MsTinaTv #39;s Myelin Repair, Genetics
GeneUtree.

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Mower Genetics - LaCannalope a znienej SAGE svilukama

By: Mower Genetics

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CEOLIVE.TV Interview | Panna Sharma / CEO of Cancer Genetics (NASDAQ:CGIX)
Cancer Genetics Inc. is an emerging leader in DNA-based cancer diagnostics, servicing some of the most prestigious medical institutions in the world. Our tests target cancers that are difficult...

By: Mike Elliott

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Image from Chiappini et. al.

Gene therapy, the delivery of genetic material to cells in the form of DNA or RNA, has been explored as a means to treat illnesses. These treatments hinge on ourability to getDNA and RNA inside cells, where they can interact with the cell's machinery. Currently, successful delivery of nucleic acids has been stalled by inefficient insertion of the molecules into cells, safety concerns, limited accessibility of the target cells, and poor scalability.

In order to overcome these limitations, a team of scientists has proposed nanoinjection through a carefully designed array of tiny needles, which they're calling nanoneedles. Nanoinjection provides a more uniform delivery due to the high density of nanoneedles that can occupy a givensurface area. The researchers fabricated biodegradable, porous nanoneedles from silicon with a geometry that was optimized for intracellular delivery.

The nanoneedles had a 5 m length, 50 m width at the sharp end, and 600 nm base diameter, providing a 300-fold increase in surface area for delivery compared to a non-porous wireof equivalent diameter. The porosity of the needles could also be tailored to modulate things likepayload volume, mechanical strength, and how long the needle persists inside cells.

Characterization of the needles demonstrated they could withstand the force required to penetrate cells and were effective in delivering either DNA or RNA. The nanoneedles progressively dissolved over 36 hours in physiological conditions; after 72 hours only the solid stump remained.

Nanoinjection was tested by either placing nanoneedles beneath or on top of a layer of cells. In both cases, nanoinjection did not induce significant toxicitycells continued tofunction and grow normally over the course of five days. Thenanoneedle constructs were also able to load, retain, and deliver nucleic acids over a 12-18 hour period, achieving uniform RNA spread inside the cellafter 48 hours.

The nanoneedles could deliver two separate types of nucleic acids using a RNA strand and a fluorescently labeled DNA strand. These constructsdemonstrated that the molecules were active once inside the cell; they couldmodulate gene activityby either expressing a gene carried on the DNAor silencing expression of genes via RNA interference.

The efficacy of the device was also tested in rats. The nanoneedles could be used for a localized injection, as shown by their ability to carry fluorescent dyes into the skin and muscle of test rats. Nanoinjection was also assessed on ear and muscle to demonstrate that tissue architecture does not influence the delivery process. Injection of fluorescent dyes did not induce local inflammation withina 24 hour period, and imagingof the skin and muscles revealed that the tissue maintained its normal appearanceafter nanoinjection.

Finally, the researchers compared efficiency of nanoinjection todirect injection of DNA. They tested this usingVEGF165, which is a gene that influences the development of blood vessels. While both injections resulted in expression of human VEGF165 for up to one week, the blood vessels formed were very different.Nano injectionpromoted the formation ofhighly interconnected blood vessels near the surface of the skin and a six-fold increase in overall blood perfusion; direct injection did not.

These nano needles could provide a new route totargeted delivery of RNA and DNA, which could lead to major improvements in efficient gene therapy strategies.

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From left: Tushar Menon, Inder Verma and Amy Firth. Salk Institute

From left: Tushar Menon, Inder Verma and Amy Firth. / Salk Institute

Those born with the immune disorder SCID-X1, or "bubble boy disease" may one day benefit from a new treatment to give them a functioning immune system, if new research from the Salk Institute succeeds.

Working with cultures of induced pluripotent stem cells from a patient, Salk scientists led by gene therapy expert Inder Verma repaired the genetic defect that causes the disease. Infants born with this inherited condition have virtually no immune resistance, and can be killed by infections easily defeated by normal immune systems.

Researchers were able to generate what appear to be mature NK, or "natural killer" immune cells, the first time this has been done. They also generated progenitors of T cells. This doesn't repair all the immune system, but it's a big step in that direction.

