StemCell Therapy

SAN DIEGO (CNS) - Researchers at San Diego-based life science organizations have discovered a molecule that converts stem cells into healthy heart cells, possibly setting the stage for therapies that would replace some heart transplants, according to a study published in a scientific journal Friday.

The finding published in the journal Cell Stem Cell could lead to new treatments for heart disease. The study was conducted at Sanford-Burnham Medical Research Institute, the Human BioMolecular Research Institute, and ChemRegen Inc.

The molecule known as ITD-1 is able to generate an unlimited supply of heart cells, which would give scientists more cells to study in their research and give physicians healthy cells to use to treat diseased hearts, according to the study.

Mark Mercola, director of Sanford-Burnham's Muscle Development and Regeneration Program, said heart disease is the leading cause of death in the United States, but doctors can't replace damaged heart muscle.

"The only way to effectively replace lost heart muscle cells -- called cardiomyocytes -- is to transplant the entire heart," said Mercola, the senior author of the study. "Using a drug to create new heart muscle from stem cells would be far more appealing than heart transplantation."

Stem cells were targeted for the study because they can self-replicate and convert to other, specialized types of cells. The challenge for scientists is to discover the signals that direct the stem cells to turn into the types of cells they want.

The researchers said ITD-1 works by preventing a protein from sending signals to cells that regulate various functions, allowing them to re-create themselves into heart cells.

According to Sanford-Burnham, Mercola has been looking for ways to convert stem cells into heart cells for 15 years.

"This particular molecule could be useful to enhance stem cell differentiation in a damaged heart," said Erik Willems, another author of the study. "At some point, it could become the basis for a new therapeutic drug for cardiovascular disease -- one that would likely limit scar spreading in heart failure and promote new muscle formation."

According to Sanford-Burnham, Mercola, Willems, and John Cashman of the Human BioMolecular Research Institute are now working with San Diego biotech company ChemRegen Inc. to develop ITD-1 into a drug that one day might be used to treat patients.

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SD researchers find stem cells can repair damaged heart tissue

(Credit: ANNE-CHRISTINE POUJOULAT/AFP/Getty Images)

By Michelle Durham

PHILADELPHIA (CBS) - Scientists at the University of Pennsylvania have teamed up with their counterparts all over the world, working to develop human organs from the stem cells of the patient.

Using a 3-D printer, and other tools, their goal is to eradicate the risk of rejection by building organs that wont require the immunosuppressant drugs current patients have to take.

Professor of Innovation in the Department of Bioengineering at the University of Pennsylvania, Dr. Christopher Chen says he and his colleagues have been working hard on using stem cells to engineer tissues.

One of the big limitations for being able to assemble the cells into larger structures such as hearts or livers [is that] once you form a tissue that is larger then a certain size all the cells in the center of that block will starve because they are not getting access to oxygen or blood, explains Dr. Chen.

Postdoctoral fellow Jordan Miller who works with Chen saw an exhibit featuring donated human organs filled with silicone so Miller wondered if he could create the pathways for the blood flow first and then build the organs around it.

Right now they can make pathways the size of a pinky, but Chen and Miller hope that in 10 years time the technology will be advanced enough to create an organ from these gels in their lab.

But it will be many more years before they can be transplanted into a patient.

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Scientists Work To Develop Human Organs From Stem Cells

Aug. 5, 2012, 3 a.m.

A GROWING number of overseas clinics touting stem cell therapy for conditions ranging from sexual disorders to HIV are targeting Australia, where such treatments are restricted.

Australian scientists have raised concerns about so-called ''stem cell tourism'', saying many of the treatments offered are unproven, untested and potentially deadly.

The Swiss firm Fetal Cell Technologies International has been advertising in Australia since last year and Emcell, based in Ukraine, started promoting its services last month.

It is estimated as many as 200 Australians have travelled overseas for the therapy. The secretary for science policy at the Australian Academy of Science, Bob Williamson, said he empathised with the desperation of seriously ill people but warned against the unproven therapies, which can cost up to $60,000.

''The therapies are almost all untested and unproven and sometimes they have killed people,'' Professor Williamson said. The Sun-Herald's calls to Emcell's Melbourne office were not returned.

Stem Cells Australia's Megan Munsie, who is conducting a study into stem cell tourism with Monash University, said many people she interviewed were unaware of the risks of therapy overseas.

''We're not talking about rubbing something into your skin or taking a capsule, we are talking about often a very invasive procedure,'' she said.

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Fears over 'stem cell tourism' Save

Aug. 5, 2012, 3 a.m.

A GROWING number of overseas clinics touting stem cell therapy for conditions ranging from sexual disorders to HIV are targeting Australia, where such treatments are restricted.

Australian scientists have raised concerns about so-called ''stem cell tourism'', saying many of the treatments offered are unproven, untested and potentially deadly.

