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A genetically modified version of the herpes virus has shown great potential in treating advanced cancers, according to a report by the Institute of Cancer Research in London published on Thursday.

A promising therapy

Although the treatment is still in early trials, researchers have found that RP2, a modified version of the herpes simplex virus, managed to kill cancer cells in a quarter of patients. The patients had cancers so advanced and complicated that they had run out of treatments to try.

Circa 2017 face_with_colon_three

LA JOLLA—Salk scientists have created a new version of the CRISPR/Cas9 genome editing technology that allows them to activate genes without creating breaks in the DNA, potentially circumventing a major hurdle to using gene editing technologies to treat human diseases.

Continue reading “Salk scientists modify CRISPR to epigenetically treat diabetes, kidney disease, muscular dystrophy” »

According to recent research from Sweden’s Lund University, the most commonly used analytical method in population genetics is deeply flawed. This could have caused incorrect results and misconceptions regarding ethnicity and genetic relationships. The method has been used in hundreds of thousands of studies, influencing findings in medical genetics and even commercial ancestry tests. The findings were recently published in the journal Scientific Reports.

The pace at which scientific data can be gathered is increasing rapidly, resulting in huge and very complex databases, which has been nicknamed the “Big Data revolution.” Researchers employ statistical techniques to condense and simplify the data while maintaining the majority of the important information in order to make the data more manageable. PCA (principal component analysis) is perhaps the most widely used approach. Imagine PCA as an oven with flour, sugar, and eggs serving as the input data. The oven may always perform the same thing, but the ultimate result, a cake, is highly dependent on the ratios of the ingredients and how they are mixed.

“It is expected that this method will give correct results because it is so frequently used. But it is neither a guarantee of reliability nor produces statistically robust conclusions,” says Dr. Eran Elhaik, Associate Professor in molecular cell biology at Lund University.

Impaired reduction/oxidation (redox) metabolism is a key contributor to the etiology of many diseases, including primary mitochondrial disorders, cancer, neurodegeneration, and aging. However, mechanistic studies of redox imbalance remain challenging due to limited strategies which can perturb cellular redox metabolism and model pathology in various cellular, tissue, or organismal backgrounds without creating additional and potentially confounding metabolic perturbations. To date, most studies involving impaired redox metabolism have focused on oxidative stress and reactive oxygen species (ROS) production; consequently, less is known about the settings where there is an overabundance of reducing equivalents, termed reductive stress. NADH reductive stress has been modeled using pharmacologic inhibition of the electron transport chain (ETC) and ethanol supplementation. Still, both these methods have significant drawbacks. Here, we introduce a soluble transhydrogenase from E. coli (Ec STH) as a novel genetically encoded tool to promote NADH overproduction in living cells. When expressed in mammalian cells, Ec STH, and a mitochondrially-targeted version (mito Ec STH), can elevate the NADH/NAD⁺ ratio in a compartment-specific manner. Using this tool, we determine the metabolic and transcriptomic signatures of NADH reductive stress in mammalian cells. We also find that cellular responses to NADH reductive stress, including blunted proliferation, are dependent on cellular background and identify the metabolic reactions that sense changes in the cellular NADH/NAD⁺ balance. Collectively, our novel genetically encoded tool represents an orthogonal strategy to perturb redox metabolism and characterize the impact on normal physiology and disease states.

The authors have declared no competing interest.

Researchers at Mayo Clinic Comprehensive Cancer Center have identified a gene marker that may lead to a more effective, precision treatment for pancreatic ductal adenocarcinoma (PDAC). The researcher’s findings are published in Nature Cancer.

“Pancreatic ductal adenocarcinoma is one of the most lethal cancers,” says the paper’s senior author Zhenkun Lou, Ph.D. Dr. Lou says while Poly-ADP-ribose-polymerase inhibitors (PARPi) are now an FDA-approved option for standard maintenance therapy for patients with metastatic PDAC who harbor pathogenic germline BRCA1/2 mutations, only about 10 percent of patients with PDAC harbor pathogenic mutations of the homologous recombination (HR) genes. “This leaves most patients missing out on this encouraging treatment strategy,” says Dr. Lou.

In this study, Dr. Lou and his colleagues found that the protein METTL16 may be a new biomarker for PARPi treatment, and that PDAC with elevated expression of METTL16, may benefit from PARPi treatment.

Summary: In mice genetically more susceptible to PTSD following a stressful event, researchers found an increased expression of cortisol receptors on neurons in the CA1 region of the dorsal hippocampus. Those increased receptors enabled an elevated expression of the HCN1 protein and TRIP8b, reducing neural excitability.

Source: medical college of georgia at augusta university.

Social avoidance is a common symptom of PTSD, and scientists working to better understand why have laboratory evidence that while stress hormone levels consistently increase in the immediate aftermath of a traumatic event, there can be polar opposite consequences in parts of the brain down the line.

Chromosome-level engineering is a completely different beast: it’s like rearranging multiple paragraphs or shifting complete sections of an article and simultaneously hoping the changes add capabilities that can be passed onto the next generation.

Reprogramming life isn’t easy. Xiao Zhu’s DNA makeup is built from genetic letters already optimized by eons of evolutionary pressure. It’s no surprise that tinkering with an established genomic book often results in life that’s not viable. So far, only yeast have survived the rejiggering of their chromosomes.

The new study, published in Science, made the technology possible for mice. The team artificially fused together chunks from mice chromosomes. One fused pair made from chromosomes four and five was able to support embryos that developed into healthy—if somewhat strangely behaved—mice. Remarkably, even with this tectonic shift to their normal genetics, the mice could reproduce and pass on their engineered genetic quirks to a second generation of offspring.

Summary: New research in cloned pigs with a mutation of the SORL1 sheds light on Alzheimer’s development. The findings could pave the way for new treatments for the neurodegenerative disorder.

Source: Aarhus University.

For decades, researchers from all over the world have been working hard to understand Alzheimer’s disease. Now, a collaboration between the Department of Biomedicine and the Department of Clinical Medicine at Aarhus University has resulted in a flock of minipigs that could lead to a major step forward in the research and treatment of Alzheimer’s.

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As humanity reaches out to the stars and make new homes on strange new worlds, how will our genetics & DNA change under those alien planets?

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