These preliminary results may pave the way to an alternative from treating these patients, Verma said. At present, patients can be treated with bone marrow transplants, but matching donors are hard to find. Gene therapy using a viral vector to repair the defect has been successful, but has caused leukemia in some patients when the corrective gene went into the wrong place. Newer forms of this therapy appear to have reduced the risk, but long-term followups of those treated are still in progress.

Salk researchers dispensed with viruses entirely by using the TALEN technology, which allows genetic editing without viruses, and is also more precise.

The study was published in the journal Cell Stem Cell on March 12. Tushar Menon and Amy L. Firth are the first authors. Verma is the senior author.

SCID-X1 is caused by an inactivating mutation on a gene called IL-2Rg located on the X chromosome, which means it exclusively affects males. (For females who carry the mutation on one chromosome, the functional gene on the other chromosome suffices).

One-letter mutation

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Dr Schneider IU Percision Tx Initiative

By: Indiana Institute for Personalized Medicine (IIPM)

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By John ElderApril 5, 2015, 12:15 a.m.

A new frontier in stem cell therapy or a false dawn? John Elder reports.

Last week, Suzie Palmer, 44, travelled from her home in NSW to the Gold Coast for her second round of stem cell treatments for multiple sclerosis. OnTuesday morning,the wheelchair-bound poet underwent liposuction.

By 2.30pm, stem cells had been partially separated from her abdominal fat, suspended in plasma, and injected intravenously. Her doctor, Soraya Felix, is a cosmetic surgeon and molecular biologist with a sideline in regenerative medicine.

Palmer, a relentlessly upbeat and positive person, says the treatments have helped her cope better with heat, improved her mobility and flexibility and otherwise made her "feel like a normal human being". She has, she says, managed a few steps with a walker, still a long way from "running about, which is my dream".

The rapidly growing stem cell industry is aglow with similarly positive testimonials, notably on behalf of practitioners who offer little documented scientific evidence of their success.

Suzie Palmer is literally the poster girl for stem cell tourism within Australia. You can find her smiling sweetly, along with Dr Felix, on the Facebook page of a group called the Adult Stem Cell Foundation. She is one of an unknown number of unwell Australians pinning their hopes on an unregulated industry that is now under review by the Therapeutic Goods Administration.

The TGA public consultation, which closed earlier this month, was prompted by long-standing concerns raised by Stem Cells Australia that a loophole in the regulations has allowed dozens of doctors across Australia to provide experimental treatments without the ethics committee oversight that registered clinical trials are subject to. These treatments invariably cost $10,000 and up. The loophole is this: while the use of donor stem cells in therapies is tightly regulated, the use of a patient's own stem cells is not.

Professor Martin Pera is the program leader of Stem Cells Australia, which is administered by the University of Melbourne and includes scientists from Monash University, the Walter and Eliza Hall Institute for Medical Research, the Florey Institute and the CSIRO, among others. They are engaged in a seven-year Australian Research Council project to answer the big questions about stem cells and the potential for reliable therapies.

Pera's laboratory at Monash University was the second in the world to isolate embryonic stem cells, and the first to describe their differentiation into somatic cells in vitro.

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CIRM funds many projects seeking to better understand heart disease and to translate those discoveries into new therapies.

If you want to learn more about CIRM funding decisions or make a comment directly to our board, join us at a public meeting. You can find agendas for upcoming public meetings on our meetings page.

Find Out More: Stem Cell FAQ | Stem Cell Videos | What We Fund

Find clinical trials: CIRM does not track stem cell clinical trials. If you or a family member is interested in participating in a clinical trial, please visit clinicaltrials.gov to find a trial near you.

Heart disease strikes in many forms, but collectively it causes one third of all deaths in the U.S. Many forms of heart disease have a common resultcardiomyopathy. While this is commonly called congestive heart failure (CHF), it is really just the heart becoming less efficient due to any number of causes, but the most common is loss of functioning heart muscle due to the damage caused by a heart attack. An estimated 4.8 million Americans have CHF, with 400,000 new cases diagnosed each year. Half die within five years.

Numerous clinical trials are underway testing a type of stem cell found in borne marrow, called mesenchymal stem cells or MSCs, to see if they are effective in treating the form of CHF that follows a heart attack. While those trials have shown some small improvements in patients the researchers have not found that the MSCs are creating replacement heart muscle. They think the improvements may be due to the MSCs creating new blood vessels that then help make the existing heart muscle healthier, or in other ways strengthening the existing tissue.

