Archive for the ‘Gene Therapy Research’ Category

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

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

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

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

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

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

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plushberry #1 TGA Genetics week6 - Video

genetics: first draft
stop motion animation. first cut.

By: elyssa bulger

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genetics: first draft - Video

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

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Company Scientists featured on Discovery Channel - Video

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 ...

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2008 Petite Sirah Video Tasting Notes - Video

the flav trimmed.mov
TGA Genetics The Flav

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the flav trimmed.mov - Video

North Cobb High School Genetics Mitosis Lab

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North Cobb High School Genetics Mitosis Lab - Video

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

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

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

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

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

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

-- 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

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

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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Civilization V - Genetic Engineering Mod
Have you ever wanted to bring down biological war fair on your fellow civs. If you do, then this is the Mod for you! Not only are their biological weapons but you also get to make Jurassic Park!

By: crazyPotatoz

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Civilization V - Genetic Engineering Mod - Video

PALO ALTO, Calif. & CAMBRIDGE, England--(BUSINESS WIRE)--

Today, Open Monoclonal Technology, Inc. (OMT) and Recombinant Antibody Technology, Ltd (RAT) announced a publication about OmniRat in the Journal of Immunology (www.jimmunol.org/content/early/2013/01/09/jimmunol.1203041). The publication by scientists from OMT, RAT and Pfizer is entitled High-Affinity IgG Antibodies Develop Naturally in Ig- Knockout Rats Carrying Germline Human IgH/Igk/Igl Loci Bearing the Rat CH Region and covers eighteen months of close collaboration between the teams.

The manuscript describes a comprehensive comparison of wild type animals with OmniRat, the first genetically engineered rat to generate fully human antibody specificities. While there have been numerous transgenic mice expressing human antibodies, this is the first genetic engineering project that resulted in an animal that makes antibodies with fully human idiotypes as well as wild type animals make their own antibodies.

Antibodies from transgenic animals have proven to be the most productive platform for human antibody drug discovery and development. Six of eight currently approved human monoclonal antibodies are from transgenic animals and many more are in the pharmaceutical industry pipeline.

Dr. Marianne Brggemann, senior author of the manuscript, Research Director of RAT and scientific advisor to OMT, said: "We generated the first mouse expressing human antibodies 25 years ago. Many others followed but none of these worked as well as normal animals. I am pleased that we finally managed to generate an animal that makes antibodies with human idiotypes as well as wildtype animals. The data convinced Pfizer that OmniRat is a valuable tool for routine generation of high affinity human antibodies."

Open Monoclonal Technology, Inc.

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

OMT has created OmniRat, the first fully human monoclonal antibody platform based on transgenic rats. OMTs genetic engineering is based on an improved understanding of B cell development and a new approach to inactivation of endogenous antibody expression, which enables OmniRat to make antibodies with human idiotypes as efficiently as wild type rats make normal antibodies. OmniRat represents a novel and proprietary technology with unrestricted development options for fully human monoclonal antibodies, available worldwide for all targets and indications.

OMT also develops a transgenic mouse, OmniMouse, to complement OmniRat and further increase epitope coverage in human antibody development.

OmniAb integrates OMTs transgenic animal platforms, proven protein and DNA immunization and Gel-Encapsulated Microenvironment (GEM) deep antibody screening to enable fast and costefficient generation and identification of preferred human therapeutic antibody candidates.

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Open Monoclonal Technology and Recombinant Antibody Technology Announce OmniRat™ Scientific Publication

Thousands of people braved the cold and demonstrated in the streets of Berlin as politicians and policymakers met to discuss changes to global agricultural policies.

Under the slogan, We are fed up, the protesters called for an end to food scandals, genetic engineering and animal cruelty in industrial livestock farming.

We are from the Friends of the Earth and we demonstrate for the peace of animals, small farmers, ecological farming, non-genetic produce animals and non-genetic food, Viola Wagner said, as she marched and chanted.

We got up at 4 oclock to come six hours by bus. Im here for my children and my grandchildren, to make sure they have a future and good food.

More than 120 groups representing farmers, industry, and animal rights and environmental activists organized the demonstration. It was timed to coincide with International Green Week, the Agriculture Ministers' Summit and the Global Forum for Agriculture, which are all taking place in Berlin this week.

