PUBLIC RELEASE DATE:

6-Oct-2014

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

CAMBRIDGE, MA -- Deep within the bone marrow resides a type of cells known as mesenchymal stem cells (MSCs). These immature cells can differentiate into cells that produce bone, cartilage, fat, or muscle a trait that scientists have tried to exploit for tissue repair.

In a new study that should make it easier to develop such stem-cell-based therapies, a team of researchers from MIT and the Singapore-MIT Alliance in Research and Technology (SMART) has identified three physical characteristics of MSCs that can distinguish them from other immature cells found in the bone marrow. Based on this information, they plan to create devices that could rapidly isolate MSCs, making it easier to generate enough stem cells to treat patients.

Until now, there has been no good way to separate MSCs from bone marrow cells that have already begun to differentiate into other cell types, but share the same molecules on the cell surface. This may be one reason why research results vary among labs, and why stem-cell treatments now in clinical trials are not as effective as they could be, says Krystyn Van Vliet, an MIT associate professor of materials science and engineering and biological engineering and a senior author of the paper, which appears in the Proceedings of the National Academy of Sciences this week.

"Some of the cells that you're putting in and calling stem cells are producing a beneficial therapeutic outcome, but many of the cells that you're putting in are not," Van Vliet says. "Our approach provides a way to purify or highly enrich for the stem cells in that population. You can now find the needles in the haystack and use them for human therapy."

Lead authors of the paper are W.C. Lee, a former graduate student at the National University of Singapore and SMART, and Hui Shi, a former SMART postdoc. Other authors are Jongyoon Han, an MIT professor of electrical engineering and biological engineering, SMART researchers Zhiyong Poon, L.M. Nyan, and Tanwi Kaushik, and National University of Singapore faculty members G.V. Shivashankar, J.K.Y. Chan, and C.T. Lim.

Physical markers

MSCs make up only a small percentage of cells in the bone marrow. Other immature cells found there include osteogenic cells, which have already begun the developmental path toward becoming cartilage- or bone-producing cells. Currently, researchers try to isolate MSCs based on protein markers found on the cell surfaces. However, these markers are not specific to MSCs and can also yield other types of immature cells that are more differentiated.

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New technique allows scientists to find rare stem cells within bone marrow

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Stem-cell-based therapies could soon become a lot easier to develop as researchers have found a way to identify a type of immature stem cells within the bone marrow that can help in tissue repair.

These cells known as mesenchymal stem cells (MSCs) can differentiate into cells that produce bone, cartilage, fat, or muscle.

The team of researchers has identified three physical characteristics of MSCs that can distinguish them from other immature cells found in the bone marrow.

"You can now find the needles in the haystack and use them for human therapy," senior study author Krystyn Van Vliet, an associate professor at Massachusetts Institute of Technology in the US.

Based on this information, they plan to create devices that could rapidly isolate MSCs, making it easier to generate enough stem cells to treat patients.

Until now, there has been no good way to separate MSCs from bone marrow cells.

After measuring several other physical traits, the researchers found two that could be combined with size to completely distinguish MSCs from other stem cells: stiffness of the cell, and the degree of fluctuation in the cell's nuclear membrane.

"You do not need more than these three, but you also cannot use fewer than these three," Van Vliet added.

"We now have a triplet of characteristics that identifies populations of cells that are going to be multipotent versus populations of cells that are only going to be able to become bone or cartilage cells."

The researchers tested the regenerative abilities of the isolated MSCs in mice. They found that these cells could help repair both muscle and bone injuries, while cells identified as osteogenic stromal cells were able to repair bone but not muscle.

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New technique to identify rare stem cells

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The family of brave toddler Margot Martini launched a new bone marrow donor appeal this morning exactly a year after she was diagnosed with leukaemia.

Her relatives said the first Team Margot Stem Cell and Bone Marrow Awareness Day would be held in another 12 months, on Wednesday October 7, 2015.

The two-year-old underwent a bone marrow transplant in February after her dad, Yaser, from Essington, and mum Vicki launched a desperate appeal for help.

Margot Martini with mum Vicky

But she relapsed and her parents decided to end her treatment after being told her chances of survival were less than one per cent.

The awareness day is designed to promote awareness around the need for more potential stem cell donors to join the UK and worldwide registries.

