Leukemia cells have a remembrance of things past
ScienceDaily (Apr. 24, 2012) Although people generally talk about cancer, it is clear that the disease occurs in a bewildering variety of forms. Even single groups of cancers, such as those of the white blood cells, may show widely differing properties. How do the various cancers arise and what factors determine their progression? Clues to these two issues, at least for leukemias, have now been provided by Boris Kovacic and colleagues at the University of Veterinary Medicine, Vienna (Vetmeduni Vienna). The results are published in the current issue of the journal EMBO Molecular Medicine and have extremely important consequences for the treatment of a particularly aggressive type of leukemia.
It is well known that many types of cancer arise as a result of a mutation within a cell and prevailing wisdom has held that the stage of differentiation of this cell determines exactly what form of cancer develops. For example, it was believed that so-called chronic myeloid leukemia or CML arises from bone marrow stem cells, while a different type of leukemia, known as B-cell acute lymphoid leukemia or B-ALL, results from B-cell precursors. This belief has been spectacularly refuted by the latest results from Boris Kovacic and colleagues in the Vetmeduni Viennas institutes of Animal Breeding and Genetics and of Pharmacology and Toxicology.
The researchers have now shown that both CML and B-ALL arise from the most primordial kind of blood cell (long-term haematopoietic stem cells), although the pathways by which the diseases progress are different. The usual causes of CML and B-ALL are two highly related versions of the same oncogene, BCR/ABL. If the primordial blood cells are transformed or made potentially cancerous by a particular version of BCR/ABL, for technical reasons termed BCR/ABLp210, the result is chronic myeloid leukemia or CML. The long-term haematopoietic stem cells remain and act as the dreaded cancer stem cells, or CSCs, which ensure that the disease persists. Curing chronic myeloid leukemia requires the complete elimination of the CSCs. However, if the long-term haematopoietic stem cells are transformed by a related version of BCR/ABL, BCR/ABLp185, the result is a highly aggressive form of leukemia, B-ALL. The finding that B-ALL actually originates from the same stem cells as CML was both unexpected and highly provocative.
Kovacic and colleagues have shown further that B-ALL only develops if the transformed stem cell is exposed to a particular growth factor, interleukin-7. If interleukin-7 is present (it usually is), the transformed long-term haematopoietic stem cells undergo a differentiation step to CSCs, which in this case correspond to pro-B cells. If interleukin-7 is absent during the initial phase of transformation, B-ALL cannot develop.
In other words, two distinct types of cell are involved in leukemia development, the primordial cells (also termed the cells of origin of cancer) and the cancer stem cells that cause the disease to progress. Unless the CSCs are eliminated, fresh cancer cells can arise at any time and the leukemia will recur. The problem is that current leukemia therapies are not designed to target CSCs. The primordial CSCs in CML are highly quiescent and thus difficult to target. In contrast, the CSCs in B-ALL are abundant and have a high turnover rate, which makes them susceptible to treatment. Treatment of B-ALL may thus succeed in eliminating most CSCs but if even a single cell remains intact it is likely that the patient will relapse, possibly with an even more aggressive form of leukemia. A therapy that targets the bulk of tumour cells will not work, as Kovacic succinctly summarizes his results. To treat B-ALL successfully it will be necessary for us to learn much more about the development of the disease. A combined therapy is required, so future work should aim at developing drugs that target the long-term haematopoietic stem cells from which B-ALL is derived.
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The above story is reprinted from materials provided by Veterinrmedizinische Universitt Wien, via AlphaGalileo.
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Leukemia cells have a remembrance of things past
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VistaGen Secures Key U.S. Patent Covering Stem Cell Technology Methods Used to Test Drug Candidates for Liver Toxicity
SOUTH SAN FRANCISCO, CA--(Marketwire -04/25/12)- VistaGen Therapeutics, Inc. (VSTA.OB - News) (VSTA.OB - News), a biotechnology company applying stem cell technology for drug rescue, has secured a new United States patent covering the company's proprietary methods used to measure and type the toxic effects produced by drug compounds in liver stem cells.
Test methods included in this new patent, (U.S. Patent 11/445,733), titled "Toxicity Typing Using Liver Stem Cells," cover all mammalian liver stem cells -- rat and mouse cells, for example, in addition to human cells. Liver stem cells used in drug testing can be derived from in vivo tissue or produced from embryonic stem cells (ES) or induced pluripotent stem cells (iPS).
H. Ralph Snodgrass, Ph.D., VistaGen's President and Chief Scientific Officer, said, "This patent covers the monitoring of changes in gene expression as an assay for predicting drug toxicities. It is well known that drugs activate and suppress specific genes, and that the changes in gene expression reflect the mechanism of drug toxicities. The specific sets of genes that are affected become a profile of that drug."
VistaGen's new patent also covers techniques used to develop a database of gene expression profiles of drugs that have the same type of liver toxicity. Using sophisticated "pattern matching" database tools, drug developers can analyze these related profiles to determine "gene expression signatures" that are common and predictive of drugs that produce specific types of toxicity.
"Without this database capability, a drug's single gene expression profile could not be interpreted," Dr. Snodgrass added. "The ability to use liver stem cells to differentiate drug-dependent gene expression profiles, and to compare those profiles of drugs known to induce toxic liver effects, provides a powerful tool for predicting liver toxicity of new drug candidates, including drug rescue variants."
Shawn K. Singh, VistaGen's Chief Executive Officer, stated, "Strong and enforceable intellectual property rights are critical components of our plan to optimize the commercial potential of our Human Clinical Trials in a Test Tube platform. This new liver toxicity typing patent further solidifies our growing IP portfolio, and supports the continuing development of LiverSafe 3D, our human liver cell-based bioassay system, which complements our CardioSafe 3D human heart cell-based bioassay system for heart toxicity."
About VistaGen Therapeutics
VistaGen is a biotechnology company applying human pluripotent stem cell technology for drug rescue and cell therapy. VistaGen's drug rescue activities combine its human pluripotent stem cell technology platform, Human Clinical Trials in a Test Tube, with modern medicinal chemistry to generate new chemical variants (Drug Rescue Variants) of once-promising small-molecule drug candidates. These are drug candidates discontinued due to heart toxicity after substantial development by pharmaceutical companies, the U.S. National Institutes of Health (NIH) or university laboratories. VistaGen uses its pluripotent stem cell technology to generate early indications, or predictions, of how humans will ultimately respond to new drug candidates before they are ever tested in humans, bringing human biology to the front end of the drug development process.
Additionally, VistaGen's small molecule drug candidate, AV-101, is in Phase 1b development for treatment of neuropathic pain. Neuropathic pain, a serious and chronic condition causing pain after an injury or disease of the peripheral or central nervous system, affects approximately 1.8 million people in the U.S. alone. VistaGen is also exploring opportunities to leverage its current Phase 1 clinical program to enable additional Phase 2 clinical studies of AV-101 for epilepsy, Parkinson's disease and depression. To date, VistaGen has been awarded over $8.5 million from the NIH for development of AV-101.
Visit VistaGen at http://www.VistaGen.com, follow VistaGen at http://www.twitter.com/VistaGen or view VistaGen's Facebook page at http://www.facebook.com/VistaGen
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VistaGen Secures Key U.S. Patent Covering Stem Cell Technology Methods Used to Test Drug Candidates for Liver Toxicity
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Research and Markets: Recent Advances in Cancer Research and Therapy – Increased Research on one of the Major Causes …
DUBLIN--(BUSINESS WIRE)--
Research and Markets (http://www.researchandmarkets.com/research/msjp88/recent_advances_in) has announced the addition of Elsevier Science and Technology's new report "Recent Advances in Cancer Research and Therapy" to their offering.
Cancer continues to be one of the major causes of death throughout the developed world, which has led to increased research on effective treatments. Because of this, in the past decade, rapid progress in the field of cancer treatment has been seen. Recent Advances in Cancer Research and Therapy reviews in specific details some of the most effective and promising treatments developed in research centers worldwide. While referencing advances in traditional therapies and treatments such as chemotherapy, this book also highlights advances in biotherapy including research using Interferon and Super Interferon, HecI based and liposome based therapy, gene therapy, and p53 based cancer therapy. There is also a discussion of current cancer research in China including traditional Chinese medicine. Written by leading scientists in the field, this book provides an essential insight into the current state of cancer therapy and treatment.
Key Topics Covered:
1. Biotherapy of Cancer: Progress in China
2. Cancer Targeting Gene-Viro-Therapy (CTGVT) and Its Promising Future
3. Relationship Between Antiproliferative Activities and Class I MHC Surface Expression of Mouse Interferon Proteins on B16-F10 Melanoma Cells
4. Mitotic Regulator Hec1 as a Potential Target for Developing Breast Cancer Therapeutics
5. Advances in Liposome-based Targeted Gene Therapy of Cancer
6. Re-wiring the Intracellular Signaling Network in Cancer
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Research and Markets: Recent Advances in Cancer Research and Therapy - Increased Research on one of the Major Causes ...
