SINGAPORE: Australia-based stem cell therapy firm Mesoblast has announced plans to accelerate commercial manufacturing operations in Singapore.

This is to prepare for new product launches in the United States and other major markets over the next couple of years.

Its existing operations in Singapore include making stem cell products for clinical trials under its contract with its partner, pharmaceutical company Lonza.

One of its key products still awaiting full approval is Prochymal, which Mesoblast says can help to more than double the survival rate of patients suffering from complications after receiving tissue transplants from donors -- known as graft versus host disease.

The global stem cell market is expected to grow at an average annual rate of 12 per cent between 2011 and 2016 to reach more than S$8 billion by 2016.

Mesoblast said commercial manufacturing requires a much larger capacity and operations must be scaled-up to meet regulatory demands.

Silviu Itescu, chief executive at Mesoblast, said: "We are now in a phase of making more investments in order to get our processes to commercial scale. That anticipates successful commercial launches.

"If we're successful in that over the next 18-24 months, then we're going to leverage the investment in our commercial facilities to be able to build up and prepare for launching of much larger opportunities in cardiovascular medicine, orthopaedics and diseases of immunity and inflammation which would require purpose-built facilities."

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Mesoblast to accelerate operations in S'pore

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Washington, DC (PRWEB) May 28, 2014

Catherine M. Bollard, MBChB, MD, director of Childrens National Health Systems Program for Cell Enhancement and Technologies for Immunotherapy (CETI), and her team have performed the hospitals first treatment using T-cell therapy for a 6-month-old patient with congenital immune deficiency and a life-threatening virus infection.

Not only does this therapy offer a potentially curative treatment for patients who have failed conventional therapies for infections and cancer, the procedure sets the stage for avoiding potentially toxic drugs which can ultimately reduce inpatient stays and medical costs.

Its extremely important, offering a novel therapeutic thats not available at the majority of hospitals worldwide, said Dr. Bollard, a member of the Division of the Blood and Marrow Transplantation and senior scientist at Childrens Nationals Center for Cancer and Immunology Research at Childrens Research Institute. She is also the Principal Investigator and the Sheik Zayed Institute for Pediatric Surgical Innovation.

Childrens National is one of the few hospitals in the world to offer cellular therapy to treat life-threatening infections in patients with immune deficiencies as well as preventing or treating relapse in children with cancer. Cellular therapy uses the bodys own immune system to fight cancer and/or infections.

Patients from other hospitals and childrens facilities have been referred to Childrens National because of the uniqueness of the cell therapies we can now offer here, Dr. Bollard said. This kind of procedure reduces the amount of time for care and is not only cost effective for a hospital but also more tolerable for the patient, said Dr. Bollard. None of this could have been achieved without every one of those members within the CETI Program pulling together as a team to make it happen.

In the first of its kind cellular therapy achievement at Childrens National, Dr. Bollard and her team have shown that in the laboratory they can train nave or inexperienced immune system cells (T-cells) to kill cancer and/or viruses. In the first patient treated here, T-cells were grown from the patients mother and then injected into the young patient, who had severe combined immunodeficiency and a potentially life threatening virus infection. The T-cells the patient received (cytotoxic T lymphocytes) are a type of white blood cell that can kill virus-infected cells or cancer cells infected or cells that are damaged in other ways.

The babys immunodeficiency ailments included SCID, or severe combined immunodeficiency, a primary immune deficiency, which can result in the onset of one or more serious infections within the first months of life. Early in life, the child was infected with cytomegalovirus (CMV), a latent virus related to herpes that has significant morbidity and high mortality rates in immune compromised people. Initially, the patient had received a bone marrow transplant, but the CMV could not be cleared with the drug therapy he received after transplant, Dr. Bollard said.

Conventional treatment using antiviral agents is expensive and toxic and can be ineffective. Transfer of virus-specific T cytotoxic cells is seen as an alternative means of preventing and treating these infections. The hospital takes donor cells and manufactures them in the lab to fight specific viruses and/or cancer. The cells are given to the patients in the outpatient clinic, in a procedure that takes less than five minutes. The cytotoxic T-cells usually take within two to six weeks after which time the patient may no longer need other medications to treat or prevent infection.

We give these cells to the patient and then we hope that in a couple of weeks the CMV viral load falls to very low levels or even zero, Dr. Bollard said. This patient is 6 months old. By giving these T-cells, he can get off the drug therapy and spare his kidneys from the toxicity of the antiviral drugs.

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Catherine M. Bollard, MBCHB, MD, of Childrens National Performs Its First Treatment Using T-Cell Therapy On Child ...