The event also comes as another scandal in Germany has shaken consumer confidence in the safety and quality of the countrys food. Animal feed fats contaminated with the carcinogenic compound dioxin has again been discovered in the food chain, causing some countries to block German pork and egg imports.

Organizers said 22,000 people came from all over Germany, although police estimated turnout closer to 15,000.

Following about 50 tractors, they marched from Berlins main train station, along one of the main shopping streets, through the government district, and ended with a rally in front of German Chancellor Angela Merkels offices.

The current dioxin scandal has suddenly highlighted the backlog of reforms in agricultural policy, Hubert Weiger, chairman of BUND (Friends of the Earth Germany), said in a speech.

In her weekly video message on Saturday, Merkel said the government would tighten controls in the animal feed industry.

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Berlin protests focus on farming and food safety

--Johns Hopkins scientists identify epigenetic changes that referee genetic risk

Newswise In one of the first genome-wide studies to hunt for both genes and their regulatory tags in patients suffering from a common disease, researchers have found a clear role for the tags in mediating genetic risk for rheumatoid arthritis (RA), an immune disorder that afflicts an estimated 1.5 million American adults. By teasing apart the tagging events that result from RA from those that help cause it, the scientists say they were able to spot tagged DNA sequences that may be important for the development of RA. And they suspect their experimental method can be applied to predict similar risk factors for other common, noninfectious diseases, like type II diabetes and heart ailments.

In a report published in Nature Biotechnology Jan. 20, the researchers at Johns Hopkins and the Karolinska Institutet say their study bridges the gap between whole-genome genetic sequencing and diseases that have no single or direct genetic cause. Most genetic changes associated with disease do not occur in protein-coding regions of DNA, but in their regulatory regions, explains Andrew Feinberg, M.D., M.P.H., a Gilman scholar, professor of molecular medicine and director of the Center for Epigenetics at the Johns Hopkins University School of Medicines Institute for Basic Biomedical Sciences. Our study analyzed both and shows how genetics and epigenetics can work together to cause disease, he says.

Rheumatoid arthritis is a debilitating disease that causes inflammation, stiffness, pain and disfigurement in joints, especially the small joints of the hands and feet. It is thought to be an autoimmune disease, meaning that the bodys immune system attacks its own tissues, an assault led primarily by white blood cells. According to Feinberg, several DNA mutations are known to confer risk for RA, but there seem to be additional factors that suppress or enhance that risk. One probable factor involves chemical tags that attach to DNA sequences, part of a so-called epigenetic system that helps regulate when and how DNA sequences are read, how theyre used to create proteins and how they affect the onset or progress of disease.

To complicate matters, Feinberg notes, the attachment of the tags to particular DNA sequences can itself be regulated by genes. The details of what causes a particular sequence to be tagged are unclear, but it seems that some tagging events depend on certain DNA sequences. In other words, those tagging events are under genetic control, he says. Other tagging events, however, seem to depend on cellular processes and environmental changes, some of which could be the result, rather than the cause, of disease.

To tease apart these two types of tagging events, the researchers catalogued DNA sequences and their tagging patterns in the white blood cells of more than 300 people with and without one form of RA.

The team then began filtering out the tags that did not appear to affect RA risk. For example, if tags were seen on the same DNA sequence in those with and without RA, it was assumed that the tags at those sites were irrelevant to the cause or development of the disease. Then, from among the RA-relevant tags, they narrowed in on tags whose placement seemed to be dependent on DNA sequence. Finally, they made sure that the DNA sequences identified were themselves more prevalent in patients with RA. In this way, they created a list of DNA sequences associated with altered DNA tagging patterns, both of which were associated with RA.

Ultimately, the team identified 10 DNA sites that were tagged differently in RA patients and whose tagging seemed to affect risk for RA. Nine of the 10 sites were within a region of the genome known to play an important role in autoimmune diseases, while the 10th was on a gene that had never before been associated with the disease. Since RA is a disease in which the bodys immune system turns on itself, current treatments often involve suppressing the entire immune system, which can have serious side effects, Feinberg says. The results of this study may allow clinicians to instead directly target the culpable genes and/or their tags.

Our method allows us to predict which tagging sites are most important in the development of a disease. In this study, we looked for tagging sites under genetic control, but similar tags can be triggered by environmental exposures, like smoking, so there are many applications for this type of work, says Yun Liu, Ph.D., a lead researcher on the project.

