SALT LAKE CITY, Oct. 29, 2013 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) today announced that it has launched a new prognostic test, Myriad myPlan Lung Cancer, for patients diagnosed with early-stage lung adenocarcinoma. myPlan Lung Cancer is an RNA expression panel of 31 cell-cycle-progression genes, in combination with tumor staging information, to determine a patient's risk of dying from lung cancer within five years.

The myPlan Lung Cancer test has been extensively studied in more than 1,500 patients. In these studies, myPlan Lung Cancer was shown to be significantly predictive of five-year lung cancer mortality and considerably more predictive than tumor staging information alone. In a large validation study presented at the IASLC annual meeting, patients with a high-risk myPlan Lung Cancer score had nearly twice the rate of lung cancer deaths (35 percent) than patients with a low-risk score (18 percent). These findings build on data published in Clinical Cancer Research that showed the myPlan Lung Cancer test is the strongest independent predictor of survival in patients with early-stage lung cancer as compared to the conventional clinical variables of disease progression including age, stage of disease, gender, smoking status and tumor size.

"Post-surgical treatment decisions for early-stage lung cancer patients are largely guided by tumor staging. However, the prognostic power of tumor stage alone is limited and there remain unacceptably high mortality rates for this patient population," said Mark C. Capone, president of Myriad Genetics Laboratories. "Myriad myPlan Lung Cancer is a powerful new prognostic test that stratifies patients based on their risk of lung cancer-related, five-year mortality. Our test will empower physicians to know with confidence which patients should receive surgery alone versus those who may need more aggressive therapy."

Myriad myPlan Lung Cancer is being launched in a phased approach beginning with an early-access, clinical-experience program to medical and scientific thought leaders, followed by a full commercial launch in calendar year 2014. myPlan Lung Cancer will be sold through Myriad's own specialty sales force to assist physicians in providing their lung cancer patients with the most appropriate healthcare management. myPlan Lung Cancer has a list price of $3,400.

Myriad myPlan Lung Cancer is the second molecular diagnostic test launched by Myriad this fiscal year. In September, the Company launched Myriad myRisk(TM) Hereditary Cancer, a new multi-gene diagnostic test for eight major hereditary cancers including breast, colorectal, ovarian, endometrial, pancreatic, prostate, gastric and melanoma.

About Myriad Genetics

Myriad Genetics is a leading molecular diagnostic company dedicated to making a difference in patients' lives through the discovery and commercialization of transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess risk of disease progression and recurrence. Myriad's molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a commitment to improving an individual's decision making process for monitoring and treating disease. Myriad is focused on strategic directives to introduce new products, including companion diagnostics, as well as expanding internationally. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

Myriad, the Myriad logo and Myriad myPlan Lung Cancer, Myriad myRisk Hereditary Cancer, are trademarks or registered trademarks of Myriad Genetics, Inc. in the United States and foreign countries. MYGN-F, MYGN-G.

Safe Harbor Statement

This press release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to Myriad myPlan Lung Cancer being launched in a phased approach beginning with an early-access, clinical-experience program to medical and scientific thought leaders, followed by a full commercial launch in calendar year 2014; Myriad myPlan Lung Cancer being sold through Myriad's own specialty sales force to assist physicians in providing their lung cancer patients with the most appropriate healthcare management; Myriad myPlan Lung Cancer being an important new molecular diagnostic tool that will help physicians in predicting the aggressiveness of early-stage lung adenocarcinoma in conjunction with conventional clinical parameters; and the Company's strategic directives under the caption "About Myriad Genetics". These "forward-looking statements" are management's present expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those described in the forward-looking statements. These risks include, but are not limited to: the risk that sales and profit margins of our existing molecular diagnostic tests and companion diagnostic services may decline or will not continue to increase at historical rates; risks related to changes in the governmental or private insurers reimbursement levels for our tests; the risk that we may be unable to develop or achieve commercial success for additional molecular diagnostic tests and companion diagnostic services in a timely manner, or at all; the risk that we may not successfully develop new markets for our molecular diagnostic tests and companion diagnostic services, including our ability to successfully generate revenue outside the United States; the risk that licenses to the technology underlying our molecular diagnostic tests and companion diagnostic services tests and any future tests are terminated or cannot be maintained on satisfactory terms; risks related to delays or other problems with operating our laboratory testing facilities; risks related to public concern over our genetic testing in general or our tests in particular; risks related to regulatory requirements or enforcement in the United States and foreign countries and changes in the structure of the healthcare system or healthcare payment systems; risks related to our ability to obtain new corporate collaborations or licenses and acquire new technologies or businesses on satisfactory terms, if at all; risks related to our ability to successfully integrate and derive benefits from any technologies or businesses that we license or acquire; risks related to increased competition and the development of new competing tests and services; the risk that we or our licensors may be unable to protect or that third parties will infringe the proprietary technologies underlying our tests; the risk of patent-infringement claims or challenges to the validity of our patents; risks related to changes in intellectual property laws covering our molecular diagnostic tests and companion diagnostic services and patents or enforcement in the United States and foreign countries, such as the Supreme Court decision in the lawsuit brought against us by the Association for Molecular Pathology et al; risks of new, changing and competitive technologies and regulations in the United States and internationally; and other factors discussed under the heading "Risk Factors" contained in Item 1A of our most recent Annual Report on Form 10-K filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in our Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.

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Google Exec Ray Kurzweil Says Robots Will Keep Us Alive | The Rubin Report
Google engineering director and futurist Ray Kurzweil believes we are close to realizing everlasting life and is making it his mission to get us there. This ...

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Bolton, UK (PRWEB UK) 29 October 2013

According to the BBC, the University Hospital in Birmingham are trialing a new gene therapy hospital treatment, aiding in the fight against prostate cancer (1). The pioneering treatment could help prevent the incidence of surgical errors, increasing the success rate associated with treating the disease.