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By Joel Ceausu, May 28th, 2014

An East End Montreal hospital is home to a new national network on regenerative medicine and cell therapy research. CellCAN will be based at Maisonneuve-Rosemont Hospital and directed by renowned cell therapy researcher Dr. Denis Claude Roy. The objective is to unite efforts of researchers, clinicians, funders, industry, charities, government members, patient representatives and the public. Specifically, CellCAN will promote exchanges, cooperation, partnership development and innovation in regenerative medicine and cell therapy, explained Roy. As the hub of a network of cell therapy centers and labs in Toronto, Ottawa, Quebec City, Edmonton, and Vancouver, CellCAN will propel Canadian stem cell research and clinical development forward thanks to a $3 million grant over four years. Discoveries in stem cell research make their way to clinical trials bringing researchers closer to new treatments for patients with cancer, diabetes, cardiovascular and ocular diseases, neurological and blood disorders and other health issues. Regenerative cell therapies have almost unlimited possibilities, said Roy, director of the cellular therapy laboratory at Maisonneuve-Rosemonts research centre. This will transform the nature of medicine and have significant impact on our health care systems. The Universit de Montral-affiliated hospital in Rosemont is an internationally recognized leader in hematology-oncology, stem cell transplants, ophthalmology, nephrology and kidney transplants. The funds come from the federally financed Networks of Centres of Excellence, Maisonneuve-Rosemont Foundation, Ronald and Herbert Black, and various organizations across Canada.n

Click here to see the full newspaper. Updated on May 28, 2014

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East End home for cell network

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Charlottesville, VA (PRWEB) May 27, 2014

Researchers at the University of Virginia School of Medicine have devised a way to detect unintended side effects of manipulating genes using a revolutionary new system that is sweeping the scientific world by storm.

The gene targeting system, called CRISPR, allows editing of genetic information at specifically targeted sites in the genome. UVAs new approach reveals the system has the potential to bind to unintended sites and cause gene mutations at some of these sites mutations that could have serious consequences for research and efforts to develop medical treatments. UVAs new approach, however, also identifies ways to help prevent those potentially dangerous off-target effects, allowing scientists to improve their results with this important new gene-editing system.

A primary goal of gene manipulation is to correct harmful mutations, so it is vital to avoid introducing mutations unintentionally, explained UVAs Mazhar Adli, PhD, of the Department of Biochemistry and Molecular Genetics. We know that genetic mutations are hallmarks of disease. The whole aim is to change these apparent genetic mutations, to go and correct these mutations, he said. We want to change this information only at the targeted space, at the targeted locus. If you change any other information, basically you are introducing mutations that you dont want. You are correcting one gene and potentially you might be introducing mutations in 10 other genes and maybe many other places in the genome.

Adlis new research sheds light on the potential off-target effects of the CRISPR/Cas9 gene editing system. The system has proved extremely popular because it allows scientists to manipulate specific sections of the genome of living mammals, making it a tool of tremendous importance for scientific research. It has been adopted quickly and widely, including for work in human cells, because it is comparatively simple and because many labs have the resources to use it. You can basically target any genomic region in living cells and change the genetic information, which has been the holy grail of research for the past several decades, Adli said. To be able to go and change the genetic information in living cells was a dream, basically.

UVAs new research helps explain the mechanism that underpins the CRISPR system and why it is vulnerable to off-target gene mutations. We not only found where it binds in the genome, we also investigated why it goes to these regions in the genome. By analyzing specific sequences underlying these off-targets, we also found out the determinants why it goes to the on-targets and also to these off-target regions, and our research shows that it goes there because of some sequence similarity to the original targeted regions, Adli said. So our results will help improve the specificity of the system so that we can minimize the off-targets.

Adlis work also showed that the naturally occurring form of a key enzyme used in the CRISPR system introduces far more mutations than an altered form of that enzyme that is less commonly used. The former cuts both strands of DNA during gene editing, allowing mutations to occur, while the latter snips only one strand, allowing cells to repair the damage without introducing mutations.

Unfortunately the wild-type form [the naturally occurring form] is much easier to deal with. Everyone in the field is using the wild type. Now with this paper, and with additional papers coming out, they will have to stop using the wild type form of the enzyme. They have to use the [altered form] to overcome the off-targets. It is much superior and the off-targets are very dangerous.

The findings have been published online by the journal Nature Biotechnology and will appear in a forthcoming print edition. The paper was authored by UVAs Cem Kuscu and Sevki Arslan, sharing credit as the lead authors; Ritambhara Singh; Jeremy Thorpe; and Adli.

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UVA Detects Unwanted Effects of Important Gene ...

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Scientists armed with a supercomputer and a vast trove of newly collected data on the body's most potent "tumor suppressor" gene have created the best map yet of how the gene works, an accomplishment that could lead to new techniques for fighting cancers, which are adept at disabling the gene in order to thrive.

Scientists from the University of Colorado Cancer Center and the University of Colorado Boulder used a new technology to tease out how the p53 gene -- which is responsible for recognizing damaged DNA in cells and then marking them for death -- is actually able to suppress tumors by determining what other genes p53 regulates. The study, published in the journal eLife, describes dozens of new genes directly regulated by p53.

The study authors say further research can explore which of these genes are necessary for p53's cancer-killing effect, how cancer cells evade these p53-activated genes, and how doctors may be able to moderate cancer cells' ability to stay safe from these genetic attempts at suppression.

The exhaustively studied p53 gene -- which has been the subject of 50,000 papers over more than 30 years of research -- is the most commonly inactivated gene in cancers. When p53 acts, cells are stopped or killed before they can survive, grow, replicate and cause cancer.

As such, all cancers must deal with p53's anti-tumor effects. Generally, there are two ways that cancer cells do this: by mutating p53 directly or by making a protein called MDM2, which stops p53 from functioning

The current study explores cancer cells' second strategy of blocking p53 function by producing the protein MDM2. Researchers have reasoned that treating a patient with an MDM2 inhibitor should allow p53 to restart its anti-cancer activities.

