Archive for October, 2013

Gene therapy patient on new trial
Gene therapy patient on new trial Heart gene therapy patient on new trial A trial of a gene therapy to treat heart failure has started at a London hospital.

By: Spab Fi

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Gene therapy patient on new trial - Video

ScienceLIVE: Treating Spinal Cord Injury
ScienceLIVE: Treating Spinal Cord Injury.

By: Sci Mag

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ScienceLIVE: Treating Spinal Cord Injury - Video

SIKESTON, MO (KFVS) -

Stem cell therapycan bea very controversial issue, but now some veterinarians are using new techniques to harvest those cells.

The cutting edge procedure helps fight degenerative diseases and has only been performed a few times in Missouri.

Experts say regenerative medicine using stem cells is a less invasive and more cost effective alternative for dogs suffering from osteoarthritis and cartilage injuries.

Googus is an 8 year old Boxer mix diagnosed with degenerative myelopathy.

This terminal disease affects the spinal cord causing loss of control in the hind legs.

"Even though they're unable to use their back legs they're still normal in their brain and they just don't understand why they can't walk," said Dr. Stephen Williams, Animal Health Center. "There's just not a good connection and transmission from the nerves to the back legs."

But new technology could slow, if not stop, its progression. Dr. Williams is using stem cell therapy to counteract this and other degenerative diseases in dogs.

"The stem cells from the patient are the ones that are going to benefit that same patient versus trying to take stem cells from a different dog and putting them in this dog," said Dr. Williams. "By harvesting the stem cells from the fat versus people have heard of stem cells from umbilical cords and stuff like that we're taking it from the fat tissue and harvesting those and actually activating with a fluorescent light."

Once the fat is extracted it's a two hour process to prepare the new stem cells. Those are then injected back into the patient along with platelets that work with the immune system to fight the disorder.

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Stem cell therapy used locally in dogs

SIKESTON, MO (KFVS) -

Stem cell therapycan bea very controversial issue, but now some veterinarians are using new techniques to harvest those cells.

The cutting edge procedure helps fight degenerative diseases and has only been performed a few times in Missouri.

Experts say regenerative medicine using stem cells is a less invasive and more cost effective alternative for dogs suffering from osteoarthritis and cartilage injuries.

Googus is an 8 year old Boxer mix diagnosed with degenerative myelopathy.

This terminal disease affects the spinal cord causing loss of control in the hind legs.

"Even though they're unable to use their back legs they're still normal in their brain and they just don't understand why they can't walk," said Dr. Stephen Williams, Animal Health Center. "There's just not a good connection and transmission from the nerves to the back legs."

But new technology could slow, if not stop, its progression. Dr. Williams is using stem cell therapy to counteract this and other degenerative diseases in dogs.

"The stem cells from the patient are the ones that are going to benefit that same patient versus trying to take stem cells from a different dog and putting them in this dog," said Dr. Williams. "By harvesting the stem cells from the fat versus people have heard of stem cells from umbilical cords and stuff like that we're taking it from the fat tissue and harvesting those and actually activating with a fluorescent light."

Once the fat is extracted it's a two hour process to prepare the new stem cells. Those are then injected back into the patient along with platelets that work with the immune system to fight the disorder.

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Stem cell therapy used in Sikeston in dogs

Assistant Professor Cecilia Williams is doing double duty finding ways to combat triple-negative breast cancer and helping students get hands-on experience with scientific research. | Courtesy of uh.edu

A research team at the University is working on finding new ways to treat triple-negative breast cancer, the only subtype of breast cancer that doesnt have a targeted gene therapy.

Triple-negative breast cancer receives its name from its lack of the three receptors that fuel most breast cancers. Biology senior Marisa Simon, who received an undergraduate research fellowship this summer to work on the project, explained the added difficulties of this form of cancer.

Unlike the other breast cancer subtypes, TNBC does not over-express progesterone, estrogen or human epidermal growth factor receptors, Simon said. Therefore, the cancer cant be targeted based on the receptors for these hormones.

The research team, led by assistant professor Cecilia Williams, is working with the maternal embryonic leucine-zipper kinase protein to find a different way of treating TNBC.

Williams discovered that MELK was found in stem-like cells, but disappeared as those cells developed. Then, the team found that the mammary stem-like cells shared major gene expression with the TNBC subtype and that MELK expression correlates with poor prognosis in breast cancer.

We believe that targeting MELK, or the mechanism that MELK is involved in, can help improving the poor prognosis of this breast cancer subtype, Williams said. Now, our first aim (is) to understand the role of MELK for mammary stem cells and for TNBC and then to explore its use for better treatments.

Simon said Williams is a well-known cancer researcher who has authored many publications and her work has greatly contributed to the knowledge and understanding of various types breast cancer.

She was extremely generous in allowing me to join her lab, Simon said. Through her mentoring and the help of her experienced graduate students, I have developed a passion for research.

Cell and molecular biology graduate student Jun Wang, who is also working with Williams, is researching other methods to treat TNBC.

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UH researcher works to crack breast cancer treatment

PUBLIC RELEASE DATE:

24-Oct-2013

Contact: Genevieve Maul gm349@admin.cam.ac.uk 44-012-237-65542 University of Cambridge

Researchers from the University of Cambridge have discovered a novel genetic cause of severe obesity which, although relatively rare, demonstrates for the first time that genes can reduce basal metabolic rate how the body burns calories.

Previous studies (performed by David Powell and colleagues at Lexicon Pharmaceuticals in Texas) demonstrated that when the gene KSR2 (Kinase Suppressor of Ras 2) was deleted in mice, the animals became severely obese. As a result of this research, Professor Sadaf Farooqi from the University of Cambridge's Wellcome Trust-MRC Institute of Metabolic Science decided to explore whether KSR2 mutations might also lead to obesity in humans.

In collaboration with Dr Ines Barroso's team at the Wellcome Trust Sanger Institute, the researchers sequenced the DNA from over 2,000 severely obese patients and identified multiple mutations in the KSR2 gene. The research was published online today, 24 October, in the journal Cell.

KSR2 belongs to a group of proteins called scaffolding proteins which play a critical role in ensuring that signals from hormones such as insulin are correctly processed by cells in the body to regulate how cells grow, divide and use energy. To investigate how KSR2 mutations might lead to obesity, Professor Farooqi's team performed a series of experiments which showed that many of the mutations disrupt these cellular signals and, importantly, reduce the ability of cells to use glucose and fatty acids.