Her family said they hoped mixed race people would sign up to plug a gaping hole on the lists.

Just sixty per cent of the 37,000 patients needing a stem cell donor worldwide receives a perfect match.

But that figure plunges to barely 20 per cent for those from black, Asian or ethnic minority communities.

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By Jon Cohen October 6 at 5:00 PM

Researchers are closer to unraveling the mystery of how Timothy Ray Brown, the only human cured of HIV, defeated the virus, according to a new study. Although the work doesnt provide a definitive answer, it rules out one possible explanation.

Brown remains one of the most studied cases in the HIV epidemics history. In 2006, after living with the virus for 11 years and controlling his infection with antiretroviral drugs, he learned that he had developed acute myeloid leukemia. (The leukemia has no known relationship to HIV infection or treatment.) Chemotherapy failed, and the next year Brown received the first of two bone marrow transplants a common treatment for this cancer and ditched his antiretrovirals. (An American then living in Berlin, Brown has been known to researchers for years as the Berlin patient.

When HIV-infected people stop taking these drugs, levels of HIV typically skyrocket within weeks. Yet researchers scouring Browns blood over the past seven years have found only traces of the viral genetic material, none of which can replicate.

Today, researchers point to three factors that might independently or in combination have ridden Browns body of HIV. The first is the process of conditioning, in which doctors destroyed Browns immune system with chemotherapy and whole-body irradiation to prepare him for his bone marrow transplant.

Second, his oncologist, Gero Htter, took an extra step that he thought might not only cure the leukemia but also help rid Browns body of HIV. He found a bone marrow donor who had a rare mutation in a gene that cripples a key receptor on white blood cells that the virus uses to establish an infection.

The third possible explanation is that Browns new immune system attacked remnants of his old one that held HIV-infected cells, a process known as graft vs. host disease.

In the new study, a team led by immunologist Guido Silvestri of Emory University in Atlanta designed an unusual monkey experiment to test these possibilities.

Bone marrow transplants work because of stem cells. Modern techniques avoid actually aspirating bone marrow and instead can sift through blood and pluck out the stem cells needed for a transplant to engraft. So the researchers first drew blood from three rhesus macaque monkeys, removed stem cells and put the cells in storage. They then infected these animals and three control monkeys with a hybrid virus, known as SHIV, that contains parts of the simian and human AIDS viruses. All six animals soon began receiving antiretroviral drugs, and SHIV levels in the blood quickly dropped below the level of detection on standard tests, as expected.

A few months later, the three monkeys with stored stem cells underwent whole-body irradiation to condition their bodies and then had their own stem cells reinfused. After the cells engrafted, a process that took a few more months, the researchers stopped antiretrovirals in the three animals and in the three controls. SHIV quickly came screaming back in the three controls and two of the transplanted animals. (One of the transplanted monkeys did not have the virus rebound, but its kidneys failed and the researchers euthanized it.)

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(PRWEB UK) 7 October 2014

Stem cell treatments take place in countries all around the world every day. Thousands of lives have already been saved, and advancements in this area of medicine means that future healthcare treatments look set to further prolong and improve life.

But specialist stem cell bank BioEden warn that there is a risk of thinking of stem cell therapy in terms of the future alone. 'The need to have a stem cell match is vital', says Group CEO Mr Tony Veverka. 'Without access to a stem cell match, the work of stem cell scientists could be at risk. That is the reason why BioEden was set up, to ensure that anyone could bank and have access to their own stem cells. We also wanted to ensure that the brilliant work being carried out by stem cell scientists and medical professionals could continue unhindered'.

BioEden's services are being promoted by Health Care Professionals including specialist insurance intermediaries, and dentists. This week to highlight Stem Cell Awareness week, members of their specialist teams will be on the road visiting dentists, schools and healthcare insurance companies.

'Let's make everyone aware of the opportunities they have to store their own cells during stem cell awareness week. Perhaps we need to re name it Stem Cell Self-Awareness week'.

For more information visit http://www.bioeden.com

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BioEden the specialist tooth stem cell bank plan to shake up public perception as Stem Cell Awareness week takes hold.

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GenapSys has appointed Mark Pratt as vice president of product development. Most recently, Pratt was senior director of accuracy R&D at Personalis. Before that, he served at Illumina, where he was responsible for engineering research, including holding leadership positions in the development of the HiSeq and MiSeq systems.

