Archive for March, 2015

Spring Fling Genetics Conference Brian VanDoormaal Speaking
Spring Fling Genetics Conference Brian VanDoormaal Speaking.

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Spring Fling Genetics Conference Brian VanDoormaal Speaking - Video

Spinal Cord Injury Spotlight - Damien M. at Project Walk Houston
Damien Maya suffered a T-12 incomplete spinal cord injury in May of 2011 as a result of multiple gunshots. This is a video of his hard work and dedication to recovering. Damien has said that...

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Spinal Cord Injury Spotlight - Damien M. at Project Walk Houston - Video

An injection of a patient's bone marrow stem cells during rotator cuff surgery significantly improved healing and tendon durability, according to a study presented today at the 2015 Annual Meeting of the American Academy of Orthopaedic Surgeons (AAOS).

Each year in the U.S., more than 2 million people have rotator cuff surgery to re-attach their shoulder tendon to the head of the humerus (upper arm bone). Rotator cuff tears can occur during a fall or when lifting an extremely heavy object; however, most tears are the result of aging and overuse.

The French study, of which a portion appeared in the September 2014 issue of International Orthopaedics, included 90 patients who underwent rotator cuff surgery. Researchers tried to make the two groups as equivalent as possible based on rotator cuff tear size, tendon rupture location, dominate shoulder, gender and age. Forty-five of the patients received injections of bone marrow concentrate (BMC) mesenchymal stem cells (MSCs) at the surgical site, and 45 had their rotator cuff repaired or reattached without MSCs.

Patient ultrasound images were obtained each month following surgery for 24 months. In addition, MRI images were obtained of patient shoulders at three and six months following surgery, and at one year, two years, and 10 years following surgery.

At six months, all 45 of the patients who received MSCs had healed rotator cuff tendons, compared to 30 (67 percent) of the patients who did not receive MSCs. The use of bone marrow concentrate also prevented further ruptures or retears. At 10 years after surgery, intact rotator cuffs were found in 39 (87 percent) of the MSC patients, but just 20 (44 percent) of the non-MSC patients.

In addition, "some retears or new tears occurred after one year," said Philippe Hernigou, MD, an orthopaedic surgeon at the University of Paris and lead study author. "These retears were more frequently associated with the control group patients who were not treated with MSCs.

"While the risk of a retear after arthroscopic repair of the rotator cuff has been well documented, publications with long-term follow-up (more than three years) are relatively limited," said Dr. Hernigou. "Many patients undergoing rotator cuff repair surgery show advanced degeneration of the tendons, which are thinner and atrophic (more likely to degenerate), probably explaining why negative results are so often reported in the literature, with frequent post-operative complications, especially retear. Observations in the MSC treatment group support the potential that MSC treatment has both a short-term and long-term benefit in reducing the rate of tendon retear."

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The above story is based on materials provided by American Academy of Orthopaedic Surgeons. Note: Materials may be edited for content and length.

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Stem cells may improve tendon healing, reduce retear risk in rotator cuff surgery

LAS VEGAS, March 26, 2015 /PRNewswire-USNewswire/ -- An injection of a patient's bone marrow stem cells during rotator cuff surgery significantly improved healing and tendon durability, according to a study presented today at the 2015 Annual Meeting of the American Academy of Orthopaedic Surgeons (AAOS).

Each year in the U.S., more than 2 million people have rotator cuff surgery to re-attach their shoulder tendon to the head of the humerus (upper arm bone). Rotator cuff tears can occur during a fall or when lifting an extremely heavy object; however, most tears are the result of aging and overuse.

The French study, of which a portion appeared in the September 2014 issue of International Orthopaedics, included 90 patients who underwent rotator cuff surgery. Researchers tried to make the two groups as equivalent as possible based on rotator cuff tear size, tendon rupture location, dominate shoulder, gender and age. Forty-five of the patients received injections of bone marrow concentrate (BMC) mesenchymal stem cells (MSCs) at the surgical site, and 45 had their rotator cuff repaired or reattached without MSCs.

Patient ultrasound images were obtained each month following surgery for 24 months. In addition, MRI images were obtained of patient shoulders at three and six months following surgery, and at one year, two years, and 10 years following surgery.

At six months, all 45 of the patients who received MSCs had healed rotator cuff tendons, compared to 30 (67 percent) of the patients who did not receive MSCs. The use of bone marrow concentrate also prevented further ruptures or retears. At 10 years after surgery, intact rotator cuffs were found in 39 (87 percent) of the MSC patients, but just 20 (44 percent) of the non-MSC patients.

In addition, "some retears or new tears occurred after one year," said Philippe Hernigou, MD, an orthopaedic surgeon at the University of Paris and lead study author. "These retears were more frequently associated with the control group patients who were not treated with MSCs.

"While the risk of a retear after arthroscopic repair of the rotator cuff has been well documented, publications with long-term follow-up (more than three years) are relatively limited," said Dr. Hernigou. "Many patients undergoing rotator cuff repair surgery show advanced degeneration of the tendons, which are thinner and atrophic (more likely to degenerate), probably explaining why negative results are so often reported in the literature, with frequent post-operative complications, especially retear. Observations in the MSC treatment group support the potential that MSC treatment has both a short-term and long-term benefit in reducing the rate of tendon retear."

Study abstract

View 2015 AAOS Annual Meeting disclosure statements

About AAOS

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Stem cells may significantly improve tendon healing, reduce retear risk in rotator cuff surgery

Tampa, FL. (PRWEB) March 26, 2015

This month, the Lung Institute has started treating people suffering from chronic lung diseases with stem cells extracted from their bone marrow. This treatment protocol is added to the two other treatment options offered by the Lung Institute: venous (blood-derived) and adipose (fat-derived) stem cell therapy.

The bone marrow and adipose treatments offer the highest concentration of stem cells and allow for the cells to be reintroduced directly into the lungs through a nebulizer. Given this added benefit, most patients in the past opted to receive the adipose treatment over venous. However, many patients have other medical conditions that preclude them from choosing the adipose treatment. Since the number of stem cells harvested from a bone marrow procedure matches that of the adipose procedure, patients that have previously only qualified for the venous procedure are now eligible for a treatment option that produces the highest chance of success.

