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Category: genetics – Page 375

BERKELEY, Calif., Aug. 20, 2019 /PRNewswire/ — Today, the U.S. Patent and Trademark Office has awarded a new patent (U.S. 10,385,360) to the University of California (UC), University of Vienna, and Dr. Emmanuelle Charpentier covering nucleic acid molecules encoding single-molecule guide RNAs, as well as CRISPR-Cas9 compositions comprising single-molecule guide RNAs or nucleic acid molecules encoding single-molecule guide RNAs.

Over the past six months, UC’s U.S. CRISPR-Cas9 portfolio has sharply increased, and to date includes 11 separate patents for methods and compositions related to the gene-editing technology. Looking ahead, UC anticipates at least six additional related patents issuing in the near future, bringing UC’s total portfolio to 17 patents and spanning various compositions and methods including targeting and editing genes in any setting, such as within plant, animal, and human cells. The portfolio also includes patents related to the modulation of transcription.

“The USPTO has continually acknowledged the Doudna-Charpentier team’s groundbreaking work,” said Eldora L. Ellison, Ph.D., lead patent strategist on CRISPR-Cas9 matters for UC and a Director at Sterne, Kessler, Goldstein & Fox. “True to UC’s mission as a leading public university, the patent granted today and others in its CRISPR-Cas9 portfolio will be applied for the betterment of society.”

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Neurotoxic anticancer drugs, such as platinum-based anticancer drugs, taxanes, vinca alkaloids, and proteasome/angiogenesis inhibitors are responsible for chemotherapy-induced peripheral neuropathy (CIPN). The health consequences of CIPN remain worrying as it is associated with several comorbidities and affects a specific population of patients already impacted by cancer, a strong driver for declines in older adults. The purpose of this review is to present a comprehensive overview of the long-term effects of CIPN in cancer patients and survivors. Pathophysiological mechanisms and risk factors are also presented. Neurotoxic mechanisms leading to CIPNs are not yet fully understood but involve neuronopathy and/or axonopathy, mainly associated with DNA damage, oxidative stress, mitochondria toxicity, and ion channel remodeling in the neurons of the peripheral nervous system. Classical symptoms of CIPNs are peripheral neuropathy with a “stocking and glove” distribution characterized by sensory loss, paresthesia, dysesthesia and numbness, sometimes associated with neuropathic pain in the most serious cases. Several risk factors can promote CIPN as a function of the anticancer drug considered, such as cumulative dose, treatment duration, history of neuropathy, combination of therapies and genetic polymorphisms. CIPNs are frequent in cancer patients with an overall incidence of approximately 38% (possibly up to 90% of patients treated with oxaliplatin). Finally, the long-term reversibility of these CIPNs remain questionable, notably in the case of platinum-based anticancer drugs and taxanes, for which CIPN may last several years after the end of anticancer chemotherapies. These long-term effects are associated with comorbidities such as depression, insomnia, falls and decreases of health-related quality of life in cancer patients and survivors. However, it is noteworthy that these long-term effects remain poorly studied, and only limited data are available such as in the case of bortezomib and thalidomide-induced peripheral neuropathy.

Platinum-based anticancer drugs (i.e., cisplatin, oxaliplatin), proteasome/angiogenesis inhibitors (bortezomib/thalidomide), vinca alkaloids (i.e., vincristine, vinorelbine) and taxanes (i.e., paclitaxel, docetaxel) are the most common anticancer drugs used as first-line chemotherapy for several cancers, including colorectal, gastric, breast and lung cancers, and multiple myeloma. Despite their different action mechanisms, all these anticancer drugs share a common adverse and disabling effect for patients, namely CIPN (Balayssac et al., 2011). CIPN has a considerable impact on cancer treatments and their related symptoms severely affect patients’ daily activities and quality of life. Thus CIPN is often the main adverse effect leading to the reduction or discontinuation of chemotherapy.

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The evolving gene-editing technology CRISPR-Cas9 is useful for changing one gene, or maybe a few genes at a time. A team at ETH Zurich has tweaked the technology so they can change 25 different gene sites at once. Instead of using the Cas9 enzyme to do the DNA cutting, though, they used Cas12a. That allowed them to create a long “address list” of gene sites to target, they explained in the journal Nature Methods. They created a DNA molecule called a plasmid to store the list, inserted it in human cells and were able to modify several genes, they reported. (Release)

Chemotherapy and radiation suppress blood stem cells, often for several weeks or even months after cancer treatments are complete. This leaves patients vulnerable to infections and other health problems. Scientists at the University of California, Los Angeles have created a new drug that targets the protein tyrosine phosphatase-sigma (PTP-sigma), which is prevalent on blood stem cells. They showed that blocking the protein in rodent models with the drug, called DJ009, helped blood cells recover more quickly after they were damaged by radiation. They published their findings in the journal Nature Communications. (Release)

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Researchers at the Stanford University School of Medicine report in a new study that they found a way to help rats recover neurons in the brain’s center of learning and memory. They accomplished the feat by blocking a molecule that controls how efficiently genetic instructions are used to build proteins.