The Personalized Medicine Coalition announced that Daryl Pritchard will be its new VP of science policy, in charge of promoting the organization's science-related policies and of raising awareness of precision healthcare issues among policymakers, providers, and patients. Before joining PMC, Pritchard was director of policy research at the National Pharmaceutical Council; director of research programs advocacy and personalized medicine at the Biotechnology Industry Organization; and the director of government affairs for the American Association for Dental Research.

Nabsys has appointed Steve Lombardi to president, CEO, and to its board of directors. Previously, he was CEO of Real Time Genomics, and before that he was CEO of Helicos BioSciences. He has also served as senior vice president of Affymetrix and vice president of genetic analysis at Applied Biosystems.

Roche said this week that Arthur Levinson has resigned from its board of directors, effective immediately. The drugmaker said Levinson, who was chairman and CEO at Genentech from 1999 to 2014, made the decision to avoid any conflict with his post as CEO at Calico, a Google-backed startup. Levinson has served on Roche's board since 2010.

Sanford Burnham Medical Research Institute said this week it has named Perry Nisen as its CEO and as holder of the Donald Bren Chief Executive Chair. Nisen joins Sanford Burnham from GlaxoSmithKline, where he was senior VP of science and innovation.

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Genetic Technologies Reports 'Consistent' Q1 BREVAGen Volume, Launches Second Generation Dx

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PUBLIC RELEASE DATE:

6-Oct-2014

Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News @LiebertOnline

New Rochelle, NY, October 6, 2014While poker is a game of chance, there is skill and decision-making involved, and the quality of those decisions depends on both knowledge of the game and the ability to control one's emotions. The results of a new study that evaluates emotionality, experience level, and success among online poker players are presented 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 November 6, 2014.

In the article "Experienced Poker Players are Emotionally Stable," Michael Laakasuo, Jussi Palomki, and Mikko Salmela, University of Helsinki, Finland, propose that emotional stability is both a predictive and enabling factor for becoming an experienced and successful poker player. The authors' assessments of emotionality also led to the conclusion that poker players who prefer live play rather than online games are more likely to be extroverted and open to experiences.

"Previous studies have shown that online poker players tend to be introverted individuals and that those who perform better at poker are less neurotic," says Editor-in-Chief Brenda K. Wiederhold, PhD, MBA, BCB, BCN, Interactive Media Institute, San Diego, California. "This study, however, takes research a step further by comparing online and offline players."

###

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

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PUBLIC RELEASE DATE:

6-Oct-2014

Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News @LiebertOnline

New Rochelle, NY, October 6, 2014Self-management of diabetes, including medication, nutrition, and lifestyle strategies, is essential for optimal glycemic control and minimizing complications of the disease. Education to teach and improve self-management skills is critical for success and, when delivered via the Internet, can lead to better glycemic control and enhanced diabetes knowledge compared to usual care, according to a Review article in Diabetes Technology & Therapeutics (DTT), a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the DTT website at http://online.liebertpub.com/doi/full/10.1089/dia.2014.0155 until November 6, 2014.

Katherine Pereira, DNP, Beth Phillips, MSN, Constance Johnson, PhD, and Allison Vorderstrasse DNSc, Duke University School of Nursing (Durham, NC), review various methods of delivering diabetes education via the Internet and compare their effectiveness in improving diabetes-related outcomes. In the article "Internet Delivered Diabetes Self-Management Education: A Review" the authors describe some of the benefits of this method of educating patients, including ease of access and the ability to self-pace through the materials.

"With the increasing prevalence of diabetes globally and a decreasing number of available healthcare providers, alternative approaches and better education in self-management are necessary to improve diabetes outcomes," says DTT Editor-in-Chief Satish Garg, MD, Professor of Medicine and Pediatrics at the University of Colorado Denver. "This study evaluates the role of Internet-based self-management in diabetes-related outcomes."