Patients are often surprised by the simplicity of these minimally invasive procedures, but with cutting-edge technology and the patient-centric clinical team at the Lung Institute, patients can rest assured that they are in good hands. Throughout the entire treatment process, patients have the opportunity to get any questions immediately answered by our knowledgeable medical staff. The Lung Institute clinical team remains in contact with patients after treatment and works together with the patients physician and pulmonologist to create a strong support system for the patient.

About the Lung Institute At the Lung Institute, we are changing the lives of hundreds of people across the nation through the innovative technology of regenerative medicine. We are committed to providing patients a more effective way to address pulmonary conditions and improve their quality of life. Our physicians, through their designated practices, have gained worldwide recognition for the successful application of revolutionary minimally invasive stem cell therapies. With over a century of combined medical experience, our doctors have established a patient experience designed with the highest concern for patient safety and quality of care. For more information, visit our website at LungInstitute.com, like us on Facebook, follow us on Twitter or call us today at (855) 313-1149.

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Lung Institute Announces New Treatment with Bone Marrow

Beneath several blankets and a stuffed giraffe in her UC San Francisco hospital bed, 11-year-old Myla Cunanan is resting after a morning of dialysis to treat a kidney-related complication from her bone marrow transplant last year.Myla is sedated and tired, but not enough to silence her spritely personality.Mom, you put the cover on backwards! she exclaimed, disassembling her iPhone from its case and flipping it around as her mother, Leyna Cunanan, laughed and lovingly stroked the hand of her youngest daughter.She makes us all brave around her, Leyna said of her daughter. She knows that there is a purpose for her for being here. Tuesday marked one year to the day since Myla was diagnosed with myeloid sarcoma, a rare cancer in which a solid collection of leukemic cells occur outside of the bone marrow. The last year also thrust Myla into the spotlight as she and her family sought to find a bone marrow donor, a mission that turned out to be impossible due to a severe lack of Asian donors worldwide.Myla is Filipino-American, and when doctors told her after three rounds of chemotherapy in spring 2014 that she urgently needed a bone marrow transplant, her family learned just how difficult it is to find a match.In fact, Asians comprise just 6 percent of donors with Be The Match Registry, the largest and most diverse marrow registry in the world.The rarer your ethnic subtype is, at least in the U.S., the less likely we are to find you a good donor, said Dr. Christopher Dvorack, who has treated Myla since last year and is an assistant professor of clinical pediatrics in the Division of Allergy, Immunology, and Blood and Marrow Transplant at UC San Francisco.Last summer, her family registered about 300 donors through drives at their church, Mylas school and local shopping centers, and shared Mylas plight on social media with a photo of Myla holding a sign that reads, Will you marrow me?But a match was not found, and by August, doctors told Mylas family they would need to use a half-match donor, which was Mylas father.There are two main ways to donate bone marrow. The first is to have needles inserted into hip bones to extract a small amount of bone marrow. The second requires four days of injections of medicine designed to stimulate bone marrow and cause it to release stem cells from the bone marrow into the blood.The problem with half-match donors is the patients immune system can reject the donated bone marrow, which is what happened to Myla, Dvorack explained.She initially did well, she then later developed a complication that has kept her in the hospital, he said.The complication, thrombotic microangiopathy with renal involvement, means Mylas kidneys function less than 15 percent. She was subsequently diagnosed as chronic kidney disease Stage 5, and has been receiving hemodialysis several times a week.But her family remain advocates for the need for more bone marrow donors, particularly among ethnic minorities.We didnt find a match for Myla ... but we would like to continue to [hold] drives for other patients, her mother said.Ruby Law, a recruitment director for the Asian American Donor Program based in Alameda, worked with Myla and her family last year to seek a donor and said their efforts have extended beyond simply finding a match.Mylas family is very passionate about raising awareness of marrow and blood stem cell donation, Law said.Since Mylas most recent hospitalization, which began a week before Thanksgiving, her mother has lived with her at UCSF. Myla was among the 126 patients transferred from the UCSF Parnassus Campus to the new complex at Mission Bay on Feb. 1.Recently, Myla has been writing a book to help other kids going through similar journeys.When you read this book, I want you to think positive always, the last line of the opening letter states.And that pretty much sums up Mylas attitude, according to her doctor and family. Despite having been hospitalized for the majority of the past year, Myla insists she has plenty to be thankful for. While hospitalized, Myla has held book, bracelet and band-aid drives.There are days, of course, when she doesnt feel good, her mother said. But she always thinks about other people. She likes to give.To sign up as a donor, visit http://www.aadp.org or call (510) 568-3700.

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One year after cancer diagnosis, Bay Area girl continues to highlight need for Asian bone marrow donors

Julie Gramyk 3 21 2015 Youtube
Julie Gramyk, Medical Esthetic, explains how Momentis #39; new skincare system is the first in the world to penetrate beyond the skin #39;s barrier and target the skin #39;s stem cells resulting in rebuilding...

By: judyrstak

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Julie Gramyk 3 21 2015 Youtube - Video

Stemologica Review - Reduce Wrinkles Appearance Using Stemologica
Click the link below to get a risk free trial; http://skincarebeautyshop.com/go/have-your-stemologica-free-trial/ Read the Terms and Condition before you order. Click the link below to read...

By: Mher Barbs

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Stemologica Review - Reduce Wrinkles Appearance Using Stemologica - Video

Celprogen Released Stem Cell Active Ingredients for the Cosmetic Industry Tested and Validated in Cosmetic Products for a Decade

The present invention relates to culturing stem cells in animal free conditions has been developed and optimized by Celprogen utilizing single use bioreactor technology. The cosmetic industry has benefited from this technology for their regenerative skin care product lines. The topical application of these skin care products utilizing Celprogens Stem Cell Derived Conditioned Media have been in the market for 10 plus years.

