Oct. 20, 2013 Research led by St. Jude Children's Research Hospital scientists has linked an inherited gene variation to a nearly four-fold increased risk of developing a pediatric acute lymphoblastic leukemia (ALL) subtype that is associated with a poor outcome. The study appears today in the online edition of the scientific journal Nature Genetics.

The high-risk variant was found in the GATA3 gene. Researchers reported the high-risk version of the gene was more common among Hispanic Americans and other individuals with high Native American ancestry than those of other ethnic backgrounds. Forty percent of Hispanic Americans carried the high-risk variant, compared to 14 percent of individuals of European ancestry. For this study, ethnicity was defined by genetic variations associated with ancestry rather than individual self-reports.

Hispanic children are known to be at a higher risk of developing ALL and of dying from the disease. This is the latest in a series of St. Jude studies to report an association between inherited DNA variations in a handful of genes and an increased risk of childhood ALL among those of Hispanic ethnicity.

This is the first study to link an inherited genetic variation to an elevated risk of developing the leukemia subtype known as Philadelphia chromosome-like ALL (Ph-like ALL). Individuals with the high-risk version of GATA3 were 3.85 times more likely than those who inherited a different version of the gene to develop Ph-like ALL. Patients with the high-risk variant were also more likely to have a poor treatment response and have their cancer eventually return.

A significant percentage of patients with the high-risk GATA3 variant also had the tumor genetic alterations -- including mutations, gene deletions and chromosomal re-arrangements -- that are hallmark of Ph-like ALL. The changes occur in genes, including CRLF2, JAK and IKZF1 that regulate how blood cells grow and mature.

"Until recently, little was known about why a child develops a specific subtype of ALL in the first place and whether inherited genetic variations that predispose an individual to a subtype also influence how he or she responds to the therapy," said corresponding author Jun J. Yang, Ph.D., an assistant member of the St. Jude Department of Pharmaceutical Sciences. "In this study, we discovered a genetic basis for susceptibility to Ph-like ALL, but even more importantly, the evidence that host and tumor genomes may interact with each other to influence the risk of developing and surviving ALL."

The study was done in collaboration with the Children's Oncology Group, a U.S.-based research cooperative study group focused on childhood cancer research and clinical trials. The research included 680 patients enrolled in COG clinical trials.

Ph-like ALL accounts for as much as 15 percent of childhood ALL and is associated with a high risk of relapse and a poor outcome. ALL is the most common childhood cancer. While overall cure rates for pediatric ALL are now about 90 percent, only 63 percent of children with Ph-like ALL are alive and cancer free after five years. Yang added that larger population studies are needed to assess risks associated with these inherited variations.

GATA3 carries instructions for assembling a protein called a transcription factor that turns other genes on and off. The GATA3 protein, and other members of the GATA gene family, plays a crucial role in normal development of a variety of blood cells. Alterations in GATA3 have been linked to other blood cancers, including Hodgkin lymphoma.

The high-risk GATA3 variation was identified using a library of 718,890 common genetic variations known as single nucleotide polymorphisms, or SNPs, to screen the DNA of 75 children with Ph-like ALL, 436 children with other ALL subtypes and 6,661 individuals without ALL. Fifty-eight percent of patients with Ph-like ALL carried the high-risk version of the gene, compared to 29 percent of patients with other ALL subtypes and 20 percent of those without ALL. When researchers checked for the high-risk variant in additional patients with the Ph-like ALL subtype as well as other young ALL patients and individuals without the disease, they found the similar percentages carried the high-risk version.

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Inherited gene variation tied to high-risk pediatric leukemia, risk of relapse

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Frantz entered the first round competition by submitting a two-minute video clip singing a rap song about her current work on the development of vaccine combating Porcine Epidemic Diarrhoea Virus (PEDV). She was among the five finalists chosen from 40 video submissions.

"The lyrics in the rap are easy-to-understand language, and free of technical jargons, relying on items listeners are familiar with in their everyday lives, in order to get the audience to understand what I want to explain. Making a fun-filled rap song fun makes my presentation more interesting," she said.

The final round of the competition was held in Singapore on September 25, in which each finalist made a 10-minute presentation in front of a live audience of 150.

"I was very happy once the top award was announced for me. I was very anxious and excited seconds before the announcement was made because there were many Singaporean supporters attending the event held in the host country," she said.

Dr Frantz was awarded a trip to Brussels in Belgium, where she will attend the Euraxess Voice of Researchers Conference along with the winners of the other Euraxess Science Slams, which are organised in the US, Japan, India, China and Brazil.

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Thai researcher wins Euraxess Science Slam Asean 2013

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Oct. 20, 2013 In a biological quirk that promises to provide researchers with a new approach for studying and potentially treating Fragile X syndrome, scientists at the University of Massachusetts Medical School (UMMS) have shown that knocking out a gene important for messenger RNA (mRNA) translation in neurons restores memory deficits and reduces behavioral symptoms in a mouse model of a prevalent human neurological disease. These results, published today in Nature Medicine, suggest that the prime cause of the Fragile X syndrome may be a translational imbalance that results in elevated protein production in the brain. Restoration of this balance may be necessary for normal neurological function.

"Biology works in strange ways," said Joel Richter, PhD, professor of molecular medicine at UMMS and senior author on the study. "We corrected one genetic mutation with another, which in effect showed that two wrongs make a right. Mutations in each gene result in impaired brain function, but in our studies, we found that mutations in both genes result in normal brain function. This sounds counter-intuitive, but in this case that seems to be what has happened."

Fragile X syndrome, the most common form of inherited mental retardation and the most frequent single-gene cause of autism, is a genetic condition resulting from a CGG repeat expansion in the DNA sequence of the Fragile X (Fmr1) gene required for normal neurological development. People with Fragile X suffer from intellectual disability as well as behavioral and learning challenges. Depending on the length of the CGG repeat, intellectual disabilities can range from mild to severe.