It is believed, that if the treatment works, surgery for prostate cancer will become a thing of the past, eliminating the surgical errors associated with the procedure.

According to the BBC, the University Hospital in Birmingham is among the first to trial the new treatment, stimulating the bodys own immune system to attack the tumor (1). With studies on mice showing complete eradication of the cancer, hopes are high for the imminent human trials.

A new form of gene therapy, the treatment requires a virus to be injected directly into the prostate cancer tumour; a gene attached to the virus (GM-CSF,) is then released, activating the body's own immune system, attracting white blood cells to attack the cancer (1). As reported by the BBC, the virus also carries an enzyme - nitroreductase - which sits inside the cancer cell.

Two days after the injection, the patient in question will be put on a drip, which contains a cancer drug (CB1954), which is initially inactive. When the drug comes into contact with the enzyme, it reacts and starts killing the cancer cells. The inactive drug, CB1954, does not harm cells which do not have the enzyme inside, protecting the healthy tissue surrounding the tumour (1).

Urology Specialist, Prashant Patel, is hopeful that gene therapy could provide real hope for patients who are running out of treatment options (1).

"I have to stress that this is only a phase one safety trial to test that there are no side effects. However, we are excited by this."

"If this works, 15 to 20 years from now, we could be using the patient's own immune system in this way to fight early onset prostate cancer so that patients won't need painful treatments or even surgery."

Considering the procedure, Asons Executive, Laura Williams

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Newswise Scientists in The Research Institute at Nationwide Childrens Hospital have found a way to overcome one of the biggest obstacles to using viruses to deliver therapeutic genes: how to keep the immune system from neutralizing the virus before it can deliver its genetic payload. In a study published recently in Molecular Therapy, researchers found that giving subjects a treatment to temporarily rid the body of antibodies provides the virus safe passage to targeted cells, allowing it to release a corrective or replacement gene to treat disease.

Gene therapy is among the most promising treatment options for such genetic disorders as muscular dystrophy, congenital blindness and hemophilia. Scientists also are investigating gene therapy as a cure for some cancers, neurodegenerative diseases, viral infections and other acquired illnesses. To get the therapeutic gene into cells, researchers have turned to viruses, which deliver their genetic material into cells as part of their normal replication process. Time and time again, these efforts have been thwarted by the bodys own immune system, which attacks the viral vector. The therapeutic genes arent delivered and disease rages on.

Now, a team led by Louis G. Chicoine, MD, Louise Rodino-Klapac, PhD, and Jerry R. Mendell, MD, principal investigators in the Center for Gene Therapy at Nationwide Childrens, has shown for the first time that using a process called plasmapheresis just before delivering a virus-packed gene therapy protects the virus long enough for it to enter the cell and deliver the gene.

Plasmapheresis, widely used to treat patients with autoimmune disorders, removes blood from the body, separates the plasma and cells, filters out antibodies, and returns the blood to the patient. The antibody loss is temporary; the body begins producing new antibodies within a few hours of the procedure.

In a study of a gene therapy designed to treat Duchenne muscular dystrophy (DMD), Drs. Chicoine and Rodino-Klapac used plasmapheresis in a large animal model, then injected a virus packed with a micro-dystrophin gene. When they examined the levels of micro-dystrophin gene expression in the animals, they found a 500 percent percent increase over gene expression in animals that did not receive plasmapheresis. Dr. Mendell, director of the Center for Gene Therapy, helped conceive of this treatment for DMD patients based on experience with autoimmune diseases such as myasthenia gravis and inflammatory nerve diseases.

Right now, gene therapy seems to work best in patients who have no antibodies for the virus being used to deliver the gene, Dr. Mendell says. That limits the number of patients who can benefit from gene therapy.

Using plasmapheresis would increase the potential for gene therapy, Dr. Chicoine adds, by eliminating one obstacle of immune reaction.

As gene therapy becomes more prevalent, patients may need to receive more than one treatment, Dr. Rodino-Klapac says. The problem is that when they get the first treatment, their body will develop antibodies to the virus used to deliver the gene. Using plasmapheresis on someone who previously received gene therapy could allow them to be treated again.

Full citation: L. G. Chicoine, C. L. Montgomery, W. G. Bremer, K. M. Shontz, D. A. Griffin, K. N. Heller, S. Lewis, V. Malik, W.E. Grose, C. J. Shilling, K. J. Campbell, T. J. Preston, B. D. Coley, P. T. Martin, C. M. Walker, K. R. Clark, Z. Sahenk, J. R. Mendell, and L. R. Rodino-Klapac, Plasmapheresis eliminates the negative impact of AAV antibodies on micro-dystrophin gene expression following vascular delivery. Molecular Therapy. Epub 2013 Oct 23. doi:10.1038/mt.2013.244.

Funding: This research was supported by grants from the Childrens Hospital Foundation; National Institutes of Health; Senator Paul D. Wellstone Muscular Dystrophy Cooperative Research Center Grant at Nationwide Childrens Hospital; Muscular Dystrophy Association; and Jesses Journey Foundation for Gene and Cell Therapy.

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THURSDAY, Oct. 24 (HealthDay News) -- Obesity is on the rise among children, and a particular genetic mutation might play a role for some kids, a new study suggests.

Researchers in Britain conducted genetic analyses of more than 2,100 severely obese youngsters. They found that those with mutations in the KSR2 gene had larger appetites and slower metabolism than those with a normal copy of the gene, according to the study published in the Oct. 24 issue of the journal Cell.

"Changes in diet and levels of physical activity underlie the recent increase in obesity; however, some people gain weight more easily than others," study author Sadaf Farooqi, of the University of Cambridge, noted in a journal news release. "This variation between people is largely influenced by genetic factors. The discovery of a new obesity gene, KSR2, demonstrates that genes can contribute to obesity by reducing metabolic rate -- how well the body burns calories."