About Celprogen Inc. Celprogen Inc. is a global Stem Cell Research & Therapeutics company which is developing a proprietary portfolio of unique therapeutics products and life science research tools that includes genetic engineering technologies, stem cell technologies for regenerative medicine, as well as bio-engineering products for tissue & organ transplants. Headquartered in Torrance, California, Celprogen is committed to the research, development, and manufacture of quality Stem Cell, Cancer Stem Cell and Primary Cell Culture products to serve our global community. Additional information about Celprogen is available at http://www.celprogen.com.

For additional information on the product line contact: Jay Sharma Phone: 310 542 8822 info@celprogen.com http://www.celprogen.com

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Celprogen Released Stem Cell Active Ingredients for the Cosmetic Industry Tested and Validated in Cosmetic Products ...

Mar 25, 2015

Scientists at the University of Copenhagen have captured thousands of progenitor cells of the pancreas on video as they made decisions to divide and expand the organ or to specialize into the endocrine cells that regulate our blood sugar levels.

The study reveals that stem cells behave as people in a society, making individual choices but with enough interactions to bring them to their end-goal. The results could eventually lead to a better control over the production of insulin-producing endocrine cells for diabetes therapy.

The research is published in the scientific journal PLOS Biology.

Why one cell matters

In a joint collaboration between the University of Copenhagen and University of Cambridge, Professor Anne Grapin- Botton and a team of researchers including Assistant Professor Yung Hae Kim from DanStem Center focused on marking the progenitor cells of the embryonic pancreas, commonly referred to as 'mothers', and their 'daughters' in different fluorescent colours and then captured them on video to analyse how they make decisions.

Prior to this work, there were methods to predict how specific types of pancreas cells would evolve as the embryo develops. However, by looking at individual cells, the scientists found that even within one group of cells presumed to be of the same type, some will divide many times to make the organ bigger while others will become specialized and will stop dividing.

The scientists witnessed interesting occurrences where the 'mother' of two 'daughters' made a decision and passed it on to the two 'daughters' who then acquired their specialization in synchrony. By observing enough cells, they were able to extract logic rules of decision-making, and with the help of Pau Ru, a mathematician from the University of Cambridge, they developed a mathematical model to make long-term predictions over multiple generations of cells.

Stem cell movies

'It is the first time we have made movies of a quality that is high enough to follow thousands of individual cells in this organ, for periods of time that are long enough for us to follow the slow decision process. The task seemed daunting and technically challenging, but fascinating", says Professor Grapin-Botton.

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Stem cells make similar decisions to humans

Researchers at the University of Cambridge have grown functional "mini-lungs" using stems cells derived from the skin cells of patients with a debilitating lung disease. Not only can the development help them in coming up with effective treatments for specific lung diseases like cystic fibrosis, but the process has the potential to be scaled up to screen thousands of new compounds to identify potential new drugs.

Creating miniature organoids has been the focus of many a research group, as it allows scientists to better understand the processes that take place inside an organ, figure out how specific diseases occur and develop or even work towards creating bioengineered lungs.

The research team from the Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute studied a lung disease called cystic fibrosis, which is caused by genetic mutation and shortens a patient's average lifespan. Patients have great difficulty breathing as the lungs are overwhelmed by thickened mucus.

To create working mini-lungs, the researchers took skin cells from patients with the most common form of cystic fibrosis and reprogrammed them to an induced pluripotent state (iPS), which allows the cells to grow into a different type of cell inside the body.

They then activated a process called gastrulation which pushes the cells to form distinct layers such as the endoderm and foregut. The cells were then pushed further to form distal airway tissue, the part of the lung that deals with exchange of gases.

In a sense, what weve created are mini-lungs," says Dr Nick Hannan, the lead researcher. While they only represent the distal part of lung tissue, they are grown from human cells and so can be more reliable than using traditional animal models, such as mice."

To find out whether the mini lungs could actually be used to screen drugs, the team tested them out with the aid of chloride-sensitive fluorescent dye. Cells from cystic fibrosis patients typically malfunction and don't allow the chloride to pass through, so there's no change in fluorescence levels.

The team added a molecule that's currently undergoing clinical trials and noted a change in fluorescence, signaling that it was effective in getting the diseased lung cells to function properly and that the mini lungs could, in principle, be used to test potential new drugs.

"Were confident this process could be scaled up to enable us to screen tens of thousands of compounds and develop mini-lungs with other diseases such as lung cancer and idiopathic pulmonary fibrosis," says Dr Hannan. "This is far more practical, should provide more reliable data and is also more ethical than using large numbers of mice for such research."

The research was published in the journal Stem Cells and Development.

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Scientists create functioning "mini-lungs" to study cystic fibrosis

CRISPR-Cas9 is a powerful new tool for editing the genome. For researchers around the world, the CRISPR-Cas9 technique is an exciting innovation because it is faster and cheaper than previous methods. Now, using a molecular trick, Dr. Van Trung Chu and Professor Klaus Rajewsky of the Max Delbrck Center for Molecular Medicine (MDC) Berlin-Buch and Dr. Ralf Khn, MDC and Berlin Institute of Health (BIH), have found a solution to considerably increase the efficiency of precise genetic modifications by up to eightfold.

"What we used to do in years, we can now achieve in months," said gene researcher and immunologist Klaus Rajewsky, indicating the power of this new genome-editing technology. CRISPR-Cas9 not only speeds up research considerably - at the same time it is much more efficient, cheaper and also easier to handle than the methods used so far.

The CRISPR-Cas9 technology allows researchers to transiently introduce DNA double-strand breaks into the genome of cells or model organisms at genes of choice. In these artificially produced strand breaks, they can insert or cut out genes and change the genetic coding according to their needs.

Mammalian cells are able to repair DNA damage in their cells using two different repair mechanisms. The homology-directed repair (HDR) pathway enables the insertion of preplanned genetic modifications using engineered DNA molecules that share identical sequence regions with the targeted gene and which are recognized as a repair template. Thus, HDR repair is very precise but occurs only at low frequency in mammalian cells.

The other repair system, called non-homologous end-joining (NHEJ) is more efficient in nature but less precise, since it readily reconnects free DNA ends without repair template, thereby frequently deleting short sequences from the genome. Therefore, NHEJ repair can only be used to create short genomic deletions, but does not support precise gene modification or the insertion and replacement of gene segments.