###

About the Journal

Diabetes Technology & Therapeutics (DTT) is a monthly peer-reviewed journal that covers new technology and new products for the treatment, monitoring, diagnosis, and prevention of diabetes and its complications. Led by Editor-in-Chief Satish Garg, MD, the Journal covers topics that include noninvasive glucose monitoring, implantable continuous glucose sensors, novel routes of insulin administration, genetic engineering, the artificial pancreas, measures of long-term control, computer applications for case management, telemedicine, the Internet, and new medications. Tables of contents and a free sample issue may be viewed on the Diabetes Technology & Therapeutics (DTT) website at http://www.liebertpub.com/DTT. DTT is the official journal of the Advanced Technologies & Treatments for Diabetes (ATTD) Conference.

About ATTD

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PUBLIC RELEASE DATE:

6-Oct-2014

Contact: Robert Perkins perkinsr@usc.edu 213-740-9226 University of Southern California @USC

Imagine being able to take a pill that lets you eat all of the ice cream, cookies, and cakes that you wanted without gaining any weight.

New research from USC suggests that dream may not be impossible. A team of scientists led by Sean Curran of the USC Davis School of Gerontology and the Keck School of Medicine of USC found a new way to suppress the obesity that accompanies a high-sugar diet, pinning it down to a key gene that pharmaceutical companies have already developed drugs to target.

So far, Curran's work has been solely on the worm Caenorhabditis elegans and human cells in a petri dish but the genetic pathway he studied is found in almost all animals from yeast to humans. Next, he plans to test his findings in mice.

Curran's research is outlined in a study that will be published on Oct. 6 by Nature Communications.

Building on previous work with C. elegans, Curran and his colleagues found that certain genetic mutants those with a hyperactive SKN-1 gene could be fed incredibly high-sugar diets without gaining any weight, while regular C. elegans ballooned on the same diet.

"The high-sugar diet that the bacteria ate was the equivalent of a human eating the Western diet," Curran said, referring to the diet favored by the Western world, characterized by high-fat and high-sugar foods, like burgers, fries and soda.

The SKN-1 gene also exists in humans, where it is called Nrf2, suggesting that the findings might translate, he said. The Nrf2 protein, a "transcription factor" that binds to a specific sequence of DNA to control the ability of cells to detox or repair damage when exposed to chemically reactive oxygen (a common threat to cells' well being), has been well studied in mammals.

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Genetics in Motion: Putting T Cells in Their Place
The mysterious onset of type 1 diabetes may have to do with what #39;s in your genes. Studies of twins show that if one twin has type 1 diabetes, the other has a...

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Genetics - The Carpet Crawlers - Coliseo - 04/10/2014
Genetics en el Teatro Coliseo el sabado 4/10/2014. Tributo al album "The lamb lies down on Broadway" en su 40 aniversario. Aqui en "The Carpet Crawlers" Imagenes: Panasonic FZ200 Audio: Zoom H6.

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Genetics - Firth of Fifth - Coliseo - 04/10/2014
Genetics en el Teatro Coliseo el sabado 4/10/2014. Tributo al album "The lamb lies down on Broadway" en su 40 aniversario. Esto es parte del encore, del disco "Selling England..." el tema...

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Genetics Promo
Covering all the fundamental facets of genetics, including the biological construction of genes and how they work, how dominant and recessive genes influence the passing on of particular inherited...

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Minecraft: Glacticraft 2 Ep.6 (LT) "Advanced Genetics"
Ai, kad irjote!!!!! Nepamirkite LIKE, SHARE, COMMENT IR SUBSCRIBE!!!!!! Mod #39;ai: Galacticraft: http://micdoodle8.com/mods/galacticraft/downloads Advanced Genetics Applied Energisti...

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F#ck Your Genetics
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Foundation Genetics Logo Reveal

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WASHINGTON Its no secret that if your dad is tall and your mother is tall, you are probably going to be tall. But fully understanding the genetics of height has been a big order for scientists.

Researchers on Sunday unveiled what they called the biggest such study to date, analyzing genome data from more than a quarter million people to identify nearly 700 genetic variants and more than 400 genome regions linked to height.

How tall or short a person becomes is estimated to be 80 percent genetic, with nutrition and other environmental factors accounting for the rest. The worlds people on average have become taller over the past few generations because of factors including improved nutrition.

We study height for two main reasons, said Dr. Joel Hirschhorn, a geneticist and pediatric endocrinologist at Boston Childrens Hospital and the Broad Institute of Massachusetts Institute of Technology and Harvard University.

