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BRCA1 gene patent ruling to be appealed

Part of the sequence of BRCA1.

A decision that private companies can control human genes will be appealed in the Federal Court.

Cancer groups have applauded the move, and say a win is vital to protect patient access to new tests and treatments.

Law firm Maurice Blackburn has lodged documents to appeal a decision last month by Federal Court justice John Nicholas that upheld a patent on the so-called breast cancer gene mutations in a gene known as BRCA1.

Lost the case ... Yvonne D'Arcy. Photo: Peter Rae

Cancer Council head Ian Olver said it was important to have the decision clarified.

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"Everyone will be watching this," he said. "If the appeal is lost, it's very clear we will need to use the political process to change the legislation to ensure it is in the best interest of patients," he said.

Maurice Blackburn principal Rebecca Gilsenan said she believed the firm had a good basis under which to appeal the decision.

She said Justice Nicholas had erred in his decision that isolating the gene outside the body should be considered a form of new manufacture.

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BRCA1 gene patent ruling to be appealed

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Fat gene 'linked with skin cancer'

4 March 2013 Last updated at 02:52 ET

A gene previously shown to be linked to obesity may also increase the risk of a deadly form of skin cancer, say researchers writing in Nature Genetics.

Analysis of data from 73,000 people, led by the University of Leeds, found a specific section of the "fat gene" was associated with malignant melanoma.

It is the first time the gene has been linked with a specific disease independently of weight.

The results suggest a wider role for the gene than originally thought.

Malignant melanoma is the fifth most common cancer in the UK with about 12,800 new cases and about 2,200 deaths each year.

An international team analysed genetic data from the tumours of 13,000 malignant melanoma patients and 60,000 unaffected individuals.

They found that those with particular variations in a stretch of DNA within the "fat gene" or FTO gene, called intron 8, could be at greater risk of developing melanoma.

Previous research linking the FTO gene with obesity found that variants in a section called intron 1 are linked with being overweight and overeating.

It's now clear we don't know enough about what this intriguing gene does

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Gene discovery reveals importance of eating your greens

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

Contact: Liz Williams williams@wehi.edu.au 61-405-279-095 Walter and Eliza Hall Institute

Eating your greens may be even more important that previously thought, with the discovery that an immune cell population essential for intestinal health could be controlled by leafy greens in your diet.

The immune cells, named innate lymphoid cells (ILCs), are found in the lining of the digestive system and protect the body from 'bad' bacteria in the intestine. They are also believed to play an important role in controlling food allergies, inflammatory diseases and obesity, and may even prevent the development of bowel cancers.

Dr Gabrielle Belz, Ms Lucie Rankin, Dr Joanna Groom and colleagues from the Walter and Eliza Hall Institute's Molecular Immunology division have discovered the gene T-bet is essential for producing a population of these critical immune cells and that the gene responds to signals in the food we eat.

Dr Belz said the research team revealed T-bet was essential for generating a subset of ILCs which is a newly discovered cell type that protects the body against infections entering through the digestive system. "In this study, we discovered that T-bet is the key gene that instructs precursor cells to develop into ILCs, which it does in response to signals in the food we eat and to bacteria in the gut," Dr Belz said. "ILCs are essential for immune surveillance of the digestive system and this is the first time that we have identified a gene responsible for the production of ILCs."

The research was published today in the journal Nature Immunology.

Dr Belz said that the proteins in green leafy (cruciferous) vegetables are known to interact with a cell surface receptor that switches on T-bet, and might play a role in producing these critical immune cells. "Proteins in these leafy greens could be part of the same signalling pathway that is used by T-bet to produce ILCs," Dr Belz said. "We are very interested in looking at how the products of these vegetables are able to talk to T-bet to make ILCs, which will give us more insight into how the food we eat influences our immune system and gut bacteria."

