Stem cell stories that caught our eye: a good review at the NY Times, expanding cord blood and leukemia

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

Review paints picture of the field today.
A writer I have respected for many years, Karen Weintraub, wrote a nice review of the current state of stem cell clinical trials in the Tuesday Science Times in the New York Times. She discusses the steady, methodical progress being made:

“Researchers have been slowly learning how to best use stem cells, what types to use and how to deliver them to the body — findings that are not singularly transformational, but progressive and pragmatic.”

She quotes our senior VP Ellen Feigal about the safety seen so far in clinical trials and notes that CIRM should have 10 clinical trials enrolling patients by the end of the year. She also covers the dangers of clinics offering unproven therapies and the power of using iPS-type stem cells to model diseases in the laboratory. Overall, a nicely balanced piece.

Making mitochondrial disease and 3-parent embryos personal. A little newspaper in Oregon called the Willamet Week has published a story that makes the issues around so-called “three-parent” babies very personal. The controversial procedure aims to allow women with rare mitochondrial diseases to have normal children.

Mitochondria, known as the powerhouses of the cell, have the unusual trait of being the only part of the cell besides the nucleus to have any DNA. It is these few genes in the mitochondria that we inherit solely from our mothers because when the DNA from the egg and sperm fuse, the mother’s mitochondria stay in the fluid outside the nucleus. So, to avoid passing along faulty mitochondrial genes, a team in Oregon devised a way to insert the DNA from the mother’s nucleus into a donor egg that had its nucleus removed, a process called nuclear transfer.

Guided by a microscope researchers insert the nucleus from one woman into the egg of another

Guided by a microscope researchers insert the nucleus from one woman into the egg of another

The paper provides a long read—nearly 4,000 words—that goes into great detail about the procedure, the ethics, the research team’s views on the ethics, and the personal story of a patient living with a disease of exhaustion she calls “mitochondrial crash.” The writer lets the patient have the last word on ethics:

“To me it’s win-win because you’re not messing with God’s child. You’re just taking out the bad parts. I don’t want to pick out a blond-haired, blue-eyed tall kid, picking your child’s traits, but to rule out a potentially lethal chronic illness brings in a whole different story.”


Cord blood might now save more adult cancer patients.
Umbilical cord blood is a literal lifesaver for many pediatric cancer patients allowing them to withstand harsh chemotherapy and be rescued by the stem cells in the cord blood. But the procedure is used in few adults because the vast majority of cord blood samples don’t have enough stem cell for an adult requiring the use of two cord samples and doubling the chance for potentially deadly immune reactions.

A team at the University of Montreal screened more than 5,000 molecules looking for one that would let them expand the number of stem cells from one sample in the lab. They hit upon one that they say could allow a 10-fold increase in the number of single cord samples suitable for adults. They expect to begin clinical trials in December.

Science News ran a brief review of the work and the blog Science 2.0 ran the university’s press release with a bit more detail.

Trial begins with cancer drug named for CIRM
Researchers at the University of California, San Diego, announced this week that they had begun a clinical trial with leukemia patients using a drug named for our agency cirmtuzumab. This molecule, in the class of drugs called antibodies, disables a protein that cancer stem cells use to accelerate the growth of cancer.

This trial, for patients with recurrence of their chronic lymphocytic leukemia, became the third CIRM funded team this month announcing plans to start clinical trials. In addition to our blog post the San Diego Union Tribune wrote about the latest trial, and we issued press releases on the trials for spinal cord injury and diabetes.

Don Gibbons

New formula a more efficient way to reprogram adult cells to become like embryonic stem cells

Shinya Yamanaka won the Nobel Prize for developing a recipe of genetic factors that can turn back the clock of adult cells and make them behave like embryonic stem cells. But he would be the first to tell you his recipe ultimately may not be the best one for making these stem cells called iPS cells.

Virtually from the day he published his groundbreaking work, teams around the world have tried to develop new formulas that get around some problems with the original. One issue is the low efficiency of getting true stem cells. Another is the high rate of genetic aberrations that can be produced in the resulting stem cells.