Many researchers, including Van Trung Chu, Klaus Rajewsky and Ralf Khn, are seeking to promote the HDR repair pathway to make gene modification in the laboratory more precise in order to avoid editing errors and to increase efficiency. The MDC researchers succeeded in increasing the efficiency of the more precisely working HDR repair system by temporarily inhibiting the most dominant repair protein of NHEJ, the enzyme DNA Ligase IV. In their approach they used various inhibitors such as proteins and small molecules.

"But we also used a trick of nature and blocked Ligase IV with the proteins of adeno viruses. Thus we were able to increase the efficiency of the CRISPR-Cas9 technology up to eightfold," Ralf Khn explained. For example, they succeeded in inserting a gene into a predefined position in the genome (knock-in) in more than 60 per cent of all manipulated mouse cells. Khn has just recently joined the MDC and is head of the research group for "iPS cell based disease modeling." Before coming to the MDC, he was on the research staff of Helmholtz Zentrum Mnchen. "The expertise of Ralf Khn is very important for gene research at MDC and especially for my research group," Klaus Rajewsky said.

Concurrent with the publication of the article by the MDC researchers, Nature Biotechnology published another, related paper on CRISPR-Cas9 technology. It comes from the laboratory of Hidde Ploegh of the Whitehead Institute in Cambridge, MA, USA.

Somatic gene therapy with CRISPR-Cas9 is a goal

The new CRISPR-Cas9 technology, developed in 2012, is already used in the laboratory to correct genetic defects in mice. Researchers also plan to modify the genetic set up of induced pluripotent stem cells (iPS), which can be differentiated into specialized cell types or tissues. That is, researchers are able to use the new tool to introduce patient-derived mutations into the genome of iPS cells for studying the onset of human diseases. "Another future goal, however, is to use CRISPR-Cas9 for somatic gene therapy in humans with severe diseases," Klaus Rajewsky pointed out.

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Researchers greatly increase precision of new genome editing tool

CRISPR-Cas9 is a powerful new tool for editing the genome. For researchers around the world, the CRISPR-Cas9 technique is an exciting innovation because it is faster and cheaper than previous methods. Now, using a molecular trick, Dr. Van Trung Chu and Professor Klaus Rajewsky of the Max Delbrck Center for Molecular Medicine (MDC) Berlin-Buch and Dr. Ralf Khn, MDC and Berlin Institute of Health (BIH), have found a solution to considerably increase the efficiency of precise genetic modifications by up to eightfold (Nature Biotechnology: doi:10.1038/nbt.3198)**.

"What we used to do in years, we can now achieve in months," said gene researcher and immunologist Klaus Rajewsky, indicating the power of this new genome-editing technology. CRISPR-Cas9 not only speeds up research considerably - at the same time it is much more efficient, cheaper and also easier to handle than the methods used so far.

The CRISPR-Cas9 technology allows researchers to transiently introduce DNA double-strand breaks into the genome of cells or model organisms at genes of choice. In these artificially produced strand breaks, they can insert or cut out genes and change the genetic coding according to their needs.

Mammalian cells are able to repair DNA damage in their cells using two different repair mechanisms. The homology-directed repair (HDR) pathway enables the insertion of preplanned genetic modifications using engineered DNA molecules that share identical sequence regions with the targeted gene and which are recognized as a repair template. Thus, HDR repair is very precise but occurs only at low frequency in mammalian cells.

The other repair system, called non-homologous end-joining (NHEJ) is more efficient in nature but less precise, since it readily reconnects free DNA ends without repair template, thereby frequently deleting short sequences from the genome. Therefore, NHEJ repair can only be used to create short genomic deletions, but does not support precise gene modification or the insertion and replacement of gene segments.

Many researchers, including Van Trung Chu, Klaus Rajewsky and Ralf Khn, are seeking to promote the HDR repair pathway to make gene modification in the laboratory more precise in order to avoid editing errors and to increase efficiency. The MDC researchers succeeded in increasing the efficiency of the more precisely working HDR repair system by temporarily inhibiting the most dominant repair protein of NHEJ, the enzyme DNA Ligase IV. In their approach they used various inhibitors such as proteins and small molecules.

"But we also used a trick of nature and blocked Ligase IV with the proteins of adeno viruses. Thus we were able to increase the efficiency of the CRISPR-Cas9 technology up to eightfold," Ralf Khn explained. For example, they succeeded in inserting a gene into a predefined position in the genome (knock-in) in more than 60 per cent of all manipulated mouse cells. Khn has just recently joined the MDC and is head of the research group for "iPS cell based disease modeling". Before coming to the MDC, he was on the research staff of Helmholtz Zentrum Mnchen. "The expertise of Ralf Khn is very important for gene research at MDC and especially for my research group," Klaus Rajewsky said.

Concurrent with the publication of the article by the MDC researchers, Nature Biotechnology published another, related paper on CRISPR-Cas9 technology. It comes from the laboratory of Hidde Ploegh of the Whitehead Institute in Cambridge, MA, USA.

Somatic gene therapy with CRISPR-Cas9 is a goal

The new CRISPR-Cas9 technology, developed in 2012, is already used in the laboratory to correct genetic defects in mice. Researchers also plan to modify the genetic set up of induced pluripotent stem cells (iPS), which can be differentiated into specialized cell types or tissues. That is, researchers are able to use the new tool to introduce patient-derived mutations into the genome of iPS cells for studying the onset of human diseases. "Another future goal, however, is to use CRISPR-Cas9 for somatic gene therapy in humans with severe diseases," Klaus Rajewsky pointed out.

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MDC researchers greatly increase precision of new genome editing tool

Stem Cell Therapy For Multiple Sclerosis
Back for round 2. After treatment in 2014 Beverly had improvement in her energy level, balance, walking and had colors come into her vision for the first time in 10 years. Beverly went blind...

By: Stem Cell Patient

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Stem Cell Therapy For Multiple Sclerosis - Video

Bobby Chia (Foto by Allan Defensor)

THERE is a lot of hype going on in some circles about stem cell therapy: Is it a cure-all? Is it the elusive fountain of youth?

