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Category: genetics – Page 260

“Our studies in mice revealed how genes co-operate to cause cancer in different organs. We identified main players, the order in which they occur during tumor progression, and the molecular processes how they turn normal cells into threatening cancers. Such processes are potential targets for new treatments”.

Why do alterations of certain genes cause cancer only in specific organs of the human body? Scientists at the German Cancer Consortium (DKTK), the Technical University of Munich (TUM), and the University Medical Center Göttingen have now demonstrated that cells originating from different organs are differentially susceptible to activating mutations in cancer drivers: The same mutation in precursor cells of the pancreas or the bile duct leads to fundamental different outcomes. The team discovered for the first time that tissue specific genetic interactions are responsible for the differential susceptibility of the biliary and the pancreatic epithelium towards transformation by oncogenes. The new findings could guide more precise therapeutic decision making in the future.

There have been no major improvements in the treatment of pancreatic and in the last decades and no effective targeted therapies are available to date. “The situation for patients with pancreatic and extrahepatic bile duct cancer is still very depressing with approximately only 10% of patients surviving five years,” says Dieter Saur, DKTK Professor for Translational Cancer Research at TUM’s university hospital Klinikum rechts der Isar, DKTK partner site Munich.

DKTK is a consortium centered around the German Cancer Research Center (DKFZ) in Heidelberg, which has long-term collaborative partnerships with specialist oncological centers at universities across Germany.

Continue reading “Why identical mutations cause different types of cancer” | >

Encouraging Mid Trial data update! Great to know Dr. Katcher is applying for IRB approval for their human clinical trial for E5.

In this video we provide an update on Dr. Katcher’s experiment where he is treating rats with E5 (formerly called Elixer) on a regular schedule to see how long they will live for. Dr Katcher’s team have kindly provided some intermediate updates that we share in the video.
0:00 — 00:50 Introduction.
00:51 — 04:02 Project Background/Overview.
04:03 — Project Update.

Papers referred to in this newsletter.

Continue reading “Reverse Aging of 54% Study Extension — Dr. Harold Katcher’s E5 Project Update July 2021” | >

NYU Abu Dhabi (NYUAD) researchers have uncovered a code that sets the genome of the liver to account for the remarkable ability for this organ to regenerate. This finding offers new insight into how the specific genes that promote regeneration can be activated when part of the liver is removed. These findings have the potential to inform the development of a new form of regenerative medicine that could help non-regenerative organs regrow in mice and humans.

While other animals can regenerate most organs, humans, mice, and other mammals can only regenerate their liver in response to an injury or when a piece is removed. NYUAD researchers hypothesized that the that drive in the liver would be controlled by a specific code that allows them to be activated in response to injury or resection. They home in on the epigenome, which is the modifications on the DNA that alter the gene expression, as opposed to changing the itself.

Using a mouse liver model, the team of NYUAD researchers, led by Professor of Biology Kirsten Sadler Edepli, identified the elements of the present in quiescent liver cells—cells that are currently not replicating but have the ability to proliferate under the right conditions—that activate to regenerate. Genes involved in liver cell proliferation are silenced in livers that are not regenerating, but the surprising finding was that they reside in parts of the genome where most genes are active. The researchers found that these pro-regenerative genes were marked with a specific modification—H3K27me3. During regeneration, H3K27me3 is depleted from these genes, enabling their dynamic expression and driving proliferation.

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New research from the RIKEN Center for Brain Science (CBS) in Japan shows that a deficit in histone methylation could lead to the development of autism spectrum disorders (ASD). A human variant of the SUV39H2 gene led researchers to examine its absence in mice. Published in Molecular Psychiatry, the study found that when absent, adult mice exhibited cognitive inflexibility similar to what occurs in autism, and embryonic mice showed misregulated expression of genes related to brain development. These findings represent the first direct link between the SUV39H2 gene and ASD.

Genes are turned on and off throughout our development. But genetic variation means that what is turned off in some people remains turned on in others. This is why, for example, some adults can digest dairy products and others are lactose intolerant; the gene for making the enzyme lactase is turned off when some people become adults, but not others. One way that genes can be turned on and off is through a process called histone methylation in which special enzymes transfer methyl groups to histone proteins that are wrapped around DNA.

Variations in genes related to methylation during brain development can lead to serious problems. One such variation occurs in a rare disorder called Kleefstra Syndrome, in which a mutation prevents methylation of H3K9—a specific location on histone H3. Because Kleefstra Syndrome resembles autism in some ways, RIKEN CBS researchers led by Takeo Yoshikawa looked for autism-specific variations in genes that can modify H3K9. Among nine such genes, they found one variant in an H3K9 methyltransferase gene— SUV39H2 —that was present in autism, and the mutated SUV39H2 prevented methylation when tested in the lab. Similar loss-of-function results were found for the mouse version of the variant.

