PUBLIC RELEASE DATE:

24-Nov-2014

Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News @LiebertOnline

New Rochelle, NY, November 24, 2014--Genetically engineered pigs, minipigs, and microminipigs are valuable tools for biomedical research, as their lifespan, anatomy, physiology, genetic make-up, and disease mechanisms are more similar to humans than the rodent models typically used in drug discovery research. A Comprehensive Review article entitled "Current Progress of Genetically Engineered Pig Models for Biomedical Research," describing advances in techniques to create and use pig models and their impact on the development of novel drugs and cell and gene therapies, is published in BioResearch Open Access, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available on the BioResearch Open Access website at http://online.liebertpub.com/doi/full/10.1089/biores.2014.0039.

Gkhan Gn and Wilfried Kues, Friedrich-Loeffler-Institute (Neustadt, Germany), Istanbul Technical University, and Istanbul University Faculty of Veterinary Medicine (Turkey), discuss the technologies that have made it possible to develop transgenic pig models of human diseases, such as targeted gene transfer and genome sequencing. The authors review current progress in creating transgenic pig models for cancer, cardiovascular diseases, diabetes, neurodegenerative diseases, ophthalmology, and xenotransplantation. These models will enable researchers to study disease processes, identify new drug targets, test novel cell therapies to restore diseased tissues and organs, and assess methods to correct or replace mutated genes.

"This review provides an excellent update of recent progress in the field of pig transgenics for biomedical research," says BioResearch Open Access Editor Jane Taylor, PhD, MRC Centre for Regenerative Medicine, University of Edinburgh, Scotland.

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About the Journal

BioResearch Open Access is a bimonthly peer-reviewed open access journal led by Editor-in-Chief Robert Lanza, MD, Chief Scientific Officer, Advanced Cell Technology, Inc. and Editor Jane Taylor, PhD. The Journal provides a new rapid-publication forum for a broad range of scientific topics including molecular and cellular biology, tissue engineering and biomaterials, bioengineering, regenerative medicine, stem cells, gene therapy, systems biology, genetics, biochemistry, virology, microbiology, and neuroscience. All articles are published within 4 weeks of acceptance and are fully open access and posted on PubMed Central. All journal content is available on the BioResearch Open Access website at http://www.liebertpub.com/biores.

About the Publisher

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New treatments for cancer, diabetes, and heart disease -- you may have a pig to thank

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With an MBA from the University of Chicago (2006) and an MSc from the Compigne University of Technology (1997), David Del Bourgo has combined education in management and biomedical engineering. He has acquired 17 years of experience in marketing and sales development within the healthcare industry.

Before joining Genomic Vision, David Del Bourgo was VP Sales and Marketing at Theraclion, which specializes in therapeutic ultrasound equipment. After joining the company in 2009, he instigated Theraclions marketing strategy, developed the network of key opinion leaders and deployed the direct and indirect sales of an innovative echotherapy solution, which established the company as a major player in the treatment of tumors by ultrasound.

From 2006 to 2009, David was Director of Corporate Development and Marketing at Orbotech, a NASDAQ-listed Israeli electronics company, where he notably contributed to the growth of their medical division and led the acquisition of a Danish company specializing in nuclear cardiology (turnover of $30 million). His other positions have included Manager in Strategic Consulting at Advention Business Partners (2005-2006) and various positions at General Electric Healthcare, where he was initially a researcher (1997) before being appointed International Product Marketing Manager (2001-2003).

At Genomic Vision, Davids mission has begun with the setting up of a Sales and Marketing team, which is already operational, consisting of product specialists and a field team whose aim will be to promote the Companys innovative genetic tests among the main European diagnostic centers.

Aaron Bensimon, Genomic Visions co-founder and Chairman, says: We are very pleased to be able to count on a manager with such experience at Genomic Vision. David and his team are highly driven by their objective of deploying our international marketing strategy. His expertise and knowledge of the sector represent real assets in identifying sales opportunities for the genetic tests we are developing, and notably those targeting breast and colon cancer, which are scheduled to be launched in 2015.

Next financial press release

ABOUT GENOMIC VISION A spinoffof the Institut Pasteur, Genomic Vision is a molecular diagnostics company specialized in developing diagnostic tests for genetic diseases and cancers. Using molecular combing, an innovative technology that allows the direct visualization of individual DNA molecules, Genomic Vision detects quantitative and qualitative variations in the genome that are at the origin of numerous serious pathologies. Having benefited from the financial support of the Institut Pasteur, SGAM AI, Vesalius Biocapital and Quest Diagnostics, the Company is developing a solid portfolio of tests that notably target breast cancer and cancer of the colon. Since 2013, the Company has marketed the CombHeliX FSHD test for identifying a myopathy that is difficult to detect, Facio-scapulo-humeral dystrophy (FSHD), in the United States thanks to a strategic alliance with Quest Diagnostics, the American leader in diagnostic laboratory tests, and in France.

ABOUT MOLECULAR COMBING DNA molecular combing technology considerably improves the structural and functional analysis of DNA molecules. DNA fibers are stretched out on glass slides, as if combed, and uniformly aligned over the whole surface. It is then possible to identify genetic anomalies by locating genes or specific sequences in a patients genome using genetic markers, an approach developed by Genomic Vision and patented under the name Genomic Morse Code. This exploration of the entire genome at high resolution via a simple analysis enables the direct visualization of genetic anomalies that are undetectable by other technologies.

