Oct. 22, 2013 The first evidence that the underlying genetic defect responsible for trisomy 21, also known as Down syndrome, can be suppressed in laboratory cultures of patient-derived stem cells was presented today (Oct. 22) at the American Society of Human Genetics 2013 annual meeting in Boston.

People with Down syndrome are born with an extra chromosome 21, which results in a variety of physical and cognitive ill effects. In laboratory cultures of cells from patients with Down syndrome, an advanced genome editing tool was successfully used to silence the genes on the extra chromosome, thereby neutralizing it, said Jeanne Lawrence, Ph.D., Professor of Cell & Developmental Biology at the University Massachusetts Medical School, Worcester, MA.

Dr. Lawrence and her team compared trisomic stem cells derived from patients with Down syndrome in which the extra chromosome 21 was silenced to identical cells from patients that were untreated. The researchers identified defects in the proliferation, or rapid growth, of the untreated cells and the differentiation, or specialization, of untreated nervous system cells. These defects were reversed in trisomic stem cells in which the extra chromosome 21 was muted.

"Silencing of trisomy 21 by manipulation of a single gene in living cells in laboratory cells surmounts the first major obstacle to development of potential 'chromosome therapy,'" said Dr. Lawrence, whose presentation today provided an update to the results that she and her colleagues reported earlier this year in the journal Nature.

In her ASHG presentation, Dr. Lawrence described the use of the novel editing tool to examine changes in gene expression that result from the silencing of the extra chromosome. The changes in gene expression were not limited to chromosome 21 but were genome-wide.

"In fact, the results indicate that the most prominent changes are in genes not encoded on chromosome 21," said Dr. Lawrence, who also provided more perspective about the various avenues of research that the results have created and that are now being and will be pursued in her lab.

The approach used by Dr. Lawrence and her team was inspired by the natural process that silences one copy of the female mammals' two sex-determining X chromosomes during embryonic development. In males, the sex-determining chromosomes are X and Y, and gene silencing helps maintain similar expression patterns of X chromosome genes in females and males.

To understand this biological process, Dr. Lawrence and her collaborators several years ago began studying the X-inactivation gene (XIST), which encodes a large non-coding RNA molecule. In laboratory cultures of cells, this molecule was shown to cover the surface of one of the X chromosomes of female mammals. XIST's actions permanently blocked the expression, or activity level, of the genes on the affected X chromosome.

Dr. Lawrence and her team mimicked this natural process by inserting the XIST gene into the gene-rich core of the extra chromosome 21 in lab cultures of pluripotent stem cells from patients with Down syndrome. Before taking this step, they first demonstrated that a large transgene could be successfully inserted at a specific site by using zinc-finger nuclease technology.

In the laboratory cells, they found that the RNA from the inserted XIST gene induced a host of epigenetic modifications that transcriptionally silenced the genes of the extra chromosome 21.

Originally posted here:
Gene-silencing strategy opens new path to understanding Down Syndrome

Recommendation and review posted by Bethany Smith

A Children Hospital of Philadelphia gene therapy spinout is taking over development of a Phase 3 gene therapy program to treat inherited blindness by counteracting retinal degeneration. Its one of the most common causes of blindness in children.

Spark Therapeutics is advancing the work of CHOPs Center for Cellular and Molecular Therapeutics. The center was set up in 2004 as a center for gene therapy translational research and manufacturing. CHOP is giving it $50 million to advance its genetic therapies.

Inherited blindness is caused by mutations in the RPE65 gene. There is currently no drug or therapeutic treatment for this form of inherited retinal degeneration, according to the hospital statement. It ultimately causes irreversible blindness.

The treatment has produced some encouraging results. A clinical study of 12 patients with RPE65-related blindness demonstrated notable improvement in visual function. In some cases, children who were profoundly blind were able to recognize faces and move independently, according to the statement.All school-age patients enrolled in the trial were able to transfer from Braille classrooms to sighted classrooms. The next step is a Phase 3 open-label, randomized, controlled study that will expand on the study.

The gene mutation in one of 14 genes that cause Lebers congenital amaurosis. It disrupts development of the retina, causing people with the disease to have severe vision deficits from birth that progress slowly over time to total blindness.

Many of the centers leaders will take on management roles in Spark or work with the company as scientific advisers. Among those advisers is Dr. Katherine A. High, a gene therapy pioneer who has worked as the director of the center from the start.

The group is also developing a gene therapy for hemophilia B. The goal is to eliminate or reduce the need for regular infusions of clotting factor. It might even be able to help hemophilia B patients with inhibiting antibodies.

The company is also advancing toward the clinic with gene therapy programs to address neurodegenerative diseases and additional hematologic disorders and other forms of inherited blindness.

The company was co-founded by CEO Jeffrey D. Marrazzo, who has served as an entrepreneurial consultant to the hospital for the past three years. He said: The creation of Spark is the culmination of a decade-long commitment by CHOP and our founding team to drive the field of gene therapy forward during a time when many in the industry had moved away.

Last month, CHOP formed a partnership with Osage University Partners in a move to develop more partnership opportunities. One spin-off company CHOP has produced is Vascular Magnetics to treat peripheral artery disease. A rotovirus vaccine called RotaTeq produced through joint research between CHOP and Wistar Institute is now sold by Merck.

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Late stage gene therapy for inherited blindness part of Children’s Hospital spinout

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Spark Therapeutics hopes to commercialize multiple gene-based treatments developed at the Childrens Hospital of Philadelphia.

A new biotechnology company will take over human trials of two gene therapies that could offer one-time treatments for a form of childhood blindness and hemophilia B.

The gene therapies were developed by researchers at the Childrens Hospital of Philadelphia, which has committed $50 million to the new company called Spark Therapeutics. The launch is the latest hint that after decades of research and some early setbacks, gene therapy may be on its way to realizing its potential as a powerful treatment for inherited disease.

In December 2012, the European Union gave permission to Dutch company Uniqure to sell its gene therapy for a fat-processing disorder, making Glybera the first gene therapy to make its way into a Western market (see Gene Therapy on the Mend as Treatment Gets Western Approval). However, Glybera has not been approved by the U.S., nor has any other gene therapy.