Patients who had the mutations in KSR2 had an increased drive to eat in childhood, but also a reduced metabolic rate, indicating that they have a reduced ability to use up all the energy that they consume. A slow metabolic rate can be found in people with an underactive thyroid gland, but in these patients thyroid blood tests were in the normal range - eliminating this as a possible explanation for their low metabolic rate. People have speculated for a long time that some individuals may burn calories more slowly than others. The findings in this study provide the first evidence that defects in a particular gene, KSR2, can affect a person's metabolic rate and how their bodies processed calories.

Professor Farooqi said: "Up until now, the genes we have identified that control body weight have largely affected appetite. However, KSR2 is different in that it also plays a role in regulating how energy is used in the body. In the future, modulation of KSR2 may represent a useful therapeutic strategy for obesity and type 2 diabetes."

Changes in diet and levels of physical activity underlie the recent increase in obesity in the UK and worldwide. However, there is a lot of variation in how much weight people gain. This variation between people is largely influenced by genetic factors, and many of the genes involved act in the brain. The discovery of a new obesity gene, KSR2, adds another level of complexity to the body's mechanisms for regulating weight. The Cambridge team is continuing to study the genetic factors influencing obesity, findings which they hope to translate into beneficial therapies in the future.

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Novel genetic mutations cause low metabolic rate and obesity

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24-Oct-2013

Contact: Cathy Yarbrough press@ashg.org 858-243-1814 American Society of Human Genetics

An international team of scientists has identified an association between heritable, rare mutations in the RINT1 gene and increased risk of early onset breast cancer, according to research reported today (Oct. 24) at the American Society of Human Genetics 2013 annual meeting in Boston.

The rare mutations in RINT1, a tumor suppressor gene, were detected in three of 49 families participating in a study that sequenced the whole exome, the protein-coding DNA, of families with multiple individuals affected by breast cancer.

"Although mutations in RINT1 are rare, it is most likely that the remaining unknown breast cancer susceptibility genes will account for similar small proportions of the disease," said Daniel J Park, Ph.D., who presented the study at ASHG 2013 and is Senior Research Fellow in genetic epidemiology at the University of Melbourne, Australia.

Only about 35 percent of the familial risk for breast cancer has been explained, according to Dr. Park and his collaborators, who added that the discovery of the RINT1 variants' association with the disease could help members of families with multiple cases of breast cancer to identify their individual risk for developing the cancer.

Dr. Park's collaborators in the search for unidentified breast cancer susceptibility genes are scientists at the Institute Curie in Paris, International Agency for Research on Cancer in Lyon, France, Huntsman Cancer Institute in Salt Lake City, Utah, as well as the University of Melbourne.

After pinpointing the first three mutations in RINT1 (p.Q115X, p.M378del and p.D403Y), the international team of scientists assessed the association between the variants and breast cancer risk by conducting a population-based case-control study of 1,313 women diagnosed with early-onset breast cancer. Rare RINT1 variants were uncovered in 23 individuals in this group, but in only 6 women out of 1,123 who did not have breast cancer, demonstrating a significant association between RINT1 mutations and risk of early onset breast cancer, according to the researchers.

In parallel, an additional 684 women with breast cancer who are members of multiple-case breast cancer families were screened for RINT1 mutations, and six additional rare mutations were identified.

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Mutations in novel tumor suppressor gene associated with early onset breast cancer

Newswise HOUSTON -- ( Oct. 24, 2013 ) -- Just 13 days in space may be enough to cause profound changes in eye structure and gene expression, report researchers from Houston Methodist, NASA Johnson Space Center, and two other institutions in the October 2013 issue of Gravitational and Space Research.

The study, which looked at how low gravity and radiation and oxidative damage impacts mice, is the first to examine eye-related gene expression and cell behavior after spaceflight.

"We found many changes in the expression of genes that help cells cope with oxidative stress in the retina, possibly caused by radiation exposure," said Houston Methodist pathologist Patricia Chvez-Barrios, M.D., the study's principal investigator. "These changes were partially reversible upon return to Earth. We also saw optic nerve changes consistent with mechanical injury, but these changes did not resolve. And we saw changes in the expression of DNA damage repair genes and in apoptotic pathways, which help the body destroy cells that are irreparably damaged."

Since 2001, studies have shown astronauts are at increased risk of developing eye problems, like premature age-related macular degeneration. Experts suspect the cause is low gravity, heightened exposure to solar radiation, or a combination of the two.

In Nov. 2011, a NASA-sponsored Ophthalmology study of seven astronauts showed that all seven had experienced eye problems after spending at least six months in space. Doctors saw a flattening of the back of the eyeball, folding of the choroid (vascular tissue behind the retina), excess fluid around and presumed swelling of the optic nerve, or some combination of these.

High-energy radiation from the Sun can cause nasty, extremely damaging chemical reactions in cells, collectively called oxidative stress. Earth's atmosphere reflects or absorbs much of this radiation and is, ironically, a much better shield than the thick metal hulls of space shuttles and the International Space Station.

Damage to eyes isn't merely a long-term health issue for some astronauts back on Earth -- it could interfere with future missions in which any loss of focus or vision makes it difficult for humans to complete long missions, such as round-trip travel to Mars (12 to 16 months) or to the moons of Jupiter (about two years). If both radiation exposure and gravity loss are to blame, one solution to save astronauts' eyes might be a spacecraft with a more protective hull and inside, a spinning hamster wheel that simulates gravity similar to those envisioned by futurist author Arthur C. Clarke and realized in Stanley Kubrick's film, 2001: A Space Odyssey.

To determine the impact of radiation exposure on eyes, Chvez-Barrios and lead author Susana Zanello, Ph.D., a space life scientist at NASA Johnson Space Center, examined mouse retinal gene expression on the 1st, 5th, and 7th days following a 13-day trip aboard space shuttle Discovery (STS-133), measuring indicators of oxidative and cellular stress. The researchers also examined the eyes and surrounding tissues for broad changes in structure and shape that could relate to low gravity. They maintained two controls on Earth -- one in which mice were kept in the same general conditions as those aboard the shuttle, and one in which mice were maintained in typical, Earth-based care facilities.

Mice returning to Earth showed immediate evidence of oxidative stress in their retinas. But the increased expression of six oxidative stress response genes appeared to return to normal by the seventh day on Earth. An indicator of oxidative stress in the cornea was also elevated one day after mice had returned from orbit, but returned to near-normal levels by the seventh day.

"This suggests oxidative stress in the retina and lens are at least partially reversible under the circumstances of the experiment," Chvez-Barrios said. "This was after a relatively short time in orbit. We dont know if damage caused by longer periods of oxidative stress will be more severe. Only more studies with longer exposure times may help answer this question."

