Category Archives: Massachusetts Stem Cells

9 hours ago by Hannah L. Robbins In the top image the frog embryo is developing normally. In the bottom image the frog embryo is lacking a head and brain as a result of the suppression of the Notum protein. Credit: Nathalia G. Amado

A protein that is necessary for the formation of the vertebrate brain has been identified by researchers at the Harvard Stem Cell Institute (HSCI) and Boston Children's Hospital, in collaboration with scientists from Oxford and Rio de Janeiro.

The researchers say the finding, which has been successfully demonstrated in frog embryos, will help scientists control differentiation of various cell types.

Their study was given early online Thursday and is being published in print in the March 23 issue of the journal Developmental Cell. Xinjun Zhang and Seong-Moon Cheong, both postdoctoral fellows in the laboratory of HSCI-affiliated faculty member Xi He at Boston Children's Hospital, are co-first authors.

The protein, Notum, first discovered in fruit flies in 2002 and then found in mice and humans, is one of many that help determine embryonic development. For some time, researchers have known that Notum regulates wing formation in flies. But until recently, it was not known how Notum affected vertebrate embryo development. In collaboration with researchers from University of Oxford and Federal University of Rio de Janeiro, He and colleagues compared how frog embryoswhich are considered models for human embryosdeveloped with and without Notum.

When the researchers injected frog embryos with Notum, the embryos grew bigger brains and heads. When Notum was not present, the embryos would become a sack of skin cells with no head and a tiny brain, a result of embryonic progenitor cells making only epidermal but not neural cells.

Simply put, said He, "The frog brain cannot be properly formed without Notum."

These findings could benefit stem cell researchers trying to create specific tissue types or organs in the lab. In order to guide or direct stem cells to differentiate into a given cell type, such as neural cells or muscle cells, researchers continue to alter their experimental recipes, fine-tuning which molecules should be added to their dishes in what sequence and amount.

For those trying to create neural cells, "Notum is a necessary ingredient and new tool in the kit box for researchers to instruct human progenitor cells to become neural tissues," said He, who is also an American Cancer Society research professor.

Additionally, the researchers were able to demonstrate how Notum deactivates Wnt, which is a family of proteins that direct stem cells to "self-renew," or make more stem cells, among other things. If left unchecked, Wnt could cause certain types of cancer, such as gastrointestinal, brain, and blood cancers.

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Researchers identify a vital protein that can determine head and brain development

Scientists at Tuft University in Massachusetts grew bone marrow on silk They were able to generate functioning platelet cells that form blood clots The cells could be used to stop bleeding in injured patients in ER rooms It has raised hopes that man-made blood can be created for transfusions However some say it could be up to 15 years before stem cells can be used to create blood that can be safely used for transfusions during surgery

By Richard Gray for MailOnline

Published: 11:46 EST, 19 February 2015 | Updated: 12:50 EST, 23 February 2015

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A major component of blood has been grown in the laboratory by scientists, bringing man-made blood transfusions a step closer.

Biomedical engineers have for the first time produced functional blood platelets - the cells that cause clots to form - from human bone marrow grown in the laboratory.

The achievement raises hopes that it will soon be possible to produce fully functional blood in a similar way.

Scientists have managed to grow fully functioning platelets like the one above surrounded by red blood cells

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Could we soon have man-made blood?

Transplanting islets encapsulated with CXCL12 restores blood sugar control without immunosuppression in animal models of diabetes

An approach developed by Massachusetts General Hospital (MGH) investigators may provide a solution to the limitations that have kept pancreatic islet transplantation from meeting its promise as a cure for type 1 diabetes. In the March issue of the American Journal of Transplantation, the research team reports that encapsulating insulin-producing islets in gel capsules infused with a protein that repels key immune cells protected islets from attack by the recipient's immune system without the need for immunosuppressive drugs, restoring long-term blood sugar control in mouse models. The technique was effective both for islets from unrelated mice and for islets harvested from pigs.

"Protecting donor islets from the recipient's immune system is the next big hurdle toward making islet transplantation a true cure for type 1 diabetes," says Mark Poznansky, MD, PhD, director of the MGH Vaccine and Immunotherapy Center, who led the study. "The first was generating enough insulin-producing islets, which has been addressed by several groups using pig islets or - as announced last fall by Doug Melton's team at the Harvard Stem Cell Institute - with islet cells derived from human stem cells. Now our technology provides a way to protect islets or other stem-cell-derived insulin-producing cells from being destroyed as soon as they are implanted into a diabetic individual without the need for high-intensity immunosuppression, which has its own serious side effects."

