Category Archives: Cell Medicine

PUBLIC RELEASE DATE:

4-Dec-2014

Contact: John Wallace wallacej@vcu.edu 804-628-1550 Virginia Commonwealth University @vcunews

Is the human immune system similar to the weather, a seemingly random yet dynamical system that can be modeled based on past conditions to predict future states? Scientists at VCU Massey Cancer Center's award-winning Bone Marrow Transplant (BMT) Program believe it is, and they recently published several studies that support the possibility of using next-generation DNA sequencing and mathematical modeling to not only understand the variability observed in clinical outcomes of stem cell transplantation, but also to provide a theoretical framework to make transplantation a possibility for more patients who do not have a related donor.

Despite efforts to match patients with genetically similar donors, it is still nearly impossible to predict whether a stem cell transplant recipient will develop potentially fatal graft-versus-host disease (GVHD), a condition where the donor's immune system attacks the recipient's body. Two studies recently published by the online journal Frontiers in Immunology explored data obtained from the whole exome sequencing of nine donor-recipient pairs (DRPs) and found that it could be possible to predict which patients are at greatest risk for developing GVHD and, therefore, in the future tailor immune suppression therapies to possibly improve clinical outcomes. The data provides evidence that the way a patient's immune system rebuilds itself following stem cell transplantation is representative of a dynamical system, a system in which the current state determines what future state will follow.

"The immune system seems chaotic, but that is because there are so many variables involved," says Amir Toor, M.D., member of the Developmental Therapeutics research program at Massey and associate professor in the Division of Hematology, Oncology and Palliative Care at the VCU School of Medicine. "We have found evidence of an underlying order. Using next-generation DNA sequencing technology, it may be possible to account for many of the molecular variables that eventually determine how well a donor's immune system will graft to a patient."

Toor's first study revealed a large and previously unmeasured potential for developing GVHD for which the conventional approach used for matching DRPs does not account. The conventional approach for donor-recipient compatibility determination uses human leucocyte antigen (HLA) testing. HLA refers to the genes that encode for proteins on the surface of cells that are responsible for regulating the immune system. HLA testing seeks to match DRPs who have similar HLA makeup.

Specifically, Toor and his colleagues used whole exome sequencing to examine variation in minor histocompatibility antigens (mHA) of transplant DRPs. These mHA are protein fragments presented on the HLA molecules, which are the receptors on cells' surface to which these fragments of degraded proteins from within a cell bind in order to promote an immune response. Using advanced computer-based analysis, the researchers examined potential interactions between the mHA and HLA and discovered a high level of mHA variation in HLA-matched DRPs that could potentially contribute to GVHD. These findings may help explain why many HLA-matched recipients experience GVHD, but why some HLA-mismatched recipients experience none remains a mystery. This seeming paradox is explained in a companion paper, also published in the journal Frontiers in Immunology. In this manuscript, the team suggests that by inhibiting peptide generation through immunosuppressive therapies in the earliest weeks following stem cell transplantation, antigen presentation to donor T cells could be diminished, which reduces the risk of GVHD as the recipients reconstitute their T-cell repertoire.

Following stem cell transplantation, a patient begins the process of rebuilding their T-cell repertoire. T cells are a family of immune system cells that keep the body healthy by identifying and launching attacks against pathogens such as bacteria, viruses or cancer. T cells have small receptors that recognize antigens. As they encounter foreign antigens, they create thousands of clones that can later be called upon to guard against the specific pathogen that presented the antigen. Over the course of a person's life, they will develop millions of these clonal families, which make up their T-cell repertoire and protect them against the many threats that exist in the environment.

This critical period where the patient rebuilds their immune system was the focus of the researchers' efforts. In previous research, Toor and his colleagues discovered a fractal pattern in the DNA of recipients' T-cell repertoires. Fractals are self-similar patterns that repeat themselves at every scale. Based on their data, the researchers believe that the presentation of minor histocompatability antigens following transplantation helps shape the development of T-cell clonal families. Thus, inhibiting this antigen presentation through immunosuppressive therapies in patients who have high mHA variation can potentially reduce the risk of GVHD by influencing the development of their T-cell repertoire. This is backed by data from clinical studies that show immune suppression soon after transplantation improves outcomes in unrelated DRPs.