ILCs are essential for maintaining the delicate balance between tolerance, immunity and inflammation. Ms Rankin said the discovery had given the research team further insight into external factors responsible for ILC activation. "Until recently, it has been difficult to isolate or produce ILCs," Ms Rankin said. "So we are very excited about the prospect for future research on these cells which are still poorly understood."

ILCs produce a hormone called interleukin-22 (IL-22), which can protect the body from invading bacteria, Dr Belz said. "Our research shows that, without the gene T-bet, the body is more susceptible to bacterial infections that enter through the digestive system. This suggests that boosting ILCs in the gut may aid in the treatment of these bacterial infections," she said.

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Gene discovery reveals importance of eating your greens

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Gene Simpson Named Vice President of Underwriting and Marketing for CompWest Insurance Company

SAN FRANCISCO, March 4, 2013 /PRNewswire/ --CompWest Insurance Company, a subsidiary of Accident Fund Holdings, Inc., announces the appointment of Gene J. Simpson as vice president of Underwriting and Marketing.

(Logo: http://photos.prnewswire.com/prnh/20100727/DE40865LOGO )

Simpson recently joined CompWest's senior management team and is responsible for company-wide underwriting and marketing practices. In this position, Simpson coordinates the development and implementation of company underwriting and marketing programs; manages and directs the execution of all sales plans and production initiatives; as well as the research, strategy and implementation of new markets.

"The CompWest team has made significant strides in stabilizing our financial results, despite challenging environmental factors," Bryan Bogardus, president of CompWest Insurance Company, said. "As we look forward, we see a significant role for CompWest in the workers' compensation marketplace and the addition of Gene is an investment in our future. Gene has a proven track record of developing and deploying successful go-to-market strategies and he is excited about working with our employees and partner brokers to grow our company."

Simpson most recently served as vice president of Workers' Compensation Product Management for Seabright Holdings, Inc. Prior to that, he served as vice president of General Liability and Product Line Manager for Liberty Mutual Insurance and for 11 years in a variety of capacities for Safeco Insurance Company, including assistant vice president of Product Development,; assistant director of Workers' Compensation; commercial manager of National Programs and commercial underwriter of Multiline and Workers' Compensation.

Simpson graduated from Western Washington University with a Bachelor of Science in applied mathematics and holds the designations of Chartered Property Casualty Underwriter (CPCU) and Certified Insurance Counselor (CIC). Simpson is an active member of his community, participating in various fundraising efforts to support several charitable organizations with a particular interest in Susan G. Komen for the Cure.

About CompWest Insurance CompanyCompWest is one of the most innovative underwriters of workers' compensation insurance in California and the Western States.Its industry-leading claims management model, called Workers' Compensation with Care, coupled with outstanding loss prevention services and ability-based return to work programs has produced lower insurance costs and competitive rates for more than 2,000 policyholders.CompWest is rated "A-" (Excellent) by A.M. Best Company.To learn more about the 'CompWest Difference' go to http://www.compwestinsurance.com.

Accident Fund Holdings, Inc.Accident Fund Holdings, Inc. is a workers compensation insurance holding company conducting business through four operating units: Accident Fund Companies, located in Lansing, Michigan; United Heartland, located in New Berlin, Wisconsin; CompWest, located in San Francisco, California; and Third Coast Underwriters, located in Chicago, Illinois. Its insurance company subsidiaries are rated "A-" (Excellent) by A.M. Best. Accident Fund Holdings is a wholly-owned subsidiary of Blue Cross Blue Shield of Michigan. For more information, visit Accident Fund Holdings' website at http://www.afhi.com.

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Gene Simpson Named Vice President of Underwriting and Marketing for CompWest Insurance Company

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Obesity gene 'linked to melanoma'

A gene linked to obesity and over-eating may also increase the risk of the most deadly form of skin cancer, research has shown.

People with a particular DNA modification within the FTO gene may be more likely to develop malignant melanoma.

Previous research has shown that variations in a different part of the gene are a major risk factor for obesity.