Wikipedia definesstem cell therapy as the use of stem cells to treat or prevent a disease or condition.The process involves the administration of live whole cells or maturation of a specific cell population in a patient for the treatment of the disease as has been done in bone marrow transplants.

Bobby Chia, a Thai national who was in Cebu for a brief visit, said that stem cell therapy has been done in Villa Medica, Germany, since the 1960s. He learned about it 10 years ago when his mother had cancer and he looked around for the best medical care for her and found it in Villa Medica. It made her so much better (she can even play tennis now) that four years ago, Chia bought the clinic being run by Dr. Geoffrey Huertgen, a third generation doctor of that clinic.

The stem cell can be taken from the patient himself, but Chia says this stem source is naturally as old as the patient himself. Villa Medica chooses to use stem cells from fetuses of sheep (he said that stem cells from any mammal would be the same, but sheep stem cells are the ones more readily available). The process for Villa Medica, says Chia, involves the designing of a cocktail of stem cells to address whatever needs correction. If the eyes are not good, we choose the eyes. If the ears are not good, we choose the ears. If the heart is not good, we choose the heart. The procedure has been known to treat diseases and ailments like Parkinsons, diabetes, hypertension, migraine, allergies etc.

It (stem cell therapy) does not make you 18 years old all over again but it energizes you; from not being able to walk to walking again. It gives you a better quality of life. It is not a quick cure, but for a lot of people it is. We offer a choice for people who have no hope, Chia shares. But my main target is people who are not sick, Chia states, referring to athletes, models, professionals who want to have a better quality of life.

Chia says there are four doctors in Villa Medica. Since the cell therapy is patient-specific, the patient needs to stay four days and four nights at the clinic: for a detox program, for physical check-up, for interview, for determining the cocktail of stem cells to be used and how. The result, Chia says,is not immediate. It may take six weeks or even longer for the stem cells to do their work.

Chia says he has had about 150 patients coming from Cebu. Leaf through the pages of the local papers, one of them might just be there!

Published in the Sun.Star Cebu newspaper on March 27, 2015.

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On stem cell therapy, benefits

A federal public servant has lost a legal bid to have taxpayers pay for experimental stem cell treatment on his dodgy knees.

The Administrative Appeals Tribunal has knocked back an appeal by Customs officer Vic Kaplicas to force insurer Comcare to pay $13,400 for the new treatment, instead saying he could have a tried-and-tested double knee replacement.

But the 49-year-old border official says he worries he cannot pass his department's fitness tests if he undergoes the knee replacements, which will leave him unable to run.

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The former triathlete, who had to give up his sport because of his bad knees, said he was keen to avoid the "radical but effective" replacements for as long as possible.

Mr Kaplicas hurt his left knee working at Sydney's Mascot Airport in 2000, then injured his right knee 10 years later at Kingsford-Smith.

He managed the pain in his knees, which have since developed osteoarthritis, for years using over-the-counter painkillers, physio, exercises and injections but Mr Kaplicas' doctors say a more permanent solution is now needed.

In June 2012, Sydney knee specialist Sam Sorrenti asked Comcare to pay for bilateral knee stem cell assisted arthroscopic surgery for Mr Kaplicas.

The cost of the procedure was estimated at $13,464.00 for arthroscopy, stem cell harvesting and injection, and a "HiQCell procedure".

Dr Sorrenti said the knee replacements were not a good idea for a man of Mr Kaplicas' age, arguing the new knees would last 15 years at best, were intended for older people who are less concerned with physical activity, and left no further options.

Originally posted here:
No stem cell treatment for public servant's dodgy knee

Scientists have revealed a brand new function for one of the first cancer genes ever discovered - the retinoblastoma gene - in a finding that could open up exciting new approaches to treatment.

The retinoblastoma gene is so called because mutations to it cause a rare children's eye cancer of the same name, and is known to play a central role in stopping healthy cells from dividing uncontrollably.

Now the new study - jointly led by scientists at The Institute of Cancer Research, London, and UCL (University College London) - has found that the gene also has another important function, in helping to 'glue' severed strands of DNA back together.

The research suggests that existing drugs that exploit the weaknesses of some cancers in repairing their DNA could be effective against tumours with mutations to the retinoblastoma gene.

The study, published today (Thursday) in the journal Cell Reports, was funded by a range of organisations including Cancer Research UK, Worldwide Cancer Research, the Wellcome Trust and The Institute of Cancer Research (ICR) itself.

Researchers found that mutations to the retinoblastoma gene or RB1 - which are found in many cancers - prevent the effective fixing of broken DNA strands. This results in chromosome abnormalities which can lead to the development of tumours and drive cancers to evolve into more aggressive forms.

Numerous common cancer types have RB1 mutations, including hard-to-treat cancers such as triple-negative breast cancer, small cell lung cancer, glioblastoma, and aggressive types of prostate cancer.

Researchers deleted the RB1 gene from lab-grown human and mouse cancer cells, and looked at a variety of measures that indicate defective DNA repair. They found substantially more double-stranded DNA breaks and chromosome abnormalities in cells that lacked RB1 than those where the gene was functional.

In another experiment, the researchers demonstrated that the RB1 protein attaches to two other protein called XRCC5 and XRCC6, forming a cluster of molecules that mend broken strands of DNA.

RB1 was first discovered in the 1980s and has long been known to have an important role in controlling cell division. It was discovered through studies of the rare eye cancer retinoblastoma, which in around half of cases is caused by inherited mutations to the RB1 gene.

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New role uncovered for 'oldest' tumor suppressor gene

Large genome databases are starting to reveal critical health informationeven about people who have not contributed their DNA.

Maps show how common certain risk-causing DNA mutations are around Iceland.

The CEO of an Icelandic gene-hunting company says he is able to identify everyone from that country who has a deadly cancer risk, but has been unable to warn people of the danger because of ethics rules governing DNA research.

The company, DeCode Genetics, based in Reykjavk, says it has collected full DNA sequences on 10,000 individuals. And because people on the island are closely related, DeCode says it can now also extrapolate to accurately guess the DNA makeup of nearly all other 320,000 citizens of that country, including those who never participated in its studies.

