the areas of cancer, heart disease, viral disease, genetic disease, and neurological disease, as well as ethical, legal, and regulatory issues related to the gene transfer in humans. Its sister journals are Human Gene Therapy Methods, published bimonthly and focused on the application of gene therapy to product testing and development, and Human Gene Therapy Clinical Development, published quarterly and featuring data relevant to the regulatory review and commercial development of cell and gene therapy products. Tables of content for all three publications and a sample issue may be viewed on the Human Gene Therapy website.

About the Publisher

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Does the body's immune response to viral vector delivery systems affect the safety or efficacy of gene therapy?

Recommendation and review posted by Bethany Smith

I have frequently pointed out that pharmaceutical companies acknowledge that animal models are not predictive for human response in terms of efficacy or toxicity. More evidence for this position comes from Robert G. Hunter in an article in Genetic Engineering & Biotechnology News.[1] Hunter: Having developed over the past 20 years into a global market recently estimated at $5 billion, in vitro and in silico products and services are now about the same size as the in vivo services (contract research organization) industry. If animal models worked well, there would be no need for industry to look at other options. Pharma does not love bunnies. Pharma loves money.

Matthew Herper addressed the problems in drug development in an article in Forbes.[2] Herper:

Theres one factor that, as much as anything else, determines how many medicines are invented, what diseases they treat, and, to an extent, what price patients must pay for them: the cost of inventing and developing a new drug, a cost driven by the uncomfortable fact than 95% of the experimental medicines that are studied in humans fail to be both effective and safe.

Animal models are relied on for the evaluation of both efficacy and safety.[3-9] Herper continues:

A new analysis conducted at Forbes puts grim numbers on these costs. A company hoping to get a single drug to market can expect to have spent $350 million before the medicine is available for sale. In part because so many drugs fail, large pharmaceutical companies that are working on dozens of drug projects at once spend $5 billion per new medicine. . . . This is crazy. For sure its not sustainable, says Susan Desmond-Hellmann, the chancellor at UCSF and former head of development at industry legend Genentech, where she led the testing of cancer drugs like Herceptin and Avastin. Increasingly, while no one knows quite what to do instead, any businessperson would look at this and say, You cant make a business off this. This is not a good investment. I say that knowing that this has been the engine of wonderful things.

This, in part, is why disease-specific drugs like Kalydeco, a drug for cystic fibrosis (CF) patients that have a specific genetic mutation, costs $294,000 per patient per year.

The reason animal models fail for drug development is that animals and humans are evolved systems that are differently complex. While morphological similarities exist, very small differences in the genetic make-up between species and between individuals of the same species means the predictive value for extrapolation is nil in the real world. (For more on this see Trans-Species Modeling Theory.) Moreover, if the concept of evolved, complex systems invalidates trans-species extrapolation in drug development, it is going to do the same when trans-species extrapolation involves any perturbation that affects higher levels of organization. So just based on the evidence from drug development we can safely say that disease research on mice, monkeys, or dogs is not going to result in knowledge that has predictive value for human patients. The literature confirms this.[10-21][[22]p19-33, 73-77] [23-25]

Compare the above to this recent statement from Michael E. Goldberg published in the Wisconsin State Journal: Nearly every medical advance from the last century is a product of responsible animal research, and animal models will continue to be important to medical progress. . . . Activists who claim animal research does not benefit humans are wrong. Animals are essential to medical progress in all fields of human disease. [26] This illustrates the dichotomy regarding animal models. Dr Goldberg is an animal modeler who does basic research, which he sells as applied research. Not surprisingly, Goldberg thinks animal modeling is great. He does not suffer loss of income or prestige when the knowledge from animal modeling fails to translate to human patients.

Pharma on the other hand, can actually measure the success or lack thereof of animal models in the form of drugs successfully brought to market and Pharma says it doesnt work. Remember, Pharma is a business and they do not care how they develop new drugs they just want to develop new drugs so they can make money. Also remember that there are not two different theories of evolution: one for drug development and another for basic science research or basic research masquerading as applied research. If animal modeling in drug development fails to be consistent with evolutionary biology, then it fails in general as well.

Image courtesy of Wkipedia Common http://en.wikipedia.org/wiki/File:Chromosomes_mutations-en.svg

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There is Only One Evolution

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Health

Linda Carroll NBC News contributor

19 hours ago

A rare genetic mutation that disrupts the production of histamine may help researchers unravel the mystery that surrounds Tourette syndrome.

The mutation discovered by Yale researchers can cause the kinds of tics and other abnormalities that are the hallmark of the syndrome, according to a study published Wednesday in the journal Neuron.

Thus far the genetic anomaly has been discovered only in nine members of a single family: a father and all eight of his children who have both the mutation and Tourette syndrome.