Link:
Predicting the storm: Can computer models improve stem cell transplantation?

- As improved R&D climate supports development, stem cell therapeutics market expected to boom globally

KUALA LUMPUR, Malaysia, Dec. 2, 2014 /PRNewswire/ -- Stem cells have the potential to transform healthcare by enabling the cost-effective treatment of many conditions that currently have poor treatment options. This will be particularly important for the rapidly growing aged population as well as the rising proportion of patients with neurological and chronic conditions. Stem cells may enable regenerative treatments that avoid traditional drugs, devices and surgery for these patient groups.

New analysis from Frost & Sullivan, Analysis of the Global Stem Cell Market, finds that the market earned revenues of US$40.01 billion in 2013 and estimates this to nearly triple to US$117.66 billion in 2018 at a compound annual growth rate of 24.1 percent. The study covers human adult and embryonic stem cells. While North America is the market leader with more than half of the global stem cell market share, the Asia-Pacific is expected to record the highest compound annual growth rate (CAGR) during the forecast period. In fact, the APAC stem cell market, which was valued at US$5.60 billion in 2013, is projected to increase to US$18.71 billion by 2018.

For complimentary access to more information on this research, please visit: http://corpcom.frost.com/forms/APAC_PR_DJeremiah_P805-52_10Nov14.

"The overall R&D funding for stem cell research has increased significantly in the past 5 to 10 years and will reach desired heights in the years to come," said Frost & Sullivan Healthcare Consultant Sanjeev Kumar. "The number of venture capital firms investing in stem cell research has risen and government funding agencies have begun to acknowledge the future benefits of the stem cell industry."

While the stiff regulations that previously guarded stem cell research have begun to relax, other legal and ethical issues continue to hamper research. For instance, research institutes that adopt policies addressing concerns surrounding the use of human embryonic tissues may hinder the overall research process, which usually involves several collaborative enterprises. Other market challenges include insurers' reluctance to pay for expensive stem cell therapies and the likelihood that patients themselves will be unable to afford these treatments.

"The global stem cell industry is in an early stage of development, with a handful of small and large participants," noted Kumar. "In the near future, mergers, acquisitions and collaborations will accelerate growth, with multinational companies and larger pharmaceutical companies playing a key role in facilitating these activities. As the market evolves, standards and new regulatory frameworks are expected to ease market challenges."

In the meantime, the market's growth potential is being underlined by promising results from clinical trials and the escalating importance of stem cell banking services across the globe. Eventually, the technology is expected to play a crucial function in various areas including neurological disorders, orthopaedics, cancer, haematological disorders, injuries and wound care, cardiovascular diseases, spinal cord injuries, diabetes, incontinence and liver disorders. Therapeutics manufacturers are also likely to explore the relevance of stem cells in other areas and combine them with existing applications to enhance treatment options.

Analysis of the Global Stem Cell Market is part of the Life Sciences (http://www.lifesciences.frost.com) Growth Partnership Service program. Frost & Sullivan's related studies include: Analysis of the Global Infectious Disease Diagnostics Market, Western European Companion Diagnostics Market, Analysis of the Global Biosimilars Market, and Analysis of the US Retinal Therapeutics Market. All studies included in subscriptions provide detailed market opportunities and industry trends evaluated following extensive interviews with market participants.

About Frost & Sullivan

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Stem Cells to Revolutionise the Future of Diagnostic and Therapeutic Medicine

MIAMI (PRWEB) December 01, 2014

GlobalStemCellsGroup.com has announced plans to team with Portal Medestetica, the largest physician portal in Lain America, to launch Portalstemcells.com, a new portal dedicated to providing physicians in Spain and Latin America with relevant information, clinical research news and products relating to stem cells and regenerative medicine.

The new collaboration between Global Stem Cells Group and Portal Medestetica will answer a growing need to expand the reach of high-impact news, studies and breakthroughs, and significantly advance the clinical utilization of stem cell research and clinical trials throughout Latin America. The Portalstemcells.com site is designed to help promote the latest state-of-the-art developments in regenerative medicine as they become available, and to share educational content with physicians throughout the region.