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Gene Ray, Founder of $2.6 Billion Titan Corp, Invests in Medistem's ERC Technology and Joins Advisory Board
SAN DIEGO, CA--(Marketwire -04/25/12)- Medistem Inc. (MEDS.PK - News) announced Dr. Gene Ray, founder of $2.6 Billion Titan Corp, has invested in and joined the Advisory Board for Medistem Inc. Dr. Ray is a Ph.D in Theoretical Physics, Inventor, and Entrepreneur who founded and sold Titan Corp for $2.6 Billion. Dr. Ray has a long track record of success in developing science and technology solutions for the Department of Defense and Homeland Security.
"When Dr. Ichim presented Medistem's story to me two years ago, I was intrigued by the possibility of security and military applications of the Universal Donor adult stem cell that Medistem has discovered," said Dr. Ray. "Since that time, Medistem has obtained FDA approval for clinical trials, numerous publications in peer-reviewed journals with top-notch Universities, and built an experienced management team. When Medistem asked for my help in assisting with strategic issues associated with value optimization and positioning in the arena of military/radioprotectant applications, I was eager to not only offer my expertise, but also to become an investor in the company."
A native of Kentucky, Dr. Ray's academic achievements include: B.S. in Mathematics, Physics & Chemistry, Murray State University, M.S. in Physics and Ph.D in Theoretical Physics, University of Tennessee. In addition to founding Titan Corporation, Dr. Ray has served as Executive Vice President at SAIC, Chief of the Strategic Division of the USAF and as a defense industry analyst. He is currently Chairman of the Board of Decision Sciences on the Board of Artel Corporation, and Chairman of the Cardiology Advisory Board at Scripps Clinic.
Medistem's lead product, the Endometrial Regenerative Cell (ERC), is a stem cell that is more economical to produce, due to its unique origin, and studies suggest it is more effective than other stem cell sources. In addition to the ongoing 60 patient double-blind RECOVER-ERC clinical trial for Heart Failure and its FDA approved Critical Limb Ischemia trial, the company has been investigating possibility of using its new stem cell in protection from radiation injury. Medistem filed patent number 61/625657 covering use of ERC for radiation protection. Dr. Ray's experience working with The Department of Defense and Homeland Security will significantly help Medistem position itself for potential military application of ERCs for radiation exposure.
"I have followed the work of Dr. Ray for some time now with great admiration," said Thomas Ichim, CEO of Medistem. "There are few people in the world that have the unique combination of being a genuine innovator while at the same time having the talent to transform ideas into return on investment to shareholders. Dr. Ray has successfully optimized value in businesses he founded ranging from novel computer systems, to translation services, to food pasteurization, and more recently to detection of nuclear material using muon-based technology. This ability to seamlessly transverse across disciplines, while finding means of successful commercialization, suggested to us that Dr. Ray will add great value to the breadth of applications that our stem cell product may be used for."
Commercialization of therapies for radioprotection fall under the "Animal Efficacy" rule developed by the U.S. Food and Drug Administration (FDA) in 2002 which eliminates the requirement for Phase II and Phase III clinical trials. Under this rule marketing approval is based upon efficacy studies in representative animal species and only Phase I safety data is needed. Medistem believes safety data from its current clinical trials will be sufficient in combination with animal efficacy data, thereby making the commercialization of these therapies ready for market quickly.
"We believe that Dr. Ray will be of great assistance in positioning us in the expanding market for stem cell-based therapeutics," said Dr. Vladimir Bogin, Chairman of Medistem. "Development of novel radioprotectants in the area of cell therapy has attracted significant defense interest. The company Osiris received a $4.2 million upfront grant for large animal studies along with a procurement order of $224.7 million (http://investor.osiris.com/releasedetail.cfm?releaseid=284617) while Cellarant last year received a $153 million award for development and stockpiling of their hematopoietic progenitor cells from the Biomedical Advanced Research and Development Authority (BARDA) for use in radiation sickness (http://www.cellerant.com/pr_090110.html). We plan to seek similar contracts/grants for our ongoing work in this space."
"It is our honor to have Dr. Ray personally invest in and join the Medistem Family. Through leveraging his experience, wisdom, and ingenuity, we are confident in accelerating the process of value optimization for our shareholders," said Vladimir Zaharchook, Vice Chairman and Vice President of Medistem.
About Medistem Inc. Medistem Inc. is a biotechnology company developing technologies related to adult stem cell extraction, manipulation, and use for treating inflammatory and degenerative diseases. The company's lead product, the endometrial regenerative cell (ERC), is a "universal donor" stem cell being developed for critical limb ischemia and heart failure. A publication describing the support for use of ERC for this condition may be found at http://www.translational-medicine.com/content/pdf/1479-5876-6-45.pdf.
Cautionary Statement This press release does not constitute an offer to sell or a solicitation of an offer to buy any of our securities. This press release may contain certain forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. Forward-looking statements are inherently subject to risks and uncertainties, some of which cannot be predicted or quantified. Future events and actual results could differ materially from those set forth in, contemplated by, or underlying the forward-looking information. Factors which may cause actual results to differ from our forward-looking statements are discussed in our Form 10-K for the year ended December 31, 2007 as filed with the Securities and Exchange Commission.
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Mayo Clinic identifies gene critical to development and spread of lung cancer
Public release date: 24-Apr-2012 [ | E-mail | Share ]
Contact: Paul Scotti scotti.paul@mayo.edu 904-953-2299 Mayo Clinic
JACKSONVILLE, Fla. A single gene that promotes initial development of the most common form of lung cancer and its lethal metastases has been identified by researchers at Mayo Clinic in Florida. Their study suggests other forms of cancer may also be driven by this gene, matrix metalloproteinase-10 (MMP-10).
The study, published in the journal PLoS ONE on April 24, shows that MMP-10 is a growth factor secreted and then used by cancer stem-like cells to keep themselves vital. These cells then drive lung cancer and its spread, and are notoriously immune to conventional treatment.
The findings raise hope for a possible treatment for non-small cell lung cancer, the leading cause of U.S. cancer deaths. Researchers discovered that by shutting down MMP-10, lung cancer stem cells lose their ability to develop tumors. When the gene is given back to the cells, they can form tumors again.
The power of this gene is extraordinary, says senior investigator Alan Fields, Ph.D., the Monica Flynn Jacoby Professor of Cancer Research within the Department of Cancer Biology at Mayo Clinic in Florida.
"Our data provides evidence that MMP-10 plays a dual role in cancer. It stimulates the growth of cancer stem cells and stimulates their metastatic potential,'' he says. "This helps explain an observation that has been seen in cancer stem cells from many tumor types, namely that cancer stem cells appear to be not only the cells that initiate tumors, but also the cells that give rise to metastases."
Dr. Fields says the findings were unexpected, for several reasons.
The first is that the cancer stem cells express MMP-10 themselves, and use it for their own growth. Most of the known members of the matrix metalloproteinase genes are expressed in the tumor's microenvironment, the cells and tissue that surround a tumor, he says. The enzymes produced by these genes are involved in breaking down the microenvironment that keeps a tumor in place, allowing cancer cells to spread, which is why other genes in this family have been linked to cancer metastasis.
"The fact that a gene like MMP-10, which codes for a matrix metalloproteinase that has been linked to metastasis, is actually required for the growth and maintenance of cancer stem cells is very surprising. One would not have predicted that such a gene would be involved in this process," Dr. Fields says.
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Mayo Clinic identifies gene critical to development and spread of lung cancer
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Scientists identify 'critical' gene for development and spread of lung cancer
Scientists from the Mayo Clinic have identified a single gene that appears to be a major driving force in the development and spread of the most common form of lung cancer. The study also suggested the gene may play a role in a number of other different types of cancer.
Matrix metalloproteinase-10 (MMP-10) is a growth factor gene used by cancer stem-like cells to keep themselves healthy, as well as migrate into the bloodstream or lymph nodes. Thanks in part to MMP-10, these stem cells are highly resistant to cancer treatments.
This family of [MMP] genes have been implicated for a long time in the process of metastasis the ability of tumors to migrate out of the primary site and survive and move to a distal site, Dr. Alan P. Fields, the Monica Flynn Jacoby Professor of Cancer Research at Mayo Clinic in Florida, told FoxNews.com.
According to Fields, metastasis depends on the ability of MMP genes to degrade the stroma or the environment surrounding the tumor. The stroma normally provides structure for tissues and acts as a barrier against cancer cells.
However, it was a surprise to researchers when they found that MMP was not only involved in metastasis, but also in the earliest stages of tumor growth.
In a mouse model of lung cancer, when we inhibited MMP, we found these animals were deficient in their ability to initiate tumors when we attempted to activate tumor formations, Fields said. We expected the tumors would form, but not progress to the point of metastasizing. But the tumors never started growing.
