StemCell Therapy

BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) today announced that its collaborator, Millennium: The Takeda Oncology Company, a wholly owned subsidiary of Takeda Pharmaceutical Company Limited, has received a positive recommendation from the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) for the conditional marketing authorization of ADCETRIS (brentuximab vedotin) for two indications: (1) the treatment of adult patients with relapsed or refractory CD30-positive Hodgkin lymphoma (HL) following autologous stem cell transplant (ASCT) or following at least two prior therapies when ASCT or multi-agent chemotherapy is not a treatment option, and (2) for the treatment of adult patients with relapsed or refractory systemic anaplastic large cell lymphoma (sALCL). ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30.

The positive opinion from CHMP and broad label recommendation is a key step in the European regulatory process for ADCETRIS and brings us closer to our goal of making this important new therapy globally available to patients with relapsed Hodgkin lymphoma or systemic ALCL, said Clay B. Siegall, Ph.D., President and Chief Executive Officer of Seattle Genetics. If approved in the European Union, ADCETRIS will represent the first new therapeutic advance for relapsed Hodgkin lymphoma patients in several decades and further validates the potential of ADCs in the treatment of cancer.

The European Commission, which has the authority to approve medicines for use in the European Union, generally follows the recommendations of the CHMP and typically renders a final decision within three months of the CHMP opinion. If the CHMP recommendation is formally adopted by the European Commission, ADCETRIS would be approved for marketing in all 27 member states of the European Union.

European Commission approval will trigger two milestone payments, one for each indication, totaling $25 million to Seattle Genetics under the collaboration agreement between Seattle Genetics and Millennium: The Takeda Oncology Company. Seattle Genetics is also entitled to tiered double-digit royalties with percentages starting in the mid-teens and escalating to the mid-twenties based on net sales of ADCETRIS within Millenniums territories, subject to offsets for royalties paid by Millennium to third parties.

About ADCETRIS

ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

ADCETRIS received accelerated approval from the U.S. Food and Drug Administration (FDA) in August 2011 for relapsed HL and sALCL.

Seattle Genetics and Millennium are jointly developing ADCETRIS. Under the terms of the collaboration agreement, Seattle Genetics has U.S. and Canadian commercialization rights and the Takeda Group has rights to commercialize ADCETRIS in the rest of the world. Seattle Genetics and the Takeda Group are funding joint development costs for ADCETRIS on a 50:50 basis, except in Japan where the Takeda Group will be solely responsible for development costs.

About Seattle Genetics

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Seattle Genetics Announces ADCETRIS® Receives Positive CHMP Opinion for Conditional Approval in European Union

ScienceDaily (July 19, 2012) Not all adult stem cells are created equal. Some are busy regenerating worn out or damaged tissues, while their quieter brethren serve as a strategic back-up crew that only steps in when demand shoots up. Now, researchers at the Stowers Institute for Medical Research have identified an important molecular cue that keeps quiescent mouse hematopoietic (or blood-forming) stem cells from proliferating when their services are not needed.

Publishing in the July 20, 2012 issue of Cell, the team led by Stowers Investigator Linheng Li, Ph.D., report that Flamingo and Frizzled 8, a tag team best known for its role in establishing cell polarity, are crucial for maintaining a quiescent reserve pool of hematopoietic stem cells in mouse bone marrow. Their finding adds new insight into the mechanism that controls the delicate balance between long-term maintenance of stem cells and the requirements of ongoing tissue maintenance and regeneration.

"Hematopoietic stem cells daily produce billions of blood cells via a strict hierarchy of lineage-specific progenitors," says Li. "Identifying the molecular signals that allow hematopoietic stem cell populations to sustain this level of output over a lifetime is fundamental to understanding the development of different cell types, the nature of tumor formation, and the aging process. My hope is that these insights will help scientists make meaningful progress towards new therapies for diseases of the blood."

The current working model, which grew out of earlier work by Li and others, postulates that hematopoietic stem cells (HSC), which are part of the reserve pool sit quietly and only divide a few times a year. They jump into action only when needed to replace active HSCs damaged by daily wear and tear or to increase their numbers in response to injury or disease. But how quiescent and active hematopoietic stem cell subpopulations are maintained and regulated in vivo is largely unknown.

What is known is that both populations of cells reside in adjacent specialized microenvironments, which provide many of the molecular cues that guide stem cell activity. Frequently cycling HSCs constitute around 90 percent of all hematopoietic stem cells and are found in the central marrow, where they seek the company of endothelial and perivascular cells. The main home base of quiescent hematopoietic stem cells is trabecular bone, the spongy part typically found at the end of long bones. Here, these cells engage in a constant molecular dialog with preosteoblasts, the precursors of bone-forming osteoblasts, which are characterized by the expression of N-cadherin.

Trying to decode the nature of the conversation graduate student and first author Ryohichi Sugimura focused on Flamingo (Fmi), a surface-based adhesion molecule, and Frizzled 8 (Fz8), a membrane-based receptor. Both molecules are part of the non-canonical arm of the so-called Wnt signaling pathway, a large network of secreted signaling molecules and their receptors. The canonical arm of the Wnt-signaling pathway exerts its influence through beta-catenin and helps regulate stem cell self-renewal in the intestine and hair follicles.

After in vitro experiments had revealed that Fmi and Fz8 accumulate at the interface between co-cultured quiescent hematopoietic stem cells and preosteoblasts, Sugimura and his colleagues were able to show that Fmi also regulates Fz8 distribution in vivo. This observation provided the first hint that these cooperation partners may carry at least part of the conversation that instructs hematopoietic stem cells to sit still. It also confirmed the previous finding by Li's team that a portion of HSCs resides in the N-cadherin+ osteoblastic niche.

When Sugimura examined the expression patterns of individual members of the Wnt signaling network within quiescent HSCs' microenvironment he found that levels of canonical Wnt ligands where low. Levels of non-canonical Wnt ligands and inhibitors of the canonical arm of the Wnt signaling network, on the other hand, were high.

"These observations indicated that the osteoblast niche provides a microenvironment in which non-canonical Wnt signaling prevails over canonical Wnt-signaling under normal conditions," says Sugimura. "It also suggested that Fmi and Fz8 may play a direct role in maintaining the pool of quiescent hematopoietic stem cells."

Mice that had been genetically engineered to lack either Fmi or Fz8 provided the crucial clue: Not only had the number of quiescent hematopoietic stem cells plummeted in these mice, their hematopoietic stem cell function was reduced by more than 70 percent as well.

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The yin and yang of stem cell quiescence and proliferation

ScienceDaily (July 18, 2012) To build a tooth, a detailed recipe to instruct cells to differentiate towards proper lineages and form dental cells is needed. Researchers in the group of Professor Irma Thesleff at the Institute of Biotechnology in Helsinki, Finland have now found a marker for dental stem cells. They showed that the transcription factor Sox2 is specifically expressed in stem cells of the mouse front tooth.

Despite the development of new bioengineering protocols, building a tooth from stem cells remains a distant goal. Demand for it exists as loss of teeth affects oral health, quality of life, as well as ones appearance. To build a tooth, a detailed recipe to instruct cells to differentiate towards proper lineages and form dental cells is needed. However, the study of stem cells requires their isolation and a lack of a specific marker has hindered studies so far.