The Swiss firm Fetal Cell Technologies International has been advertising in Australia since last year and Emcell, based in Ukraine, started promoting its services last month.

It is estimated as many as 200 Australians have travelled overseas for the therapy. The secretary for science policy at the Australian Academy of Science, Bob Williamson, said he empathised with the desperation of seriously ill people but warned against the unproven therapies, which can cost up to $60,000.

''The therapies are almost all untested and unproven and sometimes they have killed people,'' Professor Williamson said. The Sun-Herald's calls to Emcell's Melbourne office were not returned.

Stem Cells Australia's Megan Munsie, who is conducting a study into stem cell tourism with Monash University, said many people she interviewed were unaware of the risks of therapy overseas.

''We're not talking about rubbing something into your skin or taking a capsule, we are talking about often a very invasive procedure,'' she said.

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Fears over 'stem cell tourism' Save

A GROWING number of overseas clinics touting stem cell therapy for conditions ranging from sexual disorders to HIV are targeting Australia, where such treatments are restricted.

Australian scientists have raised concerns about so-called ''stem cell tourism'', saying many of the treatments offered are unproven, untested and potentially deadly.

The Swiss firm Fetal Cell Technologies International has been advertising in Australia since last year and Emcell, based in Ukraine, started promoting its services last month.

It is estimated as many as 200 Australians have travelled overseas for the therapy. The secretary for science policy at the Australian Academy of Science, Bob Williamson, said he empathised with the desperation of seriously ill people but warned against the unproven therapies, which can cost up to $60,000.

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''The therapies are almost all untested and unproven and sometimes they have killed people,'' Professor Williamson said. The Sun-Herald's calls to Emcell's Melbourne office were not returned.

Stem Cells Australia's Megan Munsie, who is conducting a study into stem cell tourism with Monash University, said many people she interviewed were unaware of the risks of therapy overseas.

''We're not talking about rubbing something into your skin or taking a capsule, we are talking about often a very invasive procedure,'' she said.

See the original post here:
Fears over 'stem cell tourism'

Public release date: 3-Aug-2012 [ | E-mail | Share ]

Contact: Elisabeth (Lisa) Lyons elyons@cell.com 617-386-2121 Cell Press

Human HLA genes the genes that allow our immune system to tell the difference between our own cells and foreign invaders are evolving much more rapidly than previously thought, according to an article online on August 3rd in Trends in Genetics. The resulting degree of variation improves our ability to fight off disease, but could also present challenges to current worldwide efforts aimed at identifying potential donors for patients undergoing stem cell transplantation.

"This new work makes clear the daunting and near hopeless challenge of keeping track of the continuous output from the HLA mutational spigot," says first author William Klitz, from the University of California, Berkeley.

HLA proteins sit at the surface of human cells. Every individual has a specific HLA on the surface of their cells and these proteins effectively act as an identification card. Any other cells that have the same HLA on the outside are recognized as 'self'; foreign particles like bacteria or viruses are identified as invaders and the immune system kicks in to remove them. The same system that helps us fight off germs makes organ or stem cell transplantation difficult. Our bodies treat transplanted tissue as foreign and reject it. Unless, however, the patient and the donor share the same HLA genes. As a result, worldwide efforts are underway to identify all possible HLA variants, in the hopes of more effectively matching patients with potential donors.

The difficulty is that within the human population, HLA genes are mutating rapidly and Klitz estimates that more than a million variants exist in the current population. Trying to identify all the variants will be nearly impossible and ultimately pointless, according to Klitz, because of how quickly these genes are evolving. This rapid evolution is a boon in some ways because it means that, at the population level, our immune systems are getting better at fighting off pathogens. For transplant recipients, however, the most likely implication is that the best chance for a match will be found in first-degree relatives rather than in a worldwide search for donors.

###

Klitz et al.: "New reservoirs of HLA alleles: Pools of rare variants enhance immune defense"

William Klitz, School of Public Health, University of California, Berkeley, CA, USA Philip Hedrick, School of Life Sciences, Arizona State University, Tempe, AZ, USA Ed Louis, Centre for Genetics and Genomics, University of Nottingham, UK

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Unexpected variation in immune genes poses difficulties for transplantation

SAN DIEGO (CNS) - Researchers at San Diego-based life science organizations have discovered a molecule that converts stem cells into healthy heart cells, possibly setting the stage for therapies that would replace some heart transplants, according to a study published in a scientific journal Friday.

The finding published in the journal Cell Stem Cell could lead to new treatments for heart disease. The study was conducted at Sanford-Burnham Medical Research Institute, the Human BioMolecular Research Institute, and ChemRegen Inc.