The study suggested it was the overexpression of MMP-10 specifically that drives the cancer stem cells. In normal tissues, the amount of MMP-10 is very low, but in cancerous tissues it is expressed much more highly. Besides lung cancer, MMP-10 is also suspected to play a role in colorectal, breast, prostate, ovarian and kidney cancers, as well as melanoma and renal cell carcinoma.
The finding suggests drugs or compounds that inhibit MMP-10 activity could be effective as anti-tumor agents with the potential to prevent the spread of tumors or even cause them to regress.
Current cancer treatments, such as chemotherapy, target the cells that make up the bulk of a tumor. But because the cancer-driving stem cells are left intact, the cancer can and often does return.
Tumor stem cells are very resistant to these therapeutic agents, so they remain at the site of the tumor even as the tumor regresses and the patient goes it to remission, Fields explained. Then what happens is you see a relapse or recurrence of the tumor due to these stem cells.
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Scientists identify 'critical' gene for development and spread of lung cancer
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A striking link is found between the Fragile-X gene and mutations that cause autism
Public release date: 25-Apr-2012 [ | E-mail | Share ]
Contact: Peter Tarr tarr@cshl.edu 516-367-8455 Cold Spring Harbor Laboratory
Cold Spring Harbor, NY A team led by scientists at Cold Spring Harbor Laboratory (CSHL) publishes research today indicating a striking association between genes found disrupted in children with autism and genes that are targets of FMRP, the protein generated by the gene FMR1, whose dysfunction causes Fragile-X syndrome. The new study appears online April 25 in the journal Neuron.
Fragile-X syndrome is the most common cause of inherited intellectual disability. It is also counted among the autism spectrum disorders (ASDs) owing to the co-occurrence of autism-like symptoms in patients. A usually devastating disorder, Fragile X occurs when the FRM1 gene fails to direct nerve cells to manufacture FMRP, the FMR1-encoded protein, which plays a vital role in neural development and synaptic plasticity.
"A surprising proportion -- up to 20% -- of the candidate genes we see in our sample drawn from 343 autism families appear to be regulated by FMRP," says CSHL Research Investigator Dr. Michael Ronemus, co-first author of the new study. "Because of research connecting FMRP to the phenomenon of neuroplasticity, our work indicates a possible convergence of mechanisms causing autism," adds CSHL Professor Michael Wigler, the senior author of the study. Neuroplasticity is the process by which our brains become sensitized and desensitized to repetitive inputs.
Besides team leader Wigler, a geneticist, others who worked on the study included CSHL sequencing authority Dr. W. Richard McCombie, a sequencing team at Washington University, St. Louis, and Drs. Michael Schatz, Ivan Iossifov and Dan Levy of CSHL, all computational biologists.
Families studied by the team were part of the Simons Simplex Collection. This collection is comprised of "simplex" autism families: those with at least two children, only one of whom has autism spectrum disorder or ASD. In such cases, disease causation has been previously linked to de novo, or spontaneously occurring, gene mutations.
The new research reached its conclusions based on full exome sequencing of each family member's genome. The exome is the portion of the genome less than 2% of the total -- in which DNA encodes proteins. By studying simplex families, researchers seek to discover, among other things, the fraction of autism caused by gene mutations that are not inherited.
This study focused on small-scale de novo mutations changes in DNA as small as a single DNA "letter" relative to the normal sequence, and small insertions or deletions as large as 10 or 15 letters. In the majority of children with small de novo mutations those mutations traced to the father's germ cells (sperm), in an age-dependent manner. Thus, the children of older parents were more likely to have the sorts of mutations that can cause autism.
There are many types of gene mutations, some more likely to result in biological dysfunction than others. One of the most important findings of this study concerned the type of small-scale de novo mutations most likely to play a causative role in autism. "We found that those small-scale de novo changes that disrupt genes in other words, those that disrupt the production of a normal length protein -- are twice as frequent in affected vs. unaffected children," says CSHL Assistant Professor Ivan Iossifov, a quantitative biologist who is the study's other co-first author. (In technical terms, these "disrupting" mutations include frame-shift, splice-site, and nonsense mutations, but not missense mutations.)
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A striking link is found between the Fragile-X gene and mutations that cause autism
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Gene critical to development and spread of lung cancer identified
ScienceDaily (Apr. 24, 2012) A single gene that promotes initial development of the most common form of lung cancer and its lethal metastases has been identified by researchers at Mayo Clinic in Florida. Their study suggests other forms of cancer may also be driven by this gene, matrix metalloproteinase-10 (MMP-10).
The study, published in the journal PLoS ONE on April 24, shows that MMP-10 is a growth factor secreted and then used by cancer stem-like cells to keep themselves vital. These cells then drive lung cancer and its spread, and are notoriously immune to conventional treatment.
The findings raise hope for a possible treatment for non-small cell lung cancer, the leading cause of U.S. cancer deaths. Researchers discovered that by shutting down MMP-10, lung cancer stem cells lose their ability to develop tumors. When the gene is given back to the cells, they can form tumors again.
The power of this gene is extraordinary, says senior investigator Alan Fields, Ph.D., the Monica Flynn Jacoby Professor of Cancer Research within the Department of Cancer Biology at Mayo Clinic in Florida.
"Our data provides evidence that MMP-10 plays a dual role in cancer. It stimulates the growth of cancer stem cells and stimulates their metastatic potential,'' he says. "This helps explain an observation that has been seen in cancer stem cells from many tumor types, namely that cancer stem cells appear to be not only the cells that initiate tumors, but also the cells that give rise to metastases."
Dr. Fields says the findings were unexpected, for several reasons.
The first is that the cancer stem cells express MMP-10 themselves, and use it for their own growth. Most of the known members of the matrix metalloproteinase genes are expressed in the tumor's microenvironment, the cells and tissue that surround a tumor, he says. The enzymes produced by these genes are involved in breaking down the microenvironment that keeps a tumor in place, allowing cancer cells to spread, which is why other genes in this family have been linked to cancer metastasis.
"The fact that a gene like MMP-10, which codes for a matrix metalloproteinase that has been linked to metastasis, is actually required for the growth and maintenance of cancer stem cells is very surprising. One would not have predicted that such a gene would be involved in this process," Dr. Fields says.
The researchers also did not expect to find that cancer stem cells produce much more MMP-10 than do the rest of the cells that make up the bulk of the tumor.
"MMP-10 acts to keep these cancer stem cells healthy and self renewing, which also helps explain why these cells escape conventional chemotherapy that might destroy the rest of the tumor," Dr. Fields says. "That is why lung cancer often recurs after treatment, and why its spread to other parts of the lung, as well as nearby lymph nodes, the brain, liver and spinal cord can't be stopped."
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Gene critical to development and spread of lung cancer identified
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Nano nod for lab-on-a-chip
The Domino technology uses a plastic chip that can perform 20 genetic tests from a single drop of blood.
You wouldn't know it from appearances, but a metal cube the size of a toaster, created at the University of Alberta, is capable of performing the same genetic tests as most fully equipped modern laboratoriesand in a fraction of the time.
At its core is a small plastic chip developed with nanotechnology that holds the key to determining whether a patient is resistant to cancer drugs or has viruses like malaria. The chip can also pinpoint infectious diseases in a herd of cattle.
Talk about thinking outside the box.
Dubbed the Domino, the technologydeveloped by a U of A research teamhas the potential to revolutionize point-of-care medicine. The innovation has also earned Aquila Diagnostic Systems, the Edmonton-based nano startup that licensed the technology, a shot at $175,000 as a finalist for the TEC NanoVenturePrize award.
Were basically replacing millions of dollars of equipment that would be in a conventional, consolidated lab with something that costs pennies to produce and is field portable so you can take it where needed. Thats where this technology shines, said Jason Acker, an associate professor of laboratory medicine and pathology at the U of A and chief technology officer with Aquila.
The Domino employs polymerase chain reaction technology used to amplify and detect targeted sequences of DNA, but in a miniaturized form that fits on a plastic chip the size of two postage stamps. The chip contains 20 gel postseach the size of a pinheadcapable of identifying sequences of DNA with a single drop of blood.
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Thats the real value propositionbeing able to do multiple tests at the same time, Acker said, adding that the Domino has been used in several recently published studies, showing similar accuracy to centralized labs.
The Domino effect: Personalized medicine
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Nano nod for lab-on-a-chip
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Pathway Genomics Adds Prominent Bioinformatics Experts to Scientific Advisory Board
SAN DIEGO--(BUSINESS WIRE)--
Pathway Genomics Corporation, a genetic testing laboratory specializing in nutrition and exercise response, inherited disease, prescription drug response and health condition risks, has established a world-leading scientific advisory board. Among the board members are James Fowler, Ph.D., professor of medical genetics at UCSD School of Medicine, Christoph Lange, Ph.D., associate professor of biostatistics at Harvard University School of Public Health, and Nicholas Schork, Ph.D., director of bioinformatics and biostatistics at the Scripps Translational Science Institute.
