From Stem Cells to Stomachs: Scientists Generate 3D, Functioning Human Stomach Tissue

The human stomach can be a delicate organ. For example, even the healthiest stomach can be compromised by H. pylori bacteria—a tiny but ruthless pathogen which has shown to be linked to both peptic ulcer disease and stomach cancer.

The best way to study how an H. pylori infection leads to conditions like cancer would be to recreate that exact environment, right down to the stomach itself, in the lab. But that task has proven far more difficult than originally imagined.

Part of a miniature stomach grown in the lab, stained to reveal various cells found in normal human stomachs [Credit: Kyle McCracken]

Part of a miniature stomach grown in the lab, stained to reveal various cells found in normal human stomachs [Credit: Kyle McCracken]

But now, scientists at the Cincinnati Children’s Hospital Medical Center and the University of Cincinnati College of Medicine have successfully grown functional, human stomach tissue in a dish—the first time such a feat has been accomplished.

Further, they were then able to test how human stomach tissue reacts to an invasion by H. pylori—a huge leap forward toward one day developing treatments for potentially deadly stomach disease.

Reporting in today’s issue of the journal Nature, senior author Jim Wells describes his team’s method of turning human pluripotent stem cells into stomach cells, known as gastric cells. Wells explained the importance of their breakthrough in a news release:

“Until this study, no one had generated gastric cells from human pluripotent stem cells. In addition, we discovered how to promote formation of three-dimensional gastric tissue with complex architecture and cellular composition.”

The team called this stomach tissue gastric organoids, a kind of ‘mini-stomach’ that mimicked the major cellular processes of a normal, functioning human stomach. Developing a human model of stomach development—and stomach disease—has long been a goal among scientists and clinicians, as animal models of the stomach did not accurately reflect what would be happening in a human stomach.

In this study, the research team identified the precise series of steps that can turn stem cells into gastric cells. And then they set these steps in motion.

Over the course of a month, the team coaxed the formation of gastric organoids that measured less than 1/10th of one inch in diameter. But even with this small size, the team could view the cellular processes that drive stomach formation—and discover precisely what happens when that process goes awry.

But what most intrigued the researchers, which also included first author University of Cincinnati’s Kyle McCracken, was how quickly an H. pylori infection impacted the health of the stomach tissue.

“Within 24 hours, the bacteria had triggered biochemical changes in the organ,” said McCracken.

According to McCracken, as the H. pylori infection spread from cell to cell, the researchers also recorded the activation of c-Met, a gene known to be linked to stomach cancer—further elucidating the relationship between H. pylori and this form of stomach disease.

Somewhat surprisingly, little was known about how gastric cells play a role in obesity-related diseases, such as type 2 diabetes. But thanks to Wells, McCracken and the entire Cincinnati Children’s research team—we are that much closer to shedding light on this process.

Wells also credits his team’s reliance on years of preliminary data performed in research labs around the world with helping them reach this landmark:

“This milestone would not have been possible if it hadn’t been for previous studies from many other basic researchers on understanding embryonic organ development.”

Scientists Develop Stem Cell ‘Special Forces’ in order to Target, Destroy Brain Tumors

Curing someone of cancer is, in theory, a piece of cake: all you have to do is kill the cancer cells while leaving the healthy cells intact.

But in practice, this solution is far more difficult. In fact, it remains one of the great unsolved problems in modern oncology: how do you find, target and destroy each individual cancer cell in the body—while minimizing damage to the surrounding cells.

Encapsulated toxin-producing stem cells (in blue) help kill brain tumor cells in the tumor resection cavity (in green). [Credit: Khalid Shah, MS, PhD]

Encapsulated toxin-producing stem cells (in blue) help kill brain tumor cells in the tumor resection cavity (in green). [Credit: Khalid Shah, MS, PhD]

But luckily, Harvard Stem Cell Institute scientists at Massachusetts General Hospital may have finally struck gold: they have designed special, toxin-secreting stem cells that can target and destroy brain tumors. Their findings, which were performed in laboratory mice and which appear in the latest issue of the journal STEM CELLS, offer up an entirely unique method for eradicating deadly cancers.

Harvard Neuroscientist Khalid Shah, who led the study, explained in last Friday’s news release that the idea of engineering stem cells to kill cancer cells is not new—but there was a key difference in scientists’ ability to target individual cells vs. difficult-to-reach tumors, which is often the case with brain cancer:

“Cancer-killing toxins have been used with great success in a variety of blood cancers, but they don’t work as well in solid tumors because the cancers aren’t as accessible and the toxins have a short half-life.”