Californias stem cell agency has numerous awards looking into heart disease (the full list is below). Most of these involve looking for ways to create stem cells that can replace the damaged heart muscle, restoring the hearts ability to efficiently pump blood around the body. Some researchers are looking to go beyond transplanting cells into the heart and are instead exploring the use of tissue engineering technologies, such as building artificial scaffolds in the lab and loading them with stem cells that, when placed in the heart, may stimulate the recovery of the muscle.

Other CIRM-funded researchers are working in the laboratory, looking at stem cells from heart disease patients to better understand the disease and even using those models to discover and test new drugs to see if they are effective in treating heart disease. Other researchers are trying to make a type of specialized heart cell called a pacemaker cell, which helps keep a proper rhythm to the hearts beat.

We also fund projects that are trying to take promising therapies out of the laboratory and closer to being tested in people. These Disease Team Awards encourage the creation of teams that have both the scientific knowledge and business skills needed to produce therapies that can get approval from the Food and Drug Administration (FDA) to be tested in people. In some cases, these awards also fund the early phase clinical trials to show that they are safe to use and, in some cases, show some signs of being effective.

This team developed a way to isolate some heart-specific stem cells that are found in adult heart muscle. They use clumps of cells called Cardiospheres to reduce scarring caused by heart attacks. Initially they used cells obtained from the patients own heart but they later developed methods to obtain the cells they need from donor organs, which allows the procedure to become an off-the-shelf-therapy, meaning it can be available when and where the patient needs it rather than having to create it new each time. The company, working with the Cedars-Sinai team, received FDA approval to begin a clinical trial in June 2012.

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TRUCKEE, Calif. The Gene Upshaw Memorial Fund donated $180,557 in 2014 to further the Tahoe Institute for Rural Health Researchs pursuit to invent a device that accurately diagnoses concussions.

Since launching the fund in 2009, $323,544 has been directed specifically for traumatic brain injury research with the Tahoe Institute for Rural Health Research. Most of the money is raised through the Gene Upshaw Memorial Golf Classic conducted in July.

Upshaw, a National Football League Hall of Famer and former NFL Players Association executive director, died of pancreatic cancer in 2008 at Tahoe Forest Hospital. Upshaws wife, Terri, and sons Justin and Daniel established the fund because of the exceptional care he received at the hospital.

More than $825,000 has been raised since the inaugural golf classic in 2009. Funds have also supported the Gene Upshaw Memorial Tahoe Forest Cancer Center, pancreatic cancer research, Tahoe Forest Hospital Innovations Fund and Hospice programs at Tahoe Forest Hospital.

Led by founding director Thomas D. Hobday, the Tahoe Institute for Rural Health Research began work on developing a concussion-testing mechanism three years ago.

Hobday and his team of researchers are determined to replace the standard subjective computerized testing programs such as ImPACT with an objective mechanism for determining when a concussion has occurred and when it has healed

Research has determined that traumatic brain injuries typically occur when athletes come back to the field before the brain has healed or returned to its baseline and suffer subsequent brain trauma.

Researchers envision the device as a low-cost, compact, portable unit that will be able to determine injury severity within 10 minutes.

To further evaluate their testing device and gather more data for their research, the institute is testing student-athletes at Truckee High School and Feather River College, as well as Squaw Valley, Sugar Bowl and Northstar ski teams, during their 2014-15 sports seasons.

The institutes TBI research started five years ago following a conference of neurologists, doctors and scientists from Tahoe Forest Hospital and UC Davis.

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CANCER RESEARCH UK scientists have discovered that a vital self-destruct switch in cells is hijacked - making some pancreatic and non small cell lung cancers more aggressive, according to research published in Cancer Cell today (Thursday)*.

The team, from the Cancer Research UK Centre at the UCL (University College London) Cancer Institute, found that mutations in the KRAS gene interferes with protective self-destruct switches, known as TRAIL receptors, which usually help to kill potentially cancerous cells.

The research, carried out in cancer cells and mice, shows that in cancers with faulty versions of the KRAS gene these TRAIL receptors actually help the cancer cells to grow and spread to new areas in the body.

These KRAS faults occur in 95 per cent of pancreatic cancers** and 30 per cent of non small cell lung cancers.