Spark has a chance to be the first gene-therapy company to see FDA approval. Results for a late-stage trial of a gene therapy for Lebers Congenital Amaurosis, an inherited condition that leads to a loss of vision and eventually blindness, are expected by mid-2015. That treatment is one of several gene therapies in or nearing late-stage testing contending to be the first gene therapy approved by the FDA for sale in the U.S. (see When Will Gene Therapy Come to the U.S.).

In addition to taking the reins for two-ongoing human trials, Spark will also work on gene therapies for other eye and blood conditions as well as neurodegenerative diseases, says CEO Jeff Marrazzo. The gene therapy technology developed at the Childrens Hospital has been speeding down the tracks, he says, and the company will provide the vehicle to get these therapies to the people who need them.

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New Gene Therapy Company Launches

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Orange County, CA (PRWEB) October 21, 2013

The premier stem cell therapy clinic on the West Coast, Physician First Choice, is now offering IV stem cell treatment for numerous medical conditions. This includes stem cell treatment for Alzheimer's disease, Diabetes, Parkinson's, Liver Disease, Cardiac Disease, COPD and much more. The treatments are provided by US Board Certified Stem Cell Doctors and for more information call (888) 988-0515.

Stem cell therapy has become available for numerous medical conditions and can dramatically improve the patient's baseline. Increasing amounts of research are showing the benefits of IV stem cell therapy for conditions such as diabetes and COPD. Prior to stem cell therapy, these conditions could be managed with traditional medications, but the disease itself could not be altered. With stem cell therapy, that possibility exists.

The Board Certified stem cell doctors at Physician First Choice have over 20 combined years of experience working with patients for both stem cell injection treatment and IV therapy. The clinic treats patients at multiple Southern California locations along with an international location in Mexico. Patient treatment is performed by the same US Board Certified doctors before, during and after therapy to ensure continuity of care.

The program in Mexico involves four days worth of treatment at a first rate clinic, and patients stay at a beautiful hotel with transportation included. IV stem cell therapy is performed along with growth factor treatments to enhance the effect of the bone marrow stem cells.

For conditions such as multiple sclerosis, Alzheimer's or Parkinson's, watching a loved one deteriorate can be disheartening even when the best care is received. Physician First Choice has been having excellent results with IV stem cell treatment for diabetes and these conditions, and the program has been growing exponentially as a result.

The 4 Day Stem Cell Therapy IV Program is offered as a package. Transportation to and from San Diego is included along with the Hotel Stay, All Medical Treatment, Breakfast Each Day, and Transportation between the Gorgeous Hotel and the Stem Cell Treatment Facility. Patients must be approved for program inclusion with a full medical record review and evaluation by the Southern California doctors.

To inquire about program inclusion for IV stem cell therapy, call Physician First Choice at (888) 988-0515.

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Physician First Choice Now Offering IV Stem Cell Therapy for Numerous Medical Conditions with US Board Certified Stem ...

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Prophet TB Joshua Anointing Water Testimony Healed of Spinal Cord Injury Emmanuel TV 20 Oct 13 SCOAN
Anointing Water Testimony Healed of Spinal Cord Injury 20 October 2013 Emmanuel TV.

By: Momisi

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Prophet TB Joshua Anointing Water Testimony Healed of Spinal Cord Injury Emmanuel TV 20 Oct 13 SCOAN - Video

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Yinka Ayefele opens up on how he sustained a spinal cord injury
On December 12, 1997, popular musician Yinka Ayefele was on his way to attend a programme at OGBC, Ibadan when he was involved in a motor accident on Abeokut...

By: TheGoldMyne

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Yinka Ayefele opens up on how he sustained a spinal cord injury - Video

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Durham, NC (PRWEB) October 21, 2013

Cato Research regulatory expert William Lee, Ph.D., R.A.C., Vice President of Regulatory Affairs at Cato Research, will present in San Francisco, California at the OMICS Group Conference, 3rd International Conference on Pharmaceutical Regulatory Affairs.

Dr. Lee's presentation is titled: "Regulatory Roadmap for Initiating a Gene Therapy Drug into Clinical Trials in the United States."

Abstract of Presentation: Exciting progress has been made in the development of gene therapy, and experimental research has brought forward novel treatment opportunities for viral vectors, DNA vectors, and gene-modified cell therapies. Clinical development of a gene therapy drug is challenging, requiring understanding of controlled manufacturing, relevant nonclinical pharmacology and safety studies, and clinical risk factors. For initiating clinical trials in the United States, regulatory requirements for investigational gene therapy drugs are more stringent than those with other investigational biologics (recombinant antibodies or recombinant proteins).

This talk will highlight these requirements, including the following: (1) Submissions to regulatory authorities (2) Manufacturing (3) Nonclinical studies

Dr. William Lee received his B.A. from The Johns Hopkins University and his Ph.D. from Cornell University Graduate School of Medical Sciences. Dr. Lee has 20 years of research and industry experience. His focus is on gene therapy with retroviral vectors, adeno-associated viral vectors, and DNA vectors. He spent 9 years at the gene therapy start-up firm Viagene, Inc., followed by 2 years at Chiron. In 1999, he joined Cato Research, in Durham, North Carolina, where he is currently Vice President, Regulatory Affairs. His projects have included the design of Phase 1 and Phase 2 protocols for a gene therapy drug and interactions with the FDA and NIH/OBA. Currently, he manages projects involving regulatory strategy and submissions of investigational new drug applications and marketing applications for biologics and drugs.

For more information about this event, please visit: http://www.cato.com/events.shtml.

About Cato Research Founded in 1988 by Dr. Allen Cato and Lynda Sutton and headquartered near Research Triangle Park, North Carolina, Cato Research is a full-service, global contract research and development organization providing strategic and tactical support for clients in the pharmaceutical, biotechnology, and medical device industries. Services range from design and management of preclinical and clinical studies to submission of regulatory documents required for marketing approval. With a staff of approximately 300 and offices located in the United States, Europe, Canada, Israel, and South Africa, the Cato Research team consistently demonstrates an unsurpassed level of responsiveness, flexibility, attention to detail, and passion for bringing their clients products to market with speed and cost-effectiveness.