Additionally, the companys internal computational and bioinformatics team is led by Lixin Zhou, Ph.D., former senior scientist at Illumina and former collaborative bioinformatics investigator at The Institute for Genomic Research, an organization of The J. Craig Venter Institute.
Working with innovators in specific and technical fields helps Pathway bring highly accurate, useful and actionable information to physicians and their patients, said Michael Nova, M.D., Pathway Genomics chief medical officer. Were committed to seeking out this actionable genetic information through computational biology methods, and cloud-based bioinformatics.
An acclaimed behavioral geneticist, James Fowler, Ph.D., is currently a professor of medical genetics at UCSD School of Medicine, and is world-renowned for his breakthrough discoveries in genetics and social networking, behavioral economics, cooperation, and political behavior.
Christoph Lange, Ph.D., is an assistant professor of medicine at Harvard Medical School and an associate professor of biostatistics at Harvard School of Public Health. Langes current research interests fall into the broad areas of statistical genetics and generalized linear models.
Nicholas J. Schork, Ph.D., is a professor at The Scripps Research Institute in the department of molecular and experimental medicine and director of bioinformatics and biostatistics at the Scripps Translational Science Institute. Schorks research focuses are in quantitative human genetics and integrated approaches to complex biological and medical problems. He has published over 350 scientific articles and book chapters analyzing complex, multifactorial traits and diseases.
Pathways scientific advisory board consists of 10 leaders in various fields including behavioral genetics, bioinformatics, biostatistics, endocrinology, human epigenetics, metabolism, nutrigenomics, nutrition, obesity and exercise genetics, oncology, and weight management. To view the companys full scientific advisory board, visit http://www.pathway.com/sab.
About Pathway Genomics
Pathway Genomics owns and operates an on-site genetic testing laboratory that is accredited by the College of American Pathologists (CAP), accredited in accordance with the U.S. Health and Human Services Clinical Laboratory Improvement Amendments (CLIA) of 1988, and licensed by the state of California. Using only a saliva sample, the company incorporates customized and scientifically validated technologies to generate personalized reports, which address a variety of medical issues, including an individuals carrier status for recessive genetic conditions, food metabolism and exercise response, prescription drug response, and propensity to develop certain diseases such as heart disease, type 2 diabetes and cancer. For more information about Pathway Genomics, visit http://www.pathway.com.
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Pathway Genomics Adds Prominent Bioinformatics Experts to Scientific Advisory Board
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Genetic variants, tobacco exposure and lung cancer risk
Public release date: 25-Apr-2012 [ | E-mail | Share ]
Contact: Zachary Rathner Zachary.Rathner@oup.com 301-841-1286 Journal of the National Cancer Institute
There is an association between the rs1051730-rs16969968 genotype and objective measures of tobacco exposure, which indicates that lung cancer risk is largely, if not entirely, mediated by level of tobacco exposure, according to a study published April 25 in the Journal of the National Cancer Institute.
The rs1051730-rs16969968 genotype is known to be associated with heaviness of smoking, lung cancer risk, and other smoking-related outcomes. Prior studies have generally depended on self-reported smoking behavior, which may have underestimated associations and masked the contribution of heaviness of smoking to the associations of these polymorphisms with lung cancer and other health outcomes.
In order to determine the association between the rs1051730-rs16969968 genotype and self-reported cigarette consumption and plasma or serum cotinine levels, Marcus R. Munaf, Ph.D., of the School of Experimental Psychology at the University of Bristol and colleagues, examined data from six independent studies that looked at self-reported daily cigarette consumption and plasma or serum cotinine levels among cigarette smokers and conducted a meta-analysis of pooled per-allele effects. In addition, the researchers looked at the link between the genotypes and lung cancer risk using published data on the association between cotinine levels and lung cancer risk.
The researchers found that the rs1051730-rs16969968 genotype is strongly associated with tobacco exposure measured through cotinine levels, and that the association is strong even after adjustment for self-reported cigarette consumption. "These data therefore support the conclusion that association of rs1051730-rs16969968 genotype with lung cancer risk is mediated largely, if not wholly, via tobacco exposure," the researchers write.
The researchers point out certain limitations of the study, however, namely that the data were drawn from disparate studies from various populations. The data also relies on current smoking measures, rather than lifetime exposure, which is more strongly associated with lung cancer risk.
However, they have confidence in their results, which show that phenotype precision is important to uphold in GWAS studies, rather than ever-larger sample sizes, they say. "The use of objective measures of smoking behavior in genome-wide studies may reveal novel variants associated with these outcomes, which would be undetectable using conventional self-report measures."
In an accompanying editorial, Margaret R. Spitz, M.D., MPH, of the Department of Molecular and Cellular Biology at the Dan L. Duncan Cancer Center at Baylor College of Medicine, writes that these findings "confirm that cigarettes per day is an imprecise measure of nicotine consumption, and favor the interpretation that the association between these variants and lung cancer is mediated by smoking. But the degree to which the association is mediated by smoking is yet to be determined." They add that more studies, including mouse and cellular models, along with emerging metabolic markers, "may help tease apart the direct and indirect associations of these variants with lung cancer risk."
###
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Genetic variants, tobacco exposure and lung cancer risk
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Genetic Associations with Concussions Discussed by AMSSM Researcher
Newswise ATLANTA, Ga. Thomas R. Terrell, MD presented Prospective Cohort Study of the Association of Genetic Polymorphisms and Concussion Risk and Postconcussion Neurocognitive Deficits in College Athletes at the 21st American Medical Society for Sports Medicine Annual Meeting in Atlanta, Ga. on April 23, 2012.
A multi-center prospective cohort study of over 3,200 college and high school athletes was designed to look at the association of genetic polymorphisms with risk of acute concussion and for an associative link with longer duration of symptoms. Following analysis trying to link certain genetic polymorpisms, those evaluated did not show an association with prospective concussions, although some association was found in a pooled analysis of self-reported and prospective concussions.
Dr. Terrell, a two-time AMSSM Foundation Research Award winner, commented, Although we did not find an association of these genetic factors in association prospectively with concussions, the next segment of our research is to evaluate other genetic factors, particularly for associations with severe or recurrent concussions. He was optimistic about possible associations and said, As we look at further data and expand our numbers of concussions included in the study, part of the Tau gene and other genetic polymorphisms have a link in explaining neurocognitive recovery
The AMSSM annual conference features lectures and research addressing the most challenging topics in sports medicine today including prevention of sudden death, cardiovascular issues in athletes, concussion, biologic therapies, and other controversies facing the field of sports medicine.
More than 1,200 sports medicine physicians from across the United States and 12 countries around the world are attending the meeting.
Dr. Terrell is an Associate Professor at the University of Tennessee Graduate School of Medicine and holds a Certificate of Added Qualification in Sports Medicine.
The AMSSM is a multi-disciplinary organization of sports medicine physicians whose members are dedicated to education, research, advocacy, and the care of athletes of all ages. Founded in 1991, the AMSSM is now comprised of more than 2,000 sports medicine physicians whose goal is to provide a link between the rapidly expanding core of knowledge related to sports medicine and its application to patients in a clinical setting.
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Genetic Associations with Concussions Discussed by AMSSM Researcher
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NewLink Genetics Receives Notice of Allowance From USPTO for New Patent Broadly Covering Its D-1MT IDO Pathway Inhibitor
AMES, Iowa, April 24, 2012 (GLOBE NEWSWIRE) -- NewLink Genetics Corporation (Nasdaq:NLNK - News) today announced that the United States Patent & Trademark Office (USPTO) has allowed broad claims to oral pharmaceutical compositions comprising 1-methyl-D-tryptophan (D-1MT) (US Serial No. 12/175,538) and also to oral pharmaceutical compositions comprising 1-methyl-DL-tryptophan (US Serial No. 11/603,291). The company holds exclusive rights to the allowed applications.
"These patents will strengthen our D-1MT franchise in the United States," commented Dr. Charles Link, NewLink's Chairman and CEO, "and should facilitate our ongoing discussions with potential development and marketing partners for this product candidate.
"We have studied D-1MT in multiple single-agent phase 1 studies as well as in separate phase 1 studies evaluating D-1MT in combination with either docetaxel or an autologous dendritic cell vaccine," Noted Dr. Nicholas Vahanian, NewLink's President and Chief Medical Officer. "Data from several of these studies will be presented at the ASCO annual meeting in June."