Professor Henning Walczak, lead researcher of the study and scientific director of the Cancer Research UK-UCL Centre, said: "Our research has unveiled a new strategy used by some pancreatic and non small cell lung cancers to overcome our body's natural defences against cancer. By understanding the faults in these cancers we think we can develop more tailored treatments, which could one day provide urgently-needed options for patients with these types of pancreatic and non small cell lung cancers."

Each year in Great Britain 32,500 people are diagnosed with non small cell lung cancer and around 8,600 people are diagnosed with pancreatic cancer. Survival for these cancers has not shown much improvement for 40 years.

Nell Barrie, senior science information manager at Cancer Research UK, said: "Sadly survival from pancreatic and lung cancers remains far too low, partly because these cancers are very difficult to treat once they have spread.

"We urgently need better treatments, so it's vital to delve deeper into the molecular workings of these cancers to find ways to combat them. This research may one day help us find a way to block cancer spread, which would be a vital step to save more lives."

###

For media enquiries contact Emily Head in the Cancer Research UK press office on 020 3469 6189 or, out of hours, on 07050 264 059.

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Body's cancer defenses hijacked to make pancreatic and lung cancers more aggressive

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Genetic Engineering Technology
Discussion on my research topic for ENG 2010.

By: Guintah212

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Genetic studies in humans, zebrafish and mice have revealed how two different types of genetic variations team up to cause a rare condition called Hirschsprung's disease. The findings add to an increasingly clear picture of how flaws in early nerve development lead to poor colon function, which must often be surgically corrected. The study also provides a window into normal nerve development and the genes that direct it.

The results appear in the April 2 issue of the American Journal of Human Genetics.

About one in every 5,000 babies is born with Hirschsprung's disease, which causes bowel obstruction and can be fatal if not treated. The disease arises early in development when nerves that should control the colon fail to grow properly. Those nerves are part of the enteric nervous system, which is separate from the central nervous system that enables our brains to sense the world.

The genetic causes of Hirschsprung's disease are complex, making it an interesting case study for researchers like Aravinda Chakravarti, Ph.D., a professor in the Johns Hopkins University School of Medicine's McKusick-Nathans Institute of Genetic Medicine. His research group took on the condition in 1990, and in 2002, it performed the first-ever genomewide association study to identify common variants linked to the disease.

But while Chakravarti's and other groups have identified several genetic variants associated with Hirschsprung's, those variants do not explain most cases of the disease. So Chakravarti and colleagues conducted a new genomewide association study of the disease, comparing the genetic markers of more than 650 people with Hirschsprung's disease, their parents and healthy controls. One of their findings was a variant in a gene called Ret that had not been previously associated with the disease, although other variations in Ret had been fingered as culprits.

The other finding was of a variant near genes for several so-called semaphorins, proteins that guide developing nerve cells as they grow toward their final targets. Through studies in mice and zebrafish, the researchers found that the semaphorins are indeed active in the developing enteric nervous system, and that they interact with Ret in a system of signals called a pathway.

"It looks like the semaphorin variant doesn't by itself lead to Hirschsprung's, but when there's a variant in Ret too, it causes the pathway to malfunction and can cause disease," Chakravarti says. "We've found a new pathway that guides development of the enteric nervous system, one that nobody suspected had this role."

Chakravarti notes that the genetic puzzle of Hirschsprung's is still missing some pieces, and no clinical genetic test yet exists to assess risk for the disease. Most of the genetic variants that have so far been connected to this rare disease are themselves relatively common and are associated with less severe forms of the disease. The hunt continues for rare variants that can explain more severe cases.

###

Other authors on the paper are Qian Jiang, Stacey Arnold, Betty Doan, Ashish Kapoor, Albee Yun Ling, Maria X. Sosa, Moltu Guy, Krishna Praneeth Kilambi, Qingguang Jiang, Grzegorz Burzynski, Kristen West, Seneca Bessling, Jeffrey J. Gray and Andrew S. McCallion of The Johns Hopkins University; Tiffany Heanue and Vassilis Pachnis of the MRC National Institute for Medical Research; Paola Griseri and Isabella Ceccherini of the Istituto Gaslini; Jeanne Amiel and Stanislas Lyonnet of the French National Institute of Health and Medical Research and Paris Descartes University-Sorbonne Paris Cite; Raquel M. Fernandez and Salud Borrego of the University of Seville; Joke B.G.M. Verheij of the University of Groningen; and Robert M.W. Hofstra of the University of Rotterdam.