Researchers in the group of Professor Irma Thesleff at the Institute of Biotechnology in Helsinki, Finland have now found a marker for dental stem cells. They showed that the transcription factor Sox2 is specifically expressed in stem cells of the mouse incisor (front tooth). The mouse incisor grows continuously throughout life and this growth is fueled by stem cells located at the base of the tooth. These cells offer an excellent model to study dental stem cells.

The researchers developed a method to record the division, movement, and specification of these cells. By tracing the descendants of genetically labeled cells, they also showed that Sox2 positive stem cells give rise to enamel-forming ameloblasts as well as other cell lineages of the tooth.

Although human teeth dont grow continuously, the mechanisms that control and regulate their growth are similar as in mouse teeth. Therefore, the discovery of Sox2 as a marker for dental stem cells is an important step toward developing a complete bioengineered tooth. In the future, it may be possible to grow new teeth from stem cells to replace lost ones, says researcher Emma Juuri, a co-author of the study.

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The above story is reprinted from materials provided by Helsingin yliopisto (University of Helsinki), via AlphaGalileo.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

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One step closer to growing a tooth

(Phys.org) -- New research at the Hebrew University of Jerusalem sheds light on pluripotencythe ability of embryonic stem cells to renew themselves indefinitely and to differentiate into all types of mature cells. Solving this problem, which is a major challenge in modern biology, could expedite the use of embryonic stem cells in cell therapy and regenerative medicine. If scientists can replicate the mechanisms that make pluripotency possible, they could create cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases.

To shed light on these processes, researchers in the lab of Dr. Eran Meshorer, in the Department of Genetics at the Hebrew Universitys Alexander Silberman Institute of Life Sciences, are combining molecular, microscopic and genomic approaches. Meshorer's team is focusing on epigenetic pathwayswhich cause biological changes without a corresponding change in the DNA sequencethat are specific to embryonic stem cells.

The molecular basis for epigenetic mechanisms is chromatin, which is comprised of a cell's DNA and structural and regulatory proteins. In groundbreaking research performed by Shai Melcer, a PhD student in the Meshorer lab, the mechanisms which support an open chromatin conformation in embryonic stem cells were examined. The researchers found that chromatin is less condensed in embryonic stem cells, allowing them the flexibility or "functional plasticity" to turn into any kind of cell.

A distinct pattern of chemical modifications of chromatin structural proteins (referred to as the acetylation and methylation of histones) enables a looser chromatin configuration in embryonic stem cells. During the early stages of differentiation, this pattern changes to facilitate chromatin compaction.

But even more interestingly, the authors found that a nuclear lamina protein, lamin A, is also a part of the secret. In all differentiated cell types, lamin A binds compacted domains of chromatin and anchors them to the cells nuclear envelope. Lamin A is absent from embryonic stem cells and this may enable the freer, more dynamic chromatin state in the cell nucleus. The authors believe that chromatin plasticity is tantamount to functional plasticity since chromatin is made up of DNA that includes all genes and codes for all proteins in any living cell. Understanding the mechanisms that regulate chromatin function will enable intelligent manipulations of embryonic stem cells in the future.

"If we can apply this new understanding about the mechanisms that give embryonic stem cells their plasticity, then we can increase or decrease the dynamics of the proteins that bind DNA and thereby increase or decrease the cells differentiation potential," concludes Dr. Meshorer. This could expedite the use of embryonic stem cells in cell therapy and regenerative medicine, by enabling the creation of cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases.

More information: The research appears in the journal Nature Communications as Melcer et al., Histone modifications and lamin A regulate chromatin protein dynamics in early embryonic stem cell differentiation. go.nature.com/9B33Ue

Journal reference: Nature Communications

Provided by Hebrew University of Jerusalem

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Researchers identify mechanisms that allow embryonic stem cells to become any cell in the human body

ScienceDaily (July 18, 2012) New research at the Hebrew University of Jerusalem sheds light on pluripotency -- the ability of embryonic stem cells to renew themselves indefinitely and to differentiate into all types of mature cells. Solving this problem, which is a major challenge in modern biology, could expedite the use of embryonic stem cells in cell therapy and regenerative medicine.

If scientists can replicate the mechanisms that make pluripotency possible, they could create cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases.

To shed light on these processes, researchers in the lab of Dr. Eran Meshorer, in the Department of Genetics at the Hebrew University's Alexander Silberman Institute of Life Sciences, are combining molecular, microscopic and genomic approaches. Meshorer's team is focusing on epigenetic pathways -- which cause biological changes without a corresponding change in the DNA sequence -- that are specific to embryonic stem cells.

The molecular basis for epigenetic mechanisms is chromatin, which is comprised of a cell's DNA and structural and regulatory proteins. In groundbreaking research performed by Shai Melcer, a PhD student in the Meshorer lab, the mechanisms which support an "open" chromatin conformation in embryonic stem cells were examined. The researchers found that chromatin is less condensed in embryonic stem cells, allowing them the flexibility or "functional plasticity" to turn into any kind of cell.

A distinct pattern of chemical modifications of chromatin structural proteins (referred to as the acetylation and methylation of histones) enables a looser chromatin configuration in embryonic stem cells. During the early stages of differentiation, this pattern changes to facilitate chromatin compaction.

But even more interestingly, the authors found that a nuclear lamina protein, lamin A, is also a part of the secret. In all differentiated cell types, lamin A binds compacted domains of chromatin and anchors them to the cell's nuclear envelope. Lamin A is absent from embryonic stem cells and this may enable the freer, more dynamic chromatin state in the cell nucleus. The authors believe that chromatin plasticity is tantamount to functional plasticity since chromatin is made up of DNA that includes all genes and codes for all proteins in any living cell. Understanding the mechanisms that regulate chromatin function will enable intelligent manipulations of embryonic stem cells in the future.

"If we can apply this new understanding about the mechanisms that give embryonic stem cells their plasticity, then we can increase or decrease the dynamics of the proteins that bind DNA and thereby increase or decrease the cells' differentiation potential," concludes Dr. Meshorer. "This could expedite the use of embryonic stem cells in cell therapy and regenerative medicine, by enabling the creation of cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases."

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Mechanisms that allow embryonic stem cells to become any cell in the human body identified

Public release date: 18-Jul-2012 [ | E-mail | Share ]

Contact: Sarah Dionne smdionne@partners.org 617-726-6126 Massachusetts General Hospital

One of the challenges to HIV vaccine development has been the lack of an animal model that accurately reflects the human immune response to the virus and how the virus evolves to evade that response. In the July 18 issue of Science Translational Medicine, researchers from the Ragon Institute of Massachusetts General Hospital (MGH), MIT and Harvard report that a model created by transplanting elements of the human immune system into an immunodeficient mouse addresses these key issues and has the potential to reduce significantly the time and costs required to test candidate vaccines.

"Our study showed not only that these humanized mice mount human immune responses against HIV but also that the ability of HIV to evade these responses by mutating viral proteins targeted by CD8 'killer' T cells is accurately reflected in these mice," says Todd Allen, PhD, senior author of the report. "For the first time we have an animal model that accurately reproduces critical host-pathogen interactions, a model that will help facilitate the development an effective vaccine for HIV." Recent studies by Allen's team and others have revealed that immune control of HIV is significantly limited by the ability of the virus to evade immune responses by rapidly mutating.

