Archive for the ‘Gene Therapy Research’ Category

Kinect Tech in Real Weapons
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Arthritis Treatment Center What is Stem Cell Therapy
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Last year an international team led by Cancer Research UK scientists at our Cambridge Research Institute unveiled the results of a huge research project called METABRIC . They used advanced gene sequencing techniques to analyse the patterns of gene activity in breast tumours from thousands of women, revealing the molecular signature of each tumour. The results showed that the disease could be divided into ten distinct subtypes, each with its own characteristics and outlook.

That work was just the beginning of the story. Since then, the researchers, led by Professor Carlos Caldas, have been delving into these subtypes in ever greater depth, trying to figure out what makes them different and how we can tackle each one more effectively.

In a new paper, published in the leading scientific journal Nature , the team took another look at the thousand breast cancer samples from the METABRIC study. But rather than looking at genes that bear the instructions to make proteins in our cells, the researchers focused instead on a set of genes that encode tiny lengths of RNA - a relative of the larger DNA molecules that makes up our genome.

In recent years it has become clear that these short pieces of RNA known as microRNAs, or miRNAs for short - can help to control when and where protein-making genes are switched on or off, and theyre an increasingly hot topic in the world of cancer research .

And now it looks like they may be playing a role in controlling how the immune system responds to certain breast cancers.

Small but powerful

First discovered in the 1990s in tiny worms called nematodes, microRNAs act as molecular switches inside cells, turning genes off when theyre not needed as well as fine-tuning gene activity levels. Theyre made from chopping up much longer strings of RNA a type of molecular messenger in cells.

Many hundreds of different microRNAs have now been identified, and they can recognise and act on individual genes in various ways. And thanks to projects such as ENCODE , we also know theres a lot more in the genome still to be discovered.

Researchers already know that cancer cells contain different levels of microRNAs compared to healthy cells - generally, they tend to be lower - and some types of cancer seem to have a characteristic microRNA fingerprint. This suggests that they could be useful for helping to diagnose or potentially even treat the disease.

Professor Caldas and his team wanted to find out whether the ten distinct subtypes of breast cancer theyd identified in the METABRIC study also had a telltale microRNA signature, and whether this matched up with the particular characteristics of that type.

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Genetic "fine-tuners" and breast cancer

Featured Article Academic Journal Main Category: Obesity / Weight Loss / Fitness Also Included In: Genetics Article Date: 22 Jul 2013 - 5:00 PDT

Current ratings for: Could severe obesity be in the genes?

Scientists have discovered a particular gene mutation that could be linked to a cause of severe obesity.

Researchers from Boston Children's Hospital carried out a number of genetic surveys in several groups of people suffering from obesity, as well as a series of genetic experiments in mice.

The research, published in the journal Science, analyzed a gene called Mrap2 in different groups of mice. This particular gene has a human counterpart, which according to the scientists appears to be involved in regulating metabolism and food consumption.

The researchers explained that the protein encoded by the Mrap2 gene sends a signal to a receptor in the brain called Mc4r. This receptor assists in increasing the metabolism and decreasing appetite in a "signaling chain" involved in energy regulation.

They explain that fat cells produce a hormone called leptin. This hormone triggers receptors in the brain to start the production of a second hormone called aMSH.

Mrap2 helps Mc4r detect the aMSH hormone, which essentially leads to a drop in appetite and weight. The scientists explain that any mutations in this signaling chain are likely to increase the risk of obesity.

The researchers analyzed two groups of mice. One group who had the Mrap2 gene removed from just the brain, and one group who had the gene removed from "whole-of-body."

Both groups of mice grew to around twice their normal size, but weight gain was greatest in those with the gene removed completely.

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Could severe obesity be in the genes?

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The Harmful Effects of Genetic Engineering
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We previously reported that direct-to-consumer genetic tests can spur positive lifestyle changes, but we're back to warn you that a recent study done at Emory University in Atlanta has shown that the results of the at-home kits can vary widely. Not only that, but a Google search here at ThirdAge.com revealed that two of the companies in the study, deCODEme, and Navigenics, are no longer selling their products. However, customers who had already used the kits can still get their results, which is reason enough to pay attention to divergent findings of the Emory team! The link to deCODEme leads to a page that says: "Sales of Genetic Scans direct to consumer through deCODEme have been discontinued!" The link to Navigenics takes us to a page that says: "We are no longer accepting orders or samples for the Navigenics Health Compass service." The third company, 23andMe, is still in business.

