THURSDAY - March 6, 2008-------------------------------------------------News Archive/Return to Today's News Alerts

Gene Mutations Linked to Longer Life Spans

Animal research had shown that mutations to genes involved in the IGF-I signaling pathway cause two effects: Affected animals have impaired growth - but also longer life spans.

Scientists at the Albert Einstein College of Medicine of Yeshiva University reasoned that altered signaling in this pathway might also influence human longevity. To find out, they analyzed IGF-I-related genetic variations in 384 Ashkenazi (Eastern European) Jewish centenarians. And since plasma levels of IGF-I do not reflect their levels at a younger age, the researchers also looked at two other groups: the children of these centenarians, and a control group consisting of Ashkenazi Jews the same age as the centenarians’ children but with no family history of longevity.

The present study focused on genes involved in the action of insulin-like growth factor (IGF-I), a hormone that in humans is regulated by human growth hormone. Affecting virtually every cell type in the body, IGF-I is crucially important for children’s growth and continues contributing to tissue synthesis into adulthood. The IGF-I cell-signaling pathway is triggered when IGF-I molecules circulating in blood plasma latch onto receptors on the surface of cells, causing a signal to be sent to the cell’s nucleus that may, for example, tell that cell to divide.

Remarkably, the female children of the centenarians had IGF-I plasma levels that were 35 percent higher than female controls—perhaps a sign that the body was compensating for a glitch in IGF-I signaling by secreting increased amounts of the hormone. That suspicion was strengthened by two other findings: the daughters of centenarians were 2.5 cm shorter than female controls; and when the researchers analyzed the gene coding for the IGF-I cell-surface receptor molecule to which the IGF-I hormone binds, the receptor genes of centenarians and their daughters were much more likely to have a variety of mutations than were the receptor genes of the controls.

“Our findings suggest that, by interfering with IGF-I signaling, these gene mutations somehow play a role in extending the human life span, as they do in many other organisms,” says Dr. Nir Barzilai, senior author of the study and director of the Institute for Aging Research at Einstein.
Dr. Barzilai notes that a drug that decreases IGF-I action is currently being tested as a cancer treatment and could be useful in delaying aging. “Since the subjects in our study have been exposed to their mutations since conception, it is not clear whether people would need such a therapy throughout life or if it could help people who received it at a later time.”

Published March, 2008 in the journal Nature Materials
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WEDNESDAY - March 5, 2008-------------------------------------------------News Archive/Return to Today's News Alerts

Electronic Structure of DNA Revealed For 1st Time

Utilizing a technique that combines low temperature measurements and theoretical calculations, Hebrew University of Jerusalem scientists and others have revealed for the first time the electronic structure of single DNA molecules.

The knowledge of the electronic properties of DNA is an important issue in many scientific areas from biochemistry to nanotechnology - for example in the study of DNA damage by ultraviolet radiation that may cause the generation of free radicals and genetic mutations. In those cases, DNA repair occurs spontaneously via an electronic charge transfer along the DNA helix that restores the damaged molecular bonds.

In nano-bioelectronics, which is the advanced research field devoted to the study of biological molecules (to produce electrical nanocircuits, for example), it has been suggested that DNA, or its derivatives, may become used as possible conducting molecular wires in the realization of molecular computing networks which are smaller and more efficient than those produced today with silicon technology.

The knowledge that has been acquired in this project, say the researchers, may also be relevant for current attempts to develop new sophisticated, reliable, faster and cheaper ways to decode the sequence of human DNA.

The research, published in the prestigious journal Nature Materials, is a result of an international collaboration. The research was conducted by Errez Shapir and coordinated by Dr. Danny Porath at the Department of Physical Chemistry and Center for Nanoscience and Nanotechnology at the Hebrew University and by Dr. Rosa Di Felice at the S3 Center of INFM-CNR in Modena, Italy. Also collaborating in the project were Prof. Alexander Kotlyar at Tel Aviv University, who synthesized the molecules, the CINECA supercomputing center in Italy, and Prof. Gianaurelio Cuniberti at the University of Regensburg, Germany.

In their work, the researchers were able to decode the electronic structure of DNA and to understand how the electrons distribute into the various parts of the double helix, a result that has been pursued by scientists for many years, but was previously hindered by technical problems.