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Just Two Weeks in Orbit Causes Changes in Eyes

October 24, 2013

Lee Rannals for redOrbit.com Your Universe Online

Researchers at the American Society of Human Genetics 2013 meeting in Boston say they have discovered an interaction that could explain the link between eating meat and colorectal cancer risk. The team said the newly discovered potential gene-diet interaction for colorectal cancer could shed light on the statistically significantly increased risk of the cancer that is associated with the consumption of red and processed meats.

If replicated, our findings have a relevant public health significance because diet is a modifiable risk factor for colorectal cancer, saidJane Figueiredo, Assistant Professor of Preventive Medicine at the University of Southern California Keck School of Medicine. It is conceivable that selected individuals at higher risk of colorectal cancer based on genomic profiling could be targeted for screening, diet modification and other prevention strategies.

Scientists determined that lower colorectal cancer risk associated with vegetable, fruit and fiber intake was also linked to genetic variants. Ulrike Peters, a Member of the Fred Hutchinson Cancer Research Centers Public Health Sciences Division who headed the study, said the teams research represents an important new insight into disease development.

This is the first colorectal cancer investigation with the statistical power to identify gene-dietary interactions across the genome of a large population of individuals. The study included 9,287 patients with colorectal cancer and a control group of 9,117 individuals without cancer, all of whom were participants in the 10 Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO) observational studies.

Scientists searched 2.7 million gene variants to identify those that are associated with the consumption of red meat and processed meat as well as fruits and vegetables. The genetic sequences and information about the participants medical history and diet are stored in the GECCO database.

The team found a significant interaction between the genetic variant rs4143094 and processed meat consumption. This variant can be found on the same chromosome 10 region that includes a transcription factor gene previously linked to several forms of cancer. They also found a statistically significant diet-gene interaction in another variant located on chromosome 8, which was associated with a reduced risk of colorectal cancer.

Researchers believe that digestion of processed meats may promote an immunological or inflammatory response that triggers tumor development. The transcription factor gene on chromosome 10 normally helps suppress the immunological or inflammatory response, but instead it contains a mutation that could encode a dysregulated transcription factor that impacts its ability to suppress the response.

Peters said that in addition to uncovering a novel gene-diet interaction for colorectal cancer, the study may have important implications for understanding the underlying causes and biological pathways of cancer.

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Gene-Diet Interaction Explains Link Between Meat And Colorectal Cancer

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24-Oct-2013

Contact: John Bean john.bean@eortc.be European Organisation for Research and Treatment of Cancer

Results of EORTC trial 58951 suggest that detecting ERG gene deletion at diagnosis of childhood B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) would be useful for risk stratification. The study, published in Leukemia showed that patients with the ERG gene deletion had a very good outcome with an 8-year event-free survival of 86.4% and an overall survival of 95.6%.

ALL is the most common childhood malignancy, but it is characterized by a number of recurring genetic alterations. These alterations, each with a specific gene expression profile, can influence response to treatment. For example, high hyperdiploidy and the chromosomal translocation t(12;21)/ETV6RUNX1 are the most prevalent alterations in young children and are associated with good treatment response and outcome. On the other hand, t(9;22)/BCRABL1, rearrangements of the MLL gene, low hypodiploidy, intrachromosomal amplification of chromosome 21 (iAMP21) are all associated with a high risk of relapse. In addition, IKZF1 gene deletion has been recently described as a strong marker of poor outcome.

Dr. Emmanuelle Clappier of the Hematology University Institute, St-Louis and Robert Debr Hospitals in Paris and lead author of this EORTC publication says, "The genetic basis of BCP-ALL is still unknown for a significant proportion of cases, and consequently outcome is unpredictable at the time of diagnosis. This is especially true for older children and adolescents, more than half of whom display no classifying genetic alteration. There is a clear need for new biological markers to assist in making treatment decisions and improve outcome for these patients."

A genomic deletion in the ERG gene was identified by array-CGH analysis in selected patients. Then an independent non-selected cohort of 897 children aged 1-17 years and treated for BCP-ALL in the EORTC 58951 trial between December 1998 and July 2008 was screened for ERG gene deletions. ERG gene deletion was found in 3.2% of the patients (29 out of the 897 patients) and was associated with higher age (median age 7.0 years versus 4.0 years, P=0.004) and frequent IKZF1 4-7 deletions (37.9% versus 5.3% in the remaining patients, P<0.001). For patients with an IKZF1 4-7 deletion, those who also had ERG gene deletion had a better outcome (8-year event-free survival, 85.7% vs. 51.3%, HR: 0.16, 95% CI: 0.02-1.20, P=0.04). This work allowed the description of a new genetic marker in BCP-ALL, ERG gene deletion, and to refine the prognostic impact of IKZF1 deletions.

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EORTC trial 58951 was coordinated by the EORTC Children's Leukemia Group and was conducted in 25 sites located in Belgium and France. It was an academic trial supported by the Laurette Fugain Foundation and the EORTC Charitable Trust.

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EORTC study suggests detecting ERG gene deletion useful for risk stratification in childhood ALL

PUBLIC RELEASE DATE:

24-Oct-2013

Contact: Cathy Yarbrough press@ashg.org 858-243-1814 American Society of Human Genetics

Research on the DNA of a large multi-generational family has provided a genetic clue that enabled scientists to pinpoint a gene that plays a role in mitral valve prolapse (MVP), a common cardiac disease that is a leading cause of heart failure, according to a study presented today (Thursday, Oct. 24) at the American Society of Human Genetics 2013 meeting in Boston.

The scientists who located the gene, named DCSH1, also determined how mutations in this gene disrupt the normal embryonic development of the mitral valve, one of the valves that controls blood flow in the heart.

"This work provides insights into the pathways regulating valve growth and development," said Susan Slaugenhaupt, Ph.D., Associate Professor of Neurology in the Center for Human Genetic Research at Massachusetts General Hospital and Harvard Medical School and one of the lead scientists in the collaborative group that conducted the research.

"The results implicate a previously unrecognized paradigm in the development of long-term structural integrity in the mitral valve," said Ronen Y. Durst, M.D., former member of Dr. Slaugenhaupt's lab and now a senior cardiologist at Hebrew University and Hadassah Medical Center in Jerusalem. Dr. Durst presented the study this afternoon at ASHG 2013.

The researchers' first step was to link MVP to a region on human chromosome 11 in the DNA of the group of relatives with the heart disorder. By sequencing that DNA region in family members, the scientists were able to link mutations in DCSH1 to MVP.