The traditional animal model for HIV research is the rhesus monkey, which can be infected with the related simian immunodeficiency virus (SIV). But differences in viral sequences between SIV and HIV, along with differences between the human and monkey immune systems, limit the ability of the SIV model to replicate directly key interactions between HIV and the human immune system. Development of an effective HIV vaccine will require a greater understanding of how human immune responses succeed or fail to control HIV.

The current study was designed to test the humanized BLT mouse, a model created by transplanting human bone marrow stem cells, along with other human tissue, into mice lacking a functioning immune system. Andrew Tager, MD, a co-author of the report and director of the MGH Humanized Mouse Program, explains, "Multiple researchers have contributed to dramatic improvements in the ability of humanized mice to model human diseases. Earlier studies with BLT mice performed at the University of Texas Southwestern Medical Center, the MGH and elsewhere have demonstrated that this particular humanized mouse model reproduces many aspects of the human immune response."

Timothy Dudek, PhD, of the Ragon Institute, lead author of the current study, adds, "Unlike normal mice, these humanized mice can be infected with HIV. But there has been little evidence regarding whether they reproduce the interaction between HIV and the human immune system, particularly the development of specific immune responses that exert control over HIV by targeting critical regions of the virus."

Tager's team at the MGH Center for Immunology and Inflammatory Diseases created groups of humanized BLT mice using cells and tissues from human donors with different alleles, or versions, of the immune system's HLA molecules, which flag infected cells for destruction by CD8 T cells. Particular HLA alleles, such as HLA-B57, are more common in individuals naturally able to control HIV, and some of the mice generated by Tager's group expressed this important protective allele.

Six weeks after the mice had been infected with HIV, the researchers found that the virus was rapidly evolving in regions known to be targeted by CD8 T cells. Their observation indicated that not only were the humanized mouse immune systems responding to HIV but also that the virus was mutating to avoid those responses in a manner similar to what is seen in humans. In mice expressing the protective HLA-B57 allele, just as in human patients who control viral levels, CD8 responses were directed against an essential region of the virus, preventing viral mutation and allowing the animals to more effectively contain HIV.

"We now know that these mice appear to replicate the specificity of the human cellular response to HIV and that the virus is attempting to evade these responses just as it does in humans," says Allen, an associate professor of Medicine at Harvard Medical School. "We are currently studying whether we can induce human HIV-specific immune responses in these animals by vaccination, which would provide a rapid, cost-effective model to test the ability of different vaccine approaches to control or even block HIV infection. If we can do this, we'll have a very powerful new tool to accelerate HIV vaccine development, one that also may be useful against other pathogens."

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Mouse with human immune system may revolutionize HIV vaccine research

(Phys.org) -- New research at the Hebrew University of Jerusalem sheds light on pluripotencythe ability of embryonic stem cells to renew themselves indefinitely and to differentiate into all types of mature cells. Solving this problem, which is a major challenge in modern biology, could expedite the use of embryonic stem cells in cell therapy and regenerative medicine. If scientists can replicate the mechanisms that make pluripotency possible, they could create cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases.

To shed light on these processes, researchers in the lab of Dr. Eran Meshorer, in the Department of Genetics at the Hebrew Universitys Alexander Silberman Institute of Life Sciences, are combining molecular, microscopic and genomic approaches. Meshorer's team is focusing on epigenetic pathwayswhich cause biological changes without a corresponding change in the DNA sequencethat are specific to embryonic stem cells.

The molecular basis for epigenetic mechanisms is chromatin, which is comprised of a cell's DNA and structural and regulatory proteins. In groundbreaking research performed by Shai Melcer, a PhD student in the Meshorer lab, the mechanisms which support an open chromatin conformation in embryonic stem cells were examined. The researchers found that chromatin is less condensed in embryonic stem cells, allowing them the flexibility or "functional plasticity" to turn into any kind of cell.

A distinct pattern of chemical modifications of chromatin structural proteins (referred to as the acetylation and methylation of histones) enables a looser chromatin configuration in embryonic stem cells. During the early stages of differentiation, this pattern changes to facilitate chromatin compaction.

But even more interestingly, the authors found that a nuclear lamina protein, lamin A, is also a part of the secret. In all differentiated cell types, lamin A binds compacted domains of chromatin and anchors them to the cells nuclear envelope. Lamin A is absent from embryonic stem cells and this may enable the freer, more dynamic chromatin state in the cell nucleus. The authors believe that chromatin plasticity is tantamount to functional plasticity since chromatin is made up of DNA that includes all genes and codes for all proteins in any living cell. Understanding the mechanisms that regulate chromatin function will enable intelligent manipulations of embryonic stem cells in the future.

"If we can apply this new understanding about the mechanisms that give embryonic stem cells their plasticity, then we can increase or decrease the dynamics of the proteins that bind DNA and thereby increase or decrease the cells differentiation potential," concludes Dr. Meshorer. This could expedite the use of embryonic stem cells in cell therapy and regenerative medicine, by enabling the creation of cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases.

More information: The research appears in the journal Nature Communications as Melcer et al., Histone modifications and lamin A regulate chromatin protein dynamics in early embryonic stem cell differentiation. go.nature.com/9B33Ue

Journal reference: Nature Communications

Provided by Hebrew University of Jerusalem

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Researchers identify mechanisms that allow embryonic stem cells to become any cell in the human body

ScienceDaily (July 17, 2012) Using adult stem cells, Johns Hopkins researchers and a consortium of colleagues nationwide say they have generated the type of human neuron specifically damaged by Parkinson's disease (PD) and used various drugs to stop the damage.

Their experiments on cells in the laboratory, reported in the July 4 issue of the journal Science Translational Medicine, could speed the search for new drugs to treat the incurable neurodegenerative disease, but also, they say, may lead them back to better ways of using medications that previously failed in clinical trials.

"Our study suggests that some failed drugs should actually work if they were used earlier, and especially if we could diagnose PD before tremors and other symptoms first appear," says one of the study's leaders, Ted M. Dawson, M.D., Ph.D., a professor of neurology at the Johns Hopkins University School of Medicine.

Dawson and his colleagues, working as part of a National Institute of Neurological Disorders and Stroke consortium, created three lines of induced pluripotent stem (iPS) cells derived from the skin cells of adults with PD. Two of the cell lines had the mutated LRKK2 gene, a hallmark of the most common genetic cause of PD. Induced pluripotent stem cells are adult cells that have been genetically reprogrammed to their most primitive state. Under the right circumstances, they can develop into most or all of the 200 cell types in the human body.

In the laboratory, the consortium scientists used the iPS cells to create dopamine neurons, those that bear the brunt of PD. Around age 60, people who have the disorder typically begin to show symptoms, including shaking (tremors) and difficulty with walking, movement and coordination. In the United States, at least 500,000 people are believed to have PD, and an estimated 50,000 new cases are reported annually.

Dawson says the ability to experiment with a form of "Parkinson's in a dish" should lead to further understanding of how the disease originates, develops and behaves in humans. Although scientists have been able to stop the disease in mice, the compounds used to do so have not worked in people, suggesting that human PD behaves differently than animal models of the disorder. Dawson, director of Johns Hopkins' Institute for Cell Engineering, says the researchers began with the belief that PD is strongly linked to disruption of the dopamine neurons' mitochondria, the energy-making power plants of the cells. Mitochondria undergo regular turnover in which they fuse together and then split apart. Normal neurons make new mitochondria and degrade older mitochondria in a balanced way to supply just the amount of energy needed.

PD, Dawson says, is believed to damage this system, leaving too few functional mitochondria and producing too many brain-damaging oxygen-free radicals.