Now, a team pairing researchers at the Hebrew University in Jerusalem and the Whitehead Institute in Cambridge, Massachusetts, has published a new recipe that seems to yield many more true stem cells, ones that are called pluripotent because they can make all cell types. The new cells also seem to have fewer genetic alterations, which could make them safer for clinical use in people.

They made the improved cells by moving from OSKM to SNEL—from the original genetic factors, Oct4, Sox2, Klf4 and Myc, to Sall4, Nanog, Esrrb and Lin28. An elaborate computer analysis of the function of genes helped them come up with the formula.

This work used mouse cells, so up next on their agenda is coming up with a similar formula that works in human cells. HealthCanal ran the university’s press release and Genetic Engineering & Biotechnology News ran a slightly more technical analysis of the work.

Don Gibbons

Stem cell stories that caught our eye: first iPS clinical trial, cancer metabolism and magnates helping heal hearts

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

First clinical trial with reprogrammed stem cells.
Today, a Japanese woman became the first patient to be treated with cells derived from reprogrammed iPS-type stem cells. The patient received cells matured into a type of cell damaged in the most common form of blindness, age-related macular degeneration.

Those cells, a normal part of the eye’s retina, were made from stem cells created from a skin sample donated by the patient several months ago. In the intervening time the resulting retinal cells have been tested in mice and monkeys to make sure they will not cause tumors. Because the cells have the same genes as the patient, researchers believe they may not be rejected by the patient’s immune system in the absence of immune suppressive drugs—the beauty of iPS technology.

Right now, that technology is much too cumbersome and time consuming to result in a broadly applicable therapy. But if this first clinical trial proves the immune system get-out-of-jail-free theory, it should intensify efforts to make iPS technology more efficient.

When Japanese authorities gave permission to treat the first patient earlier this week Popular Science provided an easy read version of the story and Nature News provided a bit more detail.

Cancer cells don’t handle their sugar well. Sugar has a bad rep these days. Now, it looks like manipulating sugar metabolism might lead to ways to better treat leukemia and perhaps, make therapies less toxic to normal cells. It turns out cancer cells are much more sensitive to changes in sugar level than normal blood stem cells or the intermediate cells that give rise the various branches of the blood system.

David Scadden at the Harvard Stem Cell Institute has long studied the role of the stem cell's environment in its function.

David Scadden at the Harvard Stem Cell Institute has long studied the role of the stem cell’s environment in its function.

A team led by old friend and colleague at the Harvard Stem Cell Institute, David Scadden, first looked at sugar metabolism in normal blood forming stem cells and their intermediate cells. They found that the parent stem cell and their direct offspring, those intermediate cells, behave differently when faced with various manipulations in sugar level, which makes sense since the intermediate cells are usually much more actively dividing.

But when they manipulated the genes of both types of cells to make them turn cancerous, the cancer cells from both were much more sensitive to changes in sugar metabolism. In a university press release picked up by ScienceCodex David said he hoped to interest drug companies in developing ways to exploit these differences to create better therapies.

Magnets and nanoparticles steer stem cells.
Getting stem cells to where they are needed to make a repair, and keeping them there is a major challenge. A team at Los Angeles’ Cedars-Sinai hospital that we fund (but not for this study) has taken an approach to this problem that is the equivalent of holding your pants up with a double set of button, a belt and suspenders.

Treating damaged hearts in rats they first loaded iron-containing nanoparticles with two types of antibodies, one that recognizes and homes to injured heart tissue and one that attracts healing stem cells. After infusing them into the animal’s blood stream, they placed a magnet over its heart to hold the iron nanoparticles near by. The iron provided the added benefit of letting the team track the cells via magnetic resonance imaging (MRI) to verify they did get to and stay where they were needed.

In a press release from the hospital picked up by ScienceDaily the lead researcher Eduardo Marban said:

“The result is a kind of molecular matchmaking,”

The study was published in Nature Communications and you can read about other work we fund in Marban’s lab trying to figure out once you get the stem cells to the heart exactly how do they create the repair.

Reprogrammed stem cells turned into white blood cells. We have written often about the difficulties of getting stem cells to create fully mature blood cells. Last week we talked about a Wisconsin team breaking the barrier for red blood cells. Now, a team at the Salk Institute is reporting success for white blood cells.

