Lifeboat Foundation

Two recently published studies are raising new concerns that the breakthrough CRISPR-Cas9 gene editing system could potentially trigger an increased cancer risk in cells edited using the technique. With human trials using the gene-editing technique set to commence this year, the scientists behind these new studies urge researchers to be aware of this newly discovered and dangerous cancer-driving mechanism.

It has been less than a decade since the revolutionary CRISPR-Cas9 gene-editing technique was discovered, allowing scientists an unprecedented way to accurately edit DNA. For the most part, the technique has proved promising, safe and effective. Last year, a controversial study was published claiming the technique could introduce unintended, off-target mutations, but after a flurry of criticism attacking the veracity of the work it was ultimately retracted.

These two new studies raise entirely new concerns regarding the technique’s potential for triggering cancer in edited cells. One study comes from a collaboration between the University of Cambridge and the Karolinska Institutet, while the other is led by a team of researchers at pharmaceutical company Novartis.

Advances in reproductive technology have put genetic choices within reach of perspective parents. But critics warn of ethical peril.

For the first time, researchers have mapped the cell nucleus in 3D, revealing the packaging and organization of a cell’s DNA in unprecedented detail.

June 8 (UPI) — The nucleus of the cell is where the action happens, but it’s not easy to analyze the behavior of a massive genome inside an area 50 times smaller than the width of a human hair.

Now, for the first time, researchers have mapped the cell nucleus in 3D, revealing the packaging and organization of a cell’s DNA in unprecedented detail.

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A quick 4-minute overview of Epigenetic Rejuvenation – a breakthrough approach to whole-body rejuvenation that can potentially add decades to our lives.

New video from Undoing Aging 2018: Matthew Scholz, founder and CTO of Immusoft, on their work developing a breakthrough platform for treating a variety of genetic diseases.

Accelerating rejuvenation therapies to repair the damage of aging. Berlin, March, 15 — 17.

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Study based upon human skeletal muscle aging, mutagenesis, and the role of #satellite cells.

“A more comprehensive understanding of the interplay of stem cell–intrinsic and extrinsic factors will set the stage for improving cell therapies capable of restoring tissue homeostasis and enhancing muscle repair in the aged.”

Human aging has multiple effects on the human body. One of the effects of human aging is the reduction in skeletal muscle (SkM) function and a reduction in the number and activity of satellite cells (SCs), the resident stem cells. The whole genome of single SC clones of the leg muscle vastus lateralis from healthy individuals of different ages (21–78 years) was analyzed, to study the specific connection between SC aging and muscle impairment. In healthy adult muscle rapid increase of SCs is consistent with the accumulation rate of 13 somatic mutations per genome per year. Mutations typically do not happen in SkM-expressed genes because they are protected. However, as mutations in exons and promoters increase, genes involved in SC activity and muscle function are targeted which results in aging. Exons are coding sections of an RNA transcript, or the DNA encoding it, that are translated into protein. Proteins are the synthesis of molecules. A change in of a single base pair that caused the substitution of a different amino acid in the resulting protein (missense mutation) that was propagated to the muscle and detected in association with SC mutations affecting the whole tissue. #Somatic mutagenesis in SCs as a result is the driving force in the age related decline of SkM function.

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A new class of patients could soon be treated for breast cancer, no chemotherapy required. That’s because they don’t really benefit from it, according to a study published Sunday in the New England Journal of Medicine.

Those patients: those diagnosed with early-stage, invasive, hormone-receptor-positive breast cancer who scored in a specific range of a genetic test. They benefit just as much from chemotherapy, which many don’t tolerate well and can have long-term consequences, as they do from hormone treatments, which have many fewer side effects.

But before this study came out, many people in this group were prescribed chemotherapy because doctors had, based on the best information available, assumed it would help them. For those people, the side effects of chemotherapy could have been avoided, without making the treatment any less effective.

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Today, we will be taking a look at a new study showing that an NAD+ precursor was able to improve mitochondrial function in cells and flies with a model of Parkinson’s disease.

Summary

While mitochondrial dysfunction is emerging as key in Parkinson’s disease (PD), a central question remains whether mitochondria are actual disease drivers and whether boosting mitochondrial biogenesis and function ameliorates pathology. We address these questions using patient-derived induced pluripotent stem cells and Drosophila models of GBA-related PD (GBA-PD), the most common PD genetic risk. Patient neurons display stress responses, mitochondrial demise, and changes in NAD+ metabolism. NAD+ precursors have been proposed to ameliorate agerelated metabolic decline and disease. We report that increasing NAD+ via the NAD+ precursor nicotinamide riboside (NR) significantly ameliorates mitochondrial function in patient neurons. Human neurons require nicotinamide phosphoribosyltransferase (NAMPT) to maintain the NAD+ pool and utilize NRK1 to synthesize NAD+ from NAD+ precursors. Remarkably, NR prevents the age-related dopaminergic neuronal loss and motor decline in fly models of GBA-PD.

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