The solution, Shah and his team argued, was stem cells. Previously, Shah and his team discovered that stem cells could be used to circumvent these problems. The fact that stem cells continuously renew meant that they could also be used to continually deliver toxins to brain tumors.

“But first, we needed to genetically engineer stem cells that could resist being killed themselves by the toxins,” said Shah.

In this study, the research team introduced a small genetic change, or mutation, into the stem cells so that they become impervious to the toxin’s harmful effects. They then introduced a second mutation that allowed the stem cells to maintain and produce and secrete toxins throughout the cells’ lifetime—effectively giving it an unlimited supply of ammunition to use once it encountered the brain tumor.

They then employed a common technique whereby the toxins were tagged so that they only sought out and infected cancer cells—leaving healthy cells unscathed.

“We tested these stem cells in a clinically relevant mouse model of brain cancer,” Shah described. “After doing all of the molecular analysis and imaging to track the inhibition of protein synthesis within brain tumors, we do see the toxins kill the cancer cells and eventually prolonging the survival in animal models.”

While preliminary, these results are encouraging. As the team continues to refine their method of development and delivery, they are optimistic that they can bring their methods to clinical trial within the next five years.

October ICOC Board Meeting to Begin Soon

The October ICOC Board Meeting begins this morning in Los Angeles, CA.

The complete agenda can be found here, including a special Spotlight on Disease focusing on Retinitis Pigmentosa.

For those not able to attend, you are welcome to dial in!

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CIRM-Funded Scientists Make New Progress Toward Engineering a Human Esophagus

Creating tissues and organs from stem cells—often referred to as ‘tissue engineering’—is hard. But new research has discovered that the process may in fact be a little easier than we once thought, at least in some situations.

Engineered human esophageal tissue [Credit: The Saban Research Institute].

Engineered human esophageal tissue [Credit: The Saban Research Institute].

Last week, scientists at The Saban Research Institute of Children’s Hospital Los Angeles announced that the esophagus—the tube that transports food, liquid and saliva between the mouth and the stomach—can be grown inside animal models after injecting the right mix of early-stage, or ‘progenitor,’ esophageal cells.

These findings, published in the journal Tissue Engineering Part A, are an important step towards generating tissues and organs that have been damaged due to disease or—in some cases—never existed in the first place.

According to stem cell researcher Tracy Grikscheit, who led the CIRM-funded study, the researchers first implanted a biodegradable ‘scaffold’ into laboratory mice. They then injected human progenitor cells into the mice and watched as they first traveled to the correct location—and then began to grow. The ability to both migrate to the right location and differentiate into the right cell type, without the need for any external coaxing, is crucial if scientists are to successfully engineer such a critical type of tissue.

“Different progenitor cells can find the right ‘partner’ in order to grow into specific esophageal cell types—and without the need for [outside] growth factors,” explained Grikscheit in a news release. “This means that successful tissue engineering of the esophagus is simpler than we previously thought.”

Grikscheit, who is also a pediatric surgeon as Children’s Hospital Los Angeles, was particularly hopeful with how their findings might one day be used to treat children born with portions of the esophagus missing—as well as adults suffering from esophageal cancer, the fastest-growing cancer in the U.S.

“We have demonstrated that a simple and versatile, biodegradable polymer is sufficient for the growth of a tissue-engineered esophagus from human cells. This not only serves as a potential source of tissue, but also a source of knowledge—as there are no other robust models available for studying esophageal stem cell dynamics.”

Want to learn more about tissue engineering? Check out these video highlights from a recent CIRM Workshop on the field.

UCLA Study Suggests New Way to Mend a Broken Heart

When you suffer a heart attack, your heart-muscle cells become deprived of oxygen. Without oxygen, the cells soon whither and die—and are entombed within scar tissue. And once these cells die, they can’t be brought back to life.

But maybe—just maybe—there is another way to build new heart muscle. And if there is, scientists like Dr. Arjun Deb at the University of California, Los Angeles (UCLA), are hot on the trail to find it.