The molecule known as ITD-1 is able to generate an unlimited supply of heart cells, which would give scientists more cells to study in their research and give physicians healthy cells to use to treat diseased hearts, according to the study.

Mark Mercola, director of Sanford-Burnham's Muscle Development and Regeneration Program, said heart disease is the leading cause of death in the United States, but doctors can't replace damaged heart muscle.

"The only way to effectively replace lost heart muscle cells - called cardiomyocytes - is to transplant the entire heart," said Mercola, the senior author of the study. "Using a drug to create new heart muscle from stem cells would be far more appealing than heart transplantation."

Stem cells were targeted for the study because they can self-replicate and convert to other, specialized types of cells. The challenge for scientists is to discover the signals that direct the stem cells to turn into the types of cells they want.

The researchers said ITD-1 works by preventing a protein from sending signals to cells that regulate various functions, allowing them to re-create themselves into heart cells. According to Sanford-Burnham, Mercola has been looking for ways to convert stem cells into heart cells for 15 years.

"This particular molecule could be useful to enhance stem cell differentiation in a damaged heart," said Erik Willems, another author of the study. "At some point, it could become the basis for a new therapeutic drug for cardiovascular disease - one that would likely limit scar spreading in heart failure and promote new muscle formation."

According to Sanford-Burnham, Mercola, Willems, and John Cashman of the Human BioMolecular Research Institute are now working with San Diego biotech company ChemRegen Inc. to develop ITD-1 into a drug that one day might be used to treat patients.

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Stem cell research by local science organizations could lead to new treatments for heart disease

Scientists have found evidence that cancerous tumors might originate as stem cells - undifferentiated master cells which can grow into any tissue in the body. Investigators say if this proves true, it could provide a new way to prevent or cure cancer.

Stem cells are primitive structures in the human body that normally transform themselves into healthy, specialized tissue, everything from blood and bone cells to heart and liver cells. Now there is evidence that stem cells can also develop into cancer cells that multiply into life-threatening tumors.

The conventional theory of cancer formation is that it begins with the division of a single mutated cell. The new study challenges this theory with evidence that mutated, cancerous cells may develop directly from stem cells.

Luis Parada, head of developmental biology at the University of Texas Southwestern Medical Center in Dallas, and his colleagues studied an aggressive, lethal form of human brain cancer called glioblastoma multiforme in genetically bred mice. The cancer is usually fatal within a year of diagnosis. Researchers used chemotherapy on the rodents that temporarily halted the growth of their tumors. But when investigators stopped the drug, the cancer came back. Parada says a molecular analysis showed the tumors recurred because a small number of stem cells clustered within the brain tissue began dividing, producing new tumor cells.

But when a group of mice with glioblastoma were given both chemotherapy and a drug that destroyed the stem cells in their brain tissue, their cancer was cured.

Parada says the findings could radically change the way cancer is treated.

Then its no longer valid to evaluate the volume of a tumor and say whether therapy is working or not. What will be important is to know is how that therapy is affecting the cancer stem cells within the tumor, Parada said.

Two other independent studies published this week provide additional evidence that stem cells may be the starting point for cancerous tumors. One team of researchers from Universite Libre de Bruxelles in Brussels, Belgium, and the Wellcome Trust Cancer Research Institute in Britain looked at the role of the master cells in the development of squamous cell carcinoma, a form of skin cancer.

Another group of investigators at the University Medical Center in Utrecht, the Netherlands, engineered a multi-colored model of an intestinal tumor known as an adenoma so they could trace the progression of stem cells to an early-stage tumor. Researchers tagged the master cells with a red color and watched as they produced a protein that stimulated the growth of pre-cancerous blue cells.

Researcher Hugo Snippert, who created the adenoma model, says there can be many genetic mutations in cells that dont cause cancer. He says its only when the stem cells are mutated that cancer develops.

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Study Identifies Stem Cells as Cancer Source

SAN DIEGO - Researchers at a pair of San Diego-based life scienceorganizations announced Thursday the discovery of a molecule that converts stemcells into healthy heart cells, ending a 15-year hunt.

The finding, published in Friday's issue of the journal Cell Stem Cell,could lead to new treatments for heart disease. The study was performed atSanford-Burnham Medical Research Institute, the Human BioMolecular ResearchInstitute, and ChemRegen Inc.

The molecule known as ITD-1 is able to generate an unlimited supply ofheart cells, which would give scientists more heart cells to study in theirresearch, and give physicians healthy cells to use to treat diseased hearts,according to the study.

Mark Mercola, director of Sanford-Burnham's Muscle Development andRegeneration Program, said heart disease is the leading cause of death in theU.S., but doctors can't replace damaged heart muscle.

"The only way to effectively replace lost heart muscle cells -- calledcardiomyocytes -- is to transplant the entire heart," said Mercola, the seniorauthor of the study. "Using a drug to create new heart muscle from stem cellswould be far more appealing than heart transplantation."