The findings could someday lead to new treatments for obesity and type 2 diabetes, the researchers said.

Farooqi and colleagues had previously found that deleting the KSR2 gene led to obesity in mice, highlighting the gene's role in controlling energy balance and metabolism. These findings confirm KSR2's role in the regulation of weight and metabolism in humans.

"This work adds to a growing body of evidence that genes play a major role in influencing a person's weight and may be useful for developing new ways to treat people who are heavy and develop diabetes," Farooqi said.

More information

The American Academy of Pediatrics has more about childhood obesity.

Copyright 2013 HealthDay. All rights reserved.

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A rare childhood disease may hold clues to treating Alzheimer's and Parkinson's, a study has found.

Scientists analysing A-T disease, which leaves youngsters unable to walk by adolescence, have found new ways of understanding the more common neurodegenerative diseases, according to the report in the online journal Nature Neuroscience.

Children born with A-T have mutations in both of their copies of the ATM gene and cannot make normal ATM protein, and experts at Rutgers University in New Jersey in the US hope their research will lead to new therapies for Alzheimer's and Parkinson's.

The rare genetic childhood disorder - which occurs in about one in 40,000 births - leads to problems in movement, co-ordination, equilibrium and muscle control as well as a number of other deficiencies outside the nervous system.

Using mouse and human brain tissue studies, the researchers from Rutgers found that without ATM, the levels of a regulatory protein known as EZH2 go up.

Looking through the characteristics of A-T disease in cells in tissue culture and in brain samples from both humans and mice with ATM mutation, they found that the increase in EZH2 was a major contributing factor to the neuromuscular problems caused by A-T.

Plan a conversation in a familiar, non-threatening environment

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PUBLIC RELEASE DATE:

28-Oct-2013

Contact: Holly Evarts holly.evarts@columbia.edu 347-453-7408 Columbia University

New York, NYOctober 28, 2013: Researchers at Columbia Engineering, led by Chemical Engineering Professors Venkat Venkatasubramanian and Sanat Kumar, have developed a new approach to designing novel nanostructured materials through an inverse design framework using genetic algorithms. The study, published in the October 28 Early Online edition of Proceedings of the National Academy of Sciences (PNAS), is the first to demonstrate the application of this methodology to the design of self-assembled nanostructures, and shows the potential of machine learning and "big data" approaches embodied in the new Institute for Data Sciences and Engineering at Columbia.

"Our framework can help speed up the materials discovery process," says Venkatasubramanian, Samuel Ruben-Peter G. Viele Professor of Engineering, and co-author of the paper. "In a sense, we are leveraging how nature discovers new materialsthe Darwinian model of evolutionby suitably marrying it with computational methods. It's Darwin on steroids!"

Using a genetic algorithm they developed, the researchers designed DNA-grafted particles that self-assembled into the crystalline structures they wanted. Theirs was an "inverse" way of doing research. In conventional research, colloidal particles grafted with single-stranded DNA are allowed to self-assemble, and then the resulting crystal structures are examined. "Although this Edisonian approach is useful for a posteriori understanding of the factors that govern assembly," notes Kumar, Chemical Engineering Department Chair and the study's co-author, "it doesn't allow us to a priori design these materials into desired structures. Our study addresses this design issue and presents an evolutionary optimization approach that was not only able to reproduce the original phase diagram detailing regions of known crystals, but also to elucidate previously unobserved structures."

The researchers are using "big data" concepts and techniques to discover and design new nanomaterialsa priority area under the White House's Materials Genome Initiativeusing a methodology that will revolutionize materials design, impacting a broad range of products that affect our daily lives, from drugs and agricultural chemicals such as pesticides or herbicides to fuel additives, paints and varnishes, and even personal care products such as shampoo.

"This inverse design approach demonstrates the potential of machine learning and algorithm engineering approaches to challenging problems in materials science," says Kathleen McKeown, director of the Institute for Data Sciences and Engineering and Henry and Gertrude Rothschild Professor of Computer Science. "At the Institute, we are focused on pioneering such advances in a number problems of great practical importance in engineering."

Venkatasubramanian adds, "Discovering and designing new advanced materials and formulations with desired properties is an important and challenging problem, encompassing a wide variety of products in industries addressing clean energy, national security, and human welfare." He points out that the traditional Edisonian trial-and-error discovery approach is time-consuming and costlyit can cause major delays in time-to-market as well as miss potential solutions. And the ever-increasing amount of high-throughput experimentation data, while a major modeling and informatics challenge, has also created opportunities for material design and discovery.

The researchers built upon their earlier work to develop what they call an evolutionary framework for the automated discovery of new materials. Venkatasubramanian proposed the design framework and analyzed the results, and Kumar developed the framework in the context of self-assembled nanomaterials. Babji Srinivasan, a postdoc with Venkatasubramanian and Kumar and now an assistant professor at IIT Gandhinagar, and Thi Vo, a PhD candidate at Columbia Engineering, carried out the computational research. The team collaborated with Oleg Gang and Yugang Zhang of Brookhaven National Laboratory, who carried out the supporting experiments.

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PALO ALTO, Calif.--(BUSINESS WIRE)--

EMD Serono, a subsidiary of Merck KGaA, Darmstadt, Germany, and Open Monoclonal Technology, Inc. (OMT), a leader in the genetic engineering of animals for development of human therapeutic antibodies, today announced expansion of their collaboration agreement from June 2012. Under the terms of the new agreement, EMD Serono will make an upfront payment to secure unlimited access to the OmniRat platform as well as success-based development milestones and royalties. Further details of the contract are not being disclosed.

The expansion of our collaboration with OMT is reflective of its strong quality and the significant progress we've made together over the last 15 months," said Dr. Annalisa Jenkins, Executive Vice President and head of Global Research & Development for Merck Serono, a biopharmaceutical division of Merck KGaA, Darmstadt, Germany. This is a good example of our focus on exploring targeted partnerships with innovative companies such as OMT, with the goal of generating access to technologies that advance our capabilities in biotech development.