Scar forming cells (in red) in a region of the injured heart expressing blood vessel cell marker in green and thus appearing yellow (see arrows). This study observed that approximately a third of the scar-forming cells in the injured region of the heart adopted "blood vessel" cell-like characteristics. [Credit: Dr. Arjun Deb/Nature]

Scar forming cells (in red) in a region of the injured heart expressing blood vessel cell marker in green and thus appearing yellow (see arrows). This study observed that approximately a third of the scar-forming cells in the injured region of the heart adopted “blood vessel” cell-like characteristics. [Credit: Dr. Arjun Deb/Nature]

Published yesterday in the journal Nature, Deb and his team at UCLA’s Eli & Edythe Broad Center for Regenerative Medicine and Stem Cell Research have found some scar-forming cells in the heart have the ability to become blood vessel-forming cells—if given the proper chemical ‘boost.’

“It is well known that increasing the number of blood vessels in the injured heart following a heart attack improves its ability to heal,” said Deb. “We know that scar tissue in the heart is associated with poor prognosis. Reversing or preventing scar tissue from forming has been one of the major challenges in cardiovascular medicine.”

Tackling the ever-growing problem in heart disease can seem an almost insurmountable task. While heart disease claims more lives worldwide than any other disease, advances in modern medicine in recent decades mean that more and more people are surviving heart attacks, and living with what’s called ‘heart failure,’ for their hearts can no longer beat at full capacity, and they have trouble taking long walks or even going up a flight of stairs.

Transforming this scar tissue into functioning heart muscle has therefore been the focus of many research teams, including CIRM grantees such as Drs. Deepak Srivastava and Eduardo Marbán, who have each tackled the problem from different angles. Late last year, treatment first designed by Marbán and developed by Capricor Therapeutics got the green light for a Phase 2 Clinical Trial.

In this study, Deb and his team focused on scar-forming cells, called fibroblasts, and blood-vessel forming cells, called endothelial cells. Previously, experiments in mice revealed that many fibroblasts literally transformed into endothelial cells—and helped contribute to blood vessel formation in the injured area of the heart. The team noted this phenomenon has been called the mesenchymal-endothelial transition, or MEndoT.

In this study, the researchers identified the molecular mechanism behind MEndoT—and further identified a small molecule that can enhance this transition, thus boosting the formation of blood vessels in the injured heart. This study bolsters the idea of focusing on the creation of blood vessels as a way to help reverse damage caused by a heart attack. Said Deb:

“Our findings suggest the possibility of coaxing scar-forming cells in the heart to change their identity into blood vessel-forming cells, which could potentially be a useful approach to better heart repair.”

Cranking it Up to Eleven: Heightened Growth of Neural Stem Cells Linked to Autism-like Behavior

Autism is not one single disease but a suite of many, which is why researchers have long struggled to understand its underlying causes. Often referred to as the Autism Spectrum Disorders, autism has been linked to multiple genetic and environmental factors—different combinations of which can all result in autism or autistic-like behavior.

Could an unusual boost in neural stem cell growth during pregnancy be linked to autistim-like behavior in children?

Could an unusual boost in neural stem cell growth during pregnancy be linked to autitism-like behavior in children?

But as we first reported in last week’s Weekly Roundup, scientists at the University of California, Los Angeles (UCLA) have identified a new factor that can occur during pregnancy and that may be linked to the development of autism-like behavior. These results shed new light on a notoriously murky condition.

UCLA scientist Dr. Harley Kornblum led the study, which was published last week in the journal Stem Cell Reports.

In it, Kornblum and his team describe how inflammation in pregnant mice, known as ‘maternal inflammation’ caused a spike in the production of neural stem cells—cells that one day develop into mature brain cells, such as neurons and glia cells. This abnormal growth, the team argues, led to enlarged brains in the newborn mice and, importantly, autism-like behavior such as decreased vocalization and social behavior, as well as overall increase in anxiety and repetitive behaviors, such as grooming. As Kornblum explained in a news release:

“We have now shown that one way maternal inflammation could result in larger brains and, ultimately, autistic behavior is through the activation of the neural stem cells that reside in the brain of all developing and adult mammals.”

However, Kornblum notes that many environmental factors may cause inflammation during pregnancy—and the inflammation itself is not thought to directly cause autism.

“Autism is a complex group of disorders, with a variety of causes. Our study shows a potential way that maternal inflammation could be one of those contributing factors, even if it is not solely responsible, through interactions with known risk factors.”

These known risk factors include genetic mutations, such as those to a gene called PTEN, which have been shown to increase one’s risk for autism.