Stem cells were targeted for the study because they can self-replicateand convert to other, specialized types of cells. The challenge for scientistsis to discover the signals that direct the stem cells to turn into the types ofcells they want.

Link:
15 Year Stem Cell Study Yields Healthy Heart Cells

Researchers have discovered a molecule that converts stem cells into heart cells, which could be used to replace diseased or damaged tissue in patients suffering from heart disease.

Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham), the Human BioMolecular Research Institute, and ChemRegen, Inc. have been searching for molecules that convert stem cells to heart cells for about eight yearsand now they've found one.

In the new study, the researchers have described how they sifted through a large collection of drug-like chemicals and uncovered ITD-1, a molecule that can be used to generate unlimited numbers of new heart cells from stem cells.

"Heart disease is the leading cause of death in this country. Because we can't replace lost cardiac muscle, the condition irreversibly leads to a decline in heart function and ultimately death. The only way to effectively replace lost heart muscle cellscalled cardiomyocytesis to transplant the entire heart," Mark Mercola, senior author of the study, said.

"Using a drug to create new heart muscle from stem cells would be far more appealing than heart transplantation," he said.

Stem cells are important because they do two unique things self-renew, producing more stem cells and differentiate, becoming other, more specialized cell types.

To obtain a large number of a certain cell type, such as heart cells, the hard part is figuring out the signals that direct them to become the desired cell type.

Mercola's group has been hunting for heart-inducing signals for 15 yearsin embryos and in stem cells.

To find a synthetic molecule that might one day lead to a drug therapy to regenerate the heart, they joined forces with a team of medicinal chemists at the Human BioMolecular Research Institute led by John Cashman, Ph.D.

With funding from the California Institute for Regenerative Medicine, they used sophisticated robotic technology to methodically test a large collection of drug-like chemicals, looking for that needle in a haystack that, when added to stem cells, results in cardiomyocytes.

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How to mend a broken heart

Stem cells fuel cancer

There's new information on just how powerful cancer cells can be. Three new studies are out that could answer just how cancer can return even after chemotherapy.

Scientists believe cancer returns because the cancer cells themselves contain their own pool of stem cells that can multiply and fuel the cancer.

Stem cells in healthy tissues are known for their ability to produce any kind of cell. The new research deals with a different kind, cancer stem cells. Some researchers, but not all, believe they lurk as a persisting feature in tumors.

Over the last decade, studies have found evidence for them in tumors like breast and colon cancers. But this research has largely depended on transplanting human cancer cells into mice that don't have immune systems, an artificial environment that raises questions about the relevance of the results.

Now, three studies reported online Wednesday in the journals Nature and Science present evidence for cancer stem cells within the original tumors. Again, the research relies on mice. That and other factors mean the new findings still won't convince everyone that cancer stem cells are key to finding more powerful treatments.

Exercise benefits depression

Your daily trip to the gym may be more beneficial than you think. A new study out shows exercise is an effective tool in warding off depression.

Researchers looked at participants who were depressed and had heart disease. Those who combined the medication Zoloft within 90 minutes of exercise, got more relief than those who took a placebo pill.

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Health Headlines: Stem cells fuel cancer

Public release date: 2-Aug-2012 [ | E-mail | Share ]

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

STANFORD, Calif. Stem cells are special. Nestled in muscle and skin, organ and bone, they bide their time over years or decades until called to replace damaged or lost tissue. One secret to their longevity is an enzyme called telomerase, which stills the relentless ticking of the molecular clock that limits the life span of other cells.

This cellular fountain of youth prevents the progressive shortening of the tips of our chromosomes that occurs with each cell division. But the presence of telomerase can be a double-edged sword: The same activity that ensures long life for stem cells can also keep a cancer cell dividing long after its aging neighbors have thrown in the towel. Conversely, a malfunction can prevent stem cells from doing their job and lead to devastating diseases.

Now, for the first time, researchers at the Stanford University School of Medicine have identified how telomerase is recruited to chromosome ends and figured out a way to block it.

"If telomerase is unable to maintain the ends of the chromosomes, cells will stop multiplying," said professor of medicine Steven Artandi, MD, PhD. "This would be advantageous in cancer cells, but in normal stem cells it can cause severe dysfunction and lead to diseases such as pulmonary fibrosis, aplastic anemia and a genetic condition called dyskeratosis congenita. We want to understand how telomerase works, and to develop therapies for cancer and these other diseases."

Artandi is the senior author of the research, which will be published Aug. 3 in Cell. He is also a member of the Stanford Cancer Institute. Graduate student Franklin Zhong is the first author of the study.