Portalstemcells.com will be the ideal vehicle to promote education and cutting-edge science throughout the region, says Ricardo de Cubas, founder of Global Stem Cells Group. The potential of regenerative medicine and stem cells therapies inspiring the medical community to find real opportunities to repair or replace tissue damaged from disease, relieve pain and provide the potential for curing chronic diseases where no cure existed before.

The Portalstemcells.com site is aimed at fostering growth and ethical development in the fast-moving field of stem cell medicine by filling a gap in the resources available throughout Latin America. The goal is to elevate the delivery of stem cell science in order to impact the lives of many patients worldwide.

For more information visit the Global Stem Cells website, email bnovas(at)regenestem(dot)com, or call 305-224-1858.

About the Global Stem Cells Group:

Global Stem Cells Group, Inc. is the parent company of six wholly owned operating companies dedicated entirely to stem cell research, training, products and solutions. Founded in 2012, the company combines dedicated researchers, physician and patient educators and solution providers with the shared goal of meeting the growing worldwide need for leading edge stem cell treatments and solutions.

With a singular focus on this exciting new area of medical research, Global Stem Cells Group and its subsidiaries are uniquely positioned to become global leaders in cellular medicine.

Global Stem Cells Groups corporate mission is to make the promise of stem cell medicine a reality for patients around the world. With each of GSCGs six operating companies focused on a separate research-based mission, the result is a global network of state-of-the-art stem cell treatments.

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Global Stem Cells Group and Portal Medestetica to Launch Latin American Stem Cell Portal

Okayama City, Japan (PRWEB UK) 2 December 2014

Researchers at Okayama University Graduate School of Medicine and Kyorin University School of Medicine have successfully generated a kidney-like structure from just a single cell.

It has been predicted that the kidney will be among the last organs successfully regenerated in vitro due to its complex structure and multiple functions, states Shinji Kitamura, Hiroyuki Sakurai and Hirofumi Makino at the beginning of their latest report, before continuing to describe results suggesting a far more positive prognosis for the pace of kidney regeneration research. Despite the anatomical challenges posed by the kidney anatomy and the complexities understood from embryonic kidney development processes, the researchers have demonstrated that kidney-like structures can be generated from just a single adult kidney stem cell.

In embryos, kidney development requires two types of primordial cells cells at the earliest stage of development. However by generating kidney-like structures from a single type of kidney stem cell the researchers provide evidence for differences in the organ development in adults and embryos.

Kitamura, Sakurai and Makino researchers from Okayama and Kyorin Universities - took kidney stem cells from the different kidney components of microdissected adult rats and grew them in culture. A method for growing three-dimensional cell clusters showed that kidney-like structures could form so long as the initial cell cluster was large enough.

The minimum cluster size required might suggest that not all the kidney stem cells have stem cell characteristics. Therefore the researchers cloned kidney stem cells and confirmed that kidney-like structures still formed from the clusters of clone cells after a few weeks.

The researchers add, Although the physiological roles of such cells are currently unclear, analogous cells in the adult human kidney would be a valuable resource for the regeneration of kidneys in vitro.

Background Kidney structure There are more than a dozen distinct types of cell in the kidneys. The basic structural unit of the kidney is the nephron, which filters the blood to regulate the concentration of water and soluble substances such as sodium salts. Each nephron comprises several well-defined segments: the glomerulus, the proximal tubule, the loop of Henle, the distal tube and the collecting duct.

In embryo kidney organogenesis two primordial cell types are required to differentiate into all the different cell types in the kidney: metanephric mesenchymal cells and uteric bud cells. Kitamura, Sakurai and Makino produced kidney cells that could differentiate into a kidney-like structure without these primordial cell types, suggesting these are adult kidney stem cells.

Obtaining kidney stem cells The researchers microdissected adult rat kidneys into segments from the glomeruli, proximal convoluted tubule (S1/PCT), proximal straight tubule (S2, S3), medullary thick ascending limb of Henles loop and the collecting duct. They then grew the cells on mouse mesenchymal cells. While there is no known single biomarker for adult kidney stem cells, immunohistochemical anaylysis identified a number of markers in the kidney stem cells- that are found in embryonic or adult kidneys.

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Kidney organ regeneration research leaps forward

November 25, 2014

Provided by Peter Bracke, UCLA

Understanding the self-replication mechanisms is critical for improving stem cell therapies for blood-related diseases and cancers

Led by Dr. Hanna Mikkola, a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, UCLA scientists have discovered a protein that is integral to the self-replication of hematopoietic stem cells during human development.

