Category Archives: Stem Cells

BRUSSELS - Belgian medical researchers have succeeded in repairing bones using stem cells from fatty tissue, with a new technique they believe could become a benchmark for treating a range of bone disorders.

The team at the Saint Luc university clinic hospital in Brussels have treated 11 patients, eight of them children, with fractures or bone defects that their bodies could not repair, and a spin-off is seeking investors to commercialise the discovery.

Doctors have for years harvested stem cells from bone marrow at the top of the pelvis and injected them back into the body to repair bone.

The ground-breaking technique of Saint Luc's centre for tissue and cellular therapy is to remove a sugar cube sized piece of fatty tissue from the patient, a less invasive process than pushing a needle into the pelvis and with a stem cell concentration they say is some 500 times higher.

The stem cells are then isolated and used to grow bone in the laboratory. Unlike some technologies, they are also not attached to a solid and separate 'scaffold'.

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Stem cells from fatty tissue show potential for bone repair

Belgian medical researchers have succeeded in repairing bones using stem cells from fatty tissue, with a new technique they believe could become a benchmark for treating a range of bone disorders.

The team at the Saint Luc university clinic hospital in Brussels have treated 11 patients, eight of them children, with fractures or bone defects that their bodies could not repair, and a spin-off is seeking investors to commercialize the discovery.

Doctors have for years harvested stem cells from bone marrow at the top of the pelvis and injected them back into the body to repair bone.

The ground-breaking technique of Saint Luc's centre for tissue and cellular therapy is to remove a sugar cube sized piece of fatty tissue from the patient, a less invasive process than pushing a needle into the pelvis and with a stem cell concentration they say is some 500 times higher.

The stem cells are then isolated and used to grow bone in the laboratory. Unlike some technologies, they are also not attached to a solid and separate 'scaffold'.

"Normally you transplant only cells and you cross your fingers that it functions," the centre's coordinator Denis Dufrane told Reuters television.

His work has been published in Biomaterials journal and was presented at an annual meeting of the International Federation for Adipose Therapeutics and Science (IFATS) in New York in November.

BONE FORMATION

"It is complete bone tissue that we recreate in the bottle and therefore when we do transplants in a bone defect or a bone hole...you have a higher chance of bone formation."

The new material in a lab dish resembles more plasticine than bone, but can be molded to fill a fracture, rather like a dentist's filling in a tooth, hardening in the body.

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Belgian researchers use groundbreaking surgery to repair bones

Art of Science: Montage of Stem Cells by Peter Tonge
A montage of stem cells called "All for One - One for All" by Peter Tonge.

By: Mount Sinai Hospital

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Art of Science: Montage of Stem Cells by Peter Tonge - Video

HealthWACH - Banking baby #39;s stem cells
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HealthWACH - Banking baby's stem cells - Video

Jan. 14, 2014 Breast cancer stem cells exist in two different states and each state plays a role in how cancer spreads, according to an international collaboration of researchers. Their finding sheds new light on the process that makes cancer a deadly disease.

"The lethal part of cancer is its metastasis so understanding how metastasis occurs is critical," says senior study author Max S. Wicha, M.D., Distinguished Professor of Oncology and director of the University of Michigan Comprehensive Cancer Center. "We have evidence that cancer stem cells are responsible for metastasis -- they are the seeds that mediate cancer's spread. Now we've discovered how the stem cells do this."

First, on the outside of the tumor, a type of stem cell exists in a state called the epithelial-mesenchymal transition (EMT) state. These stem cells appear dormant but are very invasive and able to get into the bloodstream, where they travel to distant parts of the body.

Once there, the stem cells transition to a second state that displays the opposite characteristics, called the mesenchymal-epithelial transition state (MET). These cells are capable of growing and making copies of themselves, producing new tumors.

"You need both forms of cancer stem cells to metastasize and grow in distant organs. If the stem cell is locked in one or the other state, it can't form a metastasis," Wicha says.

The findings, which are published in the January issue of Stem Cell Reports, raise a number of questions about how to treat or prevent metastatic breast cancer. Researchers must now understand whether new therapies must attack both forms of the stem cell to be successful. Different pathways regulate each type of stem cell, which suggests that effective therapies must be able to target multiple pathways.

In addition, current tests that look at tumor cells circulating in the blood to help determine whether the cancer is spreading do not appear to capture the EMT stem cells, which are the cancer cells that travel through the blood. U-M researchers are working with colleagues from the U-M College of Engineering to develop new tools to isolate the EMT stem cells from the blood of cancer patients.