Thats raising complex medical and ethical issues about whether DeCode, which is owned by the U.S. biotechnology company Amgen, will be able to inform members of the public if they are at risk for fatal diseases.

Kri Stefnsson, the doctor who is founder and CEO of DeCode, says he is worried about mutations in a gene called BRCA2 that convey a sharply increased risk of breast and ovarian cancers. DeCodes data can now identify about 2,000 people with the gene mutation across Icelands population, and Stefnsson saidthat the company has been in negotiations with health authorities about whether to alert them.

We could save these people from dying prematurely, but we are not, because we as a society havent agreed on that, says Stefnsson. I personally think that not saving people with these mutations is a crime. This is an enormous risk to a large number of people.

The Icelandic Ministry of Welfare said a special committee had been formed to regulate such incidental findings and would propose regulations by the end of the year.

Kri Stefnsson

The technique used by DeCode to predict peoples genes offers clues to the future of so-called precision medicine in other countries, including the U.S., where this year President Barack Obama called for researchers to assemble a giant database of one million people (see U.S to Develop DNA Study of One Million People). A large enough U.S. database could also be used to infer genes of people whether or not they had joined it, says Stefnsson, and could raise similar questions about whether and how to report health hazards to the public.

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Genome Study Predicts DNA of the Whole of Iceland

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Newswise New Brunswick, N.J., March 25, 2015 Nearly 10,000 deaths from melanoma the deadliest of all skin cancers occurred in the U.S. last year, according to the National Cancer Institute. And while treatment advances have been made in fighting melanoma, a majority of these patients will die from their disease. In an aim to build upon these advances, investigators at Rutgers Cancer Institute of New Jersey have demonstrated that removal of a gene involved in the cellular self-cannibalization process of autophagy could provide therapeutic benefit to patients with melanoma.

Half of all melanomas harbor an activating mutation in the BRAF gene that turns on the cancer signaling pathway in cells known as the MAP kinase pathway. Activation of the MAP kinase pathway promotes tumor growth and survival. Drugs designed to selectively block activated BRAF have led to significant improvement in clinical response and overall survival in melanoma patients, but resistance to these drugs often develops leading to recurrence. With this study, published in the current online edition of Cancer Discovery (doi: 10.1158/2159-8290.CD-14-1473), senior author Janice M. Mehnert, MD, medical oncologist in the Melanoma and Soft Tissue Oncology Program at the Cancer Institute of New Jersey, in collaboration with Eileen White, PhD, associate director for basic science at the Cancer Institute and distinguished professor of molecular biology and biochemistry at Rutgers School of Arts and Sciences, aimed to identify mechanisms critical for melanoma that could be targeted in conjunction with BRAF inhibition.

Investigators tested the consequence of removing the autophagy gene known as ATG7 from laboratory models of BRAF-driven melanoma. Autophagy is a process in which intracellular components are recycled in order to help sustain cell growth. When ATG7 was removed from melanomas they found much smaller tumors with increased senescence, which is a known barrier to cancer that causes tumor cells to stop proliferating. Thus ATG7 promotes development of BRAF-mutated melanoma by overcoming senescence. They went on to show that loss of ATG7 potentiated the anti-tumor activity of a BRAF inhibitor in melanoma. The work demonstrates that BRAF-mutated melanoma requires autophagy for tumor development and blocking autophagy could have therapeutic value, particularly in combination with BRAF inhibition.

This discovery that ATG7 promotes the growth of melanoma tumors underscores that the development of agents targeting autophagy may effectively inhibit melanoma growth, notes Dr. Mehnert, who is an associate professor of medicine at Rutgers Robert Wood Johnson Medical School. Clinical trials seeking to block the process of autophagy are ongoing at the Cancer Institute.

Other authors on the study include: Xiaoqi Xie, Ju Yong Koh and Sandy Price, all Cancer Institute and Robert Wood Johnson Medical School.

The work was supported by funding from the V Foundation for Cancer Research, National Institutes of Health (R01CA163591, R01CA130893), the Val Skinner Foundation and Rutgers Cancer Institute of New Jersey (pilot grant P30CA072720).

About Rutgers Cancer Institute of New Jersey Rutgers Cancer Institute of New Jersey (www.cinj.org) is the states first and only National Cancer Institute-designated Comprehensive Cancer Center. As part of Rutgers, The State University of New Jersey, the Cancer Institute of New Jersey is dedicated to improving the detection, treatment and care of patients with cancer, and to serving as an education resource for cancer prevention. Physician-scientists at the Cancer Institute engage in translational research, transforming their laboratory discoveries into clinical practice, quite literally bringing research to life. To make a tax-deductible gift to support the Cancer Institute of New Jersey, call 848-932-3637 or visit http://www.cinj.org/giving. Follow us on Facebook at http://www.facebook.com/TheCINJ.

The Cancer Institute of New Jersey Network is comprised of hospitals throughout the state and provides the highest quality cancer care and rapid dissemination of important discoveries into the community. Flagship Hospital: Robert Wood Johnson University Hospital. System Partner: Meridian Health (Jersey Shore University Medical Center, Ocean Medical Center, Riverview Medical Center, Southern Ocean Medical Center, and Bayshore Community Hospital). Major Clinical Research Affiliate Hospitals: Carol G. Simon Cancer Center at Morristown Medical Center and Carol G. Simon Cancer Center at Overlook Medical Center. Affiliate Hospitals: JFK Medical Center, Robert Wood Johnson University Hospital Hamilton (CINJ Hamilton), and Robert Wood Johnson University Hospital Somerset.

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Research Shows Gene Removal May Aid Melanoma Treatment

Biotechnology Part I - Mr Pauller
This video presents the topic of biotechnology. Included in the discussion are: genetic engineering, PCR, plasmids, cloning, and restriction enzymes.

By: Noel Pauller

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Biotechnology Part I - Mr Pauller - Video

Using high-performance computing and genetic engineering to boost the photosynthetic efficiency of plants offers the best hope of increasing crop yields enough to feed a planet expected to have 9.5 billion people on it by 2050, researchers report in the journal Cell.