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Genetics I Notes Bio
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Strike Force Heroes 2 - Mission.10 "Gene Therapy"
Iagi

By: AntilTheIkaring

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bluebird bio
Jim DeTore, CFO (NASDAQ: BLUE) Headquarters: Cambridge, MA With its lentiviral-based gene therapy and gene editing capabilities, bluebird bio has built an integrated product platform with...

By: Alliance for Regenerative Medicine

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Oxford BioMedica
Paul Blake, M.D., Chief Development Officer (LON: OXB) Headquarters: Oxford, UK Oxford BioMedica is a leading gene and cell therapy company with an unrivaled portfolio of gene therapy products...

By: Alliance for Regenerative Medicine

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Spinal Cord Injury Spotlight - Emily H. at Project Walk San Francisco
Emily suffered a C5 spinal cord injury in 2010 as a result of a diving accident. She joined our San Francisco location last Spring and has made remarkable strides. See her progression here....

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Paraplegic Walks With Robotic Legs. Re Walk Training
My names Josh im 24 from south jersey. I have a spinal cord injury from the t8-t12 vertebra a complete paralysis from my stomach down. I currently train using Re Walk Robotic Legs at Bacharach...

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Inovio Pharmaceuticals
Niranjan Sardesai, Ph.D., Chief Operating Officer (NASDAQ: INO) Headquarters: Plymouth Meeting, PA Inovio is revolutionizing the fight against cancer and infectious diseases. Our immunotherapies...

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Researchers map chromosomal changes that must take place before stem cells can be used to produce pancreatic and liver cells

IMAGE:These are pancreatic cells derived from embryonic stem cells. view more

Credit: UC San Diego School of Medicine

Stem cells hold great promise for treating a number of diseases, in part because they have the unique ability to differentiate, specializing into any one of the hundreds of cell types that comprise the human body. Harnessing this potential, though, is difficult. In some cases, it takes up to seven carefully orchestrated steps of adding certain growth factors at specific times to coax stem cells into the desired cell type. Even then, cells of the intestine, liver and pancreas are notoriously difficult to produce from stem cells. Writing in Cell Stem Cell April 2, researchers at University of California, San Diego School of Medicine have discovered why.

It turns out that the chromosomes in laboratory stem cells open slowly over time, in the same sequence that occurs during embryonic development. It isn't until certain chromosomal regions have acquired the "open" state that they are able to respond to added growth factors and become liver or pancreatic cells. This new understanding, say researchers, will help spur advancements in stem cell research and the development of new cell therapies for diseases of the liver and pancreas, such as type 1 diabetes.

"Our ability to generate liver and pancreatic cells from stem cells has fallen behind the advances we've made for other cell types," said Maike Sander, MD, professor of pediatrics and cellular and molecular medicine and director of the Pediatric Diabetes Research Center at UC San Diego. "So we haven't yet been able to do things like test new drugs on stem cell-derived liver and pancreatic cells. What we have learned is that if we want to make specific cells from stem cells, we need ways to predict how those cells and their chromosomes will respond to the growth factors."

Sander led the study, together with co-senior author Bing Ren, PhD, professor of cellular and molecular medicine at UC San Diego and Ludwig Cancer Research member.

Chromosomes are the structures formed by tightly wound and packed DNA. Humans have 46 chromosomes - 23 inherited from each parent. Sander, Ren and their teams first made maps of chromosomal modifications over time, as embryonic stem cells differentiated through several different developmental intermediates on their way to becoming pancreatic and liver cells. Then, in analyzing these maps, they discovered links between the accessibility (openness) of certain regions of the chromosome and what they call developmental competence - the ability of the cell to respond to triggers like added growth factors.

"We're also finding that these chromosomal regions that need to open before a stem cell can fully differentiate are linked to regions where there are variations in certain disease states," Sander says.

In other words, if a person were to inherit a genetic variation in one of these chromosomal regions and his or her chromosome didn't open up at exactly the right time, he or she could hypothetically be more susceptible to a disease affecting that cell type. Sander's team is now working to further investigate what role, if any, these chromosomal regions and their variations play in diabetes.

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'Open' stem cell chromosomes reveal new possibilities for diabetes

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A particular molecular pathway permits stem cells in pediatric bone cancers to grow rapidly and aggressively, according to researchers at NYU Langone Medical Center and its Laura and Isaac Perlmutter Cancer Center.

