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Inhibiting NLK in cancers with mutated PTEN could turn the cancer's strength against it

Inhibiting NLK in cancers with mutated PTEN could turn the cancer's strength against it | Longevity science | Scoop.it

A mutation that allows cells to grow out of control could also provide a new way to target and destroy cancer cells. This potential Achilles’ heel comes from a mutation in a gene called PTEN, which is found in a wide range of cancers.

 

PTEN is one of many tumor suppressor genes that we have to prevent our cells from growing out of control. If the PTEN gene stops working because of a mutation, it can cause tumours to develop – indeed many tumors have a mutated form of PTEN. However when a door closes, a window opens: the PTEN mutation helps the tumor to grow, but it could also mark it out as a target.

 

Researchers from the Institute of Cancer Research, London, found that switching off another gene known as NLK (Nemo-like kinase) killed tumor cells that had the PTEN mutation. This makes NLK a good target for drug developers to create a new cancer treatment.

 

Initially, the researchers took samples of tumor cells with and without the mutation, and switched off genes for important proteins that are used for regulating lots of processes in the cell. To do this they used small interfering RNA (or siRNA) which interfere with the processes of specific genes. These siRNAs block the chain of events that allow a gene to produce a protein, effectively switching it off. By switching off 779 genes individually, they could look for ones where cells with the PTEN mutation died and cells without the mutation survived.

 

This is how the researchers discovered the powerful effect of switching off the NLK gene. They are not certain how this works but it appears to protect a protein called FOXO1 that can act as a backup tumor suppressor and cause the cancer cell to die. When PTEN is mutated, the FOXO1 protein becomes vulnerable to a process called phosphorylation, which means it is ejected from the cell nucleus and destroyed. NLK is one of the proteins that phosphorylates FOXO1 and so by switching off the NLK gene, FOXO1 is able to do its job.

 


Via Dr. Stefan Gruenwald
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Extracting human DNA with full genetic data in minutes | KurzweilAI

Extracting human DNA with full genetic data in minutes | KurzweilAI | Longevity science | Scoop.it

University of Washington engineers and NanoFacture, a Bellevue, Wash., company, have created a device that can extract human DNA from fluid samples in a simpler, more efficient and environmentally friendly way than conventional methods.

The device will give hospitals and research labs a much easier way to separate DNA from human fluid samples, which will help with genome sequencing, disease diagnosis and forensic investigations.

 

 

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Vitamin D might help some Parkinson's patients

Vitamin D might help some Parkinson's patients | Longevity science | Scoop.it

 

NEW YORK (Reuters Health) - Depending on their genes, some Parkinson's patients may be able to slow their deterioration by taking vitamin D supplements, according to a small study from Japan.Researchers...

 

Franklin Delano Williams's curator insight, March 28, 12:03 PM

I take my Vitamin D every day. My father had Parkinson's Disease in his 40's.  I'm 67 and counting...

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Caloric restriction has a protective effect on chromosomes

Caloric restriction has a protective effect on chromosomes | Longevity science | Scoop.it

According to a study carried out by a team led by María Blasco, the director of the Spanish National Cancer Research Centre (CNIO) and head of the Telomeres and Telomerase Group, a sustained lowering of food intake over time results in an increase of telomere length -- the ends of chromosomes -- in adult mice, which has a protective effect on the DNA and genetic material.

 

 

Ray and Terry's 's insight:

Caloric restriction is step 6 of the Transcend program. Moderate CR (10%) is manageable and easier to sustain over the long term.

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A noninvasive avenue for Parkinson’s disease gene therapy | KurzweilAI

A noninvasive avenue for Parkinson’s disease gene therapy | KurzweilAI | Longevity science | Scoop.it

Researchers at Northeastern University in Boston have developed a gene therapy approach that may one day stop Parkinson’s disease (PD) in it tracks, preventing disease progression and reversing its symptoms.

The novelty of the approach lies in the nasal route of administration and nanoparticles containing a gene capable of rescuing dying neurons in the brain.

 

 

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Receptor for Tasting Fat is CD36

Receptor for Tasting Fat is CD36 | Longevity science | Scoop.it
For the first time, a team of scientists at Washington University School of Medicine has identified a human receptor that can taste fat.

 

CD36 is a membrane protein found on the surface of many cell types in humans, mice, rats and many vertebrate animals. The findings also suggest that variations in the CD36 gene can make people more or less sensitive to the taste of fat.

 

“The ultimate goal is to understand how our perception of fat in food might influence what foods we eat and the quantities of fat that we consume,” said Dr. Nada Abumrad, senior investigator and the Dr. Robert A. Atkins Professor of Medicine and Obesity Research.

 

“In this study, we’ve found one potential reason for individual variability in how people sense fat. It may be, as was shown recently, that as people consume more fat, they become less sensitive to it, requiring more intake for the same satisfaction. What we will need to determine in the future is whether our ability to detect fat in foods influences our fat intake, which clearly would have an impact on obesity.”

 

The CD36 discovery follows research that had identified a role for the gene in rats and mice. Scientists had learned that when animals are genetically engineered without a working CD36 gene, they no longer display a preference for fatty foods. In addition, animals that can’t make the CD36 protein have difficulty digesting fat.

 

Up to 20 percent of people are believed to have the variant in the CD36 gene that is associated with making significantly less CD36 protein. That, in turn, could mean they are less sensitive to the presence of fat in food.

 

Dr. Abumrad was the first to identify CD36 as the protein that facilitates the uptake of fatty acids. She explained that better understanding of how the protein works in people could be important in the fight against obesity.

“Diet can affect sensitivity to fat, and in animals, diet also influences the amount of CD36 that’s made,” added Dr. Pepino. “If we follow the results in animals, a high-fat diet would lead to less production of CD36, and that, in turn, could make a person less sensitive to fat. From our results in this study, we would hypothesize that people with obesity may make less of the CD36 protein. So it would seem logical that the amounts of the protein we make can be modified, both by a person’s genetics and by the diet they eat.”


Via Dr. Stefan Gruenwald
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