Until now there has been no evidence that obesity and melanoma are linked.

The new findings, published in the journal Nature Genetics, suggest that FTO has more wide-ranging functions than previously thought.

Lead scientist Dr Mark Iles, from the University of Leeds, said: "This is the first time to our knowledge that this major obesity gene, already linked to multiple illnesses, has been linked to melanoma. This raises the question whether future research will reveal that the gene has a role in even more diseases.

"When scientists have tried to understand how the FTO gene behaves, so far they've only examined its role in metabolism and appetite. But it's now clear we don't know enough about what this intriguing gene does.

"This reveals a hot new lead for research into both obesity-related illnesses and skin cancer."

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Obesity gene 'linked to melanoma'

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First evidence that obesity gene is risk factor for melanoma

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

Contact: Rachel Barson r.barson@leeds.ac.uk 01-133-432-060 University of Leeds

The research shows that people with particular variations in a stretch of DNA within the FTO gene, called intron 8, could be at greater risk of developing melanoma.

Variations in a different part of the FTO gene, called intron 1, are already known to be the most important genetic risk factor for obesity and overeating. These variants are linked to Body Mass Index (BMI) a measure of a person's shape based on their weight and height. Having a high BMI can increase the risk of various diseases including type 2 diabetes, kidney disease, womb (endometrial) cancer and more.

But this research is the first to reveal that the gene affects a disease melanoma which isn't linked to obesity and BMI.

The results, published in Nature Genetics, suggest that FTO has a more wide-ranging role than previously suspected, with different sections of the gene being involved in various diseases.

Study author, Dr Mark Iles, Cancer Research UK scientist at the University of Leeds, said: "This is the first time to our knowledge that this major obesity gene, already linked to multiple illnesses, has been linked to melanoma. This raises the question whether future research will reveal that the gene has a role in even more diseases?

"When scientists have tried to understand how the FTO gene behaves, so far they've only examined its role in metabolism and appetite. But it's now clear we don't know enough about what this intriguing gene does.

"This reveals a hot new lead for research into both obesity-related illnesses and skin cancer."

The researchers examined tumour samples in more than 13,000 melanoma patients and almost 60,000 unaffected people from around the world.

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First evidence that obesity gene is risk factor for melanoma

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February 28th 2013 time lapse and Chemtrail photos – Video


February 28th 2013 time lapse and Chemtrail photos
February 28th 2013 recorded data from Virginia, USA. Please subscribe for more videos uploaded frequently. Share to spread awareness of Geo-engineering and genetic modification. Music by Bone Thugs n Harmony: Change The World

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Phonophani – End Of All Things – Video


Phonophani - End Of All Things
Phonophani - End Of All Things from Genetic Engineering (2001)

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New Guidance Issued on Genetic Testing of Children

Newswise For the first time, the American Academy of Pediatrics (AAP) and the American College of Medical Genetics and Genomics (ACMG) spoke with one voice and released a set of recommendations and guidelines on best practices for genetic testing and screening of children.

Genetic screening is done more on children than on any other group, with about 4 million newborns screened every year for nearly 40 metabolic and endocrine disorders including phenylketonuria, cystic fibrosis and hypothyroidism, as well as hemoglobinopathies, such as sickle cell disease. Most states have adopted the uniform panel, although some states include a variety of additional conditions.

Despite gains in technology and the study of genetics, such guidelines had not been updated by either group in at least a decade.

We now have geneticists, pediatricians and ethicists all in consensus about what are the best guidelines for genetic testing and screening of children, said pediatrician Lainie Ross, MD, PhD, Carolyn and Matthew Bucksbaum professor and associate director at the MacLean Center for Clinical Medical Ethics at the University of Chicago.

Ross is the lead author of the policy statement, published by AAP, and the companion technical paper, published by the ACMG. The new guidelines were released on Feb. 21, 2013.

