Cancer Therapy - Therapy for Cancer
Cancer Therapy. http://www.CancerUncensored.com. Welcome to today #39;s issue of cancer uncensored. Hi, I #39;m Chris, and I am the author of cancer uncensored, a step-by-step guide to cancer prevention, early detection and cancer survival. In today #39;s video,I would like to present you with an overview of cancer. I #39;m going to briefly talk about exactly what cancer is, what triggers it, what the symptoms are, how you can avoid it. We #39;ll also go over current treatment procedures and alternative treatment. I #39;m going to also let you know where you can go to get the most up-to-date news and breakthroughs. Before we get stuck in, I ought to address two points Firstly, people are afraid of cancer. I can fully understand that, as my wife has cancer, but as a society, we must not allow the fear of the condition stop us from taking steps to understand it, because that way we can actively prevent it. One in three of us will be diagnosed with cancer within our lifetimes, yet 85% of cancer is preventable! This video, and my book, cancer uncensored, can tell you how. So take in as much of this information as you can, because it could save your life. Secondly, you must understand that cancer is not entirely understood. We have quite a few very solid theories, and lots of study data, but if cancer was fully understood, we would be even closer to a cure. As Thomas Edison once said, "The doctor of the future will no longer treat the human frame with drugs, but rather will cure and prevent disease with ...

By: CancerUncensored

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Cancer Therapy - Therapy for Cancer - Video

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How Do You Get Cancer?
How Do You Get Cancer? http://www.CancerUncensored.com. Welcome to today #39;s issue of cancer uncensored. Hi, I #39;m Chris, and I am the author of cancer uncensored, a step-by-step guide to cancer prevention, early detection and cancer survival. In today #39;s video,I would like to give you an overview of cancer. I am going to briefly go over what cancer is, what causes it, what the symptoms are, what you can do to actively avoid it. We will also go over current treatment methods and alternative medicine. I #39;ll also tell you where you should go to get the most up-to-date news and advancements. Before we get stuck in, I should address two points Firstly, people are afraid of cancer. I can fully understand that, as my wife has recently been diagnosed with cancer, but as a society, we must not let the dread of the disease prevent us from taking steps to understand it, as that way we can actively prevent it. One in three of us will be diagnosed with cancer during our lifetimes, yet 85% of cancer is preventable! This video, and my book, cancer uncensored, can tell you how. So take in as much of this data as you can, because it could save your life. Secondly, you need to realise that cancer is not entirely understood. We have a number of very solid theories, and lots of study data, but if cancer was fully understood, we would be closer to a cure. To quote Thomas Edison, "The doctor of the future will no longer treat the human frame with drugs, but rather will cure and prevent disease with ...

By: CancerUncensored

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How Do You Get Cancer? - Video

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Prevention Of Cancer - Cancer Prevention
Prevention Of Cancer. http://www.CancerUncensored.com. Welcome to today #39;s issue of cancer uncensored. Hi, I #39;m Chris, and I am the author of cancer uncensored, a step-by-step guide to cancer prevention, early detection and cancer survival. In today #39;s video,I want to present you with an overview of cancer. I am going to briefly talk about exactly what cancer is, what causes it, what symptoms there are, what you can do to prevent it. We will also go over current treatment options and alternative medicine. I #39;ll also let you know where you should go to get the most up-to-date news and breakthroughs. Before we get stuck in, I should address two points Firstly, people are terrified of cancer. I can fully understand that, as my wife has cancer, but as a society, we must not allow the dread of the disease stop us from taking steps to understand it, because that way we can actively prevent it. One in three of us will be diagnosed with cancer during our lifetimes, yet 85% of cancer is preventable! This video, and my book, cancer uncensored, will tell you how. So absorb as much of this data as you can, as it could save your life. Secondly, you need to realise that cancer is not totally understood. We have a number of very solid theories, and a lot of study data, but if cancer was fully understood, we would be closer to a cure. To quote Thomas Edison, "The doctor of the future will no longer treat the human frame with drugs, but rather will cure and prevent disease with nutrition." But as ...

By: CancerUncensored

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Prevention Of Cancer - Cancer Prevention - Video

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Introduction To Genetics and Heredity
This video discusses the basics of genetics and heredity. It discusses why offspring have shared characteristics and the role alleles play in that. It also reviews the basics of Mendelian genetics addressing the differences between purebreeds and hybrids and dominant and recessive alleles. You will be shown how to fill out a Punnett Square and how to read it.