While transplantation of pancreatic islets has been investigated for several decades as a treatment and potential cure for type 1 diabetes, its success has been limited. Along with the risk of rejection that accompanies all organ transplants - a risk that is even greater for cross-species transplants - donated islets are subject to the same autoimmune damage that produced diabetes in the first place. The immunosuppressive drugs used to prevent organ rejection significantly increase the risk of infections and some cancers, and they also can contribute directly to damaging the islets. Among the strategies investigated to protect transplanted islets are enclosing them in gel capsules and manipulating the immune environment around the implant. The MGH-developed approach includes aspects of both approaches.

Previous research from the MGH team demonstrated that elevated expression of a chemokine - a protein that induces the movement of other cells - called CXCL12 repels the effector T cells responsible for the rejection of foreign tissue while attracting and retaining regulatory T cells that suppress the immune response. For the current study they investigated how either coating islets with CXCL12 or enclosing them in CXCL12 gel capsules would protect islets transplanted into several different mouse models.

Their experiments revealed that islets from nondiabetic mice, either coated with CXCL12 or encapsulated in a CXCL12-containing gel, survived and restored long-term blood sugar control after transplantation into mice with diabetes that was either genetically determined or experimentally induced. CXCL12-encapsulated islets were even protected against rejection by recipient animals previously exposed to tissue genetically identical to that of the donor, which usually would sensitize the immune system against donor tissue. CXCL12-encapsulated pig islets successfully restored blood sugar control in diabetic mice without being rejected. The ability of CXCL12 - either as a coating or encapsulating gel - to repel effector T cells and attract regulatory T cells was also confirmed.

"While studying this procedure in larger animals is an essential next step, which is currently underway with the support of the Juvenile Diabetes Research Foundation, we expect that this relatively simple procedure could be readily translatable into clinical practice when combined with technologies such as stem-cell-derived islets or other insulin-producing cells and advanced encapsulation devices," says Poznansky, an associate professor of Medicine at Harvard Medical School. "We also hope that CXCL12 will have a role in protecting other transplanted organs, tissues and cells as well as implantable devices, a possibility we are actively investigating."

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Tao Chen, MD, of the MGH Vaccine and Immunotherapy Center (VIC) is lead author of the American Journal of Transplantation report. Additional co-authors include James Markmann, MD, PhD, and David Sachs, MD, of the MGH Center for Transplantation Sciences. The study was supported by grants from the Juvenile Diabetes Research Foundation and the Friends of VIC. A patent covering the approach described in this paper has been issued to the MGH and exclusively licensed to the biotech startup company VICapsys.

Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $785 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.

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Protein that repels immune cells protects transplanted pancreatic islets from rejection

2 hours ago by Deirdre Branley Credit: CDC

Each year nearly 600,000 peoplemostly children under age five and pregnant women in sub-Saharan Africadie from malaria, caused by single-celled parasites that grow inside red blood cells. The most deadly malarial speciesPlasmodium falciparumhas proven notoriously resistant to treatment efforts. But thanks to a novel approach developed by scientists at Albert Einstein College of Medicine of Yeshiva University and described in the January 20 online edition of ACS Chemical Biology, researchers can readily screen thousands of drugs to find those potentially able to kill P. falciparum.

Scientists have known for more than a decade that malaria parasites have an Achilles heel: Like all cells, they require two key building blockspurines and pyrimidinesto synthesize their DNA and RNA. But malaria parasites can't synthesize purines on their own. Instead, they must import purines from the host red blood cells that they invade. A parasite protein called PfENT1 transports purines from blood cell into the parasites. So drugs that block PfENT1 could conceivably kill the parasites by depriving them of purines they needbut an experimental approach for identifying PfENT1 inhibitors didn't exist, until now.

Einstein's Myles Akabas, M.D., Ph.D., developed a novel yeast-based high-throughput assay for identifying inhibitors of the PfENT1 transporter. Dr. Akabas worked with two MSTP students in his lab (I.J. Frame and Roman Deniskin) as well as colleagues at Einstein (Drs. Ian Willis and Robyn Moir) and Columbia University (Drs. Donald Landry and David Fidock). The researchers used their technique to screen 64,560 different compounds. They identified 171 potential antimalarial drugs. Studies of nine of the most potent drugs showed that they kill P. falciparum parasites in laboratory culture.