About D-1MT and inhibition of the IDO pathway
IDO pathway inhibitors, including D-1MT, represent a potential breakthrough approach to cancer therapy using small-molecule, anti-toleragenic product candidates intended to counteract a key mechanism by which tumors evade immune-mediated destruction. IDO is an enzyme that regulates immune response by suppressing T-cell function and enabling local tumor immune escape. Recent studies have demonstrated that IDO is overexpressed in many cancers, within both tumor cells as a direct defense against T-cell attack, and also within antigen presenting cells in tumor draining lymph nodes whereby IDO promotes peripheral tolerance to tumor associated antigens (TAAs). When hijacked by developing cancers in this manner, IDO may facilitate the survival, growth, invasion, and metastasis of malignant cells expressing TAAs that might otherwise be recognized and attacked by the immune system as foreign. D-1MT is currently in multiple Phase 1B/2 studies evaluating the addition of D-1MT to Taxotere in the treatment of breast cancer and the addition of D-1MT to an autologous P-53 dendritic cell vaccine also in the treatment of breast cancer patients. In addition to its clinical D-1MT product candidate, NewLink has an active program directed at discovering and developing other IDO pathway inhibitors.
About NewLink Genetics Corporation
NewLink Genetics Corporation is a biopharmaceutical company focused on discovering, developing and commercializing novel immunotherapeutic products to improve cancer treatment options for patients and physicians. NewLink's portfolio includes biologic and small molecule immunotherapy product candidates intended to treat a wide range of oncology indications. NewLink's product candidates are designed with an objective to harness multiple components of the innate immune system to combat cancer, either as a monotherapy or in combination with current treatment regimens, without incremental toxicity. NewLink's lead product candidate, HyperAcute Pancreas cancer immunotherapy is being studied in a Phase 3 clinical trial in surgically resected pancreatic cancer patients (patient information is available at http://www.pancreaticcancer-clinicaltrials.com). This clinical trial is being performed under a Special Protocol Assessment with the U.S. Food and Drug Administration. NewLink and its collaborators have completed patient enrollment for a Phase 1/2 clinical trial evaluating its HyperAcute Lung cancer immunotherapy product candidate for non-small cell lung cancer and a Phase 2 clinical trial for its HyperAcute Melanoma cancer immunotherapy product candidate. NewLink also is developing d-1-methyltryptophan, or D-1MT, a small molecule, orally bioavailable product candidate from NewLink's proprietary indoleamine (2, 3) dioxygenase, or IDO, pathway inhibitor technology. Through NewLink's collaboration with the National Cancer Institute, NewLink is studying D-1MT in various chemotherapy and immunotherapy combinations in two Phase 1B/2 safety and efficacy clinical trials. For more information please visit http://www.linkp.com.
Safe Harbor Statement
This press release contains "forward-looking statements" for purposes of the safe harbor provided by the Private Securities Litigation Reform Act of 1995. These statements include, but are not limited to, statements regarding the issuance of, and protection provided by, the above described patents (U.S. Serial Nos. 12/175,538 and 11/603,291) and statements regarding the potential for the patents to facilitate development, marketing and partnering efforts. Such statements are based on management's current expectations and involve risks and uncertainties. Actual results and performance could differ materially from those projected in the forward-looking statements as a result of many factors, including, without limitation, the risks and uncertainties associated with: the protection and market exclusivity provided by the Company's intellectual property; risks related to the drug discovery and the regulatory approval process; and, the impact of competitive products and technological changes. These and other factors are identified and described in more detail in the Company's filings with the Securities and Exchange Commission, including without limitation the Company's annual report on Form 10-K for the year ended December 31, 2011, as amended, and subsequent filings. The Company disclaims any intent or obligation to update these forward-looking statements.
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Seattle Genetics to Host Conference Call and Webcast Discussion of First Quarter 2012 Financial Results on May 8, 2012
BOTHELL, Wash.--(BUSINESS WIRE)--
Seattle Genetics, Inc. (SGEN - News) announced today that it will report its first quarter 2012 financial results on Tuesday, May 8, 2012, after the close of financial markets. Following the announcement, company management will host a conference call and webcast discussion of the results and provide a general corporate update. Access to the event can be obtained as follows:
LIVE access on Tuesday, May 8, 2012
1:30 p.m. Pacific Time (PT) / 4:30 p.m. Eastern Time (ET)
REPLAY access
About Seattle Genetics
Seattle Genetics is a biotechnology company focused on the development and commercialization of monoclonal antibody-based therapies for the treatment of cancer. The U.S. Food and Drug Administration granted accelerated approval of ADCETRIS in August 2011 for two indications. ADCETRIS is being developed in collaboration with Millennium: The Takeda Oncology Company. In addition, Seattle Genetics has three other clinical-stage ADC programs: SGN-75, ASG-5ME and ASG-22ME. Seattle Genetics has collaborations for its ADC technology with a number of leading biotechnology and pharmaceutical companies, including Abbott, Bayer, Celldex Therapeutics, Daiichi Sankyo, Genentech, GlaxoSmithKline, Millennium, Pfizer and Progenics, as well as ADC co-development agreements with Agensys, an affiliate of Astellas, and Genmab. More information can be found at http://www.seattlegenetics.com.
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Seattle Genetics to Host Conference Call and Webcast Discussion of First Quarter 2012 Financial Results on May 8, 2012
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Will we ever correct diseases before birth? | Not Exactly Rocket Science
Heres the sixth piece from my new BBC column
Every year, millions of people are born with debilitating genetic disorders, a result of inheriting just one faulty gene from their parents. They may have been dealt a dud genetic hand, but they do not have to stick with it. With the power of modern genetics, scientists are developing ways of editing these genetic errors and reversing the course of many hard-to-treat diseases.
These gene therapies exploit the abilities of viruses biological machines that are already superb at penetrating cells and importing genes. By removing their ability to reproduce, and loading them with the genes of our choice, we can transform viruses from causes of disease into vectors for cures.
After a few shaky starts, some of these approaches are beginning to hit their stride. Thirteen children with SCID, an immune disorder that leaves people fatally vulnerable to infections, now have working immune systems. Several British patients with haemophilia, which prevents their blood from clotting properly, can now produce a clotting protein called factor IX, which they once had to inject. A British man and three Americans with inherited forms of progressive blindness can see again.
It is still early days as far as trumpeting gene therapy cures are concerned, but even if they do succeed there is still one significant limitation that cannot be overlooked. Treating adults and children in this way will do for some disorders, but genetic disorders cause irreparable organ damage, or even death, very early. With some of the diseases that we look at, five years old is too late. Sometimes, you dont get to the age of five, says Simon Waddington from University College London. Every single one is a little bit niche but when you list them all out, theres quite a lot of them.
To treat such conditions, we need to intervene as early as possible, and this means correcting genetic disorders in the womb. There are advantages to such prenatal gene therapy. Organs that are hard to target after birth, such as airways blocked with mucus in cystic fibrosis patients, may be easier to reach in the womb. Being smaller, foetuses need a relatively smaller amount of delivery vector. And their immune systems are naive, so they are unlikely to mount an immune response to these vectors.
Risk assessment
So far, several teams have tested prenatal gene therapy in animals, including mice, monkeys and sheep. The results have been promising. In several cases, the animals produce decent levels of foreign proteins for many months, and their immune systems tolerate the added genes. Some have even been cured of their diseases.
Despite these successes, the research has reached an impasse. No one has tried prenatal gene therapy in humans, and no clinical trials are in the works. This is understandable. Altering a foetus genes is a sombre prospect, especially as gene therapy is still a relatively immature technology. It hasnt been embedded enough yet, says Waddington. If these treatments can prove their safety and effectiveness in adults, the field will move towards trials in newborn babies, and from there to prenatal tests.
For now, there are still many potential risks to address. Were still very much looking at which is the right vector to use, says Anna David, from University College London. Lentiviruses and retroviruses (such as HIV) shunt their genes into those of their host. They would seem to provide an ideal way of correcting a faulty gene, either by overwriting it, or providing a cell with working copies.
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Will we ever correct diseases before birth? | Not Exactly Rocket Science
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Research and Markets: Breaking the Gene Therapy Barrier for Life-Threatening Red Blood Cell Disorders
DUBLIN--(BUSINESS WIRE)--
Research and Markets (http://www.researchandmarkets.com/research/xvg9rk/breaking_the_gene) has announced the addition of GlobalData's new report "Breaking the Gene Therapy Barrier for Life-Threatening Red Blood Cell Disorders" to their offering.
Breaking the Gene Therapy Barrier for Life-Threatening Red Blood Cell Disorders takes a look at gene therapy for the treatment of blood disorders such as beta-thalassemia and sickle cell anemia. An international team of researchers led by scientists at Weill-Cornell Medical College in New York City have designed a novel gene therapy strategy with potentially curative implications for patients with beta-thalassemia and sickle cell anemia. This development represents an important advance in addressing significant unmet market needs regarding the future development of therapeutic products for these two serious red blood cell disorders.