The discovery lays the groundwork for researchers to generate hematopoietic stem cells in the lab that better mirror those that develop in their natural environment. This could in turn lead to improved therapies for blood-related diseases and cancers by enabling the creation of patient-specific blood stem cells for transplantation.

The findings are reported online ahead of print in the journal Cell Stem Cell.

Researchers have long been stymied in their efforts to make cell-based therapies for blood and immune diseases more broadly available, because of an inability to generate and expand human hematopoietic stem cells (HSCs) in lab cultures. They have sought to harness the promise of pluripotent stem cells (PSCs), which can transform into almost any cell in the human body, to overcome this roadblock. HSCs are the blood-forming cells that serve as the critical link between PSCs and fully differentiated cells of the blood system. The ability of HSCs to self-renew (replicate themselves) and differentiate to all blood cell types, is determined in part by the environment that the stem cell came from, called the niche.

In the five-year study, Mikkola, Dr. Sacha Prashad and Dr. Vincenzo Calvanese, members of Mikkolas lab and lead authors of the study, investigated a HSC surface protein called GPI-80. They found that it was produced by a specific subpopulation of human fetal hematopoietic cells that were the only group that could self-renew and differentiate into various blood cell types. They also found that this subpopulation of hematopoietic cells was the sole population able to permanently integrate into and thrive within the blood system of a recipient mouse.

Mikkola and colleagues further discovered that GPI-80 identifies HSCs during multiple phases of human HSC development and migration. These include the early first trimester of fetal development when newly generated human hematopoietic stem cells can be found in the placenta, and the second trimester when HSCs are actively replicating in the fetal liver and the fetal bone marrow.

We found that whatever HSC niche we investigated, we could use GPI-80 as the best determinant to find the stem cell as it was being generated or colonized different hematopoietic tissues, said Mikkola, associate professor of molecular, cell and development biology at UCLA and also a member of the Jonsson Comprehensive Cancer Center. Moreover, loss of GPI-80 caused the stem cells to differentiate into mature blood cells rather than HSCs. This essentially tells us that GPI-80 must be present to make HSCs. We now have a very unique marker for investigating how human hematopoietic cells develop, migrate and function.

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UCLA Researchers Identify Protein Key To The Development Of Blood Stem Cells

Cambridge stem cell pioneer DefiniGEN is in China this week showcasing technology that arguably gives the UK a world lead in countering liver and pancreatic cancer.

The young company is seeking Chinese partners to broaden the reach of the technology which holds a potentially significant payback in regenerative medicine.

With US global stem cell innovator Roger Pedersen among its technology founders, DefiniGEN was founded two years ago to commercialise a stem cell production platform developed at the University of Cambridge.

The platform generates human liver and pancreatic cell types using Nobel Prize winning human Induced Pluripotent Stem Cell (iPSC) technology.

DefiniGEN is visiting Shanghai and Beijing on a trade mission organised by UKTI East of England in partnership with the China-Britain Business Council.

The company is actively looking to partner with Life Science distributors and pharmaceutical drug discovery companies in China. CEO Dr Marcus Yeo and Dr Masashi Matsunaga business development manager for Asia Pacific - are spearheading the initiative.

The visit includes a range of medically-focused ventures from one to one meetings with key players to presentations at UK consulates.

DefiniGEN cells are provided to the drug discovery sector for use in lead optimisation and toxicity programmes.

The companys OptiDIFF platform produces validated libraries of disease-modelled human liver cells for a range of diseases. The phenotype (the composite of an organisms traits) and pathology of the diseases is pre-confirmed in the cells.

The technology provides pharmaceutical companies with more predictive in vitro cell products enabling the development of safer and more effective treatments.

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Cambridge stem cell pioneer targets China partners

PUBLIC RELEASE DATE:

20-Nov-2014

Contact: Scott LaFee slafee@ucsd.edu 619-543-5232 University of California - San Diego @UCSanDiego

While investigating a rare genetic disorder, researchers at the University of California, San Diego School of Medicine have discovered that a ubiquitous signaling molecule is crucial to cellular reprogramming, a finding with significant implications for stem cell-based regenerative medicine, wound repair therapies and potential cancer treatments.

