June 6, 2013 A novel gene variant found in human and animal tissue may be a promising treatment for cancer, including breast and brain cancer, according to scientists from the Icahn School of Medicine at Mount Sinai. The variant, called PTEN-long, may contribute to a cell's healthy function and also suppress tumor cell development.

This landmark study is published in the June 6, 2013 issue of the journal Science.

Ramon Parsons, MD, PhD, Professor and Chair of Oncological Sciences led the team that discovered a mutation in the tumor suppressor gene PTEN, which has subsequently been recognized as the second most common mutation in cancer, especially in breast, prostate, and brain cancers. PTEN encodes a 403 amino acid lipid phosphatase protein that is critical to cellular growth, proliferation, and survival. Genetic inactivation of PTEN causes tumor development.

In the current study, Dr. Parsons and his team analyzed human cells and discovered a PTEN variant that has an additional protein sequence and is 43 percent longer than normal PTEN. They called this new variant PTEN-Long. Like PTEN, the long form has the same enzymatic activity, but unlike PTEN, it is secreted by the cell and can enter other cells, indicating that the added protein sequence acts as a delivery system for the tumor suppressor gene.

"This study culminates more than a decade of research that began soon after we learned the therapeutic potential of PTEN and the PI3K pathway," said Dr. Parsons. "We are excited about the potential of PTEN-Long as a therapy for multiple cancer types."

Using human breast and brain tumor cells that lacked PTEN and PTEN-Long, the research team introduced and overexpressed PTEN-Long and PTEN into the cells. They found that, similar to PTEN, PTEN-Long decreased the signaling activity on the PI3K pathway, thus reducing cellular proliferation. They also found that PTEN-Long was reduced in breast tumor tissue compared to healthy breast tissue.

To test the therapeutic potential of PTEN-Long, Dr. Parsons and his team injected mice with tumor cells, then administered PTEN-Long or a control preparation to the mice. For one of their tumor models, after five days of treatment, the tumors disappeared completely. The authors conclude that PTEN-Long alters signaling on the PI3K pathway to inhibit tumor growth and that its ability to enter other cells is critical to this process. As insulin operates on the PI3K pathway as well, the research team also noticed a brief increase in glucose concentration in the PTEN-Long treated mice.

"These findings indicate that PTEN-Long may contribute to cell homeostasis and suppression of cancer," said Dr. Parsons. "This gene variant has significant potential as a protein-based therapy to treat cancer, and may have implications in diseases such as diabetes."

Next, Dr. Parsons plans to study the normal functions of PTEN-Long, how tumors become resistant to it, what happens when it is missing, and how it can be used as a tool for therapy.

The work was funded by the NCI, The Octoberwoman Foundation, and the Avon Foundation.

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Gene variant may provide novel therapy for several cancer types

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Able to Walk Slowly After Severe Spinal Cord Injury by Instay Rehabilitation Center, Dubai
TSB, one of our patients for instay rehabilitation was admitted in Rochestter Wellness after severe spinal cord injury and had a RTA.Look how he is trying to walk slowly with support after...

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Able to Walk Slowly After Severe Spinal Cord Injury by Instay Rehabilitation Center, Dubai - Video

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June 4, 2013 In a pair of distinct but complementary papers, researchers at the University of California, San Diego School of Medicine and colleagues illuminate the functional importance of a relatively new class of RNA molecules. The work, published online this week in the journal Nature, suggests modulation of enhancer-directed RNAs or eRNAs could provide a new way to alter gene expression in living cells, perhaps affecting the development or pathology of many diseases.

Enhancers are sequences in the genome that act to boost or enhance the activity or expression of nearby genes. They often behave in a cell-specific manner and play an important role in establishing a cell's identity and functional potential, said Christopher Glass, MD, PhD, a professor in the department of Medicine and Cellular and Molecular Medicine at UC San Diego and principal investigator of one of the papers.

Although enhancers have been recognized for more than 25 years, scientists have labored to fully flesh out the breadth and complexity of what enhancers do and how they do it. In 2010, it was discovered that enhancers directed expression of RNA on a broad scale in neurons and macrophages, a type of immune system cell. Dubbed eRNAs, they were different from other classes of nuclear non-coding RNAs, and raised new questions about their potential roles in the functions of enhancers. The two Nature papers attempt to answer some of these questions.

In the first, principal investigator Glass and colleagues investigated a pair of related transcriptional repressors called Rev-Erb-alpha and Rev-Erb-beta (proteins with important roles in regulating the circadian rhythm in many cell types) in mouse macrophages. Using genome-wide approaches, they found that the Rev-Erb proteins repressed gene expression in macrophages primarily by binding to enhancers. Collaboration with researchers at the Salk Institute for Biological Studies revealed that the repressive function of Rev-Erbs was highly correlated with their ability to repress the production of eRNAs.

In the second paper, principal investigator Michael G. Rosenfeld, MD, a professor in the UC San Diego Department of Medicine and Howard Hughes Medical Institute investigator, and colleagues looked at estrogen receptor binding in human breast cancer cells and its impact on enhancer transcription. In contrast to the repressive functions of Rev-Erbs, estrogen receptors (ERs) activate gene expression; but, like Rev-Erbs, they primarily function by also binding to enhancers. ER binding was shown to be associated with increases in enhancer-directed eRNAs in the vicinity of estrogen-induced genes, and to exert roles on activation of coding target genes.

Both papers offer new evidence that eRNAs significantly contribute to enhancer activity, and therefore to expression of nearby genes. Because many broadly expressed genes that play key roles in essential cellular functions are under the control of cell-specific enhancers, the ability to affect enhancer function by knocking down eRNAs could potentially provide a new strategy for altering gene expression in vivo in a cell-specific manner, said Glass, noting that in his research, anti-sense oligonucleotides were developed in conjunction with Isis Pharmaceuticals, which suppressed enhancer activity and reduced expression in nearby genes.

Co-authors of the Glass paper are Michael T. Y. Lam, Hanna P. Lesch, David Gosselin, Sven Heinz, Yumiko Tanaka-Oishi, Christopher Benner, Minna U. Kaikkonen, Mika Kosaka and Cindy Y. Lee, Department of Cellular and Molecular Medicine, UCSD; Han Cho, Salk Institute for Biological Studies; Aneeza S. Kim, Andy Watt and Tamar R. Grossman, Isis Pharmaceuticals, Inc.; and Ronald M. Evans, Salk Institute for Biological Studies and Howard Hughes Medical Institute; and Michael G. Rosenfeld.