In normal cell growth, the Hippo pathway, which controls organ size in animals, works as a dam, regulating cell proliferation. What the researchers found is that the transcription factor of a DNA binding protein called sex determining region Y box 2, or Sox2 for short, which normally maintains cell self-renewal, actually releases the floodgates in the Hippo pathway in osteosarcomas and other cancers, permitting the growth of highly aggressive, tumor-forming stem cells.

Results from the study are to be published in the journal Nature Communications online April 2.

"This study is one of the first to identify the mechanisms that underlie how an osteosarcoma cancer stem cell maintains its tumor-initiating properties," says senior study investigator Claudio Basilico, MD, the Jan T. Vilcek Professor of Molecular Pathogenesis at NYU Langone and a member of its Perlmutter Cancer Center.

In the study, the investigators used human and mouse osteosarcomas to pinpoint the molecular mechanisms that inhibit the tumor-suppressive Hippo pathway. The researchers concluded that Sox2 represses the functioning of the Hippo pathway, which, in turn, leads to an increase of the potent growth stimulator Yes Associated Protein, known as YAP, permitting cancer cell proliferation.

"Our research is an important step forward in developing novel targeted therapies for these highly aggressive cancers," says study co-investigator Alka Mansukhani, PhD, an associate professor at NYU Langone and also a member of the Perlmutter Cancer Center. "One possibility is to develop a small molecule that could knock out the Sox2 transcription factor and free the Hippo pathway to re-exert tumor suppression."

Mansukhani adds that the research suggests that drugs such as verteporfin, which interfere with cancer-promoting YAP function, might prove useful in Sox2-dependent tumors.

The study expands on previous work in Basilico's and Mansukhani's molecular oncology laboratories at NYU Langone and on earlier work by Upal Basu Roy, PhD, MPH, the lead study investigator, who found that Sox2 was an essential transcription factor for the maintenance of osteosarcoma stem cells.

The NYU group has shown that, i addition to playing a role in osteosarcoma, Sox2 operates in other tumors, such as glioblastomas, an aggressive type of brain cancer.

###

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Key mechanism identified in tumor-cell proliferation in pediatric bone cancers

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Can PRP and Stem Cell Therapy Help You? | Orlando Orthopaedic Center
How can PRP and stem cell therapy help you heal? Orlando Orthopaedic Center #39;s Dr. Matthew R. Willey explains. For more visit http://www.OrlandoOrtho.com.

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DALLAS, April 2, 2015 /PRNewswire/ --

Lifescienceindustryresearch.com adds "Complete 2015-16 Induced Pluripotent Stem Cell (iPSC) Industry Report" in its store. Recent months have seen the first iPSC clinical trial in humans, creation of the world's largest iPSC Biobank, major funding awards, a historic challenge to the "Yamanaka Patent", a Supreme Court ruling affecting industry patent rights, the announcement of an iPSC cellular therapy clinic scheduled to open in 2019, and much more. Furthermore, iPSC patent dominance continues to cluster in specific geographic regions, while clinical trial and scientific publication trends give clear indicators of what may happen in the industry in 2015 and beyond.

Is it worth it to get informed about rapidly-evolving market conditions and identify key industry trends that will give an advantage over the competition?

BrowsetheReportComplete 2015-16 Induced Pluripotent Stem Cell (iPSC) Industry Reportathttp://www.lifescienceindustryresearch.com/complete-2013-14-induced-pl ....

Induced pluripotent stem cells represent a promising tool for use in the reversal and repair of many previously incurable diseases. The cell type represents one of the most promising advances discovered within the field of stem cell research during the past decade, making this a valuable industry report for both companies and investors to claim in order to optimally position themselves to sell iPSC products. To profit from this lucrative and rapidly expanding market, you need to understand your key strengths relative to the competition, intelligently position your products to fill gaps in the market place, and take advantage of crucial iPSC trends.

Report Applications

This global strategic report is produced for: Management of Stem Cell Product Companies, Management of Stem Cell Therapy Companies, Stem Cell Industry Investors

It is designed to increase your efficiency and effectiveness in:

Four Primary Areas of Commercialization

There are currently four major areas of commercialization for induced pluripotent stem cells, as described below:

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Induced Pluripotent Stem Cell (iPSC) Industry Complete Report 2015 - 2016

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Children's Healthcare of Atlanta and Winship Cancer Institute target graft-versus-host-disease through immune cell therapy

An innovative clinical trial using the science of "personalized" cellular therapy has begun enrolling children and adults suffering from graft-versus-host-disease (GVHD), a life-threatening complication of bone marrow transplantation in which donor immune lymphocytes attack the organs of the bone marrow transplant recipient.

