Lifeboat Foundation: Safeguarding Humanity
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Category: genetics – Page 58

Inside every cell, inside every nucleus, your continued existence depends on an incredibly complicated dance. Proteins are constantly wrapping and unwrapping DNA, and even minor missteps can lead to cancer. A new study from the University of Chicago reveals a previously unknown part of this dance—one with significant implications for human health.

In the study, published Oct. 2 in Nature, a team of scientists led by UChicago Prof. Chuan He, in collaboration with University of Texas Health Science Center at San Antonio Prof. Mingjiang Xu, found that RNA plays a significant role in how DNA is packaged and stored in your cells, via a gene known as TET2. The paper is titled “RNA m5C oxidation by TET2 regulates chromatin state and leukaemogenesis.”

This pathway also appears to explain a long-standing puzzle about why so many cancers and other disorders involve TET2-related mutations—and suggests a set of new targets for treatments.

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Unlocking the complexities of the fruit fly brain is a crucial step toward understanding the human brain. Fruit flies share many genetic similarities with humans, making them a valuable model organism for studying brain functions as well as diseases.

“An estimated 75% of human genes related to diseases have homologs in the fly genome,” Sebastian Seung, co-leader of the research team, told Interesting Engineering (IE).

“We’ve long known about the molecular similarities between fly and human brains. We have been slower to realize that there are also similarities at the circuit level, revealed by examining patterns of connectivity. We now know that fly circuits for olfaction, vision, and navigation have architectural similarities with mammalian circuits for the same functions,” Seung added.

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The same technique could also be applied to studies of brain damage, Ruetz said. “Neural stem cells in the subventricular zone are also in the business of repairing brain tissue damage from stroke or traumatic brain injury.”

The glucose transporter connection “is a hopeful finding,” Brunet said. For one, it suggests not only the possibility of designing pharmaceutical or genetic therapies to turn on new neuron growth in old or injured brains, but also the possibility of developing simpler behavioral interventions, such as a low carbohydrate diet that might adjust the amount of glucose taken up by old neural stem cells.

The researchers found other provocative pathways worthy of follow-up studies. Genes relating to primary cilia, parts of some brain cells that play a critical role in sensing and processing signals such as growth factors and neurotransmitters, also are associated with neural stem cell activation. This finding reassured the team that their methodology was effective, partly because unrelated previous work had already discovered associations between cilia organization and neural stem cell function. It is also exciting because the association with the new leads about glucose transmission could point toward alternative avenues of treatment that might engage both pathways, Brunet said.

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CRISPR-Cas systems help to protect bacteria from viruses. Several different types of CRISPR-Cas defense systems are found in bacteria, which differ in their composition and functions. Among them, the most studied proteins today are Cas9 and Cas12, also known as DNA or “gene scissors,” which have revolutionized the field of genome editing, enabling scientists to edit genomes and correct disease-causing mutations precisely.

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The foundation hopes to prevent extinctions, and obtain the necessary biological material to safeguard genetic diversity.

Already backed by a confirmed $50 million in funding, its goal is to halt the extinction crisis through three key conservation focus points.

The Colossal Foundation’s first key…

Who ever said you can’t save a few species on the way to de-extincting a mammoth?

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Pathogen encounter can result in epigenetic remodeling that shapes disease caused by heterologous pathogens.

The therapeutic potential of antigen-independent innate immune memory (IIM) is of particular relevance in the context of respiratory viruses with pandemic potential. Lercher et al. find that antiviral IIM in alveolar macrophages following SARS-CoV-2 infection ameliorates disease caused by a secondary unrelated pathogen, influenza A virus.

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U.S. researchers developed CheekAge, a tool that reliably estimates mortality risk.

Researchers in the United States have created a next-generation tool named CheekAge, which uses methylation patterns found in easily obtainable cheek cells.

In a groundbreaking discovery, the team has demonstrated that CheekAge can reliably estimate mortality risk, even when epigenetic data from different tissues are utilized for analysis.

Epigenetic markers are chemical changes to DNA that don’t alter the genetic code but can affect how genes work. Methylation is one such change, often linked to aging. Scientists use these patterns to create “age clocks” that estimate biological age, revealing how fast someone is aging.

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A powerful new analytical tool offers a closer look at how tumor cells “shape-shift” to become more aggressive and untreatable, as shown in a study from researchers at Weill Cornell Medicine and the New York Genome Center.

A tumor cell shape-shifts by changing its cell type or state, thus altering its basic pattern of activity and perhaps even its appearance. This changeability or “plasticity” is a characteristic of cancer that leads to diverse tumor-cell populations and ultimately the emergence of cell types enabling treatment resistance and metastatic spread.

The new tool, described Sept. 24 in a paper in Nature Genetics, can be used to quantify this plasticity in samples of tumor cells. The researchers demonstrated it with analyses of tumor samples from animal models and human patients, identifying, for example, a key transitional cell state in glioblastoma, the most common form of brain cancer.

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The FDA has approved a new targeted drug specifically for brain tumors called low-grade gliomas. The drug, vorasidenib, was shown in clinical trials to delay progression of low-grade gliomas that had mutations in the IDH1 or IDH2 genes.

“Although there have been other targeted therapies for the treatment of brain tumors with the IDH mutation, [this one] has been one of the most successful in survival prolongation of brain tumor patients,” said Darell Bigner, MD, PhD, the E. L. and Lucille F. Jones Cancer Distinguished Research Professor and founding director of the Preston Robert Tisch Brain Tumor Center at Duke.

In clinical trials, progression-free survival was estimated to be 27.7 months for people in the vorasidenib group versus 11.1 months for those in the placebo group.

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