Funding for this research came, in part, from National Institutes of Health grants CA17390, U19DK62434, DK091183, DK063491 and CA52599.

Co-authors of the Rosenfeld paper are Wenbo Li, Dimple Notani, Esperanza Nunez, Aaron Yun Chen, Jie Zhang, Kenneth Ohgi, Xiaoyuan Song and Hong-Sook Kim, Howard Hughes Medical Institute, Department of Medicine, UCSD; Qi Ma and Daria Merkurjev, Howard Hughes Medical Institute, Department of Medicine, UCSD and Graduate Program in Bioinformatics, UCSD; Bogdan Tanasa, Howard Hughes Medical Institute, and The Scripps Research Institute; and Soohwan Oh, Howard Hughes Medical Institute, School of Biology, UCSD; and Christopher Glass.

Funding for this research came, in part, from the Howard Hughes Medical Institute and the National Institutes of Health grant CA17390.

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Enhancer RNAs alter gene expression: New class of molecules may be key emerging 'enhancer therapy'

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BALTIMORE, MD--(Marketwired - Jun 5, 2013) - Goldman Small Cap Research, a stock market research firm focused on the small cap and microcap sectors, believes that the low level of toxicity in the Nuvilex Inc. (OTCQB: NVLX)pancreatic cancertherapy could have a major impact in its cancer therapy emerging as a therapy of choice, if it is ultimately awarded FDA approval. The Company is an international firm engaged in live-cell encapsulation technology to treat pancreatic cancer along with the development and study of the use of medical marijuana for the treatment of oncology patients.

The results of Nuvilex's oft-cited Phase II pancreatic cancer trial of 14 patients demonstrated that the patients' median survival rate doubled compared to historical control and results of the current gold standard used today, which is Gemzar. Plus, the 1-year survival rate was triple that of control and double that of the standard Gemzar therapy. Perhaps the most telling component of the trial was the fact that only one-third of the standard chemotherapy dosage was used, thereby measurably increasing the patient quality of life as compared to other therapies.

For example, according to the Gemzar.com website, the side effects of using the treatment for pancreatic cancer are many, with varying ranges of severity.On the mild side, nausea, diarrhea, fever and hair loss are common in anywhere from 3:10 to 7:10 of patients.In addition, 7 out of 10 patients suffered from anemia, low white blood cell count, and changes in their liver function tests.

In future tests, Nuvilex will likely use stand-alone Gemzar therapy as a comparator. But, if earlyNuvilex results are an indication, it is not just efficacy that could serve patients well, but if combined with an approved low toxicity due to the reduced chemotherapy dosage, clinicians and patients could seek out the treatment in droves.

A copy of this article as well as other articles and Nuvilex reports can be accessed by visiting http://www.goldmanresearch.com.

About Goldman Small Cap Research: Led by former Piper Jaffray analyst and mutual fund manager Rob Goldman, Goldman Small Cap Research produces small cap and micro cap stock research reports, daily stock market blogs, and popular investment newsletters.For more information, visit http://www.goldmanresearch.com.

A Goldman Small Cap Research report is not intended as an offering, recommendation, or a solicitation of an offer to buy or sell the securities mentioned or discussed.Please read the report's full disclosures and analyst background on our website before investing. Neither Goldman Small Cap Research nor its parent is a registered investment adviser or broker-dealer with FINRA or any other agency. To download our research, view our disclosures, or for more information, visit http://www.goldmanresearch.com.

About Nuvilex, Inc. (OTCQB: NVLX): Nuvilex, Inc. has been a provider of all-natural products for many years, has expanded its company to increase its natural product based footprint through medical marijuana studies and is becoming an international biotechnology provider of live, therapeutically valuable, encapsulated cells and services for treatments, research and medicine. The Company's offerings will ultimately include cancer, diabetes and other clinical treatments using the company's natural product knowledge, product base, cell and gene therapy expertise, and live-cell encapsulation technology in addition to other new products currently under development. For more information visit: http://www.nuvilex.com.

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Low Level of Toxicity a Major Plus for Nuvilex's Pancreatic Cancer Therapy

Recommendation and review posted by Bethany Smith

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/cn2vq9/cell_therapy) has announced the addition of Jain PharmaBiotech's new report "Cell Therapy - Technologies, Markets and Companies" to their offering.

This report describes and evaluates cell therapy technologies and methods, which have already started to play an important role in the practice of medicine. Hematopoietic stem cell transplantation is replacing the old fashioned bone marrow transplants. Role of cells in drug discovery is also described. Cell therapy is bound to become a part of medical practice.

Stem cells are discussed in detail in one chapter. Some light is thrown on the current controversy of embryonic sources of stem cells and comparison with adult sources. Other sources of stem cells such as the placenta, cord blood and fat removed by liposuction are also discussed. Stem cells can also be genetically modified prior to transplantation.

Cell therapy technologies overlap with those of gene therapy, cancer vaccines, drug delivery, tissue engineering and regenerative medicine. Pharmaceutical applications of stem cells including those in drug discovery are also described. Various types of cells used, methods of preparation and culture, encapsulation and genetic engineering of cells are discussed. Sources of cells, both human and animal (xenotransplantation) are discussed. Methods of delivery of cell therapy range from injections to surgical implantation using special devices.

Cell therapy has applications in a large number of disorders. The most important are diseases of the nervous system and cancer which are the topics for separate chapters. Other applications include cardiac disorders (myocardial infarction and heart failure), diabetes mellitus, diseases of bones and joints, genetic disorders, and wounds of the skin and soft tissues.

Regulatory and ethical issues involving cell therapy are important and are discussed. Current political debate on the use of stem cells from embryonic sources (hESCs) is also presented. Safety is an essential consideration of any new therapy and regulations for cell therapy are those for biological preparations.

The cell-based markets was analyzed for 2012, and projected to 2022. The markets are analyzed according to therapeutic categories, technologies and geographical areas. The largest expansion will be in diseases of the central nervous system, cancer and cardiovascular disorders. Skin and soft tissue repair as well as diabetes mellitus will be other major markets.

The number of companies involved in cell therapy has increased remarkably during the past few years. More than 500 companies have been identified to be involved in cell therapy and 289 of these are profiled in part II of the report along with tabulation of 278 alliances. Of these companies, 160 are involved in stem cells. Profiles of 72 academic institutions in the US involved in cell therapy are also included in part II along with their commercial collaborations. The text is supplemented with 55 Tables and 12 Figures. The bibliography contains 1,050 selected references, which are cited in the text.