"Now that we know we are looking at two different states of cancer stem cells, we can use markers that distinguish these states to get a better sense of where the cancer stem cells are and to determine the effectiveness of our treatments," Wicha says.

The study looked specifically at breast cancer stem cells but the researchers believe the findings likely have implications for other cancer types as well.

Breast cancer statistics: 234,580 Americans will be diagnosed with breast cancer this year and 40,030 will die from the disease, according to the American Cancer Society.

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New breast cancer stem cell findings explain how cancer spreads

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Newswise While the ability of human embryonic stem cells (hESCs) to become any type of mature cell, from neuron to heart to skin and bone, is indisputably crucial to human development, no less important is the mechanism needed to maintain hESCs in their pluripotent state until such change is required.

In a paper published in this weeks Online Early Edition of PNAS, researchers from the University of California, San Diego School of Medicine identify a key gene receptor and signaling pathway essential to doing just that maintaining hESCs in an undifferentiated state.

The finding sheds new light upon the fundamental biology of hESCs with their huge potential as a diverse therapeutic tool but also suggests a new target for attacking cancer stem cells, which likely rely upon the same receptor and pathway to help spur their rampant, unwanted growth.

The research, led by principal investigator Karl Willert, PhD, assistant professor in the Department of Cellular and Molecular Medicine, focuses upon the role of the highly conserved WNT signaling pathway, a large family of genes long recognized as a critical regulator of stem cell self-renewal, and a particular encoded receptor known as frizzled family receptor 7 or FZD7.

WNT signaling through FZD7 is necessary to maintain hESCs in an undifferentiated state, said Willert. If we block FZD7 function, thus interfering with the WNT pathway, hESCs exit their undifferentiated and pluripotent state.

The researchers proved this by using an antibody-like protein that binds to FZD7, hindering its function. Once FZD7 function is blocked with this FZD7-specific compound, hESCs are no longer able to receive the WNT signal essential to maintaining their undifferentiated state.

FZD7 is a so-called onco-fetal protein, expressed only during embryonic development and by certain human tumors. Other studies have suggested that FZD7 may be a marker for cancer stem cells and play an important role in promoting tumor growth. If so, said Willert, disrupting FZD7 function in cancer cells is likely to interfere with their development and growth just as it does in hESCs.

Willert and colleagues, including co-author Dennis Carson, MD, of the Sanford Consortium for Regenerative Medicine and professor emeritus at UC San Diego, plan to further test their FZD7-blocking compound as a potential cancer treatment.

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Keeping Stem Cells Pluripotent

New technology developed by Cambridge UK researchers could rewire stem cells and help fight conditions such as heart & liver disease as well as cancer.

The fast-working technique determines what causes stem cells to convert into other cell types and could revolutionise understanding of how genes function.

The method uses stem cells with a single set of chromosomes, instead of the two sets found in most cells, to reveal what causes the circuitry of stem cells to be rewired as they begin the process of conversion into other cell types. The same method could also be used to understand a range of biological processes.

Embryonic stem cells rely on a particular gene circuitry to retain their original, undifferentiated state, making them self-renewing. The dismantling of this circuitry is what allows stem cells to start converting into other types of cells - a process known as cell differentiation - but how this happens is poorly understood.

The method uses stem cells with a single set of chromosomes to uncover how cell differentiation works.

Cells in mammals contain two sets of chromosomes one set inherited from the mother and one from the father. This can present a challenge when studying the function of genes, however: as each cell contains two copies of each gene, determining the link between a genetic change and its physical effect, or phenotype, is immensely complex.

The conventional approach is to work gene by gene, and in the past people would have spent most of their careers looking at one mutation or one gene, said Dr Martin Leeb, who led the research, in collaboration with Professor Austin Smith.

Today, the process is a bit faster, but its still a methodical gene by gene approach because when you have an organism with two sets of chromosomes thats really the only way you can go.

Dr Leeb used unfertilised mouse eggs to generate embryonic stem cells with a single set of chromosomes, known as haploid stem cells. These haploid cells show all of the same characteristics as stem cells with two sets of chromosomes, and retain the same full developmental potential, making them a powerful tool for determining how the genetic circuitry of mammalian development functions.

The researchers used transposons jumping genes to make mutations in nearly all genes. The effect of a mutation can be seen immediately in haploid cells because there is no second gene copy.