Scope
- Introduction and detail on two red blood cell disorders - sickle cell anemia and beta-thalassemia
- Current gene therapy initiatives for beta-thalassemia and sickle cell anemia
- Challenges to Gene Therapy
- Market Implications
Reasons to buy
- Understand the effectiveness of gene therapy in the treatment of red blood cell disorders
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Research and Markets: Breaking the Gene Therapy Barrier for Life-Threatening Red Blood Cell Disorders
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Leukaemia cells have a remembrance of things past
Public release date: 24-Apr-2012 [ | E-mail | Share ]
Contact: Dr Boris Kovacic Boris.Kovacic@vetmeduni.ac.at 43-125-077-5622 University of Veterinary Medicine -- Vienna
Although people generally talk about "cancer", it is clear that the disease occurs in a bewildering variety of forms. Even single groups of cancers, such as those of the white blood cells, may show widely differing properties. How do the various cancers arise and what factors determine their progression? Clues to these two issues, at least for leukaemias, have now been provided by Boris Kovacic and colleagues at the University of Veterinary Medicine, Vienna (Vetmeduni Vienna). The results are published in the current issue of the journal EMBO Molecular Medicine and have extremely important consequences for the treatment of a particularly aggressive type of leukaemia.
It is well known that many types of cancer arise as a result of a mutation within a cell and prevailing wisdom has held that the stage of differentiation of this cell determines exactly what form of cancer develops. For example, it was believed that so-called chronic myeloid leukaemia or CML arises from bone marrow stem cells, while a different type of leukaemia, known as B-cell acute lymphoid leukaemia or B-ALL, results from B-cell precursors. This belief has been spectacularly refuted by the latest results from Boris Kovacic and colleagues in the Vetmeduni Vienna's institutes of Animal Breeding and Genetics and of Pharmacology and Toxicology.
The researchers have now shown that both CML and B-ALL arise from the most primordial kind of blood cell (long-term haematopoietic stem cells), although the pathways by which the diseases progress are different. The usual causes of CML and B-ALL are two highly related versions of the same oncogene, BCR/ABL. If the primordial blood cells are transformed or made potentially cancerous by a particular version of BCR/ABL, for technical reasons termed BCR/ABLp210, the result is chronic myeloid leukaemia or CML. The long-term haematopoietic stem cells remain and act as the dreaded cancer stem cells, or CSCs, which ensure that the disease persists. Curing chronic myeloid leukaemia requires the complete elimination of the CSCs. However, if the long-term haematopoietic stem cells are transformed by a related version of BCR/ABL, BCR/ABLp185, the result is a highly aggressive form of leukaemia, B-ALL. The finding that B-ALL actually originates from the same stem cells as CML was both unexpected and highly provocative.
Kovacic and colleagues have shown further that B-ALL only develops if the transformed stem cell is exposed to a particular growth factor, interleukin-7. If interleukin-7 is present (it usually is), the transformed long-term haematopoietic stem cells undergo a differentiation step to CSCs, which in this case correspond to pro-B cells. If interleukin-7 is absent during the initial phase of transformation, B-ALL cannot develop.
In other words, two distinct types of cell are involved in leukaemia development, the primordial cells (also termed the cells of origin of cancer) and the cancer stem cells that cause the disease to progress. Unless the CSCs are eliminated, fresh cancer cells can arise at any time and the leukaemia will recur. The problem is that current leukaemia therapies are not designed to target CSCs. The primordial CSCs in CML are highly quiescent and thus difficult to target. In contrast, the CSCs in B-ALL are abundant and have a high turnover rate, which makes them susceptible to treatment. Treatment of B-ALL may thus succeed in eliminating most CSCs but if even a single cell remains intact it is likely that the patient will relapse, possibly with an even more aggressive form of leukaemia. "A therapy that targets the bulk of tumour cells will not work," as Kovacic succinctly summarizes his results. "To treat B-ALL successfully it will be necessary for us to learn much more about the development of the disease. A combined therapy is required, so future work should aim at developing drugs that target the long-term haematopoietic stem cells from which B-ALL is derived."
###
The paper "Diverging fates of cells of origin in acute and chronic leukemia" by Boris Kovacic, Andrea Hoelbl, Gabriele Litos, Memetcan Alacakaptan, Christian Schuster, Katrin M. Fischhuber, Marc A. Kerenyi, Gabriele Stengl, Richard Moriggl, Veronika Sexl and the late Hartmut Beug is published in the current issue of the journal "EMBO Molecular Medicine" (2012, Vol. 4 pp. 283-297).
The work was initiated at the Research Institute of Molecular Pathology (IMP) and was performed together with groups at the Medical University of Vienna and the Ludwig Boltzmann Institute for Cancer Research in Vienna.
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Leukaemia cells have a remembrance of things past
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Leukemia cells have a remembrance of things past
ScienceDaily (Apr. 24, 2012) Although people generally talk about cancer, it is clear that the disease occurs in a bewildering variety of forms. Even single groups of cancers, such as those of the white blood cells, may show widely differing properties. How do the various cancers arise and what factors determine their progression? Clues to these two issues, at least for leukemias, have now been provided by Boris Kovacic and colleagues at the University of Veterinary Medicine, Vienna (Vetmeduni Vienna). The results are published in the current issue of the journal EMBO Molecular Medicine and have extremely important consequences for the treatment of a particularly aggressive type of leukemia.
It is well known that many types of cancer arise as a result of a mutation within a cell and prevailing wisdom has held that the stage of differentiation of this cell determines exactly what form of cancer develops. For example, it was believed that so-called chronic myeloid leukemia or CML arises from bone marrow stem cells, while a different type of leukemia, known as B-cell acute lymphoid leukemia or B-ALL, results from B-cell precursors. This belief has been spectacularly refuted by the latest results from Boris Kovacic and colleagues in the Vetmeduni Viennas institutes of Animal Breeding and Genetics and of Pharmacology and Toxicology.
The researchers have now shown that both CML and B-ALL arise from the most primordial kind of blood cell (long-term haematopoietic stem cells), although the pathways by which the diseases progress are different. The usual causes of CML and B-ALL are two highly related versions of the same oncogene, BCR/ABL. If the primordial blood cells are transformed or made potentially cancerous by a particular version of BCR/ABL, for technical reasons termed BCR/ABLp210, the result is chronic myeloid leukemia or CML. The long-term haematopoietic stem cells remain and act as the dreaded cancer stem cells, or CSCs, which ensure that the disease persists. Curing chronic myeloid leukemia requires the complete elimination of the CSCs. However, if the long-term haematopoietic stem cells are transformed by a related version of BCR/ABL, BCR/ABLp185, the result is a highly aggressive form of leukemia, B-ALL. The finding that B-ALL actually originates from the same stem cells as CML was both unexpected and highly provocative.
Kovacic and colleagues have shown further that B-ALL only develops if the transformed stem cell is exposed to a particular growth factor, interleukin-7. If interleukin-7 is present (it usually is), the transformed long-term haematopoietic stem cells undergo a differentiation step to CSCs, which in this case correspond to pro-B cells. If interleukin-7 is absent during the initial phase of transformation, B-ALL cannot develop.
In other words, two distinct types of cell are involved in leukemia development, the primordial cells (also termed the cells of origin of cancer) and the cancer stem cells that cause the disease to progress. Unless the CSCs are eliminated, fresh cancer cells can arise at any time and the leukemia will recur. The problem is that current leukemia therapies are not designed to target CSCs. The primordial CSCs in CML are highly quiescent and thus difficult to target. In contrast, the CSCs in B-ALL are abundant and have a high turnover rate, which makes them susceptible to treatment. Treatment of B-ALL may thus succeed in eliminating most CSCs but if even a single cell remains intact it is likely that the patient will relapse, possibly with an even more aggressive form of leukemia. A therapy that targets the bulk of tumour cells will not work, as Kovacic succinctly summarizes his results. To treat B-ALL successfully it will be necessary for us to learn much more about the development of the disease. A combined therapy is required, so future work should aim at developing drugs that target the long-term haematopoietic stem cells from which B-ALL is derived.
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The above story is reprinted from materials provided by Veterinrmedizinische Universitt Wien, via AlphaGalileo.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
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Leukemia cells have a remembrance of things past
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VistaGen Secures Key U.S. Patent Covering Stem Cell Technology Methods Used to Test Drug Candidates for Liver Toxicity
SOUTH SAN FRANCISCO, CA--(Marketwire -04/25/12)- VistaGen Therapeutics, Inc. (VSTA.OB - News) (VSTA.OB - News), a biotechnology company applying stem cell technology for drug rescue, has secured a new United States patent covering the company's proprietary methods used to measure and type the toxic effects produced by drug compounds in liver stem cells.
Test methods included in this new patent, (U.S. Patent 11/445,733), titled "Toxicity Typing Using Liver Stem Cells," cover all mammalian liver stem cells -- rat and mouse cells, for example, in addition to human cells. Liver stem cells used in drug testing can be derived from in vivo tissue or produced from embryonic stem cells (ES) or induced pluripotent stem cells (iPS).