The two groups also were unified in their call for greater parental involvement in the genetic testing and screening of children.

Currently, genetic screening of newborns is mandatory and this has led to minimal or no engagement of parents. Parents are often not told that screening is happening. When they are told, very little information typically is provided, even though they had the right to refuse screening in most states.

The new statement promotes mandatory offering of screening. A mandatory offer means parents must be informed that screening is available and should be provided with an overview of what will be screened for, the type of results they may get, the minor risks involved and the potential benefits if their child is found to have a disorder that requires immediate treatment.

After such education and counseling, parents then would be asked to give permission for screening. While there are no guidelines on what form that consent would take, it could be as easy as a verbal agreement to go ahead.

In our world, we want every baby to be screened. The move from mandatory screening to mandatory offering is to engage parents, to make sure that parents know about screening and give permission for it, Ross said. If they say no, the next step is not to say OK but to engage in further conversation because refusal should be a very rare event given the high benefit-to-risk ratio.

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Seven Genetic Risk Factors Associated with Common Eye Disorder

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Newswise A professor from Case Western Reserve University School of Medicine is one of the lead authors of a study identifying seven new regions of the human genome that are associated with increased risk of age-related macular degeneration (AMD), a leading cause of blindness among older adults.

The AMD Gene Consortium, a network of international investigators representing 18 research groups, also confirmed the existence of 12 other regions called loci that had been identified in previous studies. The authors report their findings online in the journal Nature Genetics. Supported by the National Eye Institute (NEI), a part of the National Institutes of Health, the study represents the most comprehensive genome-wide analysis of genetic variations associated with AMD.

This work represents a big step forward toward solving why some people get AMD, while others do not, said Sudha Iyengar, PhD, professor of epidemiology and biostatistics at Case Western Reserve School of Medicine and a member of the consortiums senior executive committee. This disease is not caused by a single change in the DNA, but represents many events that accumulate over the lifetime of a patient. Identification of these genes provides molecular windows into the AMD disease process.

AMD affects the macula, a region of the retina responsible for central vision. The retina is the layer of light-sensitive tissue in the back of the eye that houses rod and cone photoreceptor cells. Compared with the rest of the retina, the macula is especially dense with cone photoreceptors; humans rely on the macula for tasks that require sharp vision, such as reading, driving, and recognizing faces. As AMD progresses, such tasks become more difficult and eventually impossible. Some kinds of AMD are treatable, but no cure exists. An estimated 2 million Americans suffer from AMD.

Since the 2005 discovery that certain variations in the gene for complement factor Ha component of the immune systemare associated with major risk for AMD, research groups around the world have conducted genome-wide association studies to identify other loci that affect AMD risk. These studies were made possible by tools developed through the Human Genome Project, which mapped human genes, and related projects, such the International HapMap Project, which identified common patterns of genetic variation within the human genome.

The consortiums analysis included data from more than 17,100 people with the most advanced and severe forms of AMD, which were compared to data from more than 60,000 people without AMD. The 19 loci that were found to be associated with AMD implicate a variety of biological functions, including regulation of the immune system, maintenance of cellular structure, growth and permeability of blood vessels, lipid metabolism, and atherosclerosis.

As with other common diseases, such as Type 2 diabetes, an individual persons risk for getting AMD is likely determined not by one but many genes. Further comprehensive DNA analysis of the areas around the 19 loci identified by the AMD Gene Consortium could turn up undiscovered rare genetic variants with a disproportionately large effect on AMD risk. Discovery of such genes could greatly advance scientists understanding of AMD pathogenesis and their quest for more effective treatments.

This compelling analysis by the AMD Gene Consortium demonstrates the enormous value of effective collaboration, said NEI director Paul A. Sieving, MD, PhD. Combining data from multiple studies, this international effort provides insight into the molecular basis of AMD, which will help researchers search for causes of the disease and will inform future development of new diagnostic and treatment strategies.