By: mrfox218

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Introduction To Genetics and Heredity - Video

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Signs Of Cancer - Cancer Signs
Signs Of Cancer. http://www.CancerUncensored.com. Welcome to today #39;s issue of cancer uncensored. Hi, I #39;m Chris, and I am the author of cancer uncensored, a step-by-step guide to cancer prevention, early detection and cancer survival. In today #39;s video,I want to present you with an overview of cancer. I am going to briefly go over what cancer is, what triggers it, what symptoms there are, what you can do to actively avoid it. I #39;ll also go over current treatment methods and alternative medicine. I #39;m going to also tell you where you can go to get the most up-to-date news and breakthroughs. Before we get stuck in, I #39;d like to address two points Firstly, people are terrified of cancer. I can fully understand that, as my wife has recently been diagnosed with cancer, but as a society, we mustn #39;t allow the dread of the condition prevent us from taking steps to understand it, as that way we can actively prevent it. One in three of us will be diagnosed with cancer within our lifetimes, yet 85% of cancer is preventable! This video, and my book, cancer uncensored, can tell you how. So take in as much of this information as you can, because it could save your life. Secondly, you need to realise that cancer isn #39;t fully understood. We have quite a few very solid theories, and a lot of study data, but if cancer was fully understood, we might be even closer to a cure. To quote Thomas Edison, "The doctor of the future will no longer treat the human frame with drugs, but rather will cure and ...

By: CancerUncensored

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Signs Of Cancer - Cancer Signs - Video

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chernobyl week 5
really bad quality sorry not the plant but the video. tga genetics

By: jeffry blodem

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chernobyl week 5 - Video

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plushberry #1 TGA Genetics week6
sorry about the quality of the video.will be hd in a couple months or so.

By: jeffry blodem

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plushberry #1 TGA Genetics week6 - Video

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genetics: first draft
stop motion animation. first cut.

By: elyssa bulger

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genetics: first draft - Video

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Company Scientists featured on Discovery Channel
Featuring Nu Skin Scientists: Joseph Chang, Ph.D., Chief Scientific Officer, Vice President of Product Development Jia-Shi (Josh) Zhu, Ph.D., Senior Director of Pharmacology and Clinical Affairs Richard Weindruch, Ph.D., Co-founder, LifeGen Technologies, Professor of Geriatrics and Gerontology, University of Wisconsin Department of Medicine Tomas A. Prolla, Ph.D, Co-founder, LifeGen Technologies, Professor, departments of Genetics and Medical Genetics, University of Wisconsin To view our company #39;s Scientific Advisory Board, see bit.ly

By: EndlessVitality

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Company Scientists featured on Discovery Channel - Video

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2008 Petite Sirah Video Tasting Notes
Winemaker Robert Foley discusses the Terroir, Vinification, Flavor Profile, and Cellar-ability of his 2008 Petite Sirah -- a dark and inky combination of Valley Floor and Mountain fruit that will, as Bob says, "tattoo you from the inside out." For lovers of big, extracted red wines, packed with flavor and fine tannins, this is the variety for you! Not to be con- fused with Syrah... Petite Sirah was originally discovered by a French botanist Francois Durif, working at the Montpel- lier Viticultural Institute in southern France. He found this variety growing in a Peloursin vineyard and discovered that it had good resistance to downy mildew and named it for himself, Durif. Unfortunately, the tight clusters were prone to bunch rot and the wines that were produced were considered too big and tannic for the French palate and the variety was eliminated and is no longer found in France. It did make its way to California and other parts of the world where it is known as Petite Sirah. There is nothing "petite" about it -- even the berries are very large and the wines can be enormous. The key to user friendliness is patience to allow the seeds to ripen, allowing the tannins to relax. Through genetics, it was determined that this variety was the result of pollination of a Peloursin flower with Syrah pollen. With Petite Sirah mountain and valley-floor vineyards pro- ducing remarkably different character in recent vintages, we just had to celebrate these different personalities and ...