Further research by Kornblum’s team further clarified the connection between inflammation and neural stem cell overgrowth. Specifically, they noticed a series of chemical reactions, known as a molecular pathway, appeared to stimulate the growth of neural stem cells in the developing mice. The identification of pathways such as these are vital when exploring new types of therapies—because once you know the pathway’s role in disease, you can then figure out how to change it.

“The discovery of these mechanisms has identified new therapeutic targets for common autism-associated risk factors,” said Dr. Janel Le Belle, the paper’s lead author. “The molecular pathways that are involved in these processes are ones that can be manipulated and possibly even reversed pharmacologically.”

These findings also support previous clinical findings that the roots of autism likely begin in the womb and continue to develop after birth.

One key difference between this work and previous studies, however, was that most studies point to irregularities in the way that neurons are connected as a key factor that leads to autism. This study points to not just a network ‘dysregulation,’ but also perhaps an overabundance of neurons overall.

“Our hypothesis—that one potential means by which autism may develop is through an overproduction of cells in the brain, which then results in altered connectivity—is a new way of thinking about autism.”

Advances in the fields of stem cell biology and regenerative medicine have given new hope to families caring for autistic loved ones. Read more about one such family in our Stories of Hope series. You can also learn more about how CIRM-funded researchers are building our understanding of autism in our recent video: Reversing Autism in the Lab with help from Stem Cells and the Tooth Fairy.

Scientists Reach Yet Another Milestone towards Treating Type 1 Diabetes

There was a time when having type 1 diabetes was equivalent to a death sentence. Now, thanks to advances in science and medicine, the disease has shifted from deadly to chronic.

But this shift, doctors argue, is not good enough. The disease still poses significant health risks, such as blindness and loss of limbs, as the patients get older. There has been a renewed effort, therefore, to develop superior therapies—and those based on stem cell technology have shown significant promise.

Human stem cell-derived beta cells that have formed islet like clusters in a mouse. Cells were transplanted to the kidney capsule and photo was taken two weeks later by which time the beta cells are making insulin and have cured the mouse's diabetes. [Credit: Douglas Melton]

Human stem cell-derived beta cells that have formed islet like clusters in a mouse. Cells were transplanted to the kidney capsule and photo was taken two weeks later by which time the beta cells are making insulin and have cured the mouse’s diabetes. [Credit: Douglas Melton]

Indeed, CIRM-funded scientists at San Diego-based Viacyte, Inc. recently received FDA clearance to begin clinical trials of their VC-01 product candidate that delivers insulin via healthy beta cells contained in a permeable, credit card-sized pouch.

And now, scientists at Harvard University have announced a technique for producing mass quantities of mature beta cells from embryonic stem cells in the lab. The findings, published today in the journal Cell, offer additional hope for the millions of patients and their families looking for a better way to treat their condition.

The team’s ability to generate billions of healthy beta cells—cells within the pancreas that produce insulin in order to maintain normal glucose levels—has a particular significance to the study’s senior author and co-scientific director of the Harvard Stem Cell Institute, Dr. Doug Melton. 23 years ago, his infant son Sam was diagnosed with type 1 diabetes and since that time Melton has dedicated his career to finding better therapies for his son and the millions like him. Melton’s daughter, Emma, has also been diagnosed with the disease.

Type 1 diabetes is an autoimmune disorder in which the body’s immune system systematically targets and destroys the pancreas’ insulin-producing beta cells.

In this study, the team took human embryonic stem cells and transformed them into healthy beta cells. They then transplanted them into mice that had been modified to mimic the signs of diabetes. After closely monitoring the mice for several weeks, they found that their diabetes was essentially ‘cured.’ Said Melton:

“You never know for sure that something like this is going to work until you’ve tested it numerous ways. We’ve given these cells three separate challenges with glucose in mice and they’ve responded appropriately; that was really exciting.”

The researchers are undergoing additional pre-clinical studies in animal models, including non-human primates, with the hopes that the 150 million cells required for transplantation are also protected from the body’s immune system, and not destroyed.

Melton’s team is collaborating with Medical Engineer Dr. Daniel G. Anderson at MIT to develop a protective implantation device for transplantation. Said Anderson of Melton’s work:

“There is no question that the ability to generate glucose-responsive, human beta cells through controlled differentiation of stem cells will accelerate the development of new therapeutics. In particular, this advance opens the doors to an essentially limitless supply of tissue for diabetic patients awaiting cell therapy.”