H. Ralph Snodgrass, Ph.D., VistaGen's President and Chief Scientific Officer, said, "This patent covers the monitoring of changes in gene expression as an assay for predicting drug toxicities. It is well known that drugs activate and suppress specific genes, and that the changes in gene expression reflect the mechanism of drug toxicities. The specific sets of genes that are affected become a profile of that drug."
VistaGen's new patent also covers techniques used to develop a database of gene expression profiles of drugs that have the same type of liver toxicity. Using sophisticated "pattern matching" database tools, drug developers can analyze these related profiles to determine "gene expression signatures" that are common and predictive of drugs that produce specific types of toxicity.
"Without this database capability, a drug's single gene expression profile could not be interpreted," Dr. Snodgrass added. "The ability to use liver stem cells to differentiate drug-dependent gene expression profiles, and to compare those profiles of drugs known to induce toxic liver effects, provides a powerful tool for predicting liver toxicity of new drug candidates, including drug rescue variants."
Shawn K. Singh, VistaGen's Chief Executive Officer, stated, "Strong and enforceable intellectual property rights are critical components of our plan to optimize the commercial potential of our Human Clinical Trials in a Test Tube platform. This new liver toxicity typing patent further solidifies our growing IP portfolio, and supports the continuing development of LiverSafe 3D, our human liver cell-based bioassay system, which complements our CardioSafe 3D human heart cell-based bioassay system for heart toxicity."
About VistaGen Therapeutics
VistaGen is a biotechnology company applying human pluripotent stem cell technology for drug rescue and cell therapy. VistaGen's drug rescue activities combine its human pluripotent stem cell technology platform, Human Clinical Trials in a Test Tube, with modern medicinal chemistry to generate new chemical variants (Drug Rescue Variants) of once-promising small-molecule drug candidates. These are drug candidates discontinued due to heart toxicity after substantial development by pharmaceutical companies, the U.S. National Institutes of Health (NIH) or university laboratories. VistaGen uses its pluripotent stem cell technology to generate early indications, or predictions, of how humans will ultimately respond to new drug candidates before they are ever tested in humans, bringing human biology to the front end of the drug development process.
Additionally, VistaGen's small molecule drug candidate, AV-101, is in Phase 1b development for treatment of neuropathic pain. Neuropathic pain, a serious and chronic condition causing pain after an injury or disease of the peripheral or central nervous system, affects approximately 1.8 million people in the U.S. alone. VistaGen is also exploring opportunities to leverage its current Phase 1 clinical program to enable additional Phase 2 clinical studies of AV-101 for epilepsy, Parkinson's disease and depression. To date, VistaGen has been awarded over $8.5 million from the NIH for development of AV-101.
Visit VistaGen at http://www.VistaGen.com, follow VistaGen at http://www.twitter.com/VistaGen or view VistaGen's Facebook page at http://www.facebook.com/VistaGen
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VistaGen Secures Key U.S. Patent Covering Stem Cell Technology Methods Used to Test Drug Candidates for Liver Toxicity
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Moffitt Cancer Center Supports Personalized Medicine With Oracle Health Sciences Technology
REDWOOD SHORES, CA--(Marketwire -04/25/12)- Oracle (ORCL - News)
News Facts
Supporting Quotes
Supporting Resources
About Oracle Oracle engineers hardware and software to work together in the cloud and in your data center. For more information about Oracle (ORCL - News), visit http://www.oracle.com.
About Oracle in IndustriesOracle industry solutions leverage the company's best-in-class portfolio of products to address complex business processes relevant to health sciences, helping speed time to market, reduce costs, and gain a competitive edge.
About Moffitt Cancer CenterFollow Moffitt on Facebook: http://www.facebook.com/MoffittCancerCenter Follow Moffitt on Twitter: @MoffittNews Follow Moffitt on YouTube: MoffittNews
Located in Tampa, Moffitt Cancer Center is the only Florida-based National Cancer Institute Comprehensive Cancer Center, a designation that recognizes Moffitt's excellence in research and contributions to clinical trials, prevention and cancer control. Moffitt has 14 affiliates in Florida, one in Georgia, one in Pennsylvania and two in Puerto Rico. Moffitt is also a member of the National Comprehensive Cancer Network, a prestigious alliance of the country's leading cancer centers, and is listed in U.S. News & World Report as one of "America's Best Hospitals" for cancer.
TrademarkOracle is a registered trademark of Oracle and/or its affiliates. Other names may be trademarks of their respective owners.
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Moffitt Cancer Center Supports Personalized Medicine With Oracle Health Sciences Technology
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Neuralstem Chief Scientific Officer To Present At Spinal Cord Injury Conference In China
ROCKVILLE, Md., April 25, 2012 /PRNewswire/ --Neuralstem, Inc. (CUR) announced that Karl Johe, PhD, Chairman and Chief Scientific Officer, will present at the Fourth International Spinal Cord Injury Treatments and Trials Symposium, in Xi'an, China on Friday, May 4, at 1:00 PM (http://iscitt.org/iscitt4/). Dr. Johe's talk, entitled "Human spinal cord-derived neural stem cells (HSSC) for treatment of neurological diseases," willreview the readiness of Neuralstem's cells to enter clinical trials in China, as well as provide an overview of the US clinical programs in amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease) and in spinal cord injury. Neuralstem has an ongoing FDA-approved Phase I trial testing the safety of its cells in the treatment of ALS and has submitted an IND (Investigational New Drug) to the FDA to initiate trials with its cells in chronic spinal cord injury. Neuralstem's wholly-owned subsidiary in China, Neuralstem China(Suzhou Neuralstem Biopharmaceutical Company Ltd.), is developing cell therapy treatments for chronic motor disorder from stroke in collaboration with BaYi Brain Hospital in Beijing.
(Logo: http://photos.prnewswire.com/prnh/20061221/DCTH007LOGO )
About Neuralstem
Neuralstem's patented technology enables the ability to produce neural stem cells of the human brain and spinal cord in commercial quantities, and the ability to control the differentiation of these cells constitutively into mature, physiologically relevant human neurons and glia. Neuralstem is in an FDA-approved Phase I safety clinical trial for amyotrophic lateral sclerosis (ALS), often referred to as Lou Gehrig's disease, and has been awarded orphan status designation by the FDA.
In addition to ALS, the company is also targeting major central nervous system conditions with its cell therapy platform, including spinal cord injury, ischemic spastic paraplegia and chronic stroke. The company has submitted an IND (Investigational New Drug) application to the FDA for a Phase I safety trial in chronic spinal cord injury.
Neuralstem also has the ability to generate stable human neural stem cell lines suitable for the systematic screening of large chemical libraries. Through this proprietary screening technology, Neuralstem has discovered and patented compounds that may stimulate the brain's capacity to generate new neurons, possibly reversing the pathologies of some central nervous system conditions. The company has received approval from the FDA to conduct a Phase Ib safety trial evaluating NSI-189, its first small molecule compound, for the treatment of major depressive disorder (MDD). Additional indications could include schizophrenia, Alzheimer's disease and bipolar disorder.
For more information, please visit http://www.neuralstem.com or connect with us on Twitter and Facebook.
Cautionary Statement Regarding Forward Looking Information
This news release may contain forward-looking statements made pursuant to the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995. Investors are cautioned that such forward-looking statements in this press release regarding potential applications of Neuralstem's technologies constitute forward-looking statements that involve risks and uncertainties, including, without limitation, risks inherent in the development and commercialization of potential products, uncertainty of clinical trial results or regulatory approvals or clearances, need for future capital, dependence upon collaborators and maintenance of our intellectual property rights. Actual results may differ materially from the results anticipated in these forward-looking statements. Additional information on potential factors that could affect our results and other risks and uncertainties are detailed from time to time in Neuralstem's periodic reports, including the annual report on Form 10-K for the year ended December 31, 2011.
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Neuralstem Chief Scientific Officer To Present At Spinal Cord Injury Conference In China
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Spinal cord injury researchers win Apple Award for article on niacin for dyslipidemia
Public release date: 25-Apr-2012 [ | E-mail | Share ]
Contact: Carolann Murphy CMurphy@kesslerfoundation.org 973-324-8382 Kessler Foundation
West Orange, NJ. April 25, 2012. American Spinal Injury Association (ASIA) has awarded its 2012 Apple Award to the article by Mark Nash, PhD, et al, entitled, "Safety, tolerance, and efficacy of extended-release niacin monotherapy for treating dyslipidemia risks in persons with chronic tetraplegia: a randomized multicenter controlled trial." The article, (doi:10.1016/j.apmr.2010.06.029) which was published in Archives of Physical Medicine and Rehabilitation in March 2011, is based on a study conducted in spinal cord injury (SCI) research centers in Florida, New York, New Jersey and California. The study was supported by a SCI Collaborative Research Project (grant no. H133A111105) from the National Institute on Disability and Rehabilitation Research, and Kos Pharmaceuticals.