Originally posted here:
Cambridge learns how to rewire stem cells

Jan. 13, 2014 Geneticists from Ohio, California and Japan joined forces in a quest to correct a faulty chromosome through cellular reprogramming. Their study, published online today in Nature, used stem cells to correct a defective "ring chromosome" with a normal chromosome. Such therapy has the promise to correct chromosome abnormalities that give rise to birth defects, mental disabilities and growth limitations.

"In the future, it may be possible to use this approach to take cells from a patient that has a defective chromosome with multiple missing or duplicated genes and rescue those cells by removing the defective chromosome and replacing it with a normal chromosome," said senior author Anthony Wynshaw-Boris, MD, PhD, James H. Jewell MD '34 Professor of Genetics and chair of Case Western Reserve School of Medicine Department of Genetics and Genome Sciences and University Hospitals Case Medical Center.

Wynshaw-Boris led this research while a professor in pediatrics, the Institute for Human Genetics and the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UC, San Francisco (UCSF) before joining the faculty at Case Western Reserve in June 2013.

Individuals with ring chromosomes may display a variety of birth defects, but nearly all persons with ring chromosomes at least display short stature due to problems with cell division. A normal chromosome is linear, with its ends protected, but with ring chromosomes, the two ends of the chromosome fuse together, forming a circle. This fusion can be associated with large terminal deletions, a process where portions of the chromosome or DNA sequences are missing. These deletions can result in disabling genetic disorders if the genes in the deletion are necessary for normal cellular functions.

The prospect for effective counter measures has evaded scientists -- until now. The international research team discovered the potential for substituting the malfunctioning ring chromosome with an appropriately functioning one during reprogramming of patient cells into induced pluripotent stem cells (iPSCs). iPSC reprogramming is a technique that was developed by Shinya Yamanaka, MD, PhD, a co-corresponding author on the Nature paper. Yamanaka is a senior investigator at the UCSF-affiliated Gladstone Institutes, a professor of anatomy at UCSF, and the director of the Center for iPS Cell Research and Application (CiRA) at the Institute for Integrated Cell-Material Sciences (iCeMS) in Kyoto University. He won the Nobel Prize in Medicine in 2012 for developing the reprogramming technique.

Marina Bershteyn, PhD, a postdoctoral fellow in the Wynshaw-Boris lab at UCSF, along with Yohei Hayashi, PhD, a postdoctoral fellow in the Yamanaka lab at the Gladstone Institutes, reprogrammed skin cells from three patients with abnormal brain development due to a rare disorder called Miller Dieker Syndrome, which results from large terminal deletions in one arm of chromosome 17. One patient had a ring chromosome 17 with the deletion and the other two patients had large terminal deletions in one of their chromosome 17, but not a ring. Additionally, each of these patients had one normal chromosome 17.

The researchers observed that, after reprogramming, the ring chromosome 17 that had the deletion vanished entirely and was replaced by a duplicated copy of the normal chromosome 17. However, the terminal deletions in the other two patients remained after reprogramming. To make sure this phenomenon was not unique to ring chromosome 17, they reprogrammed cells from two different patients that each had ring chromosomes 13. These reprogrammed cells also lost the ring chromosome, and contained a duplicated copy of the normal chromosome 13.

"It appears that ring chromosomes are lost during rapid and continuous cell divisions during reprogramming," said Yamanaka. "The duplication of the normal chromosome then corrects for that lost chromosome."

"Ring loss and duplication of whole chromosomes occur with a certain frequency in stem cells," explained Bershteyn. "When chromosome duplication compensates for the loss of the corresponding ring chromosome with a deletion, this provides a possible avenue to correct large-scale problems in a chromosome that have no chance of being corrected by any other means."

"It is likely that our findings apply to other ring chromosomes, since the loss of the ring chromosome occurred in cells reprogrammed from three different patients," said Hayashi.

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Study discovers chromosome therapy to correct severe chromosome defect

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In a paper published in this week's Online Early Edition of the Proceedings of the National Academy of Sciences, researchers from the University of California, San Diego School of Medicine identify a key gene receptor and signaling pathway essential to maintaining human embryonic stem cells in an undifferentiated state.

While the ability of human embryonic stem cells (hESCs) to become any type of mature cell, from neuron to heart to skin and bone, is indisputably crucial to human development, no less important is the mechanism needed to maintain hESCs in their pluripotent state until such change is required.