To understand the normal biological functions altered by the mutated copy of DCSH1, the researchers turned to two animal models, zebrafish and mice. Experimentally reducing the expression level of the zebrafish version of DCSH1 resulted in abnormal heart development.

"Treating the zebrafish embryos with the normal copy of the DCHS1 gene rescued the lesion, while the mutated human DCHS1 gene did not," said Dr. Slaugenhaupt. "This finding constitutes strong evidence that the mutation disrupts the normal function of DCHS1."

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First gene detected for most common form of mitral valve prolapse

PUBLIC RELEASE DATE:

24-Oct-2013

Contact: Kathryn Ruehle kruehle@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, October 24, 2013Performing surgery to take pressure off the spine after a traumatic injury soon after the event could prevent or reverse some of the secondary damage caused by swelling and decreased blood flow to the injured spine. However, strong evidence to support early spinal surgery is lacking, mainly because the available study data cannot be easily compared, as explained in a review of this controversial field published in Journal of Neurotrauma, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available on the Journal of Neurotrauma website.

Joost van Middendorp, Allard Hosman, and Suhail Doi, Stoke Mandeville Hospital (Aylesbury, UK), University of Oxford, UK, University of Queensland (Brisbane, Australia), and Radboud University Nijmegen Medical Center (the Netherlands), performed a systematic review of the literature on spinal decompression surgery following traumatic spinal cord injury (SCI).

Although debate continues over the effects of the timing of surgery, the authors found that "early" compared to "late" spinal surgery was associated with significantly greater motor and neurological improvement and shorter length of hospital stay. As the authors report, though, the evidence supporting early spinal surgery "lack robustness" due to various sources of bias within the studies and heterogeneity within and between the studies. For example, the studies being compared include patients with various severities and levels of spinal cord injuries.

They report their findings in "The Effects of the Timing of Spinal Surgery after Traumatic Spinal Cord Injury: A Systematic Review and Meta-Analysis."

"This timely article contributes additional data and discussion to the general topic of decompression surgery as an effective strategy to protect against traumatic SCI," says W. Dalton Dietrich, III, PhD, Deputy Editor of Journal of Neurotrauma and Kinetic Concepts Distinguished Chair in Neurosurgery, Professor of Neurological Surgery, Neurology and Cell Biology, University of Miami Leonard M. Miller School of Medicine. "This well done meta-analysis of published data should therefore be of great interest to the readership of the Journal, including spinal surgeons."

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Does the timing of surgery to treat traumatic spinal cord injury affect outcomes?

Oct. 24, 2013 A common genetic variant that affects 1 in 3 people significantly increases the risk of colorectal cancer from the consumption of red meat and processed meat, according to a study presented today at the annual American Society of Human Genetics 2013 meeting.

In addition to identifying a gene that raises risk for colorectal cancer from eating red or processed meat, the study -- the first to identify the interactions of genes and diet on a genome-wide scale -- also reveals another specific genetic variation that appears to modify whether eating more vegetables, fruits and fiber actually lowers your colorectal cancer risk.

"Diet is a modifiable risk factor for colorectal cancer. Our study is the first to understand whether some individuals are at higher or lower risk based on their genomic profile. This information can help us better understand the biology and maybe in the future lead to targeted prevention strategies," said lead author Jane Figueiredo, Ph.D., Assistant Professor of Preventive Medicine at the Keck School of Medicine of USC.

"But we are not saying that if you don't have the genetic variant that you should eat all the red meat you'd like," Figueiredo added. "People with the genetic variant allele have an even higher increased risk of colorectal cancer if they consume high levels of processed meat, but the baseline risk associated with meat is already pretty bad."

We've all heard reports about how certain foods may lower or raise the risk for certain diseases, such as cancer. But how our personal genetic variations modify the effects of diet on disease has not yet been thoroughly investigated, said senior author Ulrike Peters, Ph.D., M.P.H, of the Fred Hutchinson Cancer Research Center's Public Health Sciences Division.

The researchers systematically searched the more than 2.7 million genetic sequences for interactions with consumption of red and processed meat. The study looked at 9,287 patients with colorectal cancer and a control group of 9,117 individuals without cancer.

The risk of colorectal cancer associated with processed meat was significantly higher among people with the genetic variant rs4143094, the study shows. This variant is located on the same chromosome 10 region that includes GATA3, a transcription factor gene previously linked to several forms of cancer. The transcription factor encoded by this gene normally plays a role in the immune system, but carries this genetic variant in about 36 percent of the population.

The researchers speculate that the digestion of processed meat may promote an immunological or inflammatory response that may trigger tumor development. The GATA3 transcription factor normally would help suppress the immunological or inflammatory response. However, if the GATA3 gene region contains a genetic variant, it may encode a dysregulated transcription factor that impacts its ability to suppress the response.

But other genetic vatiants may be beneficial: On chromosome 8, another statistically significant diet-gene interaction was found in variant rs1269486. For people with this variant, eating your fruits and veggies may be even better for you when it comes to colorectal cancer risk, the research shows.

The study is part of an ongoing collaboration among multiple institutions worldwide, the international NIH-funded Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO).

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Gene variant that raises risk for colorectal cancer from eating processed meat present in one-in-three people

PUBLIC RELEASE DATE:

24-Oct-2013

Contact: Suzanne Wu suzanne.wu@usc.edu 213-740-0252 University of Southern California

A common genetic variant that affects 1 in 3 people significantly increases the risk of colorectal cancer from the consumption of red meat and processed meat, according to a study presented today at the annual American Society of Human Genetics 2013 meeting, the largest gathering of human geneticists in the world.

In addition to identifying a gene that raises risk for colorectal cancer from eating red or processed meat, the study the first to identify the interactions of genes and diet on a genome-wide scale also reveals another specific genetic variation that appears to modify whether eating more vegetables, fruits and fiber actually lowers your colorectal cancer risk.

"Diet is a modifiable risk factor for colorectal cancer. Our study is the first to understand whether some individuals are at higher or lower risk based on their genomic profile. This information can help us better understand the biology and maybe in the future lead to targeted prevention strategies," said lead author Jane Figueiredo, Ph.D., Assistant Professor of Preventive Medicine at the Keck School of Medicine of USC.

"But we are not saying that if you don't have the genetic variant that you should eat all the red meat you'd like," Figueiredo added. "People with the genetic variant allele have an even higher increased risk of colorectal cancer if they consume high levels of processed meat, but the baseline risk associated with meat is already pretty bad."