There has never been a better time to try this, said University of Illinois plant biology professor Stephen P. Long, who wrote the report with colleagues from Illinois and the CAS-MPG Partner Institute of Computational Biology in Shanghai.

"We now know every step in the processes that drive photosynthesis in C3 crop plants such as soybeans and C4 plants such as maize," Long said. "We have unprecedented computational resources that allow us to model every stage of photosynthesis and determine where the bottlenecks are, and advances in genetic engineering will help us augment or circumvent those steps that impede efficiency."

Substantial progress has already been made in the lab and in computer models of photosynthesis, Long said.

"Our lab and others have put a gene from cyanobacteria into crop plants and found that it boosts the photosynthetic rate by 30 percent," he said.

Photosynthetic microbes offer other clues to improving photosynthesis in plants, the researchers report. For example, some bacteria and algae contain pigments that utilize more of the solar spectrum than plant pigments do. If added to plants, those pigments could bolster the plants' access to solar energy.

Some scientists are trying to engineer C4 photosynthesis in C3 plants, but this means altering plant anatomy, changing the expression of many genes and inserting new genes from C4 plants, Long said.

"Another, possibly simpler approach is to add to the C3 chloroplast the system used by blue-green algae," he said. This would increase the activity of Rubisco, an enzyme that catalyzes a vital step of the conversion of atmospheric carbon dioxide into plant biomass. Computer models suggest adding this system would increase photosynthesis as much as 60 percent, Long said.

Computer analyses of the way plant leaves intercept sunlight have revealed other ways to improve photosynthesis. Many plants intercept too much light in their topmost leaves and too little in lower leaves; this probably allows them to outcompete their neighbors, but in a farmer's field such competition is counterproductive, Long said.

Studies headed by U. of I. plant biology professor Donald Ort aim to make plants' upper leaves lighter, allowing more sunlight to penetrate to the light-starved lower leaves. Computer modeling of photosynthesis also shows researchers where the traffic jams occur -- the steps that slow the process down and reduce efficiency.

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Photosynthesis hack is needed to feed the world by 2050

IMAGE:This photo shows University of Illinois field trials of various photosynthesis hacks. view more

CHAMPAIGN, Ill. -- Using high-performance computing and genetic engineering to boost the photosynthetic efficiency of plants offers the best hope of increasing crop yields enough to feed a planet expected to have 9.5 billion people on it by 2050, researchers report in the journal Cell.

There has never been a better time to try this, said University of Illinois plant biology professor Stephen P. Long, who wrote the report with colleagues from Illinois and the CAS-MPG Partner Institute of Computational Biology in Shanghai.

"We now know every step in the processes that drive photosynthesis in C3 crop plants such as soybeans and C4 plants such as maize," Long said. "We have unprecedented computational resources that allow us to model every stage of photosynthesis and determine where the bottlenecks are, and advances in genetic engineering will help us augment or circumvent those steps that impede efficiency."

Substantial progress has already been made in the lab and in computer models of photosynthesis, Long said.

"Our lab and others have put a gene from cyanobacteria into crop plants and found that it boosts the photosynthetic rate by 30 percent," he said.

Photosynthetic microbes offer other clues to improving photosynthesis in plants, the researchers report. For example, some bacteria and algae contain pigments that utilize more of the solar spectrum than plant pigments do. If added to plants, those pigments could bolster the plants' access to solar energy.

Some scientists are trying to engineer C4 photosynthesis in C3 plants, but this means altering plant anatomy, changing the expression of many genes and inserting new genes from C4 plants, Long said.

"Another, possibly simpler approach is to add to the C3 chloroplast the system used by blue-green algae," he said. This would increase the activity of Rubisco, an enzyme that catalyzes a vital step of the conversion of atmospheric carbon dioxide into plant biomass. Computer models suggest adding this system would increase photosynthesis as much as 60 percent, Long said.

Computer analyses of the way plant leaves intercept sunlight have revealed other ways to improve photosynthesis. Many plants intercept too much light in their topmost leaves and too little in lower leaves; this probably allows them to outcompete their neighbors, but in a farmer's field such competition is counterproductive, Long said.

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Report: Photosynthesis hack needed to feed the world by 2050

IMAGE:Cyberpsychology, Behavior, and Social Networking is an authoritative peer-reviewed journal published monthly online with Open Access options and in print that explores the psychological and social issues surrounding... view more

Credit: Mary Ann Liebert, Inc., publishers

New Rochelle, NY, March 25, 2015--The photo-sharing app Snapchat is not yet as popular as Facebook for social networking, but the greater privacy Snapchat may offer could motivate users to share more intimate types of content for different purposes. A new study comparing Snapchat and Facebook use and their effect on romantic relationships is published in Cyberpsychology, Behavior, and Social Networking, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Cyberpsychology, Behavior, and Social Networking website until April 25, 2015.

The article "Snapchat Elicits More Jealousy Than Facebook: A Comparison of Snapchat and Facebook Use" describes a study comparing how individuals use the two social networking apps, and whether Snapchat, with which messages disappear after only a few seconds and are typically sent to a smaller number of people, affords more private communication and intimate, personal content that could evoke greater jealousy. Authors Sonja Utz and Nicole Muscanell, Knowledge Media Research Center (Tbingen, Germany), and Cameran Khalid (Glasgow University, Scotland), found that behaviors of romantic partners on Snapchat evoked higher levels of jealousy than did the same behaviors on Facebook.

"Although a small preliminary study, this is an important foray into a new communication platform," says Editor-in-Chief Brenda K. Wiederhold, PhD, MBA, BCB, BCN, Interactive Media Institute, San Diego, California and Virtual Reality Medical Institute, Brussels, Belgium. "And with the January 2015 Snapchat update, which made Best Friends Lists private, one wonders if we will now see the fire of jealousy further inflamed."

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About the Journal

Cyberpsychology, Behavior, and Social Networking is an authoritative peer-reviewed journal published monthly online with Open Access options and in print that explores the psychological and social issues surrounding the Internet and interactive technologies, plus cybertherapy and rehabilitation. Complete tables of content and a sample issue may be viewed on the Cyberpsychology, Behavior, and Social Networking website.