Starting with iPS-type stem cells they got the mature white cells via a two-step process. First they manipulated one gene called Sox2 to get the stem cells to become the right intermediate cells. Then they used a gene-regulating molecule called a micro-RNA to get the middleman cells to mature into white blood cells.

In a press release from the Salk, lead researcher Juan Carlos Izpisua Belmonte noted the clinical importance of the work:

“In terms of potential clinical applications, the hematopoietic system represents one of the most suitable tissues for stem cell-based therapies. . .”

The team published the research in the journal Stem Cells and the web portal BioSpace picked up the release.

Book on early spinal cord injury clinical trial. The title of a book on the first ever clinical trial using cells from embryonic stem cells kind of says it all: Inevitable Collision: The Inspiring Story that Brought Stem Cell Research to Conservative America.

Katy Sharify's experience in the first embryonic stem cell trial is featured in a new book and she discussed it in a video from a CIRM workshop.

Katy Sharify’s experience in the first embryonic stem cell trial is featured in a new book and she discussed it in a video from a CIRM workshop.


The book details the personal stories of the first and fifth patients in the spinal cord injury trial conducted by Geron. That company made the financial decision to end its stem cell product development in favor of its cancer products. But the spinal cord injury trial is now set to restart, modified to treat neck injuries instead of back injuries and at higher doses, through CIRM funding to the company that bought the Geron stem cell business, Asterias.

In a press release from the publisher, the book’s author explained her goal:

“Through this book I hope to bridge the gap between science and religion and raise awareness of the importance and power of stem cell research.”

The fifth patient in the Geron study, Katie Sharify, is featured in our “Stories of Hope” that have filled The Stem Cellar this week.

Don Gibbons

Stem cell stories that caught our eye: heart stem cells, lizard tails and mapping progress in the field

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

Could cells in arteries be elusive heart stem cells?
Our hearts have a modest limited ability to regenerate and repair themselves, suggesting we must have a few heart stem cells. But no one has figured out where those cells hang out. Now, a team at Vanderbilt in Nashville has shown that cells in the lining of the heart’s arteries can contribute to new heart muscle.

They made the discovery using a labeling technique that let them tag those cells, called endothelial cells, and show that the same tag showed up in new muscle in the heart. This suggests those cells have the properties of heart stem cells.

The finding also suggests that coronary heart disease, where plaque builds up inside the arteries, could damage the heart with a one-two-punch. Besides narrowing the artery it may also make it more difficult to mobilize these heart stem cells that reside inside the artery lining. The research published in Cell Reports was written up by Genetic Engineering & Biotechnology News.

Secrets of the lizard’s tail. Most folks who have spent any time watching nature programing on TV have seen the handy trick of the green anole lizard. If a predator catches it by the tail it can shed its tail and grow a new one. A team at Arizona State University has uncovered the genetic recipe for how the lizard pulls off this trick.

anole_5They analyzed various segments of tails as they were regrowing to see which genes were turned on that would not normally be turned on in adult tissue. They identified 325 genes. The beauty of the finding is 302 of those genes have matching genes in humans. Those genes become immediate candidates for research into finding ways to allow humans to regrow lost or damaged tissue.

Discover did a nice job of explaining how this lizard is a better model for human comparisons than other animals such as salamanders and fish that can also regrow body parts but use a very different process. And the university press release offers a bit more detail of what the team did.

Review maps where the field is going. Six leaders in the stem cell field wrote a review in the journal Science this week of what to expect in the next few years from research with pluripotent stem cells—those stem cells that can become any tissue in the body, both embryonic stem cells and reprogrammed iPS type stem cells. The authors included researchers from the University of Rochester, the University of Pittsburgh, Harvard, and the University of Wisconsin.

The main hurdles researchers are working to overcome involve maturing the stem cells to the right adult tissue, making sure they are purely those cells, and getting them to integrate with the patient’s own tissue after transplant. They note progress is each of these areas, but in most cases much more work needs to be done.

The University of Rochester put out a press release detailing their faculty member’s contribution to the paper focusing on neural diseases. He suggests that complex diseases that impact multiple types of cells, such as Alzheimer’s, would be the most difficult to treat with stem cells. But diseases impacting a single type of nerve cell, such as Huntington’s, Parkinson’s and multiple sclerosis would be the first to benefit from cells generated from pluripotent stem cells. HealthCanal picked up the university’s release.