Dr. Roland Buelow, founder and CEO of OMT, said: "EMD Seronos transition to unlimited platform access is evidence of their success with OmniRat on multiple therapeutic targets during the past 15 months. The expansion illustrates how OMT provides its partners with access to complementary platforms for discovery of superior antibodies against challenging targets in a cost-effective fashion.

About Merck KGaA

Merck is a leading pharmaceutical, chemical and life science company with total revenues of 11.2 billion in 2012, a history that began in 1668, and a future shaped by approximately 38,000 employees in 66 countries. Its success is characterized by innovations from entrepreneurial employees. Merck's operating activities come under the umbrella of Merck KGaA, in which the Merck family holds an approximately 70% interest and free shareholders own the remaining approximately 30%. In 1917 the US subsidiary Merck & Co. was expropriated and has been an independent company ever since. For more information, please visit http://www.merckserono.com or http://www.merckgroup.com.

About EMD Serono, Inc.

EMD Serono, Inc., a subsidiary of Merck KGaA, Darmstadt, Germany, is a specialized biopharmaceutical company dedicated to developing therapies with ground breaking potential. The company has strong market positions in neurology, endocrinology and reproductive health. In addition, EMD Serono has an enduring commitment to solve the unsolvable, with state-of-the-art science dedicated to developing new therapies in the core focus areas of neurology, oncology, immune oncology and immunology. With a long-standing history of industry expertise and a dedication to shape the future of healthcare, the companys US footprint continues to grow, with approximately 1,000 employees around the country and fully integrated commercial, clinical and research operations in its home state, Massachusetts. For more information, please visit http://www.emdserono.com.

Open Monoclonal Technology, Inc.

Open Monoclonal Technology, Inc. (OMT) is a leader in genetic engineering of animals for discovery of human therapeutic antibodies naturally optimized human antibodies.

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EMD Serono and Open Monoclonal Technology Expand Collaboration to Include Unlimited Access to OmniRat® Human Antibody ...

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SALT LAKE CITY, Oct. 28, 2013 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) today announced that validation data for the Myriad myPlan Lung Cancer test showed that it significantly predicted patients' risk of death from early-stage lung adenocarcinoma within five years of being diagnosed. A key finding of the validation study is that patients with a high-risk myPlan prognostic score had approximately twice the number of lung cancer related deaths compared to patients with a low-risk score.

Myriad is presenting these results and another myPlan clinical study this week at the International Association for the Study of Lung Cancer (IASLC) 15th World Conference on Lung Cancer in Sydney, Australia. myPlan Lung Cancer is the only prognostic test on the market today that can assess a patient's risk of lung cancer mortality and thereby guide the physician in determining which patients may benefit from post-surgical chemotherapy.

"The Myriad myPlan Lung Cancer test provides new information that can identify people at high risk of lung cancer recurrence and will enable us to offer these patients additional therapy to improve their survival," said Raphael Bueno, M.D., Associate Chief of Thoracic Surgery at Brigham and Women's Hospital and Harvard Medical School. "Once we know a patient's risk profile, we can align our clinical management strategies to achieve better medical outcomes and save more lives."

The two studies being presented at the IASLC annual meeting are:

Validation of a Proliferation-based Expression Signature as Prognostic Marker in Early Stage Lung Adenocarcinoma. [Bueno et al., Poster: Oct. 28, 2013, 3:30 p.m. -- 4:15 p.m. AEDT]

This study evaluated the association of cell cycle progression (CCP) genes with five-year lung cancer mortality in 650 patients diagnosed with stage 1 or 2 lung adenocarcinoma. In this clinical validation study, patients with a high-risk Myriad myPlan Lung Cancer prognostic score had a significantly higher average five-year mortality rate (35 percent) than patients with a low-risk score (18 percent). The prognostic score (CCP + tumor stage) segregated stage 1A to 2B patients with five-year risk estimates ranging from 11 percent to 68 percent. This study demonstrated that the myPlan Lung Cancer prognostic score was statistically significant in predicting five-year lung cancer mortality, and was significantly more predictive than tumor staging information alone. These data strongly support the use of the Myriad myPlan Lung Cancer test to help stratify patients' risk profiles and determine which patients are candidates for conservative management with surgery alone versus more intensive therapy based on a higher personal risk profile.

Integrated Prognosis in Early-Stage Resectable Lung Adenocarcinoma. [Kim et al., Poster: Oct. 30, 2013, 3:30 p.m. -- 4:15 p.m. AEDT]

This study evaluated a prognostic model that combines a cell cycle progression (CCP) score with tumor stage in order to maximize the prognostic utility of both predictive markers. The primary outcome measure was cancer specific death within five years of surgery. The results for this study show that both tumor stage and CCP score are statistically significant independent predictors of lung cancer death. However, the combination of tumor stage and the CCP expression score was a more powerful predictor of post-surgical risk of cancer-specific death than tumor stage alone. Myriad myPlan Lung Cancer is a prognostic test that combines CCP score and tumor stage and offers clinicians a more precise risk assessment of patients with early-stage lung cancer, which may improve medical management of these patients.

About Myriad Genetics

Myriad Genetics is a leading molecular diagnostic company dedicated to making a difference in patients' lives through the discovery and commercialization of transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess risk of disease progression and recurrence. Myriad's molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a commitment to improving an individual's decision making process for monitoring and treating disease. Myriad is focused on strategic directives to introduce new products, including companion diagnostics, as well as expanding internationally. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

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LOS ANGELES--(BUSINESS WIRE)--

Life Stem Genetics Inc., an emerging innovator in the advancement of Adult Stem Cell therapy, is pleased to announce that Matthew Sullivan, COO of global heath products company Asana International, and Shahab Bakhtyar, an independent medical business consultant with global experience, have joined Life Stems Executive Advisory Board.

