Lifeboat Foundation

With liquid biopsies, detecting cancer and tracking treatment progress can be as easy as taking a blood test. This is an increasingly popular way of monitoring cancer, because it’s much less invasive than solid tumour biopsies. And liquid biopsies can become even more sensitive if they capture methylation information as well as genetic data.

Usually, liquid biopsies for cancer rely on the detection of small amounts of DNA that are shed from a tumour into the bloodstream. But especially in the disease’s early stages, circulating tumour DNA (ctDNA) levels are very low and point mutations linked to cancer can be easy to miss.

“If we want to develop assays to detect cancer earlier, we need very sensitive detection of these rare tumour fragments,” says Charlotte Proudhon, group leader at the Research Institute for Environmental and Occupational Health in Rennes, France, whose team are among those now developing liquid biopsy methods that include epigenetic markers, such as methylation.

A new University of Maryland-led discovery could spur the development of new and improved treatments for Hutchinson-Gilford progeria syndrome (HGPS), often simply called “progeria”—a rare genetic disorder with no known cure that causes accelerated aging in children.

Publishing in the journal Aging…

Researchers identify protein that could improve cardiovascular health of those with progeria.

Continue reading “UMD-led Study Could Lead to Lengthened Lives for Patients With Premature Aging Disease” »

An achievement that was deemed impossible has successfully become accomplished. For the first time in history, DNA can be edited. One of the goals is to be able to get rid of genetic diseases. This whole concept in genomic science has opened up a whole new revolutionary way of dealing with such critical health issues. There is a possibility that illnesses that were once incurable have a chance to be curable.

MedlinePlus provides a definition and states that a collection of tools known as genome editing, or gene editing, allows researchers to alter an organism’s DNA. These technologies enable the addition, deletion, or modification of genetic material at specific genomic regions. A person’s DNA can be altered through gene editing to fix mistakes that lead to illnesses.

CRISPR-Cas9, short for CRISPR-associated protein 9 and clustered regularly interspaced short palindromic repeats, is a well-known example as one of the approaches used and developed by scientists to edit DNA. The scientific community is very excited about the CRISPR-Cas9 system since it is more accurate, efficient, quicker, and less expensive than existing genome editing techniques.

Summary: Researchers have discovered that the protein USP50 regulates DNA replication by managing which enzymes—nucleases or helicases—cleave or unwind DNA strands during replication. This control is crucial for stable replication, especially when the process encounters issues that need restarting. When USP50 is absent, cells struggle to coordinate enzyme use, leading to replication errors and potential genetic instability.

The findings provide new insights into genome maintenance and may help explain some hereditary conditions, such as early-onset aging and certain cancers. Understanding USP50’s role opens doors to potential therapeutic strategies aimed at protecting DNA integrity.

To support the data generated in Il11ra1-deleted mice on a mixed C57BL6/129 genetic background³⁰ and to more deeply dissect age-related effects, we studied young (3-month-old) and aged (2-year-old) female mice with deletion of Il11 (Il11^−/−) on a C57BL6/J background³¹.

Immunoblots confirmed IL-11 up-regulation across tissues in old age in this additional strain (Fig. 1m). Old female Il11^−/− mice had lower body weights and fat mass and preserved lean mass (Fig. 2a–c). The frailty score¹⁵ of old female Il11^−/− mice was lower than that of old wild-type mice and their body temperatures were mildly increased (Fig. 2d and Extended Data Fig. 5a). Lower frailty scores were largely driven by improvements in tremor, loss of fur colour, gait disorders and vestibular disturbance (Supplementary Table 1). Muscle strength was higher in both young and old Il11^−/− mice (a phenomenon that was observed for some other phenotypes) compared with age-matched controls (Fig. 2e and Extended Data Fig. 5b).

Chronic inhibition of mTORC1 with rapamycin can cause glucose intolerance owing to indirect inhibition of mTORC2³⁵. It was therefore important to more fully assess the effects of IL-11 inhibition on liver function, metabolism and glucose utilization in old mice. As wild-type mice aged, there were increases in serum AST, ALT, cholesterol and triglycerides, which were collectively mitigated in old Il11^−/− mice (Fig. 2f and Extended Data Fig. 5c, d). Glucose tolerance test (GTT) and insulin tolerance test (ITT) profiles of old Il11^−/− mice were similar to those of young wild-type mice, whereas GTTs and ITTs of old wild-type mice showed impairment (Fig. 2g and Extended Data Fig. 5e, f). Indexed skeletal muscle mass was greater in both young and old Il11^−/− mice compared with the equivalent wild-type mice (Extended Data Fig. 5g).

Bryan Johnson, a millionaire tech entrepreneur dedicated to reversing ageing, recently took to social media to boast about his “super clean plasma.” In a detailed post on X, he shared that a lab technician couldn’t bring himself to dispose of the plasma after a total plasma exchange (TPE) procedure.

Johnson claims to have reduced his epigenetic age through his comprehensive regimen called Project Blueprint. He follows a strict diet and exercise routine, spends over $2 million annually on a team of doctors and medical equipment, and undergoes both experimental and conventional treatments-including the recent TPE procedure.

TPE, a procedure often used in regenerative medicine and anti-ageing treatments, involves replacing a patient’s plasma with donor plasma or a substitute fluid. In Johnson’s case, his plasma was replaced with albumin.

Genetic testing company settles with plaintiffs over breach that was revealed when hacker published link to database labeled ‘ashkenazi DNA Data of Celebrities’

The breach, which occurred last October, affected more than 6.9 million customers and included users’ personal details such as their location, name and birthdate, as well as some information about their family trees. That data was shared on BreachForums, an online forum used by cybercriminals.

According to court documents, the data breach was revealed October 6 after a hacker going by the pseudonym Golem, a reference to the Jewish mythical defender made of clay, published a link to a database labeled ashkenazi DNA Data of Celebrities. According to the lawsuit, the hacker referred to the list as the most valuable data you’ll ever see, though most of the names were not famous.

CRISPR-Cas is used broadly in research and medicine to edit, insert, delete or regulate genes in organisms. TnpB is an ancestor of this well-known “gene scissors” but is much smaller and thus easier to transport into cells.

Using protein engineering and AI algorithms, University of Zurich researchers have now enhanced TnpB capabilities to make DNA editing more efficient and versatile, paving the way for treating a genetic defect for high cholesterol in the future. The work has been published in Nature Methods.

CRISPR-Cas systems, which consist of protein and RNA components, were originally developed as a natural defense mechanism of bacteria to fend off intruding viruses. Over the last decade, re-engineering these so-called “gene scissors” has revolutionized genetic engineering in science and medicine.

A Ludwig Cancer Research study has punctured a longstanding assumption about the source of the most common type of DNA mutation seen in the genome—one that contributes to many genetic diseases, including cancer.

Led by Ludwig Oxford Leadership Fellow Marketa Tomkova, postdoc Michael McClellan, Assistant Member Benjamin Schuster-Böckler and Associate Investigator Skirmantas Kriaucionis, the study has implications not only for basic cancer biology but also for such things as assessments of carcinogenic risk associated with environmental factors and our understanding of the emergence of drug resistance during cancer therapy. Its findings are reported in the current issue of Nature Genetics.

The mutation in question—in which cytosine ©, one of the four bases of DNA that spell out our genes, is erroneously switched to thymine (T)—was thought to be primarily the result of a spontaneous chemical reaction with water. This reaction, deamination, is about twice as likely to happen when a cytosine is chemically tagged by the addition of a molecule known as a methyl group to create 5-methylcytosine, which occurs in DNA at so-called “CpG” positions, where C is followed by the base guanine (G).