For over 100 years, its been a great model for studying the genetics of diseases like obesity, diabetes, asthma that are also caused by the combined influence of many genes acting together. So by understanding how the genetics of height works, we can understand how the genetics of human disease works, he said.

In addition, short stature in childhood is a major clinical issue for pediatric endocrinologists. Knowing genes and their variants that are important for height eventually may help doctors diagnose children who have a single major underlying cause for short stature, Hirschhorn added.

The international team of researchers analyzed data from the genomes of 253,288 people of European ancestry, all from Europe, North America and Australia. They perused about 2 million common genetic variants in these individuals and identified 697 gene variants in 424 gene regions as related to height.

Many genes pinpointed in the study, published in the journal Nature Genetics, are probably important regulators of skeletal growth, but were not previously known to be involved, the researchers said.

Some were related to collagen, a component of bone; a component of cartilage called chondroitin sulfate; and growth plates, the area of growing tissue near the ends of the bodys long bones.

The researchers said there is much more to learn.

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Study on genetics of height provides elusive answers

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Gene therapy (1 of 5)
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Xenon Pharmaceuticals, an early-stage biotech with a gene therapy discovery platform for rare diseases, announced terms for its IPO on Monday. The Burnaby, Canada-based company plans to raise $44 million by offering 4.0 million shares at a price range of $10 to $12. At the midpoint of the proposed range, Xenon Pharmaceuticals would command a market value of $159 million.

Xenon has a number of collaboration and licensing agreements with large pharmaceuticals including Teva, Genentech and Merck for its preclinical research.The company's discovery platform was used to develop uniQure's Glybera treatment for orphan disease lipoprotein lipase deficiency, the first gene therapy approved in the EU. February IPO uniQure ( QURE ) priced above its range but ended the first day down 14% and now trades 40% below the IPO price.Xenon is eligible to receive mid single-digit royalties on net sales of Glybera.

Teva is in Phase 2 trials for a gene therapy discovered by Xenon that is being developed to treat osteoarthritis. Genentech was cleared to begin a Phase 1 trial for Xenon's pain treatment and Merck is in preclinical development for cardiovascular disease. Xenon also has a variety of preclinical therapies for both orphan diseases (such as Dravet Syndrome) and large-market conditions (including acne).

Primary shareholders include Medpace, Lipterx, InterWest Partners, Fidelity, Invesco and CEO Simon Pimstone. Collaboration partner Teva ( TEVA ) intends to purchase $10 million worth of shares on the offering (23% of float at the midpoint) and Genentech (owned by Roche) plans to invest $5 million in a concurrent private placement at the offer price.

Xenon Pharmaceuticals, which was founded in 1996, plans to list on the NASDAQ under the symbol XENE. Jefferies and Wells Fargo Securities are the joint bookrunners on the deal. It is expected to price during the week of October 13, 2014.

Investment Disclosure: The information and opinions expressed herein were prepared by Renaissance Capital's research analysts and do not constitute an offer to buy or sell any security. Renaissance Capital, the Renaissance IPO ETF (symbol: IPO) or the Global IPO Fund (symbol: IPOSX) , may have investments in securities of companies mentioned.

The views and opinions expressed herein are the views and opinions of the author and do not necessarily reflect those of The NASDAQ OMX Group, Inc.

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Researchers at Cincinnati Childrens Hospital Medical Center have discovered a new gene and cell therapy that could treat a rare lung disease in children.

In the study, published in the journal Nature, researchers found that transplanting pulmonary macrophages immune cells into the lungs of mice corrected hereditary pulmonary alveolar proteinosis (hPAP).

The lung disease is caused by a build-up of surfactant, an oily substance in the air sacs of the lungs, which results in reduced lung function and eventually failure. The condition is the opposite of a common condition in premature babies, whose lungs are at a higher risk of collapsing because their air sacs will not stay open. Children with hPAP, on the other hand, have such high levels of surfactants that the childrens air sacs overinflate, and they drown internally as a result.

Between 2,000 and 3,000 children in the U.S. have hPAP, senior study author Bruce Trapnell, a physician in the division of neonatology and pulmonary biology at Cincinnati Children's Hospital Medical Center, told FoxNews.com.