Policy Matters: Stem Cells and the Public Interest

Guest Author Geoff Lomax is CIRM’s Senior Officer for Medical and Ethical Standards.

In the spirit of Stem Cell Awareness Day, Cell Stem Cell has compiled a “Public Interest” collection of articles covering ethical, legal, and social implications of stem cell research and made it freely available. The collection may be found here.

shutterstock_169882310

The collection covers issues ranging from research involving human embryos to the use of stem cell therapies in patients. For those of you interested in a good primer on the history of stem cell controversies, Herbert Gottweis provides a detailed review of the federal policy debate in the United States. This debate has resulted in inconsistent policy and disrupted research. Gottweis uses this history to support his message that a “comprehensive, and proactive policy approach in this field beyond the quick legal fix” is needed for patients to ultimately benefit from the science.

What I found most interesting about this collection was the focus on stem cell treatments and “tourism.” A majority of the articles address the use of stem cells in patients. This focus is an indicator of how far the field has progressed. Stem cells clinical trials are now a reality and this results in two separated but related considerations. First, is how to make sure prospective patients are well informed should they participate in a clinical trial. Second, how to avoid stem cell “snake oil” where someone is pitching an unproven procedure. These issues are related by their solution that involves empowerment and education of patients and their support networks.

For example, in Stem Cell Tourism and Public Education: The Missing Elements, Master writes:

“It is important for the scientific, medical, ethics, and policy communities to continue to promote accurate patient and public information on stem cell research and tourism and to ensure that it is effectively disseminated to patients by working alongside patient advocacy groups.”

Master’s team found that groups committed to the advancement of good science, including patient advocates and researchers, often lacked basic information about clinical trials and other options for patients. This lack of information may contribute to patients being wooed by those pitching unproven procedures. Thus, the research community should continue to work with patients and advocacy organizations to identity options for treatment.

Another aspect of patient empowerment is what Insoo Huyn refers to as “therapeutic hope” in his piece: Therapeutic Hope, Spiritual Distress, and the Problem of Stem Cell Tourism. Huyn suggests that a supportive system for delivering cell therapies should includes nurturing hope. He writes, “patients might understand when an intervention’s chances of success are extremely remote at best, but may still want to ‘‘give it a shot’’ as long as a beneficial outcome cannot be ruled out as categorically impossible.” Huyn recognizes that well developed early-stage clinical trials are not expected to provide a benefit to patients (they are designed to evaluate safety), but the nature of the therapeutic (often cells) means there may be some real effect.

A third piece by the ISSCR Ethics Taskforce titled Patients Beware: Commercialized Stem Cell Treatments on the Web presents a guide to evaluating therapies. They present five principles that patients, researchers and advocates can rally around to identify credible interventions. The taskforce states:

The guiding principles for the development of the recommended process were that (1) the standards for identifying and reviewing clinics and suppliers should be objective and clear; (2) the inquiry and review process should be publicly transparent and relatively straight- forward for any clinic or practitioner to comply with; (3) conflicts of interest, if any, of the declarant ought to be disclosed to the ISSCR; (4) there should be no actual or apparent conflicts of interest of staff or others involved in the inquiry or review process for any particular matter; and (5) any findings that a clinic fails to meet standards should be communicated in a specific factual way, rather than with broad conclusions of fraudulent practices.

While the Cell Stem Cell Public Interest series covers a range of issues related to stem cells and society, the emphasis on treatments and patients is a reminder of how far the field has come. There is broad consensus that patients, researchers and advocates have roles to play in advancing safe and effective cell therapies.

Geoff Lomax

These Are the Cells You’re Looking for: Scientists Devise New Way to Extract Bone-Making Stem Cells from Fat

Buried within our fat tissue are stashes of stem cells—a hidden reservoir of cells that, if given the right cues, can transform into cells that make up bone, cartilage or fat. These cells therefore represent a much-needed store for regenerative therapies that rebuild bone or cartilage lost to disease or injury.