We know that Tourette is about 90 percent genetic, said study coauthor Dr. Christopher Pittenger, an associate professor of psychiatry and psychology at the Yale University School of Medicine and director of the Yale OCD research clinic. But its been incredibly hard to find any genetic abnormalities that cause the syndrome. We have proven that this gene really is the cause of Tourette in this family and also looked at some of its downstream effects.

Courtesy Jeffrey Kramer

Jeffrey Kramer and his three sons. Kramer and two of his grown-up sons have been living with Tourette for decades. Hes excited by the new findings, but realistic about their impact on patients with the syndrome.

What isnt known yet is how, or if, this finding can be extended to other people with Tourette, Pittenger and other experts said.

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Rare genetic mutation discovered in Tourette syndrome family

Recommendation and review posted by Bethany Smith

(MENAFN - Muscat Daily) A Weill Cornell Medical College study that analysed the DNA of Qatar's native population has discovered genetic variations that could help doctors target interventions to reduce the prevalence of a variety of debilitating hereditary disorders

Researchers at Weill Cornell Medical College in Qatar (WCMC-Q) and Weill Cornell Medical College in New York (WCMC-NY), working with colleagues from Cornell University in Ithaca and Hamad Medical Corporation, identified 37 genetic variants in 33 genes known to play causal roles in a total of 36 diseases, including such devastating conditions as cystic fibrosis, sickle cell anemia and muscular dystrophy. The study points the way to more comprehensive screening for a host of inherited diseases, which could significantly reduce their incidence.

The project titled, 'Exome Sequencing Identifies Potential Risks Variants for Mendelian Disorders at High Prevalence in Qatar' sequenced the DNA of 100 Qatari nationals representing the three major ethnic subgroups of the country the Bedouin (termed Q1 for the purposes of the study), those of Persian-South Asian descent (Q2), and those of African descent (Q3). By analysing the individuals' exomes important sections of the DNA containing the code that is translated into proteins and comparing them to the genetic data of the participants in the worldwide 1,000 Genomes Project (1000G), the researchers were able to identify the variations that cause disease among the Qatari population.

All the conditions targeted in the study were so-called Mendelian diseases'. Named after Gregor Mendel, the 19th century researcher widely regarded as the founder of genetic science, Mendelian diseases are those caused by a single mutated gene and are also known as monogenic disorders.

Dr Khalid Fakhro, postdoctoral associate in genetic medicine at WCMC-Q, and Dr Juan L Rodriguez-Flores of WCMC-NY, were co-lead principal investigators in the study, which is part of a group of research projects investigating the Qatari genome led by Dr Ronald Crystal, chairman of Genetic Medicine at Weill Cornell Medical College in New York. The study has been accepted for publication in the journal Human Mutation, appearing online in December 2013 and in print in January 2014.

Dr Crystal explained the study: ''There are about 3.2bn letters that comprise the human genome and about two percent of those letters code for the actual proteins. This two per cent is found in regions called exomes,'' he said. ''A Mendelian or monogenic disease is caused by a change in a single letter out of the 3.2bn.

''The reason this is relevant for Qatar is that the structure of the society encourages a high degree of consanguineous marriage, so the frequency of these monogenic diseases is quite high,'' he said.

Pre-marital counseling and screening is one method of decreasing the likelihood of children being born with monogenic diseases. Parents undergo screening to see if either or both carry genetic variations that cause disease before having children. The individuals that carry the disorder do not necessarily have the conditions themselves, but may carry them on recessive genes.

Dr Crystal added, ''Disorders are present in all populations around the world, so Qatar is no different. Qatar is only different in that its variations and the frequency with which they occur are unique to its population. By finding out what these variations are and taking appropriate action we can save people from the trauma of some very unpleasant disorders. We're talking here about things like brain malformation, diabetes, blindness, deafness, cardiovascular disorders, inflammatory disorders and many other conditions. While these conditions are not common, they do occur, some are untreatable and many are very difficult to live with, for both the sufferer and their families.''

Currently, pre-marital counseling in Qatar screens for four genetic variations out of the 37 identified by the study, so incorporating the newly discovered variations into the screening process could have a significant impact.

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Mapping the Qatari shows way to prevention of inherited diseases

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Dragon Genetics Game
Simple arcade game which focuses strictly on dragon genetics. It #39;s pretty simple and there isnt that much variation but interesting. Royalty Free Music by: h...

By: IamJaylew

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Dragon Genetics Game - Video

Recommendation and review posted by Bethany Smith

Originally published January 8, 2014 at 11:38 AM | Page modified January 8, 2014 at 6:13 PM

NEW YORK Seattle Genetics said Wednesday it expanded a cancer treatment collaboration with drugmaker AbbVie.

