Lifeboat Foundation

The role of epigenetics, which determine how your genes are expressed, is being increasingly implicated in aging, as is the potential of therapies that revert epigenetics back to those of a younger person.

What are epigenetic alterations?

The DNA in each of our cells is identical, with only some small variations, so why do our various organs and tissues look so different, and how do cells know what to become?

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A study published today in the journal Nature Medicine led by researchers at Huntsman Cancer Institute (HCI) at the University of Utah (U of U) describes a new therapeutic approach with potential for patients with pancreatic cancer. These researchers discovered a combination drug therapy that may effectively combat the disease. HCI researchers first observed anti-cancer impacts in a laboratory setting and, subsequently, in its first use in a human patient.

The study has already progressed to a clinical trial that is now open at HCI and will soon be open at other sites in the United States. Details about the clinical trial, called THREAD, are available under National Clinical Trial Number 03825289. The combination therapy uses two drugs already approved for use by the Food and Drug Administration for other diseases, including cancer. The new drug combination is administered through pills taken orally.

Pancreatic tumors are characterized by mutations in a gene called KRAS. When KRAS is mutated in this way, it sends constant signals that promote abnormal cell division and growth in cancer cells. As a result, tumors grow out of control. At the same time, like all cells, pancreatic cancer cells must recycle their components to provide building blocks for new growth in an essential cell function known as autophagy. Previous studies to combat pancreatic cancer that were focused either on the role of KRAS or on impacting autophagy were not effective.

Accumulation of fat in the liver, known as fatty liver disease, is experienced by over 5.5 million Australians, including more than 40% of all adults over the age of 50.

Fatty liver develops from a combination of both genetic and environmental causes, which influence the age of onset and severity of the disease. Experts are now describing the condition as a hidden epidemic, which is driving up rates of liver transplant, contributing to a range of illnesses and ultimately death.

Fatty liver disease usually has no early symptoms and diagnoses with current technologies mostly comes when it’s too late to prevent major illness. But now, for the first time in a study published in the prestigious scientific journal, Nature, a team of researchers from the Baker Heart and Diabetes Institute, University of California, and University of Sydney, have discovered biomarkers in the blood that can predict the accumulation of toxic fats in the liver, which are a sign of early fatty liver disease. These predictions can be made based on the lipid (fats) profile in the blood.

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Your genome literally identifies you, but researchers and genetic firms keep saying that DNA data is anonymous. It’s a privacy scandal waiting to happen.

By Chelsea Whyte

EVERY person in the world is issued with a unique code before they are even born. Governments, insurance firms and indeed pretty much anyone can use this code to catalogue us throughout our entire lives. This isn’t a sci-fi dystopia – it is just genetics.

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Jennifer Doudna, one of CRISPR’s primary innovators, stays optimistic about how the gene-editing tool will continue to empower basic biological understanding.

What is less known is that a more problematic source of DNA damage is normal cellular processes such as DNA replication. These cannot be avoided because they are inevitably in action every time cells divide. The scale of this problem is best illustrated by realizing that our bodies are made up by successive divisions of trillions of cells, all originating from a single fertilized egg. Every day, a quarter of a trillion cells in the adult human body continue to divide to replenish old or damaged tissue. Amongst the multitude of DNA damage incurred during each such cell division process, the most dangerous are those that can be passed on from mother cells to newly born daughter cells. This inherited DNA damage is the true ‘enemy within’ that cannot be simply avoided by changing one’s lifestyle.

Researchers from the University of Copenhagen have identified a specific mechanism that protects our cells from natural DNA errors — an ‘enemy within’ — which could permanently damage our genetic code and lead to diseases such as cancer. The study has just been published in one of the most influential scientific journals, Nature Cell Biology.

Researchers from the University of Copenhagen have discovered a mechanism that gives human cells a chance to stop piling up mutations cells replicate and divide in the body. The discovery could prove to be very useful in the development of new treatments against diseases caused by changes in human DNA such as cancer.

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Researchers in the US have built an “alien” DNA system from eight building block letters, so expanding the genetic code from four and doubling its information density. The new system meets all of the requirements for Darwinian evolution and can also be transcribed to RNA. It will be important for future synthetic biology applications and expands the scope of molecular structures that might be capable of supporting life, both here on Earth and more widely in the universe.

One of the main characteristics of life is that it can store and pass on genetic information. In modern-day organisms, this is done by DNA using just four building blocks: guanine, cytosine, adenine and thymine (G, A, C and T). Pairs of DNA strands form a double helix with A bonding to T and C bonding to G.

Four more building blocks .