A release from Emory quotes lead researcher Cecile Janssens as confirming the demise of deCODEme and Navigencis "Although two of the companies that we studied are no longer operating, genotyping and sequencing is becoming less expensive and testing such as this is increasingly popular," she said. "The methods used for predicting these types of results are of important concern."

Janssens and colleagues published their findings online in the journal Genetics in Medicine. Test results provided by the three companies at the time of the study indicated an individual's risks for a large number of diseases. The study was conducted by creating DNA datafor a hypothetical population of 100,000 individuals, which is "a less expensive and equally valid method for demonstrating the variations in predicted risk among the companies," according to the release. Predicted risks, which were calculated using the methods of the three companies detailed on their websites, were assessed and compared for six diseases:type 2 diabetes, prostate cancer, celiac disease, Crohn disease, age-related vision loss, and abnormal heart rhythm. The variations in predicted risks were explained by three factors: *The companies considered a different number of genetic variants in the risk calculations.Generally a larger difference in the number of variants implied more variation in predicted risks. *All three companies used an estimate for the average population disease risk as a starting point for their predictions. Differences in average risks affect predicted risks of all consumers to the same extent.For example, when the average odds is two times higher, all predicted odds are also two times higher.

*The companies applied different mathematical formulas. The formulas of two companies led to an overestimation of risks when predicted risks were higher and even predicted risks that were higher than 100 percent. "Our study provides insight into the methodology and performance of risk estimation for personal genome tests," Janssens explains. "Future efforts to design predictive models will benefit from understanding the strengths and limitations of these current models and formulas."

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Genetic Test Kit Results Vary

Marshall Summar, MD Introduces Genetics Program (1 of 3) | Children #39;s National
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Marshall Summar, MD Introduces Genetics Program (2 of 3) | Children #39;s National
Dr. Summar discussing genetics department (2 of 3) http://www.childrensnational.org/departmentsandprograms/default.aspx?Id=378 Type=Dept Name=Genetics%20and%...

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Genetics: The Study of Heredity - Mendel #39;s Experiments
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Pentagon Tests Virus that Destroys Human Genetics
Funvax is called a vaccine against being religious, it destroys the part of our genetics they have named the "God gene". In this leaked video, they describe ...

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Let #39;s Play The Sims 3 - Perfect Genetics Challenge - Episode 22
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FAQ1-Stem Cell Therapy
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Myriad Genetics - DNA Patentability
Professor David Schwartz (IIT Chicago-Kent College of Law) discusses the decision in the Supreme Court case Association for Molecular Pathology v. Myriad Gen...

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Genetics: The Study of Heredity - Making a Pedigree
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Let #39;s Play Metal Gear Solid - Part 1 This is Snake
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HONOLULU (HawaiiNewsNow) -

Breakthrough research has created excitement in the genetics field. The University of Massachusetts Medical School has found a way to turn off the chromosome that causes down syndrome.

In Hawaii five to eight babies a year are born with Down syndrome. It is the most common birth defect. Doctors say the new research is exciting because it's the first time someone has been able to shut off a gene, although not everyone agrees that's the right thing to do.

"Not too high," said Emily Keane, as her father Darryl pushed her on a swing.

Emily is 22 years old and brings a world of joy to her family.

"She is very social, she likes to have friends," said Karen Keane, Emily's mom.

Emily was born with Down syndrome and cerebral palsy which makes it difficult for her to have a job. So when the family heard about the breakthrough research that doctors found a way to turn off the extra chromosome that causes the Down syndrome they were excited and would have done it had it been an option for Emily.

"Yes absolutely because it would open up more possibilities for her. She wants to do everything, she wants to be like everybody else and that would make that possible for her," said Karen Keane.

"The universal thing is that the kids are a blessing but the other side of it is we're always looking for ways to help improve their quality of life," said Darryl Keane, Emily's dad. "The medical research if it can help we are definitely open to that."

We also met five year old Gracie McComas.