The Bothell company said it will receive a $25 million upfront payment from AbbVie, and it could get $255 million in license and milestones payment per drug. AbbVie also agreed to pay Seattle Genetics royalties in the single digits on sales of any drugs that are approved.

Shares of Seattle Genetics rose $1.04, or 2.6 percent, to $41.04 Wednesday.

Seattle Genetics and Abbott Laboratories started working together in March 2011 on experimental antibodies designed to fight cancer. The antibodies are designed to selectively deliver anticancer drugs to tumor cells. Abbott made an $8 million upfront payment. In October 2012 the companies agreed to expand their partnership, and Abbott paid Seattle Genetics an additional 25 million.

AbbVie was spun off from Abbott a year ago. It sells branded prescription drugs, including the blockbuster anti-inflammatory drug Humira, which is used to treat rheumatoid arthritis, psoriasis and Crohns disease.

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Seattle Genetics, AbbVie broaden partnership

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Phoenix, AZ (PRWEB) January 08, 2014

The top Phoenix stem cell clinic in the Valley, Arizona Pain Stem Cell Institute, is now offering PRP therapy for joint arthritis relief. Platelet rich plasma therapy offers the potential for relieving the pain from knee, hip, shoulder and spinal arthritis. For more information and scheduling with the Board Certified Phoenix pain management doctors, call (602) 507-6550.

Platelet rich plasma therapy, known as PRP therapy, involves a simple blood draw. The blood is then spun in a centrifuge, which then concentrates platelets and growth factors for immediate injection into the arthritic joint. The PRP therapy then acts as an attractant for the body's stem cells.

Recent published studies have shown that PRP therapy offers significant pain relief for arthritic knees and helps preserve existing cartilage. One to three injections may be necessary to obtain optimal results, which are performed as an outpatient and entail minimal risk.

In addition to PRP therapy, the Arizona Pain Stem Cell Institute offers several other regenerative medicine treatments for both joint and spinal arthritis. This includes bone marrow and fat derived stem cell injections along with amniotic stem cell rich injections. These injections are offered for patients as part of numerous clinical research studies.

The stem cell injection studies are enrolling now at the Institute. The studies are industry subsidized, with the procedures performed by the Board Certified pain management physicians.

The Arizona Pain Stem Cell Institute is part of Arizona Pain Specialists. With 5 locations accepting over 50 insurances, the pain clinics offer comprehensive treatment options for patients with both simple and complicated pain conditions.

Call (602) 507-6550 for more information and scheduling.

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Arizona Pain Stem Cell Institute Now Offering PRP Therapy for Joint Arthritis Relief

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Researchers have developed a new way to study bone disorders and bone growth, using stem cells from patients afflicted with a rare, genetic bone disease. The approach, based on Nobel-Prize winning techniques, could illuminate the illness, in which muscles and tendons progressively turn into bone, and addresses the similar destructive process that afflicts a growing number of veterans who have suffered blast injuries including traumatic amputations or injuries to the brain and nervous system. This insidious hardening of tissues also grips some patients following joint replacement or severe bone injuries.

The disease model, described in a new study by a UC San Francisco-led team, involves taking skin cells from patients with the bone disease, reprogramming them in a lab dish to their embryonic state, and deriving stem cells from them.

Edward Hsiao, MD, PhD

Once the team derived the stem cells, they identified a cellular mechanism that drives abnormal bone growth in the thus-far untreatable bone disease, calledfibrodysplasiaossificansprogressiva(FOP). Furthermore, they found that certain chemicals could slow abnormal bone growth in the stem cells, a discovery that might help guide future drug development.

Clinically, the genetic and trauma-caused conditions are very similar, with bone formation in muscle leading to pain and restricted movement, according to the leader of the new study, Edward Hsiao, MD, PhD, an endocrinologist who cares for patients with rare and unusual bone diseases at the UCSF Metabolic Bone Clinic in the Division of Endocrinology and Metabolism.

The human cell-based disease model is expected to lead to a better understanding of these disorders and other illnesses, Hsiao said.

The new FOP model already has shed light on the disease process in FOP by showing that the mutated gene can affect different steps of bone formation, Hsiao said. These different stages represent potential targets for limiting or stopping the progression of the disease, and may also be useful for blocking abnormal bone formation in other conditions besides FOP. The human stem-cell lines we developed will be useful for identifying drugs that target the bone-formation process in humans."

The teams development of, and experimentation with, the human stem-cell disease model for FOP, published in the December issue of theOrphanetJournal of Rare Diseases, is a realization of the promise of research using stem cells of the type known as induced pluripotent stem (iPS) cells, immortal cells of nearly limitless potential, derived not from embryos, but from adult tissues.