If the approach described in the study can be applied to humans, it may one day help patients who’ve suffered a stroke, or major loss and are thus at higher risk of memory loss.

In the study, to be published online Aug. 19 in eNeuro, researchers induced extremely —as would happen when the heart stops beating—in rats. These rats lost neurons in a specific region of the hippocampus critical to learning and memory, but the researchers improved the animals’ recovery of the by injecting a molecule that blocks a microRNA: a short molecule that tweaks gene activation by preventing the conversion of genetic blueprints into proteins. Interestingly, the scientists found that a microRNA blockade potentially causes astrocytes—cells that support neurons and make up 50% of the cells in the brain—to turn into neurons.

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A letter was recently published in Nature on 329,000 young people identifying 74 genetic variants—spelling mistakes in single nucleotides in the six billion letter human genome—which can be used to predict nearly 20 percent of the variation in school years completed, a quantitative trait of fortitude which is correlated to general intelligence, and which you can learn about by sequencing your own genome.

Staple that to your college application.

Even before the “molecular age,” we were on guard for the slightest tips that show we are more or less valued than our peers. But there was also caution from the academics that there was actually very little we could do to leverage our biology for improvement. In 1924, the Harvard geneticist William Castle quipped that “we are scarcely as yet in a position to do more than make ourselves ridiculous in this matter. We are no more in a position to control eugenics than the tides of the ocean.”

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Some people live much longer than average, partly thanks to their DNA. A study, published in the European Heart Journal, shows that it could be possible to replicate this genetic gift even for those lacking it. The way is now open to an innovative therapy model capable of preventing and fighting cardiovascular diseases through a real rejuvenation of blood vessels.

The study, conducted by the I.R.C.C.S. Neuromed, the I.R.C.C.S. Multimedica and the Department of Medicine, Surgery, and Dentistry, Salerno Medical School University of Salerno, with the support of the Cariplo Foundation and the Italian Ministry of Health, focuses on the gene that encodes the BPIFB4 . In the past, the same research group had identified a variant of this gene, the so-called LAV (“longevity associated variant”), which prevails in people over 100 years of age. Now, through a , researchers have inserted the LAV-BPIFB4 gene into the DNA of animal models particularly susceptible to atherosclerosis and, consequently, to cardiovascular diseases.

“The results—says Annibale Puca, coordinator of a research team at the University of Salerno and at I.R.C.C. MultiMedica—were extremely encouraging. We observed an improvement in the functionality of the endothelium (the inner surface of blood vessels), a reduction of atherosclerotic plaques in the arteries and a decrease in the inflammatory state.”

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For a core of longevity true believers, the time to intervene is now.

“How old are you?” James Clement wanted to know.

I turn 50 this year. There’s a new creaking in my bones; my skin doesn’t snap back the way it used to. It’s developed a dull thickness—you can’t tickle me at all. My gums are packing it in and retreating toward my jaw. These changes have been gradual or inexplicably sudden, like the day when I could no longer see the typed words that are my profession. Presbyopia, the ophthalmologist told me. Totally normal. You’re middle-aged.

To Clement, though, my age was great news. “Yep, you are going to live forever,” he said. “I think anybody under 50 who does not have a genetic liability will make it to longevity escape velocity.”

Continue reading “The transhumanists who want to live forever” | >

A team of scientists at UC San Francisco and the National Institutes of Health have achieved another CRISPR first, one which may fundamentally alter the way scientists study brain diseases.

In a paper published August 15 in the journal Neuron, the researchers describe a technique that uses a special version of CRISPR developed at UCSF to systematically alter the activity of in human neurons generated from , the first successful merger of stem cell-derived cell types and CRISPR screening technologies.

Though mutations and other genetic variants are known to be associated with an increased risk for many , technological bottlenecks have thwarted the efforts of scientists working to understand exactly how these genes cause .

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A new study outlines multiple ways in which epiblast stem cells can be reprogrammed back into a fully pluripotent state, paving the way for a better understanding of epigenetics.

The role of epigenetics

Epigenetics are why our cells, which all have the same DNA, differ in function. A bone cell has the same genetics as a nerve cell, but its epigenetic switches instruct it to perform the functions of a bone cell and not a nerve cell. Epigenetic alterations, however, are one of the primary hallmarks of aging. As we age, harmful epigenetic switches are activated and beneficial ones are deactivated, causing age-related dysfunction. This may even lead to inflammation, which causes further epigenetic damage, leading to a dangerous feedback loop.

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A research group at ETH Zurich, Switzerland, has made it possible to edit hundreds of genes at once with CRISPR gene editing.

CRISPR gene editing has revolutionized the biotech industry by providing an easy and quick way to genetically modify organisms. So far, however, CRISPR techniques have only managed to edit a maximum of seven genes at once. This limits the potential of the technique in creating cell therapies, since whole networks of genes need to be reprogrammed to control each cell’s fate.

The Swiss research group devised a way to overcome this limitation with a CRISPR technique able to edit 25 genes in one go. This number could also be increased to up to hundreds of genes at a time. This method therefore makes it possible to edit gene networks, and reprogram stem cells to become cell therapies such as skin cells or insulin-producing pancreatic cells.

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