Dr. Nash accepted the award at the annual ASIA meeting on behalf of the authors. Drs. Nash, John Lewis, and Armando J. Mendez are affiliated with the University of Miami, Miller School of Medicine, Miami, Florida. Their co-authors are Trevor A. Dyson-Hudson, MD, of Kessler Foundation, West Orange, NJ, Yaga Szlachcic, MD, and Florence Yee, PharmD of Rancho Los Amigos National Research Center, Downey, CA, and Ann M. Spungen, EdD, and William A. Bauman, MD, of the James Peters VA Medical Center, Bronx, NY. Dr. Dyson-Hudson acknowledged the many challenges to carrying out a multi-center clinical trial. "However," he commented, "results from rigorously controlled collaborative studies like this one provide the necessary evidence to support the usage of interventions in persons with SCI and provide the foundation for clinical guidelines in this population."
The Apple Award is named for David Apple, Jr., MD, medical director emeritus of Shepherd Center and a well known SCI researcher. The Apple Award acknowledges excellence in publishing in SCI rehabilitation research. This annual prize is given at the ASIA meeting,. The award for the best published paper by a clinician or researcher in the preceding calendar year is now in its sixth year. The award is sponsored by ASIA, Shepherd Center, and Thomas Land Publishers, Inc.
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About the SCI Model System
The Spinal Cord Injury Model System program, sponsored by the National Institute on Disability and Rehabilitation Research (NIDRR), Office of Special Education and Rehabilitative Services, US Dept of Education, provides assistance to establish innovative projects for the delivery , demonstration, and evaluation of comprehensive medical, vocational, and other rehabilitation services to meet the needs of individuals with spinal cord injury. Model system centers across the United States work together to demonstrate improved care, maintain a national database, participate in independent and collaborative research and provide continuing education relating to spinal cord injury.
About Kessler Foundation
Trevor Dyson-Hudson, MD, is interim director of Spinal Cord Injury Research at Kessler Foundation. He is also co-director of the Northern New Jersey SCI Model System, one of 14 NIDRR- funded regional systems in the U.S. Kessler Foundation is one of six centers in the US with model systems for both spinal cord injury and traumatic brain injury (Northern New Jersey TBI System).
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Spinal cord injury researchers win Apple Award for article on niacin for dyslipidemia
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Living Longer: The Power of Regenerative Medicine – Video
24-04-2012 01:41 Scientists at UNSW's School of Biomedical Engineering have discovered what speeds up the healing process. In studying white blood cells, a short form of the molecule perlecan was discovered which not only promotes healing, but could promote bone growth.
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Living Longer: The Power of Regenerative Medicine - Video
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ACT Announces Data and Safety Monitoring Board (DSMB) Approval to Increase RPE Dosage for Stargardt’s Disease Patients …
MARLBOROUGH, Mass.--(BUSINESS WIRE)--
Advanced Cell Technology, Inc. (ACT; OTCBB: ACTC), a leader in the field of regenerative medicine, announced today that the Data and Safety Monitoring Board (DSMB), an independent group of medical experts closely monitoring the Companys three ongoing clinical trials, have recently authorized the Company to move forward with enrollment and treatment of additional patients with Stargardts disease (SMD). In the U.S. SMD trial, ACT will screen and enroll patients for the second cohort, who, in keeping with trial protocol, will be injected with 100,000 retinal pigment epithelial (RPE) cells - as compared with the 50,000 cell dose used in the patients of the first cohort. The Company has also been approved to treat the final two patients to round out the initial dosing arm in its European trial. The use of pluripotent stem cells to derive RPE cells, and the use of the resulting RPE cells for treating a wide range of macular degenerative disorders, are covered by a robust patent portfolio owned by ACT, including a number of issued broad patents in key world markets.
DSMB authorization to move to the next higher dosage of cells in our U.S. clinical trial and complete the treatment of the first cohort of patient in our European trial represents yet another significant advancement for our clinical programs, commented Gary Rabin, chairman and CEO of ACT. We are pleased with the pace of progress and the continued finding of safety amongst the participants in both the U.S. and European trials. The results so far have been encouraging, and with our SMD programs having been granted orphan medicinal product designation in both the U.S. and Europe, we look forward to eventually reaching a stage at which we can further avail ourselves of all the regulatory and financial benefits this designation brings.
The three procedures comprising the first cohort of patients in the U.S. SMD trial were all conducted at University of California at Los Angeles (UCLA), by Steven Schwartz, M.D., Ahmanson Professor of Ophthalmology at the David Geffen School of Medicine at UCLA and retina division chief at UCLA's Jules Stein Eye Institute. The first procedure in the E.U. trial was conducted at Moorfields Eye Hospital in London, by a team of surgeons led by Professor James Bainbridge, consultant surgeon at Moorfields and Chair of Retinal Studies at University College London.
We are gratified to be moving to the next stage in both of our SMD trials, commented Robert Lanza, M.D., ACTs chief scientific officer. We remain very encouraged by the preliminary data in the first four SMD patients treated with the lowest dose of RPE cells at UCLA and Moorfields Eye Hospital. We are doubling the number of cells that will be transplanted in the next group of patients in the U.S. trial. We will be anxious to see if the higher dosage of RPE cells will impact visual function and photoreceptor rescue.
ACT is conducting three clinical trials in the U.S. and Europe using hESC-derived RPE cells to treat forms of macular degeneration. Each trial will enroll a total of 12 patients, with cohorts of three patients each in an ascending dosage format. These trials are prospective, open-label studies, designed to determine the safety and tolerability of hESC-derived RPE cells following sub-retinal transplantation into patients with dry-AMD or Stargardt's macular dystrophy (SMD) at 12 months, the studys primary endpoint. On January 20, 2012, the first SMD patient enrolled in the Companys U.K. clinical trial was treated at Moorfields Eye Hospital in London. The final patient of the first cohort in the companys SMD trial in the U.S. was treated on February 13, 2012.
Further information about patient eligibility for the dry AMD study and the concurrent study on SMD is also available on http://www.clinicaltrials.gov; ClinicalTrials.gov Identifiers: NCT01345006, NCT01469832 and NCT01344993.
About Advanced Cell Technology, Inc.
Advanced Cell Technology, Inc., is a biotechnology company applying cellular technology in the field of regenerative medicine. For more information, visit http://www.advancedcell.com.
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ACT Announces Data and Safety Monitoring Board (DSMB) Approval to Increase RPE Dosage for Stargardt’s Disease Patients ...
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Cryo-Save Hires Stem Cell Expert in the Flagship Lab in Niel, Belgium
ZUTPHEN, the Netherlands, April 24, 2012 /PRNewswire/ --
In line with its continuous efforts to improve internal stem cell procedures, Cryo-Save proudly announces the appointment of the highly knowledgeable stem cell expert Dr. Marcin Jurga. Dr. Jurga will supervise new process validation at the Cryo-Save labs and study new processing techniques for umbilical cord blood, cord tissue and fat tissue, to ensure quality and use of the highest technology available on the market.
Marcin Jurga is specialized in adult stem cells biology, neuroscience and tissue engineering. His field of interest focuses on developing new methods for adult stem cell applications in in-vitro toxicology and regenerative medicine. Part of his validation study and internal research at Cryo-Save includes studies on fresh and frozen cells isolated from fat tissue and cord tissue, to explain the quality of these and their ability for extensive growth in vitro and multilineage differentiation.
"Cryo-Save is truly committed to the advancement of stem cell therapy. Storing stem cells is utterly important and our core business, but we are also committed to increasing the potential use of these stem cells and building the tools needed to tackle un-met medical needs with stem cells", said Arnoud Van Tulder, CEO of Cryo-Save.
Dr. Jurga is an experienced stem cell researcher with broad international experience; he was team leader and senior researcher at the Cell Therapy Research Institute in Lyon, France and previously completed a post doc at the Centre for Life, Newcastle University in the UK. He got Ph.D. degree in Poland, at the Mossakowski Medical Research Centre of Polish Academy of Sciences in Warsaw. In May, Dr. Jurga is also planning to get a habilitation degree at Lyon 1 Claude-Bernard University in France. The habilitation thesis entitled: "Stem Cell Therapy and Neutral Tissue Engineering in Regeneration of Central Nervous System".
Cryo-Save, the leading international family stem cell bank, stores more than 200,000 samples from umbilical cord blood, cord tissue and adipose tissue. There are already many diseases treatable by the use of stem cells, and the number of treatments will only increase. Driven by its international business strategy, Cryo-Save is now represented in over 40 countries on four continents, with ultra-modern processing and storage facilities in the United States, Belgium, Germany, Dubai, India, South Africa and France (validation in progress).
Cryo-Save: http://www.cryo-save.com/group
Cryo-Save Group N.V.
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Cryo-Save Hires Stem Cell Expert in the Flagship Lab in Niel, Belgium
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