Established earlier this year, the Executive Advisory Board has become a cornerstone of Life Stems global stem-cell growth model by actively retaining influential business leaders with broad backgrounds in corporate development and finance in our targeted industries with a focus on business expansion into Canada, Europe, Asia, and the Middle East.

Matthew Sullivan, BA, MBA, is a corporate finance specialist who has worked with numerous early-stage and well-established companies in operations as well as strategic and financial planning. Matthews background is in venture capital and business analysis. His role has ranged from business planning/implementation, M&A, market analysis to operational implementation. He is currently COO of Asana International, a global health products company, CFO of Kat Gold Holdings, a publicly traded gold production and exploration company based in Ghana, and CFO of Travelvu, a business that places smart devices in hotel rooms. Matthew holds a Bachelor of Arts degree from the University of British Columbia, Canada, and an MBA from Dalhousie University, Canada.

Shahab Bakhtyar, MBA, is an independent business consultant with a focus on expansion and financing of small to medium sized businesses. In the last 15 years, Mr. Bakhtyars consultancy has focused mainly on Western Canada where he includes medical/health service providers among his clientele. Prior to establishing his business in Canada, Mr. Bakhtyar worked in Dubai, UAE. Included among his clients were Emirate Air and FIFA to whom he provided marketing and advertising services. Mr. Bakhtyar holds an MBA from Queens University, Canada. He has traveled to over 63 countries and maintains a strong international network of business contacts with a focus throughout the Middle East and Canada.

The addition of Matthew and Shahab to our advisory board aligns with our goal of developing a team of advisors who share our core values and can help us attain our growth initiatives in the rapidly advancing Adult Stem Cell therapy business sector, says Gloria Simov, president and CEO of Life Stem Genetics. Life Stem will greatly benefit from the depth of industry expertise and overall business acumen that both Matthew and Shahab bring, and we look forward to their value-added contributions as we continue to build our base of stem cell clinics throughout the world.

About Life Stem Genetics

Life Stem Genetics (LSG) is a progressive healthcare company focused on Adult Stem Cell (ASC) healing therapies. For decades, stem cells have been utilized in the successful treatment of a variety of ailments. Today, advanced ASC therapies are being offered to patients as an efficient and painless alternative treatment for a wide range of ailments including, but not limited to, orthopedic injuries, neurological disorders such as Parkinsons and Alzheimers, cancer, arthritis, diabetes, multiple sclerosis, as well as age management. Adult Stem Cell therapies and LSGs proprietary techniques are experiencing some of the best results in the industry in helping to repair or reprogram damaged or diseased tissues and organs. Life Stems ASC specialist has performed thousands of stem cell treatments including some of the top names in PGA golf, NFL football, NBA basketball, and Major League Baseball. LSG will offer its proprietary treatments through a series of affiliate doctors and medical clinics with 60 affiliated clinics thus far. LSGs mission is to develop a comprehensive approach to the treatment and maintenance of diseases while breaking free from the medical insurance maze by tapping into an affordable private-pay sector.

Contrarian Press, the publisher, has been engaged by Life Stem Genetics to assist with identification of potential market participants who may be interested in learning more about the company and its securities. Updated disclaimer and disclosure information is available at the publisher's website listed above and at the following link:

http://www.contrarianwealthcoalition.com/guide/LIFS.pdf

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RUTHERFORD, N.J., Oct. 28, 2013 (GLOBE NEWSWIRE) -- Cancer Genetics, Inc. (CGIX), a diagnostics company focused on developing genomic-based, oncology tests and services, today announced the closing of its previously announced public offering of 3,286,700 shares of its common stock (including 428,700 shares that were offered and sold by Cancer Genetics pursuant to the exercise in full of the underwriters' over-allotment option) at a price to the public of $14.00 per share. The gross proceeds to Cancer Genetics from the offering were $46 million, before underwriting discounts and commissions and other offering expenses payable by Cancer Genetics.

Aegis Capital Corp. acted as sole book-running manager for the offering.

Feltl and Company, Inc., Cantor Fitzgerald & Co. and Dougherty & Company acted as co-managers for the offering.

This offering was made only by means of a prospectus.

A copy of the prospectus relating to this offering may be obtained by contacting Aegis Capital Corp., Prospectus Department, 810 Seventh Avenue, 18th Floor, New York, NY 10019, telephone: 212-813-1010, e-mail: prospectus@aegiscap.com.

A registration statement relating to these securities was declared effective by the Securities and Exchange Commission on October 22, 2013. This press release shall not constitute an offer to sell or a solicitation of an offer to buy, nor shall there be any sale of these securities in any state or jurisdiction in which such an offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of any such state or jurisdiction.

About Cancer Genetics:

Cancer Genetics, Inc. is an emerging leader in DNA-based cancer diagnostics and services some of the most prestigious medical institutions in the world. Our tests target cancers that are difficult to diagnose and predict treatment outcomes. These cancers include hematological, urogenital and HPV-associated cancers. We also offer a comprehensive range of non-proprietary oncology-focused tests and laboratory services that provide critical genomic information to healthcare professionals as well as biopharma and biotech. Our state-of-the-art reference lab is focused entirely on maintaining clinical excellence and is both CLIA certified and CAP accredited and has licensure from several states including New York State. We have established strong research collaborations with major cancer centers such as Memorial Sloan-Kettering, The Cleveland Clinic, Mayo Clinic and the National Cancer Institute. For further information, please see http://www.cancergenetics.com.

