Archive for October, 2013

Matric revision: Life Sciences: Genetics (4/8): DNA replication (1/5): mitoses and meiosis
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Matric Revision: Life Sciences: Genetics: Biotechnology (4/9): Recombinant DNA Technology (3/3)
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Matric Revision: Life Sciences: Genetics: Biotechnology (4/9): Recombinant DNA Technology (3/3) - Video

Matric Revision: Life Sciences: Genetics: Biotechnology (3/9): DNA (2/3) insulin (2/2)
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Matric Revision: Life Sciences: Genetics: Biotechnology (3/9): DNA (2/3) insulin (2/2) - Video

Matric Revision: Life Sciences: Genetics: Biotechnology (1/9): Introduction
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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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Myriad myPlan(TM) Lung Cancer Test Meets Primary Endpoint in Validation Study

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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Life Stem Genetics Strengthens Its Executive Advisory Board by Adding MBAs Matthew Sullivan and Shahab Bakhtyar

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

Matric Revision: Life Sciences: Genetics: Biotechnology (9/9): Gene therapy
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Matric Revision: Life Sciences: Genetics: Biotechnology (9/9): Gene therapy - Video

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

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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stem cell therapy treatment for autism from united kingdom by dr alok sharma, mumbai, india - Video

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

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

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

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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International Group Finds 11 New Alzheimer's Genes to Target for Drug Discovery, Adding New Clues Into Complex Disease ...

Matric revision: Life Sciences: Genetics (6/8): DNA replication (3/5): protein synthesis (2/4)
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Matric Revision: Life Sciences: Genetics: Biotechnology (8/9): Cloning (4/4): pro and con
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PUBLIC RELEASE DATE:

27-Oct-2013

Contact: Kim Menard kim.menard@uphs.upenn.edu 215-662-6183 University of Pennsylvania School of Medicine

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 Alzheimer's 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 Alzheimer's 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 Alzheimer's 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."

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Started in 2011, IGAP includes the contributions from the European Alzheimer's 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 Alzheimer's 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 Alzheimer's 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.

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International group finds 11 new Alzheimer's genes to target for drug discovery

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Next spring, students at local high schools will dive into the study of the marine bacterium Kytococcus sedentarius, thanks to a $1.1 million National Science Foundation grant to UB.

Stephen Koury and his colleagues in the School of Medicine and Biomedical Sciences, received the grant to educate regional high school teachers and recruit high school students to pursue careers in STEM (science, technology, engineering and mathematics) fields. The new program focuses on bioinformatics, an interdisciplinary field that uses software tools to store, retrieve, organize and analyze biologic information. Bioinformatics is a field of rapid growth that provides tools for better health care through improvement in prevention, detection, diagnosis and treatment of diseases.

Koury, research assistant professor in the Department of Biotechnical and Clinical Laboratory Sciences, notes that new jobs on the Buffalo Niagara Medical Campus likely will require training in biotechnology and bioinformatics; the new program will provide a pipeline for educator and student recruitment, training and mentorship in STEM fields at the high school level.

For us to be successful, we need to create the environment where children not only want to get involved, but want to stay in Buffalo, says Norma Nowak, professor of biochemistry, director of science and technology at UBs New York State Center of Excellence in Bioinformatics and Life Sciences, and associate professor of oncology at Roswell Park Cancer Institute. This needs to be the spark that lights the fire.

Over the next three years, the grant will allow 450 high school students and 90 teachers to conduct and present scientific research in bioinformatics. The program will involve educators and students from 13 counties, including Niagara, Erie, Chautauqua, Cattaraugus, Wyoming, Genesee, Orleans, Monroe, Livingston, Allegany, Ontario, Wayne and Steuben.

The educational program will begin with a two-week workshop at UB, where high school teachers will receive training in microbial genome annotation. The teachers then will pass on their new skills to selected students in their schools, with support from UB faculty and staff.

During the first semester, students will be introduced to basic aspects of genetics and genomics. They also will receive career mentoring through a partnership with the New York State Area Health Education Center System (AHEC), a unit of UBs Department of Family Medicine that addresses health care workforce needs.

The second semester will focus on conducting Web-based research in microbial annotation through a program called IMG-ACT, a bioinformatics tool kit available through the U.S. Department of Energys Joint Genome Institute. The program will end with a capstone symposium at which students will present the results of their research to university faculty, researchers and employers in the biosciences fields.

For many local students, this will be their first real-world taste of scientific experimentation. And since its an unscripted project, students will learn to rely on themselves, rather than the specific direction of instructors.

We cant say for sure what they should find, says Koury. They will actually be doing a research project, and by the time they are done, they will probably be the expert on the particular gene sequence they have studied. It will give them that joy of discovery.

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