While scientists have identified the genetic mutation that causes Fragile X, on a molecular level they still don't know much about how the disease works or what precisely goes wrong in the brain as a result. What is known is that the Fmr1 gene codes for the Fragile X protein (FMRP). This protein probably has several functions throughout the neuron but its main activity is to repress the translation of as many as 1,000 different mRNAs. By doing this, FMRP controls synaptic plasticity and higher brain function. Mice without the Fragile X gene, for instance, have a 15 to 20 percent overall elevation in neural protein production. It is thought that the inability to repress mRNA translation and the resulting increase in neural proteins may somehow hamper normal synaptic function in patients with Fragile X. But because FMRP binds so many mRNAs, and some proteins become more elevated than others, parsing which mRNA or combination of mRNAs is responsible for Fragile X pathology is a daunting task.

From Frog Egg to Fragile X

For years, Dr. Richter had been studying how translation, the process in which cellular ribosomes create proteins, went from dormant to active in frog eggs. He discovered the key gene controlling this process, the RNA binding protein CPEB. In 1998, Richter found the CPEB protein in the rodent brain where it played an important role in regulating how synapses talk to each other. At this point, his work began to move from exploring the role of CPEB in the developmental biology of the frog to how the CPEB protein impacted learning and memory. A serendipitous research symposium with colleagues at Cold Spring Harbor got him thinking about CPEB and Fragile X syndrome.

"Here I was, an outsider, a molecular biologist who had worked for years with frog eggs, in the same room with neurobiologists and neurologists, when they started talking about Fragile X syndrome and translational activity," said Richter. "It got me thinking that the CPEB protein might be a path to restoring the translational imbalance they were discussing."

Richter knew that CPEB stimulated translation and that FMRP repressed it. He also knew that animal models lacking the CPEB protein had memory deficits and that both proteins bound to many of the same mRNAs -- the overlap may be as higher as 33 percent. The thought was that by taking away a protein that stimulated translation might counterbalance the loss of the repressor FMRP protein, thereby restoring translational homeostasis in the brain and normal neurological function.

"It was one of those kind of goofy 'what if' sort of things," said Richter.

To test his hypothesis, Richter developed a double knockout mouse model that lacked both the FMRP gene that caused Fragile X and the CPEB gene. When they began measuring for Fragile X pathologies what they found was almost too good to be true.

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Two genetic wrongs make a biochemical right

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PUBLIC RELEASE DATE:

20-Oct-2013

Contact: Jim Fessenden james.fessenden@umassmed.edu 508-856-2000 University of Massachusetts Medical School

WORCESTER, MA In a biological quirk that promises to provide researchers with a new approach for studying and potentially treating Fragile X syndrome, scientists at the University of Massachusetts Medical School (UMMS) have shown that knocking out a gene important for messenger RNA (mRNA) translation in neurons restores memory deficits and reduces behavioral symptoms in a mouse model of a prevalent human neurological disease. These results, published today in Nature Medicine, suggest that the prime cause of the Fragile X syndrome may be a translational imbalance that results in elevated protein production in the brain. Restoration of this balance may be necessary for normal neurological function.

"Biology works in strange ways," said Joel Richter, PhD, professor of molecular medicine at UMMS and senior author on the study. "We corrected one genetic mutation with another, which in effect showed that two wrongs make a right. Mutations in each gene result in impaired brain function, but in our studies, we found that mutations in both genes result in normal brain function. This sounds counter-intuitive, but in this case that seems to be what has happened."

Fragile X syndrome, the most common form of inherited mental retardation and the most frequent single-gene cause of autism, is a genetic condition resulting from a CGG repeat expansion in the DNA sequence of the Fragile X (Fmr1) gene required for normal neurological development. People with Fragile X suffer from intellectual disability as well as behavioral and learning challenges. Depending on the length of the CGG repeat, intellectual disabilities can range from mild to severe.

While scientists have identified the genetic mutation that causes Fragile X, on a molecular level they still don't know much about how the disease works or what precisely goes wrong in the brain as a result. What is known is that the Fmr1 gene codes for the Fragile X protein (FMRP). This protein probably has several functions throughout the neuron but its main activity is to repress the translation of as many as 1,000 different mRNAs. By doing this, FMRP controls synaptic plasticity and higher brain function. Mice without the Fragile X gene, for instance, have a 15 to 20 percent overall elevation in neural protein production. It is thought that the inability to repress mRNA translation and the resulting increase in neural proteins may somehow hamper normal synaptic function in patients with Fragile X. But because FMRP binds so many mRNAs, and some proteins become more elevated than others, parsing which mRNA or combination of mRNAs is responsible for Fragile X pathology is a daunting task.

From Frog Egg to Fragile X

For years, Dr. Richter had been studying how translation, the process in which cellular ribosomes create proteins, went from dormant to active in frog eggs. He discovered the key gene controlling this process, the RNA binding protein CPEB. In 1998, Richter found the CPEB protein in the rodent brain where it played an important role in regulating how synapses talk to each other. At this point, his work began to move from exploring the role of CPEB in the developmental biology of the frog to how the CPEB protein impacted learning and memory. A serendipitous research symposium with colleagues at Cold Spring Harbor got him thinking about CPEB and Fragile X syndrome.

"Here I was, an outsider, a molecular biologist who had worked for years with frog eggs, in the same room with neurobiologists and neurologists, when they started talking about Fragile X syndrome and translational activity," said Richter. "It got me thinking that the CPEB protein might be a path to restoring the translational imbalance they were discussing."

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2 genetic wrongs make a biochemical right

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Natural Bodybuilder - INSANE Genetics (Preview) bodybuilding fitness 2013 bodybuilding fitness 2013
Natural bodybuilder fitness model Stephen - Preview video of his upcoming training videos where he will be showing himself working out in the gym and will ...

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[BIOS 332] Introduction to Genetics - Jason Tresser
August 31, 2013.

By: BiolaUniversity

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By RTT News, October 21, 2013, 09:24:00 AM EDT

(RTTNews.com) - Seattle Genetics, Inc.( SGEN ), Monday announced the initiation of a phase 1 clinical trial evaluating SGN-LIV1A for patients with LIV-1-positive metastatic breast cancer. SGN-LIV1A utilizes Seattle Genetics' antibody-drug conjugate or ADC technology. The trial will assess the safety and antitumor activity of SGN-LIV1A, targeted to LIV-1, a protein which is expressed in most subtypes of metastatic breast cancer. The primary endpoint of the trial is safety, with key secondary endpoints of objective response, duration of response and progression-free survival.