For further information, please go to http://www.genomicvision.com

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Genomic Vision Appoints David Del Bourgo as Head of Sales and Marketing

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A Newcastle research centre has been renamed in honour of a North East expert in muscular dystrophy and related neuromuscular conditions.

The John Walton Muscular Dystrophy Research Centre, which is part of the Institute of Genetic Medicine at Newcastle University, officially adopted its new name yesterday.

Born in Rowlands Gill, Lord Walton qualified from Newcastle Medical School, and went on to become both a consultant neurologist and professor of neurology in Newcastle, and from 1971-1981 was Dean of Medicine at the University.

The 92-year-old has spent his career helping improve the lives of people with muscle-wasting conditions, as well as other neurological conditions, first through medicine and then through Parliamentary campaigning.

Lord Walton said: I am deeply touched and honoured that it was decided that the centre should be called after me. It is more than 60 years since I began work on muscular dystrophy here in Newcastle and it is thrilling to see the way in which a whole area of research and management of patients has matured and developed.

I have often said that I am a simple Geordie lad, born in Rowlands Gill, brought up in this area, my father a school teacher, my mother a school teacher, my grandfather a miner, and to have been able to be at the forefront of the developments of muscular dystrophy is very exciting.

Newcastle and its reputation in the whole field of muscular dystrophy research stands very high in the world and that is something which I personally, and all the team, have every right to be proud of.

The John Walton Muscular Dystrophy Research Centre is a collaboration between Newcastle University and Newcastle Hospitals NHS Foundation Trust.

Pioneering research is carried out at the centre to develop treatments to help those with the debilitating condition.

Kate Bushby, professor of genetics at Newcastle University said: The renaming of the centre is very exciting. Lord Walton laid the foundation for the whole speciality of muscular dystrophy and he raised the profile of the condition; he started the research and he got the initial funding from the different charities and medical research council.

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Newcastle research centre renamed in honour of muscular dystrophy expert

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PUBLIC RELEASE DATE:

25-Nov-2014

Contact: Amy Blustein ablustein@wihri.org 401-681-2822 Women & Infants Hospital @womenandinfants

There has been much recent debate on the benefits and risks of screening for breast cancer using BRCA1 and BRCA2 mutations in the general adult population. With an estimated 235,000 new breast cancer diagnoses each year in the U.S. and more than 40,000 deaths, it is clearly important to be able to determine which women may be genetically predisposed to breast cancer.

Glenn E. Palomaki, PhD, associate director of the Division of Medical Screening and Special Testing in the Department of Pathology and Laboratory Medicine at Women & Infants Hospital of Rhode Island has recently published an invited commentary in the November issue of Genetics in Medicine. The commentary is entitled "Is it time for BRCA1/2 mutation screening in the general adult population? Impact of population characteristics."

A family history of breast or ovarian cancer or a personal history of early-onset cancer are strong risk factors for breast cancer. Systematic criteria when caring for a patient with a positive family history have been well established by such agencies as the U.S. Preventive Services Task Force and the National Comprehensive Cancer Network.

Dr. Palomaki said, "With the identification of the tumor suppressor genes BRCA1 and BRCA2 in the 1990s, the scientific community has extensively explored both the personal and population impact of carrying a deleterious mutation in these genes. Any new population-based screening test, such as testing for BRCA1 and BRCA2 mutations, requires consideration of key performance characteristics that evaluate both strengths and shortcomings before its introduction."

In his commentary, Dr. Palomaki cited two recent publications that present perspectives on routine, population-based screening for breast cancer using BRCA1/2 mutations in different populations.

"Together, these two publications offer an unusual opportunity to compare and contrast how distinct population differences, such as the mutations carrier rate, might influence the feasibility of population-based screening," said Dr. Palomaki. "Because founder mutations are more common in Ashkenazi Jewish women, are more easily identified and account for a higher proportion of all breast cancer cases, pilot trials in that population are indicated before launching widespread screening in Israel to identify and resolve implementation issues. Such screening in the United States, however, is more complicated, tilting the balance away from routine population screening, as least for the moment."

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Pathology specialist contributes to debate on breast cancer gene screening

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PUBLIC RELEASE DATE:

25-Nov-2014

Contact: Gina DiGravio ginad@bu.edu 617-638-8480 Boston University Medical Center @BostonUNews

(Boston)-- In the largest study of the genetics of memory ever undertaken, an international researcher team including scientists from Boston University School of Medicine (BUSM), have discovered two common genetic variants that are believed to be associated with memory performance. The findings, which appear in the journal Biological Psychiatry, are a significant step towards better understanding how memory loss is inherited.

Longer life spans and the increased prevalence of memory impairment and dementia world-wide underscore the critical public health importance of efforts aimed at deciphering the underlying mechanisms of human memory.

The Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium was developed to facilitate the study of the entire genome through pooling of data from research centers all across the world. Nearly 30,000 participants who did not have dementia were included in the study. Each participant completed memory tests, such as word recall, and their entire genome was genotyped. Using sophisticated statistical analysis, the genome was examined for segments that were associated with low memory scores.

The researchers found genetic variants near the Apolipoprotein E gene, known to harbor an increased risk of dementia (especially Alzheimer disease), were associated with poorer memory performance, mostly so in the oldest participants and for the short story recall. In a sub-study with post-mortem brain samples, participants with an increasing load of memory risk variants also had more pathological features of Alzheimer disease, perhaps reflecting in some instances early pre-clinical stages of the disease.