"We've shown that the PfENT1 transporter is a potential drug target for developing novel antimalarial drugs," said Dr. Akabas, senior author of the ACS Chemical Biology paper and a professor of physiology & biophysics, of medicine and in the Dominick P. Purpura Department of Neuroscience at Einstein. "By using our rather simple approach, scientists could create similar high-throughput screens to identify inhibitors for killing other parasites that rely on transporters to import essential nutrients."

Explore further: Malaria-in-a-dish paves the way for better treatments

Massachusetts Institute of Technology (MIT) researchers have engineered a way to use human liver cells, derived from induced pluripotent stem cells, to screen potential antimalarial drugs and vaccines for ...

An antimalarial agent developed by researchers at Albert Einstein College of Medicine of Yeshiva University proved effective at clearing infections caused by the malaria parasite most lethal to humans by literally ...

Malaria is one of the most deadly infectious diseases in the world today, claiming the lives of over half a million people every year, and the recent emergence of parasites resistant to current treatments ...

Scientists searching for new drugs to fight malaria have identified a number of compoundssome of which are currently in clinical trials to treat cancerthat could add to the anti-malarial arsenal.

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Scientists develop novel technique for finding drugs to combat malaria

Researchers at the Massachusetts Institute of Technology (MIT) have developed a new method for tackling diabetes that could represent a significant breakthrough in treating the condition. The team's engineered insulin stays in the patients bloodstream, but is only activated when sugar levels start to tip the scales.

There have been some promising developments in diabetes research over recent months. Back in October, stem cell researchers at Harvard University revealed a breakthrough on the road towards a cure for the condition via a means of creating human insulin-producing beta cells. More recently, a University of Alabama at Birmingham study showed that high blood pressure drugs have the ability to reverse the disease in animal models.

The new MIT study isnt centered on a cure for the condition, but focuses instead on developing a better method of treatment for patients.

Type 1 diabetes patients use insulin injections to make up for a lack of the hormone in their bloodstream. Some make use of a long-acting treatment that stays in the system for 24 hours, while others keep tabs on their calorie intake and blood sugar levels to determine how much to inject. Both of these methods act independently of the patients blood sugar levels.

Researchers at MIT have developed a new form of treatment that not only circulates for a long period of time, but is only activated when blood sugar levels get too high. This would provide a more efficient method of dealing with glucose spikes over extended periods of time.

To create the new, glucose-responsive treatment, the researchers made two modifications. Firstly, in order to ensure that the engineered hormone stays in the bloodstream for the required length of time, a hydrophobic molecule known as an aliphatic domain was added. Its not known for certain why the chain of fatty molecules prolong the molecules lifespan in the bloodstream, though its thought that it may bind to proteins, preventing the insulin from tackling sugar molecules.

Secondly, researchers added PBA a chemical group that reversibly binds to glucose, thus bringing it into contact with the insulin when high levels of sugar present themselves. The team created four different variants of the engineered molecule, each containing PBA with a different chemical modification, such as fluorine or nitrogen.

To test the effectiveness of the treatment, experiments were carried out on insulin-deficient mice, measuring the response of their blood sugar levels to surges in glucose over 10 hours. The results showed that the engineered insulin containing PBA with fluorine responded fastest to the spikes, winning out against the other chemically-modified treatments, as well as traditional regular and long-acting insulin.

While further testing is required before the engineered insulin could be used in routine treatment, it could mark a significant advance in how the condition is tackled, providing a more efficient alternative to existing treatments. The MIT team plans to continue its research, working to improve the performance of the modified insulin, making it safer and more efficient.

Source: MIT

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MIT researchers develop glucose-responsive diabetes treatment

Washington, DC (PRWEB) February 04, 2015

New Organ, a collective initiative for biomedical engineering and regenerative medicine, announced today that two new teams have joined the field competing for the New Organ Liver Prize, a global competition sponsored by the Methuselah Foundation, a biomedical charity. The prize challenge will award $1,000,000 to the first team that creates a regenerative or bioengineered solution that enables a large animal to live 90 days without native liver function.

These two distinguished teams, led by Dr. Hiro Nakauchi of Stanford University/University of Tokyo and Dr. John Geibel of Yale University, join five others representing scientists and clinicians from Harvard Medical School, Massachusetts General Hospital, Northwick Park Institute for Medical Research, University College London, University of Florida, University of Oxford, University of Pittsburgh, and Yokohama City University.