For more information, please contact: Cato Research Phone: 919-361-2286 http://www.cato.com

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Cato Research Presents at OMICS Group Conference, 3rd International Conference on Pharmaceutical Regulatory Affairs

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For centuries, yogurt has been known as a healthy food. Now, new checkoff-funded research aims to make it even healthier.

Through a process known as gene mapping, researchers at the Minnesota-South Dakota Dairy Foods Research Center have discovered a way to increase the longevity of the beneficial bacterial culture in yogurt.

Bifidobacterium longum, the main bacteria in yogurt, has been found to keep the intestinal tract healthy and even to help prevent colon cancer. However, in the past, these beneficial bacteria sometimes expired by the time the product reached consumers, thereby limiting its health benefits. The new research helps these bacteria maintain their beneficial properties after the yogurt leaves the grocery store.

"This new step forward in yogurt research will help establish the importance of including this nutritious dairy food in the diet of more Americans," said Lloyd Metzger, director of the Minnesota-South Dakota Dairy Foods Research Center in St. Paul. "The bottom line is that more health-conscious consumers will have another reason to choose dairy products when shopping in the grocery store."

According to the USDA, per capita consumption of yogurt increased by 5.7 percent from 7 pounds to 7.4 pounds in 2002, the last year for which information is available. Hopefully, this new research will push that figure even higher.

The research was funded by checkoff dollars from the Midwest Dairy Association, a non-profit organization funded by dairy producers.

Midwest Dairy Association

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Research aims to increase yogurt’s health value

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PUBLIC RELEASE DATE:

20-Oct-2013

Contact: Lauren Riley lauren.riley@aacr.org 215-446-7155 American Association for Cancer Research

BOSTON PF-06463922, an investigational drug being developed by Pfizer Inc., has the potential to become a new treatment option for patients who have lung cancer harboring abnormalities in the ALK gene, according to preclinical results presented here at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics, held Oct. 19-23.

About 3 to 5 percent of lung cancers harbor ALK gene abnormalities. The drug crizotinib (Xalkori), which blocks ALK protein kinase activity, was approved in August 2011 by the U.S. Food and Drug Administration for the treatment of patients who have these lung cancers. Although robust responses to crizotinib are observed for lung cancers harboring ALK gene abnormalities, the majority eventually become resistant to the effects of the drug. In many cases, resistance arises because of genetic mutations in ALK.

"Resistance to targeted therapies such as crizotinib is a major challenge when treating patients with cancer," said Tod Smeal, Ph.D., associate research fellow in the Oncology Research Unit at Pfizer Inc. in San Diego, Calif. "Our goal is to take advantage of everything we have learned about designing drugs that target kinases like ALK and the ways in which lung cancers become resistant to crizotinib to develop the best next-generation ALK inhibitor we can.

"Our preclinical studies suggest that we are making progress toward achieving our goal: PF-06463922 has potent ALK-inhibiting activity, it is capable of inhibiting all the crizotinib-resistant ALK mutants so far detected in patients, and it can efficiently access the brain. We are excited about these preclinical results and very hopeful that they will translate into meaningful responses in the clinic."

After carefully designing PF-06463922, Smeal and colleagues first showed in cell assays that it potently inhibited the activity of ALK and all eight of the mutant forms of ALK known to cause resistance to crizotinib in patients with lung cancer. They then showed that PF-06463922 inhibited the growth of tumors harboring three of the crizotinib-resistant ALK mutants, including the most resistant ALK mutant, G1202R, in mice.

Further analysis indicated that PF-06463922 readily entered the brains of mice, rats, and dogs. In mice, levels of PF-06463922 in the brain were 20-30 percent of levels of PF-06463922 in the blood. This is potentially clinically relevant because a significant number of lung cancer patients will develop brain metastasis during the course of their disease, according to Smeal, although he noted that it will be important to see if these results in animals hold true in humans.

Smeal and colleagues also found that PF-06463922 potently inhibited the protein ROS1, a close relative of ALK recently implicated in a number of cancer types, including some lung and brain cancers. Further, PF-06463922 had antitumor effects in two mouse models of cancers driven by ROS1 gene abnormalities, leading the researchers to suggest that PF-06463922 has potential as a treatment for this subgroup of cancers, in addition to its promise as a new treatment for ALK-driven cancers.

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Targeted investigational therapy potential to overcome crizotinib resistance in lung cancers

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Oct. 18, 2013 A gene important in skin tanning has been linked to higher risk for testicular cancer in white men, according to a study led by scientists from the U.S. National Institutes of Health and the University of Oxford in England. Nearly 80 percent of white men carry a variant form of this gene, which increased risk of testicular cancer up to threefold in the study.

The research appeared online October 10, 2013 in the journal Cell, and is the result of an integrated analysis of big data supported by laboratory research. The team suspected that variations in a gene pathway controlled by the tumor suppressor gene p53 could have both positive and negative effects on human health.

"Gene variations occur naturally, and may become common in a population if they convey a health benefit," said Douglas Bell, Ph.D., author on the paper and researcher at the National Institute of Environmental Health Sciences (NIEHS), part of NIH. "It appears that this particular variant could help protect light-skinned individuals from UV skin damage, like burning or cancer, by promoting the tanning process, but it permits testicular stem cells to grow in the presence of DNA damage, when they are supposed to stop growing."

Bell explained that p53 stimulates skin tanning when ultraviolet light activates it in the skin. It then must bind a specific sequence of DNA located in a gene called the KIT ligand oncogene (KITLG), which stimulates melanocyte production, causing the skin to tan.

To conduct the analysis, Xuting Wang, Ph.D., of NIEHS, co-author and lead bioinformatics scientist on the paper, led a data mining expedition to sieve through many different data sets. The team selected possible leads from the intersection of more than 20,000 p53 binding sites in the human genome, 10 million inherited genetic variations genotyped in the 1000 Genomes Project, and 62,000 genetic variations associated with human cancers identified in genome-wide association studies (GWAS). These data sets were gathered through joint efforts of thousands of researchers from around the world.