According to the researchers two additional regions of the genome, pointing to genes involved in immune response, were associated with the ability to recall word lists, providing new support for an important role of immune system dysfunction in age-related memory decline. "Interestingly genetic variants associated with memory performance also predicted altered levels of expression of certain genes in the hippocampus, a key region of the brain for the consolidation of information. These were mainly genes involved in the metabolism of ubiquitin that plays a pivotal role in protein degradation," explained lead author Stphanie Debette, MD, PhD, adjunct associate professor of neurology at BUSM.

This unprecedented world-wide collaboration has generated novel important hypotheses on the biological underpinnings of memory decline in old age, however the researchers caution that more research is clearly needed to confirm these findings. "The differential associations according to memory test characteristics and age should be accounted for in future studies. Exploring other types of genetic variation, including rare variants and epigenetic modifications, will be crucial to decipher the full spectrum of memory heritability," added Debette.

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Researchers shed new light on the genetics of memory performance

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PUBLIC RELEASE DATE:

24-Nov-2014

Contact: Vanessa Wasta wasta@jhmi.edu 410-614-2916 Johns Hopkins Medicine @HopkinsMedicine

After mining the genetic records of thousands of breast cancer patients, researchers from the Johns Hopkins Kimmel Cancer Center have identified a gene whose presence may explain why some breast cancers are resistant to tamoxifen, a widely used hormone treatment generally used after surgery, radiation and other chemotherapy.

The gene, called MACROD2, might also be useful in screening for some aggressive forms of breast cancers, and, someday, offering a new target for therapy, says Ben Ho Park, M.D., Ph.D., an associate professor of oncology in the Kimmel Cancer Center's Breast Cancer Program and a member of the research team.

The drug tamoxifen is used to treat estrogen receptor-positive breast cancers. Cells in this type of breast cancer produce protein receptors in their nuclei which bind to and grow in response to the hormone estrogen. Tamoxifen generally blocks the binding process of the estrogen-receptor, but some estrogen receptor-positive cancers are resistant or become resistant to tamoxifen therapy, finding ways to elude its effects. MACROD2 appears to code for a biological path to tamoxifen resistance by diverting the drug from its customary blocking process to a different way of latching onto breast cancer cell receptors, causing cancer cell growth rather than suppression, according to a report by Park and his colleagues published online Nov. 24 in the Proceedings of the National Academy of Sciences.

Specifically, the team's experiments found that when the gene is overexpressed in breast cancer cells--producing more of its protein product than normal--the cells become resistant to tamoxifen.

One piece of evidence for the gene's impact was demonstrated when the Johns Hopkins scientists blocked MACROD2's impact in breast cancer cell cultures by using an RNA molecule that binds to the gene to "silence," or turn off, the gene's expression. But the technique only partially restored the cells' sensitivity to tamoxifen.

To conduct the study, the scientists examined two well-known databases of breast cancer patients' genetic information, The Cancer Genome Atlas and the Molecular Taxonomy of Breast Cancer International Consortium study. Patients who had MACROD2 overexpressed in primary breast cancers at the original breast cancer site had significantly worse survival rates than those who did not, according to an analysis of the patient databases.

With this in mind, the Johns Hopkins scientists suggest that clinicians may be able to look at MACROD2 activity to help them identify aggressive breast cancers at early stages of growth.

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Johns Hopkins scientists link gene to tamoxifen-resistant breast cancers

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CSF Colloquium: "Chiari Heritable Connective Tissue Disorders - Genetics"
Help share more videos like this by supporting CSF: http://csfinfo.org/donate-online/ Dr. Allison Ashley-Koch talks more about the genetics of Chiari malformation and heritable connective tissue...

By: Chiari Syringomyelia Foundation

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CSF Colloquium: "Chiari & Heritable Connective Tissue Disorders - Genetics" - Video

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CHAPTER 34 - Glaucoma and genetics Glaucoma Sensor

By: Geno Academy

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CHAPTER 34 - Glaucoma and genetics Glaucoma Sensor - Video

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Geoffrey Ondrich and Waylon Cude are both 16 years old. Both boys have autism, and both would rather use their computers than do almost anything else in the world.

But thats just about all they have in common.

Waylon is serious and intense, and so is the way he uses his computer: He spends hours immersed in online role-playing games, and he interned last summer at IBM, programming Linux for websites.

On a sunny Friday in October, he leans toward a computer monitor in a testing room at the University of Washington in Seattle, where he is part of a study on the genetics of autism. Waylon focuses diligently on his reaction-time test, frowning to himself when he makes a mistake. Throughout the day, he responds politely to questions, especially factual ones, but doesnt engage in chitchat or commentary. At one point, a clinician who has been testing Waylons motor skills remarks that he is almost as nimble at rearranging tiny plastic pegs with his left hand as he is with his dominant right. Waylon doesnt respond.

By contrast, when Geoffrey completes a task for the same study, he gets a few minutes on his iPad, his passport to fun and pleasure. He watches bits of a movie or scrolls through his collection of music until he finds a particular song with a catchy, disco-y beat, and dances happily in his chair.