Telomerase is normally expressed in adult stem cells and immune cells, as well as in cells of the developing embryo. In these cells, the enzyme caps off the ends of newly replicated chromosomes, allowing unfettered cell division. Without telomerase, cells stop dividing or die when the ends called telomeres fall below a minimum length. Unfortunately, the enzyme is also active in nearly all cancer cells.

Earlier research in Artandi's lab identified a protein called TCAB1 that brings the telomerase complex (actually a large clump of many proteins) to a processing area in the cell's nucleus called a Cajal body. But no one knew how the complex was then ferried to the ends of telomeres, and research was stymied by the complex's large size, multiple components and relative scarcity.

"This problem has been really intractable," said Artandi. "The enzyme is extremely hard to study. But we've now found that telomerase is recruited to the telomeres through an interaction with a protein called TPP1 that coats the ends of chromosomes." What's more, the researchers have identified the exact region of TPP1 to which telomerase binds a section called an OB-fold.

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Research shows how protein component that enables cell replication gets ferried to chromosome tips

ScienceDaily (Aug. 2, 2012) Stem cells are special. Nestled in muscle and skin, organ and bone, they bide their time over years or decades until called to replace damaged or lost tissue. One secret to their longevity is an enzyme called telomerase, which stills the relentless ticking of the molecular clock that limits the life span of other cells.

This cellular fountain of youth prevents the progressive shortening of the tips of our chromosomes that occurs with each cell division. But the presence of telomerase can be a double-edged sword: The same activity that ensures long life for stem cells can also keep a cancer cell dividing long after its aging neighbors have thrown in the towel. Conversely, a malfunction can prevent stem cells from doing their job and lead to devastating diseases.

Now, for the first time, researchers at the Stanford University School of Medicine have identified how telomerase is recruited to chromosome ends -- and figured out a way to block it.

"If telomerase is unable to maintain the ends of the chromosomes, cells will stop multiplying," said professor of medicine Steven Artandi, MD, PhD. "This would be advantageous in cancer cells, but in normal stem cells it can cause severe dysfunction and lead to diseases such as pulmonary fibrosis, aplastic anemia and a genetic condition called dyskeratosis congenita. We want to understand how telomerase works, and to develop therapies for cancer and these other diseases."

Artandi is the senior author of the research, published Aug. 3 in Cell. He is also a member of the Stanford Cancer Institute. Graduate student Franklin Zhong is the first author of the study.

Telomerase is normally expressed in adult stem cells and immune cells, as well as in cells of the developing embryo. In these cells, the enzyme caps off the ends of newly replicated chromosomes, allowing unfettered cell division. Without telomerase, cells stop dividing or die when the ends -- called telomeres -- fall below a minimum length. Unfortunately, the enzyme is also active in nearly all cancer cells.

Earlier research in Artandi's lab identified a protein called TCAB1 that brings the telomerase complex (actually a large clump of many proteins) to a processing area in the cell's nucleus called a Cajal body. But no one knew how the complex was then ferried to the ends of telomeres, and research was stymied by the complex's large size, multiple components and relative scarcity.

"This problem has been really intractable," said Artandi. "The enzyme is extremely hard to study. But we've now found that telomerase is recruited to the telomeres through an interaction with a protein called TPP1 that coats the ends of chromosomes." What's more, the researchers have identified the exact region of TPP1 to which telomerase binds -- a section called an OB-fold.

"When we mutated this site in TPP1," said Artandi, "we blocked the interaction between the two proteins and prevented telomerase from going to the telomeres. And when we interfered with this interaction in human cancer cells, the telomeres began to shorten." The researchers are now assessing whether the life span of the cancer cells, and their ability to divide unchecked, will also be affected by the treatment.

To confirm their finding, Artandi and his colleagues used cells from patients with pulmonary fibrosis -- a debilitating scarring or thickening of lung tissue associated with telomerase mutations. The disease had been troubling to researchers and clinicians, however, because the patients' mutated telomerase seemed to be fully active when tested in the laboratory. Zhong and Artandi found that the disease-associated mutations occurred in the portion of telomerase that interacted with TPP1, and interfered with their binding. As a result the enzyme, although active, couldn't get to where it was needed.

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How protein component that enables cell replication gets ferried to chromosome tips

Multicolored intestine tissue in genetically modified mice allow scientists to track which cells give rise to tumors. Image: A. G. Schepers et al., Science (2012)

By Gretchen Vogel, ScienceNOW

All too often, cancer that seems to have been wiped out by treatment comes back. Some scientists have blamed so-called cancer stem cells, a subset of cancer cells that might be able to remain dormant, evading chemotherapy or radiation treatments, only to form new tumors months or years later. The idea has been controversial, but three papers published today report evidence that in certain brain, skin, and intestinal tumors, cancer stem cells are the source of tumor growth.