Other lead authors of the study include: Gonalo R. Abecasis, D. Phil., University of Michigan; Lindsay A. Farrer, PhD, Boston University; Iris Heid, PhD, University of Regensburg, Germany; and Jonathan L. Haines, PhD, Vanderbilt University.

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Seven Genetic Risk Factors Associated with Common Eye Disorder

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7 genetic risk factors found to be associated with common eye disorder

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

Contact: Jessica Studeny jessica.studeny@case.edu 216-368-4692 Case Western Reserve University

A professor from Case Western Reserve University School of Medicine is one of the lead authors of a study identifying seven new regions of the human genome that are associated with increased risk of age-related macular degeneration (AMD), a leading cause of blindness among older adults.

The AMD Gene Consortium, a network of international investigators representing 18 research groups, also confirmed the existence of 12 other regions called loci that had been identified in previous studies. The authors report their findings online in the journal Nature Genetics. Supported by the National Eye Institute (NEI), a part of the National Institutes of Health, the study represents the most comprehensive genome-wide analysis of genetic variations associated with AMD.

"This work represents a big step forward toward solving why some people get AMD, while others do not," said Sudha Iyengar, PhD, professor of epidemiology and biostatistics at Case Western Reserve School of Medicine and a member of the consortium's senior executive committee. "This disease is not caused by a single change in the DNA, but represents many events that accumulate over the lifetime of a patient. Identification of these genes provides molecular windows into the AMD disease process."

AMD affects the macula, a region of the retina responsible for central vision. The retina is the layer of light-sensitive tissue in the back of the eye that houses rod and cone photoreceptor cells. Compared with the rest of the retina, the macula is especially dense with cone photoreceptors; humans rely on the macula for tasks that require sharp vision, such as reading, driving, and recognizing faces. As AMD progresses, such tasks become more difficult and eventually impossible. Some kinds of AMD are treatable, but no cure exists. An estimated 2 million Americans suffer from AMD.

Since the 2005 discovery that certain variations in the gene for complement factor Ha component of the immune systemare associated with major risk for AMD, research groups around the world have conducted genome-wide association studies to identify other loci that affect AMD risk. These studies were made possible by tools developed through the Human Genome Project, which mapped human genes, and related projects, such the International HapMap Project, which identified common patterns of genetic variation within the human genome.

The consortium's analysis included data from more than 17,100 people with the most advanced and severe forms of AMD, which were compared to data from more than 60,000 people without AMD. The 19 loci that were found to be associated with AMD implicate a variety of biological functions, including regulation of the immune system, maintenance of cellular structure, growth and permeability of blood vessels, lipid metabolism, and atherosclerosis.

As with other common diseases, such as Type 2 diabetes, an individual person's risk for getting AMD is likely determined not by one but many genes. Further comprehensive DNA analysis of the areas around the 19 loci identified by the AMD Gene Consortium could turn up undiscovered rare genetic variants with a disproportionately large effect on AMD risk. Discovery of such genes could greatly advance scientists' understanding of AMD pathogenesis and their quest for more effective treatments.

"This compelling analysis by the AMD Gene Consortium demonstrates the enormous value of effective collaboration," said NEI director Paul A. Sieving, MD, PhD. "Combining data from multiple studies, this international effort provides insight into the molecular basis of AMD, which will help researchers search for causes of the disease and will inform future development of new diagnostic and treatment strategies."

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7 genetic risk factors found to be associated with common eye disorder

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Genzyme’s Head of Rare Diseases Honored by the Genetic Disease Foundation

CAMBRIDGE, Mass.--(BUSINESS WIRE)--

Genzyme, a Sanofi company (EURONEXT: SAN and NYSE: SNY), today announced that Genzymes Head of Rare Diseases, Rogerio Vivaldi, MD, has been honored as the Genetic Disease Foundations Industry Person of the Year. The award is given to an individual in the life sciences industry who has made outstanding contributions to advancing medical research and bringing new therapies to people living with rare genetic diseases.

