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Washington, March 18 : Researchers have discovered a previously unrecognized gene variation that makes humans have healthier blood lipid levels and reduced risk of heart attacks.

Researchers from the University of Michigan and the Norwegian University of Science and Technology scanned the genetic information available from a biobank of thousands of Norwegians, focusing on variations in genes that change the way proteins function.

Most of what they found turned out to be already known to affect cholesterol levels and other blood lipids.

But one gene, dubbed TM6SF2, wasn't on the radar at all. In a minority of the Norwegians who carried a particular change in the gene, blood lipid levels were much healthier and they had a lower rate of heart attack.

And when the researchers boosted or suppressed the gene in mice, they saw the same effect on the animals' blood lipid levels.

Cristen Willer, Ph.D., the senior author of the paper and an assistant professor of Internal Medicine, Human Genetics and Computational Medicine and Bioinformatics at the U-M Medical School, said that while genetic studies that focused on common variations may explain as much as 30 percent of the genetic component of lipid disorders, they still don't know where the rest of the genetic risk comes from.

She said that this approach of focusing on protein-changing variation may help them zero in on new genes faster.

Willer and Kristian Hveem of the Norwegian University of Science and Technology suggested the same gene may also be involved in regulating lipid levels in the liver.

The study has been published in the journal Nature Genetics.

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New gene linked to reduced heart attack risk discovered

Scientists have discovered a previously unrecognized gene variation that makes humans have healthier blood lipid levels and reduced risk of heart attacks -- a finding that opens the door to using this knowledge in testing or treatment of high cholesterol and other lipid disorders.

But even more significant is how they found the gene, which had been hiding in plain sight in previous hunts for genes that influence cardiovascular risk.

This region of DNA where it was found had been implicated as being important in controlling blood lipid levels in a report from several members of the same research team in 2008. But although this DNA region had many genes, none of them had any obvious link to blood lipid levels. The promise of an entirely new lipid-related gene took another six years and a new approach to find.

In a new paper in Nature Genetics, a team from the University of Michigan and the Norwegian University of Science and Technology report that they zeroed in on the gene in an entirely new way.

The team scanned the genetic information available from a biobank of thousands of Norwegians, focusing on variations in genes that change the way proteins function. Most of what they found turned out to be already known to affect cholesterol levels and other blood lipids.

But one gene, dubbed TM6SF2, wasn't on the radar at all. In a minority of the Norwegians who carried a particular change in the gene, blood lipid levels were much healthier and they had a lower rate of heart attack. And when the researchers boosted or suppressed the gene in mice, they saw the same effect on the animals' blood lipid levels.

"Cardiovascular disease presents such a huge impact on people's lives that we should leave no stone unturned in the search for the genes that cause heart attack," says Cristen Willer, Ph.D., the senior author of the paper and an assistant professor of Internal Medicine, Human Genetics and Computational Medicine & Bioinformatics at the U-M Medical School.

"While genetic studies that focused on common variations may explain as much as 30 percent of the genetic component of lipid disorders, we still don't know where the rest of the genetic risk comes from," Willer adds. "This approach of focusing on protein-changing variation may help us zero in on new genes faster."

Willer and Kristian Hveem of the Norwegian University of Science and Technology led the team that published the new result. Intriguingly, Willer and colleagues suggest the same gene may also be involved in regulating lipid levels in the liver -- a finding confirmed by the observations of a team led by Jonathan Cohen and Helen Hobbs, who propose a role for the gene in liver disease in the same issue of Nature Genetics.

Hveem, a gastroenterologist, says that "more research into the exact function of this protein will be needed to understand the role it plays in these two diseases, and whether it can be targeted with new drug therapies to reduce risk -- or treat -- one or both diseases."

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New gene linked to key heart attack risk factor found by novel gene-finding approach

A gene-by-gene examination of cells from one of the deadliest forms of brain cancer may have uncovered a new treatment option.

Neurosurgeon Clark Chen and his colleagues at the University of California San Diego School of Medicine decided to use a form of genetic engineering in which individuals genes in a cell are, in effect, turned off to see what impact this has on the cell.

In this case, Chen and his teams were applying this gene-silencing technique on cells from glioblastoma, one of the most aggressive and hard-to-treat malignant brain tumors. They were trying to find which genes played a key role in helping the cancerous brain cells grow and survive.

After compiling their list of genetic suspects, the U.C. San Diego researchers made an interesting discovery: Many of the genes involved in glioblastoma growth help regulate the effect of the neurochemical dopamine, they reported recently online in the journal Oncotarget.

Chen and his team made their discovery by using shRNA in a molecular engineering technique known as RNA interference. Called short-hairpin RNA by some and small-hairpin RNA by others, shRNA can keep a gene from turning the genetic blueprint encoded in its DNA into a specific protein molecule. Scientists use viruses to insert the shRNA into a target gene and block its role in the production of the protein.

ShRNAs are invaluable tools in the study of what genes do. They function like molecular erasers, said Chen, the vice chairman of the division of neurosurgery at the U.C. San Diego School of Medicine. We can design these erasers against every gene in the human genome.

Because of the similarities in the lists of genes involved in glioblastoma growth and dopamine regulation, the researchers decided to see what effect dopamine antagonist drugs would have on the brain cancer cells. They discovered these drugs have significant anti-tumor effects on glioblastoma cells grown in laboratory dishes and in lab mice.

The anti-glioblastoma effects of these drugs are completely unexpected and were only uncovered because we carried out an unbiased genetic screen, said Chen.

In addition to psychosis, dopamine antagonists are used to treat other disorders, including anxiety-panic and Parkinsons disease and to control nausea and vomiting and already have a stamp of approval from the U.S. Food and Drug Administration.

First, these drugs are already FDA-cleared for human use in the treatment of other diseases, so it is possible these drugs may be re-purposed for glioblastoma treatment, thereby bypassing years of pre-clinical testing, said Bob Carter, chairman of the U.C. San Diego School of Medicine division of neurosurgery.

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