Dawson and his colleagues looked for -- and found -- evidence of impaired mitochondria in the neurons they derived from PD patients.

They also found that the neurons they generated from PD patients were more susceptible to stressors, such as the pesticide rotenone, placed on them in the lab. Those neurons were more likely to become damaged or to die than the neurons derived from the skin of healthy individuals.

Satisfied that their stem cell-generated neurons were behaving like dopamine brain cells, the scientists next set out to see if they could slow the damage occurring in the PD neurons by introducing various compounds to the cells. They tested Coenzyme Q10, rapamycin and the LRRK2 kinase inhibitor GW5074, all of which are known to reverse mitochondrial defects in animals. The cells responded favorably to all three treatments, preventing stressors from continuing to damage the mitochondria.

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Researchers turn skin cells into brain cells, a promising path to better Parkinson's treatment

Eighteen top science students from northern Wisconsin high schools have earned the opportunity to hone their laboratory skills and work alongside leading researchers from the University of Wisconsin-Madison at a summer science camp focused on stem cells.

Hosted by the Morgridge Institute for Research, a nonprofit biomedical research institute affiliated with UW-Madison, the four-day summer science camp starts today and will cover a number of hands-on activities. Students will participate in neural and cardiac differentiation labs, attend lectures from top UW-Madison researchers and enjoy some time for fun and relaxation at campus attractions including Union South and the Kohl Center.

Students will work with both human embryonic stem cells and induced pluripotent stem cells. Human embryonic stem cells are blank-slate, or pluripotent, cells that have the capacity to differentiate into any of the more than 220 cell types in the human body. Induced pluripotent stem cells derived from reprogrammed skin cells show some differences from human embryonic stem cells and also are the focus of much promising research for human health and pharmaceutical development.

Human embryonic stem cells were first isolated on the UW-Madison campus by James Thomson, who also was among the first to create induced pluripotent stem cells. Today, Wisconsin researchers are considered leaders in developing an understanding of these cells as they search for treatments and cures for diseases such as diabetes, Parkinson's and heart disease. Wisconsin scientists also are pioneering the use of stem cells to help develop better and safer medicines.

Students will use stem cell lines that were established approximately 10 years ago. These cells continue to play a vital role in international research because of their flexibility and well-documented performance characteristics.

The students participating in the camp, held July 16-19, attend schools and educational centers including Cornell High School; Forward Service Corp.; Oconto Falls High School; Oneida Nation High School; and Rhinelander High School. The students earned the honor of attending through their classroom performance and dedication during months of preparatory study.

Students participating in the stem cell camp are:

The stem cell science camp was designed to provide an enrichment experience in an advanced scientific field while introducing promising students to the variety of academic opportunities on the UW-Madison campus.

"Through the camp, we are able to provide students with an in-depth opportunity to broaden their horizons in science, technology and medicine while highlighting the tremendous career opportunities in these rapidly growing fields," says Rupa Shevde, a senior scientist and director of outreach experiences for the Morgridge Institute for Research. "The students benefit from learning about the cutting-edge research that is going on while at the same time gaining hands-on experience with stem cells and other critically important research tools. Introducing the students to stem cells allows us to teach a variety of concepts including the genetic aspects of human diseases and important ethical considerations for researchers."

This summer's stem cell science camp also will feature lectures and presentations from a number of UW-Madison stem cell researchers, including:

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Northern Wisconsin high schoolers learn with stem cells, UW researchers

Newswise Johns Hopkins tissue engineers have used tiny, artificial fiber scaffolds thousands of times smaller than a human hair to help coax stem cells into developing into cartilage, the shock-absorbing lining of elbows and knees that often wears thin from injury or age. Reporting online June 4 in the Proceedings of the National Academy of Sciences, investigators produce an important component of cartilage in both laboratory and animal models. While the findings are still years away from use in people, the researchers say the results hold promise for devising new techniques to help the millions who endure joint pain.

Joint pain affects the quality of life of millions of people. Rather than just patching the problem with short-term fixes, like surgical procedures such as microfracture, were building a temporary template that mimics the cartilage cells natural environment, and taking advantage of natures signals to biologically repair cartilage damage, says Jennifer Elisseeff, Ph.D., Jules Stein Professor of Ophthalmology and director of the Translational Tissue Engineering Center at the Johns Hopkins University School of Medicine.

Unlike skin, cartilage cant repair itself when damaged. For the last decade, Elisseeffs team has been trying to better understand the development and growth of cartilage cells called chondrocytes, while also trying to build scaffolding that mimics the cartilage cell environment and generates new cartilage tissue. This environment is a 3-dimensional mix of protein fibers and gel that provides support to connective tissue throughout the body, as well as physical and biological cues for cells to grow and differentiate.

In the laboratory, the researchers created a nanofiber-based network using a process called electrospinning, which entails shooting a polymer stream onto a charged platform, and added chondroitin sulfatea compound commonly found in many joint supplementsto serve as a growth trigger. After characterizing the fibers, they made a number of different scaffolds from either spun polymer or spun polymer plus chondroitin. They then used goat bone marrow-derived stem cells (a widely used model) and seeded them in various scaffolds to see how stem cells responded to the material.

Elisseeff and her team watched the cells grow and found that compared to cells growing without scaffold, these cells developed into more voluminous, cartilage-like tissue. The nanofibers provided a platform where a larger volume of tissue could be produced, says Elisseeff, adding that 3-dimensional nanofiber scaffolds were more useful than the more common nanofiber sheets for studying cartilage defects in humans.

The investigators then tested their system in an animal model. They implanted the nanofiber scaffolds into damaged cartilage in the knees of rats, and compared the results to damaged cartilage in knees left alone.

They found that the use of the nanofiber scaffolds improved tissue development and repair as measured by the production of collagen, a component of cartilage. The nanofiber scaffolds resulted in greater production of a more durable type of collagen, which is usually lacking in surgically repaired cartilage tissue. In rats, for example, they found that the limbs with damaged cartilage treated with nanofiber scaffolds generated a higher percentage of the more durable collagen (type 2) than those damaged areas that were left untreated.

Whereas scaffolds are generally pretty good at regenerating cartilage protein components in cartilage repair, there is often a lot of scar tissue-related type 1 collagen produced, which isnt as strong, says Elisseeff. We found that our system generated more type 2 collagen, which ensures that cartilage lasts longer.

Creating a nanofiber network that enables us to more equally distribute cells and more closely mirror the actual cartilage extracellular environment are important advances in our work and in the field. These results are very promising, she says.

Other authors included Jeannine M. Coburn, Matthew Gibson, Sean Monagle and Zachary Patterson, all from Johns Hopkins University.

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Nanoscale Scaffolds And Stem Cells Show Promise In Cartilage Repair

Human neural stem cells. Courtesy UC Irvine radiation oncology professor Charles Limoli.

Human neural stem cells restored memory in mice with brain symptoms similar to Alzheimers disease, UC Irvine scientists reported Tuesday, opening the door to eventual treatment for human sufferers.

The announcement, made at an Alzheimers science conference in Vancouver, involves versatile though still largely mysterious neural stem cells grown in the lab by StemCells Inc., of Newark, Ca.

The cells, researchers at UCI and elsewhere have shown, can become many types of cells once injected into the body restoring limb movement in mice with crushed spines, halting blindness in rats and, now, improving memory and brain function in mice bred to exhibit the kinds of impairment seen in Alzheimers.