For more than 20 years, Dr. Vivaldi has worked to identify the unmet needs of those living with rare genetic diseases, such as Gaucher disease, said Elisa Ross, President of the Genetic Disease Foundation (GDF). We are pleased to recognize Dr. Vivaldi for his dedication and commitment to improving patients lives.

The award will be presented tonight at the GDF Gala at New Yorks Gotham Hall.The eventwill raise funds for the Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai.

I am truly honored by this award. As a physician in Brazil, I saw firsthand the importance of diagnosis and treatment for rare genetic diseases, said Dr. Vivaldi. At Genzyme we continue the mission to develop and deliver transformative therapies to all patients affected by rare genetic diseases.

The Genetic Disease Foundation is a non-profit organization established in 1997 by patients and families affected by genetic disorders. The Foundations mission is to help prevent and treat genetic diseases by supporting research and counseling and conducting educational initiatives.

About Genzyme, a Sanofi Company

Genzyme has pioneered the development and delivery of transformative therapies for patients affected by rare and debilitating diseases for over 30 years. We accomplish our goals through world-class research and with the compassion and commitment of our employees. With a focus on rare diseases and multiple sclerosis, we are dedicated to making a positive impact on the lives of the patients and families we serve. That goal guides and inspires us every day. Genzymes portfolio of transformative therapies, which are marketed in countries around the world, represents groundbreaking and life-saving advances in medicine. As a Sanofi company, Genzyme benefits from the reach and resources of one of the worlds largest pharmaceutical companies, with a shared commitment to improving the lives of patients. Learn more at http://www.genzyme.com.

About Sanofi

Sanofi, a global and diversified healthcare leader, discovers, develops and distributes therapeutic solutions focused on patients needs. Sanofi has core strengths in the field of healthcare with seven growth platforms: diabetes solutions, human vaccines, innovative drugs, consumer healthcare, emerging markets, animal health and the new Genzyme. Sanofi is listed in Paris (SAN) and in New York (SNY).

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Genzyme’s Head of Rare Diseases Honored by the Genetic Disease Foundation

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ME3: Extended Cut Analysis Part 6 – Video


ME3: Extended Cut Analysis Part 6
The Synthesis ending. TED: Bonnie Bassler: The secret, social lives of bacteria http://www.youtube.com The ending to Life Story, the best genetics movie ever made: http://www.youtube.com

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Katy Perry vs Little Mix – ET vs DNA – Video


Katy Perry vs Little Mix - ET vs DNA
Songs Used: Katy Perry - ET (Acapella)(Pitch Altered)(Teenage Dream) Little Mix - DNA (Instrumental Glamour Simple Genetics Acapella)(DNA) No Copyright Infringement Intended. For entertainment purposes only. "Copyright Disclaimer Under Section 107 of the Copyright Act 1976, allowance is made for "fair use" for purposes such as criticism, comment, news reporting, teaching, scholarship, and research. Fair use is a use permitted by copyright statute that might otherwise be infringing. Non-profit, educational or personal use tips the balance in favor of fair use." I DO NOT OWN THE RIGHTS TO THE SONGS IN THIS VIDEO. ALL RIGHTS RESERVED TO ITS RIGHTFUL OWNERS.

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McCabe Genetics Lot 16 2013 – Video


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McCabe Genetics Lot 18 2013 – Video


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McCabe Genetics Lot 21 2013 – Video


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McCabe Genetics Lot 50 2013 – Video


McCabe Genetics Lot 50 2013

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McCabe Genetics Lot 114 2013 – Video


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McCabe Genetics Lot 138 2013 – Video


McCabe Genetics Lot 138 2013

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McCabe Genetics Lot 139 2013 – Video


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The Genetics Behind Age-related Macular Degeneration Detailed In New Study

March 4, 2013

redOrbit Staff & Wire Reports Your Universe Online

A coalition of 18 different research organizations has identified seven new genetic regions associated with an eye disorder that is a common cause of blindness in older individuals, according to a study published online Sunday in the journal Nature Genetics.