The cancer stem cell model differs from the traditional idea that tumor growth is equal opportunitythat is, any and all cancerous cells can divide and cause the tumor to grow and spread. The stem cell model says that tumor growth is more hierarchical, mainly driven by a subset of cells that can make new copies of themselves and give rise to the other cell types the tumor contains. Some of the first evidence for cancer stem cells came from studies of leukemia in the 1990s, which showed that only a small subset of the cancerous blood cells could propagate the disease in mice. But it has been harder to test whether cancer stem cells fuel the growth of tumors in other tissues.

In the new studies, three independent groups used genetic cell-marking techniques to trace the proliferation of certain cells within growing tumors. The method gives researchers a glimpse of what happens in the real life of a tumor, says Cdric Blanpain, a stem cell researcher at the Universit Libre de Bruxelles in Belgium. He and his colleagues report online in Nature that in mouse papilloma tumors, a precursor to skin cancer, most of the tumor growth came from a few cells, which in some ways resembled the stem cells that maintain healthy skin.

In a second paper, also published online today in Nature, developmental biologist Luis Parada and his colleagues at the University of Texas Southwestern Medical Center (UTSMC) in Dallas show that in mice that develop glioma, a form of brain cancer, tumor growth seems to come from a small subset of cells in the tumor. They find that the cells can remain dormant during chemotherapy that kills off most of the cancer and can give rise to new tumors once the drug treatment stops.

And in the third paper, published online today in Science, developmental biologists and stem cell researchers Hugo Snippert, Arnout Schepers, Hans Clevers, and their colleagues at the Hubrecht Institute in Utrecht, the Netherlands, used mice with multicolored intestines to look at the kinds of cells that form intestinal adenomas, a precursor to intestinal cancer. The rodents, which the scientists have nicknamed confetti mice, carry genetic markers that can label intestinal cells blue, green, red, or yellow depending on which cell they originate from. The team reports that the adenomas grow from cells that express a gene called Lgr5+, which is also active in normal intestinal stem cells. The tumor is really like a caricature of normal tissue, Snippert says.

Such cell-tracing techniques are the right approach to test the cancer stem cell model, says Sean Morrison, who studies stem cells and cancer at UTSMC and who was not involved in any of the studies. There is now enough evidence to be fairly sure that the model explains at least some types of cancer, he says. Morrison cautions, however, that the studies on papilloma and adenoma looked at precancerous tumors. Indeed, when Blanpain and his colleagues examined mice with squamous cell carcinoma, a malignant outgrowth of the papilloma, they found that most of the cells were actively dividing, not just a small subset of stem-cell-like cells.

Understanding which cancers might grow fromor simply harborcancer stem cells is key to more effective treatments, the researchers say. That is no easy task, however. Morrison notes that tumor growth differs even among patients with the same type of cancer. Still, says Parada, having three examples in which tumors seem to harbor cancer stem cells suggests there will be more. I hope it will bolster and stimulate the community to figure out how to better study the cancer stem cell model, he says. Lets bring this level of scrutiny to all solid tumors.

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Cancer Stem Cells Can Fuel Tumor Growth

(AP) Why does cancer come back after a tumor has been seemingly eradicated? Three new studies from American, Belgian, British and Dutch researchers may have an answer.

Study: Stem cells boost brain tumor treatments

The studies bolster a long-debated idea that tumors contain their own pool of stem cells that can multiply and keep fueling the cancer, seeding regrowth. If that's true, scientists will need to find a way to kill those cells, apart from how they target and attack the rest of the tumor.

Stem cells in healthy tissues are known for their ability to produce any kind of cell. The new research deals with a different kind, cancer stem cells. Some researchers, but not all, believe they lurk as a persisting feature in tumors.

Over the past decade, studies have found evidence for them in tumors like breast and colon cancers. But this research has largely depended on transplanting human cancer cells into mice that don't have immune systems, an artificial environment that raises questions about the relevance of the results.

Now, three studies reported online Wednesday in the journals Nature and Science present evidence for cancer stem cells within the original tumors. Again, the research relies on mice. That and other factors mean the new findings still won't convince everyone that cancer stem cells are key to finding more powerful treatments.

But researcher Luis Parada, of the University of Texas Southwestern Medical Center in Dallas, believes his team is onto something. He says that for the type of brain tumor his team studied, "we've identified the true enemy."

If his finding applies to other cancers, he said, then even if chemotherapy drastically shrinks a tumor but doesn't affect its supply of cancer stem cells, "very little progress has actually been made."

The three studies used labeling techniques to trace the ancestry of cells within mouse tumors.

Collectively, they give "very strong support" to the cancer stem cell theory, said Jeffrey M. Rosen, a professor of molecular and cellular biology at Baylor College of Medicine in Houston. He did not participate in the work but supports the theory, which he said is widely accepted.