About the Publisher

Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Games for Health Journal, Telemedicine and e-Health, and Journal of Child and Adolescent Psychopharmacology. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 80 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc., publishers website.

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Snapchat or Facebook -- which one is more likely to elicit romantic jealousy?

Using a novel approach that homes in on rare families severely affected by autism, a Johns Hopkins-led team of researchers has identified a new genetic cause of the disease. The rare genetic variant offers important insights into the root causes of autism, the researchers say. And, they suggest, their unconventional method can be used to identify other genetic causes of autism and other complex genetic conditions.

A report on the study appears in the April 2 issue of the journal Nature.

In recent years, falling costs for genetic testing, together with powerful new means of storing and analyzing massive amounts of data, have ushered in the era of the genomewide association and sequencing studies. These studies typically compare genetic sequencing data from thousands of people with and without a given disease to map the locations of genetic variants that contribute to the disease. While genomewide association studies have linked many genes to particular diseases, their results have so far failed to lead to predictive genetic tests for common conditions, such as Alzheimer's, autism or schizophrenia.

"In genetics, we all believe that you have to sequence endlessly before you can find anything," says Aravinda Chakravarti, Ph.D. , a professor in the Johns Hopkins University School of Medicine's McKusick-Nathans Institute of Genetic Medicine. "I think whom you sequence is as important -- if not more so -- than how many people are sequenced."

With that idea, Chakravarti and his collaborators identified families in which more than one female has autism spectrum disorder, a condition first described at Johns Hopkins in 1943. For reasons that are not understood, girls are far less likely than boys to have autism, but when girls do have the condition, their symptoms tend to be severe. Chakravarti reasoned that females with autism, particularly those with a close female relative who is also affected, must carry very potent genetic variants for the disease, and he wanted to find out what those were.

The research team compared the gene sequences of autistic members of 13 such families to the gene sequences of people from a public database. They found four potential culprit genes and focused on one, CTNND2, because it fell in a region of the genome known to be associated with another intellectual disability. When they studied the gene's effects in zebrafish, mice and cadaveric human brains, the research group found that the protein it makes affects how many other genes are regulated. The CTNND2 protein was found at far higher levels in fetal brains than in adult brains or other tissues, Chakravarti says, so it likely plays a key role in brain development.

Specifically, mutations in CNNTD2 disrupted the connections called synapses that form among brain cells. "This is consistent with recent findings that many gene mutations associated with autism are involved in synapse development," says Richard Huganir, Ph.D. , director of the Solomon H. Snyder Department of Neuroscience, who participated in the research. "The results of this study add to the evidence that abnormal synaptic function may underlie the cognitive defects in autism."

While autism-causing variants in CTNND2 are very rare, Chakravarti says, the finding provides a window into the general biology of autism. "To devise new therapies, we need to have a good understanding of how the disease comes about in the first place," he says. "Genetics is a crucial way of doing that."

Chakravarti's research group is now working to find the functions of the other three genes identified as possibly associated with autism. They plan to use the same principle to look for disease genes in future studies of 100 similar autism-affected families, as well as other illnesses. "We've shown that even for genetically complicated diseases, families that have an extreme presentation are very informative in identifying culprit genes and their functions -- or, as geneticists are taught, 'treasure your exceptions.'" Chakravarti says.

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New autism-causing genetic variant identified

(New York - March 25, 2015) Induced pluripotent stem cells (iPSCs) -- adult cells reprogrammed back to an embryonic stem cell-like state--may better model the genetic contributions to each patient's particular disease. In a process called cellular reprogramming, researchers at Icahn School of Medicine at Mount Sinai have taken mature blood cells from patients with myelodysplastic syndrome (MDS) and reprogrammed them back into iPSCs to study the genetic origins of this rare blood cancer. The results appear in an upcoming issue of Nature Biotechnology.

In MDS, genetic mutations in the bone marrow stem cell cause the number and quality of blood-forming cells to decline irreversibly, further impairing blood production. Patients with MDS can develop severe anemia and in some cases leukemia also known as AML. But which genetic mutations are the critical ones causing this disease?

In this study, researchers took cells from patients with blood cancer MDS and turned them into stem cells to study the deletions of human chromosome 7 often associated with this disease.

"With this approach, we were able to pinpoint a region on chromosome 7 that is critical and were able to identify candidate genes residing there that may cause this disease," said lead researcher Eirini Papapetrou, MD, PhD, Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai.

Chromosomal deletions are difficult to study with existing tools because they contain a large number of genes, making it hard to pinpoint the critical ones causing cancer. Chromosome 7 deletion is a characteristic cellular abnormality in MDS and is well-recognized for decades as a marker of unfavorable prognosis. However, the role of this deletion in the development of the disease remained unclear going into this study.

Understanding the role of specific chromosomal deletions in cancers requires determining if a deletion has observable consequences as well as identifying which specific genetic elements are critically lost. Researchers used cellular reprogramming and genome engineering to dissect the loss of chromosome 7. The methods used in this study for engineering deletions can enable studies of the consequences of alterations in genes in human cells.

"Genetic engineering of human stem cells has not been used for disease-associated genomic deletions," said Dr. Papapetrou. "This work sheds new light on how blood cancer develops and also provides a new approach that can be used to study chromosomal deletions associated with a variety of human cancers, neurological and developmental diseases."

Reprogramming MDS cells could provide a powerful tool to dissect the architecture and evolution of this disease and to link the genetic make-up of MDS cells to characteristics and traits of these cells. Further dissecting the MDS stem cells at the molecular level could provide insights into the origins and development of MDS and other blood cancers. Moreover, this work could provide a platform to test and discover new treatments for these diseases.

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This study was supported by grants from the National Institutes of Health, the American Society of Hematology, the Sidney Kimmel Foundation for Cancer Research, the Aplastic Anemia & MDS International Foundation, the Ellison Medical Foundation, the Damon Runyon Cancer Research Foundation, the University of Washington Royalty Research Fund, and a John H. Tietze Stem Cell Scientist Award.

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Researchers discover genetic origins of myelodysplastic syndrome using stem cells