We've all heard reports about how certain foods may lower or raise the risk for certain diseases, such as cancer. But how our personal genetic variations modify the effects of diet on disease has not yet been thoroughly investigated, said senior author Ulrike Peters, Ph.D., M.P.H, of the Fred Hutchinson Cancer Research Center's Public Health Sciences Division.

The researchers systematically searched the more than 2.7 million genetic sequences for interactions with consumption of red and processed meat. The study looked at 9,287 patients with colorectal cancer and a control group of 9,117 individuals without cancer.

The risk of colorectal cancer associated with processed meat was significantly higher among people with the genetic variant rs4143094, the study shows. This variant is located on the same chromosome 10 region that includes GATA3, a transcription factor gene previously linked to several forms of cancer. The transcription factor encoded by this gene normally plays a role in the immune system, but carries this genetic variant in about 36 percent of the population.

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Researchers identify gene variant that raises risk for colorectal cancer from eating processed meat

BOSTON & LEUVEN, Belgium--(BUSINESS WIRE)--

Cartagenia, the world leader in providing genetic labs and clinicians with software-based workflow support for variant assessment, lab reporting, and integration of diagnostic knowledge-bases, today announced that more than 120 labs and clinics across three continents have now adopted and are relying on its Bench platform genetics diagnostics solution for use in daily practice. Bench is a web-based software and database platform with features and knowledge sources that allows clinicians to analyze, interpret and manage genomic variations in routing diagnostics.

Cartagenia CEO Herman Verrelst said the marked success of the Bench platform underscores a true need for clinical grade tools for lab variant assessment and reporting support in the rapidly expanding world of genetic diagnostics.

It is very rewarding to see the enthusiastic response we are receiving for our Bench solutions in all our key markets and across three continents, Verrelst said. We believe this reflects very strong growth in NGS adoption and a clear need for diagnostic-grade solutions in lab interpretation and reporting workflow automation, integration with the referring physician and hospital IT, and linking to the community through data sharing initiatives all tools that Cartagenia Bench platform provides.

Cartagenia also announced that it has released a new version of its Bench Lab NGS module, the powerful software and database solution for robust and reliable NGS variant analysis, interpretation and reporting pipelines.

The new version of the NGS module is focused on increasing a labs efficiency through faster report generation and has added:

Greenwood Genetic Center, a South Carolina-based, non-profit institute that provides genetic services and diagnostic laboratory testing, adopted Bench Lab NGS in 2012. Mike Friez, Greenwoods Director of Diagnostic Laboratories, noted that his lab generates DNA sequencing data on large portions of the genome and Cartagenias Bench Lab product facilitates the sorting, filtering and organization of these data.

Implementing the Cartagenia Bench Lab NGS platform has significantly impacted our ability to effectively manage and interpret data for our targeted NGS panels as well as the exomes generated from our undiagnosed patients, Friez said. By pooling a variety of powerful resources, Cartagenia really does enable us to make progress in assisting the families we serve.

Jean-Louis Mandel, Professor of Genetics at the Faculty of Medicine of Strasbourg, France, and Head of the Human Molecular Genetic Group at the IGBMC, noted that he is impressed by the collaborative approach set up with Cartagenia.

We have seen the Bench Lab NGS platform evolve rapidly over the period of time weve worked with Cartagenia to evaluate the software and run it on our own research and diagnostic samples, Prof. Mandel said. Cartagenia speaks the language of clinical geneticists, and Im looking forward to having many fruitful and constructive discussions that will undoubtedly lead to yet more new analysis and interpretation support features of wide interest.

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Cartagenia Announces More Than 120 Labs and Clinics Globally Now Relying on Its Bench Platform for Routine Genetic ...

Oct. 24, 2013 Researchers from the Institute of Genomic Medicine (Inmegen) carried out a study on genetic factors that can be associated to metabolic syndrome, main trigger of cardiovascular diseases, type II diabetes and obesity, with the goal of identifying high risk populations and influence its treatment in the most effective way.

Under the lead of Lorena Orozco, the objective of the research is to know the genetic susceptibility of the mixed and indigenous Mexican populations to developing metabolic syndrome or one of its components and the relationship of this risk with its indigenous, Caucasian or African origins.

The researcher explained that the metabolic syndrome is characterized by the simultaneous presence or sequence of at least three of the next components: increment in glucose levels, triglycerides, arterial hypertension, low levels of benefic cholesterol (HDL) and rise of the waist circumference.

She also said that the study includes individuals from different Mexican states throughout the country, like Chiapas, San Luis Potos, Mexico State, Yucatn, Chihuahua, Oaxaca, Puebla and Mexico City.

The project's study group was integrated by 800 mixed race individuals and 400 natives more than 30 years old, from both sexes. Blood samples were taken from this groups in order to know their cholesterol, triglycerides, glucose and blood pressure levels, as well as their body mass, size, weight and height.

In this stage of the study, it was founded that 42 per cent of the mixed population suffered from metabolic syndrome and 10 per cent had type II diabetes.

Regarding the indigenous group, the results showed that there were communities like the Tojolabales form Chiapas, where type II diabetes was barely present, contrasting with other groups like the Totonacas from Veracruz, were the prevalence of this disease was near a 25 per cent. It was also found that 45 per cent of the Tarahumaras from Chihuahua that were tested had high blood pressure.

In another phase of the project, DNA from each individual was analyzed to evaluate the intervention of three genes (AKT1, GCKR and ADIPOQ) that participate in the metabolism of glucose or fatty acids.

"We are heirs of a genetics that in a hostile environment, thousands of years ago, helped us survive long periods of famine and other hardships. However, in the present, this genetics is the detonator of diseases such as diabetes, obesity and metabolic syndrome," emphasized the researcher.

Regarding the main discoveries, the researchers observed that in the mixed population there are variations in the sequence of ADIPOQ and GCKR genes that are associated to the rise of triglycerides in the blood stream. Meanwhile, the variations of the gene AKT1 are related with low levels of benefic cholesterol.

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Genetic factors predispose metabolic syndrome in mixed races

Newswise BOSTON/CHICAGO An international research consortium led by investigators at Massachusetts General Hospital (MGH) and the University of Chicago has answered several questions about the genetic background of obsessive-compulsive disorder (OCD) and Tourette syndrome (TS), providing the first direct confirmation that both are highly heritable and also revealing major differences between the underlying genetic makeup of the disorders. Their report is being published in the October issue of the open-access journal PLOS Genetics.