By: RobertFoleyVineyards

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2008 Petite Sirah Video Tasting Notes - Video

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the flav trimmed.mov
TGA Genetics The Flav

By: vlr12285

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the flav trimmed.mov - Video

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North Cobb High School Genetics Mitosis Lab

By: lovemoe001

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North Cobb High School Genetics Mitosis Lab - Video

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Gene predicts cancer development, BYU study finds

By Celeste Tholen Rosenlof

January 22nd, 2013 @ 8:22pm

PROVO A team of Brigham Young University researchers has identified a gene that could predict a cancer patient's chance of survival.

BYU biology professor David Bearss and co-author of the BYU-University of Iowa study found that a handful of genes in a tumor can predict how the cancer will progress and how patients will respond to therapy throughout the cancer's progression.

Bearss and his colleagues, including a team of BYU undergraduate students, studied 19 multiple myeloma cancer patients by taking biopsied cell samples throughout their cancer treatment and looking at them on the genetic level.

Multiple myeloma is a cancer that transforms white blood cells in bone marrow and destroys its function. About 20,000 people in the U.S. are diagnosed with the disease each year, resulting in about 11,000 deaths, Bearss said.

"We're still not very good at treating it, is the bottom line," he said.

Bearss set out to understand what happens to the cancerous cells at a genetic level throughout treatment. He found that a set of genes or markers consistently and dramatically changed as patients became resistant to therapy. Moreover, they found that one gene called NEK2, is a predictor of poor therapy response in multiple myeloma patients.

That, Bearss said, is a big breakthrough for patients and doctors faced with treatment decisions.

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Gene predicts cancer development, BYU study finds

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AMSTERDAM, January 22, 2013 /PRNewswire/ --

uniQure B.V., the leader in the field of human gene therapy, today announced the appointment of Philip Astley-Sparke, former President and CEO of BioVex, as President US to provide strategic leadership and help build uniQure's clinical, regulatory, and commercial infrastructure in the US.

Since May 2012, Philip is a venture partner at Forbion Capital Partners, uniQure's largest investor. As a venture partner he works with selected portfolio companies to help management execute on their business plans. Philip served as Vice President and General Manager at Amgen, Inc. until December 2011, following the acquisition of BioVex, Inc. in March 2011. Philip had been President and CEO of BioVex since 2005, during which he achieved several milestones for the company: its relocation from the UK to the US, the formation of a commercial grade manufacturing facility and nascent commercial capabilities, and the successful negotiation with Amgen to acquire BioVex for up to $1bn. BioVex focused on the development of pioneering first-in-class oncolytic vaccines. Prior to BioVex, Philip was an investment banker with JP Morgan H&Q (Robert Fleming) where he advised on a number of high profile mergers and public financings. He qualified as a Chartered Accountant with Arthur Andersen in London and holds a Bachelor's Degree in Cellular Pathology and Molecular Pathology from Bristol University (UK).

"Philip's experience and expertise will be invaluable in building a successful US infrastructure for uniQure," says Jrn Aldag, CEO of uniQure. "He is to devote an important part of his time to uniQure, and will become a key member of our management team. We look forward to establishing a foothold in the US, and developing uniQure to full commercial maturity."

About uniQure

uniQure is a world leader in the development ofhuman gene based therapies.uniQure's Glybera, a gene therapy for the treatment of lipoprotein lipase deficiency has been approved in the European Union, and is the first approved gene therapy in the Western world. uniQure's product pipeline of gene therapy products in development comprise hemophilia B, acute intermittent porphyria, Parkinson's disease and SanfilippoB. Using adeno-associated viral (AAV) derived vectors as the delivery vehicle of choice for therapeutic genes, the company has been able to design and validate probably the world's first stable and scalable AAV manufacturing platform.This proprietary platform can be applied to a large number of rare(orphan) diseases caused by one faulty gene. uniQure's largest shareholders are Forbion Capital Partners and Gilde Healthcare, two of the leading life sciences venture capital firms in the Netherlands. Further information can be found at http://www.uniqure.com.

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uniQure Appoints Philip Astley-Sparke President US

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Jan. 21, 2013 Independent clinical trials, including one conducted at the Scheie Eye Institute at the Perelman School of Medicine, have reported safety and efficacy for Leber congenital amaurosis (LCA), a congenital form of blindness caused by mutations in a gene (RPE65) required for recycling vitamin A in the retina. Inherited retinal degenerative diseases were previously considered untreatable and incurable. There were early improvements in vision observed in the trials, but a key question about the long-term efficacy of gene therapy for curing the retinal degeneration in LCA has remained unanswered.

