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A large case-control study by international researchers at the RIKEN Center for Integrative Medical Sciences (IMS) in Japan has found that people who carry certain genetic risk factors for gastric (stomach) cancer have a much greater risk if they have also been infected by the bacterium Helicobacter pylori. The study, published in The New England Journal of Medicine, could contribute to the development of tailored genomic medicine for treating stomach cancer.

Stomach cancer is the fourth leading cause of cancer death worldwide and has both environmental and genetic risk factors. Environmentally, infection by H. pylori increases the risk of stomach cancer. Because the virulence of H. pylori in East Asia is high, the incidence of stomach cancer is higher in countries like Japan. Genetically, while hereditary gene variation is why we have different colored eyes and are unique as individuals, sometimes gene variants are associated with the risk of disease. For example, individuals who carry a certain hereditary pathogenic variant of the CDH1 gene have an increased risk of gastric cancer.

Testing for the presence of pathogenic variants is now one of several measures being taken for cancer prevention, surveillance, and treatment selection. However, because large-scale, case-control studies are lacking, and because those that exist have not assessed how the risk for stomach cancer changes when pathogenic variants interact with environmental factors like H. pylori, it remains unclear what actual clinical measures can be taken. To address this issue, researchers therefore evaluated the risk of gastric cancer in a large case-control study of Japanese people, considering whether they were carriers of pathogenic variants and whether they had been infected by H. pylori.

Altered dystrophin expression was found in some tumors and recent studies identified a developmental onset of Duchenne muscular dystrophy (DMD). Given that embryogenesis and carcinogenesis share many mechanisms, we analyzed a broad spectrum of tumors to establish whether dystrophin alteration evokes related outcomes. Transcriptomic, proteomic, and mutation datasets from fifty tumor tissues and matching controls (10,894 samples) and 140 corresponding tumor cell lines were analyzed. Interestingly, dystrophin transcripts and protein expression were found widespread across healthy tissues and at housekeeping gene levels. In 80% of tumors, DMD expression was reduced due to transcriptional downregulation and not somatic mutations. The full-length transcript encoding Dp427 was decreased in 68% of tumors, while Dp71 variants showed variability of expression.

Do you really want to live forever? Futurist Ray Kurzweil has predicted that humans will achieve immortality in just seven years. Genetic engineering company touts ‘Jurassic Park’-like plan to ‘de-extinct’ dodo bird Elon Musk ‘comfortable’ putting Neuralink chip into one of his kids.

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One can only hope.

A former Google engineer has just predicted that humans will achieve immortality in eight years, something more than likely considering that 86% of his 147 predictions have been correct.

Ray Kurzweil visited the YouTube channel Adagio, in a discussion on the expansion of genetics, nanotechnology and robotics, which he believes will lead to age-reversing ‘nanobots’.

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The actor Bruce Willis was diagnosed with aphasia in April 2022—updated in February 2023 to frontotemporal dementia (FTD). Now, a major advancement is helping develop new treatments for some people with motor neuron diseases, including FTD and ALS, possibly including a nasal spray that could help prevent the genetic disease.

A recently patented genome editing tool called PASTE holds genuine promise for expanding the universe of treatable genetic diseases. The approach combines elements of CRISPR and prime editing with a pair of enzymes designed to enable the integration of large segments of DNA without incurring double-stranded DNA breaks.

U.S. Patent No. 11,572,556, assigned to MIT, covers systems, methods, and compositions for programmable addition via site-specific targeting elements (PASTE). The patent describes site-specific integration of a nucleic acid into a genome, using a CRISPR–Cas9 nickase fused to a reverse transcriptase (RT) and a serine integrase. These enzymes target specific genome sequences known as attachment sites, binding to them before integrating their DNA payload.

PASTE can insert DNA fragments as large as 50,000 base pairs, which puts it on a different plane compared to other genome editing tools such as prime editing.

A new CRISPR tool corrected a genetic mutation that causes vision loss, in an experiment in mice — and its creators at the Wuhan University of Science and Technology (WUST) in China think it could be a safe way to treat countless other genetic diseases in people.

The challenge: Vision starts with light entering the eye and traveling to the retina. There, light-sensitive cells, called photoreceptors, convert light into electrical signals that are sent to the brain.

Retinitis pigmentosa is a rare — and, currently, incurable — genetic disease that can be caused by mutations in more than 100 different genes. These mutations destroy the cells of the retina, leading to vision loss, and for most people, there’s no way to stop the disease or reverse its damage (the exception is a gene therapy approved to treat mutations in the RPE65 gene).

Scientists at St. Jude Children’s Research Hospital and Rockefeller University have combined their expertise to gain a better understanding of the cystic fibrosis transmembrane conductance regulator (CFTR). Mutations in CFTR cause cystic fibrosis, a fatal disease with no cure.

Current therapies using a drug called a potentiator can enhance CFTR functions in some patients; but how the potentiators work is not well understood. The new findings reveal how CFTR functions mechanistically and how disease mutations and potentiators affect those functions. With this information, researchers may be able to design more effective therapies for cystic fibrosis. The study was published today in Nature.

Cystic fibrosis is a genetic disorder that causes people to produce mucus that is too thick and sticky. This can block airways and lead to lung damage as well as cause problems with digestion. The disease affects about 35,000 people in the United States. CFTR is an anion channel, a passageway that maintains the right balance of salts and fluid across epithelial and other membranes. Mutations in CFTR are what cause cystic fibrosis, but these mutations can affect CFTR function differently. Therefore, some drugs used to treat the disease can only partially restore function of specific mutant forms of CFTR.

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