When he doesnt have music to dance to, Geoffrey often rocks back and forth in his chair, slapping the top of his left wrist with his right hand. The clinician who is working with him struggles to engage his attention as Geoffrey picks up a plate from a toy tea set and peers at it closely. He bites the plate, then rolls a Matchbox car back and forth over the table in front of him.

Its no surprise that these two boys, at the same age and with the same diagnosis, are so different. Clinicians are fond of saying, If youve seen one kid with autism, youve seen one kid with autism, meaning that its impossible to draw conclusions by looking at just a few people.

This diversity has been a major hurdle for understanding autism and for coming up with treatments that can help a majority of people with the diagnosis. Most studies include individuals who share the same phenotype, or outward characteristics, but whose autism may arise from entirely different origins. Because of this, they often produce muddled results. We recognize autism is a really heterogeneous disorder and were not making a lot of headway when we try to study it as a heterogeneous disorder, says Thomas Frazier, director of the Cleveland Clinic Childrens Center for Autism.

A close look at DNA may provide a way through this muddle.

What weve learned in the last five years about the underlying genetics is that there are hundreds, if not a thousand or more, different genetic subtypes of autism, says geneticist David Ledbetter, chief scientific officer at Geisinger Health System in Danville, Pennsylvania.

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Genetics Suggest Autism Isnt Just One DisorderIts Hundreds

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Bio 298 Gene Therapy

By: Josephine Mosman

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Bio 298 Gene Therapy - Video

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UCLA Stem Cell Researchers Announce Gene Therapy Cure for 18 Bubble Baby Patients
Researchers at UCLA announced today that they had cured 18 children who were born with the so-called Bubble Baby disease, a genetic disorder that leaves the young sufferers without a working...

By: UCLA Eli Edythe Broad Center of Regenerative Medicine and Stem Cell Research

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UCLA Stem Cell Researchers Announce Gene Therapy Cure for 18 Bubble Baby Patients - Video

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Copy of HOPE, HYPE REALITY: ZINC FINGER GENE THERAPY TO CONTROL OR CURE HIV
A video to answer your questions about a gene therapy approach to an HIV cure. On Nov 5, 2014, the defeatHIV Community Advisory Board hosted a talk with Dr. ...

By: defeatHIV

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Copy of HOPE, HYPE & REALITY: ZINC FINGER GENE THERAPY TO CONTROL OR CURE HIV - Video

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The promise and potential dangers of gene therapy | Tomorrow Today - Interview
What role is gene therapy likely to play in the future? Professor Wolfgang Uckert, the president of the German Society for Gene Therapy, talks about the potential of the treatment. More tomorrow-...

By: DW (English)

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The promise and potential dangers of gene therapy | Tomorrow Today - Interview - Video

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Gene Therapy - Treating the Disease Instead of the Symptoms | Tomorrow Today
Children found to be particularly susceptible to illness could be suffering from a genetic - and potentially fatal - immune disorder. This year #39;s prestigious Robert Koch Prize has been awarded...

By: DW (English)

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Gene Therapy - Treating the Disease Instead of the Symptoms | Tomorrow Today - Video

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Duchenne Muscular Dystrophy: Ryan #39;s Story
Learn more about Duchenne Muscular Dystrophy (here: http://bit.ly/1yzusRh) or connect with a specialist (here: http://bit.ly/1xz0Cy1). When you help Ryan, you help kids everywhere. Please...

By: NationwideChildrens

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Duchenne Muscular Dystrophy: Ryan's Story - Video

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Chuck Bednar for redOrbit.com Your Universe Online

A new stem cell gene therapy developed by researchers at UCLA is set to begin clinical trials early next year after the technique reportedly cured 18 children who were born without working immune systems due to a condition known as ADA-deficient Severe Combined Immunodeficiency (SCID) or Bubble Baby disease.

The treatment was developed by Dr. Donald Kohn, a member of the UCLA Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, and his colleagues, and according to the university, it is able to identify and correct faulty genes by using the DNA of the youngsters born with this life-threatening condition.

Left untreated, ADA-deficient SCID is often fatal within the first year of a childs life, reports Peter M. Bracke for UCLA. However, after more than three decades of research, Dr. Kohns team managed to develop a gene therapy that can safely restore the immune systems of children with the disease by using their own cells and with no noticeable side effects.

All of the children with SCID that I have treated in these stem cell clinical trials would have died in a year or less without this gene therapy, instead they are all thriving with fully functioning immune systems, Dr. Kohn, who is also a professor of pediatrics and of microbiology, immunology and molecular genetics, said in a recent statement.

Children born with SCID have to be isolated in a controlled environment for their own safety, because without an immune system, they are extremely vulnerable to illnesses and infections that could be deadly. While there are other treatments for ADA-deficient SCID, Dr. Kohn noted that they are not always optimal or feasible for many children. The new technique, however, provides them with a cure, and the chance to live a full healthy life.

SCID is an inherited immunodeficiency that is typically diagnosed about six months after birth, the researchers said, and children with the condition are so vulnerable to infectious diseases that even the common cold could prove fatal to them. This particular form of the condition causes cells to not create ADA, an enzyme essential for the production of the white blood cells which are a vital component of a healthy, normally-functioning immune system.

Approximately 15 percent of all SCID patients are ADA-deficient, according to the university, and these youngsters are typically treated by being injected twice per week with the required enzyme. This is a process that must continue throughout a patients entire life, and even then it doesnt always work to bring their immune systems to optimal levels. Alternately, they could undergo bone marrow transplants from matched siblings, but those matches are rare and the transplanted cells themselves are often rejected by the childs body.