"In the end, one variant in the p53 pathway was strongly associated with testicular cancer, but also, surprisingly, displayed a positive benefit that is probably related to tanning that has occurred as humans evolved," Wang noted.

The group at the Ludwig Institute for Cancer Research at the University of Oxford, led by Gareth Bond, Ph.D., performed complex experiments to confirm the molecular mechanism that linked the variant with cancer and tanning.

"White males with a single nucleotide variation in KITLG, called the G allele, have the highest odds of having testicular cancer. In fact, the twofold to threefold increased risk is one of the highest and most significant among all cancer GWAS conducted within the past few years," said Bond. "The high frequency of this allele in light skin individuals may explain why testicular cancer is so much more frequent in people of European descent than those of African descent."

Bond said although the G allele increases testicular cancer risk, it may explain why testicular tumors are often easily cured with chemotherapy. "Most other tumors have a mutant p53, but in these testicular cell tumors, the p53 is functioning properly, and the drugs used for testicular cancer appear to work in concert with p53's tumor suppression function to kill the cancer cells."

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Tanning gene linked to increased risk of testicular cancer

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Newswise (MEMPHIS, Tenn. October 20, 2013) Research led by St. Jude Childrens Research Hospital scientists has linked an inherited gene variation to a nearly four-fold increased risk of developing a pediatric acute lymphoblastic leukemia (ALL) subtype that is associated with a poor outcome. The study appears today in the online edition of the scientific journal Nature Genetics.

The high-risk variant was found in the GATA3 gene. Researchers reported the high-risk version of the gene was more common among Hispanic Americans and other individuals with high Native American ancestry than those of other ethnic backgrounds. Forty percent of Hispanic Americans carried the high-risk variant, compared to 14 percent of individuals of European ancestry. For this study, ethnicity was defined by genetic variations associated with ancestry rather than individual self-reports.

Hispanic children are known to be at a higher risk of developing ALL and of dying from the disease. This is the latest in a series of St. Jude studies to report an association between inherited DNA variations in a handful of genes and an increased risk of childhood ALL among those of Hispanic ethnicity.

This is the first study to link an inherited genetic variation to an elevated risk of developing the leukemia subtype known as Philadelphia chromosome-like ALL (Ph-like ALL). Individuals with the high-risk version of GATA3 were 3.85 times more likely than those who inherited a different version of the gene to develop Ph-like ALL. Patients with the high-risk variant were also more likely to have a poor treatment response and have their cancer eventually return.

A significant percentage of patients with the high-risk GATA3 variant also had the tumor genetic alterationsincluding mutations, gene deletions and chromosomal re-arrangementsthat are hallmark of Ph-like ALL. The changes occur in genes, including CRLF2, JAK and IKZF1 that regulate how blood cells grow and mature.

Until recently, little was known about why a child develops a specific subtype of ALL in the first place and whether inherited genetic variations that predispose an individual to a subtype also influence how he or she responds to the therapy, said corresponding author Jun J. Yang, Ph.D., an assistant member of the St. Jude Department of Pharmaceutical Sciences. In this study, we discovered a genetic basis for susceptibility to Ph-like ALL, but even more importantly, the evidence that host and tumor genomes may interact with each other to influence the risk of developing and surviving ALL.

The study was done in collaboration with the Childrens Oncology Group, a U.S.-based research cooperative study group focused on childhood cancer research and clinical trials. The research included 680 patients enrolled in COG clinical trials.

Ph-like ALL accounts for as much as 15 percent of childhood ALL and is associated with a high risk of relapse and a poor outcome. ALL is the most common childhood cancer. While overall cure rates for pediatric ALL are now about 90 percent, only 63 percent of children with Ph-like ALL are alive and cancer free after five years. Yang added that larger population studies are needed to assess risks associated with these inherited variations.

GATA3 carries instructions for assembling a protein called a transcription factor that turns other genes on and off. The GATA3 protein, and other members of the GATA gene family, plays a crucial role in normal development of a variety of blood cells. Alterations in GATA3 have been linked to other blood cancers, including Hodgkin lymphoma.

The high-risk GATA3 variation was identified using a library of 718,890 common genetic variations known as single nucleotide polymorphisms, or SNPs, to screen the DNA of 75 children with Ph-like ALL, 436 children with other ALL subtypes and 6,661 individuals without ALL. Fifty-eight percent of patients with Ph-like ALL carried the high-risk version of the gene, compared to 29 percent of patients with other ALL subtypes and 20 percent of those without ALL. When researchers checked for the high-risk variant in additional patients with the Ph-like ALL subtype as well as other young ALL patients and individuals without the disease, they found the similar percentages carried the high-risk version.

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Inherited Gene Variation Tied to High-Risk Pediatric Leukemia and Greater Risk of Relapse

Recommendation and review posted by Bethany Smith

Oct. 20, 2013 Research led by St. Jude Children's Research Hospital scientists has linked an inherited gene variation to a nearly four-fold increased risk of developing a pediatric acute lymphoblastic leukemia (ALL) subtype that is associated with a poor outcome. The study appears today in the online edition of the scientific journal Nature Genetics.

The high-risk variant was found in the GATA3 gene. Researchers reported the high-risk version of the gene was more common among Hispanic Americans and other individuals with high Native American ancestry than those of other ethnic backgrounds. Forty percent of Hispanic Americans carried the high-risk variant, compared to 14 percent of individuals of European ancestry. For this study, ethnicity was defined by genetic variations associated with ancestry rather than individual self-reports.

Hispanic children are known to be at a higher risk of developing ALL and of dying from the disease. This is the latest in a series of St. Jude studies to report an association between inherited DNA variations in a handful of genes and an increased risk of childhood ALL among those of Hispanic ethnicity.

This is the first study to link an inherited genetic variation to an elevated risk of developing the leukemia subtype known as Philadelphia chromosome-like ALL (Ph-like ALL). Individuals with the high-risk version of GATA3 were 3.85 times more likely than those who inherited a different version of the gene to develop Ph-like ALL. Patients with the high-risk variant were also more likely to have a poor treatment response and have their cancer eventually return.