Key Topics Covered:

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Research and Markets: Cell Therapy - Technologies, Markets and Companies - Updated 2013-2022 Global Report

Recommendation and review posted by Bethany Smith

Public release date: 3-Jun-2013 [ | E-mail | Share ]

Contact: Scott LaFee slafee@ucsd.edu 619-543-6163 University of California - San Diego

In a pair of distinct but complementary papers, researchers at the University of California, San Diego School of Medicine and colleagues illuminate the functional importance of a relatively new class of RNA molecules. The work, published online this week in the journal Nature, suggests modulation of "enhancer-directed RNAs" or "eRNAs" could provide a new way to alter gene expression in living cells, perhaps affecting the development or pathology of many diseases.

Enhancers are sequences in the genome that act to boost or "enhance" the activity or expression of nearby genes. They "often behave in a cell-specific manner and play an important role in establishing a cell's identity and functional potential," said Christopher Glass, MD, PhD, a professor in the department of Medicine and Cellular and Molecular Medicine at UC San Diego and principal investigator of one of the papers.

Although enhancers have been recognized for more than 25 years, scientists have labored to fully flesh out the breadth and complexity of what enhancers do and how they do it. In 2010, it was discovered that enhancers directed expression of RNA on a broad scale in neurons and macrophages, a type of immune system cell. Dubbed eRNAs, they were different from other classes of nuclear non-coding RNAs, and raised new questions about their potential roles in the functions of enhancers. The two Nature papers attempt to answer some of these questions.

In the first, principal investigator Glass and colleagues investigated a pair of related transcriptional repressors called Rev-Erb-alpha and Rev-Erb-beta (proteins with important roles in regulating the circadian rhythm in many cell types) in mouse macrophages. Using genome-wide approaches, they found that the Rev-Erb proteins repressed gene expression in macrophages primarily by binding to enhancers. Collaboration with researchers at the Salk Institute for Biological Studies revealed that the repressive function of Rev-Erbs was highly correlated with their ability to repress the production of eRNAs.

In the second paper, principal investigator Michael G. Rosenfeld, MD, a professor in the UC San Diego Department of Medicine and Howard Hughes Medical Institute investigator, and colleagues looked at estrogen receptor binding in human breast cancer cells and its impact on enhancer transcription. In contrast to the repressive functions of Rev-Erbs, estrogen receptors (ERs) activate gene expression; but, like Rev-Erbs, they primarily function by also binding to enhancers. ER binding was shown to be associated with increases in enhancer-directed eRNAs in the vicinity of estrogen-induced genes, and to exert roles on activation of coding target genes.

Both papers offer new evidence that eRNAs significantly contribute to enhancer activity, and therefore to expression of nearby genes. "Because many broadly expressed genes that play key roles in essential cellular functions are under the control of cell-specific enhancers, the ability to affect enhancer function by knocking down eRNAs could potentially provide a new strategy for altering gene expression in vivo in a cell-specific manner," said Glass, noting that in his research, anti-sense oligonucleotides were developed in conjunction with Isis Pharmaceuticals, which suppressed enhancer activity and reduced expression in nearby genes.

###

Co-authors of the Glass paper are Michael T. Y. Lam, Hanna P. Lesch, David Gosselin, Sven Heinz, Yumiko Tanaka-Oishi, Christopher Benner, Minna U. Kaikkonen, Mika Kosaka and Cindy Y. Lee, Department of Cellular and Molecular Medicine, UCSD; Han Cho, Salk Institute for Biological Studies; Aneeza S. Kim, Andy Watt and Tamar R. Grossman, Isis Pharmaceuticals, Inc.; and Ronald M. Evans, Salk Institute for Biological Studies and Howard Hughes Medical Institute; and Michael G. Rosenfeld.

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Enhancer RNAs alter gene expression

Recommendation and review posted by Bethany Smith

A new cancer drug for patients with the same faulty gene as actress Angelina Jolie has shown "impressive responses" in a clinical trial, researchers have said.

The potential drug, called BMN 673, targets DNA repair in cancer cells and is designed to attack tumours that have been left vulnerable by genetic mutations.

BRCA genes were brought into the public consciousness last month after Jolie, 37, revealed she underwent a double mastectomy when doctors told her that her faulty gene - BRCA1 - meant she had an 87% risk of developing breast cancer and a 50% risk of ovarian cancer.

Scientists studying BMN 673 found the drug was "well tolerated" by patients and showed "excellent anti-tumour activity", the Institute of Cancer Research (ICR) and the Royal Marsden NHS Foundation Trust said.

The results of the trial - which was funded by US firm BioMarin Pharmaceutical and involved the University of Newcastle and several American institutions - were presented at the American Society of Clinical Oncology (Asco) meeting in Chicago.

Some 70 patients with a range of cancers, including ovarian or peritoneal, and breast, were monitored, and patients with cancers linked to BRCA mutations saw the most substantial improvement.

The researchers used different measures of the drug's effect on tumour instability and breakdown.

One was a clinical score called Recist, which included a range of measures such as whether visible lesions, or cracks, appear in the walls of tumours after treatment.

Some 11 of 25 evaluable ovarian cancer patients with BRCA mutations had a Recist-positive response to treatment, as did seven of 18 breast cancer patients with BRCA mutations.Signs of some clinical benefit were seen in several more patients, the experts said.

BRCA mutations reduce cells' ability to repair their DNA, and when inherited substantially increase the risk of developing a range of cancers, including breast, ovarian and prostate.

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Jolie gene drug trial 'impressive'

Recommendation and review posted by Bethany Smith

RESEARCH TRIANGLE PARK, N.C.--(BUSINESS WIRE)--

Precision BioSciences, Inc., a leader in the field of genome engineering, today announced that it has filed a patent infringement lawsuit against Lonza Group (LONN.VX) and a number of its affiliates in the U.S. District Court for the District of Delaware. The lawsuit seeks a ruling that Lonzas importation into the United States and the use, offer for sale, and sale in the United States of the GS XceedTM Gene Expression System and CHOK1SV knock-out cell line infringe U.S. Patent No. 8,377,674 (the 674 patent), which applies Precision BioSciences Directed Nuclease EditorTM genome editing technology. The lawsuit requests monetary damages as well as a permanent injunction preventing Lonza from importing the GS XceedTM Gene Expression System and CHOK1SV knock-out cell line into the United States and from using, selling or offering to sell those materials in the United States.