The study, which is excepted to enroll up to 70 patients, is enrolling patients with triple negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting, or patients with ER-positive and/or PR-positive and HER2-negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting, and at least three prior hormonal therapies.

ADCs are designed to harness the targeting ability of antibodies to deliver cell-killing agents directly to cancer cells. This approach is intended to spare non-targeted cells and thus reduce many of the toxic effects of traditional chemotherapy while enhancing antitumor activity.

For comments and feedback: contact editorial@rttnews.com

http://www.rttnews.com

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Seattle Genetics Begins Phase 1 Trial Of ADC Candidate SGN-LIV1A

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BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) today announced the initiation of a phase 1 clinical trial evaluating SGN-LIV1A for patients with LIV-1-positive metastatic breast cancer. SGN-LIV1A utilizes Seattle Genetics industry-leading antibody-drug conjugate (ADC) technology. The trial is designed to assess the safety and antitumor activity of SGN-LIV1A, an ADC targeted to LIV-1 (SLC39A6), a protein which is expressed in most subtypes of metastatic breast cancer.

ADCs represent a novel treatment approach that have demonstrated activity in both hematologic and solid tumors. SGN-LIV1A is one of four ADCs that we are advancing into the clinic during 2013, demonstrating our significant investment in this approach for the treatment of cancer, said Jonathan Drachman, M.D., Chief Medical Officer and Executive Vice President, Research and Development, at Seattle Genetics. The target expression in breast cancer, preclinical antitumor activity, and need for novel therapeutic options for advanced breast cancer patients all support the clinical evaluation of SGN-LIV1A.

ADCs are designed to harness the targeting ability of antibodies to deliver cell-killing agents directly to cancer cells. This approach is intended to spare non-targeted cells and thus reduce many of the toxic effects of traditional chemotherapy while enhancing antitumor activity.

The study is a phase 1, open-label, dose-escalation clinical trial to evaluate the safety and antitumor activity of SGN-LIV1A in patients with LIV-1-positive metastatic breast cancer. The trial is enrolling patients with triple negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting, or patients with ER-positive and/or PR-positive and HER2-negative disease who have previously been treated with at least two prior cytotoxic regimens in the metastatic setting, and at least three prior hormonal therapies. The primary endpoint of the trial is safety, with key secondary endpoints of objective response, duration of response and progression-free survival (PFS). The study is expected to enroll up to 70 patients at multiple centers in the United States.

The treatment of cancer is changing with the introduction of more targeted agents and understanding disease-specific prognostic factors. Antibody-drug conjugates are an example of this evolving landscape, representing a rational approach to targeted drug delivery, said Howard A. Burris, M.D., Chief Medical Officer, Executive Director of Drug Development at Sarah Cannon Research Institute and investigator for this phase 1 clinical trial. We are eager to evaluate SGN-LIV1A in this phase 1 trial for advanced breast cancer.

At the American Association of Cancer Research (AACR) Annual Meeting in April 2013, preclinical data demonstrated that up to 92 percent of breast tumors analyzed expressed LIV-1, with limited expression in normal tissue. SGN-LIV1A demonstrated significant antitumor activity in multiple preclinical models at well-tolerated doses (AACR 2013 Abstract 3962).

More information about the trial, including enrolling centers, will be available by visiting http://www.clinicaltrials.gov.

About SGN-LIV1A

SGN-LIV1A is an ADC comprised of an anti-LIV-1 monoclonal antibody linked to a synthetic cytotoxic cell-killing agent, monomethyl auristatin E (MMAE), using Seattle Genetics proprietary technology. The ADC is designed to be stable in the bloodstream, and to release its cytotoxic agent upon internalization into LIV-1-expressing tumor cells, which is expressed in most subtypes of metastatic breast cancer. This approach is intended to spare non-targeted cells and thus reduce many of the toxic effects of traditional chemotherapy while enhancing the antitumor activity.

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Seattle Genetics Initiates Phase 1 Trial of ADC Candidate, SGN-LIV1A, for Patients with LIV-1-Positive Metastatic ...

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By Traci Pedersen Associate News Editor Reviewed by John M. Grohol, Psy.D. on October 20, 2013

A genetic variation that impacts how quickly smokers process nicotine can help predict whether those who try to quit are likely to respond to nicotine replacement therapy, according to a new study published in the journal Addiction.

The gene, however, has very little effect on the success of treatment with the drug buproprion (Zyban), an antidepressant that is often prescribed help people quit smoking by reducing their cravings and other withdrawal effects.

Smokers often struggle with cravings and withdrawal when stopping smoking. said lead researcher Laura Jean Bierut, M.D., professor of psychiatry.

This study gives us insights into who may respond to different types of smoking cessation medications so that we can improve the odds of quitting.

Clinically, we often observe that responses to medication vary from one patient to another, said first author Li-Shiun Chen, M.D., assistant professor of psychiatry. To understand those differences, we studied a gene called CYP2A6, which controls nicotine metabolism in our bodies.

It turns out that most of us metabolize nicotine rapidly, but others can metabolize it much more slowly.

Earlier research has shown that roughly 70 percent of individuals have a variation of the CYP2A6 gene that helps them metabolize nicotine quickly, while 30 percent metabolize nicotine more slowly.

Nicotine levels drop more quickly in fast metabolizers after they quit smoking, Chen said.

In slow metabolizers, nicotine stays in the body longer. We have found that fast metabolizers of nicotine are more likely to relapse when they try to quit because when their nicotine levels drop rapidly, they can fall victim to cravings, but theyre also more likely to be helped by nicotine replacement therapy, which can increase nicotine levels and help control those cravings.

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In Smokers, Gene Impacts Success in Nicotine Replacement Therapy

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If one of two packages of, say, frozen edamame you are looking at on the supermarket shelf says, partially-produced with genetic engineering, which of those packages would you buy?