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New Down syndrome research gets mixed reactions from parents

Medically, obesity is now considered a disease. Socially, the condition is regarded differently. In the latter realm, being extremely overweight can seem like a symptom of laziness or lack of willpower.

Research into the genetics of obesity, however, is revealing that judgment may be unfair. Researchers at Boston Childrens Hospital have discovered a gene that, when deleted, causes extreme obesity in mice. Although an initial survey showed that disease-causing mutations in the gene are quite rare in people, scientists think that less severe mutations in this and other rare genes associated with obesity may cause subtle differences in energy regulation and metabolism. Those differences may cause some people to be predisposed to weight gain.

In an unusual twist, the mice in the study published Thursday in the journal Science didnt gain weight simply because they ate more. Rodents lacking the gene must be fed about 15 percent less than normal mice to have the same amount of weight gain.

The mice we have made that are obese, while theyre children and adolescents and in that phase, theyre getting very obese, but not eating more than brothers and sisters, said Dr. Joseph Majzoub, chief of endocrinology at Childrens Hospital. Its quite different from other types of obesity.

Dr. Michael Schwartz, director of the Diabetes and Obesity Center of Excellence at the University of Washington, said that the new study was a valuable addition to the growing knowledge about the genetic underpinnings of obesity. Schwartz, who was not involved in the work, said that in addition to genes that cause severe obesity, there are genes that protect against gaining weight. The genetic predisposition to gain weight was probably influenced not only by genes that make people gain weight, he said, but in flaws in those that protect against gaining weight.

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New gene associated with severe obesity - Boston.com

Toronto, ON (PRWEB) July 20, 2013

Bel Marra Health, who offers high-quality, specially formulated vitamins and nutritional supplements, reports on a new study revealing a gene found to determine prognosis of breast cancer.

As Bel Marra Health reports in its article, (http://www.belmarrahealth.com/cancer/breast-cancer-prognosis-determined-by-this-one-gene/) receiving a confirmed breast cancer diagnosis is difficult, and discovering an aggressive form of this disease can be utterly devastating. But new research just published in Cell may provide some hope for those diagnosed with aggressive forms of breast cancer. The researchers identified a particular gene, called ZEB1, with the power to convert non-cancer stem cells into cancer stem cells, and thus ultimately influence whether a breast cancer will exhibit as a benign form or as an aggressive and rapidly spreading form. This discovery has major implications on the future of breast cancer treatment, allowing brand new options to begin to be devised for patients fighting this devastating disease.

There are various categories of breast cancer, differing according to their molecular structure. Less aggressive types of breast cancer are grouped into the luminal category, while more aggressive types are categorized into the basal category. Patients that are diagnosed with a luminal type of breast cancer have a better prognosis than those diagnosed with a basal type of the disease. Aggressive basal types of breast cancer often metastasize, spreading and creating tumors in other areas of the body. This may be due to the fact that non-cancer stems cells from basal type breast cancer are able to turn into cancer stem cells relatively easily, while those from luminal types of breast cancer usually stay in a non-cancer stem cell state.

Genes that control the expression of other genes are known as transcriptor factors. Therefore, they have a significant role in various cell activities. ZEB1 is one type of transcriptor factor, responsible for transitioning certain types of cells into other forms. The researchers found that the ZEB1 gene is found in a poised state in basal non-cancer stem cells, which means that they are ready to respond to environmental cues that would put them into action. Essentially, the ZEB1 gene converts non-cancer stem cells into cancer stem cells. This may be the basis that determines whether breast cancer cells will exhibit benign or aggressive behavior in the future. The researchers discovered that the ZEB1 gene acts differently in luminal and basal breast cancer cells. In luminal breast cancer cells, the ZEB1 gene is basically shut down whereas, in basal breast cancer cells, the ZEB1 gene is more active, allowing for easier conversion of non-cancer stem cells into cancer stem cells.

The results from the current research suggest that breast cancer cells are very adaptable. Treatment options for breast cancer should look at targeting cancer stem cells and preventing non-cancer stem cells from transitioning into cancer stem cells. One way in which this may be accomplished is by discovering new treatment options that inhibit the adaptability of breast cancer cells. This may help to control the spread of cancer throughout the body, resulting in a better prognosis.