A significant percentage of patients with the high-risk GATA3 variant also had the tumor genetic alterations -- including mutations, gene deletions and chromosomal re-arrangements -- that are hallmark of Ph-like ALL. The changes occur in genes, including CRLF2, JAK and IKZF1 that regulate how blood cells grow and mature.

"Until recently, little was known about why a child develops a specific subtype of ALL in the first place and whether inherited genetic variations that predispose an individual to a subtype also influence how he or she responds to the therapy," said corresponding author Jun J. Yang, Ph.D., an assistant member of the St. Jude Department of Pharmaceutical Sciences. "In this study, we discovered a genetic basis for susceptibility to Ph-like ALL, but even more importantly, the evidence that host and tumor genomes may interact with each other to influence the risk of developing and surviving ALL."

The study was done in collaboration with the Children's Oncology Group, a U.S.-based research cooperative study group focused on childhood cancer research and clinical trials. The research included 680 patients enrolled in COG clinical trials.

Ph-like ALL accounts for as much as 15 percent of childhood ALL and is associated with a high risk of relapse and a poor outcome. ALL is the most common childhood cancer. While overall cure rates for pediatric ALL are now about 90 percent, only 63 percent of children with Ph-like ALL are alive and cancer free after five years. Yang added that larger population studies are needed to assess risks associated with these inherited variations.

GATA3 carries instructions for assembling a protein called a transcription factor that turns other genes on and off. The GATA3 protein, and other members of the GATA gene family, plays a crucial role in normal development of a variety of blood cells. Alterations in GATA3 have been linked to other blood cancers, including Hodgkin lymphoma.

The high-risk GATA3 variation was identified using a library of 718,890 common genetic variations known as single nucleotide polymorphisms, or SNPs, to screen the DNA of 75 children with Ph-like ALL, 436 children with other ALL subtypes and 6,661 individuals without ALL. Fifty-eight percent of patients with Ph-like ALL carried the high-risk version of the gene, compared to 29 percent of patients with other ALL subtypes and 20 percent of those without ALL. When researchers checked for the high-risk variant in additional patients with the Ph-like ALL subtype as well as other young ALL patients and individuals without the disease, they found the similar percentages carried the high-risk version.

Read more:
Inherited gene variation tied to high-risk pediatric leukemia, risk of relapse

Recommendation and review posted by Bethany Smith

Frantz entered the first round competition by submitting a two-minute video clip singing a rap song about her current work on the development of vaccine combating Porcine Epidemic Diarrhoea Virus (PEDV). She was among the five finalists chosen from 40 video submissions.

"The lyrics in the rap are easy-to-understand language, and free of technical jargons, relying on items listeners are familiar with in their everyday lives, in order to get the audience to understand what I want to explain. Making a fun-filled rap song fun makes my presentation more interesting," she said.

The final round of the competition was held in Singapore on September 25, in which each finalist made a 10-minute presentation in front of a live audience of 150.

"I was very happy once the top award was announced for me. I was very anxious and excited seconds before the announcement was made because there were many Singaporean supporters attending the event held in the host country," she said.

Dr Frantz was awarded a trip to Brussels in Belgium, where she will attend the Euraxess Voice of Researchers Conference along with the winners of the other Euraxess Science Slams, which are organised in the US, Japan, India, China and Brazil.

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Thai researcher wins Euraxess Science Slam Asean 2013

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Oct. 20, 2013 In a biological quirk that promises to provide researchers with a new approach for studying and potentially treating Fragile X syndrome, scientists at the University of Massachusetts Medical School (UMMS) have shown that knocking out a gene important for messenger RNA (mRNA) translation in neurons restores memory deficits and reduces behavioral symptoms in a mouse model of a prevalent human neurological disease. These results, published today in Nature Medicine, suggest that the prime cause of the Fragile X syndrome may be a translational imbalance that results in elevated protein production in the brain. Restoration of this balance may be necessary for normal neurological function.

"Biology works in strange ways," said Joel Richter, PhD, professor of molecular medicine at UMMS and senior author on the study. "We corrected one genetic mutation with another, which in effect showed that two wrongs make a right. Mutations in each gene result in impaired brain function, but in our studies, we found that mutations in both genes result in normal brain function. This sounds counter-intuitive, but in this case that seems to be what has happened."

Fragile X syndrome, the most common form of inherited mental retardation and the most frequent single-gene cause of autism, is a genetic condition resulting from a CGG repeat expansion in the DNA sequence of the Fragile X (Fmr1) gene required for normal neurological development. People with Fragile X suffer from intellectual disability as well as behavioral and learning challenges. Depending on the length of the CGG repeat, intellectual disabilities can range from mild to severe.

While scientists have identified the genetic mutation that causes Fragile X, on a molecular level they still don't know much about how the disease works or what precisely goes wrong in the brain as a result. What is known is that the Fmr1 gene codes for the Fragile X protein (FMRP). This protein probably has several functions throughout the neuron but its main activity is to repress the translation of as many as 1,000 different mRNAs. By doing this, FMRP controls synaptic plasticity and higher brain function. Mice without the Fragile X gene, for instance, have a 15 to 20 percent overall elevation in neural protein production. It is thought that the inability to repress mRNA translation and the resulting increase in neural proteins may somehow hamper normal synaptic function in patients with Fragile X. But because FMRP binds so many mRNAs, and some proteins become more elevated than others, parsing which mRNA or combination of mRNAs is responsible for Fragile X pathology is a daunting task.

From Frog Egg to Fragile X

For years, Dr. Richter had been studying how translation, the process in which cellular ribosomes create proteins, went from dormant to active in frog eggs. He discovered the key gene controlling this process, the RNA binding protein CPEB. In 1998, Richter found the CPEB protein in the rodent brain where it played an important role in regulating how synapses talk to each other. At this point, his work began to move from exploring the role of CPEB in the developmental biology of the frog to how the CPEB protein impacted learning and memory. A serendipitous research symposium with colleagues at Cold Spring Harbor got him thinking about CPEB and Fragile X syndrome.