Dr. Kohn and his colleagues tested two therapy regimens on 18 ADA-deficient SCID over the course of two multi-year clinical trials starting in 2009. During the trials, the blood stem cells of the patients were removed from their bone marrow and genetically modified in order to correct the defect. All 18 of the patients were cured.

The technique used a virus delivery system first developed in Dr. Kohns laboratory in the 1990s a technique which inserts the corrected gene that produces the ADA into the blood forming stem cells in the bone marrow. The genetically corrected blood-forming stem cells will then produce the T-cells required to combat infections.

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New Stem Cell Treatment Found To Cure 'Bubble Baby' Disease

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ORLANDO, Fla. -

Little Hunter Miller's motor is always running. Like most toddlers, he's sometimes one step away from trouble, but for Hunter, being rough and tumble can have serious side effects. Hunter has severe hemophilia.

Three days after he was born, a routine circumcision caused a major scare.

"You know, a baby gets up in the morning and their diapers are just full," said Hunter's grandmother, Tina Miller. "Well, his was full, but it was full of blood."

Doctors diagnosed Hunter with hemophilia A, which means his blood is missing a protein, known as clotting factor VIII. When he gets hurt, doctors need to inject the clotting factor to stop the bleeding. He's had eight emergency room visits in 19 months.

"Him falling, bumping his head too hard, little cuts. He cut the roof of his mouth with a tortilla chip and that was a hospital trip," said Heather Frederick, Hunter's mother.

Dr. Katherine Ponder studies gene therapy treatment for hemophilia and other blood disorders. Her lab treated hemophilia A in animals, but she said the therapy isn't quite ready for humans yet.

"I think that the big question is going to be the safety," said Katherine Ponder, hematologist at Washington University School of Medicine in St. Louis.

But gene therapy has proven effective for some patients with hemophilia B. Researchers at St. Jude's Children's Research Hospital and University College of London have added the missing protein -- factor IX -- to a specially-engineered virus, which travels to the patients liver and transfers the gene.

"This modifies the disease from a situation where they might bleed once a week to a situation where they hardly ever bleed," Ponder explained.

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Health Beat: Gene therapy: From bench to bedside: Hemophilia

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Cambridge stem cell pioneer DefiniGEN is in China this week showcasing technology that arguably gives the UK a world lead in countering liver and pancreatic cancer.

The young company is seeking Chinese partners to broaden the reach of the technology which holds a potentially significant payback in regenerative medicine.

With US global stem cell innovator Roger Pedersen among its technology founders, DefiniGEN was founded two years ago to commercialise a stem cell production platform developed at the University of Cambridge.

The platform generates human liver and pancreatic cell types using Nobel Prize winning human Induced Pluripotent Stem Cell (iPSC) technology.

DefiniGEN is visiting Shanghai and Beijing on a trade mission organised by UKTI East of England in partnership with the China-Britain Business Council.

The company is actively looking to partner with Life Science distributors and pharmaceutical drug discovery companies in China. CEO Dr Marcus Yeo and Dr Masashi Matsunaga business development manager for Asia Pacific - are spearheading the initiative.

The visit includes a range of medically-focused ventures from one to one meetings with key players to presentations at UK consulates.

DefiniGEN cells are provided to the drug discovery sector for use in lead optimisation and toxicity programmes.

The companys OptiDIFF platform produces validated libraries of disease-modelled human liver cells for a range of diseases. The phenotype (the composite of an organisms traits) and pathology of the diseases is pre-confirmed in the cells.

The technology provides pharmaceutical companies with more predictive in vitro cell products enabling the development of safer and more effective treatments.

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Cambridge stem cell pioneer targets China partners

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Chuck Bednar for redOrbit.com Your Universe Online

A new stem cell gene therapy developed by researchers at UCLA is set to begin clinical trials early next year after the technique reportedly cured 18 children who were born without working immune systems due to a condition known as ADA-deficient Severe Combined Immunodeficiency (SCID) or Bubble Baby disease.

The treatment was developed by Dr. Donald Kohn, a member of the UCLA Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, and his colleagues, and according to the university, it is able to identify and correct faulty genes by using the DNA of the youngsters born with this life-threatening condition.

Left untreated, ADA-deficient SCID is often fatal within the first year of a childs life, reports Peter M. Bracke for UCLA. However, after more than three decades of research, Dr. Kohns team managed to develop a gene therapy that can safely restore the immune systems of children with the disease by using their own cells and with no noticeable side effects.

All of the children with SCID that I have treated in these stem cell clinical trials would have died in a year or less without this gene therapy, instead they are all thriving with fully functioning immune systems, Dr. Kohn, who is also a professor of pediatrics and of microbiology, immunology and molecular genetics, said in a recent statement.

Children born with SCID have to be isolated in a controlled environment for their own safety, because without an immune system, they are extremely vulnerable to illnesses and infections that could be deadly. While there are other treatments for ADA-deficient SCID, Dr. Kohn noted that they are not always optimal or feasible for many children. The new technique, however, provides them with a cure, and the chance to live a full healthy life.

SCID is an inherited immunodeficiency that is typically diagnosed about six months after birth, the researchers said, and children with the condition are so vulnerable to infectious diseases that even the common cold could prove fatal to them. This particular form of the condition causes cells to not create ADA, an enzyme essential for the production of the white blood cells which are a vital component of a healthy, normally-functioning immune system.