Precision prefers to focus its business development efforts in a positive and productive manner, said Matthew Kane, CEO of Precision BioSciences. However, willful infringement of Precisions proprietary gene editing technology cannot be tolerated. The GS XceedTM Gene Expression System competes directly with Precision's GS knockout system that we developed using our award-winning Directed Nuclease EditorTM technology. We cannot allow Lonza to import, market, and sell a product developed using our intellectual property to customers in the United States without a license to do so.

Today, Precision controls a rapidly growing patent estate consisting of eighteen issued genome engineering patents. Precisions European and Australian patents claim methods that are similar to those claimed in the 674 patent. Certain of the European and Australian patent claims describe methods for modifying DNA in cells, such as the CHOK1SV cell line, using an engineered meganuclease.

About Precision BioSciences

Precision BioSciences mission is to continually provide, improve, and enable the worlds most powerful genome engineering technology. Precisions proprietary Directed Nuclease EditorTM (DNE) technology enables the production of genome editing enzymes that can insert, remove, modify, and regulate essentially any gene in mammalian or plant cells.

Precision BioSciences vision is to be the conduit through which the worlds greatest genome engineering challenges are solved. Precision has successfully utilized its DNE technology to create innovative products in partnerships with many of the worlds largest biopharmaceutical and agbiotech firms. Internally, Precision is developing DNE-based products for biologics manufacturing and human therapeutics. For additional information, please visit http://www.precisionbiosciences.com.

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Precision BioSciences Files Patent Infringement Lawsuit against Lonza Related to GS XceedTM Gene Expression System

Recommendation and review posted by Bethany Smith

Public release date: 5-Jun-2013 [ | E-mail | Share ]

Contact: Press Office comunicacion@cnio.es Centro Nacional de Investigaciones Oncologicas (CNIO)

Researchers are still fascinated by the idea of the possibility of reprogramming the cells of any tissue, turning them into cells with the capacity to differentiate into cells of a completely different type pluripotent cellsand they are still striving to understand how it happens.

A group from the Spanish National Cancer Research Centre (CNIO), headed by researcher Ralph P. Schneider, from the Telomeres and Telomerase Group led by Maria A. Blasco, publishes this week an article in Nature Communications on the discovery of a new gene called TRF1 that is essential for nuclear reprogramming.

It is also known that TRF1 is indispensable for protecting telomeres, the ends of chromosomes. Existing evidence suggests that the length of telomeres and pluripotencythe capacity of a cell to differentiate into multiple cell typesare related. Pluripotent cells, for example, have very long telomeresa previous finding at CNIObut until now no protective protein for the telomeres had been found that was essential for pluripotency.

To investigate the connection between telomeres and pluripotency, researchers generated a 'reporter' mouse: they linked together the TRF1 gene and the gene coding for a green fluorescent protein and created a lineage of mice carrying this new genetic baggage. In these animals, the green fluorescent protein acts as a label to show expression of TRF1.

They discovered that TRF1 is an excellent marker for stem cells, both in adult stem cellsthose that are found in tissues and the different organs of the bodyand embryonic stem cells. It is also the case with 'induced pluripotent' stem cells (iPS cells), which are pluripotent cells that come from artificially reprogrammed specialised cells.

In the case of tissues, the authors write: "TRF1 distinguishes adult stem cells and is indispensable for their functioning". The discovery is useful for both identifying and eventually isolating the stem cell population in tissues, something that is important for the development of regenerative medicine. The cells in which TRF1 is expressed are also the most pluripotent.

In iPS cells, the same thing happens. The authors explain that: "The expression of TRF1 is an indicator of pluripotency. Those iPS cells that express the highest levels of TRF1 are also the most pluripotent. Furthermore, we demonstrate that TRF1 is necessary for the induction and maintenance of pluripotency, inhibiting the triggering of DNA damage responses and apoptosis ('cell suicide')".

###

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CNIO researchers identify a new gene that is essential for nuclear reprogramming

Recommendation and review posted by Bethany Smith

Beijing, June 5 (IANS) Scientific experts and representatives from the World Anti-Doping Agency (WADA) and the International Olympic Committee (IOC) Wednesday met here to review the progress in combatting gene and cell doping.

Two of the experts, one in anti-doping area and another in gene therapy, believed that gene doping may not exist right now but the threat looms, reports Xinhua.

"Gene therapy is still in a very early stage, which makes me believe that there should not be athletes gene doping. But WADA is right to prepare a test as gene therapy is developing so fast that this sort of doping is a potential threat," said Beijing anti-doping lab head Xu Youxuan.

More than 70 experts, both home and abroad, attended the June 5-6 Gene and Cell Doping Symposium to discuss recent findings and solutions to combat the threat of athletes manipulating their genes to enhance their sports performance.

The symposium was organised by WADA in conjunction with China Anti-Doping Agency and Beijing Olympic City Development Association.

A difference from previous three meetings in New York in 2002, Stockholm in 2005 and St. Petersburg in 2008 is that discussion on cell doping became one of the meeting's agenda.

Beijing You'an Hospital chief Li Ning considered cell doping a more realistic threat than gene doping.

"The science for cell doping is less complicated than gene doping," said Li, taking blood transfusion as an example.

"After blood cells are tampered outside an athlete's body, the blood can have increased red blood cells and be transferred back to the body which is liking using EPO for an athlete," he said.

"As for gene doping, I believe it does not exist now but will appear in a near future," he added. Li heads a research project on the cutting-edge gene therapy to cure cancer. His research group has discovered the ADV-TK virus that can stop cancer cells from reproducing.

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Experts think gene doping not yet in existence

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Javascript is currently disabled in your web browser. For full site functionality, it is necessary to enable Javascript. In order to enable it, please see these instructions. 57 minutes ago by Lisa M. Krieger

The world's last passenger pigeons perished a century ago. But a Santa Cruz, Calif.-based research project could send them flocking into the skies again, using genetic engineering to restore the once-abundant species and chart a revival for other long-gone creatures.

The promise and peril of "resurrection biology" - which could bring back other long-gone species such as the woolly mammoth and Tasmanian tiger but runs the risk of undermining conservation efforts - was the topic for experts who gathered Friday at Stanford University's Center for Law and the Biosciences.

"The grand goal is to bring the passenger pigeon back to life," said researcher Ben Novak of Revive and Restore, supported by entrepreneur Stewart Brand's Long Now Foundation of San Francisco and conducted at the University of California at Santa Cruz. "We're at the baby step of stage one."

After studying old and damaged gene fragments of 70 dead passenger pigeons in the lab of UCSC professor Beth Shapiro, the team will assemble - in computers - the genetic code of the bird once hunted to extinction. They hope to complete that within a year.