"Here I was, an outsider, a molecular biologist who had worked for years with frog eggs, in the same room with neurobiologists and neurologists, when they started talking about Fragile X syndrome and translational activity," said Richter. "It got me thinking that the CPEB protein might be a path to restoring the translational imbalance they were discussing."

Richter knew that CPEB stimulated translation and that FMRP repressed it. He also knew that animal models lacking the CPEB protein had memory deficits and that both proteins bound to many of the same mRNAs -- the overlap may be as higher as 33 percent. The thought was that by taking away a protein that stimulated translation might counterbalance the loss of the repressor FMRP protein, thereby restoring translational homeostasis in the brain and normal neurological function.

"It was one of those kind of goofy 'what if' sort of things," said Richter.

To test his hypothesis, Richter developed a double knockout mouse model that lacked both the FMRP gene that caused Fragile X and the CPEB gene. When they began measuring for Fragile X pathologies what they found was almost too good to be true.

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Two genetic wrongs make a biochemical right

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PUBLIC RELEASE DATE:

20-Oct-2013

Contact: Jim Fessenden james.fessenden@umassmed.edu 508-856-2000 University of Massachusetts Medical School

WORCESTER, MA In a biological quirk that promises to provide researchers with a new approach for studying and potentially treating Fragile X syndrome, scientists at the University of Massachusetts Medical School (UMMS) have shown that knocking out a gene important for messenger RNA (mRNA) translation in neurons restores memory deficits and reduces behavioral symptoms in a mouse model of a prevalent human neurological disease. These results, published today in Nature Medicine, suggest that the prime cause of the Fragile X syndrome may be a translational imbalance that results in elevated protein production in the brain. Restoration of this balance may be necessary for normal neurological function.

"Biology works in strange ways," said Joel Richter, PhD, professor of molecular medicine at UMMS and senior author on the study. "We corrected one genetic mutation with another, which in effect showed that two wrongs make a right. Mutations in each gene result in impaired brain function, but in our studies, we found that mutations in both genes result in normal brain function. This sounds counter-intuitive, but in this case that seems to be what has happened."

Fragile X syndrome, the most common form of inherited mental retardation and the most frequent single-gene cause of autism, is a genetic condition resulting from a CGG repeat expansion in the DNA sequence of the Fragile X (Fmr1) gene required for normal neurological development. People with Fragile X suffer from intellectual disability as well as behavioral and learning challenges. Depending on the length of the CGG repeat, intellectual disabilities can range from mild to severe.

While scientists have identified the genetic mutation that causes Fragile X, on a molecular level they still don't know much about how the disease works or what precisely goes wrong in the brain as a result. What is known is that the Fmr1 gene codes for the Fragile X protein (FMRP). This protein probably has several functions throughout the neuron but its main activity is to repress the translation of as many as 1,000 different mRNAs. By doing this, FMRP controls synaptic plasticity and higher brain function. Mice without the Fragile X gene, for instance, have a 15 to 20 percent overall elevation in neural protein production. It is thought that the inability to repress mRNA translation and the resulting increase in neural proteins may somehow hamper normal synaptic function in patients with Fragile X. But because FMRP binds so many mRNAs, and some proteins become more elevated than others, parsing which mRNA or combination of mRNAs is responsible for Fragile X pathology is a daunting task.

From Frog Egg to Fragile X

For years, Dr. Richter had been studying how translation, the process in which cellular ribosomes create proteins, went from dormant to active in frog eggs. He discovered the key gene controlling this process, the RNA binding protein CPEB. In 1998, Richter found the CPEB protein in the rodent brain where it played an important role in regulating how synapses talk to each other. At this point, his work began to move from exploring the role of CPEB in the developmental biology of the frog to how the CPEB protein impacted learning and memory. A serendipitous research symposium with colleagues at Cold Spring Harbor got him thinking about CPEB and Fragile X syndrome.

"Here I was, an outsider, a molecular biologist who had worked for years with frog eggs, in the same room with neurobiologists and neurologists, when they started talking about Fragile X syndrome and translational activity," said Richter. "It got me thinking that the CPEB protein might be a path to restoring the translational imbalance they were discussing."

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[BIOS 332] Introduction to Genetics - Jason Tresser
August 31, 2013.

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By RTT News, October 21, 2013, 09:24:00 AM EDT

(RTTNews.com) - Seattle Genetics, Inc.( SGEN ), Monday announced the initiation of a phase 1 clinical trial evaluating SGN-LIV1A for patients with LIV-1-positive metastatic breast cancer. SGN-LIV1A utilizes Seattle Genetics' antibody-drug conjugate or ADC technology. The trial will assess the safety and antitumor activity of SGN-LIV1A, targeted to LIV-1, a protein which is expressed in most subtypes of metastatic breast cancer. The primary endpoint of the trial is safety, with key secondary endpoints of objective response, duration of response and progression-free survival.

The study, which is excepted to enroll up to 70 patients, is enrolling patients with triple negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting, or patients with ER-positive and/or PR-positive and HER2-negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting, and at least three prior hormonal therapies.

ADCs are designed to harness the targeting ability of antibodies to deliver cell-killing agents directly to cancer cells. This approach is intended to spare non-targeted cells and thus reduce many of the toxic effects of traditional chemotherapy while enhancing antitumor activity.

For comments and feedback: contact editorial@rttnews.com

http://www.rttnews.com

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Seattle Genetics Begins Phase 1 Trial Of ADC Candidate SGN-LIV1A

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

Seattle Genetics, Inc. (SGEN) today announced the initiation of a phase 1 clinical trial evaluating SGN-LIV1A for patients with LIV-1-positive metastatic breast cancer. SGN-LIV1A utilizes Seattle Genetics industry-leading antibody-drug conjugate (ADC) technology. The trial is designed to assess the safety and antitumor activity of SGN-LIV1A, an ADC targeted to LIV-1 (SLC39A6), a protein which is expressed in most subtypes of metastatic breast cancer.