The findings are published in the Nov. 20 online issue of Cell Reports.

Karl Willert, PhD, assistant professor in the Department of Cellular and Molecular Medicine, and colleagues were attempting to use induced pluripotent stem cells (iPSC) to create a "disease-in-a-dish" model for focal dermal hypoplasia (FDH), a rare inherited disorder caused by mutations in a gene called PORCN. Study co-authors V. Reid Sutton and Ignatia Van den Veyver at Baylor College of Medicine had published the observation that PORCN mutations underlie FDH in humans in 2007.

FDH is characterized by skin abnormalities such as streaks of very thin skin or different shades, clusters of visible veins and wartlike growths. Many individuals with FDH also suffer from hand and foot abnormalities and distinct facial features. The condition is also known as Goltz syndrome after Robert Goltz, who first described it in the 1960s. Goltz spent the last portion of his career as a professor at UC San Diego School of Medicine. He retired in 2004 and passed away earlier this year.

To their surprise, Willert and colleagues discovered that attempts to reprogram FDH fibroblasts or skin cells with the requisite PORCN mutation into iPSCs failed using standard methods, but succeeded when they added WNT proteins - a family of highly conserved signaling molecules that regulate cell-to-cell interactions during embryogenesis.

"WNT signaling is ubiquitous," said Willert. "Every cell expresses one or more WNT genes and every cell is able to receive WNT signals. Individual cells in a dish can grow and divide without WNT, but in an organism, WNT is critical for cell-cell communication so that cells distinguish themselves from neighbors and thus generate distinct tissues, organs and body parts."

WNT signaling is also critical in limb regeneration (in some organisms) and tissue repair.

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Signaling molecule crucial to stem cell reprogramming

PUBLIC RELEASE DATE:

20-Nov-2014

Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center @sumedicine

Mouse cells and tissues created through nuclear transfer can be rejected by the body because of a previously unknown immune response to the cell's mitochondria, according to a study in mice by researchers at the Stanford University School of Medicine and colleagues in Germany, England and at MIT.

The findings reveal a likely, but surmountable, hurdle if such therapies are ever used in humans, the researchers said.

Stem cell therapies hold vast potential for repairing organs and treating disease. The greatest hope rests on the potential of pluripotent stem cells, which can become nearly any kind of cell in the body. One method of creating pluripotent stem cells is called somatic cell nuclear transfer, and involves taking the nucleus of an adult cell and injecting it into an egg cell from which the nucleus has been removed.

The promise of the SCNT method is that the nucleus of a patient's skin cell, for example, could be used to create pluripotent cells that might be able to repair a part of that patient's body. "One attraction of SCNT has always been that the genetic identity of the new pluripotent cell would be the same as the patient's, since the transplanted nucleus carries the patient's DNA," said cardiothoracic surgeon Sonja Schrepfer, MD, PhD, a co-senior author of the study, which will be published online Nov. 20 in Cell Stem Cell.

"The hope has been that this would eliminate the problem of the patient's immune system attacking the pluripotent cells as foreign tissue, which is a problem with most organs and tissues when they are transplanted from one patient to another," added Schrepfer, who is a visiting scholar at Stanford's Cardiovascular Institute. She is also a Heisenberg Professor of the German Research Foundation at the University Heart Center in Hamburg, and at the German Center for Cardiovascular Research.

Possibility of rejection

A dozen years ago, when Irving Weissman, MD, professor of pathology and of developmental biology at Stanford, headed a National Academy of Sciences panel on stem cells, he raised the possibility that the immune system of a patient who received SCNT-derived cells might still react against the cells' mitochondria, which act as the energy factories for the cell and have their own DNA. This reaction could occur because cells created through SCNT contain mitochondria from the egg donor and not from the patient, and therefore could still look like foreign tissue to the recipient's immune system, said Weissman, the other co-senior author of the paper. Weissman is the Virginia and D.K. Ludwig Professor for Clinical Investigation in Cancer Research and the director of the Stanford Institute for Stem Cell Biology and Regenerative Medicine.

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Pluripotent cells created by nuclear transfer can prompt immune reaction, researchers find

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Newswise Delivering stem cell factor directly into damaged heart muscle after a heart attack may help repair and regenerate injured tissue, according to a study led by researchers from Icahn School of Medicine at Mount Sinai presented November 18 at the American Heart Association Scientific Sessions 2014 in Chicago, IL.

