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Sponsored Video: Ambry Genetics – "Fully Automated"

An international collaboration between researchers at the University of Washington in Seattle, Duke University, Harvard University, the Oxford University Clinical Research Unit in Vietnam and Kings College London reported these findings Feb. 3 in the journal Cell.

These results suggest the possibility of tailoring tuberculosis treatment, based on a patient's genetic sequence at a gene called LTA4H, which controls the balance between pro-inflammatory and anti-inflammatory substances produced during an infection.

Tuberculosis can take hold if disease-fighting inflammation is either too weak or too strong. The strength of the response is in part the result of a person's LTA4H gene sequence. Knowing whether a patient has the gene sequence for one extreme response or the other could help guide medication decisions.

Lalita Ramakrishnan, professor of microbiology, medicine and immunology at the University of Washington and the senior author of the study, said that the study suggested that that increased TB disease severity in humans can occur for fundamentally opposite reasons. “The ability to tailor therapies to these divergent inflammatory states, based on a patient's sequence at LTA4H, could improve patient outcomes.”

This important observation for people began with a study of the tiny zebrafish. In these animals, the researchers linked mutations in the zebrafish version of the LTA4H gene to increased susceptibility to a TB-like infection. David Tobin, now on the faculty of the Department of Molecular Genetics and Microbiology at Duke University, is first author of the study. He performed the research while he was a postdoctoral fellow in the University of Washington laboratory of Dr. Ramakrishnan, working closely with another postdoctoral fellow Francisco Roca.

After they understood the biological basis of susceptibility to infection in the zebrafish, the researchers turned to the same gene in humans. They identified a sequence of the gene that led to higher activity and increased inflammation. They then collaborated with other researchers at the University of Washington, including Mary-Claire King, and researchers in Vietnam and the U.K., including Guy Thwaites, to study the gene among patients in Vietnam with TB. They discovered that patients carrying one copy of the high-activity sequence of the gene and one copy of the low-activity sequence were relatively protected from TB meningitis, a particularly deadly form of TB. Surprisingly, people with two copies of the high-activity sequence of the gene fared just as poorly as people with two copies of the low-activity sequence. This “heterozygous advantage,” or “Goldilocks effect,” is an unusual finding in human genetics.

King commented “Throughout human history, people with both forms of the LTA4H gene have probably been more likely to survive when exposed to TB than people with only one form of the LTA4H gene. This advantage may have led to both forms of the gene persisting in human populations. Selection by infectious diseases has had an enormous impact on the evolution of our species.”

This surprising finding, the researchers noted, implicated both insufficient and overly abundant inflammation as different ways TB could take hold in the body. By analyzing clinical data from patients in Vietnam with a particularly severe form of TB called TB meningitis, the researchers found that anti-inflammatory therapy only benefited patients with the gene sequence that corresponds to excess inflammation. The patients with the insufficient inflammation gene sequence derived no benefit from what has been adopted as a standard therapy for TB meningitis.

Given the clinical and therapeutic implications of these findings, the researchers sought the underlying molecular mechanisms for both extremes. For this they turned back to the zebrafish.

In collaboration with Charles Serhan, of Harvard University they showed that one gene variant weakened inflammation through the overproduction of substances called lipoxins. Hyperinflammation results from a gene variant that leads to an excess of leukotriene B4. Either can interfere with the overall levels of tumor necrosis factor, a substance that, when present in normal amounts, protects against TB infection and other diseases.

Paradoxically, either a deficiency or an overkill of tumor necrosis factor can cause macrophages, the host cells that gobble up pathogens, to die by bursting and releasing the TB pathogens into a “permissive extracellular milieu where they can grow exuberantly into corded mats” the researchers said.

The researchers then discovered that corticosteroids, which are in wide clinical use, as well the active ingredient in aspirin decreased TB infection in zebrafish with the “hot responder” genotype, but increased TB infection in their “cold responder” genotype siblings.

The researchers concluded, “If patients succumb to TB for two fundamentally different reasons, then it is imperative to design therapeutic strategies that reflect this dichotomy. For example, if evaluating the treatment effects of dexamethasone on TB meningitis doesn't take into account host genotype, the very substantial benefits of the drug for the high-reactive genotype may be diluted by its neutral or possibly detrimental effects on individuals with the low-activity genotype.”