Were thrilled that Stanford, Yale, and the University of Tokyo have joined this vital competition, New Organ Founder and Methuselah CEO David Gobel said. We launched the Liver Prize because organ disease, and the associated organ shortage, represents one of the greatest medical challenges that can be solved. With millions of people in dire need of new organs, and the scientific foundations now in place to pursue a vision of organs on demand, the time has come to solve the organ crisis once and for all.

Dr. Hiro Nakauchi has been working on the challenge of generating functional organs from pluripotent stem cells since 2007. His team has been joined by Dr. Sheikh Tamir Rashid from the University of Cambridge and Dr. Takanori Takebe of Yokohama City University, prominent researchers known for their innovative in vitro culture systems for growing hepatocytes and liver buds from human iPSCs, respectively (Nature 2011, Nature 2013).

"Generating a stem-cell-derived human liver is one of the most pressing goals for regenerative medicine, said Nakauchi. Despite great advances in tissue engineering such as 3D printer technology and decellularized scaffolds, it has still not been possible to overcome this challenge. Our approach to organ generation uses as much of the natural in vivo environment as possible. We have therefore assembled an international team of liver experts at Stanford to exploit this platform in combination with other new in vitro based techniques to achieve our goal of human liver generation.

Dr. John Geibel has over 30 years of experience in translational research, with broad expertise in physiology and pathophysiology.

According to Geibel, The need for liver transplantation has always outpaced the number of donor organs available. When looking at new means to address this problem, the idea of developing a 3D-bioprinted organ is the first truly novel approach that will allow the patient to take cells from their own body to generate the replacement liver in vitro, dramatically reducing both transplantation wait times and the need for immunosuppression. This is what intrigued our team at Yale, and we are excited to develop a model that will be the dawn of a new age in transplant surgery and patient care.

About New Organ:

New Organ is a collective initiative addressing organ disease and injury by building a prize portfolio and coalition of partners committed to advancing breakthroughs in engineering, banking, and regenerating solid organs, starting with the liver. It is a growing global network of academic, government, industry, and philanthropic stakeholders focusing on the common goal of organs on demand. The New Organ Liver Prize was launched at the 2013 World Stem Cell Summit with $1 million in initial funding from the Methuselah Foundation. Learn more at http://neworgan.org.

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New Organ Liver Prize Gathers Momentum

Massachusetts excels in the biomedical field. The commonwealth has strong, internationally recognized academic research institutions and clinical centers, as well as a growing biomedical industry, with stem cell and regenerative medicine companies. The legislation is supportive of stem cell research, and the state is setting aside funds for embryonic stem cell research. Past successes have included performing the first skin graft grown from human stem cells in 1983.

The only federal legislation regulation of stem cell research is an executive order prohibiting federal funds from being used for embryonic stem cell research, except those using embryonic stem cell lines created before August 9, 2001. Each state is therefore responsible for determining its policy and funding for stem cell research.

Stem cell research in Massachusetts falls under the 2005 act enhancing regenerative medicine, which permits and encourages stem cell research on adult, placental, umbilical cord blood, and human embryonic stem cells. The law permits the creation of embryos for research by therapeutic cloning, using somatic cell nuclear transfer. Cloning for human reproductive purposes is prohibited, and the law includes penalties for violating regulations.

To clarify the regulations for creating embryos for research, an act on biotechnology regulation also was enacted in 2006. This act makes it clear that creating embryos for research may be done only by somatic cell nuclear transfer, parthenogenesis, or other asexual means. Though embryos may not be created for research through in vitro fertilization procedures, excess embryos from assisted reproduction may be donated for research with the informed consent of the donors. Regulations prohibit payment for embryos, human gametes, or cadaveric tissue.

The legislature also overrode a governors veto to create an institute for stem cell research and regenerative medicine at the University of Massachusetts and established an investment fund to create a life science center for regenerative medicine and biotechnology in 2006. With a planned investment of $1 billion over 10 years, the Massachusetts Life Sciences Initiative will provide investment to public and private institutions, growing life sciences research, development, and commercialization, as well as building ties between sectors of the Massachusetts life sciences community. In addition to funding, this strategy of focusing on medicine and science research will provide funds to researchers for work before NIH grant funding, build an infrastructure for research, and support the translation of Massachusetts research innovation into clinical applications with tax incentives and other assistance.