Published March, 2008 in the journal Nature Materials
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Autism: Mother's Antibody Production May Affect Fetal Brain

The mothers of some autistic children may have made antibodies against their fetuses’ brain tissue during pregnancy that crossed the placenta and caused changes that led to autism, suggests research led by Johns Hopkins Children’s Center investigators and published in the February issue of the Journal of Neuroimmunology.

The causes of autism, a disorder manifesting itself with a range of brain problems and marked by impaired social interactions, communication disorders and repetitive behaviors, remain unknown for an estimated 90 percent of children diagnosed with it. Genetic, metabolic and environmental factors have been implicated in various studies of autism, a disorder affecting 1 in 150 U.S. children, according to estimates by the Centers for Disease Control and Prevention.

“Now our research suggests that the mother’s immune system may be yet another factor or a trigger in those already predisposed,” says lead investigator Harvey Singer, M.D., director of pediatric neurology at Hopkins Children’s.

Researchers caution that the findings needn’t be cause for alarm, but should be viewed instead as a step forward in untangling the complex nature of autism.

Mostly anecdotal past evidence of immune system involvement has emerged from unusual antibody levels in some autistic children and from postmortem brain tissue studies showing immune abnormalities in areas of the brain. Antibodies are proteins the body makes in response to viruses and bacteria or sometimes mistakenly against its own tissues. Yet, the majority of children with autism have no clinical evidence of autoimmune diseases, which prompted researchers to wonder whether the antibodies transferred from mother to child during pregnancy could interfere with the fetal brain directly.

To test their hypothesis, the research team used a technique called immunoblotting (or Western blot technology), in which antibodies derived from blood samples are exposed to adult and fetal brain tissue to check whether the antibodies recognize and react against specific brain proteins.

Comparing the antibody-brain interaction in samples obtained from 100 mothers of autistic children and 100 mothers of children without autism, researchers found either stronger reactivity or more areas of reactivity between antibodies and brain proteins in about 40 percent of the samples obtained from the mothers of autistic children. Further, the presence of maternal antibodies was associated with so-called developmental regression in children, increasingly immature behaviors that are a hallmark of autism.

While the findings suggest an association between autism and the presence of fetal brain antibodies, the investigators say further studies are needed to confirm that particular antibodies do indeed cross the placenta and cause damage to the fetal brain.

“The mere fact that a pregnant woman has antibodies against the fetal brain doesn’t mean she will have an autistic child,” Singer says. “Autism is a complex condition and one that is likely caused by the interplay of immune, genetic and environmental factors.”

Researchers are also studying the effect of maternal antibodies in pregnant mice. Preliminary results show that the offspring of mice injected with brain antibodies exhibit developmental and social behaviors consistent with autism.

Published March 3, 2008 in the Journal of Neuroimmunology

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A Molecular Alliance Sustains Embryonic Stem Cell State

Four ingredients are in the genetic recipe that scientists in Japan and the U.S. followed last year to persuade human skin cells to revert to an embryonic stem cell state - Oct4, Sox2, c-Myc, and Klf4. One, the reprogramming factor Klf4, determines whether a cell's genes are active or silent - but has at least two other sibling molecules that will substitute for it in order to maintain the pluripotent embryonic stem (ES) cell state, says the Genome Institute of Singapore (GIS) research team leader Ng Huck Hui, Ph.D.

Klf4 (also known as gut-enriched Krüppel-like factor or Gklf) belongs to the Krüppel-like factor (Klf) family of transcription factors regulating biological processes including proliferation, differentiation, development and apoptosis (programmed cell death). As reprogramming mature cells into an ES state may provide a ready source of tissue for biomedical research and clinical treatment of disease, several laboratories, including GIS, are trying to unravel and finely tune the reprogramming process.

GIS research found that when Klf4 was depleted, Klf2 and Klf5 took over Klf4's role. So the scientists studied the DNA binding and transcription properties of the three and found their profiles strikingly similar. "Most important, the data showed that the other Klfs were bound to the target sites when one of them was depleted." said Dr. Ng. "These Krüppel-like factors form a very powerful alliance that work together on regulating common targets. The impact of losing one of them is masked by the other two sibling molecules."

For example, Klfs were found to regulate the Nanog gene and other key genes that must be active for ES cells to be pluripotent. Nanog is one of the key pluripotency genes in ES cells.