A simple gene test for the high-responding variant, they said, could provide a rapid, inexpensive way to determine which patients would benefit from dexamethasone therapy added to standard infection-fighting drugs. They also believe clinical studies are urgently needed to be sure patients with the low-reactive genotype are not harmed by unnecessary dexamethasone treatment, and to find alternative treatment strategies for this group, such as agents that limit lipoxin production or boost inflammation.

Because the basic inflammatory biochemical pathways affected by the LTA4H gene are common to many infections, the researchers said TB treatment strategies suggested by their findings may hold promise for other serious infections.

Provided by University of Washington (news : web)

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Treatment for tuberculosis can be guided by patients' genetics

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New Governance Structure Approved by AMP Membership

SALT LAKE CITY, Feb. 6, 2012 (GLOBE NEWSWIRE) — Myriad Genetics, Inc. (Nasdaq:MYGN – News) announced today that Jim Evans, Chief Financial Officer, is scheduled to present at the Leerink Swann 2012 Global Healthcare Conference, at 11:00 a.m. Eastern Time on Thursday, February 16, 2012. The conference is being held at the Waldorf Astoria Hotel in New York, New York.

The presentation will be available to interested parties through a live webcast accessible on the investor relations section of Myriad's website at www.myriad.com.

About Myriad Genetics

Myriad Genetics, Inc. (Nasdaq:MYGN – News) is a leading molecular diagnostic company dedicated to developing and marketing transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess a patient's risk of disease progression and disease recurrence. Myriad's portfolio of nine molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a focus on improving an individual's decision making process for monitoring and treating disease. With fiscal year 2011 annual revenue of over $400 million and more than 1,000 employees, Myriad is working on strategic directives, including new product introductions, companion diagnostics, and international expansion, to take advantage of significant growth opportunities. For more information on how Myriad is making a difference, please visit the Company's website: www.myriad.com.

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Myriad Genetics to Present at the Leerink Swann 2012 Global Healthcare Conference

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Response Genetics to Present at the 22nd Annual UBS Global Healthcare Services Conference

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Signal Genetics to Buy ChipDx, Gaining Cancer Test Pipeline, Bioinformatics Resources

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Viral Genetics Inc. Issues 2011 Year in Review and 2012 Outlook

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Plant and Microbial Biology 160 – Lecture 1 – Video

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Signal Genetics Agrees to Purchase ChipDX to Gain Cancer Diagnostics

NEW YORK–(BUSINESS WIRE)– Signal Genetics, a privately held predictive genetic testing company focused on oncology, today announced an agreement with New York based ChipDX LLC (“ChipDX”), under which Signal will acquire all of the assets of ChipDX, including patents for prognostic tests in lung, breast, and colon cancers. As part of the transaction, Signal will acquire BreastGeneDX®, ColonGeneDX®, and LungGeneDX®, all diagnostic and prognostic tests in development by ChipDX. Signal believes that these genetic tests represent novel products or improvements over other products currently on the market in these cancer types. Signal will also acquire ChipDX’s web-based interface, which will be used to enhance Signal’s physician web portal and allow for remote interpretation of test algorithms. Ryan VanLaar, Ph.D., CEO and Founder of ChipDX, will join Signal as the Head of BioInformatics. Financial details of the transaction were not disclosed.

ChipDX has been recognized by leading molecular diagnostics companies and academic centers for its work in various types of cancer, including most recently for its work on the BreastGeneDX® prognostic test. The acquired tests will leverage the technology platform currently in use by Signal Genetics and its subsidiaries and will provide economies of scale to the Company’s currently commercialized Multiple Myeloma prognostic test, MyPRS Plus™. Additionally, Signal Genetics will leverage its recently established sales team as well as its commercial partners to launch the acquired products.

“The acquisition of the intellectual property and patents of ChipDX dramatically expands and enhances our oncology pipeline,” said Joe Hernandez, President and CEO of Signal. “The addition of ChipDX’s bioinformatics capabilities drastically reduces our time to market with novel molecular tests designed to facilitate better patient outcomes at a lower cost profile. We are also thrilled to have Ryan VanLaar join our team and we welcome him to Signal. This transaction is consistent with our strategy to develop and acquire innovative tools that both complement and enhance our product portfolio.”