Bone marrow transplantation is performed in some patients with cancers of the blood or bone marrow, including multiple myeloma and leukemia, as well as in some patients with sickle cell disease, thallesemia, aplastic anemia and inherited immune deficiency.

Physician-researchers at the Aflac Cancer and Blood Disorders Center at Children's Healthcare of Atlanta and Winship Cancer Institute of Emory University will harvest bone marrow cells from children and adults (12 to 65 years) with GVHD. Those cells will be used to manufacture large numbers of personalized autologous marrow mesenchymal stromal cells in the Emory Personalized Immunotherapy Center (EPIC), a dedicated pharmaceutical grade facility located within Emory University Hospital.

By infusing large doses of these personalized bone marrow cells into bone marrow transplant recipients, the physician-researchers aim to target sites of inflammation, potentially reducing GVHD in the intestine, liver and skin and limiting long-term organ damage.

Muna Qayed, MD, MSc. a pediatric hematologist-oncologist at the Aflac Cancer Center at Children's and an assistant professor at Emory School of Medicine, will lead the clinical trial, which is offered only in Atlanta and is supported by CURE Childhood Cancer.

"For patients with GVHD who do not respond to first line therapy, there is no reliable cure, and GVHD can be life threatening or a life-long disabling condition," says Dr. Qayed, "But we hope that through our clinical research, we will be able to significantly impact the course of this disease."

"This trial represents one of the most innovative clinical trials to arise from the growing partnership between the Hematology & Medical Oncology and Pediatrics departments at Emory School of Medicine, Emory Healthcare, and Children's Healthcare of Atlanta," says William (Bill) G. Woods, MD, director of the Aflac Cancer Center.

Blood and bone marrow cells have been used for more than a quarter century to treat life-threatening hematological conditions and are now used in established therapies worldwide. The current clinical trial will use mesenchymal stromal cells from the bone marrow. These cells have been studied more recently for treatment of a wide array of diseases, including autoimmune diseases.

"The beginning of this clinical trial is the culmination of two years' of collaborative effort by a terrific multidisciplinary team at Emory Healthcare, Children's Healthcare of Atlanta and the Aflac Cancer Center," says Edmund Waller, MD, director of Winship's Bone Marrow and Stem Cell Transplant Program and investigator on this trial.

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Clinical trial uses patients' own cells for treatment after bone marrow transplant

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This Saturday when the University of Kentucky basketball team faces off with the University of Wisconsin in the NCAA tournament semi-finals, die-hard Kentucky fan Scott Logdon may think twice about rooting against the Wisconsin Badgers.

Nearly two years ago, Logdon was given a life-saving donation of stem cells that helped combat his acute myeloid leukemia. The donor of those cells turned out to be 22-year-old Chris Wirz, a student at the University of Wisconsin.

Logdon, 44, learned the identity of his donor last April, more than a year after the stem cell treatment and just days after the University of Kentucky squeaked past the University of Wisconsin at the NCAA semi-finals with a score of 74 to 73.

Logdon remembers feeling mixed emotions when the Kentucky wildcats won. Later, when he found out about his donor, he joked, That must have been the Badger blood in me.

Courtesy Angela Logdon

PHOTO: Chris Wirz gave life saving stem cells to Scott Logdon, who was suffering from leukemia.

Logdons ordeal started in the fall of 2012, when he was diagnosed with acute myeloid leukemia after mistaking early symptoms for strep throat. Logdon said his doctors told him chemotherapy could only keep the cancer at bay. A full stem cell transplant would be needed to cure him of the deadly disease.

Logdons doctors hoped one of his two siblings might be a match, but neither was able to donate. Longons family and community rallied in the small town of Saldasia, Kentucky, and registered over 120 people who would be willing to donate stem cells or bone marrow.

But no one who registered was a good match for Logdon.

[The doctors] went to the national bone marrow registry to try and find the match, the father of four said. I had to go back to the hospital every 30 days [for] maintenance chemo; it was a very long wait.

Read more:
Kentucky Fan Gets Life-Saving Stem Cell Donation From Univ. of Wisconsin Student

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