"MDM2 inhibitors, which are through phase I human trials, effectively activate p53 but manage to kill only about one-in-20 tumors," said Joaqun Espinosa, an investigator at the CU Cancer Center, an associate professor of molecular, cellular and developmental biology at CU-Boulder, and the paper's co-senior author. "The question is why. What else is happening in these cancer cells that allow them to evade p53?"

The answer is in what are called "downstream" effects of this gene, Espinosa said. The gene p53 doesn't act against cancer alone. Instead, it is the master switch that sets in motion a cascade of genetic events that lead to the destruction of cancer cells. And until now, it was unclear exactly which other genes were directly activated by p53.

The imperfect knowledge of p53's effects isn't for lack of research interest. Researchers have written thousands of papers exploring p53's targets and, in fact, many genetic targets are previously known. Most of these studies determine genetic targets by measuring levels of RNA.

When a gene is activated, it creates a protein. But between the gene and its protein product is the measurable step of RNA -- the more gene-specific RNA, the more often a gene's informational blueprint is carried to the cell's manufacturing centers, and the more protein is eventually made. Researchers measure RNA to see which genes are being turned up or down by any other gene.

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How a cancer-killing gene may actually work

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Student Work:Genetically Modified Organisms:ChiChi (G8)
After learning about genetic engineering and genetically modified organisms, grade 8 students were asked to write a script and create a GMO animation to discuss the ethical implications of...

By: Springs Pacelli

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Student Work:Genetically Modified Organisms:ChiChi (G8) - Video

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NEW YORK (TheStreet) --Foundation Medicine (FMI) is a good company in what many believe is an almost-impossible sector -- diagnostics. Bears believe diagnostic tests become commoditized with vanishing profit margins and no real winners. Diagnostic companies are simply providers of hardware (or a simple operator of hardware) vulnerable to relatively low barriers to entry. Even if a company roils out a successful diagnostic test, fast followers introduce similar tests and profit margins disappear. There is certainly a kernel of truth to these bearish arguments but Foundation Medicine has a comparative advantage over other diagnostic companies which investors are failing to recognize.

The price of a particular diagnostic test may fall over time (the rapidly diminishing cost to sequence the whole genome is a great example) but more important is what happens when adoption of these tests accelerates and the Big Data assembled from them are put to use treating patients.

Foundation Medicine's current FoundationOne cancer diagnostic examines about 236 genes and four types of alterations. While you can tout the advantage of a single test that comprehensively analyses information versus a series of more specific tests, the point is this is a lot of data. If you take the low end of the company's guidance -- 22,000 tests in 2014 -- this implies information on about 5.2 million genetic alterations generated in only one year. If you include how these patients are treated and the efficacy of these treatments, you can see how Foundation Medicine is putting Big Data to good use.

Foundation Medicine's advantage comes from taking its data and combining it with the latest research and clinical practices to provide information to a doctor about 1) the specific genetic makeup of their patients' cancers, and 2) potentially effective treatments using approved drugs or experimental drugs in clinical trials. The value Foundation Medicine provides is not the diagnostics, itself, but analyzing the data that comes out of the diagnostics.

These data are exceptionally useful for oncologists, who likely have little time to follow all of the clinical trials and changing treatment paradigms or new molecular targets. This means the real barrier of entry Foundation Medicine builds is not the testing but its ability to collect and analyze the data. These data are proprietary, so each additional test and refinement of the analysis puts the company further ahead and increases that barrier. A competitor might come along and create a similar test, but the diagnostic results themselves are not meaningful unless put into a useful context. It is that useful context Foundation Medicine constantly attempts to develop and improve, making it difficult for others to enter into the space and compete in a meaningful way.

Foundation Medicine is not without its challenges. Foremost, the company must convince insurance companies to pay for tests like FoundationOne. While one can talk in the abstract about the utility of having a single test that examines all potentially important genetic mutations and the utility it provides to oncologists and patients, it is something different to change the way payers reimburse for diagnostics. The reimbursement process will be slow and there is always the risk Foundation Medicine isn't successful. This weekend's American Society of Clinical Oncology (ASCO) annual meeting is important in this regard.

Neither of these challenges will happen overnight so don't expect Foundation Medicine to be a quick-hit winner. Investing in the company requires patience.Ultimately, Foundation Medicine looks like a nice risk/reward at its current valuation.

Sobek is long Foundation Medicine.

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Bull Thesis on Foundation Medicine: Using Big Data to Improve Treatment Decisions for Cancer Patients

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PUBLIC RELEASE DATE:

28-May-2014

Contact: Stephanie Desmon sdesmon1@jhmi.edu 410-955-8665 Johns Hopkins Medicine

A multicenter team of researchers report that a commercial test designed to rule out the presence of genetic biomarkers of prostate cancer may be accurate enough to exclude the need for repeat prostate biopsies in many if not most men.

"Often, one biopsy is not enough to definitively rule out prostate cancer," says study researcher Jonathan Epstein, M.D., director of the Division of Surgical Pathology and a professor of pathology, urology and oncology at the Johns Hopkins University School of Medicine. "Our research finds that by looking for the presence or absence of cancer in a different way, we may be able to offer many men peace of mind without putting them through the pain, bleeding and risk of infection that can come with a repeat biopsy."