Ryan van Laar, CEO and Founder of ChipDX LLC, said, “Joining forces with Signal Genetics provides us with a vehicle to ultimately commercialize our strong portfolio of predictive molecular diagnostic tests. I look forward to leveraging the experience gained in the development of ChipDX to help Signal Genetics achieve its goals, and ultimately improve patient outcomes.”

About ChipDX LLC

ChipDX LLC is a privately held molecular diagnostics and personalized medicine company based in New York City. It was founded and is currently lead by Ryan VanLaar, Ph.D.

About Signal Genetics

Signal Genetics, the parent company of Myeloma Health LLC, CC Health, Respira Health, and ChipDX, is a privately held predictive genetic testing company focused on helping cancer patients. The goal of Signal Genetics is to provide cancer patients and their physicians with novel and innovative insights into their disease, including predicting outcomes, accurately staging disease, providing odds of relapse, and identifying the optimal treatment regimen based on their specific genetic expression profile. Additional information is available at www.signalgenetics.com

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Signal Genetics Announces Acquisition of ChipDX LLC and Expansion of Molecular Diagnostics Assets in Oncology

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Ambry Genetics, Looking to Entice Pharma, Rolls out CHO Cell Expression Array

(RTTNews.com) – Myriad Genetics Inc. (MYGN) Tuesday reported a 17 percent rise in second-quarter earnings on double-digit revenue growth at Molecular diagnostic testing segment and contribution of Companion diagnostic acquired last May. Both earnings and revenue for the quarter topped analysts estimates.

Looking ahead, the company also raised its outlook for full year 2012. Buoyed by the results, Myriad Genetics shares gained more than 5 percent in extended trade on the Nasdaq.

Net income for the second quarter rose to $28.3 million or $0.33 per share from $24.2 million or $0.26 per share in the prior year. On average, 19 analysts polled by Thomson Reuters expected earnings of $0.31 per share for the quarter. Analysts' estimates typically exclude special items.

Revenues for the quarter grew 22 percent to $123 million from $100.4 million a year ago. Analysts expected revenues of $115.29 million.

Molecular diagnostic testing revenue grew 17 percent and accounted for most of the revenues, as all segments and products saw growth. Within the segment, Oncology revenue rose 15 percent, and Women's Health revenue by 22 percent. Revenue from Companion diagnostic service was $5.2 million.

Myriad Genetics now expects 2012 earnings in a range of $1.24 to $1.28 per share and revenues of $465 million to $475 million. Analysts currently expect earnings of $1.24 per share and revenues of $461.45 million for the year.

The company had earlier forecast 2012 earnings in the range of $1.20 to $1.25 per share with revenues of $465 million to $475 million.

Salt Lake City, Utah-based Myriad Genetics is a molecular diagnostic company that focuses on the development of novel predictive medicine, personalized medicine, and prognostic medicine tests primarily in the U.S.

MYGN closed Tuesday on the Nasdaq at $23.66, up $0.40 or 1.72%, on a volume of about 1.8 million shares. In after hours, the stock further gained $1.24 or 5.24%.

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Myriad Genetics Profit Up, Lifts FY12 Outlook; Stock Up

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Myriad Genetics Reports Second Quarter Fiscal Year 2012 Results

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Genetics Pioneer Was UConn Professor, Mentor

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Genetics study reveals how bacteria behind serious childhood disease evolve to evade vaccines

Pneumococcus (Streptococcus pneumoniae) causes
potentially life-threatening diseases including pneumonia and meningitis. Pneumococcal infections
are thought to kill around a million young children worldwide
each year, though the success of vaccination programmes has led
to a dramatic fall in the number of cases in countries such as
the UK and US. These vaccines recognise the bacteria by its
polysaccharide, the material found on the outside of the
bacterial cell. There are over ninety different kinds – or
'serotypes' – of the bacteria, each with a different
polysaccharide coating.