Forward Looking Statements:

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. All statements pertaining to future financial and/or operating results, future growth in research, technology, clinical development and potential opportunities for Cancer Genetics, Inc. products and services, along with other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management constitute forward-looking statements. In addition, the offering is subject to market and other conditions and there can be no assurance as to the estimated proceeds from the offering and the anticipated use of proceeds from the offering. Any statements that are not historical fact (including, but not limited to, statements that contain words such as "will," "believes," "plans," "anticipates," "expects," "estimates") should also be considered to be forward-looking statements. Forward-looking statements involve risks and uncertainties, including, without limitation, risks inherent in the development and/or commercialization of potential products, uncertainty in the results of clinical trials or regulatory approvals, need and ability to obtain future capital, and maintenance of intellectual property rights and other risks discussed in the Company's Form 10-Q for the quarter ended June 30, 2013 and other filings with the Securities and Exchange Commission. These forward-looking statements speak only as of the date hereof. Cancer Genetics disclaims any obligation to update these forward-looking statements.

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Cancer Genetics Announces Closing of Public Offering of $46 Million of Shares of Common Stock

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Matric Revision: Life Sciences: Genetics: Biotechnology (9/9): Gene therapy
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CAMBRIDGE, Mass.--(BUSINESS WIRE)--

bluebird bio, Inc. (BLUE) a clinical-stage company committed to developing potentially transformative gene therapies for severe genetic and orphan diseases, today announced that the first subject in its phase 2/3 childhood cerebral adrenoleukodystrophy (CCALD) study, Starbeam (ALD-102) has undergone infusion with bluebird bios Lenti-D drug product in an autologous hematopoietic stem cell transplantation.

Treating our first subject in this study reflects the recent advances in the field of gene therapy and is the culmination of years of collaborative effort between the team at Dana-Farber/Boston Childrens Cancer and Blood Disorders Center and our colleagues at Massachusetts General Hospital, INSERM in Paris, and bluebird bio, stated David A. Williams, MD, Chief of hematology/oncology at Boston Childrens Hospital and Associate Chairman of pediatric oncology at Dana-Farber Cancer Institute. Boys with CCALD face significant risks of mortality and morbidity with allogeneic stem cell transplantation, the current standard of care treatment, if an optimally matched donor cannot be identified. bluebirds autologous Lenti-D drug product has the potential to circumvent this challenge and address an important unmet medical need for patients with this devastating disease.

Successfully initiating treatment in the Starbeam study represents an important step towards improving outcomes for patients with CCALD and is a major milestone for bluebird and its lentiviral gene therapy platform, stated Dave Davidson, MD, bluebird bios Chief Medical Officer.

About the Starbeam study (ALD-102)

The phase 2/3 study is designed to evaluate the safety and efficacy of Lenti-D drug product in the treatment of subjects with childhood cerebral adrenoleukodystrophy, or CCALD, a rare, hereditary neurological disorder affecting young boys that is often fatal. The trial study is planned to enroll up to 15 boys who will be followed for 24 months following a transplant with bluebird bios lentiviral transduced stem cells, Lenti-D. During this 24 month period, patients will be assessed for the onset of major functional disabilities, and other key assessments of disease progression.

For more information please contact clinicaltrials@bluebirdbio.com.

About Childhood Cerebral Adrenoleukodystrophy (CCALD)

Childhood Cerebral Adrenoleukodystrophy is an X-linked disease caused by the aberrant expression of the ABCD1 gene in boys leading to the inability of patients to metabolize very long chain fatty acids in cells of the brain. The disease is characterized by progressive destruction of myelin, leading to severe loss of neurological function and eventual death. The worldwide incidence of adrenoleukodystrophy (ALD) is approximately one in 20,000 newborns. CCALD accounts for about 30-40% of patients diagnosed with ALD.

About bluebird bio, Inc.

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bluebird bio Announces First Patient Transplanted in Phase 2/3 Starbeam ALD-102 Study for the Treatment of CCALD

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stem cell therapy treatment for autism from united kingdom by dr alok sharma, mumbai, india
amazing improvement seen in just 1 months after stem cell therapy treatment for autism from united kingdom by dr alok sharma, mumbai, india. After Stem Cell ...

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PUBLIC RELEASE DATE:

27-Oct-2013

Contact: Peggy Vaughn nianews3@mail.nih.gov 301-496-1752 NIH/National Institute on Aging

An international group of researchers has identified 11 new genes that offer important new insights into the disease pathways involved in Alzheimer's disease. The highly collaborative effort involved scanning the DNA of over 74,000 volunteersthe largest genetic analysis yet conducted in Alzheimer's researchto discover new genetic risk factors linked to late-onset Alzheimer's disease, the most common form of the disorder.

By confirming or suggesting new processes that may influence Alzheimer's disease developmentsuch as inflammation and synaptic functionthe findings point to possible targets for the development of drugs aimed directly at prevention or delaying disease progression.

Supported in part by the National Institute on Aging (NIA) and other components of the National Institutes of Health, the International Genomic Alzheimer's Project (IGAP) reported its findings online in Nature Genetics on Oct. 27, 2013. IGAP is comprised of four consortia in the United States and Europe which have been working together since 2011 on genome-wide association studies (GWAS) involving thousands of DNA samples and shared datasets. GWAS are aimed at detecting the subtle gene variants involved in Alzheimer's and defining how the molecular mechanisms influence disease onset and progression.

"Collaboration among researchers is key to discerning the genetic factors contributing to the risk of developing Alzheimer's disease," said Richard J. Hodes, M.D., director of the NIA. "We are tremendously encouraged by the speed and scientific rigor with which IGAP and other genetic consortia are advancing our understanding."

The search for late-onset Alzheimer's risk factor genes had taken considerable time, until the development of GWAS and other techniques. Until 2009, only one gene variant, Apolipoprotein E-e4 (APOE-e4), had been identified as a known risk factor. Since then, prior to today's discovery, the list of known gene risk factors had grown to include other playersPICALM, CLU, CR1, BIN1, MS4A, CD2AP, EPHA1, ABCA7, SORL1 and TREM2.