Youve probably heard about the God particle scientists have been working on, said Martin McGlynn, president and CEO of StemCells Inc. This isnt quite the God cell, but its an incredibly fascinating biological agent.

Over the past 12 to 18 months, scientists including Frank LaFerla, director of UCI MIND, worked on a treatment involving injection of the human neural stem cells into the brains of two kinds of mouse models those bred to model the effects of Alzheimers, and those bred to model the loss of neurons in a part of the brain known as the hippocampus.

Both animal models reported improvement in memory function, in a statistical way, McGlynn said.

Matthew Blurton-Jones, an assistant professor of neurobiology and behavior at UCI, presented the results of the Alzheimers work Tuesday at the Alzheimers Association International Conference.

Part of the scientists aim was to learn whether human neural cells placed in mice functioned as well as mouse neural cells.

That is one of the fascinating things about this, McGlynn said. They look like, smell like, walk like, dance like a human neural stem cell, (but) theyre fully regulated and submissive to the mouse, to the host.

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Stem-cell discovery: reversing Alzheimer's?

ScienceDaily (July 17, 2012) Scientists at the California Institute of Technology (Caltech) pioneered the study of the link between irregularities in the immune system and neurodevelopmental disorders such as autism a decade ago. Since then, studies of postmortem brains and of individuals with autism, as well as epidemiological studies, have supported the correlation between alterations in the immune system and autism spectrum disorder.

What has remained unanswered, however, is whether the immune changes play a causative role in the development of the disease or are merely a side effect. Now a new Caltech study suggests that specific changes in an overactive immune system can indeed contribute to autism-like behaviors in mice, and that in some cases, this activation can be related to what a developing fetus experiences in the womb.

The results appear in a paper this week in the Proceedings of the National Academy of Sciences (PNAS).

"We have long suspected that the immune system plays a role in the development of autism spectrum disorder," says Paul Patterson, the Anne P. and Benjamin F. Biaggini Professor of Biological Sciences at Caltech, who led the work. "In our studies of a mouse model based on an environmental risk factor for autism, we find that the immune system of the mother is a key factor in the eventual abnormal behaviors in the offspring."

The first step in the work was establishing a mouse model that tied the autism-related behaviors together with immune changes. Several large epidemiological studies -- including one that involved tracking the medical history of every person born in Denmark between 1980 and 2005 -- have found a correlation between viral infection during the first trimester of a mother's pregnancy and a higher risk for autism spectrum disorder in her child. To model this in mice, the researchers injected pregnant mothers with a viral mimic that triggered the same type of immune response a viral infection would.

"In mice, this single insult to the mother translates into autism-related behavioral abnormalities and neuropathologies in the offspring," says Elaine Hsiao, a graduate student in Patterson's lab and lead author of the PNAS paper.

The team found that the offspring exhibit the core behavioral symptoms associated with autism spectrum disorder -- repetitive or stereotyped behaviors, decreased social interactions, and impaired communication. In mice, this translates to such behaviors as compulsively burying marbles placed in their cage, excessively self grooming, choosing to spend time alone or with a toy rather than interacting with a new mouse, or vocalizing ultrasonically less often or in an altered way compared to typical mice.

Next, the researchers characterized the immune system of the offspring of mothers that had been infected and found that the offspring display a number of immune changes. Some of those changes parallel those seen in people with autism, including decreased levels of regulatory T cells, which play a key role in suppressing the immune response. Taken together, the observed immune alterations add up to an immune system in overdrive -- one that promotes inflammation.

"Remarkably, we saw these immune abnormalities in both young and adult offspring of immune-activated mothers," Hsiao says. "This tells us that a prenatal challenge can result in long-term consequences for health and development."

With the mouse model established, the group was then able to test whether the offspring's immune problems contribute to their autism-related behaviors. In the most revealing test of this hypothesis, the researchers were able to correct many of the autism-like behaviors in the offspring of immune-activated mothers by giving the offspring a bone-marrow transplant from typical mice. The normal stem cells in the transplanted bone marrow not only replenished the immune system of the host animals but altered their autism-like behavioral impairments.

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New evidence links immune irregularities to autism, mouse study suggests

Public release date: 17-Jul-2012 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, July 16, 2012A small, naturally occurring nucleic acid sequence, called a microRNA, known to regulate a number of different cancers, appears to alter the activity of the androgen receptor, which plays a critical role in prostate cancer. Directly targeting microRNA-125b to block androgen receptor activity represents a novel approach for treating castrate-resistant prostate cancer. This promising new strategy for improving the effectiveness of anti-androgenic and other hormonal therapies is described in an article in BioResearch Open Access, a new bimonthly peer-reviewed open access journal from Mary Ann Liebert, Inc.. The article is available free online at the BioResearch Open Access website.

Prostate cancer is the most common non-skin cancer affecting men and the second most common cause of cancer death among men. In the article "miR-125b Regulation of Androgen Receptor Signaling Via Modulation of the Receptor Complex Co-Repressor NCOR2," Xiaoping Yang, Lynne Bernis, Lih-Jen Su, Dexiang Gao, and Thomas Flaig, University of Colorado Denver (Aurora) and University of Minnesota (Duluth), looked for targets of microRNA-125b that might shed light on its role in regulating prostate cancer and found that it directly inhibits NCOR2, which acts to repress the androgen receptor. The authors point out that "the androgen receptor is a critical therapeutic target in prostate cancer" and that alterations in the receptor are essential for the development of castrate-resistant prostate cancer, in which the disease no longer responds to hormonal therapies.

"This research provides new insight into the mechanism of miR-125b regulation of castrate-resistance prostate cancer through the identification of a novel target for miR-125b," says Editor-in-Chief Jane Taylor, PhD, MRC Centre for Regenerative Medicine, University of Edinburgh, Scotland. "The clinical implications of this study are that targeted regulation of this miRNA may lead to more effective anticancer therapies."

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About the Journal

BioResearch Open Access is a bimonthly peer-reviewed open access journal that provides a new rapid-publication forum for a broad range of scientific topics including molecular and cellular biology, tissue engineering and biomaterials, bioengineering, regenerative medicine, stem cells, gene therapy, systems biology, genetics, biochemistry, virology, microbiology, and neuroscience. All articles are published within 4 weeks of acceptance and are fully open access and posted on PubMedCentral. All journal content is available online at the BioResearch Open Access website.

About the Publisher

Mary Ann Liebert, Inc., is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Tissue Engineering, Stem Cells and Development, Human Gene Therapy and HGT Methods, and AIDS Research and Human Retroviruses. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 70 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc. website.

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New therapeutic target for prostate cancer identified

LEUVEN, BELGIUM--(Marketwire -07/17/12)- TiGenix (EURONEXT:TIG), the European leader in cell therapy, announced today that after obtaining national reimbursement for ChondroCelect in the Netherlands last month, the company has now contracted with four major hospitals to make its innovative cartilage repair therapy available to their patients on a routine basis: University Medical Center Utrecht, University Hospital Maastricht, Martini Hospital Groningen, and, most recently, the Elisabeth Hospital Tilburg. Discussions with other Cartilage Expert Centers are ongoing. Reimbursement for ChondroCelect in the Netherlands is retroactive per January 1, 2011.