In 2000, the US introduced a pneumococcal vaccine which targeted seven of the ninety
serotypes. This '7-valent' vaccine was extremely effective and
had a dramatic effect on reducing disease amongst the age
groups targeted. Remarkably, the vaccine has also prevented
transmission from young children to adults, resulting in tens
of thousands fewer cases of pneumococcal disease each year. The
same vaccine was introduced in the UK in 2006 and was similarly
successful.

In spite of the success of the vaccine programmes, some
pneumococcal strains managed to continue to cause disease by
camouflaging themselves from the vaccine. In research funded by
the Wellcome Trust, scientists at the University of Oxford and
at the Centers for Disease Control and Prevention in Atlanta
studied what happened after the introduction of this vaccine in
the US. They used the latest genomic techniques combined with
epidemiology to understand how different serotypes of the
pneumococcus bacteria evolve to replace those targeted by the
initial vaccine.

The researchers found bacteria that had evaded the vaccine by
swapping the region of the genome responsible for making the
polysaccharide coating with the same region
from a different serotype, not targeted by the vaccine. This
effectively disguised the bacteria, making it invisible to the
vaccine. This exchange of genome regions occurred during a
process known as recombination, whereby one of the bacteria
replaces a piece of its own DNA with a piece from another
bacterial type.

Dr Rory Bowden, from the University of Oxford, explains:
“Imagine that each strain of the pneumococcus bacteria is a
class of schoolchildren, all wearing the school uniform. If a
boy steals from his corner shop, a policeman – in this case the
vaccine – can easily identify which school he belongs to by
looking at his uniform. But if the boy swaps his sweater with a
friend from another school, the policemen will no longer be
able to recognise him and he can escape. This is how the
pneumococcus bacteria evade detection by the vaccine.”

Dr Bowden and colleagues identified a number of recombined
serotypes that had managed to evade the vaccine. One in
particular grew in frequency and spread across the US from east
to west over several years. They also showed that during
recombination, the bacteria also traded a number of other parts of
the genome at the same time, a phenomenon never before observed
in natural populations of pneumococcus. This is of particular
concern as recombination involving multiple fragments of DNA
allows rapid simultaneous exchange of key regions of the genome
within the bug, potentially allowing it to quickly develop
antibiotic resistance.

The original 7-valent vaccine in the US has now been replaced
by a 13-valent vaccine, which targets thirteen different
serotypes, including the particular type which had escaped the
original vaccine. In the UK, the 7-valent vaccine resulted in a
substantial drop in disease overall. This overall effect was a
mixture of a large drop in frequency of the serotypes targeted
by the vaccine with some growth in serotypes not targeted by
the vaccine. The 13-valent vaccine was introduced in the UK in
2010.

Derrick Crook, Professor of Microbiology at the University of
Oxford and Infection Control Doctor at the Oxford University
Hospitals NHS Trust, adds: “Childhood vaccines are very
effective at reducing disease and death at a stage in our lives
when we are susceptible to serious infections. Understanding
what makes a vaccine successful and what can cause it to fail
is important. We should now be able to understand better what
happens when a pneumococcal vaccine is introduced into a new
population. Our work suggests that current strategies for
developing new vaccines are largely effective but may not have
long term effects that are as successful as hoped.”

Dr Bernard Beall, a scientist at the Centers for Disease
Control and Prevention commented: “The current vaccine strategy
of targeting predominant pneumococcal serotypes is extremely
effective, however our observations indicate that the organism
will continue to adapt to this strategy with some measurable
success.”

The Wellcome Trust, which part-funded this research, views
combating infectious disease and maximising the health benefits
of genetic research as two of its strategic priorities. Dr
Michael Dunn, Head of Molecular and Physiological Sciences at
the Wellcome Trust commented: “New technologies allow us to
rapidly sequence disease-causing organisms and see how they
evolve. Coupled with collaborations with epidemiologists, we
can then track how they spread and monitor the potential impact
this will have on vaccine efficiency. This will provide useful
lessons for vaccine implementation strategies.”

More information: Golubchik, T et al. Pneumococcal
genome sequencing tracks a vaccine escape variant formed
through a multi-fragment recombination event. Nature
Genetics; e-pub Jan 29, 2012.

Provided by Wellcome Trust (news : web)

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Genetics study reveals how pneumococcus bacteria evolve to evade vaccines

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