Because companies such as Monsanto, the nations leading producer of genetically-modified seeds, believe you would choose the non-GMO food, they are spending record amounts against Initiative 522, which would require labeling of genetically-engineered foods and seeds offered for retail sale in Washington.

Thats also the reason local and state groups supporting the initiative such as Label It WA. and GMO-Free San Juans want you to vote for the initiative.

Proponents address this issue directly: We also should have a right to choose whether we want to buy and eat genetically engineered food. Labels matter. They ensure transparency and preserve the freedom to make our own decisions about the food we eat. I-522 is a step in the right direction, says the pro voters statement.

Opponents point to increased costs: from Washington Wire, Advocates of Washingtons Initiative 522 say it wont cost a dime, but a new opposition report says that if voters require warning labels on genetically modified food products, the typical family of four would pay an additional $490 a year for groceries.

Local supporters of the voter-approved ban on use of genetically-modified seeds in San Juan County are hoping the 62 percent majority of county voters who supported Initiative 2012-4 last year will vote yes on Initiative 522.

But a local opponent of the GMO seed ban initiative, molecular biologist Larry Soll, says there are bigger things to worry about than a GMO label. Soll, reflecting on the fact that something close to 80 percent of food products now contain some element of GMO technology, points out that both the local and the state initiative are a back door method of getting rid of GMO crops.

The initiative imposes labeling requirements on genetically engineered foods and seeds offered for retail sale in this state. Genetically engineered is defined as foods or seeds produced by techniques that insert DNA or RNA into organisms or that use cell fusion techniques to overcome natural barriers to cell multiplication or recombination, according to the official statement in the voters pamphlet.

Genetically engineered agricultural commodities would be labeled genetically engineered, and genetically engineered packaged processed foods would be labeled partially produced with genetic engineering.

Many foods would be exempt, including alcoholic beverages, certified organic foods, foods not produced using genetic engineering, as certified by an approved independent organization, and foods served in restaurants.

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Health risks vs. higher costs; supporters, critics clash over impact of I-522

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Alien Anatomy Species Genetics part 1 of 2)

By: ?? ???

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Bodybuilding Genetics?
What is one of the biggest factors that determines bodybuilding success that people don #39;t realize? For complementary info in these videos see Muscle: Shape, ...

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LOS ANGELES--(BUSINESS WIRE)--

Life Stem Genetics Inc. (the Company), an emerging innovator in the advancement of Adult Stem Cell therapy announces that the Company's new stock symbol, LIFS, is now active.

The Company is also pleased to release the general details of its recent financing commitment. This financing is for $1 million (the Private Placement) of 1,000,000 units (each, a Unit) at a price of $1 per Unit. Each Unit will consist of one common share of the Company and one warrant to purchase an additional common share of the Company (each, a Warrant Share) at $1 per Warrant Share for a period of one year. The Company is to close the Private Placement within 45 calendar days of this press release.

Gloria Simov, CEO of Life Stem Genetics, commented, "Our new trading symbol and recent financing are key components to provide future value to our shareholders and to our fulfillment of our long term objectives in the emerging Adult Stem Cell therapy industry."

All shareholders of the Company are encouraged to view the Company's complete filings at the following link:

http://www.sec.gov/cgi-bin/browse-edgar?company=Life+Stem+Genetics HYPERLINK "http://www.sec.gov/cgi-bin/browse-edgar?company=Life+Stem+Genetics&owner=exclude&action=getcompany"& HYPERLINK "http://www.sec.gov/cgi-bin/browse-edgar?company=Life+Stem+Genetics&owner=exclude&action=getcompany"owner=exclude HYPERLINK "http://www.sec.gov/cgi-bin/browse-edgar?company=Life+Stem+Genetics&owner=exclude&action=getcompany"& HYPERLINK "http://www.sec.gov/cgi-bin/browse-edgar?company=Life+Stem+Genetics&owner=exclude&action=getcompany"action=getcompany

About Life Stem Genetics

Life Stem Genetics (LSG) is a progressive health care company that focuses on healing with a patients own Stem Cells. Stem Cells for years have been known to heal a variety of ailments successfully and now it is being offered as an efficient and painless way to treat many different illnesses ranging from orthopedic Injuries, neurological disorders such as Parkinsons, and Alzheimers, Cancer, Plastic Surgery, Age Management, Arthritis, Diabetes, Cardiology, COPD, MS, Urology, and many more. Stem Cell Therapy and LSGs proprietary techniques have experienced some of the best results in the industry, helping to repair or re-program damaged or diseased tissues and organs.

LSGs stem cell specialist has performed thousands of stem cell treatments, including the top names in PGA golf, NFL football, NBA basketball, and Major League Baseball. LSG will offer their proprietary treatments through a series of affiliate doctors, and medical clinics, with 60 affiliated clinics so far.

LSGs mission is to create a solid comprehensive approach to the treatment and maintenance of diseases and to break free from the medical insurance world by tapping into an affordable private- pay sector delivering exceptional healthcare free from the medical insurance maze.

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Life Stem Genetics Has New Stock Symbol and New Financing Commitment

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MOLOGEN AG: Clinical study with MGN1404 in malignant melanoma initiated

- Phase I trial to evaluate safety and tolerability

- Trial is under supervision of Charit - Universitaetsmedizin Berlin

Berlin, October 18, 2013 - The phase I clinical trial with the cancer immune therapy MGN1404 has been started. The trial evaluates the safety and tolerability of MGN1404 for the treatment of malignant melanoma. Furthermore data on the mechanism of action will be collected. MGN1404 will be applied in different dosages needle-free by jet-injection into skin metastases. It is planned to overall enroll nine patients in the trial. The study is a translational project for non-viral gene therapy and will be conducted by Charit in collaboration with Charit Comprehensive Cancer Center (CCCC), Experimental and Clinical Research Center (ECRC), Max Delbrueck Center for Molecular Medicine Berlin-Buch (MDC) as well as Skin Cancer Center Charit (SCCC). Principial investigator is Dr. med. Felix Kiecker, Specialist of Dermatology and Venerology, Skin Cancer Center Charit and scientific coordinator is Prof. Wolfgang Walther, ECRC, Charit.