Don Gibbons

Tiny transparent zebra fish yields big clue to black box of Alzheimer’s disease

The PR folks at the Flanders Institute for Biotechnology in Belgium produced an unusual press release to describe recent work there published in Developmental Cell. They devoted the first half to the marvels of their animal model the zebra fish.

zebrafish1For those who have only seen these nearly transparent little guys in a home aquarium the story provides a nice explanation for why they are such popular lab models. It is not unusual to walk into a lab with dozens of small fish tanks holding thousands of zebra fish. A couple key reasons: their DNA matches 90 percent of ours and the guys reproduce quickly, just three months after birth.

Nerve stem cells, key players to brain development in the embryo, become few in number in adults. More important, those few we have left seem to be less active when we need them most, when Alzheimer’s disease or other neurodegenerative disease destroys some of our existing nerves. Evgenia Salta at the Institute used the fish to try to discern why.

We have known for some time that the genes in a pathway known as Notch regulate the ability of nerve stem cells to mature into adult nerves. But we don’t know why that goes awry in disease. She focused on a genetic regulatory molecule called a microRNA that is known to be in abnormally low supply in cells from patients with Alzheimer’s.

When they manipulated the fish to lower the levels of this microRNA, the nerve stem cells in the fish failed to mature properly into nerve cells. In the press release published on ScienceDaily Salta is quoted saying:

“To our surprise, the reduced activity of miRNS-132 in the zebra fish blocks the further ripening of the stem cell into nerves cells. This new knowledge about the molecular signaling pathway that underlies this process gives us an insight into the exact blocking mechanism. Thanks to this work in zebra fish, we can now examine in detail what exactly goes wrong in the brains of patients with Alzheimer’s disease.”

You can read about CIRMM-funded projects seeking solutions to Alzheimer’s Disease on our fact sheet.

Don Gibbons

Stem cell stories that caught our eye: Willie Nelson’s contribution to muscular dystrophy, cell fate maps and funding

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

Cell fate map can show quality of cells.
The phrase “there is more than one way to skin a cat” fits much of science. It is quite true for using stem cell science to generate a needed type of adult cell to repair damaged tissue. The most traditional way, directing early stem cells, the ones called pluripotent, to mature into the desired tissue is often cumbersome and has the potential of leaving behind a few of those early cells that could cause a tumor. More recently, many teams have been starting with one type of adult tissue and reprogramming them to directly convert into a different adult tissue without passing through that potentially tumor causing state. But we have not had a good way to measure which route produces the higher quality cells—which one yield cells most like those in our body.

credit: Samantha Morris, Ph.D./Boston Children's Hospital

credit: Samantha Morris, Ph.D./Boston Children’s Hospital

Some of the biggest potential differences between cells grown in a dish and those in us, is the state of the various genetic switches that turn our genes on and off. Now, a team at Boston Children’s Hospital, the Wyss Institute at Harvard and Boston University has developed a computer algorithm to compare our natural cells to various types of cells grown in the lab.

Many in the field had hoped that the direct conversion of adult cells to other cell types would prove to be the way to go. Unfortunately, the computer program showed that those cells were not nearly as good at mimicking natural cells as cells matured from early stem cells were. However, the team suggests their system points to ways to improve direct conversion. The researchers published two paper on the system they are calling CellNet in the journal Cell August 14 and Genetic Engineering and Biotechnology News did a nice write up of the work.

Willie Nelson advances stem cells for muscular dystrophy.
Really! No, Willie is not in the lab, but he was named an honorary member of the lab and had an endowed chair held by the lab director named for him. He had performed at a concert to raise money to fund the work at UT Southwestern Medical Center in Dallas and the university decided to honor him with the named chair.

In the current paper the lab used the most trendy form of gene modification out there right now, called CRISPR. Researchers are excited about the technology because it can specifically go into our DNA and permanently cut out a mutation. Then our natural genetic machinery can go about making the correct gene. In this case they used it to cut out the error that caused Duchenne muscular dystrophy in a mouse model. After the correction, the mice grew new muscle and got stronger.