The new research, called the Detection of Cancer Using Methylated Events in Negative Tissue (DOCUMENT) study, suggests that an initial biopsy complemented with an epigenetic diagnostic test accurately rules out the existence of cancer up to 88 percent of the time. The test, developed by MDxHealth, which paid for the study, was described online in April in The Journal of Urology.

The test specifically captures the presence of chemical modifications to non-nuclear DNA sequences within cells that commonly appear when prostate cancer is present. These so-called epigenetic changes, which add a methyl group to the biochemical makeup of the DNA, alter the way genes function without changing their foundational DNA sequence. The researchers analyzed tissue from biopsies from 320 men with elevated prostate-specific antigen (PSA) levels whose results were negative for prostate cancer. The men were patients at The Johns Hopkins Hospital; the University of California, Los Angeles; the Cleveland Clinic; Eastern Virginia Medical School; and Lahey Hospital & Medical Center.

The epigenetic biomarkers the test detects reflect a process called DNA hypermethylation, in which a methyl group is chemically attached to DNA in this case, to genes called GSTP1, APC and RASSF1. These genes are known to play prominent tumor suppressive roles in key cancer-related pathways. When these genes are hypermethylated, they are commonly silenced, which can lead to a loss of this tumor-suppressing function and the emergence of cancer.

Specifically, the GSTP1 gene acts as a detoxifying agent, preventing genomic damage by carcinogens. Studies find that GSTP1 is methylated in up to 90 percent of prostate cancer cases, making it a strong indicator of the disease.

For the study, pathologists compared methylation levels between the subjects' initial tissue biopsies and later tissue samples taken from each man done within 24 months of the first biopsy. They found that average levels of APC and RASSF1 were about twice as high in the 92 subjects whose second biopsies yielded positive results, as compared to the 228 with two negative biopsies. For GSTP1, the levels were more than eight times higher in the cancerous biopsies.

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Study affirms value of epigenetic test for markers of prostate cancer

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Researchers used an emerging technique to correct the gene behind a fatal immune system disorder in an infant.

A new kind of gene therapy which involves editing, rather than replacing, faulty genes in sick people, is being used experimentally in patients. The latest report shows how scientists can correct a broken gene as it sits in the patients genome. How the health of the patient, a 4-month old infant, will change is yet to be reported.

Genome editing technology is considered a promising new tool for curing disease. For decades, gene therapy has meant that a virus delivers a functional copy of a gene that is dysfunctional in a patient. The dysfunctional copy remains and the therapeutic version typically remains separate from the rest of the genome.

The technology has drawbacks. First, by sitting outside of the genome, the activity of therapeutic gene isnt regulated properly. In some cases, the therapeutic copy is delivered by a retrovirus the plunks the new gene down near randomly in the patients genome, which risks disrupting another gene, potentially causing cells to turn cancerous. Second, some diseases, such as Huntingtons, cant be treated this way because the broken copy of the gene causes harm. To treat these kinds of conditions, the original copy of the gene must be corrected. Using genome editing to repair genes could circumvent these issues (see Genome Surgery).

In the new study, published today in the journal Nature, researchers in Milan treated a condition known as Severe Combined Immunodeficiency Syndrome, or SCID (this condition is sometimes referred to as bubble boy disease because children afflicted may live in protected environments because the risk of death from infectious disease is extremely likely). Children with this genetic condition have been treated with the additive gene therapy method in the past, and some suffered leukemia-like diseases as a side effect (see The Glimmering Promise of Gene Therapy). In the new report, researchers describe treating a single infant with zinc-finger nucleases designed to repair a defective copy of an important immune system gene.

The report does not look at the long term health effects for the infant. But the team shows that the genome editing did reconstitute a functional copy of the immune system gene in a small fraction of bone marrow cells (which give rise to immune cells). This work is undoubtedly a step towards using gene repair for gene therapy, writes immunologist Alain Fischer in an accompany article also published in Nature. Fischer led the first successful gene therapy trials for SCID patients.

In March, researchers reported an even more dramatic example of gene repair. Scientists used zinc fingers to engineer the immune cells of patients with HIV to resist the virus (see Can Gene Therapy Cure HIV?). In a few patients, the amount of virus in the blood decreased and in one patient, the virus could no longer be found.

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Genome Editing to Reverse Bubble Boy Syndrome

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

28-May-2014

Contact: Robert Miranda cogcomm@aol.com Cell Transplantation Center of Excellence for Aging and Brain Repair

Tampa, Fla. (May 28, 2014) To be suitable for medical transplantation, one idea is that human embryonic stem cells (hESCs) need to remain "undifferentiated" i.e. they are not changing into other cell types. In determining the best way to culture hESCs so that they remain undifferentiated and also grow, proliferate and survive, researchers have used blood cell "feeder-layer" cultures using animal-derived feeder cells, often from mice (mouse embryonic fibroblasts [MEFs]). This approach has, however, been associated with a variety of contamination problems, including pathogen and viral transmission.

To avoid contamination problems, a Brazilian research team has investigated the use of human menstrual blood-derived mesenchymal cells (MBMCs) as feeder layers and found that "MBMCs can replace animal-derived feeder systems in human embryonic stem cell culture systems and support their growth in an undifferentiated stage."