Dr. Matthias Schroff, Chief Executive Officer of MOLOGEN AG, stated, 'With this study the third drug candidate from our broad pipeline of cancer immune therapies is entering the clinical development phase. I am especially glad that the longtime collaboration with the Max Delbrueck Center for Molecular Medicine, one of the best German institutes in the field of molecular biology, has now led to this trial. MGN1404 is addressing a severe disease with high unmet medical need. We are looking forward to the outcome of the trial.'

http://www.mologen.com

Additional information:

MGN1404 - MIDGE(R) vector for TNF-alpha expression Tumor necrosis factor alpha (abbreviated TNF-alpha) is a signaling substance (cytokine) of the immune system. TNF-alpha can stimulate cell death and therefore has - in the case of application into the tumor - a direct antitumoral effect. It also leads to the sensitization of tumors toward other therapies, such as chemotherapy or radiation therapy. MGN1404 is a minimalistic, non-viral DNA expression vector encoding for TNF-alpha, based on MOLOGEN'S proprietary MIDGE(R) platform technology. The needle-free, intratumoral jet injection of MGN1404 conveys the MIDGE(R) vectors directly into the tumor cells. The expression of TNF-alpha is triggered there by the MIDGE(R) vectors aiming to induce cell death in the tumor.

Malignant melanoma Malignant melanomas are one of the most malignant forms of skin cancer. The worldwide occurrence of malignant melanoma in the white population has increased continually and considerably in recent decades. Approximately 77,000 people in the USA and 100,000 people in Europe develop malignant melanoma each year. Despite the lack of symptoms and a relatively small size, melanomas can metastasize early in the lymph nodes and other organs. If diagnosed when there are already distant metastases the five-year survival rate is approximately 10-20%. Treatments of late stage malignant melanoma include chemotherapy, immunotherapy or radiation therapy.

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A gene important in skin tanning has been linked to higher risk for testicular cancer in white men, according to a study led by scientists from the U.S. National Institutes of Health and the University of Oxford in England. Nearly 80 percent of white men carry a variant form of this gene, which increased risk of testicular cancer up to threefold in the study.

The research appeared online October 10, 2013 in the journal Cell, and is the result of an integrated analysis of big data supported by laboratory research. The team suspected that variations in a gene pathway controlled by the tumor suppressor gene p53 could have both positive and negative effects on human health.

The Prevalence of the G allele in African and European Populations: The G allele of the gene KITLG is associated with a greater risk of testicular cancer and is more frequent in whites than Africans or those of African descent. (Courtesy of the KITLG researchers)

Gene variations occur naturally, and may become common in a population if they convey a health benefit, said Douglas Bell, Ph.D., author on the paper and researcher at the National Institute of Environmental Health Sciences (NIEHS), part of NIH. It appears that this particular variant could help protect light-skinned individuals from UV skin damage, like burning or cancer, by promoting the tanning process, but it permits testicular stem cells to grow in the presence of DNA damage, when they are supposed to stop growing.

Bell explained that p53 stimulates skin tanning when ultraviolet light activates it in the skin. It then must bind a specific sequence of DNA located in a gene called the KIT ligand oncogene (KITLG), which stimulates melanocyte production, causing the skin to tan.

To conduct the analysis, Xuting Wang, Ph.D., of NIEHS, co-author and lead bioinformatics scientist on the paper, led a data mining expedition to sieve through many different data sets. The team selected possible leads from the intersection of more than 20,000 p53 binding sites in the human genome, 10 million inherited genetic variations genotyped in the 1000 Genomes Project, and 62,000 genetic variations associated with human cancers identified in genome-wide association studies (GWAS). These data sets were gathered through joint efforts of thousands of researchers from around the world.

In the end, one variant in the p53 pathway was strongly associated with testicular cancer, but also, surprisingly, displayed a positive benefit that is probably related to tanning that has occurred as humans evolved. Wang noted.

The group at the Ludwig Institute for Cancer Research at the University of Oxford, led by Gareth Bond, Ph.D., performed complex experiments to confirm the molecular mechanism that linked the variant with cancer and tanning.

White males with a single nucleotide variation in KITLG, called the G allele, have the highest odds of having testicular cancer. In fact, the twofold to threefold increased risk is one of the highest and most significant among all cancer GWAS conducted within the past few years, said Bond. The high frequency of this allele in light skin individuals may explain why testicular cancer is so much more frequent in people of European descent than those of African descent.

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PUBLIC RELEASE DATE:

18-Oct-2013

Contact: Robin Mackar rmackar@niehs.nih.gov 919-541-0073 NIH/National Institute of Environmental Health Sciences

A gene important in skin tanning has been linked to higher risk for testicular cancer in white men, according to a study led by scientists from the U.S. National Institutes of Health and the University of Oxford in England. Nearly 80 percent of white men carry a variant form of this gene, which increased risk of testicular cancer up to threefold in the study.

The research appeared online October 10, 2013 in the journal Cell, and is the result of an integrated analysis of big data supported by laboratory research. The team suspected that variations in a gene pathway controlled by the tumor suppressor gene p53 could have both positive and negative effects on human health.

"Gene variations occur naturally, and may become common in a population if they convey a health benefit," said Douglas Bell, Ph.D., author on the paper and researcher at the National Institute of Environmental Health Sciences (NIEHS), part of NIH. "It appears that this particular variant could help protect light-skinned individuals from UV skin damage, like burning or cancer, by promoting the tanning process, but it permits testicular stem cells to grow in the presence of DNA damage, when they are supposed to stop growing."

Bell explained that p53 stimulates skin tanning when ultraviolet light activates it in the skin. It then must bind a specific sequence of DNA located in a gene called the KIT ligand oncogene (KITLG), which stimulates melanocyte production, causing the skin to tan.