The Massachusetts Biotechnology Research Park was created in 1985 in Worcester for biotechnology research and production. The park is across the street from the University of Massachusetts Medical Center and is home to over a dozen biotechnology companies, not-for-profits, and academic institutions. The facilities include wet laboratory space and locations for buildings designed for the business. CenTech Park-Emerging Technology Research and Manufacturing located in Grafton is near the Tufts University School of Veterinary Medicine. The park is intended for emerging technology companies.

The Harvard Stem Cell Institute, founded in 2004, supports the collaborative work of the university, medical school, teaching hospitals, and researchers to bring together basic science innovation with clinical expertise to translate innovations into clinical applications. The institute supports research into all aspects of stem cell biology, including both embryonic and adult stem cells. Their primary emphasis is on the search for new therapies for serious diseases, including, among others, diabetes, neurological diseases, cardiovascular diseases, blood diseases, and cancer. The institute receives private donation support and National Institutes of Health grant funds.

The University of Massachusetts is a public research university system with campuses statewide and a medical school and a teaching hospital in Worcester. The University of Massachusetts Memorial Healthcare is home to the commonwealths public cord blood bank, as well as researchers in cell biology, stem cell research for use in bone disease and blood disorders, and clinical research with the goal of translation of their findings to clinical application in cardiovascular and blood disease, cancer, and diabetes.

The Massachusetts legislature set aside funding for an institute for stem cell research and regenerative medicine at the university, which will integrate the system-wide strengths in human and animal stem cell research as well as biological material and cell/tissue engineering. The hope is to build core lab facilities, enhance the academic programs, and use the strength of the Massachusetts Biologic laboratories in translating basic science innovations into clinical applications.

Massachusetts Biologic Laboratories became part of the University of Massachusetts in 1997. The laboratory manufactures vaccines and other biologic products at locations in Jamaica Plain and Mattapan. The laboratory is licensed by the U.S. Food and Drug Administration for vaccine manufacturing.

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Massachusetts (Stem Cell) - what-when-how

PUBLIC RELEASE DATE:

15-Dec-2014

Contact: Sarah McDonnell s_mcd@mit.edu 617-253-8923 Massachusetts Institute of Technology @MIT

CAMBRIDGE, MA -- A new study from MIT implicates a family of RNA-binding proteins in the regulation of cancer, particularly in a subtype of breast cancer. These proteins, known as Musashi proteins, can force cells into a state associated with increased proliferation.

Biologists have previously found that this kind of transformation, which often occurs in cancer cells as well as during embryonic development, is controlled by transcription factors -- proteins that turn genes on and off. However, the new MIT research reveals that RNA-binding proteins also play an important role. Human cells have about 500 different RNA-binding proteins, which influence gene expression by regulating messenger RNA, the molecule that carries DNA's instructions to the rest of the cell.

"Recent discoveries show that there's a lot of RNA-processing that happens in human cells and mammalian cells in general," says Yarden Katz, a recent MIT PhD recipient and one of the lead authors of the new paper. "RNA is processed at several points within the cell, and this gives opportunities for RNA-binding proteins to regulate RNA at each point. We're very interested in trying to understand this unexplored class of RNA-binding proteins and how they regulate cell-state transitions."

Feifei Li of China Agricultural University is also a lead author of the paper, which appears in the journal eLife on Dec. 15. Senior authors of the paper are MIT biology professors Christopher Burge and Rudolf Jaenisch, and Zhengquan Yu of China Agricultural University.

Controlling cell states

Until this study, scientists knew very little about the functions of Musashi proteins. These RNA-binding proteins have traditionally been used to identify neural stem cells, in which they are very abundant. They have also been found in tumors, including in glioblastoma, a very aggressive form of brain cancer.

"Normally they're marking stem and progenitor cells, but they get turned on in cancers. That was intriguing to us because it suggested they might impose a more undifferentiated state on cancer cells," Katz says.

Continued here:
Proteins drive cancer cells to change states

Nik Spencer/Nature

Eggs and sperm do it when they combine to make an embryo. John Gurdon did it in the 1960s, when he used intestinal cells from tadpoles to generate genetically identical frogs. Ian Wilmut did it too, when he used an adult mammalian cell to make Dolly the sheep in 1996. Reprogramming reverting differentiated cells back to an embryonic state, with the extraordinary ability to create all the cells in the body has been going on for a very long time.