The AMD Gene Consortium study also confirmed that 12 regions of the human genome (also known as loci) previously identified by scientists were also associated with age-related macular degeneration (AMD).

According to the National Eye Institute (NEI), the research which was led by experts from the University of Michigan, Boston University, Vanderbilt University, and the University of Regensburg in Germany represents the most comprehensive genome-wide analysis of genetic variations associated with AMD.

Officials with Vanderbilt University Medical Center said that the research could point to new biological pathways and therapeutic targets for AMD. In addition, Jonathan Haines, Ph.D., director of the Nashville, Tennessee-based universitys Center for Human Genetics Research, said that their efforts have made it possible to explain nearly two-thirds of the genetics associated with the development of this degenerative eye condition.

The NEI, which is a part of the US National Institutes of Health and supported the AMD Gene Consortiums efforts, explained that the condition targets a persons macula, or the part of the retina responsible for central vision. The macula typically helps people in tasks that require sharp vision, including reading and driving. However, AMD makes those tasks more difficult and eventually impossible as it progresses, and there is no known cure.

In their research, the consortium looked at data for more than 17,000 of the estimated two million Americans currently suffering from AMD. The test subjects each had more advanced, severe forms of the condition, and their genetic information was compared to that of over 60,000 people not suffering from the condition.

The 19 loci that were found to be associated with AMD implicate a variety of biological functions, including regulation of the immune system, maintenance of cellular structure, growth and permeability of blood vessels, lipid metabolism and atherosclerosis, researchers from Boston University Medical Center explained in a statement.

Further comprehensive DNA analysis of the areas around the 19 loci identified by the AMD Gene Consortium could turn up undiscovered rare genetic variants with a disproportionately large effect on AMD risk, they added. Discovery of such genes could greatly advance scientists understanding of AMD pathogenesis and their quest for more effective treatments.

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Cancer Genetics, Inc. Receives Regulatory Approvals for MatBA®-DLBCL, A Proprietary Microarray Test for the Diagnosis …

RUTHERFORD, N.J.--(BUSINESS WIRE)--

Cancer Genetics, Inc. (CGI), a leader in oncology-focused personalized medicine, today announced it has received CLIA and New York State approvals for clinical use of its proprietary mature B-cell neoplasm array or MatBA (patent 13/475,034) for diffuse large B-cell lymphoma. MatBA-DLBCL will assist clinicians in the diagnosis and prognosis of DLBCL.

DLBCL is the most common form of non-Hodgkin lymphoma (NHL), a diverse group of hematological malignancies. An estimated 190,000 people in the United State suffer from DLBCL, and up to 24,500 new U.S. cases diagnosed each year, which accounts for up to 40% of all NHL cases. Newly-diagnosed patients have a median age of 64 years, and disease progression and outcomes vary widely, due in part to the genomic characteristics of each individual patients cancer. This creates a strong clinical need for accurate and molecularly-informed prognostic testing both at the time of initial diagnosis and throughout ongoing disease monitoring efforts to ensure selection of the best treatment plan for an individual patient. However, current prognostic modalities rely primarily on clinical features.

CGIs MatBA-DLBCL microarray provides clinicians with information on genomic alterations in DLBCL, including regions of gain and loss that are associated with disease outcome.