Now, new research from the Scheie Eye Institute, published this week in the Proceedings of the National Academy of Sciences, finds that gene therapy for LCA shows enduring improvement in vision but also advancing degeneration of affected retinal cells, both in LCA patients and animal models of the same condition.

LCA disease from RPE65 mutations has two-components: a biochemical blockade leading to impaired vision, and a progressive loss of the light-sensing photoreceptor cells throughout life of the affected patient. The authors of the new study explain that until now gene therapy has been optimistically assumed, but not proven, to solve both disease components at the same time.

"We all hoped that the gene injections cured both components -- re-establishing the cycle of vision and also preventing further loss of cells to the second disease component" said Artur V. Cideciyan, PhD, lead author and co-investigator of an LCA clinical trial at Penn.

Yet, when the otherwise invisible cell layers of the retina were measured by optical imaging in clinical trial participants serially over many years, the rate of cell loss was the same in treated and untreated regions. "In other words, gene therapy improved vision but did not slow or halt the progression of cell loss," commented Cideciyan.

"These unexpected observations should help to advance the current treatment by making it better and longer lasting," commented co-author Samuel G. Jacobson, MD, PhD, principal investigator of the clinical trial. "Slowing cell loss in different retinal degenerations has been a major research direction long before the current gene therapy trials. Now, the two directions must converge to ensure the longevity of the beneficial visual effects in this form of LCA."

In a continuation of the longstanding collaboration between the Scheie investigators and the Section of Ophthalmology at Penn School of Veterinary Medicine headed by co-authors Gustavo D. Aguirre, VMD, PhD, and William A. Beltran, DVM, PhD, studies were performed to test whether the clinical results were also present in the canine model of this LCA at disease stages equivalent to those in human patients.

"Our gene treatment in this canine model provided the groundwork for the clinical trials of patients, and now we added data to confirm the fact that retinal degeneration does continue despite improved vision" said Aguirre. "The next step is to perform the relevant experiments to ask what intervention will stop the degeneration if added to the gene therapy."

"These new findings contribute to greater clarity in understanding the natural history and complexity of the RPE65 form of LCA and provide a firm foundation for future investigations," said Joan M. O'Brien MD, professor and chair of the Department of Ophthalmology and director of the Scheie Eye Institute.

Co-authors, in addition to the Penn researchers include, William W. Hauswirth, PhD, professor of Ophthalmology, at the University of Florida, Gainesville.

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Light shed on complexity of gene therapy for congenital blindness

Recommendation and review posted by Bethany Smith

Public release date: 21-Jan-2013 [ | E-mail | Share ]

Contact: Katie Delach katie.delach@uphs.upenn.edu 215-349-5964 University of Pennsylvania School of Medicine

PHILADELPHIA - Independent clinical trials, including one conducted at the Scheie Eye Institute at the Perelman School of Medicine, have reported safety and efficacy for Leber congenital amaurosis (LCA), a congenital form of blindness caused by mutations in a gene (RPE65) required for recycling vitamin A in the retina. Inherited retinal degenerative diseases were previously considered untreatable and incurable. There were early improvements in vision observed in the trials, but a key question about the long-term efficacy of gene therapy for curing the retinal degeneration in LCA has remained unanswered. Now, new research from the Scheie Eye Institute, published this week in the Proceedings of the National Academy of Sciences, finds that gene therapy for LCA shows enduring improvement in vision but also advancing degeneration of affected retinal cells, both in LCA patients and animal models of the same condition.

LCA disease from RPE65 mutations has two-components: a biochemical blockade leading to impaired vision, and a progressive loss of the light-sensing photoreceptor cells throughout life of the affected patient. The authors of the new study explain that until now gene therapy has been optimistically assumed, but not proven, to solve both disease components at the same time.

"We all hoped that the gene injections cured both components re-establishing the cycle of vision and also preventing further loss of cells to the second disease component" said Artur V. Cideciyan, PhD, lead author and co-investigator of an LCA clinical trial at Penn.