Scientific interest in reprogramming rocketed after 2006, when scientists showed that adult mouse cells could be reprogrammed by the introduction of just four genes, creating what they called induced pluripotent stem (iPS) cells1. The method was simple enough for almost any lab to attempt, and now it accounts for more than a thousand papers per year. The hope is that pluripotent cells could be used to repair damaged or diseased tissue something that moved closer to reality this year, when retinal cells derived from iPS cells were transplanted into a woman with eye disease, marking the first time that reprogrammed cells were transplanted into humans (see Nature http://doi.org/xhz; 2004).

There is just one hitch. No one, not even the dozen or so groups of scientists who intensively study reprogramming, knows how it happens. They understand that differentiated cells go in, and pluripotent cells come out the other end, but what happens in between is one of biology's impenetrable black boxes. We're throwing everything we've got at it, says molecular biologist Knut Woltjen of the Center for iPS Cell Research and Application at Kyoto University in Japan. It's still a really confusing process. It's very complicated, what we're doing.

Kerri Smith talks to researcher Andras Nagy and reporter David Cyranoski about reprogramming cells.

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One of the problems, stem-cell biologists say, is that their starting population contains a mix of cells, each in a slightly different molecular state. And the process for making iPS cells is currently inefficient and variable: only a tiny fraction end up fully reprogrammed and even these may differ from one another in subtle but important ways. What is more, the path to reprogramming may vary depending on the conditions under which cells are being grown, and from one lab to the next. This makes it difficult to compare experimental results, and it raises safety concerns should a mix of poorly characterized cells be used in the clinic.

But new techniques are starting to clarify the picture. By carrying out meticulous analyses of single cells and amassing reams of detailed molecular data, biologists are identifying a number of essential events that take place en route to a reprogrammed state. This week, the biggest such project an international collaboration audaciously called Project Grandiose unveiled its results26. The scientists involved used a battery of tests to take fine-scale snapshots of every stage of reprogramming and in the process, revealed an alternative state of pluripotency. It was the first high-resolution analysis of change in cell state over time, says Andras Nagy, a stem-cell biologist at Mount Sinai Hospital in Toronto, Canada, who led the project. I'm not shy about saying grandiose.

I'm not shy about saying grandiose.

But there is more to do if scientists want to control the process well enough to generate therapeutic cells with ease. Yes, we can make iPS cells and yes we can differentiate them, but I think we feel that we do not control them enough says Jacob Hanna, a stem-cell biologist at the Weizmann Institute of Science in Rehovot, Israel. Controlling cell behaviour at will is very cool. And the way to do it is to understand their molecular biology with great detail.

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Stem cells: The black box of reprogramming

By Sheryl Ubelacker The Canadian Press

WATCH: Dr. Andras Nagy describes the scientific breakthrough he led in solving the mystery of the stem cell reprogramming code.

TORONTO A Canadian-led international team of researchers has begun solving the mystery of just how a specialized cell taken from a persons skin is reprogrammed into an embryonic-like stem cell, from which virtually any other cell type in the body can be generated.

The research is being touted as a breakthrough in regenerative medicine that will allow scientists to one day harness stem cells to treat or even cure a host of conditions, from blindness and Parkinsons disease to diabetes and spinal cord injuries.

Besides creating the reprogramming roadmap, the scientists also identified a new type of stem cell, called an F-class stem cell due to its fuzzy appearance. Their work is detailed in five papers published Wednesday in the prestigious journals Nature and Nature Communications.

Dr. Andras Nagy, a senior scientist at Mount Sinai Hospital in Toronto, led the team of 50 researchers from Canada, the Netherlands, South Korea and Australia, which spent four years analyzing and cataloguing the day-by-day process that occurs in stem cell reprogramming.

The work builds on the 2006-2007 papers by Shinya Yamanaka, who showed that adult skin cells could be turned into embryonic-like, or pluripotent, stem cells through genetic manipulation, a discovery that garnered the Japanese scientist the Nobel Prize in 2012.

Nagy likened the roughly 21-day process to complete that transformation to a black box, so called because scientists did not know what went on within the cells as they morphed from one cell type into the other.

It was just like a black box, Nagy said Wednesday, following a briefing at the hospital. You start with a skin cell, you arrive at a stem cell but we had no idea what was happening inside the cell.

Nagys team set about cataloguing the changes as they occurred by removing cells from culture dishes at set points during the three-week period, then analyzing such cellular material as DNA and proteins present at that moment.

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Canadian scientists crack stem cell reprogramming code