Approximately 15 percent of all SCID patients are ADA-deficient, according to the university, and these youngsters are typically treated by being injected twice per week with the required enzyme. This is a process that must continue throughout a patients entire life, and even then it doesnt always work to bring their immune systems to optimal levels. Alternately, they could undergo bone marrow transplants from matched siblings, but those matches are rare and the transplanted cells themselves are often rejected by the childs body.

Dr. Kohn and his colleagues tested two therapy regimens on 18 ADA-deficient SCID over the course of two multi-year clinical trials starting in 2009. During the trials, the blood stem cells of the patients were removed from their bone marrow and genetically modified in order to correct the defect. All 18 of the patients were cured.

The technique used a virus delivery system first developed in Dr. Kohns laboratory in the 1990s a technique which inserts the corrected gene that produces the ADA into the blood forming stem cells in the bone marrow. The genetically corrected blood-forming stem cells will then produce the T-cells required to combat infections.

Read more here:
New Stem Cell Treatment Found To Cure 'Bubble Baby' Disease

Recommendation and review posted by simmons

1. Keratinocytes

There are two approaches to commit ES cells and adult stem cells (of non-epidermal origin) to the keratinocyte lineage in vitro. One approach would be to expose the cells to a cocktail of exogenous cytokines, growth factors, chemicals, and extracellular matrix (ECM) substrata over a prolonged duration of in vitro culture. Only a fraction of the stem cells would be expected to undergo commitment to the keratinocyte lineage, because many of these cytokines, growth factors, chemicals, and ECM substrata would exert non-specific pleitropic effects on stem cell differentiation into multiple lineages. At best, the cocktail combination of various cytokines, growth factors, chemicals, and ECM substrata can be optimized by trial and error, to maximize the proportion of stem cells committing to the keratinocyte lineage, while at the same time yielding a large number of other undesired lineages. Hence, extensive selection/purification and proliferation of the commited keratinocyte progenitors is likely to be required.

By using such an approach, Coraux et al.54 managed to achieve commitment and subsequent differentiation of murine ES cells into the keratinocyte lineage, in the presence of a cocktail combination of bone morphogenetic protein-4 (BMP-4), ascorbate, and ECM derived from human normal fibroblasts (HNFs) and murine NIH-3T3 fibroblasts. Nevertheless, it must be noted that the study of Coraux et al.54 also reported a high degree (approximately 80%) of non-specific differentiation into multiple uncharacterized lineages, and no attempt was made to purify differentiated keratinocytes or keratinocyte progenitors from the mixture of lineages derived from murine ES cells. Bagutti et al.61 reported that coculture with human dermal fibroblasts (HDFs) as well as HDF-conditioned media could induce beta integrin- deficient murine ES cells to commit and differentiate into the keratinocyte lineage. However, as with the study of Coraux et al.,54 the keratinocytes were interspersed with differentiated cells of other lineages. Recently, differentiation of human ES cells into the keratinocyte lineage was also reported by Green et al.62 However, this study was based on in vivo teratoma formation within a SCID mouse model, and to date, there are no parallel in vitro studies that have been reported.

With adult stem cells of non-epidermal origin, there are also few studies 63, 64 which have successfully achieved re-commitment and trans-differentiation to the keratinocyte lineage. Even so, these studies were based primarily on the transplantation of undifferentiated stem cells in vivo, with the observed trans-differentiation occurring sporadically and at extremely low frequencies. Moreover, the validity of the experimental data may be clouded by controversy over the artifact of stem cell fusion in vivo.65 To date, there are no parallel in vitro studies that have achieved recommitment and trans-differentiation of non-epidermal adult stem cells to the keratinocyte lineage. It can therefore be surmised that the use of exogenous cytokines, growth factors, chemicals, and ECM substrata to induce ES cell and nonepidermal adult stem cell commitment to the keratinocyte lineage is a relatively inefficient, time-consuming, and labor-intensive process that would require extensive selection and purification of the committed keratinocyte progenitors. Hence, it would be technically challenging to apply this to the clinical situation.

The other approach for inducing ES cell and non-epidermal adult stem cell commitment to the keratinocyte lineage is through genetic modulation. This may be achieved by transfecting stem cells with recombinant DNA constructs encoding for the expression of signaling proteins that promote commitment to the keratinocyte lineage. Of particular interest are the Lef-1/Tcf family of Wnt regulated transcription factors that act in concert with b-catenin,66, 67 c-myc which is a downstream target of the Wnt-signaling pathway,68, 69 and the transactivation domain containing isoform of transcription factor p63 (Tap63).70, 71 Interestingly, the transcription factor GATA-3, which is well known to be a key regulator of T-cell lineage determination, has also been shown to be essential for stem cell lineage determination in skin, where it is expressed at the onset of epidermal stratification and Inner Root Sheath (IRS) specification in follicles.72 Recombinant overexpression of p6373 and c-Myc74 has been reported to promote commitment and differentiation to the keratinocyte lineage.