To conduct the analysis, Xuting Wang, Ph.D., of NIEHS, co-author and lead bioinformatics scientist on the paper, led a data mining expedition to sieve through many different data sets. The team selected possible leads from the intersection of more than 20,000 p53 binding sites in the human genome, 10 million inherited genetic variations genotyped in the 1000 Genomes Project, and 62,000 genetic variations associated with human cancers identified in genome-wide association studies (GWAS). These data sets were gathered through joint efforts of thousands of researchers from around the world.

"In the end, one variant in the p53 pathway was strongly associated with testicular cancer, but also, surprisingly, displayed a positive benefit that is probably related to tanning that has occurred as humans evolved," Wang noted.

The group at the Ludwig Institute for Cancer Research at the University of Oxford, led by Gareth Bond, Ph.D., performed complex experiments to confirm the molecular mechanism that linked the variant with cancer and tanning.

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Tanning gene linked to increased risk of testicular cancer, according to NIH scientists

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I am 99.9% sure that there will never be commercial production of genetically engineered wine grapes ("GMO" to use the common misnomer). Even so, I'd like to indulge in imagining what could be if we lived in some parallel universe where rational scientific thinking prevailed.

Wine grapes are an extremely logical crop for genetic engineering because there is no tolerance for changing varieties. For annual crops like grains or vegetables, new varieties are bred on a regular basis to solve pest issues or to improve features like taste or shelf life. Breeding of perennial fruit crops is a much, much slower process, but entirely new varieties are still introduced from time to time (e.g. Jazz or Pink Lady apples). Even what we call "heirloom varieties" of most vegetable or fruit crops are mostly quite young by wine grape standards.

Chardonnay grown in Colorado

Conventional breeding just isn't a viable option for wine grapes, not because it couldn't be done, but because in an industry so focused on quality and tradition, no one would consider it. The wine industry is based on specific varieties which are hundreds of years old and for which no new variety would ever be acceptable. That is true for varieties in their original appellations (e.g. Pinot Noir and Chardonnay in Burgundy or Cabernet Sauvignon and its blending partners in Bordeaux). It is also true for those same varieties that now make great wines in "New World" (e.g. Malbec in Argentina, Zinfandel in California, or Syrah in Australia).

Therefore, wine grape varieties have been cloned for hundreds of years, specifically to avoid any genetic change (they have always been grown from rooted cuttings or from grafted buds). Grapes make seeds, but the seed won't grow up to be the same variety as the parent, thus they are never used as a way to grow new vines.

Of course, by sticking to very old varieties, wine grape growers must deal with many problems which might otherwise have been solved through breeding. Grape growers have been able to deal with some pests that attack the roots by grafting onto diverse "root stocks" with novel genetics. That was the solution to the great Phylloxera epidemic of the 19th century. But rootstocks can only help with a limited number of grape growing challenges.

Biotechnology is a perfect solution for wine grape issues because it allows changes to address one specific problem without disrupting any of the characteristics that determine quality. Of course, each variety would have to be individually transformed, but in our imaginary rational universe the regulatory regime would be made easier for multiple uses of the same basic genetic construct.

So, genetic engineering could be a very cool solution for various challenges for grapes. I'll list a few of the diseases that might be fixable this way.

As I described in an earlier post, the noble grapes of Europe must now be rather intensively sprayed with fungicides because a disease called Downy Mildew was introduced in the mid-1800s from New World grape species. Those same North American species have a good deal of resistance to that disease, and the genes for those traits could probably be identified and moved into the traditional, high-quality varieties.

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Why Genetically Engineered Grapes Would Make Great Wine

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"We can fit another stop codon over here next to the kitchen."

Yes, their creators call the Genomically Recoded Organisms they madeGROs. But they are not quite as menacing as they sound.

Genetic engineering had, until Y2K at least, was not exactly what it sounds like. No one was really engineering completely new genes that encoded completely new proteins that generated completely new life forms. But the newest generation of tinkerers thought: why not?

The genetic code that is used universally by all life on Earthgiant sequoias, daddy long legs, bakers yeast, barracudas, ring tailed lemurs, you get the idea. It dictates that specific amino acids are encoded by specific combinations of three nucleotide DNA sequences, called codons.

These tinkerers decided that this doesn't need to limit us. And ,just because this genetic code, and the entire variety of life defined by it uses only twenty amino acids; again, why should we? The researchers' attempt to work around these limits is reported in this weeks Science. These upstarts, led by Farren Isaacs at Yale but including people at Harvard, MIT, Columbia, and the Scripps Research Institute, decided to alter the genetic code and generate proteins with nonstandard amino acids.

Why would they do such a thing? The fact that all organisms share a genetic code means we can share genes, which can be good or bad. Notably, viruses hijack cellular machinery so whatever cell they are infecting makes viral proteins instead of what the cell itself needs; GROs might not have this problem. And there are those that are concerned about genetically modified organisms (GMOs) releasing DNA into the environment; if these were genomically recoded in addition to being genetically modified (GRO-GMOs?) this should pose less of a risk.

You might think that they'd start small, with a virus. But this is the super cool part: the organism they genomically recoded is a bacterium, a strain of Escherichia coli. Like all other life forms, E. coli uses three distinct stop codons to signal a halt to protein production. These researchers changed all the instances of one of these stop codons (UAG) into another, AUG. (We've covered the technology that enables this.) This enabled them to get rid of the cellular machinery that recognizes the UAG as a signal to stop making proteins.

Once that was eliminated, they reinserted UAG codons along with new machinery that recognized it as a regular codon, encoding a particular amino acidonly a nonstandard one not used by or found in any other life form. They reassigned a codon to create an alternate genetic code. Nifty right?

This GRO grew even more efficiently than the strain form which it was generated, and it exhibited significantly enhanced resistance to T7 bacteriophage, probably because it would mistranslate any viral proteins containing UAG codons. Oops from the virus' perspective, but good for the bacteria.

The authors note that they have identified an additional twelve codons that may be amenable to removal and eventual reassignment in E. coli, helping them achieve their goal of incorporating nonstandard amino acids that expand the chemical diversity of proteins in vivo. Whether or not they enhance virus resistance, the whole genomic recoding thing is cool as hell.