ADCs represent a novel treatment approach that have demonstrated activity in both hematologic and solid tumors. SGN-LIV1A is one of four ADCs that we are advancing into the clinic during 2013, demonstrating our significant investment in this approach for the treatment of cancer, said Jonathan Drachman, M.D., Chief Medical Officer and Executive Vice President, Research and Development, at Seattle Genetics. The target expression in breast cancer, preclinical antitumor activity, and need for novel therapeutic options for advanced breast cancer patients all support the clinical evaluation of SGN-LIV1A.

ADCs are designed to harness the targeting ability of antibodies to deliver cell-killing agents directly to cancer cells. This approach is intended to spare non-targeted cells and thus reduce many of the toxic effects of traditional chemotherapy while enhancing antitumor activity.

The study is a phase 1, open-label, dose-escalation clinical trial to evaluate the safety and antitumor activity of SGN-LIV1A in patients with LIV-1-positive metastatic breast cancer. The trial is enrolling patients with triple negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting, or patients with ER-positive and/or PR-positive and HER2-negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting, and at least three prior hormonal therapies. The primary endpoint of the trial is safety, with key secondary endpoints of objective response, duration of response and progression-free survival (PFS). The study is expected to enroll up to 70 patients at multiple centers in the United States.

The treatment of cancer is changing with the introduction of more targeted agents and understanding disease-specific prognostic factors. Antibody-drug conjugates are an example of this evolving landscape, representing a rational approach to targeted drug delivery, said Howard A. Burris, M.D., Chief Medical Officer, Executive Director of Drug Development at Sarah Cannon Research Institute and investigator for this phase 1 clinical trial. We are eager to evaluate SGN-LIV1A in this phase 1 trial for advanced breast cancer.

At the American Association of Cancer Research (AACR) Annual Meeting in April 2013, preclinical data demonstrated that up to 92 percent of breast tumors analyzed expressed LIV-1, with limited expression in normal tissue. SGN-LIV1A demonstrated significant antitumor activity in multiple preclinical models at well-tolerated doses (AACR 2013 Abstract 3962).

More information about the trial, including enrolling centers, will be available by visiting http://www.clinicaltrials.gov.

About SGN-LIV1A

SGN-LIV1A is an ADC comprised of an anti-LIV-1 monoclonal antibody linked to a synthetic cytotoxic cell-killing agent, monomethyl auristatin E (MMAE), using Seattle Genetics proprietary technology. The ADC is designed to be stable in the bloodstream, and to release its cytotoxic agent upon internalization into LIV-1-expressing tumor cells, which is expressed in most subtypes of metastatic breast cancer. This approach is intended to spare non-targeted cells and thus reduce many of the toxic effects of traditional chemotherapy while enhancing the antitumor activity.

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By Traci Pedersen Associate News Editor Reviewed by John M. Grohol, Psy.D. on October 20, 2013

A genetic variation that impacts how quickly smokers process nicotine can help predict whether those who try to quit are likely to respond to nicotine replacement therapy, according to a new study published in the journal Addiction.

The gene, however, has very little effect on the success of treatment with the drug buproprion (Zyban), an antidepressant that is often prescribed help people quit smoking by reducing their cravings and other withdrawal effects.

Smokers often struggle with cravings and withdrawal when stopping smoking. said lead researcher Laura Jean Bierut, M.D., professor of psychiatry.

This study gives us insights into who may respond to different types of smoking cessation medications so that we can improve the odds of quitting.

Clinically, we often observe that responses to medication vary from one patient to another, said first author Li-Shiun Chen, M.D., assistant professor of psychiatry. To understand those differences, we studied a gene called CYP2A6, which controls nicotine metabolism in our bodies.

It turns out that most of us metabolize nicotine rapidly, but others can metabolize it much more slowly.

Earlier research has shown that roughly 70 percent of individuals have a variation of the CYP2A6 gene that helps them metabolize nicotine quickly, while 30 percent metabolize nicotine more slowly.

Nicotine levels drop more quickly in fast metabolizers after they quit smoking, Chen said.

In slow metabolizers, nicotine stays in the body longer. We have found that fast metabolizers of nicotine are more likely to relapse when they try to quit because when their nicotine levels drop rapidly, they can fall victim to cravings, but theyre also more likely to be helped by nicotine replacement therapy, which can increase nicotine levels and help control those cravings.

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If one of two packages of, say, frozen edamame you are looking at on the supermarket shelf says, partially-produced with genetic engineering, which of those packages would you buy?

Because companies such as Monsanto, the nations leading producer of genetically-modified seeds, believe you would choose the non-GMO food, they are spending record amounts against Initiative 522, which would require labeling of genetically-engineered foods and seeds offered for retail sale in Washington.

Thats also the reason local and state groups supporting the initiative such as Label It WA. and GMO-Free San Juans want you to vote for the initiative.

Proponents address this issue directly: We also should have a right to choose whether we want to buy and eat genetically engineered food. Labels matter. They ensure transparency and preserve the freedom to make our own decisions about the food we eat. I-522 is a step in the right direction, says the pro voters statement.

Opponents point to increased costs: from Washington Wire, Advocates of Washingtons Initiative 522 say it wont cost a dime, but a new opposition report says that if voters require warning labels on genetically modified food products, the typical family of four would pay an additional $490 a year for groceries.

Local supporters of the voter-approved ban on use of genetically-modified seeds in San Juan County are hoping the 62 percent majority of county voters who supported Initiative 2012-4 last year will vote yes on Initiative 522.

But a local opponent of the GMO seed ban initiative, molecular biologist Larry Soll, says there are bigger things to worry about than a GMO label. Soll, reflecting on the fact that something close to 80 percent of food products now contain some element of GMO technology, points out that both the local and the state initiative are a back door method of getting rid of GMO crops.

The initiative imposes labeling requirements on genetically engineered foods and seeds offered for retail sale in this state. Genetically engineered is defined as foods or seeds produced by techniques that insert DNA or RNA into organisms or that use cell fusion techniques to overcome natural barriers to cell multiplication or recombination, according to the official statement in the voters pamphlet.