A research collaboration between the Memorial Sloan-Kettering Cancer Center and CGI using 87 patient samples, as well as the analysis of two open datasets including 171 samples (GSE11318, Lenz et al.) and 51 high risk samples (E-MEXP-3463, Taskinen) and other published datasets showed that:

CGI believes that it is the only laboratory to have a CLIA and New York State approved microarray for the genomic assessment of DLBCL. The MatBA-DLBCL Array CGH assay joins the DLBCL CompleteSM program offered by CGI, which includes a suite of esoteric tests used in the diagnosis, prognosis and clinical management of DLBCL patients. This newly-approved DLBCL test extends CGIs ongoing commitment to developing new diagnostic and disease management tools for some of the most costly and critical unmet needs in oncology today. MatBA-DLBCL joins MatBA-CLL (chronic lymphocytic leukemia) and MatBA-SLL (small lymphocytic leukemia) in CGIs suite of CLIA- and New York State-approved proprietary microarrays for the clinical management of underserved hematological malignancies.

About Cancer Genetics, Inc.

Cancer Genetics, Inc. (CGI) is an emerging leader in the field of personalized medicine, offering products and services that enable cancer diagnostics as well as treatments that are tailored to the specific genetic profile of the individual. CGI is committed to maintaining the standard of clinical excellence through its investment in outstanding facilities and equipment. Our reference laboratory is both CLIA certified and CAP accredited. In addition, we have approvals and accreditations from the states of Florida, Maryland, New York, and New Jersey. The company has been built on a foundation of world-class scientific knowledge and IP in solid and hematologic cancers, as well as strong research collaborations with major cancer centers such as Memorial Sloan-Kettering and the National Cancer Institute.

CGIs dedicated staff takes pride in our specialized laboratory services, superior turnaround time (TAT), enhanced reporting, EMR integration, and ongoing research and development for new oncology tests. CGIs full-service cancer genetic practice and path to innovation with research makes for optimal patient care management. For further information, please see http://www.cancergenetics.com.

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Cancer Genetics, Inc. Receives Regulatory Approvals for MatBA®-DLBCL, A Proprietary Microarray Test for the Diagnosis ...

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Myriad Genetics Win on Gene Patent Ownership Is Appealed

Myriad Genetics Inc. (MYGN)s Australian court victory recognizing its ownership of patents for genes linked to cancer risks will be appealed by a group representing cancer patients, a law firm said.

Cancer Voices Australia and Yvonne DArcy, a Brisbane resident diagnosed with breast cancer, sued in 2010 to stop Myriad and Genetic Technologies Ltd. (GTG) from patenting an isolated DNA associated with an increased risk of breast and ovarian cancers, according to Maurice Blackburn Lawyers. The firm said it has filed the appeal in the Federal Court of Australia today.

We intend to continue the challenge to the monopoly created by the patent held by Myriad, Rebecca Gilsenan, a lawyer at Melbourne-based Maurice Blackburn, said in an e-mailed statement.

The issue has divided the global medical community, with groups including the Association for Molecular Pathology and the American College of Medical Genetics arguing that Myriad is trying to get legal ownership of parts of the human body. The U.S. Court of Appeals for the Federal Circuit, which specializes in patent law, has twice ruled that genes can be patented.

The Myriad case returns to the U.S. Supreme Court this year after the U.S. high court agreed Nov. 30 to hear the Association for Molecular Pathologys appeal.

Australian Federal Court Justice John Nicholas ruled Feb. 15 that the method used by Myriad and Genetic Technologies of purging a gene of biological material is a manufacturing process that can be patented.

Some scientists argue they have been stymied in researching new medicines and treatments because they may come up against demands for royalties or letters demanding they stop using patented inventions. Companies such as Genomic Health Inc. (GHDX) have argued they cant attract investment dollars if they cant protect their research from competitors.

I wont give up the fight, DArcy said in todays statement. We need to continue for future generations of people who at some point in their life, may need treatment for cancer and other diseases.

The case is: Cancer Voices Australia v. Myriad Genetics. NSD643/2010. Federal Court of Australia (Sydney).

To contact the reporter on this story: Joe Schneider in Sydney at jschneider5@bloomberg.net

See the article here:
Myriad Genetics Win on Gene Patent Ownership Is Appealed

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