Finding cells that have bone-making potential is more efficiently done by looking at the genes they express (in this case, ALPL) than at proteins on their surface. The bone matrix being produced by cells is stained red in samples of cells that do not express ALPL (left), those that do express ALPL (right). [Credit: Darling lab/Brown University]

Finding cells that have bone-making potential is more efficiently done by looking at the genes they express (in this case, ALPL) than at proteins on their surface. The bone matrix being produced by cells is stained red in samples of cells that do not express ALPL (left), those that do express ALPL (right). The center image shows both types of cells prior to sorting [Credit: Darling lab/Brown University]

The only problem with these tucked-away cellular reservoirs, however, is identifying them and getting them out.

But now, researchers at Brown University have devised a unique method of identifying, extracting and then cultivating these bone-producing stem cells. Their results, published today in the journal Stem Cell Research & Therapy, seem to offer a much-needed alternative resource for growing bone.

Traditional methods attempting to locate and extract these stem cells focused on proteins that reside on the surface of the cells. Find the proteins, scientists reasoned, and you’ve found the cell.

Unfortunately, that method was not fool proof, and many argued that it wasn’t finding all the cells that reside in the fat tissue. So Brown scientists, led by Dr. Eric Darling found an alternative.

They knew that a gene called ALPL is an indicator of bone-making cells. If the gene is switched on, the cell has the potential to make bone. If it’s switched off, it does not. So Darling and his team devised a fluorescent marker, or tag, that stuck to the cells with activated ALPL. They then used a special machine to sort the cells: those that glowed went into one bucket, those that did not went into the other.

To prove that these ALPL-activated cells were indeed capable of becoming bone and cartilage, they then cultivated them for several weeks in a petri dish. Not only did they transform into the right cell types—they did so in greater numbers than cells extracted using traditional methods.

Hetal Marble, a graduate student in Darling’s lab and the paper’s first author, argues that tagging genes—rather than surface proteins—in order to distinguish and weed out cell types represents an important paradigm shift in the field. As he stated in a press release:

“Approaches like this allow us to isolate all the cells that are capable of doing what we want, whether they fit the archetype of what a stem cell is or is not. The paradigm shift is thinking about isolating populations that are able to achieve an end point rather than isolating populations that fit a strictly defined archetype.”

While their method is both precise and accurate, there is one drawback: it is slow.

Currently, it takes four days to tag, extract and cultivate the bone-making cells. In the future, the team hopes they can shorten this time frame so that they could perform the required steps within a single surgical session. As Darling stated:

“If you can take a patient into the OR, isolate a bunch of their cells, sort them and put them back in—that’s ideally where we’d like to go with this.”

See You Next Week: 2014 Stem Cell Meeting on the Mesa

Next week marks the fourth annual Stem Cell Meeting on the Mesa (SCMOM) Partnering Forum in La Jolla, California and CIRM , one of the main organizers, hopes to see you there.

SCMOM

SCMOM is the first and only meeting organized specifically for the regenerative medicine and cell therapy sectors. The meeting’s unique Partnering Forum brings together a network of companies—including large pharma, investors, research institutes, government agencies and philanthropies seeking opportunities to expand key relationships in the field. The meeting will feature presentations by 50 leading companies in the fields of cell therapy, gene therapy and tissue engineering.

Co-founded by CIRM and the Alliance for Regenerative Medicine (ARM), SCMOM has since grown both in participants and in quality. As Geoff MacKay, President and CEO of Organogenesis, Inc. and ARM’s Chairman, stated in a recent news release:

“This year the Partnering Forum has expanded to include an emphasis not only on cell therapies, but also gene and gene-modified cell therapy technologies. This, like the recent formation of ARM’s Gene Therapy Section, is a natural progression for the meeting as the advanced therapies sector expands.”

This year CIRM President and CEO Dr. C. Randal Mills, as well as Senior Vice President, Research & Development Dr. Ellen Feigal will be speaking to attendees. In addition, 12 CIRM grantees will be among the distinguished speakers, including Drs. Jill Helms, Don Kohn and Clive Svendsen, as well as leaders from Capricor, Asterias, ViaCyte, Sangamo Biosciences and others.

CIRM has made tremendous progress advancing stem cell therapies to patients and expects to have ten approved clinical trials by the end of 2014. The trials which span a variety of therapeutic areas using several therapeutic strategies such as cell therapy, monoclonal antibodies and small molecules are increasingly being partnered with major industry players. CIRM still has more than $1 billion to invest and is interested in co-funding with industry and investors—don’t miss the chance to strike the next partnership at SCMOM next week.

For more details and to view the agenda, please visit: http://stemcellmeetingonthemesa.com/