Yet, when the otherwise invisible cell layers of the retina were measured by optical imaging in clinical trial participants serially over many years, the rate of cell loss was the same in treated and untreated regions. "In other words, gene therapy improved vision but did not slow or halt the progression of cell loss," commented Cideciyan.

"These unexpected observations should help to advance the current treatment by making it better and longer lasting," commented co-author Samuel G. Jacobson, MD, PhD, principal investigator of the clinical trial. "Slowing cell loss in different retinal degenerations has been a major research direction long before the current gene therapy trials. Now, the two directions must converge to ensure the longevity of the beneficial visual effects in this form of LCA."

In a continuation of the longstanding collaboration between the Scheie investigators and the Section of Ophthalmology at Penn School of Veterinary Medicine headed by co-authors Gustavo D. Aguirre, VMD, PhD, and William A. Beltran, DVM, PhD, studies were performed to test whether the clinical results were also present in the canine model of this LCA at disease stages equivalent to those in human patients. "Our gene treatment in this canine model provided the groundwork for the clinical trials of patients, and now we added data to confirm the fact that retinal degeneration does continue despite improved vision" said Aguirre. "The next step is to perform the relevant experiments to ask what intervention will stop the degeneration if added to the gene therapy."

"These new findings contribute to greater clarity in understanding the natural history and complexity of the RPE65 form of LCA and provide a firm foundation for future investigations," said Joan M. O'Brien MD, professor and chair of the Department of Ophthalmology and director of the Scheie Eye Institute.

###

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Penn study sheds light on the complexity of gene therapy for congenital blindness

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Head Injury Improves After Stem Cell Therapy
Stem Cell Therapy done at NeuroGen Brain and Spine Institute Surana Sethia Hospital Sion-Trombay Rd, Suman Ngr Opp Corporate Park, Chembur, Mumbai -- 71. Tel : 022 - 25283706, 022 - 25281610, Mob : +91 9920 200 400 http://www.neurogen.in http://www.stemcellsmumbai.com

By: neurogenbsi

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Head Injury Improves After Stem Cell Therapy - Video

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British Israel Research and Academic Exchange Partnership (Birax) will grant NIS 25 million over five years for seven joint Israel-UK stem cell research programs.

Prime Minister Ehud Olmert and Prime Minister Gordon Brown launched Birax in 2008 through the Ministry of Science and Technology and the British Council. The British Embassy in Israel and the UK-Israel Life Sciences Council decided that Birax would focus on regenerative medicine.

Israel and the UK are global biotechnology leaders, with expertise in stem cells. Stem cells are cells which have not completed their speciation and have unique reproductive, renewal, and regenerative capabilities for organs. The ultimate dream is to use stem cells to build new tissue and organs, but in the meantime, stem cells are being developed for drug delivery and tissue regeneration. The first stem cell-based drugs were approved in 2012.

Under Birax, joint projects have already been established by Cambridge University, Oxford University, the University of Edinburgh, and the University of Nottingham in the UK and the Weizmann Institute of Science and the Hebrew University of Jerusalem. The projects are in multiple sclerosis, Parkinson's disease, and type 1 diabetes, as well as basic research on ways to prevent the immune system from attacking stem cells.

The grants will be financed by the Israeli and UK governments, and Britain's Pears Foundation, Britain's Bonita Trust, the Charles Wolfson Charitable Trust, the Rosetrees Trust, Lord Fink, the United Jewish Israel Appeal (UJIA), the Rothschild family's Yad Hanadiv, Morris Kahn's Aurum Ventures MKI Ltd.

The British Embassy also supports the life sciences through the UK-Israel Tech Hub. The Hub Biomed Manager Dr. Iris Geffen Gloor is becoming a major power in brokering Israeli-UK academic and business ties. The Hub's recent important projects include creating access to binational foundations, establishing ties between academic institutions and new companies and British pharmaceutical commercialization companies, and establishing ties between Israeli parties and the UK's National Organization for Clinical Research Infrastructure (NOCRI), a powerhouse for clinical studies.