"Our close collaboration with the Dutch hospitals is key to making ChondroCelect available to patients in the Netherlands," said Eduardo Bravo, CEO of TiGenix. "Dutch scientists and clinicians have made important contributions to the development of this innovative cartilage repair therapy. Patients who suffer from cartilage lesions in the knee that cause recurrent pain and can be incapacitating can now be routinely treated and literally find their footing again. We expect to soon expand the number of hospitals in the Netherlands where ChondroCelect is available."

Damage to the articular cartilage in the knee can be caused by sports or professional activities in which the knee is repeatedly and forcefully impacted. It is a condition that predominantly occurs in young adults, who as a result suffer from recurrent pain, locking or limited range of motion, and risk being incapacitated. TiGenix has developed ChondroCelect as a therapy to help patients regain their mobility and fully active lives by effectively repairing the damaged cartilage in the knee.

About ChondroCelect ChondroCelect for cartilage regeneration in the knee is an implantation suspension of characterized viable autologous (from the patient her- or himself) cartilage cells. The product is administered to patients in an autologous chondrocyte implantation procedure known as Characterized Chondrocyte Implantation (CCI), a surgical procedure to treat cartilage defects, in conjunction with debridement (preparation of the defect bed), a physical seal of the lesion (placement of a biological membrane, preferentially a collagen membrane) and rehabilitation.

Cartilage defects of the knee are very common and the spontaneous healing capacity of cartilage is limited. Currently, roughly 2 million cases of articular cartilage defects of the knee are diagnosed worldwide every year. TiGenix estimates that in Europe and the United States around 130,000 patients are eligible for treatment with cartilage regeneration products such as ChondroCelect.

ChondroCelect is the first cell-based product to successfully complete the entire development track from research to clinical development, and was approved by the European Medicines Agency as an Advanced Medicinal Therapy Product in October 2009. ChondroCelect is to date the only EMA approved cartilage repair therapy, and is commercially available in Belgium, the Netherlands, Luxemburg, Germany, the United Kingdom, Finland, and Spain.

About TiGenixTiGenix NV (EURONEXT:TIG) is a leading European cell therapy company with a marketed cell therapy product for cartilage repair, ChondroCelect, and a strong pipeline with clinical stage allogeneic adult stem cell programs for the treatment of autoimmune and inflammatory diseases. TiGenix is based out of Leuven (Belgium) and has operations in Madrid (Spain), and Sittard-Geleen (the Netherlands). For more information please visit http://www.tigenix.com.

Forward-looking informationThis document may contain forward-looking statements and estimates with respect to the anticipated future performance of TiGenix and the market in which it operates. Certain of these statements, forecasts and estimates can be recognized by the use of words such as, without limitation, "believes", "anticipates", "expects", "intends", "plans", "seeks", "estimates", "may", "will" and "continue" and similar expressions. They include all matters that are not historical facts. Such statements, forecasts and estimates are based on various assumptions and assessments of known and unknown risks, uncertainties and other factors, which were deemed reasonable when made but may or may not prove to be correct. Actual events are difficult to predict and may depend upon factors that are beyond TiGenix' control. Therefore, actual results, the financial condition, performance or achievements of TiGenix, or industry results, may turn out to be materially different from any future results, performance or achievements expressed or implied by such statements, forecasts and estimates. Given these uncertainties, no representations are made as to the accuracy or fairness of such forward-looking statements, forecasts and estimates. Furthermore, forward-looking statements, forecasts and estimates only speak as of the date of the publication of this document. TiGenix disclaims any obligation to update any such forward-looking statement, forecast or estimates to reflect any change in TiGenix' expectations with regard thereto, or any change in events, conditions or circumstances on which any such statement, forecast or estimate is based, except to the extent required by Belgian law.

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TiGenix Signs Up 4th Major Hospital in the Netherlands for Innovative Cartilage Repair Therapy

VS-507 is a polyether natural product with a complex chemical structure that is currently being developed by Verastem as a Wnt inhibitor. Past research has shown that VS-507 inhibits Wnt signaling by blocking the phosphorylation of the Wnt coreceptors LPR5 and LRP6 and inducing their degradation. Under the terms of the research collaboration, Eisai will synthesize analogs of VS-507 by leveraging the natural product chemistry-based drug discovery platform it used to generate the anticancer agent Halaven(R) (eribulin mesylate) from the polyether macrolide natural product Halichondrin B. Verastem will utilize its proprietary Wnt signaling and cancer stem cell assays to evaluate the resulting analogs. Verastem will own any novel compounds generated, while Eisai earns a royalty on product sales and has a right of first negotiation to obtain commercialization rights. The identification of proteins involved in cancer has become possible due to advances being made in cancer genetics research. The integration of Eisai and Verastem's complementary platform technologies is expected to have significant synergistic effects in the development of novel compounds that regulate Wnt signaling.

Eisai defines oncology as an area of therapeutic focus and is committed to developing novel anticancer agents and treatments for supportive care. Through this research collaboration, Eisai seeks to make further contribution to address the diversified needs of, and increase the benefits provided to, cancer patients and their families as well as healthcare providers.

About Cancer Stem Cells

Cancer stem cells are cancer cells that possess characteristics associated with normal stem cells. Stem cells have two key features, namely self-renewal capacity (the ability to divide and give rise to new stem cells identical to the original stem cell) and multilineage differentiation potential (the ability to differentiate into various types of cells). Some researchers advocate the cancer stem cell theory, which puts forth the idea that cancer is caused by cancer stem cells that possess the same characteristics as stem cells. Cancer stem cells were first identified in acute myeloid leukemia in 1997, and have since been discovered in solid tumors and various other types of cancer.

About Wnt Signaling

Wnt is a glycoprotein with a molecular weight of approximately 40,000. It is stored in all types of living organisms from threadworms and drosophila to mammals, and has been reported to regulate the proliferation, differentiation and motility of cells during early development and axis formation, organogenesis, and after birth. Pathways known to comprise the Wnt signaling pathway include the Wnt/Beta-catenin pathway, which is associated with cell differentiation and dorsal formation, the Wnt/PCP pathway, which is involved in planar cell polarity and motility during gastrulation, the Wnt/Ca2+ pathway, which plays a role in embryonic isolation, and the pathway involved in the regulation of muscle regeneration. The Wnt/Beta-catenin pathway is the most well-known of all the Wnt signaling pathways. Beta-catenin acts as a Wnt signaling mediator to induce gene expression which results in the regulation of cell proliferation and differentiation.

About Verastem, Inc.

Headquartered in Massachusetts in the United States, Verastem, Inc. is a biopharmaceutical company focused on discovering and developing drugs to treat breast and other cancers by targeting cancer stem cells, an underlying cause of tumor recurrence and metastasis. For more information on Verastem, Inc., please visit http://www.verastem.com.

About Eisai

Eisai Co., Ltd. (TSE: 4523; ADR: ESALY) is a research-based human health care (hhc) company that discovers, develops and markets products throughout the world. Eisai focuses its efforts in three therapeutic areas: integrative neuroscience, including neurology and psychiatric medicines; integrative oncology, which encompasses oncotherapy and supportive-care treatments; and vascular/immunological reaction. Through a global network of research facilities, manufacturing sites and marketing subsidiaries, Eisai actively participates in all aspects of the worldwide healthcare system. For more information about Eisai Co., Ltd., please visit http://www.eisai.com.