The study will be published in a future issue of Cell Medicine, but is currently freely available on-line as an unedited early e-pub at: http://www.ingentaconnect.com/content/cog/cm/pre-prints/content-CM1019silvadosSantos.

"Human embryonic stem cells present a continuous proliferation in an undifferentiated state, resulting in an unlimited amount of cells with the potential to differentiate toward any type of cell in the human body," said study corresponding author Dr. Regina Coeli dos Santos Goldenberg of the Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro. "These characteristics make hESCs good candidates for cell based therapies."

Feeder-layers for hESCs comprised of MEFs have been efficiently used for decades but, because of the clinical drawbacks, the authors subsequently experimented with human menstrual blood cells as a potential replacement for animal-derived feeder-layers, not only for negating the contamination issues, but also because human menstrual blood is so accessible. MBMCs are without ethical encumbrances and shortages, nor are they difficult to access - a problem with other human cells, such as umbilical cord blood cells, adult bone marrow cells or placenta cells.

"Menstrual blood is derived from uterine tissues," explained the researchers. "These cells are widely available 12 times a year from women of child-bearing age. The cells are easily obtained, possess the capability of long-term proliferation and are clinically compatible with hESCs-derived cells."

The researchers found that their culture system using MBMCs as a feeder-layer for hESCs are the "closest and more suitable alternative to animal-free conditions for growing hESCs" and a "good candidate for large-expansion of cells for clinical application." They also found no difference in growth factor expression when comparing the use of growth factors in both the standard feeder system using animal cells and the feeder system they tested using hESCs.

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Brazilian researchers find human menstrual blood-derived cells 'feed' embryonic stem cells

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Block GmbH Centre for Living Cell Therapy
The fresh cell therapy/stem cell therapy is always a full body treatment. The improvement of the function of individual organs also affects all other organs positively.

By: VIPiChannel

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Block GmbH Centre for Living Cell Therapy - Video

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SINGAPORE: Australia-based stem cell therapy firm Mesoblast has announced plans to accelerate commercial manufacturing operations in Singapore.

This is to prepare for new product launches in the United States and other major markets over the next couple of years.

Its existing operations in Singapore include making stem cell products for clinical trials under its contract with its partner, pharmaceutical company Lonza.

One of its key products still awaiting full approval is Prochymal, which Mesoblast says can help to more than double the survival rate of patients suffering from complications after receiving tissue transplants from donors -- known as graft versus host disease.

The global stem cell market is expected to grow at an average annual rate of 12 per cent between 2011 and 2016 to reach more than S$8 billion by 2016.

Mesoblast said commercial manufacturing requires a much larger capacity and operations must be scaled-up to meet regulatory demands.

Silviu Itescu, chief executive at Mesoblast, said: "We are now in a phase of making more investments in order to get our processes to commercial scale. That anticipates successful commercial launches.

"If we're successful in that over the next 18-24 months, then we're going to leverage the investment in our commercial facilities to be able to build up and prepare for launching of much larger opportunities in cardiovascular medicine, orthopaedics and diseases of immunity and inflammation which would require purpose-built facilities."

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Mesoblast to accelerate operations in S'pore

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Personalized Medicine Update: Dr. Annabelle Rodriguez-Oquendo
Dr. Rodriguez-Oquendo is studying the genetic link between healthy HDL cholesterol, heart disease, and infertility in women.

By: uconnhealth

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Personalized Medicine Update: Dr. Annabelle Rodriguez-Oquendo - Video

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Spinal Cord Injury; Director of Faculty; Staff Disability Services (Employment Videos)
This video shows an individual with a spinal cord injury describing adaptive techniques she uses for work and demonstrating job tasks she performs in her job as a director of faculty and staff...

By: DACPROLab

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Spinal Cord Injury; Director of Faculty; Staff Disability Services (Employment Videos) - Video

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Family Centers President Bob Arnold and Barbara Netter.

At its annual luncheon in Darien on April 23, the Center for HOPE recognized Greenwich resident Barbara Netter for her many contributions toward the advancement of gene therapy-based cancer treatments.

As the President of the Alliance for Cancer Gene Therapy (ACGT) a nonprofit organization she founded with her late husband, Edward, in 2001 Ms. Netter has raised nearly $22.5 million for numerous gene therapy research initiatives around the world. Over the years, ACGTs support has been instrumental in launching 17 human clinical trials addressing lung, ovarian, prostate and breast cancer, as well as lymphoma and leukemia.

For her work providing millions of cancer patients with a renewed sense of optimism, Ms. Netter was presented with the Ray of HOPE Award. The Ray of HOPE is the Center for HOPEs highest honor that highlights a member of the community whose efforts assist those coping with a loss, critical illness or life-altering circumstance.

We are delighted to recognize Barbara with a Ray of HOPE Award, shinning the light on her body of work in the area of critical illness and bereavement, said Bob Arnold, Family Centers president. Barbara truly inspires us, as her bountiful efforts continue to fill our world with hope and compassion.

In addition to her work with ACGT, Ms. Netter has been involved for many years with The Den for Grieving Kids a Family Centers program providing support to children and families who have lost a loved one.