Within two years, they plan to synthesize the actual DNA code, using commercially available nucleotides. This material will be inserted into the embryo of the passenger pigeon's closest living relative, a band-tailed pigeon.

Then there will be new challenges, Shapiro said.

"We need to turn it into a creature. We have to raise a captive breeding herd. Then there is the tricky part of going from a captive breeding bird to a live, thriving population in the wild," she said.

Passenger pigeons once numbered in the billions, blackening the skies and inspiring naturalists like John James Audubon, John Muir and Aldo Leopold. They had vanished by the first World War, victims of hunting and habitat loss.

But resurrected flocks reintroduced into a modern environment could be an invasive species, noted Andrew Torrance of the University of Kansas Law School. They also would be genetically modified organisms, subject to federal regulation.

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Extinct species revival raises hopes, fears

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June 4, 2013 Using a novel genetic 'editing' technique, Duke University biomedical engineers have been able to repair a defect responsible for one of the most common inherited disorders, Duchenne muscular dystrophy, in cell samples from Duchenne patients.

Instead of the common gene therapy approach of adding new genetic material to "override" the faulty gene, the Duke scientists have developed a way to change the existing mutated gene responsible for the disorder into a normally functioning gene. The Duke researchers believe their approach could be safer and more stable than current methods of gene therapy.

The researchers are now conducting further tests of this new approach in animal models of the disease.

Duchenne muscular dystrophy is a genetic disease affecting one in 3,600 newborn males. The genetic mutation is found on the X chromosome, of which males have only one copy. (Females, with two X chromosomes, presumably have at least one good copy of the gene.)

Patients with Duchenne muscular dystrophy cannot produce the protein known as dystrophin, which is essential in maintaining the structural integrity of muscle fibers. Over time, patients with the disorder suffer gradual muscle deterioration, which leads to paralysis and eventual death, usually by age 25.

"Conventional genetic approaches to treating the disease involve adding normal genes to compensate for the mutated genes," said Charles Gersbach, assistant professor of biomedical engineering at Duke's Pratt School of Engineering and Department of Orthopaedic Surgery and member of Duke's Institute for Genome Sciences and Policy. "However, this can cause other unforeseen problems, or the beneficial effect does not always last very long.

"Our approach actually repairs the faulty gene, which is a lot simpler," said David Ousterout, the Duke biomedical engineering graduate student in the Gersbach lab who led the work. "It finds the faulty gene, and fixes it so it can start producing a functional protein again."

The results of the Duke study were published online in Molecular Therapy, the journal of the American Society for Gene and Cell Therapy. The project was supported by the Hartwell Foundation, the March of Dimes Foundation and the National Institutes of Health.

The Duke experiments, which were carried out in cell samples from Duchenne muscular dystrophy patients, were made possible by using a new technology for building synthetic proteins known as transcription activator-like effector nucleases (TALENs), which are artificial enzymes that can be engineered to bind to and modify almost any gene sequence.

These TALENs bind to the defective gene, and can correct the mutation to create a normally functioning gene.

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Genetic editing shows promise in Duchenne muscular dystrophy

Recommendation and review posted by Bethany Smith

MADISON, Wis., June 5, 2013 /PRNewswire/ --Cellular Dynamics International (CDI) today announced that it has expanded its MyCell Products line, offering access to a number of human disease models and licensing key genetic engineering patents from Life Technologies and Sigma-Aldrich. CDI's MyCell Products include custom cell products manufactured using induced pluripotent stem cell (iPSC) technology to make stem cells or differentiated cells from any individual, including those with diseases of interest to pharmaceutical and academic researchers.

CDI's MyCell Products now offer access to a number of disease models, including cardiomyopathies and arrhythmias, vision disorders, neurological disorders, and muscular dystrophies. In addition, the company is actively working on expanding its disease model offering, currently working on additional disease models for neurodegenerative disorders and drug-induced liver injury (DILI).

Within the MyCell Products line, CDI maintains the iPSC line of each of the disease models, enabling customers to request manufacture of differentiated cells, such as cardiomyocytes, neurons, hepatocytes, and endothelial cells, for their discovery research.

In addition, CDI has licensed Life Technologies' GeneArt Precision TALs (TALENs) and Sigma's CompoZr ZFN technologies, which act like genomic scissors to cut DNA in a precise location. These nuclease technologies facilitate efficient genomic editing by creating double-stranded breaks in DNA at user-specified locations, stimulating the cell's natural repair process and enabling targeted gene insertions, deletions, or modifications. CDI will use the TALENs and ZFN technologies to perform genetic engineering specified by the customer, for example to introduce or correct a specific mutation, thus creating human disease models and isogenic controls.

"This expansion of the MyCell Products line is the next step in our growing disease-in-a-dish portfolio and allows our customers more ready access to diseases of interest from our growing catalog of iPSCs," said Chris Parker, CDI chief commercial officer. "Through the MyCell Products line, researchers can now access human disease models either through creation of iPSC-derived cells directly from a patient, or through inducing a disease state via use of these TALEN or ZFN technologies."

Bob Palay, CDI chief executive officer, said, "CDI's commercial goal has been to provide access to human cells that reproduce human biology, and we see both of these developments as steps toward achieving that goal. We're pleased to license these nuclease technologies from Life Technologies and Sigma-Aldrich, and the combination of these nuclease technologies with CDI's iPSC-derived cells creates a new, powerful tool to better understand and target human disease."

About Cellular Dynamics International, Inc.Cellular Dynamics International, Inc. (CDI) is a leading developer of stem cell technologies for in vitro use in drug discovery, toxicity testing and chemical safety, in vivo and cell-based therapeutic research and stem cell banking. CDI harnesses its unique manufacturing technology to produce differentiated tissue cells in industrial quality, quantity and purity from any individual's stem cell line created from a standard blood draw. CDI was founded in 2004 by Dr. James Thomson, a pioneer in human pluripotent stem cell research at the University of Wisconsin-Madison. CDI's facilities are located in Madison, Wisconsin. CDI's headquarters are located in Madison, Wisconsin, with a second facility in Novato, California. See http://www.cellulardynamics.com.

Follow us on Twitter @CellDynamics or http://www.twitter.com/celldynamics

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Cellular Dynamics International Expands MyCell Products Line with Disease Models, Genetic Engineering Patents

Recommendation and review posted by Bethany Smith

Q: When is a Jew, not a Jew?
A: When he is Jewish, according to the latest Genetic DNA research carried out by Dr. Eran Elhaik #39; #39;a Jew" and associates at the McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins...