The study also may shed light on how evolution works, explains Feinberg. It seems that natural selection might not simply be selecting for an individuals current fitness level but also for the adaptability of future generations given an unknown future. We think that certain genetic sequences may be biologically beneficial and conserved over time because they increase the amount of variation found in tagging patterns, giving individuals a greater chance of adapting to environmental changes.

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Genes and Their Regulatory 'Tags' Conspire to Promote Rheumatoid Arthritis

Jan. 21, 2013 Cancer cells are resourceful survivors with plenty of tricks for staying alive. Researchers have uncovered one of these stratagems, showing how cells lacking the tumor suppressor BRCA1 can resume one form of DNA repair, sparing themselves from stagnation or death. The study appears in the January 21st issue of The Journal of Cell Biology.

The BRCA1 protein helps to mend double-strand DNA breaks by promoting homologous recombination. Without it, cells can amass broken, jumbled, and fused chromosomes, which may cause them to stop growing or die. Although cells lacking BRCA1 seem like they should be vulnerable, loss of the protein instead seems to boost abnormal growth.

Recent studies have shown that cells lacking BRCA1 compensate by cutting back on 53BP1. This protein helps orchestrate a different DNA repair mechanism, nonhomologous end joining (NHEJ), and it thwarts a key step in homologous recombination. Researchers think that, in cells without BRCA1, 53BP1 spurs excessive NHEJ that can cause fatal chromosomal chaos. But with 53BP1 out of the way, the cells are able to resume homologous recombination. That might explain why cells that lack BRCA1 and eliminate 53BP1 can withstand traditional chemotherapy compounds and PARP inhibitors, a new generation of anti-cancer drugs that are in clinical trials. But how do cancer cells turn down 53BP1?

Researchers previously found that certain mutant fibroblasts increase production of cathepsin L, a protease that destroys 53BP1. BRCA1-deficient cancer cells take advantage of the same mechanism, according to a team of researchers led by Susana Gonzalo from the Washington University School of Medicine. When they cultured breast cancer cells that were missing BRCA1, the cells stopped growing. After two weeks of lethargy, however, some cells, which the researchers dubbed BOGA cells (BRCA1-deficient cells that overcome growth arrest), began to divide again. These cells showed increased levels of cathepsin L and reduced amounts of 53BP1. Eliminating cathepsin L from BOGA cells or dosing them with vitamin D, a cathepsin L inhibitor, prevented the decline in 53BP1 abundance.

To find out whether boosting cathepsin L levels enabled the cancer cells to restart homologous recombination, the researchers monitored sites of DNA damage tagged by RAD51, a protein that helps promote homologous recombination. The cells that had stopped growing did not display RAD51 foci, but these foci were prevalent in BOGA cells with reduced 53BP1. Removing cathepsin L from BOGA cells increased 53BP1 levels and diminished the number of RAD51 foci.

If cells can't perform homologous recombination, they turn to repair mechanisms such as NHEJ that can lead to jumbled chromosomes. However, after DNA-breaking doses of radiation, BOGA cells exhibited few chromosome defects. The number of these flaws climbed after the researchers stabilized 53BP1 levels by inhibiting cathepsin L or trimming its abundance.

The team then analyzed tumor samples from breast cancer patients. Researchers suspect that cathepsin L attacks 53BP1 by entering the nucleus. Samples from patients with BRCA1 mutations or with triple-negative breast cancer -- an aggressive form of the disease -- showed high levels of nuclear cathepsin L and reduced quantities of 53BP1. That suggests tumors in these patients hike the amounts of cathepsin L in the nucleus to break down 53BP1 and restore homologous recombination.

"It's a new pathway that explains how breast cancer cells lose 53BP1," says Gonzalo. How cancer cells boost nuclear cathepsin L levels is unclear, she notes.

Triple-negative breast cancers are currently identified by their lack of Her2 and the estrogen and progesterone receptors. The work suggests that another trio of measurements -- the amounts of 53BP1, cathepsin L, and vitamin D receptor in the nucleus -- might help identify patients that are resistant to current breast cancer treatments. These people might respond to cathepsin inhibitors, some of which are undergoing animal testing. These compounds might steer the cells away from homologous recombination and leave them vulnerable to other therapies.

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Enzyme helps cancer cells avoid genetic instability