The Center for HOPE Luncheon also featured a keynote address from Huffington Post founder and editor-in-chief Arianna Huffington.

All proceeds from the event benefited the Center for HOPE and The Den for Grieving Kids.

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Center for HOPE honors Netter

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

27-May-2014

Contact: Garth Sundem garth.sundem@ucdenver.edu University of Colorado Denver

Scientists armed with a supercomputer and a vast trove of newly collected data on the body's most potent "tumor suppressor" gene have created the best map yet of how the gene works, an accomplishment that could lead to new techniques for fighting cancers, which are adept at disabling the gene in order to thrive.

Scientists from the University of Colorado Cancer Center and the University of Colorado Boulder used a new technology to tease out how the p53 genewhich is responsible for recognizing damaged DNA in cells and then marking them for deathis actually able to suppress tumors by determining what other genes p53 regulates. The study, published in the journal eLife, describes dozens of new genes directly regulated by p53.

The study authors say further research can explore which of these genes are necessary for p53's cancer-killing effect, how cancer cells evade these p53-activated genes, and how doctors may be able to moderate cancer cells' ability to stay safe from these genetic attempts at suppression.

The exhaustively studied p53 genewhich has been the subject of 50,000 papers over more than 30 years of researchis the most commonly inactivated gene in cancers. When p53 acts, cells are stopped or killed before they can survive, grow, replicate and cause cancer.

As such, all cancers must deal with p53's anti-tumor effects. Generally, there are two ways that cancer cells do this: by mutating p53 directly or by making a protein called MDM2, which stops p53 from functioning.

The current study explores cancer cells' second strategy of blocking p53 function by producing the protein MDM2. Researchers have reasoned that treating a patient with an MDM2 inhibitor should allow p53 to restart its anti-cancer activities.

"MDM2 inhibitors, which are through phase I human trials, effectively activate p53 but manage to kill only about one-in-20 tumors," said Joaqun Espinosa, an investigator at the CU Cancer Center, an associate professor of molecular, cellular and developmental biology at CU-Boulder, and the paper's co-senior author. "The question is why. What else is happening in these cancer cells that allow them to evade p53?"

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New University of Colorado study illuminates how cancer-killing gene may actually work

Recommendation and review posted by Bethany Smith

Charlottesville, VA (PRWEB) May 27, 2014

Researchers at the University of Virginia School of Medicine have devised a way to detect unintended side effects of manipulating genes using a revolutionary new system that is sweeping the scientific world by storm.

The gene targeting system, called CRISPR, allows editing of genetic information at specifically targeted sites in the genome. UVAs new approach reveals the system has the potential to bind to unintended sites and cause gene mutations at some of these sites mutations that could have serious consequences for research and efforts to develop medical treatments. UVAs new approach, however, also identifies ways to help prevent those potentially dangerous off-target effects, allowing scientists to improve their results with this important new gene-editing system.

A primary goal of gene manipulation is to correct harmful mutations, so it is vital to avoid introducing mutations unintentionally, explained UVAs Mazhar Adli, PhD, of the Department of Biochemistry and Molecular Genetics. We know that genetic mutations are hallmarks of disease. The whole aim is to change these apparent genetic mutations, to go and correct these mutations, he said. We want to change this information only at the targeted space, at the targeted locus. If you change any other information, basically you are introducing mutations that you dont want. You are correcting one gene and potentially you might be introducing mutations in 10 other genes and maybe many other places in the genome.

Adlis new research sheds light on the potential off-target effects of the CRISPR/Cas9 gene editing system. The system has proved extremely popular because it allows scientists to manipulate specific sections of the genome of living mammals, making it a tool of tremendous importance for scientific research. It has been adopted quickly and widely, including for work in human cells, because it is comparatively simple and because many labs have the resources to use it. You can basically target any genomic region in living cells and change the genetic information, which has been the holy grail of research for the past several decades, Adli said. To be able to go and change the genetic information in living cells was a dream, basically.

UVAs new research helps explain the mechanism that underpins the CRISPR system and why it is vulnerable to off-target gene mutations. We not only found where it binds in the genome, we also investigated why it goes to these regions in the genome. By analyzing specific sequences underlying these off-targets, we also found out the determinants why it goes to the on-targets and also to these off-target regions, and our research shows that it goes there because of some sequence similarity to the original targeted regions, Adli said. So our results will help improve the specificity of the system so that we can minimize the off-targets.

Adlis work also showed that the naturally occurring form of a key enzyme used in the CRISPR system introduces far more mutations than an altered form of that enzyme that is less commonly used. The former cuts both strands of DNA during gene editing, allowing mutations to occur, while the latter snips only one strand, allowing cells to repair the damage without introducing mutations.

Unfortunately the wild-type form [the naturally occurring form] is much easier to deal with. Everyone in the field is using the wild type. Now with this paper, and with additional papers coming out, they will have to stop using the wild type form of the enzyme. They have to use the [altered form] to overcome the off-targets. It is much superior and the off-targets are very dangerous.

The findings have been published online by the journal Nature Biotechnology and will appear in a forthcoming print edition. The paper was authored by UVAs Cem Kuscu and Sevki Arslan, sharing credit as the lead authors; Ritambhara Singh; Jeremy Thorpe; and Adli.