"We suggest that Nanog and other genes are key effectors for the biological functions of the Klfs in ES cells," says Dr. Ng. "Together, our study provides new insight into how the core Klf circuitry integrates into the Nanog transcriptional network to specify gene expression unique to ES cells. The way these factors network with key genes in ES cells suggest a way of how Klf4 (along with the other three reprogramming factors) can jump-start the ES cell gene expression engine in adult cells," he noted.

Although these three Klfs are involved in diverse biological roles, their redundant roles had not been previously appreciated.

"The mystery of the role of Klf4 has been revealed in studies by Huck Hui and colleagues," added Alan Colman, Ph.D., Executive Director of the Singapore Stem Cell Consortium, which like GIS, is part of Singapore's Agency for Science, Technology and Research (A*STAR). "They show for the first time that Klf4 itself is not needed for the maintenance of the pluripotent state in ES cells; however, this is because the cells have a number of other Klf-like transcription factors that can substitute for Klf4.

Published March, 2008 in the journal Nature Cell Biology
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TUESDAY - March 4, 2008------------------------------------------------------News Archive/Return to Today's News Alerts

Genetic Region Linked to Breast Cancer Risk

A genetic variation in a region of chromosome six appears to increase the risk of breast cancer by about 40%. The region contains at least two genes but researchers were unable to determine which of them was responsible for the effect, according to Kenneth Offit, M.D., of Memorial Sloan-Kettering Cancer Center, and colleagues.

Using the increasingly popular method of genome-wide association scanning, the study confirmed that a region on chromosome 10 is also associated with increased breast cancer risk, Dr. Offit and colleagues said in the Proceedings of the National Academy of Sciences. The 40% increase in risk associated with the newly found genetic variant pales in comparison to the 20- to 40-fold increase in risk associated with mutations in the two BRCA genes. However, "these results are exciting because they point us to new molecular pathways that may be associated with breast cancer," Dr. Offit said in a statement.

Participants in the study were Ashkenazi Jews with breast cancer and a family history of the disease but no detectable mutations in BRCA1 or BRCA2 and cancer-free controls from the same population. Ashkenazi Jews were chosen because they form a genetically isolated population in which it is easier to detect so-called founder mutations that might be missed in a more genetically diverse group.

The initial cohort (study population) consisted of 249 women with breast cancer and 299 controls. After analysis of 150,080 single nucleotide polymorphisms (SNPs) in that cohort, the researchers isolated 343 that seemed to differ between cases and controls and re-analyzed them. They also re-analyzed their results in a third cohort of 243 sporadic breast cancer cases and 187 cancer-free controls and found a 26% increase in risk associated with the region on chromosome 10 that includes the gene for fibroblast growth factor receptor 2, supporting a finding reported earlier by another group.

The novel finding was a risk locus at rs2180341 in a region of chromosome six, the researchers said. The two genes in the region are RNF146 and ECHDC1, neither of which has been well studied in breast cancer, adding that other genes may also play a role in creating the association. Researchers pointed out that the variation carried by most women in the study - the so-called major haplotype - appears to protect against breast cancer and that only a minority of the women carried the variation that increased the risk. The study still needs to be repeated in a more genetically diverse population to see if the results stand up, the researchers said.

Until more is known, Dr. Offit cautioned, "this newly identified genetic marker will not have any immediate clinical implications or impact on current screening guidelines for familial breast cancer." He added that tests for the variants "should be performed only as part of research studies."

Published March, 2008 in the journal Nature Cell Biology

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Protein in Embryonic Stem Cells Control Malignant Tumor Cells

A protein that governs development of human embryonic stem cells (hESCs) also inhibits the growth and spread of malignant melanoma, the deadliest skin cancer, Northwestern University researchers have discovered. Metastatic melanoma, which develops from the transformation of skin pigment cells or melanocytes, has a death rate of more than 80 percent and a median survival of less than 7.5 months.

The Northwestern scientists, led by researcher Mary J. C. Hendrix, M.D., additionally found that the protein, called Lefty, prevents aggressive breast cancer cells from metastasizing. Death from metastatic breast cancer exceeded 40,000 in 2007, with over 180,000 new cases diagnosed in the United States.

Importantly, Lefty is secreted only in hESCs, and not in any other stem cell type tested – including stem cells isolated from amniotic fluid, cord blood or adult bone marrow – or placental cells.

Embryonic stem cells are pluripotent, meaning they can become any of 200-plus cell types in the adult body, depending on the signals they receive from their microenvironment (surrounding cells, tissues and vasculature). During cancer progression, malignant cells also receive and release signals from their microenvironment, cues that promote tumor growth and metastasis.