Our discoveries offer insight into the power of stem cells to regenerate damaged muscle after a heart attack, says lead study author Kenneth Fish, PhD, Director of the Cardiology Laboratory for Translational Research, Cardiovascular Research Center, Mount Sinai Heart, Icahn School of Medicine at Mount Sinai.

In the study, Mount Sinai researchers administered stem cell factor (SCF) by gene transfer shortly after inducing heart attacks in pre-clinical models directly into damaged heart tissue to test its regenerative repair response. A novel SCF gene transfer delivery system induced the recruitment and expansion of adult c-Kit positive (cKit+) cardiac stem cells to injury sites that reversed heart attack damage. In addition, the gene therapy improved cardiac function, decreased heart muscle cell death, increased regeneration of heart tissue blood vessels, and reduced the formation of heart tissue scarring.

It is clear that the expression of the stem cell factor gene results in the generation of specific signals to neighboring cells in the damaged heart resulting in improved outcomes at the molecular, cellular, and organ level, says Roger J. Hajjar, MD, senior study author and Director of the Cardiovascular Research Center at Mount Sinai. Thus, while still in the early stages of investigation, there is evidence that recruiting this small group of stem cells to the heart could be the basis of novel therapies for halting the clinical deterioration in patients with advanced heart failure.

cKit+ cells are a critical cardiac cytokine, or protein receptor, that bond to stem cell factors. They naturally increase after myocardial infarction and through cell proliferation are involved in cardiac repair.

According to researchers there has been a need for the development of interventional strategies for cardiomyopathy and preventing its progression to heart failure. Heart disease is the number one cause of death in the United States, with cardiomyopathy or an enlarged heart from heart attack or poor blood supply due to clogged arteries being the most common causes of the condition. In addition, cardiomyopathy causes a loss of cardiomyocyte cells that control heartbeat, and changes in heart shape, which lead to the hearts decreased pumping efficiency.

Our study shows our SCF gene transfer strategy can mobilize a promising adult stem cell type to the damaged region of the heart to improve cardiac pumping function and reduce myocardial infarction sizes resulting in improved cardiac performance and potentially increase long-term survival and improve quality of life in patients at risk of progressing to heart failure, says Dr. Fish.

This study adds to the emerging evidence that a small population of adult stem cells can be recruited to the damaged areas of the heart and improve clinical outcomes, says Dr. Hajjar.

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Delivery of Stem Cells into Heart Muscle After Heart Attack May Enhance Cardiac Repair and Reverse Injury

PUBLIC RELEASE DATE:

13-Nov-2014

Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center @sumedicine

A protein that plays a critical role in preventing the development of many types of human cancers has been shown also to inhibit a vital stem cell property called pluripotency, according to a study by researchers at the Stanford University School of Medicine.

Blocking expression of the protein, called retinoblastoma, in mouse cells allowed the researchers to more easily transform them into what are known as induced pluripotent stem cells, or iPS cells. Pluripotent is a term used to describe a cell that is similar to an embryonic stem cell and can become any tissue in the body.

The study provides a direct and unexpected molecular link between cancer and stem cell science through retinoblastoma, or Rb, one of the best known of a class of proteins called tumor suppressors. Although Rb has long been known to control the rate of cell division, the researchers found that it also directly binds and inhibits the expression of genes involved in pluripotency.

"We were very surprised to see that retinoblastoma directly connects control of the cell cycle with pluripotency," said Julien Sage, PhD, associate professor of pediatrics and of genetics. "This is a completely new idea as to how retinoblastoma functions. It physically prevents the reacquisition of stem cellness and pluripotency by inhibiting gene expression."

Marius Wernig, MD, associate professor of pathology, said, "The loss of Rb appears to directly change a cell's identity. Without the protein, the cell is much more developmentally fluid and is easier to reprogram into an iPS cell."

Wernig and Sage, both members of the Stanford Cancer Institute, share senior authorship of the study, which will be published online Nov. 13 in Cell Stem Cell. Postdoctoral scholar Michael Kareta, PhD, is the lead author.

Tumor Suppressor

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Tumor suppressor also inhibits key property of stem cells, Stanford researchers say