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UVA Detects Unwanted Effects of Important Gene Manipulation System

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A "life-saving" programme of tests for an inherited high cholesterol condition has been launched across the UK with 1 million of funding from the British Heart Foundation.

New tests aim to identify families whose members carry the gene for familial hypercholesterolaemia

The aim is to identify the one in 200 families whose members carry the gene for familial hypercholesterolaemia (FH), which can cut decades off a person's life.

Undiagnosed FH leaves individuals at high risk of developing heart disease and dying suddenly at a young age from a heart attack.

On average, the untreated condition shortens life expectancy by 20 to 30 years. But if spotted early, treatment with cholesterol-lowering statin drugs, lifestyle advice and careful monitoring can allow people with FH to live as long as anyone else.

FH is caused by a faulty gene that raises levels of the harmful form of cholesterol, low-density lipoprotein (LDL) from birth. At least 85% of those affected by the condition are undiagnosed.

The new scheme involves specialist nurses carrying out simple DNA blood tests to see if individuals with symptoms of high cholesterol carry the FH gene.

If the gene is discovered, other family members are then referred for "cascade" testing.

Steve Humphries, British Heart Foundation (BHF) professor of cardiovascular genetics at University College London, said: "With an estimated one in 200 hundred families carrying an FH-causing faulty gene in the UK, the introduction of cascade testing represents a huge opportunity to identify and treat people before they suffer from potentially life-threatening heart problems.

"After so many years of carrying out the laboratory research on FH, I am delighted now to see genetic testing being rolled out nationwide. But with such a high number of people remaining undiagnosed there is still more to be done if we're to get a complete picture of how FH affects the UK population."

Link:
Tests for cholesterol gene start

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04 Genetic Engineering cont

By: tawkaw OpenCourseWare

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04 Genetic Engineering cont - Video

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03 Genetic Engineering

By: tawkaw OpenCourseWare

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03 Genetic Engineering - Video

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PUBLIC RELEASE DATE:

27-May-2014

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, May 27, 2014The commonly used food additive monosodium glutamate (MSG) has been linked to obesity and disorders associated with the metabolic syndrome including progressive liver disease. A new study that identifies MSG as a critical factor in the initiation of obesity and shows that a restrictive diet cannot counteract this effect but can slow the progression of related liver disease is published in Journal of Medicinal Food, a peer-reviewed journal from Mary Ann Liebert, Inc.. The paper is available on the Journal of Medicinal Food website.

Makoto Fujimoto and a team of international researchers from Japan, the U.S., and Italy monitored the weight gain and development of nonalcoholic fatty liver disease and its progression to nonalcoholic steatohepatitis in MSG-treated mice fed either a calorie-restricted or regular diet. They report their findings in the article "A Dietary Restriction Influences the Progression But Not the Initiation of MSG-Induced Nonalcoholic Steatohepatitis".

"Although MSG has been deemed a safe food additive, its dosage, interaction with other drugs, effects on vulnerable populations, and effects on chronic inflammatory diseases and neurological diseases are unknown," says Co-Editor-in-Chief Sampath Parthasarathy, MBA, PhD, Florida Hospital Chair in Cardiovascular Sciences, University of Central Florida, Orlando, in the Editorial "How Safe is Monosodium Glutamate? Exploring the Link to Obesity, Metabolic Disorders, and Inflammatory Disease" . The findings by Fujimoto et al. "may have far reaching implications, as childhood obesity is a major problem across the globe."

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About the Journal

Journal of Medicinal Food is an authoritative, peer-reviewed, multidisciplinary journal published monthly in print and online. Led by Editors-in-Chief Sampath Parthasarathy, MBA, PhD, and Young-Eun Lee, PhD, Wonkwang University, Jeonbuk, Korea, this scientific journal for leaders of the nutraceutical and functional foods revolution publishes original scientific research on the bioactive substances of functional and medicinal foods, nutraceuticals, herbal substances, and other natural products. The Journal explores the chemistry and biochemistry of these substances, as well as the methods for their extraction and analysis, the use of biomarkers and other methods to assay their biological roles, and the development of bioactive substances for commercial use. Tables of content and a free sample issue may be viewed on the Journal of Medicinal Food website.

About the Publisher

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What what role does MSG play in obesity and fatty liver disease?

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Genetically modified organisms (also called GE for genetic engineering), are plants or animals created through the gene splicing techniques of biotechnology. They take fish genes (DNA), for example, and inject them into the tomatos DNA.

Most modified foods have been grown to resist chemicals, pests or disease. Thats all fine in theory, but a growing body of evidence connects GMOs with health problems, environmental damage, and more.

Of course Monsanto and other biotech companies say GE foods are safe to eat. Promises of increased yields, drought tolerance, enhanced nutrition, or any other consumer benefit have all proved false since they started doing this in the 1990s.

Most developed nations do not consider GMOs to be safe. In more than 50 countries around the world, including Australia, Japan, China, India and all of the European Union countries, there are significant restrictions or outright bans on the production and sale of GMOs. But here in the U.S., our government has approved GMOs based on studies conducted by the same corporations that created them and profit from their sale!

If theres no risk in eating products that contain GMOs then there should be no problem labeling them.