Groundbreaking work by Hendrix and colleagues is explaining how, by becoming more like unspecialized stem cells, aggressive melanoma cells migrate, invade and metastasize while remaining virtually undetected by the immune system.

Hendrix and co-researchers in previous research demonstrated that a three-dimensional matrix conditioned with hESCs induced metastatic melanoma cells to revert to normal, skin cell-like types. “This observation allowed us to appreciate the powerful influence of the hESC microenvironment on the reprogramming of metastatic melanoma cells,” Hendrix said.

In subsequent experiments, Hendrix, Postovit and co-researchers found that aggressive melanoma and breast cancer produce a “morphogenic” protein called Nodal - essential for human embryonic stem cell pluripotency. Other researchers have found that Nodal also is present in testicular cancer. “Nodal may serve as a prognostic marker of aggressive behaviors in human cancers,” Hendrix said.

As described in the PNAS study, the Lefty protein inhibits production of Nodal and therefore plays a major role in embryonic cell differentiation and development – under normal circumstances. Hendrix and colleagues discovered that metastatic tumor cells do not express Lefty, allowing them to overproduce Nodal in an unregulated manner. But when metastatic tumor cells were exposed to the microenvironment of hESCs containing Lefty, Nodal production was dramatically reduced with decreased tumor cell growth and invasiveness and an increase in programmed cell suicide.

Although exposure to a hESC microenvironment inhibited Nodal expression and tumor growth in both metastatic melanoma and breast cancer cells, the breast cancer cells underwent more complex reprogramming. Melanoma cells responded to the hESC-derived factors within three days, but breast cancer cells required two additional days to achieve the most significant reduction in Nodal. This discrepancy is likely due to differences in signaling mechanisms between the two cell types. Despite the differences between melanoma cells and breast cancer cells, both of these divergent tumor types committed cell suicide following exposure to the hESC microenvironment.

“Further, the tumor suppressive effects of the hECs microenvironment, by neutralizing the expression of Nodal in aggressive tumor cells, provide previously unexplored novel therapeutic modalities for cancer treatment,” Hendrix said.However, while findings from the study suggest that hESC-derived Lefty may have potential to prevent metastasis, it is not the only tumor suppressive factor within the embryonic microenvironment. Observations from the study highlight the potential utility of isolating factors within the hESC microenvironment responsible for influencing tumor cell fate and reversing the cancerous properties of metastatic tumor cells, such as melanoma and breast cancer.

Published March 3, 2008 in the journal Proceedings of the National Academy of Sciences - PNAS

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Gender Differences in Language Appear Biological

For the first time - and in unambiguous findings - researchers from Northwestern University and the University of Haifa show both that areas of the brain associated with language work harder in girls than in boys during language tasks, and that boys and girls rely on different parts of the brain when performing these tasks.

“Our findings – which suggest that language processing is more sensory in boys and more abstract in girls - could have major implications for teaching children and even provide support for advocates of single sex classrooms,” said Douglas D. Burman, research associate in Northwestern’s Roxelyn and Richard Pepper Department of Communication Sciences and Disorders.

Using functional magnetic resonance imaging (fMRI), researchers measured brain activity in 31 boys and in 31 girls aged 9 to 15 as they performed spelling and writing language tasks. The tasks were delivered both visually and through auditory means. Using a complex statistical model, the researchers found that girls still showed significantly greater activation in language areas of the brain than boys. The information in the tasks got through to girls’ language areas of the brain - areas associated with abstract thinking through language. And their performance accuracy correlated with the degree of activation in some of these language areas.

To their astonishment, however, this was not at all the case for boys. In boys, accurate performance depended - when reading words - on how hard visual areas of the brain worked. In hearing words, boys’ performance depended on how hard auditory areas of the brain worked. Given boys’ sensory approach, boys might be more effectively evaluated on knowledge gained from lectures via oral tests and on knowledge gained by reading via written tests. For girls, whose language processing appears more abstract in approach, these different testing methods would appear unnecessary.

If the pattern of females relying on an abstract language network and of males relying on sensory areas of the brain extends into adulthood - a still unresolved question - it could explain why women often provide more context and abstract representation than men.