By: TheWatchman144K

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Q: When is a Jew, not a Jew? - Video

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Public release date: 4-Jun-2013 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 ext. 2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, June 4, 2013The composition of breast milk varies from mother to mother, and genetic factors may affect the levels of protective components in breast milk that could influence a newborn's outcomes. The potential to perform genomic studies on breast milk samples is explored in a Review article in Breastfeeding Medicine, the Official Journal of the Academy of Breastfeeding Medicine, published by Mary Ann Liebert, Inc., publishers. The article is available free on the Breastfeeding Medicine website at http://www.liebertpub.com/bfm.

Kelley Baumgartel and Yvette Conley, University of Pittsburgh, PA, reviewed the scientific literature to determine whether breast milk is an appropriate source for genetic materialDNA and RNAto perform gene expression and epigenetic studies.

In the article "The Utility of Breast Milk for Genetic or Genomic Studies: A Systematic Review," the authors describe the potential value of the genetic information obtained from breast milk, which can be collected easily and noninvasively. It could lead to a better understanding of the variability in breast milk and to strategies for optimizing the neonatal diet through fortification of donor breast milk, supplementation of the mother's diet, or maternal lifestyle changes that would affect breast milk composition.

"The great majority of mothers produces milk that matches the needs of her infant amazingly well," says Associate Editor David S. Newburg, PhD, Professor, Department of Biology, Boston College, Chestnut Hill, MA. "But for those few infants with exceptional needs, such as premature infants, or for mothers with uncommon mutations whose milk lacks the full complement of beneficial components, genetic and genomic analysis would both identify the mismatch and provide the information to produce a personalized complementary fortifier or supplement."

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About the Journal

Breastfeeding Medicine, the Official Journal of the Academy of Breastfeeding Medicine (http://www.bfmed.org), is an authoritative, peer-reviewed journal published bimonthly in print and online. In 2014 the Journal will be publishing 10 issues per year. The Journal publishes original scientific papers, reviews, and case studies on a broad spectrum of topics in lactation medicine. It presents evidence-based research advances and explores the immediate and long-term outcomes of breastfeeding, including the epidemiologic, physiologic, and psychological benefits of breastfeeding. Tables of content and a sample issue may be viewed on the Breastfeeding Medicine website at http://www.liebertpub.com/bfm.

About the Publisher

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Can genetic analysis of breast milk help identify ways to improve a newborn's diet?

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Newswise BIRMINGHAM, Ala. A newfound genetic marker promises to better predict warfarin dose in African-Americans, according to a study published online today in The Lancet. If confirmed in further studies, the finding may help to avert more of the bleeds and blood clots that come when a patients starting dose misses the drugs narrow safety window.

First approved for use in 1954, the blood thinner warfarin effectively prevents clots but must be dosed carefully. A too-high starting dose can cause internal bleeding, while an insufficient dose may fail to protect against clots. In a hint at the promise of pharmacogenomics, inexpensive, 59-year-old warfarin may become more valuable each time a newly identified genetic marker makes more accurate algorithms used to predict dose for each patient.

As it stands, most physicians start patients on a standard five-milligram dose, closely monitor their clotting speed and adjust their dose based on it. The effort to reach a safe dose is complicated by the 20-fold variability in dose requirements observed in African Americans. The best available dosing models miss their mark often enough that warfarin causes a third of U.S. hospital visits related to drug side effects in patients aged 65 and older, with nearly two thirds of them due to bleeds.

Seeking to fix the problem, three previous genome-wide association studies (GWAS) sought to identify genetic factors that could improve warfarin dose prediction, but none of them included patients of African ancestry. That makes the current study, a seventeen-institution effort led by the University of Florida (UF), the first GWAS of its kind. The University of Alabama at Birmingham (UAB) was the largest enrolling center in the study, with local demographics and a tradition of tackling disparities best positioning it to recruit African-American patients.

Our goal is to help more patients arrive at their optimal dose more quickly, said Nita Limdi, Pharm.D., Ph.D., associate professor in the Department of Neurology within the UAB School of Medicine and co-first author of the study. As the field continues to identify genetic variations that affect dose, knowing which patients dont have certain variations will be as valuable as knowing which do.

Genome-wide association studies look at differences at many points in the genetic code to see if, across a population, one or more variations are found more often in those with a given trait, be it high risk for a disease or lower needed drug dose. The current study found that a single genetic variation is associated with a 20 percent warfarin dose reduction in people of African ancestry, an effect not present in patients of European or Asian ancestry. When incorporated into dosing algorithms, the new variant enabled the prediction of dose with 21 percent greater accuracy than the standard formula.

Clinic by clinic, doctors are starting to check genetic codes as a first step in determining each patients disease risk, likelihood of benefiting from a given drug or best dose, said Julie Johnson, director of the Center for Pharmacogenomics at the University of Florida and corresponding author for The Lancet publication. As this revolution unfolds, we need to ensure that all share in the benefits.

Where to start?

Clotting prevents small injuries from causing extended bleeds, but it can also be triggered by diseases like atrial fibrillation and cancer, as well as by surgery, aging and inactivity. Once formed, clots can float through the circulatory system to clog blood vessels elsewhere, causing heart attacks, strokes or pulmonary emboli. For these reasons, 33 million Americans got a prescription for warfarin in 2012 for the treatment and prevention of clots.

One reason warfarin is still the most widely prescribed anticoagulant, instead of newer, more easily tolerated drugs like dabigatran, rivaroxaban and apixaban, is its low cost. As a mainstay in the treatment of the underinsured in the United States, and for patients in developing countries, especially in Africa, making warfarin safer remains a priority.

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Genetic Marker Enables Better Prediction of Warfarin Dose in Patients of African Ancestry

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Genetics Introduction Video Ryan

By: Ryan Hart

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Genetics Introduction Video Ryan - Video

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MENLO PARK, Calif.--(BUSINESS WIRE)--

Personalis, Inc. today announced that it will be exhibiting at the European Society of Human Genetics Conference in Paris, France beginning Sunday, June 9, 2013. Personalis will launch its Genome Services for Research and Clinical samples, focusing on accuracy in sequencing, analysis, and interpretation of human genomes to the European market.

Personalis Genome Services include our Accuracy and Content Enhanced (ACE) Exome technology. Using additional custom targeted capture, we aim to finish genes in the medical exome and add medically interpretable content outside the exons. This has been shown to benefit work in medical genetics, pediatrics, cardiology, neurology, psychiatry, pharmacogenomics, and other areas of medicine.