The CRISPR technology needs some refinements before it would be ready for use in humans, but the team is working on that along with many others around the country. Their goal: correct the error in patient muscle stem cells so that they can produce a lifetime supply of healthy muscle. The journal Science published their work online August 14 and the HealthCanal website picked up the university press release.

Scientists need to talk to the public. The director of the National Institutes of Health, Francis Collins, visited the University of Washington this week and delivered a message straight from my personal soapbox: Funding for research is in jeopardy and the only way it will be salvaged is for researchers to get more involved in outreach to the public. The Seattle Times quoted him as saying:

“I think it’s at a particularly crucial juncture. If there was a moment to kind of raise consciousness, this is kind of the moment to do that.”

He noted that the chances of a research proposal submitted to NIH getting funded dropped from 40 percent in 1979 to 16 percent now, saying “we’re leaving half the good science on the table.” Part of the solution he suggested was for scientists to get out to Rotary clubs, high school classrooms, and any other public speaking opportunity.

“It seems to me that we all have to spend more of our time, perhaps, as ambassadors for science literacy — trying to explain what we do and why it matters.”

Don Gibbons

Stem cell stories that caught our eye: better cell reprogramming, heart failure and false claims for stem cells

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

Improving the efficiency of creating stem cell lines.
Ever since researchers first learned to reprogram adult cells to behave like embryonic stem cells in 2007 teams have tried to do it better. The earliest reprogramming resulted in less than one percent of cells converting to the stem cell state. Many years and many reprogramming recipes later some teams have got that up to a few percent, but usually still in the single digits. CIRM-funded researchers at the University of California, San Francisco, have uncovered a path that could yield dramatic increases in efficiency in creating these stem cells. They stepped back to look at what genetic factors were acting as brakes on the reprogramming and have now mapped out multiple brake points that could be inhibited to improve the production of stem cells. HealthCanal ran the university’s press release based on the journal publication in Cell.

Does source of adult cells matter for iPS-type stem cells. When researchers turn adult tissue into embryonic-like iPS cells, they know that the reprogrammed stem cells retain some memory of the type of adult tissue they were, whether it was skin, brain or heart. So, a CIRM-funded team at Stanford set out to do a series of experiments to see if that mattered. They created iPS cells from heart tissue and from skin cells. And initially, there was a difference. The stem cells made from heart more readily matured into heart muscle than those from skin, but over time, as the cells grew in the lab the difference abated. Both types of cells began to function like normal heart muscle. Stanford’s Scope blog wrote about this and a companion paper that were published this week in the Journal of the American College of Cardiology.

Heart progenitor cells, the middlemen between stem cells and adult heart muscle, shown here in green and infected with coxsackie vurus.

Heart progenitor cells, the middlemen between stem cells and adult heart muscle, shown here in green and infected with coxsackie vurus.


Viral heart failure link may be via stem cells
. Our hearts are one of our poorest performing organs when it comes to repairing themselves. The liver does it well. The lining of our guts does it well—the heart not so much. Scientists generally attribute this to the very small number of stem cells we retain in our hearts. If you lose those few, you are in deep trouble. While there are many reasons for heart failure, we have known that a high percent of those who develop this weakening of the heart’s ability to pump blood have signs of having been infected with the coxsackie virus. Researchers at San Diego State University have found out a possible reason why. The virus appears to selectively seek out and destroy the heart stem cells and middlemen progenitor cells. HealthCanal ran the university’s press release based on work published this week in PLOS Pathogens.

Review talks about reality of stem cells in sports.
Over the past year, there has been a parade of headlines about athletes getting their sports injuries treated with stem cells. The EuroStemCell collaborative has published online a great review of the reasons why stem cells might work for some of those conditions, and might not. The piece dutifully starts by noting that none of these treatments have been approved for general use because none have had sufficient testing. Taking muscle, cartilage, tendon and bone repair individually the authors discuss what research has been done and what it shows. In general, the results have not been great, in large part because we haven’t yet figured out what is the best type of cell for each injury and the best way to deliver it.