IGAP's discovery reported today of 11 new genes strengthens evidence about the involvement of certain pathways in the disease, such as the role of the SORL1 gene in the abnormal accumulation of amyloid protein in the brain, , a hallmark of Alzheimer's disease. It also offers new gene risk factors that may influence several cell functions, to include the ability of microglial cells to respond to inflammation.

The researchers identified the new genes by analyzing previously studied and newly collected DNA data from 74,076 older volunteers with Alzheimer's and those free of the disorder from 15 countries. The new genes (HLA-DRB5/HLA0DRB1, PTK2B, SLC24A4-0RING3, DSG2, INPP5D, MEF2C, NME8, ZCWPW1, CELF1, FERMT2 and CASS4) add to a growing list of gene variants associated with onset and progression of late-onset Alzheimer's. Researchers will continue to explore the roles played by these genes, to include:

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NIH-supported study identifies 11 new Alzheimer's disease risk genes

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SAQ (4.4) Genetic Engineering and Biotechnology - IB SL Biology Past Exam Paper 2 Questions
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Newswise BOSTON A fine-grained scan of DNA in lung cancer cells has revealed a gene fusion a forced merger of two normally separate genes that spurs the cells to divide rapidly, scientists at Dana-Farber Cancer Institute and the University of Colorado Cancer Center report in a new paper in the journal Nature Medicine. Treating the cells with a compound that blocks a protein encoded by one of those genes NTRK1 caused the cells to die.

The finding suggests that the fusion of NTRK1 to other genes fuels the growth of some lung adenocarcinomas (a form of non-small cell lung cancer), and that drugs that target NTRK1s protein product could be effective in patients whose lung tumors harbor such fusions.

Treatment with targeted therapies is now superior to standard chemotherapy for many patients with lung cancers that harbor genetic changes including those with fusions involving the gene ALK, says Pasi A. Jnne, MD, PhD, of Dana-Farber, the senior co-author of the paper with Robert C. Doebele, MD, PhD, of CU Cancer Center. We know of several other genes that are fused in lung cancer and that offer attractive targets for new therapies. Our discovery places lung adenocarcinomas with NTRK1 fusions squarely within that group.

In the study, researchers performed next-generation DNA sequencing tests which read the individual elements of the genetic code over long stretches of chromosomes on tumor samples from 36 patients with lung adenocarcinomas whose tumors did not contain any previously known genetic alterations that could be found with standard clinical tests. In two of those samples both from women who had never smoked investigators found that a key region of the NTRK1 gene had become fused to normally distant genes (to the gene MPRIP in one patient; and the gene CD74 in the other).

NTRK1 holds the blueprint for a protein called TRKA, which dangles from the surface of cells and receives growth signals from other cells. The binding of NTRK1 to other genes causes TRKA to issue cell-growth orders on its own, without being prompted by outside signals.

In the laboratory, investigators mixed NTRK1-inhibiting agents into lung adenocarcinoma cells harboring NTRK1 fusions. The result was a dampening of TRKAs activity and the death of the cancer cells.

Investigators then designed a new test using fluorescence in situ hybridization (FISH) to detect NTRK1 fusions and tested an additional 56 tumor samples. In total, three of 91 tumor samples which had no other sign of cancer-causing genetic abnormalities, had fusions involving NTRK1.

These findings suggest that in a few percent of lung adenocarcinoma patients people in whose cancer cells we had previously been able to find no genetic abnormality tumor growth is driven by a fusion involving NTRK1, Jnne says. Given that lung cancer is a common cancer, even a few percent is significant and translates into a large number of patients. Our findings suggest that targeted therapies may be effective for this subset of lung cancer patients.

"This is still preclinical work," Doebele says, "but it's the first and maybe even second and third important steps toward picking off another subset of lung cancer with a treatment targeted to the disease's specific genetic weaknesses."

The co-lead authors of the study are Aria Vaishnavi, BS, of the University of Colorado School of Medicine and Marzia Capelletti, PhD, of Dana-Farber. Co-authors include Anh Le, BA, Severine Kako, Sakshi Mahale, MS, Kurtis Davies, PhD, Dara Aisner, MD, PhD, Amanda Pilling, PhD Eamon Berge, MD, and Marileila Varella-Garcia, PhD, of the University of Colorado School of Medicine; Mohit Butaney, Dalia Ercan, and Peter Hammerman, MD, PhD, of Dana-Farber; Levi Garraway, MD, PhD, of Dana-Farber and the Broad Institute of MIT and Harvard; Gregory Kryukov, PhD, of the Broad Institute; Jhingook Kim, MD, of Samsung Medical Center, Seoul, Korea; Hidefumi Sasaki, MD, of Nagoya City University, Nagoya, Japan; Seung-il Park, MD, PhD, of Asan Medical Center, Seoul, Korea; Julia Haas, PhD, and Steven Andrews, PhD, of Array BioPharma; Doron Lipson, PhD, Philip Stephens, PhD, and Vince Miller, MD, of Foundation Medicine.

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Study Finds New Genetic Error in Some Lung Cancers

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AURORA, Colo. (PRWEB) October 27, 2013

A study lead by scientists at University of Colorado Cancer Center and Dana-Farber Cancer Institute in Boston has uncovered a new sub-type of lung cancer. The study revealed a gene fusion - a forced merger of two normally separate genes that spurs the cells to divide rapidly causing non-small cell lung cancer. The study is published in the journal Nature Medicine.

Scientists from CU Cancer Center and Dana-Farber collaborated on the finding. The group went a step beyond identifying the gene mutation, NTRK1, that drives some lung cancers. The scientists also showed the abnormal cells can be targeted by several drugs.

Whether a drug is already is in clinical trials, or already approved for another cancer, or just sitting on the pharma shelf somewhere, many drugs exist that turn off these candidate genes," said Robert C. Doebele, MD, PhD, the studys senior author and investigator at the CU Cancer Center.