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Meet the genomically recoded organisms

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Researchers have identified hundreds of variants in a patient's genetic code that predict which people are more susceptible to persistent chronic pain following amputation.

Dr. Andrew D. Shaw, associate professor of anesthesiology and critical care medicine at Duke University Medical Center in Durham, NC, and colleagues conducted the study on 49 military service members who had amputations and persistent pain.

The International Association for the Study of Pain (IASP) states that 80% of all amputees experience pain in the missing body part - known as phantom limb pain.

Patients complain that the pain is similar to that prior to amputation and is more likely to occur after the amputation of a chronically painful limb.

The IASP explains that large-scale surveys of amputees have revealed that treatments for phantom limb pain are often ineffective, suggesting that they fail to address the underlying mechanisms.

The new Duke University Medical Center study claims that new DNA sequence variations may be "pathways of biological importance as the possible source of chronic, persistent pain."

Dr. Shaw explains:

"Persistent phantom pain after amputation is a serious problem with no effective treatments. By identifying these 'pain genes,' we may be able to discover the reasons why pain occurs and predict which patients are more likely to have it. In the future, we hope to discover the biology of persistent pain and develop ways to combat it."

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'Pain genes' identified by DNA sequencing

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Association of Molecular Pathology v. Myriad Genetics, Inc, SCIPR 2013

By: IIT Chicago-Kent College of Law

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Association of Molecular Pathology v. Myriad Genetics, Inc, SCIPR 2013 - Video

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Newswise BETHESDA, MD (October 18, 2013) -- The Genetics Society of America (GSA) welcomes the election of five members to its Board of Directors. The new members include a vice presidentwho will serve as president of the Society in 2015a treasurer, and three directors. They are:

Jasper Rine, PhD (University of California, Berkeley). Dr. Rine will serve as vice president in 2014 and as GSA president in 2015. Sue Jinks-Robertson, PhD (Duke University Medical School), treasurer. Angelika Amon, PhD (Howard Hughes Medical Institute and Massachusetts Institute of Technology), director. Lauren McIntyre, PhD (University of Florida), director. Dmitri Petrov, PhD (Stanford University), director.

We are gratified that such talented scientists and thoughtful educators will volunteer their expertise and limited time to provide leadership for GSA, said GSA Executive Director Adam P. Fagen, PhD. As we welcome these new Board members, we thank the outgoing officers and directors for their dedicated service and look forward to their continued involvement in the Society.

These new officers and directors begin their tenure on January 1, 2014, and will remain on the GSA Board until December 31, 2016.

New Members of the GSA Board of Directors

Vice President (and President-Elect): Jasper Rine, PhD, Professor of Genetics, Genomics and Development, University of California, Berkeley, CA

Dr. Rine investigates epigeneticschanges in gene expression or cell traits not caused by changes in DNA sequenceusing brewers yeast (Saccharomyces cerevisiae), a powerful model organism in genetics. His lab is currently focused on exploring yeast and human genetic and epigenetic variation with the eventual goal of understanding gene silencing and identifying human gene variants whose impact can be addressed through diet. Dr. Rine is an elected member of the National Academy of Sciences and the American Academy of Arts and Sciences and a fellow of the American Association for the Advancement of Science. He serves as a Reviews Editor for GSAs journal GENETICS and an associate editor for GSAs journal G3: Genes|Genomes|Genetics.

Treasurer: Sue Jinks-Robertson, PhD, Professor of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC

Dr. Jinks-Robertson and her lab are examining the regulation of DNA repair and surveillance mechanisms, essential for preventing mutagenesis and maintaining genome stability, using brewers yeast (Saccharomyces cerevisiae) as a model system. Dr. Jinks-Robertson is a fellow of the American Academy of Microbiology and the American Association for the Advancement of Science. She previously served on the GSA Board as a Director from 2010 to 2012 and is founding chair of the Societys Women in Genetics Committee.

Directors: Angelika Amon, PhD, Investigator, Howard Hughes Medical Institute, and Professor of Biology, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA

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Genetics Society of America Welcomes 2014 Board Members

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New York, NY and Stamford, CT (PRWEB) October 18, 2013

More than 100 prominent donors, scientists, biotech representatives, and physicians attended Alliance for Cancer Gene Therapys Achieving Cancer Remission with Cell and Gene Therapies Tuesday night at the Harvard Club of New York City, 35 W. 44th Street.

The evening highlighted recent tremendous strides made in combating cancer with cell and gene therapy treatments, and served as appreciation for donors who have committed time and funds to furthering research and clinical trials across the nation.

Our donors have allowed top scientific minds to explore this new and promising avenue of cancer treatment, and their philanthropy is directly linked to the lives saved so far, said Barbara Netter, who co-founded Stamford-based ACGT in 2001 alongside her husband, Edward. Mrs. Netter stressed that much additional research needs to be funded in order to achieve the goal of the fully successful treatment of all types of cancer. To further that goal, Mrs. Netter has assumed the mantle of President of ACGT to chart a strategic course for the organizations continued success.

Guests were treated to an elegant reception at the Harvard Club, followed by a salutation from host Dr. Savio Woo. Dr. Woo Chairman of ACGTs Scientific Advisory Council and Professor of Hematology and Oncology at the Tisch Cancer Institute at Mount Sinai School of Medicine in New York City was instrumental in ACGTs founding over a decade ago. Also in attendance was Connie Burnett-West, a cancer survivor who overcame a critical case lung cancer with gene and cell therapy treatment.

Surgery and radiation werent options, and I was told I had limited hope for recovery, Burnett-West said. But after a sixth-month course of gene therapy, Ive been in remission for over 10 years. I could not have imagined a treatment so easy and effective.

The evenings capstone was a presentation from three of ACGTs esteemed and award winning Research Fellows. Carl H. June (M.D., University of Pennsylvania), Laurence Cooper (M.D., Ph.D., MD Anderson Cancer Center) and Michel Sadelain (M.D., Ph.D., Memorial Sloan-Kettering Cancer Center) spoke of the breakthroughs and growing momentum that gene and cell therapy has achieved with the support of ACGT.