False claims in stem cell for plastic surgery. CIRM-grantee Michael Longaker at Stanford has called out his fellow plastic surgeons to lead the charge in evaluating the uses of stem cells in cosmetic procedures. In an article in the journal Plastic and Reconstructive Surgery he describes research he did into 50 clinics that showed up in a google search offering stem cell face lifts. While they were claiming to inject age-reversing stem cells, he suggests they were doing no more than the established practice of injecting fat to smooth out wrinkles. While fat does have a few stem cells in it, he could find no evidence that the clinics had the necessary equipment to isolate those cells, and even if they did, there is scant research into whether those stem cells could have any impact. Popular Science and ScienceNewsline both ran stories about the journal article this week.

Don Gibbons

Research points to another path toward giving diabetics the insulin-producing cells they need

Type 1 diabetes is such a life-changing illness that scores of teams around the world are looking for ways to replace the insulin-producing pancreatic cells that are destroyed in the disease.

Many of these researchers use stem cells of various types to try to generate large quantities of insulin producing cells that could be transplanted. But a few are trying to directly reprogram other pancreas cells into desired beta cells. Often called transdifferentiation, this process could be a great shortcut to getting the needed cells.


Fred Levine and his CIRM-funded colleagues at the Sanford-Burnham Medical Research Institute in La Jolla have succeeded in causing this identity change using a single peptide, which you can think of as a very small protein. The islet cells in our pancreas contain beta cells and alpha cells in close proximity. When a diabetic’s immune system destroys the insulin-producing beta cells it does not harm the alpha cells, so they are a ready supply of cells that could be reprogrammed that are already in the right location. Levine’s team did this with the peptide caerulein. In a press release Levine noted:

“We have found a promising technique for type 1 diabetics to restore the body’s ability to produce insulin. By introducing caerulein to the pancreas we were able to generate new beta cells—the cells that produce insulin—potentially freeing patients from daily doses of insulin to manage their blood-sugar levels.”

Injecting the peptide worked in both a mouse model of diabetes and in human pancreas tissue from cadavers. But it also caused enough inflammation of the pancreas that the team is now tracking down the molecular target where the peptide does its magic. With that knowledge they hope to develop a more specific drug without the side effect.

Levine is well aware that a second step would be needed to protect any new beta cells they create from immune system attack. In a video that the institute produced a collaborator talked about preliminary work to prevent this immune rejection [starting at 2:45 into the video]. She is trying to super charge the type of immune cell called T-regulatory cells that are responsible for maintaining a balanced immune response.

The team published their work online in Cell Death and Disease, July 31.

Don Gibbons

Stem Cell Stories that Caught our Eye: Multiple Sclerosis, Parkinson’s and Reducing the Risk of Causing Tumors

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

Cell therapy for Parkinson’s advancing to the clinic. A decade-long moratorium on the transplant of fetal nerve tissue into Parkinson’s patient will end in two months when the first patients in a large global trial will receive the cells. BioScience Technology did a detailed overview on the causes for the moratorium and the optimism about the time being right to try again. The publication also talks about what most people in the field believe will be the long-term solution: moving from scarce fetal tissue to nerve cells grown from readily available embryonic stem cells. The author’s jumping off point was a pair of presentations at the International Society for Stem Cell Research in June, which we wrote about at the time. But the BioScience piece provides more background on the mixed results of earlier studies and references to recent journal publications showing long term—as much as 20 year—benefit for some of those patients.

It goes on to describe multiple reasons why, once the benefit is confirmed with fetal cells, moving to stem cells might be the better way to go. Not only are they more readily available, they can be purified in the lab as they are matured into the desired type of early-stage nerve cell. Researchers believe that some of the side effects seen in the early fetal trials stemmed from the transplants containing a second type of cell that caused jerking movements known as dyskinesias. One stem cell trial is expected to start in 2017, which we discussed in June.

Immunity persists through a special set of stem cells. Our immune system involves so many players and so much cell-to-cell interaction that there are significant gaps in our understanding of how it all works. One of those is how we can have long-term immunity to certain pathogens. The T-cells responsible for destroying invading bugs remember encountering specific ones, but they only live for a few years, generally estimated at five to 15. The blood-forming stem cells that are capable of generating all our immune cells would not have memory of specific invaders so could not be responsible for the long term immunity.