Shinya Yamanaka, MD, PhD, a UCSF professor of anatomy and a senior investigator with the UCSF-affiliated Gladstone Institutes, as well as the director of the Center foriPSCell Research and Application (CiRA) and a principal investigator at Kyoto University, shared the Nobel Prize in 2012 for discovering how to makeiPScells from skin cells using a handful of protein factors. These factors guide a reprogramming process that reverts the cells to an embryonic state, in which they have the potential to become virtually any type of cell.

Link:
Stem Cells Used to Model Disease that Causes Abnormal Bone Growth

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

7-Jan-2014

Contact: David McKeon DMckeon@nyscf.org 212-365-7440 New York Stem Cell Foundation

NEW YORK, NY (January 7, 2014) Scientists at The New York Stem Cell Foundation (NYSCF) Research Institute, working in collaboration with scientists from Columbia University Medical Center (CUMC), for the first time generated induced pluripotent stem (iPS) cells lines from non-cryoprotected brain tissue of patients with Alzheimer's disease.

These new stem cell lines will allow researchers to "turn back the clock" and observe how Alzheimer's develops in the brain, potentially revealing the onset of the disease at a cellular level long before any symptoms associated with Alzheimer's are displayed. These reconstituted Alzheimer's cells will also provide a platform for drug testing on cells from patients that were definitively diagnosed with the disease. Until now, the only available method to definitively diagnose Alzheimer's disease that has been available to researchers is examining the brain of deceased patients. This discovery will permit scientists for the first time to compare "live" brain cells from Alzheimer's patients to the brain cells of other non-Alzheimer's patients.

NYSCF scientists successfully produced the iPS cells from frozen tissue samples stored for up to eleven years at the New York Brain Bank at Columbia University.

This advance, published today in Acta Neuropathologica Communications , shows that disease-specific iPS cells can be generated from readily available biobanked tissue that has not been cryoprotected, even after they have been frozen for many years. This allows for the generation of iPS cells from brains with confirmed disease pathology as well as allows access to rare patient variants that have been banked. In addition, findings made using iPS cellular models can be cross-validated in the original brain tissue used to generate the cells. The stem cell lines generated for this study included samples from patients with confirmed Alzheimer's disease and four other neurodegenerative diseases.

This important advance opens up critical new avenues of research to study cells affected by disease from patients with definitive diagnoses. This success will leverage existing biobanks to support research in a powerful new way.

iPS cells are typically generated from a skin or blood sample of a patient by turning back the clock of adult cells into pluripotent stem cells, cells that can become any cell type in the body. While valuable, iPS cells are often generated from patients without a clear diagnosis of disease and many neurodegenerative diseases, such as Alzheimer's disease, often lack specific and robust disease classification and severity grading. These diseases and their extent can only be definitively diagnosed by post-mortem brain examinations. For the first time we will now be able to compare cells from living people to cells of patients with definitive diagnoses generated from their banked brain tissue.

Brain bank networks, which combined contain tens of thousands of samples, provide a large and immediate source of tissue including rare disease samples and a conclusive spectrum of disease severity among samples. The challenge to this approach is that the majority of biobanked brain tissue was not meant for growing live cells, and thus was not frozen in the presence of cryoprotectants normally used to protect cells while frozen. NYSCF scientists in collaboration with CUMC scientists have shown that these thousands of samples can now be used to make living human cells for use in disease studies and to develop new drugs or preventative treatments for future patients.

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NYSCF scientists make living brain cells from Alzheimer's patients biobanked brain tissue

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By Cassandra Leger

Cancers are not created equal nor do they respond the same to treatment and scientists have sought after the reason why for decades. In particular, research has focused on uncovering why certain cancers are very rebellious and stubborn in response to radiation therapy. The answer may lie in studying the mitochondriathe energy power plant of the cell.

A research team lead by Maxim Frolov at the University of Illinois at Chicago has shed light on the previously unknown role that mitochondria play in cell death induced by radiation therapy, as described in a November press release.The team studied the E2F gene, a key player in the natural process of cell death. Fruit flies were fitted with a mutated version of the E2F gene which caused the cells mitochondria to be misshapen. When misshapen, mitochondria produce less energy. Importantly, the fruit flies with abnormal mitochondria were resistant to radiation therapy. The study was later introduced to human cells and yielded similar results.

This discovery may help explain why cancer patients react so differently to radiation therapy and may be a building block for pharmaceutical companies to develop drugs which target mitochondrial function to improve radiation therapy outcomes.

Other research teams at the University are focused on understanding the role of mitochondrial dysfunction in cancer, including Michelle Boland and colleagues. A recently published review in the journal Frontiers in Oncology covers research on the role of dysfunctional mitochondria in multiple aspects of cell growth and the relation to cancer diagnosis and treatment.

Source: http://news.uic.edu/dysfunctional-mitochondria-may-underlie-resistance-to-radiation-therapy

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Abnormal Mitochondria May Contribute To Radiation Resistant Cancer

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