The recent research brings hope to the future prevention and treatment of breast cancer. The fact that a specific gene has been identified as the gene responsible for the aggressive nature of certain breast cancers will allow scientists to study new treatment options for this devastating disease. Additionally, researchers can investigate whether the ZEB1 gene reacts that same way in other forms of cancer, which could possibly change the future of cancer treatment.

(SOURCE: Christine L. Chaffer, et al. Poised chromatin at the ZEB1 promoter enables breast cancer cell plasticity and enhances tumorigenicity. Cell, 2013)

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Bel Marra Health Reports on New Research Discovering Aggressiveness of Breast Cancer Determined by Gene

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Two studies zero in on DNA-based drivers of weight. Is obesity written in our genes?

In two separate papers, published in the journal Science and in the Journal of Clinical Investigation (JCI), researchers describe new genetic factors that could explain weight gain in some people. In the Science study, researchers at Boston Childrens Hospital studying mice found a rare genetic mutation that prevented the animals from burning off fat calories. They also found the same gene was mutated in a group of obese people. And a team based at University College London reported in JCI that a specific form of a gene previously linked to obesity, FTO, can increase craving for high-fat foods.

The discoveries add to the growing body of knowledge about the biology behind weight, and the results confirm that while its represented by a single number, weight is the complex combination of a multitude of different metabolic processes, from brain systems that regulate appetite to enzymes that control how efficiently calories are turned from food into energy that the body needs. Making matters even more confusing, these factors are also likely influenced by environmental contributors such as diet and lifestyle.

In the mouse study, the research team determined that mutations in theMrap2 gene led the animals to eat less initially but still gain about twice as much weight as they normally would. While their appetites returned, these mice continued to gain weight despite being fed the same number of calories as a group of control animals. That led the scientists to figure out that the mice with the mutated gene were simply sequestering fat rather than breaking it down for energy. The mice, like people, possessed two copies of the gene, and mice with even one defective copy experienced significant weight gain, although not as much as those who had two mutated versions of Mrap2.

The scientists found a similar pattern among a group of 500 obese people; they detected four mutations in the human version of Mrap2, and each of the obese individuals possessed only one bad version of the gene.

(MORE: Study Identifies Four New Genetic Markers For Severe Childhood Obesity)

In the British study, the researchers divided a group of 359 healthy men of normal weight by their FTO gene status. The majority of the men had low-risk versions of the gene, while 45 of the participants had mutations that have been linked to greater appetite and caloric consumption. To figure out how the altered genes were affecting appetite, the team measured levels of the hunger hormone ghrelin both before and after meals that the participants ate; the men with the mutated form of FTO did not show the same drop in ghrelin levels, signifying that they were full, as the men with the low-risk form of FTO.

Genome wide association studies, which compare genetic makeups of obese individuals to those of normal weight, are making it easier to flesh out important genetic factors contributing to weight, and researchers at the Harvard School of Public Health say that to date, these studies haveidentified over 30 candidate genes on 12 chromosomes associated with body mass index.

Thus far mutations in about eight genes are known to cause obesity in humans. But these mutations account for under five percent of the obesity in our society, and certainly are not, by themselves, responsible for the current obesity epidemic, since the mutation rate in these genes could not have changed dramatically during the past twenty years, says Dr.Joseph Majzoub, the chief of the division of endocrinology at BostonChildrens Hospital and an author on the Science paper. However, mutations in these genes have led to the discovery of pathways that are important in energy balance in humans, giving us hope that drugs can be developed that affect these pathways to prevent excessive weight gain, either by curbing appetite or increased burning of calories.

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The Obesity Gene: Is Weight Coded in DNA?

OMD 1983 Interview (Dazzle Ships)
Interview with Andy McCluskey in 1983 speaking about the "Dazzle Ships" album, the science of genetic engineering, OMD becoming a four member band and more.....

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NUC Ops - Apex Genetics: Resecure + Defense - Planetside 2
Apex Genetics: Resecure + Defense - 7/16/13 Perspective: [NUC]Enemy http://www.nucgaming.com Server: Waterson.

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Genetics: The Study of Heredity - How Traits are Inherited
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Genetics: The Study of Heredity - Gregor Mendel
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Genetics: The Study of Heredity - Phenotypes and Genotypes
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