The disadvantage of directing differentiation through genetic modulation is the potential risks associated with utilizing recombinant DNA technology in human clinical therapy. For example, the overexpression of any one particular protein within transfected stem cells would certainly have unpredictable physiological effects upon transplantation in vivo. This problem may be overcome by placing the recombinant expression of the particular protein under the control of switchable promoters, several of which have been developed for expression in eukaryotic systems. Such switchable promoters could be responsive to exogenous chemicals,75 heat shock,76 or even light.77 Genetically modified stem cells may also run the risk of becoming malignant within the transplanted recipient. Moreover, there are overriding safety concerns with regard to the use of recombinant viral based vectors in the genetic manipulation of stem cells.78 It remains uncertain as to whether legislation would ultimately permit the use of genetically modified stem cells for human clinical therapy. At present, the potential detrimental effects of transplanting genetically modified stem cells in vivo are not well studied. More research needs to be carried out on animal models to address the safety aspects of such an approach.

More recently, there is emerging evidence that some transcription factors (which are commonly thought of as cytosolic proteins) have the ability to function as paracrine cell to cell signaling molecules.79 This is based on intercellular transfer of transcription factors through atypical secretion and internalization pathways.79 Hence, there is an exciting possibility that transcription factors implicated in commitment to the keratinocyte lineage may in the future be genetically engineered to incorporate domains that enable them to participate in novel paracrine signaling mechanisms. This in turn would have tremendous potential for inducing the commitment of ES cells and non-epidermal adult stem cells to the keratinocyte lineage.

Skin appendages, including hair follicles, sebaceous glands and sweat glands, are linked to the epidermis but project deep into the dermal layer. The skin epidermis and its appendages provide a protective barrier that is impermeable to harmful microbes and also prevents dehydration. To perform their functions while being confronted with the physicochemical traumas of the environment, these tissues undergo continual rejuvenation through homeostasis, and, in addition, they must be primed to undergo wound repair in response to injury. The skins elixir for maintaining tissue homeostasis, regenerating hair, and repairing the epidermis after injury is its stem cells.

The hair follicle is composed of an outer root sheath that is contiguous with the epidermis, an inner root sheath and the hair shaft. The matrix surrounding the dermal papilla, in the hair root, contains actively dividing, relatively undifferentiated cells and is therefore a pocket of MSCs that are essential for follicle formation. The lower segment of each hair follicle cycles through periods of active growth (anagen), destruction (catagen) and quiescence (telogen).80 A specialized region of the outer root sheath of the hair follicle, known as the bulge, is located below the sebaceous gland, which is also the attachment site of the arrector pili muscle, receiving inputs from sensory nerve endings and blood vessels. Furthermore, the hair follicle bulge is a reservoir of slow-cycling multipotent stem cells.81, 82 Subsets of these follicle-derived multipotent stem cells can be activated and migrate out of hair follicles to the site of a wound to repair the damaged epithelium; however, they contribute little to the intact epidermis. These hair follicle stem cells can also contribute to the growth of follicles themselves and the sebaceous gland. For example, in the absence of hair follicle stem cells, hair follicle and sebaceous gland morphogenesis is blocked, and epidermal wound repair is compromised.83 In addition to containing follicle epidermal stem cells, the bulge contains melanocyte stem cells.84 Recent studies show that nestin, a marker for neural progenitor cells, is selectively expressed in cells of the hair follicle bulge and that these stem cells can differentiate into neurons,85 glia, keratinocytes, smooth muscle cells, melanocytes and even blood vessels.86, 87 Examination of close developmental and anatomical parallels between epithelial tissue and dermal tissue in skin and hair follicles has revealed dermal tissue to have stem cells. Paus et al. indicated that hair follicle dermal sheath cells might represent a source of dermal stem cells that not only incorporate into the hair-supporting papilla, low down in the follicle, but also move up and out from the follicle dermal sheath into the dermis of adjoining skin.88 Hair follicle dermal sheath cells taken from the human scalp can form new dermal papilla, induce the formation of hair follicles, and produce hair shafts when transplanted onto skin.89 There is also a clear transition from dermal sheath to dermal papilla cells.90 When the follicle dermal cells are implanted into skin wounds, they can be incorporated into the new dermis in a manner similar to that of skin wound-healing fibroblasts.91 However, these cell populations still lack specific markers for purifying and distinguishing the stem cells from their progeny. Furthermore, of prime importance is improving our understanding of the relation between bulge cells and interfollicular epidermal stem cells and between bulge cells and other stem cells inhabiting the skin and the mechanisms of hair growth.

Recently, cell replacement therapy has offered a novel and powerful medical technology for skin repair and regeneration: a new population of stem cell, called a neural crest stem cell, from adult hair follicles, was discovered to have the ability to differentiate in vitro to keratinocytes, neurons, cartilage/bone cells, smooth muscle cells, melanocytes, glial cells, and adipocytes.9296 In mammalian skin, skin-derived neural progenitors were isolated and expanded from the dermis of rodent skin and adult human scalp and could differentiate into both neural and mesodermal progeny.97, 98 Skin-derived neural progenitor cells were isolated based on the sphere formation of floating cells after 37 days of culture in uncoated flasks with epidermal growth factor and fibroblast growth factor, and characterized by the production of nestin and fibronectin, markers of neural precursors. In addition, skin-derived neural progenitor cells were identified as neural crest derived by the use of Wnt1 promoter driving LacZ expression in the mouse. Some of the LacZ-positive cells were found in the skin of the face, as well as in the dermis and dermal papilla of murine whisker.99 These skin derived neural crest cells have already shown promising results in regenerative medicine such as the promotion of regenerative axonal growth after transplantation into injured adult mouse sciatic nerves 95 or spinal cord repair,100 resulting in the recovery of peripheral nerve function. This new study marks an important first step in the development of real stem-cell-based therapies and skin tissue regeneration.