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Eisai Enters Research Collaboration with Verisam, Inc. for Small Molecule Wnt Inhibitors

NEWARK, Calif., July 17, 2012 (GLOBE NEWSWIRE) -- StemCells, Inc. (STEM), today announced preclinical data demonstrating that its proprietary human neural stem cells restored memory and enhanced synaptic function in two animal models relevant to Alzheimer's disease (AD). The data was presented today at the Alzheimer's Association International Conference 2012 in Vancouver, Canada.

The study results showed that transplanting the cells into a specific region of the brain, the hippocampus, statistically increased memory in two different animal models. The hippocampus is critically important to the control of memory and is severely impacted by the pathology of AD. Specifically, hippocampal synaptic density is reduced in AD and correlates with memory loss. The researchers observed increased synaptic density and improved memory post transplantation. Importantly, these results did not require reduction in beta amyloid or tau that accumulate in the brains of patients with AD and account for the pathological hallmarks of the disease.

The research was conducted in collaboration with a world-renowned leader in AD, Frank LaFerla, Ph.D., Director of the University of California, Irvine (UCI) Institute for Memory Impairments and Neurological Disorders (UCI MIND), and Chancellor's Professor, Neurobiology and Behavior in the School of Biological Sciences at UCI. Matthew Blurton-Jones, Ph.D., Assistant Professor, Neurobiology and Behavior at UCI, presented the study results.

"This is the first time human neural stem cells have been shown to have a significant effect on memory," said Dr. LaFerla. "While AD is a diffuse disorder, the data suggest that transplanting these cells into the hippocampus might well benefit patients with Alzheimer's. We believe the outcomes in these two animal models provide strong rationale to study this approach in the clinic and we wish to thank the California Institute of Regenerative Medicine for the support it has given this promising research."

Stephen Huhn, M.D., FACS, FAAP, Vice President and Head of the CNS Program at StemCells, added, "While reducing beta amyloid and tau burden is a major focus in AD research, our data is intriguing because we obtained improved memory without a reduction in either of these pathologies. AD is a complex and challenging disorder. The field would benefit from the pursuit of a diverse range of treatment approaches and our neural stem cells now appear to offer a unique and viable contribution in the battle against this devastating disease."

About Alzheimer's Disease

Alzheimer's disease is a progressive, fatal neurodegenerative disorder that results in loss of memory and cognitive function. Today there is no cure or effective treatment option for patients afflicted by Alzheimer's disease. According to the Alzheimer's Association, approximately 5.4 million Americans have Alzheimer's disease, including nearly half of people aged 85 and older. The prevalence of Alzheimer's disease is expected to increase rapidly as a result of the country's aging population.

About StemCells, Inc.

StemCells, Inc. is engaged in the research, development, and commercialization of cell-based therapeutics and tools for use in stem cell-based research and drug discovery. The Company's lead therapeutic product candidate, HuCNS-SC(R) cells (purified human neural stem cells), is currently in development as a potential treatment for a broad range of central nervous system disorders. In a Phase I clinical trial in Pelizaeus-Merzbacher disease (PMD), a fatal myelination disorder in children, the Company has shown preliminary evidence of progressive and durable donor-derived myelination in all four patients transplanted with HuCNS-SC cells. The Company is also conducting a Phase I/II clinical trial in chronic spinal cord injury in Switzerland and recently reported positive interim safety data for the first patient cohort. The Company has also initiated a Phase I/II clinical trial in dry age-related macular degeneration (AMD), and is pursuing preclinical studies in Alzheimer's disease. StemCells also markets stem cell research products, including media and reagents, under the SC Proven(R) brand. Further information about StemCells is available at http://www.stemcellsinc.com.

The StemCells, Inc. logo is available at http://www.globenewswire.com/newsroom/prs/?pkgid=7014

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StemCells, Inc. Announces Its Human Neural Stem Cells Restore Memory in Models of Alzheimer's Disease

THE discovery of a unique marker on stem cells from the gut, liver and pancreas could eventually allow scientists to diagnose cancer earlier and develop new treatments, a Melbourne scientist says.

Professor Martin Pera from Stem Cells Australia and an international team developed an antibody that identifies and isolates the marker, which sits on the outer surface of stem cells and another type of cell called a progenitor.

These cells are particularly hard to find in the pancreas and liver.

By identifying the markers, the cells can be isolated and extracted for study in the laboratory, where scientists can observe what happens to the cells during the disease process and in repair and regeneration.

Prof Pera, who is also chair of Stem Cell Sciences at the University of Melbourne, said the number of cells with the marker expanded during pancreatic and esophageal cancer, and liver cirrhosis.

"It may well be that they are precursors of the cancers," Prof Pera told AAP.

He said if the marker could be found in the blood of cancer patients, it could allow sufferers to be diagnosed earlier and provide new approaches to treatment, which could involve developing drugs to target the marker on cancer cells.

"Cancers of the liver, pancreas and oesophagus are often very difficult to detect and challenging to treat," Prof Pera said.

He will continue his investigations into liver, pancreatic and gut stem cells with Dr Kouichi Hasegawa, who conducts stem cell research in Japan and India.

The research was published in the journal Stem Cell.

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Stem cell discovery important for cancer

ALAMEDA, Calif.--(BUSINESS WIRE)--

BioTime, Inc. (NYSE MKT: BTX), a biotechnology company that develops and markets products in the field of regenerative medicine, today announced the signing of an exclusive sublicense agreement and a supply agreement with Jade Therapeutics, LLC, a developer of an ophthalmological therapeutic sustained-release drug delivery platform. Under the agreements, BioTime will provide Jade with clinical-grade HyStem hydrogels and certain patented technology for use by Jade Therapeutics in the development of new pharmaceutical products for ophthalmologic use. Jade plans to utilize the hydrogels to facilitate time-release topical delivery of recombinant human growth hormone to help heal lesions on the ocular surface. Jade Therapeutics will retain rights to market their product upon completion of development and obtaining marketing approval. Financial terms of the transaction were not disclosed.

William P. Tew, Ph.D., BioTimes Chief Commercialization Officer, stated that Numerous published scientific reports have established the efficacy of HyStem to facilitate cell transplantation in animal models, and we currently plan on a near-term approval to market one HyStem-related product, ReneviaTM, in the EU for reconstructive and cosmetic surgery. We believe our HyStem technology may also be useful as a device for the slow, timed release of therapeutic agents such as those being developed by Jade Therapeutics, as well as for the controlled release of proteins secreted from BioTimes stem cell lines.

The HyStem product line has potential utility in a wide array of human therapeutic products, said Michael West, Ph.D., BioTimes CEO. We intend to seek additional industry partners for applications that are not core to our own therapeutic product development.

BioTime's HyStem hydrogels are proprietary biocompatible hydrogels that mimic the human extracellular matrix (ECM), a web of molecules surrounding cells that is essential to cellular function. When cells lacking the ECM (or an ECM substitute) are introduced into the body, they typically die or fail to function correctly after transplantation. BioTime's HyStem hydrogels are currently being used by researchers at a number of leading medical schools in studies of stem cell therapies for facilitating wound healing and for the treatment of ischemic stroke, brain cancer, vocal fold scarring, and cardiac infarct.