Doebele found Array BioPharma in Boulder, Colo. happened to have several compounds specific to NTRK1. The group showed that mutated NRTK1 genes in cells treated with drug candidate ARRY-470 and others was effectively turned off. The drug blocks a protein causing cancer cells to die.

This is still preclinical work," Doebele says, "but it's the first and maybe even second and third important steps toward picking off another subset of lung cancer with a treatment targeted to the disease's specific genetic weaknesses."

Foundation Medicine, Inc. performed next-generation DNA sequencing tests which read the individual elements of the genetic code over long stretches of chromosomes on tumor samples from 36 patients with lung adenocarcinomas whose tumors did not contain any previously known genetic alterations that could be found with standard clinical tests. In two of those samples both from women who had never smoked investigators found that a key region of the NTRK1 gene had become fused to normally distant genes (to the gene MPRIP in one patient; and the gene CD74 in the other).

NTRK1 holds the blueprint for a protein called TRKA, which dangles from the surface of cells and receives growth signals from other cells. The joining of NTRK1 to other genes causes TRKA to issue cell-growth orders on its own, without being prompted by outside signals.

In the laboratory, investigators mixed NTRK1-inhibiting agents into lung adenocarcinoma cells harboring NTRK1 fusions. The result was a dampening of TRKAs activity and the death of the cancer cells.

Leila Varella-Garcia, PhD, at CU Cancer Center then designed a new test using fluorescence in situ hybridization (FISH) to detect NTRK1 fusions and tested an additional 56 tumor samples. Three of 91 tumor samples, which had no other sign of cancer-causing genetic abnormalities, had fusions involving NTRK1.

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New Genetic Error in Some Lung Cancers Identified by CU Scientists

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Newswise PHILADELPHIA - The largest international Alzheimer's disease genetics collaboration to date has found 11 new genetic areas of interest that contribute to late onset Alzheimer's Disease (LOAD), doubling the number of potential genetics-based therapeutic targets to interrogate. The study, published in Nature Genetics, provides a broader view of genetic factors contributing to the disease and expands the scope of disease understanding to include new areas including the immune system, where a genetic overlap with other neurodegenerative diseases such as multiple sclerosis and Parkinson's disease was identified.

"Human genetic studies are being used with increased frequency to validate new drug targets in many diseases. Here we greatly increased the list of possible drug target candidates for Alzheimers disease, finding as many new significant genes in this one study as have been found in the last 15 years combined," said co-senior author Gerard Schellenberg, PhD, director of the Alzheimers Disease Genetics Consortium (ADGC) and professor of Pathology and Laboratory Medicine in the Perelman School of Medicine at the University of Pennsylvania. "This international effort has given us new clues into the steps leading to and accelerating Alzheimer's disease. We can add these new genetic clues to what we already know and try to piece together the mechanism of this complex disease."

Pooling resources through the International Genomics of Alzheimers Project (IGAP), the collaborative team collected 74,076 patients and controls from 15 countries. After a two stage meta-analysis, the group found some genes which confirmed known biological pathway of Alzheimer's disease, including the role of the amyloid pathway (SORL1 , CASS4) and tau (CASS4, FERMT2). Newly discovered genes involved in the immune response and inflammation (HLA-DRB5/DRB1, INPP5D, MEF2C) reinforced a pathway implied by previous work (on CR1, TREM2). Additional genes related to cell migration (PTK2B), lipid transport and endocytosis (SORL1) were also confirmed. And new hypotheses emerged related to hippocampal synaptic function (MEF2C , PTK2B), the cytoskeleton and axonal transport (CELF1, NME8, CASS4) as well as myeloid and microglial cell functions (INPP5D).

One of the more significant new associations was found in the HLA-DRB5 - DRB1 region, one of the most complex parts of the genome, which plays a role in the immune system and inflammatory response. It has also been associated with multiple sclerosis and Parkinson's disease, suggesting that the diseases where abnormal proteins accumulate in the brain may have a common mechanism involved, and possibly have a common drug target, Dr. Schellenberg noted.

"We know that healthy cells are very good at clearing out debris, thanks in part to the immune response system, but in these neurodegenerative diseases where the brain has an inflammatory response to bad proteins and starts forming plaques and tangle clumps, perhaps the immune response can get out of hand and do damage," said Dr. Schellenberg. "Through this powerful international group as well as our own US collaborations, we'll expand the data set even further to look for rare variants and continue our analysis to find more opportunities to better understand the disease and find viable therapeutic targets. Large-scale sequencing will certainly play a part in the next phase of our genetics studies."

Started in 2011, IGAP includes the contributions from the European Alzheimers Disease Initiative (EADI) in France led by Philippe Amouyel, MD, PhD, at the Institute Pasteur de Lille and Lille University; the Genetic and Environmental Risk in Alzheimers Disease (GERAD) from the United Kingdom led by Julie Williams, PhD, at Cardiff University; the neurology subgroup of the Cohorts for Heart and Aging in Genomic Epidemiology (CHARGE) led by Sudha Seshadri, MD, at Boston University School of Medicine; the Alzheimers Disease Genetics Consortium (ADGC) from the United States led by Gerard Schellenberg, PhD, Perelman School of Medicine at the University of Pennsylvania; as well as ADGC teams from the University of Miami, Vanderbilt University, Boston University and Columbia University in the United States, among others.

The National Institute on Aging provided funding for the ADGC (U01 AG032984, R01 AG033193), and the Alzheimer's Association provided crucial support to make this international collaboration possible.

# # #

Penn Medicineis one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of theRaymond and Ruth Perelman School of Medicine at the University of Pennsylvania(founded in 1765 as the nation's first medical school) and theUniversity of Pennsylvania Health System, which together form a $4.3 billion enterprise.

The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 16 years, according toU.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $398 million awarded in the 2012 fiscal year.

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Matric revision: Life Sciences: Genetics (6/8): DNA replication (3/5): protein synthesis (2/4)
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