"Both TS and OCD appear to have a genetic architecture of many different genes perhaps hundreds in each person acting in concert to cause disease," says Jeremiah Scharf, MD, PhD, of the Psychiatric and Neurodevelopmental Genetics Unit in the MGH Departments of Psychiatry and Neurology, senior corresponding author of the report. "By directly comparing and contrasting both disorders, we found that OCD heritability appears to be concentrated in particular chromosomes particularly chromosome 15 while TS heritability is spread across many different chromosomes."

An anxiety disorder characterized by obsessions and compulsions that disrupt the lives of patients, OCD is the fourth most common psychiatric illness. TS is a chronic disorder characterized by motor and vocal tics that usually begins in childhood and is often accompanied by conditions like OCD or attention-deficit hyperactivity disorder. Both conditions have been considered to be heritable, since they are known to often recur in close relatives of affected individuals, but identifying specific genes that confer risk has been challenging.

Two reports published last year in the journal Molecular Psychiatry, with leadership from Scharf and several co-authors of the current study, described genome-wide association studies (GWAS) of thousands of affected individuals and controls. While those studies identified several gene variants that appeared to increase the risk of each disorder, none of the associations were strong enough to meet the strict standards of genome-wide significance. Since the GWAS approach is designed to identify relatively common gene variants and it has been proposed that OCD and TS might be influenced by a number of rare variants, the research team adopted a different method. Called genome-wide complex trait analysis (GCTA), the approach allows simultaneous comparision of genetic variation across the entire genome, rather than the GWAS method of testing sites one at a time, as well as estimating the proportion of disease heritability caused by rare and common variants.

"Trying to find a single causative gene for diseases with a complex genetic background is like looking for the proverbial needle in a haystack," says Lea Davis, PhD, of the section of Genetic Medicine at the University of Chicago, co-corresponding author of the PLOS Genetics report. "With this approach, we aren't looking for individual genes. By examining the properties of all genes that could contribute to TS or OCD at once, we're actually testing the whole haystack and asking where we're more likely to find the needles."

Using GCTA, the researchers analyzed the same genetic datasets screened in the Molecular Psychiatry reports almost 1,500 individuals affected with OCD compared with more than 5,500 controls, and nearly TS 1,500 patients compared with more than 5,200 controls. To minimize variations that might result from slight difference in experimental techniques, all genotyping was done by collaborators at the Broad Institute of Harvard and MIT, who generated the data at the same time using the same equipment. Davis was able to analyze the resulting data on a chromosome-by-chromosome basis, along with the frequency of the identified variants and the function of variants associated with each condition.

The results found that the degree of heritability for both disorders captured by GWAS variants is actually quite close to what previously was predicted based on studies of families impacted by the disorders. "This is a crucial point for genetic researchers, as there has been a lot of controversy in human genetics about what is called 'missing heritability'," explains Scharf. "For many diseases, definitive genome-wide significant variants account for only a minute fraction of overall heritability, raising questions about the validity of the approach. Our findings demonstrate that the vast majority of genetic susceptibility to TS and OCD can be discovered using GWAS methods. In fact, the degree of heritability captured by GWAS variants is higher for TS and OCD than for any other complex trait studied to date."

Nancy Cox, PhD, section chief of Genetic Medicine at the University of Chicago and co-senior author of the PLOS Genetics report, adds, "Despite the fact that we confirm there is shared genetic liability between these two disorders, we also show there are notable differences in the types of genetic variants that contribute to risk. TS appears to derive about 20 percent of genetic susceptibility from rare variants, while OCD appears to derive all of its susceptibility from variants that are quite common, which is something that has not been seen before."

In terms of the potential impact of the risk-associated variants, about half the risk for both disorders appears to be accounted for by variants already known to influence the expression of genes in the brain. Further investigation of those findings could lead to identification of the affected genes and how the expression changes contribute to the development of TS and OCD. Additional studies in even larger patient populations, some of which are in the planning stages, could identify the biologic pathways disrupted in the disorder, potentially leading to new therapeutic approaches.

The study is a collaboration between two consortia the Tourette Syndrome Association International Consortium for Genomics (TSAICG) and the International OCD Foundation Genetics Collaborative (IOCDFGC) representing 43 institutions across 12 countries. Scharf, an assistant professor of Neurology at Harvard Medical School, is co-chair of the TSAICG steering committee and a member of the IOCDFGC steering committee. Cox is a professor of Medicine and Human Genetics, and Davis a research assistant professor at the University of Chicago. Additional co-authors include Carol Mathews, MD, University of California at San Francisco; James Knowles, MD, University of Southern California, and Evelyn Stewart, MD, University of British Columbia.

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Genetic Analysis Reveals Novel Insights Into the Genetic Architecture of Obsessive-Compulsive Disorder, Tourette ...

PUBLIC RELEASE DATE:

24-Oct-2013

Contact: Mike Morrison mdmorrison@partners.org 617-724-6425 Massachusetts General Hospital

An international research consortium led by investigators at Massachusetts General Hospital (MGH) and the University of Chicago has answered several questions about the genetic background of obsessive-compulsive disorder (OCD) and Tourette syndrome (TS), providing the first direct confirmation that both are highly heritable and also revealing major differences between the underlying genetic makeup of the disorders. Their report is being published in the October issue of the open-access journal PLOS Genetics.

"Both TS and OCD appear to have a genetic architecture of many different genes perhaps hundreds in each person acting in concert to cause disease," says Jeremiah Scharf, MD, PhD, of the Psychiatric and Neurodevelopmental Genetics Unit in the MGH Departments of Psychiatry and Neurology, senior corresponding author of the report. "By directly comparing and contrasting both disorders, we found that OCD heritability appears to be concentrated in particular chromosomes particularly chromosome 15 while TS heritability is spread across many different chromosomes."

An anxiety disorder characterized by obsessions and compulsions that disrupt the lives of patients, OCD is the fourth most common psychiatric illness. TS is a chronic disorder characterized by motor and vocal tics that usually begins in childhood and is often accompanied by conditions like OCD or attention-deficit hyperactivity disorder. Both conditions have been considered to be heritable, since they are known to often recur in close relatives of affected individuals, but identifying specific genes that confer risk has been challenging.

Two reports published last year in the journal Molecular Psychiatry, with leadership from Scharf and several co-authors of the current study, described genome-wide association studies (GWAS) of thousands of affected individuals and controls. While those studies identified several gene variants that appeared to increase the risk of each disorder, none of the associations were strong enough to meet the strict standards of genome-wide significance. Since the GWAS approach is designed to identify relatively common gene variants and it has been proposed that OCD and TS might be influenced by a number of rare variants, the research team adopted a different method. Called genome-wide complex trait analysis (GCTA), the approach allows simultaneous comparision of genetic variation across the entire genome, rather than the GWAS method of testing sites one at a time, as well as estimating the proportion of disease heritability caused by rare and common variants.