About Jade Therapeutics

Jade Therapeutics, LLC, a privately-held company headquartered in Park City, Utah, focuses on the development of locally administered, sustained-release therapeutics that improve corneal healing following damage from disease or injury, thus improving visual function and quality of life. The Companys initial product is designed to deliver recombinant human growth hormone, a well characterized biologic that has already been demonstrated to have significant healing properties. Jade recently secured a prestigious Utah Science Technology and Research (USTAR) grant to continue to conduct preclinical and market research and is in negotiation with several prominent academic and military affiliates to further product development. Examples of ocular disorders addressed by the Companys technology includes persistent corneal epithelial defects and corneal damage due to dry eye disease.

About BioTime, Inc.

BioTime, headquartered in Alameda, California, is a biotechnology company focused on regenerative medicine and blood plasma volume expanders. Its broad platform of stem cell technologies is enhanced through subsidiaries focused on specific fields of application. BioTime develops and markets research products in the field of stem cells and regenerative medicine, including a wide array of proprietary ACTCellerateTM cell lines, HyStem hydrogels, culture media, and differentiation kits. BioTime is developing ReneviaTM (formerly known as HyStem-Rx), a biocompatible, implantable hyaluronan and collagen-based matrix for cell delivery in human clinical applications. BioTime's therapeutic product development strategy is pursued through subsidiaries that focus on specific organ systems and related diseases for which there is a high unmet medical need. BioTime's majority-owned subsidiary Cell Cure Neurosciences, Ltd. is developing therapeutic products derived from stem cells for the treatment of retinal and neural degenerative diseases. BioTime's subsidiary OrthoCyte Corporation is developing therapeutic applications of stem cells to treat orthopedic diseases and injuries. Another subsidiary, OncoCyte Corporation, focuses on the diagnostic and therapeutic applications of stem cell technology in cancer, including the diagnostic product PanC-DxTM currently being developed for the detection of cancer in blood samples. ReCyte Therapeutics, Inc. is developing applications of BioTime's proprietary induced pluripotent stem cell technology to reverse the developmental aging of human cells to treat cardiovascular and blood cell diseases. BioTime's subsidiary LifeMap Sciences, Inc. markets GeneCards, the leading human gene database, and is developing an integrated database suite to complement GeneCards that will also include the LifeMapTM database of embryonic development, stem cell research, and regenerative medicine, and MalaCards, the human disease database. LifeMap will also market BioTime research products. BioTime's lead product, Hextend, is a blood plasma volume expander manufactured and distributed in the U.S. by Hospira, Inc. and in South Korea by CJ CheilJedang Corporation under exclusive licensing agreements. Additional information about BioTime can be found on the web at http://www.biotimeinc.com.

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BioTime Signs Agreements with Jade Therapeutics for Ophthalmological Drug Delivery Applications of HyStem® Technology

CLEVELAND, July 16, 2012 /PRNewswire/ --Juventas Therapeutics, a clinical-stage regenerative medicine company, announced today that it has closed a $22.2 million Series B financing that was co-led by Triathlon Medical Venture Partners and New Science Ventures. All previous venture firms, including Fletcher Spaght Ventures, Reservoir Venture Partners and Early Stage Partners participated in the round. Also joining the syndicate are new investors Takeda Ventures, Venture Investors, Global Cardiovascular Innovation Center, Tri-State Growth Fund, Glengary and select angel investors.

The proceeds will fund completion of ongoing Phase II clinical trials investigating the use of JVS-100 in treating patients with chronic heart failure or critical limb ischemia. Both trials are actively enrolling patients. JVS-100, the Company's lead product, encodes Stromal cell-Derived Factor 1 (SDF-1) which has been shown to repair damaged tissue through recruitment of circulating stem cells to the site of injury, prevent ongoing cell death and restore blood flow.

"The funds raised through this Series B will carry us through significant clinical milestones," states Rahul Aras, Ph.D., President & CEO of Juventas Therapeutics. "The fact that the round was oversubscribed and added several new investors to an already strong syndicate speaks to the excitement that is building around regenerative medicine, and specifically, the unique factor-based strategy employed by Juventas."

Clinical studies by several companies have demonstrated that delivery of adult stem cells to patients suffering from heart failure or critical limb ischemia has the potential to promote tissue repair and improve clinical outcomes. In spite of these clinical findings, questions remain about the affordability and accessibility of cell-based therapy for the general population. Rather than deliver cells, Juventas delivers JVS-100, which activates natural stem cell based repair pathways that lie dormant in a patient. This allows the benefits of regenerative medicine without the complexity of cell therapy. While currently focused on cardiovascular disease, the clinical potential for JVS-100 is broad.

Last year, Juventas Therapeutics spun-off SironRX Therapeutics to focus on development of dermal and bone related applications for JVS-100. In 2011, SironRX raised $3.4 million through a Series A financing led by North Coast Angel Fund and received $1 million in grant funding through the Ohio Third Frontier program. The Company is currently enrolling a Phase Ib randomized, placebo-controlled, double-blinded clinical trial investigating dermal JVS-100 delivery to accelerate wound closure and reduce scar formation.

"Juventas provides a commercially viable solution to delivering regenerative therapies and has the potential to address a broad range of clinical applications" states George Emont, Managing Partner for Triathlon Medical Ventures and Chairman for Juventas. We are pleased to have raised these funds for the two Phase II clinical trials and additional development as the company looks toward its Phase III trials and eventual commercialization".

About Juventas TherapeuticsJuventas Therapeutics, (www.juventasinc.com) headquartered in Cleveland, OH, is a privately-held clinical-stage biotechnology company developing a pipeline of regenerative therapies to treat lifethreatening diseases. Founded in 2007 with an exclusive license from Cleveland Clinic, Juventas has transitioned its therapeutic platform from concept to initiation of mid-stage clinical trials for treatment of heart failure and critical limb ischemia. Investors include New Science Ventures, Takeda Ventures, Triathlon Medical Venture Partners, Venture Investors, Early Stage Partners, Fletcher Spaght Ventures, Reservoir Venture Partners, Glengary, The Global Cardiovascular Innovation Center, Tri-State Growth Fund, North Coast Angel Fund, X Gen Ltd., JumpStart Inc., and Blue Chip Venture Co. The company has received non-dilutive grant support through the Ohio Third Frontier-funded Cleveland Clinic Ohio BioValidation Fund, Global Cardiovascular Innovation Center and Center for Stem Cell & Regenerative Medicine.

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Juventas Therapeutics Raises $22.2 Million Series B Financing

Researchers at Brown University, along with colleagues at several universities, have learned how to analyze genetic markers in immune system cells. The technique allows the researchers to distinguish among several types of cancer, according to a release from the university by Mike Cohea.

The immune cells, called leukocytes, are present in the blood when a person has an illness. The new technique, described in two recent papers, lets scientists identify a unique chemical alteration to DNA of each type of leukocyte. By detecting these changes, call "methylation signatures," in a patients blood sample and applying a mathematical analysis, the researchers are able to determine the relative levels of different leukocytes and correlate those with specific diseases.

The release quotes Karl Kelsey, professor of pathology and laboratory medicine in the Warren Alpert Medical School of Brown University and a senior author on both papers, as saying, Its a way to more easily interrogate the immune system of a lot of people.

One of the papers was published in BMC Bioinformatics and the second one was published online in Cancer Epidemiology, Biomarkers, and Prevention. Our approach provides a completely novel tool for the study of the immune profiles of diseases where only DNA can be accessed, the authors wrote. That is, we believe this approach has utility not only in cancer diagnostics and risk-prediction, but can also be applied to future research (including stored specimens) for any disease where the immune profile holds medical information.

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Mix of Immune Cells Detects Cancer