Published by Globes [online], Israel business news - http://www.globes-online.com - on January 20, 2013

Copyright of Globes Publisher Itonut (1983) Ltd. 2013

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Birax grants NIS 25m for Israel-UK stem cell projects

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Mansoura University Regenerative Medicine Program (MURMP): From Bench to Bedside - 2nd Day
Medical Experimental Research Center (MERC) Annual Conference Mansoura University Regenerative Medicine Program (MURMP): From Bench to Bedside

By: mansvu

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Mansoura University Regenerative Medicine Program (MURMP): From Bench to Bedside - 2nd Day - Video

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7.10 - Regenerative Medicine
Speaker: Ms. Elizabeth Sump, Director of Research Administration for the Orthopaedic and Rheumatology Institute, and Director of Governmental Relations, Cleveland Clinic and Dr. Fehmida Kapadia, Research Program Manager, Cleveland Clinic Ms. Sump is the Director of Research Administration for the Orthopaedic and Rheumatology Institute at the Cleveland Clinic, as well as a Director of Government Relations at Cleveland Clinic. She has previously served as the Executive Director of the Clinical Tissue Engineering Center, Chief Commercialization Officer of the Armed Forces Institute of Regenerative Medicine and Vice President of Corporate Development for NetGenics Inc., an enterprise bioinformatics company. A Cleveland native, Ms. Sump has been developing technology for the Healthcare and Life Sciences industries for nearly 25 years. Dr. Kapadia is a Research Program Manager at the Cleveland Clinic responsible for managing product development and commercialization of a device used to identify and isolate stem cells. Dr. Kapadia also manages the research being conducted to develop products for the treatment of wounded warriors as a part of an Armed Forces Institute of Regenerative Medicine research grant. Dr. Kapadia has a PhD in Biochemistry and a Master #39;s in Biotech Entrepreneurship. She has worked for several years in research labs conducting research in cardiovascular and molecular biology. Before joining the Cleveland Clinic, Dr. Kapadia worked at BioEnterprise which is ...

By: NEOinnovates

Excerpt from:
7.10 - Regenerative Medicine - Video

Recommendation and review posted by sam

Public release date: 20-Jan-2013 [ | E-mail | Share ]

Contact: Rachel Salis-Silverman salis@email.chop.edu 267-426-6063 Children's Hospital of Philadelphia

An extensive genomic study of the childhood cancer neuroblastoma reinforces the challenges in treating the most aggressive forms of this disease. Contrary to expectations, the scientists found relatively few recurrent gene mutationsmutations that would suggest new targets for neuroblastoma treatment. Instead, say the researchers, they have now refocused on how neuroblastoma tumors evolve in response to medicine and other factors.

"This research underscores the fact that tumor cells often change rapidly over time, so more effective treatments for this aggressive cancer will need to account for the dynamic nature of neuroblastoma," said study leader John M. Maris, M.D., director of the Center for Childhood Cancer Research at The Children's Hospital of Philadelphia (CHOP).

Striking the peripheral nervous system, neuroblastoma usually appears as a solid tumor in a young child's chest or abdomen. It comprises 7 percent of all childhood cancers, but causes 10 to 15 percent of all childhood cancer-related deaths. Neuroblastoma is notoriously complex, with a broad number of gene changes that can give rise to the disease.

Maris headed the multicenter research collaborative, the TARGET (Therapeutically Applicable Research to Generate Effective Treatments) initiative, which released its findings today in Nature Genetics. This largest-ever study genomic study of a childhood cancer analyzed DNA from 240 children with high-risk neuroblastomas. Using a combination of whole-exome, whole-genome and transcriptome sequencing, the study compared DNA from tumors with DNA in normal cells from the same patients.

Researchers at CHOP and other centers previously discovered neuroblastoma-causing mutations, such as those in the ALK gene. In the subset of patients carrying this mutation, oncologists can provide effective treatments tailored to their genetic profile.

"A few years ago, we thought we would be able to sequence the genomes of individual patients with neuroblastoma, detect their specific cancer-causing mutations, and then select from a menu of treatments," said Maris. The oncology researchers designed the TARGET study to perform genomic analyses of a large cohort of high-risk neuroblastoma patients, with the goal of mapping out a limited number of treatment strategies. This approach would represent a significant step forward in personalizing neuroblastoma therapy.

However, while the researchers confirmed that roughly 10 percent of the study's neuroblastoma patients had ALK mutations, and found that a handful of other gene mutations each accounted for percentages in the single digits, there were relatively few recurrent mutations in somatic (non-germline) cells. "The relative paucity of recurrent mutations challenges the concept that druggable targets can be defined in each patient by DNA sequencing alone," wrote the authors.