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Stem cells in tumors may fuel cancer regrowth, new studies suggest

HOUSTON, Aug. 2, 2012 /PRNewswire/ --Celltex Therapeutics Corporation, a leader in regenerative medicine services, today announced the appointments of Andrea Ferrenz, Executive Vice President, Legal Counsel, and Jane Shen Young, Manufacturing Research Scientist. Ferrenz's primary responsibility will be overseeing operations, including compliance with federal and state regulatory agencies. Young's primary responsibility will be research and development of manufacturing processes and products in regenerative science.

"Celltex is a fast growing company. The additions of Andrea and Jane will enhance our capabilities as we continue to grow," said David Eller, Chief Executive Officer of Celltex. "At Celltex, we firmly believe in the great therapeutic potential for adult stem cells and we are committed to the highest quality banking and multiplication services for clients and physicians."

Ferrenz has more than 15 years of experience in regulatory compliance and litigation, with expertise in food, drug and health law. Prior to Celltex, Ferrenz was Principal Attorney at Emord & Associates, P.C., in Washington, D.C.There, she counseled both national and international clients in health products industries operating under the jurisdiction of the FDA and FTC.Early in her career, Ferrenz worked with the U.S. Department of Health and Human Services and Children's National Medical Center's Center for Cancer and Transplantation Biology.

Ferrenz received her Bachelor's degree in biology from University of Mary Washington in Fredericksburg, Virginia, and her juris doctorate from George Washington University Law School in Washington, D.C.

"As a pioneer in stem cell banking, Celltex is paving the way for this new frontier," said Ferrenz."I hope my background in health and FDA law will be an asset to Celltex and I look forward to helping Celltex grow while maintaining positive relationships with government regulators who work to ensure the safety of health products."

Young joins Celltex from Pharmaceutical Product Development, Inc. in Middleton, Wisconsin, where she served as Associate Research Scientist. Formerly an Internal physician in the Department of Medicine at Wang-Jiang-Shan Hospital in Zhejiang, China, and a Visiting Scientist and Ph.D. in molecular biology and biochemistry at the Lund University, Sweden, Young has expertise in cell biology, molecular genetics and biochemistry. She has also co-authored publications on the development and optimization of laboratory assays, and cell sort and flow cytometry analysis.

Young received her medical degree from Zhejiang University School of Medicine. Zhejiang, China. She received her doctoral degree from Lund University, Faculty of Medicine in Sweden.

"Stem cell banking is cutting edge technology in a field that holds great potential," noted Young. "Quality and safety are tantamount to the growth of this industry and I am excited to help Celltex provide stem cell banking and multiplication of the highest quality to its clients."

For more information on Celltex Therapeutics Corporation and its staff please visit http://www.CelltexBank.com.

About Celltex

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Celltex Therapeutics Corporation Expands Laboratory Operations And Adds Depth To Its Management Team

NEW YORK (AP) How can a cancer come back after it's apparently been eradicated? Three new studies are bolstering a long-debated idea: that tumors contain their own pool of stem cells that can multiply and keep fueling the cancer, seeding regrowth.

If that's true, scientists will need to find a way to kill those cells, apart from how they attack the rest of the tumor.

Stem cells in healthy tissues are known for their ability to produce any kind of cell. The new research deals with a different kind, cancer stem cells. Some researchers, but not all, believe they lurk as a persisting feature in tumors.

Over the past decade, studies have found evidence for them in tumors like breast and colon cancers. But this research has largely depended on transplanting human cancer cells into mice that don't have immune systems, an artificial environment that raises questions about the relevance of the results.

Now, three studies reported online Wednesday in the journals Nature and Science present evidence for cancer stem cells within the original tumors. Again, the research relies on mice. That and other factors mean the new findings still won't convince everyone that cancer stem cells are key to finding more powerful treatments.

But researcher Luis Parada, of the University of Texas Southwestern Medical Center in Dallas, believes his team is onto something. He says that for the type of brain tumor his team studied, "we've identified the true enemy."

If his finding applies to other cancers, he said, then even if chemotherapy drastically shrinks a tumor but doesn't affect its supply of cancer stem cells, "very little progress has actually been made."

The three studies used labeling techniques to trace the ancestry of cells within mouse tumors.

Collectively, they give "very strong support" to the cancer stem cell theory, said Jeffrey M. Rosen, a professor of molecular and cellular biology at Baylor College of Medicine in Houston. He did not participate in the work but supports the theory, which he said is widely accepted.

Another scientist who's skeptical about the theory, and said he has plenty of company, said the new papers did not change his mind.

The rest is here:
Cancer debate: Are tumors fueled by stem cells?

NEW YORK (AP) -- How can a cancer come back after it's apparently been eradicated? Three new studies are bolstering a long-debated idea: that tumors contain their own pool of stem cells that can multiply and keep fueling the cancer, seeding regrowth.