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Nick Saraev is 25 years old, far too young, it would seem, to be thinking about death. And yet, since he turned 21, he has taken steps to prevent the infirmities of old age. Every day, he takes 2000 mg of fish oil and 4000 IU of vitamin D to help prevent heart disease and other ailments. He steams or pressure-cooks most of his meals because, he says, charring meats creates chemicals that may increase the risk of cancer. And in the winter, he keeps the humidity of his home at 35 percent, because dry air chaps his skin and makes him cough, both of which he considers manifestations of chronic inflammation, which may be bad for longevity.

Based on the life expectancies of young men in North America, Saraev, a freelance software engineer based near Vancouver, believes he has about 55 years before he really has to think about aging. Given the exponential advances in microprocessors and smartphones in his lifetime, he insists the biotech industry will figure out a solution by then. For this reason, Saraev, like any number of young, optimistic, tech-associated men, believes that if he takes the correct preventative steps now, he might well live forever. Saraev’s plan is to keep his body in good enough shape to hit “Longevity Escape Velocity,” a term coined by English gerontologist Aubrey de Grey to denote slowing down your aging enough to reach each new medical advance as it arrives. If you delay your death by 10 years, for example, that’s 10 more years scientists have to come up with a drug, computer program, or robot assist that can make you live even longer. Keep up this game of reverse leapfrog, and eventually death can’t catch you. The term is reminiscent of “planetary escape velocity,” the speed an object needs to move in order to break free of gravity.

The science required to break free of death, unfortunately, is still at ground level. According to Nir Barzilai, M.D., director of the Institute for Aging Research at Albert Einstein College of Medicine in New York City, scientists currently understand aging as a function of seven to nine biological hallmarks, factors that change as we grow older and seem to have an anti-aging effect when reversed. You can imagine these as knobs you can turn up or down to increase or decrease the likelihood of illness and frailty. Some of these you may have heard of, including how well cells remove waste, called proteostasis; how well cells create energy, or mitochondrial function; how well cells implement their genetic instructions, or epigenetics; and how well cells maintain their DNA’s integrity, called DNA repair or telomere erosion.

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“Prime Editing is a wonderful example of the revolution in genetic medicine that we are living through,” said Robert Nelsen, co-founder and Managing Director of ARCH Venture Partners, one of several companies to fund Prime Medicine. “Gene editing technologies like this, when mature, could totally change our conception of what’s possible in treating disease.”

“This is an opportunity to take a giant step toward cures for a much wider range of diseases than previously possible,” said Stephen Knight, President and Managing Partner of F-Prime Capital, another backer of the new company.

The funds raised will be used to continue building the company, expand the capabilities of its technology platform and rapidly advance towards clinical indications. By the end of 2021, Prime Medicine expects to employ more than 100 people full-time.

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To date, there are no effective antidotes against most virus infections. An interdisciplinary research team at the Technical University of Munich (TUM) has now developed a new approach: they engulf and neutralize viruses with nano-capsules tailored from genetic material using the DNA origami method. The strategy has already been tested against hepatitis and adeno-associated viruses in cell cultures. It may also prove successful against coronaviruses.

There are antibiotics against dangerous bacteria, but few antidotes to treat acute viral infections. Some infections can be prevented by vaccination but developing new vaccines is a long and laborious process.

Now an interdisciplinary research team from the Technical University of Munich, the Helmholtz Zentrum München, and the Brandeis University (USA) is proposing a novel strategy for the treatment of acute viral infections: The team has developed nanostructures made of DNA, the substance that makes up our genetic material, that can trap viruses and render them harmless.

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Viruses that infect bacteria may drive the evolution of drug-resistant superbugs by inserting their genes into the bacterial DNA, a new study suggests.

The bacteria-attacking viruses, called phages, act as parasites in that they depend on their hosts for survival. The viral parasites often kill off their microbial hosts after infiltrating their DNA, said senior study author Vaughn Cooper, director of the Center for Evolutionary Biology and Medicine at the University of Pittsburgh School of Medicine. But sometimes, the phages slip into the bacterial genome and then lay low, making sneaky changes to the bacterium’s behavior, Cooper said.

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For the first time ever, researchers from the University of Pittsburgh School of Medicine discovered that phages — tiny viruses that attack bacteria — are key to initiating rapid bacterial evolution leading to the emergence of treatment-resistant “superbugs.” The findings were published today in Science Advances.

The researchers showed that, contrary to a dominant theory in the field of evolutionary microbiology, the process of adaptation and diversification in bacterial colonies doesn’t start from a homogenous clonal population. They were shocked to discover that the cause of much of the early adaptation wasn’t random point mutations. Instead, they found that phages, which we normally think of as bacterial parasites, are what gave the winning strains the evolutionary advantage early on.

“Essentially, a parasite became a weapon,” said senior author Vaughn Cooper, Ph.D., professor of microbiology and molecular genetics at Pitt. “Phages endowed the victors with the means of winning. What killed off more sensitive bugs gave the advantage to others.”

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