ACGT has the potential to provide less expensive and less harrowing cancer treatment and, ultimately, a cure, Dr. Carl June said. And all of ACGTs life-saving work was funded through philanthropy.

Moving forward, Barbara Netter noted that ACGT will continue its outstanding commitment to treating all forms of cancer. Exclusive interviews with Research Fellows are available on ACGTs YouTube channel.

For interview opportunities with Research Fellows and/or survivors, please contact Kat McKee at kat(at)cocommunications(dot)com, or (914) 666-0066. For additional information on the Research Fellows and Dr. Woo, see the final page of this release.

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ACGT’s Top Researchers and Physicians Discuss the Success of Gene and Cell Therapy

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Motivational speaker author and mentor. how I received my spinal cord injury, quadriplegic)
Motivational speaker author and mentor Charles Fleisher speaks about how received his spinal cord injury, quadriplegic)

By: Charles Fleisher

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Motivational speaker author and mentor. how I received my spinal cord injury, quadriplegic) - Video

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Public release date: 17-Oct-2013 [ | E-mail | Share ]

Contact: Kevin Jiang kevin.jiang@uchospitals.edu 773-795-5227 University of Chicago Medical Center

Changes in gene regulation have been used to study the evolutionary chasm that exists between humans and chimpanzees despite their largely identical DNA. However, scientists from the University of Chicago have discovered that mRNA expression levels, long considered a barometer for differences in gene regulation, often do not reflect differences in protein expressionand, therefore, biological functionbetween humans and chimpanzees. The work was published Oct. 17 in Science.

"We thought that we knew how to identify patterns of mRNA expression level differences between humans and chimpanzees that would be good candidates to be of functional importance," said Yoav Gilad, PhD, Professor of Human Genetics at the University of Chicago. "Now we see that even such mRNA patterns are not translated to the protein level. Which means that it is unlikely that they can affect a functional phenotypic difference."

For genes to be expressed, DNA must be transcribed into messenger RNA (mRNA), which then code for proteins, the biological building blocks and engines that drive cellular function. Although humans and chimpanzees share highly similar genomes, previous studies have shown that the species evolved major differences in mRNA expression levels. Many of these differences were thought to indicate areas of evolutionary divergence, thus pointing to genes important for human-specific traits.

To test this, Gilad, Jonathan Pritchard, PhD, currently at Stanford University, and their team, spearheaded by postdoctoral fellow Zia Khan, PhD, used high-resolution mass spectrometry to compare the expression levels of thousands of proteins with corresponding mRNA expression data in human and chimpanzee cell lines.

The team found 815 genes with differing mRNA expression levels but only 571 genes that differed in protein expression. In total, they identified an estimated 266 genes with mRNA differences that did not lead to changes in protein levels. They found similar results in rhesus macaque cell lines when compared to both chimpanzees and humans, confirming the trend.

"Some of these patterns of mRNA regulation have previously been thought of as evidence of natural selection for important genes in humans, but this can no longer be assumed," Gilad said.

The study raises questions over why mRNA expression levels differ between species if they do not necessarily cause protein differences. Although further study is needed, Gilad believes this study suggests that protein expression levels evolve under greater evolutionary constraint than mRNA levels, via a yet-uncharacterized compensation or buffering mechanism.

For now, research that uses mRNA expression levels as a measure of the functional importance of a gene requires reassessment, and not just in studies on evolution.

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Gene regulation differences between humans and chimpanzees more complex than thought

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Public release date: 17-Oct-2013 [ | E-mail | Share ]

Contact: Phil Sahm phil.sahm@hsc.utah.edu 801-581-2517 University of Utah Health Sciences

(SALT LAKE CITY)A 30-year-old woman with a history of upper respiratory infections had no idea she carried an immunodeficiency disorder until her 6-year-old son was diagnosed with the same illness.

After learning she has common variable immunodeficiency (CVID), a disorder characterized by recurrent infections, such as pneumonia, and decreased antibodies, the woman, her husband, their three children and parents joined a multidisciplinary University of Utah study and researchers identified a novel gene mutation that caused the disease in the mom and two of her children. The researchers discovered that a mutation in the NFKB2 gene impairs a protein from functioning properly, which interferes with the body's ability to make antibodies and fight infection. The children's father did not have the mutation, nor did a third sibling or the woman's parents.

Another 35 people with CVID were tested for the gene mutation, and one other unrelated person was found to have it. His father wasn't tested, but no one else in his family immediate family had the mutation, so the researchers don't know whether he could have inherited the disorder from his father or developed the gene mutation sporadically.

CVID typically doesn't present with symptoms until adulthood and it's not uncommon for someone to reach their 20s, 30s or beyond before being diagnosed, according to Karin Chen, M.D., co-first author of the study published Thursday, Oct. 17, 2013, in the American Journal of Human Genetics online. Identifying the NFKB2 mutation will make it easier to recognize and treat the disorder, particularly after a test developed in conjunction with the study by ARUP Laboratories becomes available as early as next May.

"If we can screen patients for genetic mutations, we can identify disease complications associated with that gene, start looking for them and treating them sooner," says Chen, instructor of pediatric immunology at the University's School of Medicine.

There's no cure for CVID, but it can be treated with monthly infusions of antibodies at a cost of $5,000 to $10,000 per treatment.

Identifying the gene mutation and developing the test for it took approximately two years, a fast turnaround made possible because of the multidisciplinary research that the University of Utah Health Sciences encourages and is known for doing. The study involved researchers from the U School of Medicine's Departments of Pediatrics, Pathology, Human Genetics and Program in Molecular Medicine and ARUP, which is a University-owned, nationwide testing laboratory.

Emily M. Coonrod, Ph.D., a research scientist with the ARUP Institute for Clinical and Experimental Pathology, is co-first author with Chen. Karl V. Voelkerding, M.D., also of the Institute for Clinical and Experimental Pathology and a U professor of pathology, is the senior author.

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Mutation in NFKB2 gene causes hard-to-diagnose immunodeficiency disorder CVID

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