In the absence of frequently altered oncogenes that drive high-risk neuroblastomas, the authors concluded that most such cases may result from other changes: rare germline mutations, copy number variations and epigenetic modifications during tumor evolution.

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Tumors evolve rapidly in a childhood cancer, leaving fewer obvious tumor targets

Recommendation and review posted by Bethany Smith

DURHAM -- Duke University researchers have found a way to diagnose infectious diseases such as flu and staph infections more quickly by looking for responses in a patients genes.

Genomics, a field of genetics that takes into account the entire gene sequence, can identify diseases more quickly and accurately than typical methods, according to studies published earlier this month in PLOS ONE, a peer-reviewed online journal of science and medicine.

The researchers examined the ribonucleic acid, or RNA, from blood samples taken from patients. They found that the RNA profiles changed in specific ways among patients exposed to infectious viruses or bacteria, according to Geoffrey Ginsburg, director of genomic medicine at Dukes Institute for Genome Sciences & Policy and an author on both studies.

Other diagnostic approaches have to be very specific as to what they think the pathogens are, Ginsburg said. Our approach doesnt care, because it takes advantage of the host response,

To conduct their research, the scientists inoculated 41 people with H1N1 or H3N2 flu before analyzing their blood samples. Specific changes to the RNA profile, called the Influenza Factor, were found in patients exposed to either flu strain. The test was able to distinguish infected from non-infected individuals with 94 percent accuracy.

In a second study, the researchers found a similar factor for diagnosing staph, a common bacterial infection.

The genomic method can reveal an infection before symptoms appear, allowing treatment to begin almost immediately, Ginsburg said.

If you have been exposed, we can make the prediction on whether you are going to get sick, and consider starting an antiviral medication, Ginsburg said. Such early intervention is likely to make the treatment more effective.

Early treatment could give schools, hospitals and other places where illness spreads quickly a better chance of controlling an outbreak.

Think back to the SARS epidemic [of 2002-2003], when entire schools were being closed and people were being quarantined because we didnt know whether they were actually going to be infected and get sick, Ginsburg said. A cheap and rapid test would have offered a distinct advantage, from a public health point of view.

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Duke researchers say gene studies can help diagnose flu, other infectious diseases

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-- CHOP Researcher Leads Large, Multicenter Gene Sequencing Study of Neuroblastoma--

Newswise Philadelphia, Jan. 20, 2013 An extensive genomic study of the childhood cancer neuroblastoma reinforces the challenges in treating the most aggressive forms of this disease. Contrary to expectations, the scientists found relatively few recurrent gene mutationsmutations that would suggest new targets for neuroblastoma treatment. Instead, say the researchers, they have now refocused on how neuroblastoma tumors evolve in response to medicine and other factors.

This research underscores the fact that tumor cells often change rapidly over time, so more effective treatments for this aggressive cancer will need to account for the dynamic nature of neuroblastoma, said study leader John M. Maris, M.D., director of the Center for Childhood Cancer Research at The Childrens Hospital of Philadelphia (CHOP).

Striking the peripheral nervous system, neuroblastoma usually appears as a solid tumor in a young childs chest or abdomen. It comprises 7 percent of all childhood cancers, but causes 10 to 15 percent of all childhood cancer-related deaths. Neuroblastoma is notoriously complex, with a broad number of gene changes that can give rise to the disease.

Maris headed the multicenter research collaborative, the TARGET (Therapeutically Applicable Research to Generate Effective Treatments) initiative, which released its findings today in Nature Genetics. This largest-ever study genomic study of a childhood cancer analyzed DNA from 240 children with high-risk neuroblastomas. Using a combination of whole-exome, whole-genome and transcriptome sequencing, the study compared DNA from tumors with DNA in normal cells from the same patients.

Researchers at CHOP and other centers previously discovered neuroblastoma-causing mutations, such as those in the ALK gene. In the subset of patients carrying this mutation, oncologists can provide effective treatments tailored to their genetic profile.

A few years ago, we thought we would be able to sequence the genomes of individual patients with neuroblastoma, detect their specific cancer-causing mutations, and then select from a menu of treatments, said Maris. The oncology researchers designed the TARGET study to perform genomic analyses of a large cohort of high-risk neuroblastoma patients, with the goal of mapping out a limited number of treatment strategies. This approach would represent a significant step forward in personalizing neuroblastoma therapy.