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Stem Cells for Skin Tissue Engineering and Wound Healing

Recommendation and review posted by Bethany Smith

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genucel - Intensive New Stem Cell Eye Therapy Treatment ...

Recommendation and review posted by Bethany Smith

Vista, Ca, (PRWEB) November 23, 2014

DC Labs, nationwide provider of the luxurious Ovation Cell Therapy, introduces new retail opportunity to their Salon Professional Division. Previously, the Ovation Hair product line was available exclusively online.

Ovation Hair launched their Salon Professional Division in 2013, to offer training and certification to licensed stylists interested in learning about the benefits of Cell Therapy as well as offer In-Salon treatments to their clients. The program was received with huge success and has grown exponentially since its inception.

Lead Stylist, Brenda Stearns explains, As Certified Cell Therapists, we have been requesting this retail opportunity with Ovation since we began offering In-Salon Cell Therapy Treatments. Based on years of salon experience, we were certain clients would want to walk out of the salon product in hand - once we introduced the amazing benefits of thicker, stronger, longer hair to them. Ms. Stearns continues, This is truly a fabulous opportunity for us as stylists as well as for our clientele.

Ovation Hair is releasing the entire line of hair care products to salons currently offering Cell Therapy Treatments. The complete Ovation hair care line includes shampoos, conditioners and styling products that address individual hair care needs based on hair condition and type.

Dallas Van Kempen, CEO at Ovation Hair and founder of the Salon Professional Division explains, When we initially launched this In-Salon program, I approached it as a unique inventory free opportunity. Allowing salon stylists to simply direct interested clients to the Ovation Hair website for purchasing product. I wanted to take the burden out of carrying inventory and stocking shelves. What we came to realize was that the salon client does not want to wait for their product to be shipped to them. Mr. Van Kempen continues, Now they dont have to. The option for non-inventory support will continue to be available.

Ovation expects in-salon retail offerings to grow as more salons nationwide provide Cell Therapy Treatments. To become a Certified Cell Therapist and offer Cell Therapy Treatments and retail product at your salon, please visit http://www.ovationpro.com.

About Ovation Hair The philosophy of Ovation Hair is to meet clients high expectations with quality, nourishing and rejuvenating products that demonstrate proven effectiveness. Ovation Hair has been helping clients achieve healthy hair since 2007. Their flagship product, Ovation Cell Therapy, is proven to deliver thicker, stronger, longer hair. Ovation products include high quality ingredients, demonstrated to be safe and effective to create healthy hair. The hair care products are developed as a natural alternative designed to rejuvenate hair to look thicker, stronger and longer. For more information visit http://www.ovationhair.com. ###

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Ovation Hair Introduces Retail Product to Salons

Recommendation and review posted by Bethany Smith

Catholic Edge Genetic Engineering HD
Video By: Austin Riordan.

By: Anna Landis

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Catholic Edge Genetic Engineering HD - Video

Recommendation and review posted by Bethany Smith

Might a GMO potato really be a better potato than can win over opponents of genetic engineering and feed the French fry minions? Image: J.R. Simply.

J.R. Simplot won federal approval for a genetically modified potato on Nov. 7, and although it is a major supplier of french fries to McDonald's , don't worry about some GMO spud showing up in your Happy Meal. The fast-food chain says it has no plans on adopting it anytime soon.

But that might not be the case for long.

Simplot says that because its new potato is made from genes derived from potatoes themselves and not bacteria or genes from other species, thus creating some sort of Frankenfood, it doesn't rise to the same level of concern activists would have over some crops, or when they thwarted Monsanto's effort to propagate a GMO potato in the 1990's.

Back then, Monsanto got the FDA to approve its New Leaf potatoes that were resistant to disease and insects through the development of a synthetic version of the bacillus thuringiensis bacterium, or Bt.

After initial acclaim, the biotech charged high premiums for its seed, which limited adoption, and then ultimately went nowhere when McDonald's and the Frito-Lay division of PepsiCo were cowed by anti-GMO activists into rejecting them. J.R. Simplot, an early adopter of the GMO potato, instructed its farmers not to plant them. Monsanto eventually stopped developing the potato in 2001.

Simplot's new Innate potatoes was developed to be especially beneficial to fast-food restaurants that sell lots of french fries. It's a little science-y, but it's important to understanding what Simplot is doing.

When potatoes and other starchy foods like bread (and even coffee!) are processed at high temperatures, such as when they're deep-fried, a carcinogenic chemical compound called acrylamide if formed.

Excerpt from:
A GMO Potato Is Approved, But Will Anyone Buy It?

Recommendation and review posted by Bethany Smith

The Blockheads Pro Tips SERIES 2: Tulip Genetics!
To start off the new series of Pro Tips, I show you how to use Tulip Genetics to make your own Tulip hybrids! SUBSCRIBE FOR A HIGH FIVE! http://bit.ly/1fPJDRC (/._.)/*(._.) JOIN SAM.BOYER...

By: Sam.Boyer

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The Blockheads Pro Tips SERIES 2: Tulip Genetics! - Video

Recommendation and review posted by Bethany Smith