"Trying to find a single causative gene for diseases with a complex genetic background is like looking for the proverbial needle in a haystack," says Lea Davis, PhD, of the section of Genetic Medicine at the University of Chicago, co-corresponding author of the PLOS Genetics report. "With this approach, we aren't looking for individual genes. By examining the properties of all genes that could contribute to TS or OCD at once, we're actually testing the whole haystack and asking where we're more likely to find the needles."

Using GCTA, the researchers analyzed the same genetic datasets screened in the Molecular Psychiatry reports almost 1,500 individuals affected with OCD compared with more than 5,500 controls, and nearly TS 1,500 patients compared with more than 5,200 controls. To minimize variations that might result from slight difference in experimental techniques, all genotyping was done by collaborators at the Broad Institute of Harvard and MIT, who generated the data at the same time using the same equipment. Davis was able to analyze the resulting data on a chromosome-by-chromosome basis, along with the frequency of the identified variants and the function of variants associated with each condition.

The results found that the degree of heritability for both disorders captured by GWAS variants is actually quite close to what previously was predicted based on studies of families impacted by the disorders. "This is a crucial point for genetic researchers, as there has been a lot of controversy in human genetics about what is called 'missing heritability'," explains Scharf. "For many diseases, definitive genome-wide significant variants account for only a minute fraction of overall heritability, raising questions about the validity of the approach. Our findings demonstrate that the vast majority of genetic susceptibility to TS and OCD can be discovered using GWAS methods. In fact, the degree of heritability captured by GWAS variants is higher for TS and OCD than for any other complex trait studied to date."

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Genetic analysis reveals insights into the genetic architecture of OCD, Tourette syndrome

SALT LAKE CITY, Oct. 24, 2013 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) today announced it will present data this week at the American Society of Human Genetics (ASHG) annual meeting in Boston showing that the Myriad myRisk Hereditary Cancer test meets rigorous quality standards and provides clinical sequencing results equivalent to 99.99 percent accuracy. Myriad myRisk Hereditary Cancer is a new diagnostic test that provides patients with information about their hereditary risk for eight major cancers including breast, colorectal, ovarian, endometrial, pancreatic, prostate, gastric cancers and melanoma.

"Next-generation DNA sequencing offers the ability to test many genes at once, but it must be optimized to ensure clinical accuracy. We've invested three years of research to optimize our Myriad myRisk Hereditary Cancer test, and the validation data show that Myriad myRisk Hereditary Cancer offers 99.99 specificity and sensitivity which means it provides unprecedented quality and accuracy equal to the gold standard Sanger sequencing," said Richard J. Wenstrup, M.D., chief medical officer of Myriad. "As next-generation technology advances, mutation classification techniques also must evolve to ensure high quality data interpretation for clinical decision making. Myriad has developed a robust variant classification program called Myriad myVision(TM) to achieve highly accurate, clinically-actionable, genetic test results for patients and healthcare providers."

The five studies being presented at the ASHG annual meeting include:

Development of a Next Generation Sequencing Panel to Assess Hereditary Cancer Risk that Includes Clinical Diagnostic Analysis of the BRCA1 and BRCA2 Genes. [Roa et al., Poster: Oct. 24, 2013, 11:30 a.m. -- 12:30 p.m. ET]

This study validated the myRisk Hereditary Cancer test, which is a 25-gene panel that uses next generation sequencing (NGS) technology. The study compared the myRisk Hereditary Cancer test to the gold standard Sanger sequencing for evaluation of BRCA1 and BRCA2 mutations in 1,864 patient samples. myRisk Hereditary Cancer detected 15,877 variants compared to 15,878 variants using Sanger sequencing, resulting in an analytic sensitivity > 99.99 percent. These data show that a NGS gene panel designed to meet rigorous quality standards can provide clinical sequencing results that are equivalent to those obtained from Sanger DNA sequencing analysis (i.e., greater sensitivity without loss of specificity). In this validation study, Myriad's myRisk Hereditary Cancer test was shown to be highly effective and provided high quality, accurate results for clinical decision-making purposes.

A Clinical History Weighting Algorithm Accurately Classifies BRCA1 and BRCA2 Variants. [Bowles et al., Poster: Oct. 25, 2013, 10:30 -- 11:30 a.m. ET]

This study evaluated a clinical history weighting algorithm designed to provide highly accurate classifications for BRCA1 and BRCA2 variants of uncertain significance and which is integral to Myriad's proprietary myVision(TM) Variant Classification Program. The algorithm is based on the premise that disease-associated mutations will be observed more often in individuals at high risk for carrying a mutation, as determined by personal and family history. Statistical analysis weights the family histories of each patient carrying a variant of interest and compares those histories to control patients carrying variants known to be benign or deleterious. Data from more than 400,000 patients were used to develop the algorithm, which was validated against 6,000 BRCA1 and BRCA2 variants. The results showed that the clinical history weighting algorithm accurately classified well-documented variants associated with BRCA1 and BRCA2 and allowed classification with fewer observations than other techniques, providing timely and accurate classifications to guide clinical care. Importantly, this clinical history weighting algorithm facilitated the accurate reclassification of BRCA1 and BRCA2 variants of uncertain significance, which will improve the clinical management of patients at risk for hereditary cancer.

Frequencies of BRCA1, BRCA2, PALB2, and CDKN2A Germline Mutations in Familial Pancreatic Cancer (FPC): A PACGENE study. [Zhen/Petersen et al., Poster: Oct. 24, 2013, 10:30 -- 11:30 a.m. ET]

This study assessed the frequency of germline mutations in four of the genes in the myRisk Hereditary Cancer panel -- BRCA1, BRCA2, PALB2, and CDKN2A -- in patients with familial pancreatic cancer. Using samples from a large pancreatic cancer registry, the DNA from 80 patients who met familial pancreatic cancer criteria was tested. The frequencies for deleterious or suspected deleterious mutations and variants of uncertain significance (VUS) among the patients tested totaled 13.8 percent: BRCA1 (2.9 percent), no VUS; BRCA2 (4.4 percent), no VUS; PALB2 (1.3 percent), no VUS; CDKN2A (5.2 percent), 3 VUS. These data show the genetic heterogeneity of germline mutations in patients with familial pancreatic cancer and strongly suggest that these patients are appropriate candidates for genetic testing using a hereditary cancer panel that tests for multiple genes to prevent a misdiagnosis.