Genetically engineered agricultural commodities would be labeled genetically engineered, and genetically engineered packaged processed foods would be labeled partially produced with genetic engineering.

Many foods would be exempt, including alcoholic beverages, certified organic foods, foods not produced using genetic engineering, as certified by an approved independent organization, and foods served in restaurants.

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Health risks vs. higher costs; supporters, critics clash over impact of I-522

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Alien Anatomy Species Genetics part 1 of 2)

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LOS ANGELES--(BUSINESS WIRE)--

Life Stem Genetics Inc. (the Company), an emerging innovator in the advancement of Adult Stem Cell therapy announces that the Company's new stock symbol, LIFS, is now active.

The Company is also pleased to release the general details of its recent financing commitment. This financing is for $1 million (the Private Placement) of 1,000,000 units (each, a Unit) at a price of $1 per Unit. Each Unit will consist of one common share of the Company and one warrant to purchase an additional common share of the Company (each, a Warrant Share) at $1 per Warrant Share for a period of one year. The Company is to close the Private Placement within 45 calendar days of this press release.

Gloria Simov, CEO of Life Stem Genetics, commented, "Our new trading symbol and recent financing are key components to provide future value to our shareholders and to our fulfillment of our long term objectives in the emerging Adult Stem Cell therapy industry."

All shareholders of the Company are encouraged to view the Company's complete filings at the following link:

http://www.sec.gov/cgi-bin/browse-edgar?company=Life+Stem+Genetics HYPERLINK "http://www.sec.gov/cgi-bin/browse-edgar?company=Life+Stem+Genetics&owner=exclude&action=getcompany"& HYPERLINK "http://www.sec.gov/cgi-bin/browse-edgar?company=Life+Stem+Genetics&owner=exclude&action=getcompany"owner=exclude HYPERLINK "http://www.sec.gov/cgi-bin/browse-edgar?company=Life+Stem+Genetics&owner=exclude&action=getcompany"& HYPERLINK "http://www.sec.gov/cgi-bin/browse-edgar?company=Life+Stem+Genetics&owner=exclude&action=getcompany"action=getcompany

About Life Stem Genetics

Life Stem Genetics (LSG) is a progressive health care company that focuses on healing with a patients own Stem Cells. Stem Cells for years have been known to heal a variety of ailments successfully and now it is being offered as an efficient and painless way to treat many different illnesses ranging from orthopedic Injuries, neurological disorders such as Parkinsons, and Alzheimers, Cancer, Plastic Surgery, Age Management, Arthritis, Diabetes, Cardiology, COPD, MS, Urology, and many more. Stem Cell Therapy and LSGs proprietary techniques have experienced some of the best results in the industry, helping to repair or re-program damaged or diseased tissues and organs.

LSGs stem cell specialist has performed thousands of stem cell treatments, including the top names in PGA golf, NFL football, NBA basketball, and Major League Baseball. LSG will offer their proprietary treatments through a series of affiliate doctors, and medical clinics, with 60 affiliated clinics so far.

LSGs mission is to create a solid comprehensive approach to the treatment and maintenance of diseases and to break free from the medical insurance world by tapping into an affordable private- pay sector delivering exceptional healthcare free from the medical insurance maze.

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MOLOGEN AG: Clinical study with MGN1404 in malignant melanoma initiated

- Phase I trial to evaluate safety and tolerability

- Trial is under supervision of Charit - Universitaetsmedizin Berlin

Berlin, October 18, 2013 - The phase I clinical trial with the cancer immune therapy MGN1404 has been started. The trial evaluates the safety and tolerability of MGN1404 for the treatment of malignant melanoma. Furthermore data on the mechanism of action will be collected. MGN1404 will be applied in different dosages needle-free by jet-injection into skin metastases. It is planned to overall enroll nine patients in the trial. The study is a translational project for non-viral gene therapy and will be conducted by Charit in collaboration with Charit Comprehensive Cancer Center (CCCC), Experimental and Clinical Research Center (ECRC), Max Delbrueck Center for Molecular Medicine Berlin-Buch (MDC) as well as Skin Cancer Center Charit (SCCC). Principial investigator is Dr. med. Felix Kiecker, Specialist of Dermatology and Venerology, Skin Cancer Center Charit and scientific coordinator is Prof. Wolfgang Walther, ECRC, Charit.

Dr. Matthias Schroff, Chief Executive Officer of MOLOGEN AG, stated, 'With this study the third drug candidate from our broad pipeline of cancer immune therapies is entering the clinical development phase. I am especially glad that the longtime collaboration with the Max Delbrueck Center for Molecular Medicine, one of the best German institutes in the field of molecular biology, has now led to this trial. MGN1404 is addressing a severe disease with high unmet medical need. We are looking forward to the outcome of the trial.'

http://www.mologen.com

Additional information:

MGN1404 - MIDGE(R) vector for TNF-alpha expression Tumor necrosis factor alpha (abbreviated TNF-alpha) is a signaling substance (cytokine) of the immune system. TNF-alpha can stimulate cell death and therefore has - in the case of application into the tumor - a direct antitumoral effect. It also leads to the sensitization of tumors toward other therapies, such as chemotherapy or radiation therapy. MGN1404 is a minimalistic, non-viral DNA expression vector encoding for TNF-alpha, based on MOLOGEN'S proprietary MIDGE(R) platform technology. The needle-free, intratumoral jet injection of MGN1404 conveys the MIDGE(R) vectors directly into the tumor cells. The expression of TNF-alpha is triggered there by the MIDGE(R) vectors aiming to induce cell death in the tumor.

Malignant melanoma Malignant melanomas are one of the most malignant forms of skin cancer. The worldwide occurrence of malignant melanoma in the white population has increased continually and considerably in recent decades. Approximately 77,000 people in the USA and 100,000 people in Europe develop malignant melanoma each year. Despite the lack of symptoms and a relatively small size, melanomas can metastasize early in the lymph nodes and other organs. If diagnosed when there are already distant metastases the five-year survival rate is approximately 10-20%. Treatments of late stage malignant melanoma include chemotherapy, immunotherapy or radiation therapy.

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