If that's true, scientists will need to find a way to kill those cells, apart from how they attack the rest of the tumor.

Stem cells in healthy tissues are known for their ability to produce any kind of cell. The new research deals with a different kind, cancer stem cells. Some researchers, but not all, believe they lurk as a persisting feature in tumors.

Over the past decade, studies have found evidence for them in tumors like breast and colon cancers. But this research has largely depended on transplanting human cancer cells into mice that don't have immune systems, an artificial environment that raises questions about the relevance of the results.

Now, three studies reported online Wednesday in the journals Nature and Science present evidence for cancer stem cells within the original tumors. Again, the research relies on mice. That and other factors mean the new findings still won't convince everyone that cancer stem cells are key to finding more powerful treatments.

But researcher Luis Parada, of the University of Texas Southwestern Medical Center in Dallas, believes his team is onto something. He says that for the type of brain tumor his team studied, "we've identified the true enemy."

If his finding

The three studies used labeling techniques to trace the ancestry of cells within mouse tumors.

Collectively, they give "very strong support" to the cancer stem cell theory, said Jeffrey M. Rosen, a professor of molecular and cellular biology at Baylor College of Medicine in Houston. He did not participate in the work but supports the theory, which he said is widely accepted.

Another scientist who's skeptical about the theory, and said he has plenty of company, said the new papers did not change his mind.

Read the rest here:
Cancer debate: Are tumors fueled by own stem cells?

How can a cancer come back after it's apparently been eradicated? Three new studies are bolstering a long-debated idea: that tumors contain their own pool of stem cells that can multiply and keep fueling the cancer, seeding regrowth.

If that's true, scientists will need to find a way to kill those cells, apart from how they attack the rest of the tumor.

Stem cells in healthy tissues are known for their ability to produce any kind of cell. The new research deals with a different kind, cancer stem cells. Some researchers, but not all, believe they lurk as a persisting feature in tumors.

Over the past decade, studies have found evidence for them in tumors like breast and colon cancers. But this research has largely depended on transplanting human cancer cells into mice that don't have immune systems, an artificial environment that raises questions about the relevance of the results.

Now, three studies reported online Wednesday in the journals Nature and Science present evidence for cancer stem cells within the original tumors. Again, the research relies on mice. That and other factors mean the new findings still won't convince everyone that cancer stem cells are key to finding more powerful treatments.

But researcher Luis Parada, of the University of Texas Southwestern Medical Center in Dallas, believes his team is onto something. He says that for the type of brain tumor his team studied, "we've identified the true enemy."

If his finding applies to other cancers, he said, then even if chemotherapy drastically shrinks a tumor but doesn't affect its supply of cancer stem cells, "very little progress has actually been made."

The three studies used labeling techniques to trace the ancestry of cells within mouse tumors.

Collectively, they give "very strong support" to the cancer stem cell theory, said Jeffrey M. Rosen, a professor of molecular and cellular biology at Baylor College of Medicine in Houston. He did not participate in the work but supports the theory, which he said is widely accepted.

Another scientist who's skeptical about the theory, and said he has plenty of company, said the new papers did not change his mind.

Read more:
Are tumors fueled by stem cells?

Featured Article Academic Journal Main Category: Cancer / Oncology Also Included In: Stem Cell Research;Biology / Biochemistry Article Date: 02 Aug 2012 - 2:00 PDT

Current ratings for: Cancer Stem Cells May Drive Tumor Growth

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Papers on all three studies appeared online on Wednesday, two in Nature and one in Science.

In all three studies, the teams used genetic cell-marking techniques to track cell lineage and show that a restricted cell population appears to be the source of new tumor cells, in much the same way as stem cells are the "master builders" of new healthy cells.

GBM is a type of brain cancer that is currently considered incurable. It is a fast-growing tumor with a median survival of about 15 months. Although initially it responds to chemotherapy, the cancer nearly always comes back.

In their study, Parada and colleagues used genetically engineered mice bred to develop GBM and found that the resting tumor cells act more like stem cells.

They used a genetic marker that labels healthy adult neural stem cells, but not their more specialized descendants, to see if it would do the same for cancer stem cells in GBM. When they did so, they found all the tumors contained at least a few labelled cells, which they presumed to be stem cells.

The tumors also contained unlabelled cells, which could be killed with standard chemotherapy, but then the tumors came back soon afterwards. When they tested them again, they found the tumors contained unlabelled cells that came from labelled predecessors.

When they applied chemotherapy with a technique that suppressed the labelled cells, the researchers found the tumors shrank back to what Parada described to Nature NEWS as "residual vestiges" that bore no resemblance to GBM.

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Cancer Stem Cells May Drive Tumor Growth