Clinical quality genome interpretation also requires accurate and comprehensive databases of genetic variation. Personalis has the largest and most comprehensive manually-curated database in the world linking genetic variation with disease. We have also signed an exclusive license for commercialization of PharmGKB, the premier database linking genetic variation with drug metabolism and adverse events. Personalis also annotates genomes with information from over 30 databases. When combined with Personalis ACE (Accuracy and Content Enhanced) Technology for exome sequencing and powerful variant calling algorithms, researchers and clinicians are able to rapidly obtain the most comprehensive sequence analysis available. Personalis CEO, John West, stated We are pleased to extend this offering to the European community and are committed to expanding our global footprint to enable researchers and clinicians worldwide to take advantage of our products.

About Personalis

Personalis provides researchers and clinicians accurate DNA sequencing and interpretation of human genomes. Our ACE (Accuracy and Content Enhanced) Technology can supplement a standard exome or genome, substantially increasing its medically-relevant coverage and accuracy. Personalis builds on that with innovativealgorithms and proprietary databases for alignment, variant calling, annotation, and analysis. With this combination, we provide genomic data and interpretation of the highest accuracy.

Personalis has an exceptional team of scientific, medical and industry experts. Our R&D team brings directly relevant commercial experience from seven different DNA sequencing companies and scientific & medical expertise from the top universities in the world. This group has been deeply involved in many of the advances of recent years, and has a long track record of peer reviewed publications. We see enormous potential in human genome sequencings next big step: accurate interpretation.

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Personalis Announces Participation in the European Society of Human Genetics Conference

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LOS ANGELES, June 4, 2013 (GLOBE NEWSWIRE) -- Response Genetics, Inc. (RGDX), a company focused on the development and sale of molecular diagnostic tests that help determine a patient's response to cancer therapy, today announced that it has achieved its second milestone payment in conjunction with the non-exclusive license agreement originated in 2010 with GlaxoSmithKline ("GSK").

Under the terms of the agreement, GSK gained certain rights to Response Genetics' proprietary PCR analysis technology and diagnostic expertise to assess BRAF gene mutations in human tumor samples. Response Genetics earned its first milestone payment of $500,000 in July of 2012 for submission of the first Premarket Approval ("PMA") under the contract. On May 29, 2013, GSK announced the FDA's approval of the PMA, thereby triggering the second milestone payment of $500,000.

The BRAF gene is responsible for a protein involved in cell signaling, growth and differentiation. Specific mutations in the gene are found in a subset of patients with melanoma.Tafinlar(R) has been approved to treat melanoma that cannot be surgically removed or metastatic melanoma in adults with the V600E mutation of BRAF. Tafinlar(R) is not indicated for patients with wild-type BRAF melanoma.

"We are extremely pleased to have assisted GSK in achieving this very important milestone," said Thomas A. Bologna, Chairman and CEO of Response Genetics. "Response Genetics supports pharmaceutical companies by providing lab-developed tests that are critical for screening and stratifying patients during clinical development. The insights that emerge from our work, such as the association between the specific mutations of BRAF and response to Tafinlar(R), enable the practice of precision medicine, the selection of a cancer treatment based on the molecular characteristics of a patient's tumor."

About Response Genetics, Inc.

Response Genetics, Inc. (the "Company") is a CLIA-certified clinical laboratory focused on the development and sale of molecular diagnostic testing services for cancer. The Company's technologies enable extraction and analysis of genetic information derived from tumor cells stored as formalin-fixed and paraffin-embedded specimens. The Company's principal customers include oncologists and pathologists. In addition to diagnostic testing services, the Company generates revenue from the sale of its proprietary analytical pharmacogenomic testing services of clinical trial specimens to the pharmaceutical industry. The Company's headquarters is located in Los Angeles, California. For more information, please visit http://www.responsegenetics.com.

Forward-Looking Statement Notice

Except for the historical information contained herein, this press release and the statements of representatives of the Company related thereto contain or may contain, among other things, certain forward-looking statements, within the meaning of the Private Securities Litigation Reform Act of 1995.

Such forward-looking statements involve significant risks and uncertainties. Such statements may include, without limitation, statements with respect to the Company's plans, objectives, projections, expectations and intentions, such as the ability of the Company, to provide clinical testing services to the medical community, to continue to strengthen and expand its sales force, to continue to build its digital pathology initiative, to attract and retain qualified management, to continue to strengthen marketing capabilities, to expand the suite of ResponseDX(R) products, to continue to provide clinical trial support to pharmaceutical clients, to enter into new collaborations with pharmaceutical clients, to enter into areas of companion diagnostics, to continue to execute on its business strategy and operations, to continue to analyze cancer samples and the potential for using the results of this research to develop diagnostic tests for cancer, the usefulness of genetic information to tailor treatment to patients, and other statements identified by words such as "project," "may," "could," "would," "should," "believe," "expect," "anticipate," "estimate," "intend," "plan" or similar expressions.

These statements are based upon the current beliefs and expectations of the Company's management and are subject to significant risks and uncertainties, including those detailed in the Company's filings with the Securities Exchange Commission. Actual results, including, without limitation, actual sales results, if any, or the application of funds, may differ from those set forth in the forward-looking statements. These forward-looking statements involve certain risks and uncertainties that are subject to change based on various factors (many of which are beyond the Company's control). The Company undertakes no obligation to publicly update forward-looking statements, whether because of new information, future events or otherwise, except as required by law.

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Response Genetics Achieves Milestone Payments Totaling $1,000,000 for Services Provided to GlaxoSmithKline in the ...

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SEATTLE, WA--(Marketwired - Jun 5, 2013) - Atossa Genetics, Inc. (NASDAQ: ATOS), The Breast Health Company, announced today that Peter J. Carbonaro has joined the Company as Senior Vice President of Operations, a newly created position. Mr. Carbonaro's primarily focus and responsibilities include regulatory, quality, manufacturing, supply chain, IT, Facilities and Human Resources. He reports to Dr. Steven Quay, Chairman, CEO & President.

A veteran diagnostic/medical device/biotechnology industry decision maker, Mr. Carbonaro brings more than 30 years' experience in process development, supply chain and manufacturing. This includes expertise in product development, technology transfer, manufacturing and supply chain at a number of prominent companies including Gilead Sciences and Hoffmann LaRoche as well as several early stage companies.

"The Company is very fortunate to have Peter Carbonaro join us as at this pivotal time as we continue to ramp up sales and manufacturing of our ForeCYTE Breast Health Test," said Dr. Quay. "Peter's extensive industry experience and in-depth operations and manufacturing expertise will be invaluable in helping us make the ForeCYTE test available to millions of women across America."