By supporting labeling, companies would say, Theres no risk, we have nothing to hide, says David Ropeik, creator and director of Improving Media Coverage of Risk.

We have the right to know how our food is grown. More people are realizing that the food they eat directly affects their health.

Vote YES for labeling of GMOs! Go to http://www.nongmoproject.org for more info.

TANYA OSTERSON

Coeur dAlene

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GMOs: Dont be confused

Recommendation and review posted by Bethany Smith

President Barack Obama quizzed students on their robots, electric cars, genetic discoveries and other projects at the White House science fair, highlighting the administrations push to boost science, technology, engineering and matheducation.

U.S. companies have lamented a shortfall of workers trained in so-called STEM fields, and the government officials want to boost enrollment in such programs.

These are the fields of the future, Mr.Obama said.This is where the good jobs are going to be.

As part of the fair, Mr. Obama announced $35 million in Department of Education grants to support training of more science, engineering and math teachers, an expansion of the AmeriCorps STEM program and a mentoring plan to link tech workers with students.

The White House said 100 students from more than 30 states came to the fair.On the same day of a major announcement about Afghanistan, a call with Ukraines president-elect and developments in policy toward Syria, the president spent more than an hour visiting with some of the students and asking them about award-winning projects.

Were so proud of you, Mr. Obama told 18-year-oldElana Simonof New York City. Ms. Simon, who survived a rare form of liver cancer, discovered a link between a common genetic mutation and the illness.

Peyton Robertson, a 12-year-old from Fort Lauderdale, Fla., developed a sandless sandbag to help protect against flooding. When dry, my bags are really lightweight, they weigh only four pounds, Mr. Robertson told the president. But then when you add water it expands and becomes heavy, it weighs 30 pounds.

Some tweets from the event:

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Obama Quizzes Kid Geniuses at White House Science Fair

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PUBLIC RELEASE DATE:

27-May-2014

Contact: Shawna Williams shawna@jhmi.edu 410-955-8236 Johns Hopkins Medicine

A genetic variant linked to sudden cardiac death leads to protein overproduction in heart cells, Johns Hopkins scientists report. Unlike many known disease-linked variants, this one lies not in a gene but in so-called noncoding DNA, a growing focus of disease research. The discovery, reported in the June 5 issue of The American Journal of Human Genetics, also adds to scientific understanding of the causes of sudden cardiac death and of possible ways to prevent it, the researchers say.

"Traditionally, geneticists have studied gene variants that cause disease by producing an abnormal protein," says Aravinda Chakravarti, Ph.D., a professor of medicine, pediatrics, molecular biology and genetics, and biostatistics in the McKusick-Nathans Institute of Genetic Medicine at the Johns Hopkins University School of Medicine. "We think there will turn out to be many DNA variants that, like this one, cause disease by making too much or too little of a normal protein."

Chakravarti's interest in sudden cardiac death emerged a decade ago, when it claimed several of his colleagues within a few months. An expert in complex common diseases, he and his team knew that sudden cardiac death can be caused by many conditions. They focused on one: abnormalities in what is known as cardiac repolarization the time it takes for the heart to gear up to beat again.

The team compared the genetic sequences of tens of thousands of people with their electrocardiogram (ECG) results, identifying several regions on the genome with genetic variations associated with lengthened QT interval, a measure of cardiac repolarization, in the ECG. "The problem is that most of these variants lie outside of genes, in the noncoding DNA that controls how genes are used," Chakravarti says, "so it's hard to tell what genes they're affecting."

Despite the challenge, Chakravarti and his colleagues were able to home in on one suspect region of the genome housing a gene called NOS1AP. "There were many variants grouped in this area," says Ashish Kapoor, Ph.D., a postdoctoral researcher in Chakravarti's laboratory, "so we catalogued all 200 that we found." The team then went through a process of elimination using genetically engineered, lab-grown cells and zebra fish to identify a variant in the noncoding DNA that affected how much protein was made by the nearby NOS1AP gene.

Next, they cultured rat heart cells and engineered them to overproduce NOS1AP. When the concentration of the protein rose in a particular type of heart cell called a cardiomyocyte, the cells' electrical properties changed in a way that is similar to the pattern seen in long QT syndrome.

Kapoor notes that 67 percent of the general population carries the NOS1AP-overproducing genetic variant. "We have observed that NOS1AP genetic variants are associated with sudden cardiac death whether or not they affect a particular person's QT interval, raising the risk by about 40 percent," he says. Chakravarti notes that the results also add to scientific understanding of how the heart and QT interval work knowledge with far-reaching implications. For example, many drugs developed for noncardiac conditions have turned out to temporarily lengthen QT interval, a side effect that only turns up after much time and money are spent on drug development. By better understanding regulation of the QT interval, researchers would be better able to predict what types of drugs could affect it.

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Quantity, not quality: Risk of sudden cardiac death tied to protein overproduction

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Halfcut - Blunts to Ashes feat. King,Genetics(seven G) Unknown Mizery
Produced by Home Brewed Release: From Dungeons To Rooftops (2014) Nocturne Records http://halfcut.bandcamp.com/album/from-dungeons-to-rooftops https://www....

By: rastaRoss420

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Halfcut - Blunts to Ashes feat. King,Genetics(seven G) & Unknown Mizery - Video

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