Ask a woman for directions and you may hear something like: “Turn left on Main Street, go one block past the drug store, and then turn right, where there’s a flower shop on one corner and a cafe across the street.” Such information-laden directions may be helpful for women because all information is relevant to the abstract concept of where to turn; however, men may require only one cue and be distracted by additional information.

Published March, 2008 in the journal Neuropsychologia

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MONDAY - March 3, 2008------------------------------------------------------News Archive/Return to Today's News Alerts

Adult Stem Cell Changes Underlie Rare Progeria Syndrome

Adult stem cells may explain the cause of a Hutchinson-Gilford Progeria Syndrome (HGPS), a rare disease that causes premature aging in children, according to researchers at the National Cancer Institute (NCI), part of the National Institutes of Health (NIH). These findings are the first to indicate a biological basis for HGPS, also known as progeria, and may also provide new insights into the biological mechanisms of normal aging.

“Studies like this of the biology of HGPS hold the potential to benefit children suffering this terrible illness and enlighten us as to the medical changes we all experience as we grow older.” said NCI Director John E. Niederhuber, M.D.

HGPS is an extremely rare hereditary genetic disease of children characterized by signs of premature aging. Children with HGPS generally experience the first symptoms by the age of one, and on average succumb around the age of 15, almost exclusively from premature, progressive heart disease. HGPS occurs in one out of four to eight million births; only 100 patients have been documented in the medical literature. Because its striking cardiovascular effects and other clinical features are so closely associated with the normal aging process, HGPS holds great interest for researchers studying age-related biological changes and disease.

Because most of the tissues affected by HGPS (e.g., skin, fat, muscles, bone, and blood vessels) arise from a common developmental pathway, Misteli and Scaffidi looked at the effects of progerin on adult mesenchymal stem cells, their common cellular ancestor. An adult stem can renew itself, and differentiate into the major specialized cell types of any tissue or organ. Their experiments revealed that progerin profoundly affects the fate of these stem cells, skewing the rate at which they mature. For instance, progerin-producing stem cells showed accelerated maturation into bone but failed to develop into fat. This could explain two of the distinguishing clinical features of HGPS: abnormal bone growth and an almost complete loss of the fatty tissues normally found just beneath the skin. The researchers were able to mimic the progerin’s effects in these stem cells by experimentally activating the same components of the Notch pathway targeted by progerin.

Taken together, the results of these experiments provide a new window into the biology behind the clinical features of HGPS. They may also hold relevance for understanding the biology of normal aging. “Progerin is present at low levels in the cells of healthy people,” said Misteli. “One could envision a scenario in which progerin’s effects on the Notch pathway and, by extension, on adult stem cells could, over time, lead to many of the tissue changes we commonly associate with the aging process.”

Published March, 2008 in the journal Nature Cell Biology

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MicroRNA-203 Helps Skin Cells Prolifferate Into Protective Barrier

Every minute, 30,000 of our outermost skin cells die so that we can live. When they do, new cells migrate from the inner layer of the skin to the surface of it, where they form a tough protective barrier. In a series of elegant experiments in mice, researchers at Rockefeller University have now discovered a tiny RNA molecule that helps create this barrier. The results not only yield new insight into how skin first evolved, but also suggest how healthy cells can turn cancerous.

Hundreds of these tiny RNA molecules, called microRNAs, are expressed in skin, "But there was something curious about one in particular, microRNA-203," says Rui Yi, a postdoc who works with Elaine Fuchs, head of the Laboratory of Mammalian Cell Biology and Development. "As an embryo develops, the expression of microRNA-203 jumps very quickly over just two days. From being barely detectable at day 13, this microRNA becomes the most abundant expressed in skin," says Yi, whose work will be published as an advance online publication in Nature March 2. MicroRNAs, which were discovered in mammals in 2001, regulate genes outside of the cell's nucleus.

Yi and Fuchs, who is also a Howard Hughes Medical Institute investigator and Rebecca C. Lancefield Professor at Rockefeller, found that during the 13th day of development, mouse skin is primarily composed of undifferentiated stem cells. Two days later, these stem cells exit the inner layer of the skin and begin to differentiate into cells that form the outermost, protective layer. MicroRNA-203's expression skyrockets precisely during this period, suggesting that it plays some key role in the barrier's development.