"Atossa Genetics has the potential to change the way we think about breast cancer risk assessment and prevention and I am excited to join the Atossa team to help make the ForeCYTE test and other products and services developed by the Company become the standard of care," said Mr. Carbonaro. "I am honored to join the Atossa team to drive our success for the benefit of women in the fight against breast cancer."

Prior to joining Atossa Genetics, Mr. Carbonaro (54) served as Vice President, Operations, at Ondine Biomedical, Inc. from 2011 to 2013. From 2006 to 2011, Mr. Carbonaro served in increasingly responsible positions at Gilead Sciences, Inc., including Director of Manufacturing in Seattle, Washington; Director of Manufacturing in Ireland; Director of Global Operational Excellence, Pharmaceutical Manufacturing and Senior Director, Pharmaceutical Manufacturing. Earlier, Mr. Carbonaro served from 2001 to 2006 as Senior Director of Manufacturing for Corus Pharma, which was acquired by Gilead Sciences in 2006. From 1997 to 2001, Mr. Carbonaro was Vice President of Operations at Bartel, Inc., which was later acquired by Trinity Biotech.

Mr. Carbonaro began his career at Roche Diagnostic Systems, Inc., Belleville, New Jersey, where he served as Production Manager, Senior Group Leader and Associate Scientist. Mr. Carbonaro also served as Vice President of Operations and Director of Operations at Aprogenix, Inc., based in Houston, prior to joining Bartels.

Mr. Carbonaro holds an MBA in Organizational Behavior from Iona College and a BS degree in biology from Siena College.

On June 3, 2013, and as an inducement to cause Mr. Carbonaro to join the Company, he was awarded an option to purchase a total of 250,000 shares of common stock of the Company, par value $0.001 per share, 163,000 of which are outside the Company's 2010 Stock Option and Incentive Plan. The stock option has an exercise price equal to $4.58 per share, the fair market value on the grant date and vests over a four-year period from his commencement of service. This stock option was granted as an inducement material to Mr. Carbonaro's entering into employment with the Company and is being reported in accordance with NASDAQ Listing Rule 5635(c)(4).

About Atossa Genetics, Inc.

Atossa Genetics, Inc. (NASDAQ: ATOS), The Breast Health Company, based in Seattle, WA, is focused on preventing breast cancer through the commercialization of patented, FDA-designated Class II diagnostic medical devices and patented, laboratory developed tests (LDT) that can detect precursors to breast cancer up to eight years before mammography.

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Peter J. Carbonaro Joins Atossa Genetics as Senior Vice President of Operations

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Transhumanism Intro - (Sneak Peek)
http://www.jeremiahfilms.com The world is shifting, the "global consciousness" is moving towards a global system of technology, innovation, and communication...

By: JeremiahFilms

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Transhumanism Intro - (Sneak Peek) - Video

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Mickey #39;s Before After Stemlogix Stem Cell Therapy
Mickey, a 13 year old German Shepherd torn both of his ACLs and suffered from severe arthritis. Mickey has been treated with Stemlogix Stem Cell Therapy Platelet Max Platelet Rich Plasma...

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Mickey's Before

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Fibroblast Growth Factor FGF Stem Cell Therapy
Fibroblast Growth Factor Heals Heart Tissue by Feeding Stem Cells present.

By: David Dolores

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Fibroblast Growth Factor FGF Stem Cell Therapy - Video

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Thumb Arthroscopy with Stem Cell Therapy
Hand surgeon Dr. Michael Fitzmaurice details the thumb arthroscopy procedure that he pioneered, involving an endoscopic approach and stem cell therapy (PRP) ...

By: Michael Fitzmaurice

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Thumb Arthroscopy with Stem Cell Therapy - Video

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Sarasota, Florida (PRWEB) June 03, 2013

Guy DaSilva, MD, ABAARM, will begin conducting clinical trials for many degenerative diseases using adipose-derived stem cell therapy at the DaSilva Institute in Sarasota, Florida. The independent review board of the International Stem Cell Society will oversee the trials.

Following the IRB-approved protocols, Dr. DaSilva will treat patients suffering from chronic obstructive pulmonary disease (COPD), Type 2 Diabetes, osteoarthritis, critical limb ischemia and erectile dysfunction. Furthermore, Alzheimers disease, dementia and Parkinsons disease are pending approval, and approximately five new protocols are added each month.

While stem cell therapy is most often associated with the controversial use of embryonic stem cells, Dr. DaSilva will be exclusively using adult autologous stem cells, harvested from the patients own adipose (fat) tissue or bone marrow if fat is not available. Because patients are receiving their own cells, there is no risk of rejection, and success rates are far greater compared to the more contentious therapies.

Autologous stem cell therapy works by mimicking the bodys natural healing process, but at a more potent, concentrated level. Stem cells, which are unspecialized cells with the potential to develop into any cell, are stored throughout the body. When disease or injury strikes, the body sends these cells to the area in need, and they begin repairing and replacing damaged tissue. Stem cell function decreases with age, along with ones ability to heal. But with autologous stem cell therapy, the body is once again empowered to heal and reverse disease, and with much greater magnitude.

Dr. DaSilva trained under scientist Kristin Comella, Chief Science Officer of Bioheart, CEO of Stemlogix, Chief Scientific Officer of the Ageless Regenerative Institute, and was recently named one of the 50 most influential people on stem cells. Dr. DaSilva will implement Comellas patented extraction process to precisely isolate and remove stem cells from fat tissue, allowing for an exceptionally high yield and viability.

During the in-office procedure, a mini liposuction is performed on the patient to remove 60 milliliters of fat, which produces approximately 8 million stem cells. The stem cells are isolated and injected back into the patients body at the site of injury or disease. Only local anesthesia is needed, and the patient will go home pain-free.

Over the next month, the patients body will repair and regenerate itself naturally. Dr. DaSilva will continue to treat the patient, with therapies that range from high dose IV nutrition and heavy metal chelation to bio-identical hormones. This helps the body maintain a healthy environment to further promote cellular and mitochondrial healing.

According to Dr. DaSilva, autologous stem cell therapy is very promising. He says, This extraordinary therapy is going to change the face of medicine. For example, it has the capability to completely reverse Type 2 Diabetes with a single dose, allowing patients to avoid amputations, premature death, and a life of food monitoring and injections. The results are truly remarkable, and this is only the beginning.

About Guy DaSilva, MD, ABAARM

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Sarasota's Dr. Guy DaSilva Introduces Cutting-Edge Stem Cell Therapy For Degenerative Diseases

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