However, while the researchers confirmed that roughly 10 percent of the studys neuroblastoma patients had ALK mutations, and found that a handful of other gene mutations each accounted for percentages in the single digits, there were relatively few recurrent mutations in somatic (non-germline) cells. The relative paucity of recurrent mutations challenges the concept that druggable targets can be defined in each patient by DNA sequencing alone, wrote the authors.

In the absence of frequently altered oncogenes that drive high-risk neuroblastomas, the authors concluded that most such cases may result from other changes: rare germline mutations, copy number variations and epigenetic modifications during tumor evolution.

Personalized medicine is more complex than we had hoped, said Maris. While there are successes such as those in treating patients whose tumors harbor ALK mutations, this study implies that we must think very differently about how well use genomics to define treatment. Maris added that neuroblastoma researchers may need to turn to functional genomics, learning which tumors will or wont respond to treatments, as well as going beyond a static picture of a cancer cell with fixed genetic contents, to devising interventions to deal with dynamic tumor cells that evolve during nervous system development.

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Tumors Evolve Rapidly in a Childhood Cancer, Leaving Fewer Obvious Treatment Targets

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The kind of DNA once known as junk may influence peoples risk of getting rheumatoid arthritis, according to a study that offers the latest look at the complex system of switches that turn disease genes on.

Using genetic information from more than 300 people with rheumatoid arthritis and another 300 without, the researchers found 10 areas that appeared to influence risk, according to the research published yesterday in the journal Nature Biotechnology.

The finding builds on a growing body of evidence that genes, small pieces of DNA that make up about 1 percent of the genome, arent the only parts of the system that matter for disease risk. In September, a group of scientists created a map of the regulatory genes, and suggested they might be important for complex diseases like rheumatoid arthritis.

This could explain why risk genes assert themselves and cause disease, and why some people are affected more easily than others, said Tomas Ekstrom, a study author and professor of cell biology at the Karolinska Institutet, in a statement.

Rheumatoid arthritis, or RA, is a disease in which the immune system attacks the body, resulting in swelling and damage in the joints, which can make tasks such as walking or holding items painful. Women are more likely than men to have rheumatoid arthritis, and an estimated 1.5 million adults have the disease, according to the U.S. Centers for Disease Control and Prevention.

Changes in the junk DNA regulatory system may explain how the environment can influences inherited genes, the researchers wrote in the paper. One way that happens is in its ability to add or subtract pieces of DNA molecules. This process, called methylation, helps the body make sure that the correct genes are working at the right times.

An example of this would be the gene variant that was previously linked to the increased risk of RA amongst smokers, Ekstrom said. His group is now checking to see if there are regulatory regions that may explain the link between the inherited risk and the environment in rheumatoid arthritis.

In the study, researchers found changes in the regulatory system were associated with rheumatoid arthritis. Some of these influenced disease risk. Using mathematical modeling, the group found that some of these changes occurred only when people had particular gene variants. That suggests that the regulatory system is playing a role, the authors wrote.

Of the 10 areas discovered by the researchers, 9 were associated with a region known to play a role in diseases where the body attacks itself. One-tenth was on a region never-before associated with the disease. The findings were double-checked in a group of 12 people with rheumatoid arthritis and 12 controls.

Rheumatoid arthritis is treated with anti-inflammatory pills such as aspirin, or drugs such as Humira that attack the disease directly by modifying the immune system. Humira is made by AbbVie Inc., split off this month from Abbott Laboratories, and had $7.9 billion in 2011 sales, according to Abbott.

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Rheumatoid Arthritis Riak Boosted by Gene Regulators

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How to Pronounce Bioengineer
Learn how to say Bioengineer correctly with EmmaSaying #39;s "how do you pronounce" free tutorials. Definition of bioengineering (oxford dictionary): noun [mass noun] 1another term for genetic engineering. 2the use of artificial tissues, organs, or organ components to replace damaged or absent body parts. 3the use in engineering or industry of organisms or biological processes. Derivatives bioengineer noun verb http://www.emmasaying.com Take a look at my comparison tutorials here http://www.youtube.com Subscribe to my channel here : http://www.youtube.com

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How to Pronounce Bioengineer - Video

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