In order to figure out its role, Yi and Fuchs needed to pinpoint exactly where microRNA-203 is expressed. Other microRNAs have been found to be specific to heart and muscle tissues; some exist almost exclusively in the brain. However, this microRNA was found only in very specific types of skin - stratified epithelial tissues, to be exact - and only in this skin type's outer layers. What's more, this expression pattern is identical to that found in humans, zebrafish, chickens and the like - in other words, vertebrates that evolved more than 400 million years apart.

"If it has been expressed in this very specific tissue for a long time and across several species, it means that it probably plays an important role there," says Yi. To find out its function, Yi, in one set of experiments, used a genetic technique to precociously express microRNA in the inner layer of the skin, where stem cells proliferate at a fast clip. In a second set of experiments, he blocked microRNA-203 from functioning in the outer layer using an antagomir, a molecule that binds directly to microRNA-203 and shuts down its ability to carry out its function.

In the first set, he found that the stem cells proliferated significantly less than they did when microRNA-203 wasn't expressed, and, as a result, the mice formed very thin skin - hardly a protective layer at all. The stem cells, the researchers saw, lost their ability to proliferate not because microRNA-203 killed them off but because it suppressed the activity of a molecule called p63, whose job is to keep cells, primarily stem cells, proliferating. In the second set of experiments, Yi found that the cells in the outer layer proliferated significantly more than they did when microRNA-203 was expressed. The reason: because microRNA-203 wasn't available to shut down p63's busy work.

"We found that microRNA-203 acts to stop the translation of the p63 protein," says Fuchs. "The result is a swift transition from proliferating stem cells within the innermost layer of the epidermis and terminally differentiating cells as they exit this layer and move outward to the skin surface."

The findings have intriguing implications for cancer, since p63 is found in excess in cancer cells. "As a next step, we are going to examine whether low expression of microRNA-203 is associated with squamous cell carcinomas," says Fuchs, "and whether by putting back microRNA-203 we can inhibit the growth of these cancer cells."

Published March 2, 2008 in the journal Nature

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Do Adult Stem Cells Warrant Clinical Trials for Cardiovascular & Autoimmune Diseases?

Stem cells harvested from an adult’s blood or marrow may provide treatment benefit to select patients for some autoimmune diseases and cardiovascular disorders, according to an article in the February 27 issue of JAMA.

In broad terms, there are two types of stem cells, embryonic stem cells and adult stem cells. Human embryonic stem cells are isolated from a 4- to 5-day-old postfertilization blastocyst (an early form in the development of an embryo). Adult stem cells are located in tissues throughout the body and function as a reservoir to replace damaged or aging cells. Stem cell therapy is rapidly developing and shows great promise, “but clinical application has lagged due to ethical concerns or difficulties in harvesting or safely and efficiently expanding sufficient quantities. In contrast, clinical indications for blood-derived (from peripheral or umbilical cord blood) and bone marrow-derived stem cells, which can be easily and safely harvested, are rapidly increasing,” the authors write.

Richard K. Burt, M.D., of the Northwestern University Feinberg School of Medicine, Chicago, and colleagues conducted a review of articles regarding clinical indications and outcomes for use of blood- and bone marrow-derived stem cells - identifing 323 reports that were examined for feasibility and toxicity, and 69 that were evaluated for outcomes. The studies were published between January 1997 and December 2007.

For autoimmune diseases, 26 reports representing 854 patients reported treatment-related mortality of less than one percent (2/220 patients) for nonmyeloablative (not causing bone marrow suppression), less than two percent (3/197) for dose-reduced myeloablative, and 13 percent (13/100) for intense myeloablative regimens, i.e., those including total body irradiation or high-dose busulfan (a drug used in the treatment of some types of chronic leukemia).

For reports involving cardiovascular diseases, including 17 reports involving 1,002 heart attack patients, 16 reports involving 493 patients with chronic coronary artery disease, and three meta-analyses, the evidence suggested that stem cell transplantation performed in patients with coronary artery disease may contribute to modest improvement in cardiac function.

“Stem cells harvested from blood or marrow, whether administered as purified HSCs or mesenchymal [cells that develop into connective tissue, blood vessels and lymphatic tissue] stem cells or as an unmanipulated or unpurified product can, under appropriate conditions in select patients, provide disease-ameliorating effects in some autoimmune diseases and cardiovascular disorders. Clinical trials are needed to determine the most appropriate cell type, dose, method, timing of delivery, and adverse effects of adult HSCs for these and other nonmalignant disorders,” the authors conclude.

Published February 26, 2008 in the Journal of the American Medical Association - JAMA

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