Detection of Large Rearrangements in PMS2. [Mancini-DiNardo et al., Podium: Oct. 25, 2013, 3:15 p.m. ET]

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Myriad myRisk(TM) Hereditary Cancer Test Is Highly Accurate in Key Validation Study

Oxford BioMedica gets go-ahead to continue its trials

5:30pm Thursday 24th October 2013 in News

GENE therapy company Oxford BioMedica has been given the go-ahead by drug regulators to recruit more volunteers for a clinical trial of a treatment for eye disease.

The trials were halted in June after low concentrations of a potential impurity were discovered in the drug.

The companys share price rose four per cent on the news, having already risen following a million-dollar milestone payment from pharmaceutical giant Pfizer and a 7.1m status recognition award from the UK Government.

BioMedica, based at Oxford Science Park, has used new analytical methods to identify the impurity as DNA from foetal bovine serum, the most widely-used growth supplement in certain laboratory techniques.

Chief executive John Dawson said: We place the highest importance on safety, and our analytical methods and quality assurance processes are continuously evolving to ensure that we remain at the forefront of gene therapy development and manufacture.

Im confident that, with significant opportunities ahead, Oxford BioMedica will continue to lead the way in delivering novel gene therapies to patients.

The eye treatment uses Biomedicas LentiVector technology, developed from research at Oxford University by the companys founders, Professors Alan and Sue Kingsman.

Before resuming the trials in France and the US, the study must be approved by ethics committees following approval by the US Food and Drug Administration and the French regulatory agency, ANSM.

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Oxford BioMedica gets go-ahead to continue its trials

Genetic Engineering as a course choice after 12th
This Video suggests Genetic Engineering as a course that can be done after doing 12th (10+2).

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(4.4) Genetic Engineering and Biotechnology - IB SL Biology Past Exam Paper 1 Questions
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(4.4) Genetic Engineering and Biotechnology - IB SL Biology Past Exam Paper 1 Questions - Video

By Eva Recinos2013-10-23 02:28:28 UTC

Genetic engineering and synthetic biology are making it easier to create everything from food ingredients to scents using unexpected sources.

That's where genetically engineered yeast comes in. A recent article in the New York Times explored its larger implications and how companies like Amyris continue to push the scope of what engineered yeast can produce.

Amyris found that it can create not only ingredients for cosmetics products but also artemisinin, a compound used in drugs to treat malaria. Artemisinin normally comes from sweet wormwood, harvested by both Asian and African farmers, as The Guardian reports. Though the artificial creation of the important compound means good news in one sense, some see it as an indication that genetically engineering it could jeopardize the livelihood of harvesters.

Amyris co-founder Jay Keasling told the New York Times that the process is "just like brewing beer, but rather than spit out alcohol, the yeast spits out these products."

Evolva also experimented with genetically engineered yeast and found that it could produce synthetic vanillin, sometimes used as an alternative to the standard, natural vanilla extract.

Vanillin could be used for everything from fragrances to dairy products. As the company's site explains, vanilla and vanillin are used in many products and therefore created at a collectively large rate, but "only a small fraction of this volume contains natural vanilla, with the vast majority being synthetic vanillin."

Yet, as the New York Times article reports, other groups see problems with the artificial creations, questioning the idea of integrating engineered ingredients into everyday foods.

In the meantime, Amyris plans to work with Michelin to produce a rubber product and will likely continue to create other partnerships for future experiments.

Have something to add to this story? Share it in the comments.

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Genetically Engineered Yeast Yields More Than Beer

PUBLIC RELEASE DATE:

23-Oct-2013

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, October 23, 2013The stem cell field is at a critical point, with the potential for a major impact on clinical medicine if stem cell-based therapies can overcome serious and immediate challenges. These challenges and key action items to overcome them are described in an article published on Fast Track as part of the World Stem Cell Report 2013, a special upcoming supplement to Stem Cells and Development, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Stem Cells and Development website.

The World Stem Cell Report is the official publication of the World Stem Cell Summit, to be held December 4-6, 2013 in San Diego, CA. More than 1,000 researchers and clinicians from around the globe will attend the Summit.

In the article "Key Action Items for the Stem Cell Field Looking to 2014," author Paul S. Knoepfler, University of California Davis School of Medicine, describes the building momentum behind stem cells, both for their impact as transformative basic science discoveries and their potential for translation to clinical medicine. At the same time, however, he outlines several critical challenges, including "stem cell tourism," the complex balance between innovation and regulatory/FDA compliance, and the need to educate physicians and patients about stem cell therapies.

"Paul Knoepfler is being honored at the World Stem Cell Summit with the Stem Cell Action 'National Advocacy Award' from the Genetics Policy Institute," says Bernard Siegel, JD, Co-Chair of the 2013 World Stem Cell Summit and Executive Director, Genetics Policy Institute (GPI, Palm Beach, FL). Siegel is also Co-Editor-in-Chief of the World Stem Cell Report."Dr. Knoepfler's unique perspective as a scientist and patient advocate provides a fresh perspective to the stem cell universe. As a communicator, Paul is unsurpassed. We are proud to include his views in the Report."

"Key opinion leaders in the field like Paul Knoepfler bring into focus where we are, and where we are not yet, in regard to the further translation of stem cell research," says Editor-in-Chief Graham C. Parker, PhD, The Carman and Ann Adams Department of Pediatrics, Wayne State University School of Medicine (Detroit, MI).

###

The World Stem Cell Summit is the flagship meeting of the international stem cell community. The Summit aims to accelerate the discovery and development of lifesaving cures and therapies, bringing global stakeholders together to solve global challenges. It builds a foundation to advance cell therapies by establishing a supportive environment of regulation, legislation, financing, reimbursement, and patient advocacy. The 2013 World Stem Cell Summit will be held at the Manchester Grand Hyatt San Diego, in San Diego, California, December 4-6, 2013. It is presented by GPI and is co-organized by the California Institute for Regenerative Medicine, Mayo Clinic, Scripps Research Institute, Sanford-Burnham Medical Research Institute, and Kyoto University Institute for Integrated Cell-Material Sciences (iCeMS). For more information, visit the World Stem Cell Summit website.

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How will stem cell therapies impact patient care?

Matric revision: Life Sciences: Genetics (3/5): homozygous ...
Homozygous, dominance, co-dominance, incomplete dominance, multiple alleles Which of the cattle will definitely be homozygous? What if both are dominant? How...

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Matric revision: Life Sciences: Genetics (3/5): homozygous ... - Video