Now, an international team from Germany and from the Hutchison Center in Washington has isolated a subset of so-called “memory T-cells” that have stem cell properties. They can renew themselves and they can generate diverse offspring cells. Researchers have assumed cells like this must exist, but could not confirm it until they had some of the latest gee-wiz technologies that allow us to study single cells over time. ScienceDaily carried a story derived from a press release from the university in Munich and it discusses the long-term potential benefits from this finding, most notably for immune therapies in cancer. The team published their work in the journal Immunity.

Method may reduce the risk of stem cells causing tumors. When teams think about transplanting cells derived from pluripotent stem cells, either embryonic or iPS cells, they have to be concerned about causing tumors. While they will have tried to mature all the cells into a specific desired adult tissue, there may be a few pluripotent stem cells still in the mix that can cause tumors. A team at the Mayo Clinic seems to have developed a way to prevent any remaining stem cells in transplants derived from iPS cells from forming tumors. They treated the cells with a drug that blocks an enzyme needed for the stem cells to proliferate. Bio-Medicine ran a press release from the journal that published the finding, Stem Cells and Development. Unfortunately, that release lacks sufficient detail to know exactly what they did and its full impact. But it is nice to know that someone is developing some options of ways to begin to address this potential roadblock.

Multiple sclerosis just got easier to study. While we often talk about the power of iPS type stem cells to model disease, we probably devote too few electrons to the fact that the process is not easy and often takes a very long time. Taking a skin sample from a patient, reprogramming it to be an iPS cell, and then maturing those into the adult tissue that can mimic the disease in a dish takes months. It varies a bit depending on the type of adult tissue you want, but the nerve tissue that can mimic multiple sclerosis (MS) takes more than six months to create. So a team at the New York Stem Cell Foundation has been working on ways to speed up that process for MS. They now report that they have cut the time in half. This should make it much easier for more teams to jump into the effort of looking for cures for the disease. ScienceCodex ran the foundations press release.

Making stem cells feel like they are growing in the right neighborhood may be key to success

An adage in real estate says that the most important thing is neighborhood, neighborhood, neighborhood. Researchers are learning that the same may be true for stem cell therapies. If you want to mature stem cells into the right adult tissue and get them to behave the way you want, you better pay attention to the environment where they are grown in the lab—before they are transplanted into people.

Two journal articles posted online this month provide good reasons to head the realtors’ advice. CIRM-grantee Shyni Varghese at the University of California, San Diego, provides an elegantly simple example. When trying to turn embryonic stem cells into bone researchers often embed them inside a hydrogel scaffold. This helps them to stay put when transplanted. But researcjers generally rely on chemical or genetic signals to get the stem cells to mature into bone. This results in a mixed population of bone cells and fat cells because both those cell types branch from the same maturation pathway.

Varghese’s team altered the scaffold to make it seem more like the neighboring bone cells the maturing stem cells would encounter in normal bone. They mineralized it with calcium and phosphate. And when they did, they got pure bone cells in the lab dish. What’s more, when they implanted those “tissues” into animals, they formed densely calcified bone—the hard kind we want. The team published the work in the Journal of Materials Chemistry online July 4.

A review article in the journal BioResearch provided a good overview of ways various groups have tried to precondition stem cells in the lab so that they will survive after transplant. One of the biggest stumbling blocks in the field remains the difficulty of getting stem cells to survive in the patient, whether those are humans or little mouse patients. It turns out from the research cited in this review that turning the lab growth environment into something more closely resembling the environment in the patient improves survival.

Stem cell researchers need their version of the Google mapping bike to reveal the natural neighborhoods where the cells would grow.

Stem cell researchers need their version of the Google mapping bike to reveal the natural neighborhoods where the cells would grow.

They looked at several aspects of typical lab cell cultures that don’t mimic real tissue. Sites of injury where stem cells are needed often are also sites of lowered oxygen levels, inflammation and a disruption of the normal cell-to-cell contact that helps guides cell behavior. They found that adjusting each of those in the lab resulted in cells that were more likely to survive after transplant.

Most notably, when they grew cells in aggregates that restored cell-to-cell contact—restored the sense of neighborhood—cell survival improved significantly. Genetic Engineering & Biotechnology News wrote a brief summary of the work.

Don Gibbons