The only available therapy for the rare disease whole-lung lavage is a difficult procedure thats invasive, requires anesthesia and involves mechanical ventilation, Trapnell said. For the surgery, doctors must attach a breathing tube to one lung and fill the other with salt water. A few days later, the procedure is repeated on the opposite lung.

Its like trying to wash butter out of a sponge by squirting it with a garden hose, Trapnell said.

Searching for a different type of therapy, researchers studied transplantation of naturally healthy macrophages or gene-corrected macrophages into the lungs of mice with hPAP. The therapy corrected the disease in mice for at least one year and prevented disease-related death.

Researchers are planning clinical trials of macrophage transplantation, but they noted that questions remain. Previous research using bone marrow transplantation was successful in animal models, but failed in human trials.

We have to address how many cells to transfer, and how the human body processes these cells," study co-author Takuji Suzuki, a scientist in the division of neonatology and pulmonary biology at Cincinnati Childrens, told FoxNews.com.

Researchers hope to begin the clinical health study in two to three years.

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19 hours ago New genetic barcoding technology allows scientists to identify differences in origin between individual blood cells. Credit: Camargo Lab

A 7-year-project to develop a barcoding and tracking system for tissue stem cells has revealed previously unrecognized features of normal blood production: New data from Harvard Stem Cell Institute scientists at Boston Children's Hospital suggests, surprisingly, that the billions of blood cells that we produce each day are made not by blood stem cells, but rather their less pluripotent descendants, called progenitor cells. The researchers hypothesize that blood comes from stable populations of different long-lived progenitor cells that are responsible for giving rise to specific blood cell types, while blood stem cells likely act as essential reserves.

The work, supported by a National Institutes of Health Director's New Innovator Award and published in Nature, suggests that progenitor cells could potentially be just as valuable as blood stem cells for blood regeneration therapies.

This new research challenges what textbooks have long read: That blood stem cells maintain the day-to-day renewal of blood, a conclusion drawn from their importance in re-establishing blood cell populations after bone marrow transplantsa fact that still remains true. But because of a lack of tools to study how blood forms in a normal context, nobody had been able to track the origin of blood cells without doing a transplant.

Boston Children's Hospital scientist Fernando Camargo, PhD, and his postdoctoral fellow Jianlong Sun, PhD, addressed this problem with a tool that generates a unique barcode in the DNA of all blood stem cells and their progenitor cells in a mouse. When a tagged cell divides, all of its descendant cells possess the same barcode. This biological inventory system makes it possible to determine the number of stem cells/progenitors being used to make blood and how long they live, as well as answer fundamental questions about where individual blood cells come from.

"There's never been such a robust experimental method that could allow people to look at lineage relationships between mature cell types in the body without doing transplantation," Sun said. "One of the major directions we can now go is to revisit the entire blood cell hierarchy and see how the current knowledge holds true when we use this internal labeling system."

"People have tried using viruses to tag blood cells in the past, but the cells needed to be taken out of the body, infected, and re-transplanted, which raised a number of issues," said Camargo, who is a member of Children's Stem Cell Program and an associate professor in Harvard University's Department of Stem Cell and Regenerative Biology. "I wanted to figure out a way to label blood cells inside of the body, and the best idea I had was to use mobile genetic elements called transposons."

A transposon is a piece of genetic code that can jump to a random point in DNA when exposed to an enzyme called transposase. Camargo's approach works using transgenic mice that possess a single fish-derived transposon in all of their blood cells. When one of these mice is exposed to transposase, each of its blood cells' transposons changes location. The location in the DNA where a transposon moves acts as an individual cell's barcode, so that if the mouse's blood is taken a few months later, any cells with the same transposon location can be linked back to its parent cell.

The transposon barcode system took Camargo and Sun seven years to develop, and was one of Camargo's first projects when he opened his own lab at the Whitehead Institute for Biomedical Research directly out of grad school. Sun joined the project after three years of setbacks, and accomplished an experimental tour de force to reach the conclusions in the Nature paper, which includes data on how many stem cells or progenitor cells contribute to the formation of immune cells in mouse blood.

With the original question of how blood arises in a non-transplant context answered, the researchers are now planning to explore many more applications for their barcode tool.

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Barcoding tool for stem cells: New technology that tracks the origin of blood cells challenges scientific dogma

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