In a paper published in this week's Online Early Edition of PNAS, researchers from the University of California, San Diego School of Medicine identify a key gene receptor and signaling pathway essential to doing just that maintaining hESCs in an undifferentiated state.

The finding sheds new light upon the fundamental biology of hESCs with their huge potential as a diverse therapeutic tool but also suggests a new target for attacking cancer stem cells, which likely rely upon the same receptor and pathway to help spur their rampant, unwanted growth.

The research, led by principal investigator Karl Willert, PhD, assistant professor in the Department of Cellular and Molecular Medicine, focuses upon the role of the highly conserved WNT signaling pathway, a large family of genes long recognized as a critical regulator of stem cell self-renewal, and a particular encoded receptor known as frizzled family receptor 7 or FZD7.

"WNT signaling through FZD7 is necessary to maintain hESCs in an undifferentiated state," said Willert. "If we block FZD7 function, thus interfering with the WNT pathway, hESCs exit their undifferentiated and pluripotent state."

The researchers proved this by using an antibody-like protein that binds to FZD7, hindering its function. "Once FZD7 function is blocked with this FZD7-specific compound, hESCs are no longer able to receive the WNT signal essential to maintaining their undifferentiated state."

FZD7 is a so-called "onco-fetal protein," expressed only during embryonic development and by certain human tumors. Other studies have suggested that FZD7 may be a marker for cancer stem cells and play an important role in promoting tumor growth. If so, said Willert, disrupting FZD7 function in cancer cells is likely to interfere with their development and growth just as it does in hESCs.

Willert and colleagues, including co-author Dennis Carson, MD, of the Sanford Consortium for Regenerative Medicine and professor emeritus at UC San Diego, plan to further test their FZD7-blocking compound as a potential cancer treatment.

Read more from the original source:
By blocking key signal, researchers maintain embryonic stem cells in vital, undifferentiated state

January 12, 2014

Image Caption: Scanning electron microscopy of stem cells (yellow / green) in a scaffold structure (blue) serving as a basis for the artificial bone marrow. Credit: C. Lee-Thedieck/KIT

Rebekah Eliason for redOrbit.com Your Universe Online

An exciting breakthrough is offering hope for the treatment of blood diseases such as leukemia using artificial bone marrow.

Specialized cells, known as hematopoietic stem cells, located within bone marrow, continuously replace and supply new blood cells such as red blood cells and white blood cells. Traditionally a blood disease like leukemia is treated with bone marrow transplants that supply the patient with new hematopoietic stem cells. Researchers have now discovered a way to artificially reproduce hematopoietic stem cells.

Since not every leukemia patient can find a suitable transplant, there is a need for other forms of treatment. The lack of appropriate transplants could be solved by artificial reproduction of hematopoietic stem cells. Previously, reproduction of the cells has been impossible due to their inability to survive anywhere but in their natural environment. Hematopoietic stem cells are found in a special niche of the bone marrow. If the cells reside out of the bone marrow, the specialized properties are modified. Consequently, to effectively reproduce the cells, the stem cell niche environment must also be created.

In the microscopic environment of the stem cell niche, there are several specific properties of importance. Areas in the bone that house the stem cells are extremely porous like a sponge. Making things even more complex, the spongy tissue is also home to other cell types which exchange signal substances with the stem cells. Also, the space among the cells creates an environment ensuring stability along with a place for the cells to anchor. Furthermore, the stem cell niche supplies the cells with nutrients and oxygen.

Dr. Cornelia Lee-Thedieck is head of the Young Investigators Group Stem Cell-Material Interactions, which consists of scientitsts from the KIT Institute of Functional Interfaces (IFG), the Max Planck Institute for Intelligent Systems, Stuttgart and Tbingen University. The team was successful at artificially reproducing major properties of bone marrow at the laboratory.

Using synthetic polymers, the researchers were able to create a porous structure that simulated the spongy environment of the blood-forming bone marrow. Also, they were able to add protein building blocks which are similar to those found naturally in the environment of the bone marrow that enable cells to anchor. Finally, they added the other types of cells needed for exchanging signaling substances.

After the artificial bone marrow was created, the scientists placed hematopoietic stem cells that had been isolated from cord blood into it. For several days the cells were bred. Various analytical methods were then used to determine that cells were able to reproduce in the artificial bone marrow. When compared with standard cell cultivation methods, a larger number of stem cells in the artificial bone marrow retained their specific properties.

Link:
New Treatment For Blood Diseases Using Artificial Bone Marrow