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A research team led by the German Cancer Research Center in Heidelberg, Germany, has discovered that the genetic sequence of a tumor can be read like a molecular clock, traced back to its most recent common ancestor cell. Extracting the duration of tumor evolution can give an accurate predictor of neuroblastoma outcomes.
In a paper published in Nature Genetics titled “Neuroblastoma arises in early fetal development and its evolutionary duration predicts outcome,” the team details the steps they took in identifying a genomic clock tested against a whole genome sequenced population combined with analysis and mathematical modeling, to identify evolution markers, traceability and a likely origin point of infant neuroblastomas.
Cancer cells start out life as heroic healthy tissues, with the sort of all for one, one for all, throw yourself on a grenade to save your mates–type attitude that is taking place throughout the body every day. At some point, something goes wrong, and a good cell goes bad.
Using a self-built inverted microscope complete with laser optical tweezers to capture DNA, Yale Cancer Center and University of California Davis researchers for the first time created a visualization of the full-length human BRCA2 protein at the single molecule level.
Mutations in the breast cancer susceptibility gene, BRCA2, can significantly increase an individual’s lifetime risk of developing cancer. Approximately one in every 400 people carry a BRCA gene mutation accounting for a significant proportion of cancer that is heritable. The study was published on March 28 in the Proceedings of the National Academy of Sciences.
“If you carry a BRCA mutation, you have this incredibly high risk for breast and ovarian cancer, and also for men, prostate and pancreatic cancer,” said Yale Cancer Center member and co-author of the paper, Ryan Jensen, Ph.D., who is also an associate professor of therapeutic Radiology at Yale School of Medicine.
Engineers at MIT and the University of Massachusetts Medical School have designed a new type of nanoparticle that can be administered to the lungs, where it can deliver messenger RNA encoding useful proteins.
With further development, these particles could offer an inhalable treatment for cystic fibrosis and other diseases of the lung, the researchers say.
“This is the first demonstration of highly efficient delivery of RNA to the lungs in mice. We are hopeful that it can be used to treat or repair a range of genetic diseases, including cystic fibrosis,” says Daniel Anderson, a professor in MIT’s Department of Chemical Engineering and a member of MIT’s Koch Institute for Integrative Cancer Research and Institute for Medical Engineering and Science (IMES).
“You won’t live forever” is a catchphrase which has often been touted and has so far remained the proven truth of life — of humans and almost every other living being on planet earth. But soon, this catchphrase may well become the truth of the past, as humanity steps forward to attain immortality.
A former Google scientist has made a prediction, which if proven right, may redefine human civilisation as we know it. Ray Kurzweil, whose over 85 per cent of 147 predictions have been proven right, has predicted that humans will become immortal by 2029.
The revelation came when the 75-year-old computer scientist dwelled upon genetics, nanotechnology, robotics and more in a YouTube video posted by channel Adagio.
Advanced age is a shared risk factor for many chronic and debilitating skeletal diseases including osteoporosis and periodontitis. Mesenchymal stem cells develop various aging phenotypes including the onset of senescence, intrinsic loss of regenerative potential and exacerbation of inflammatory microenvironment via secretory factors. This review elaborates on the emerging concepts on the molecular and epigenetic mechanisms of MSC senescence, such as the accumulation of oxidative stress, DNA damage and mitochondrial dysfunction. Senescent MSCs aggravate local inflammation, disrupt bone remodeling and bone-fat balance, thereby contributing to the progression of age-related bone diseases. Various rejuvenation strategies to target senescent MSCs could present a promising paradigm to restore skeletal aging.
Nanomedicine uses nanomaterials [e.g., carbon nanotubes (CNTs), nanoparticles, and nanodiscs] or organic nanostructures (e.g., DNA origami and liposomes) for drug delivery (8–10), medical imaging (11–14), and tissue regeneration (15). Nanomaterials offer therapeutic efficacy through their tissue permeation, interaction with an external energy source, and capability to be combined with other therapeutic modalities (16, 17). Because we recently demonstrated that GBM cells are mechanosensitive (18), we set to use nanomaterials to develop a nanoscale mechanical approach to treat GBM. Mechanical perturbation has been investigated as an approach to target cancer cells. For example, magnetic field–actuated nanomaterials compromise the integrity of plasma membrane, leading to the death of in vitro–cultured GBM cells (19) and breast cancer cells (20). GBM cells, which were preincubated with magnetic nanoparticles, were implanted into mice to generate xenograft tumors. A rotating magnetic field, which was then applied to these magnetic particles–harboring tumors, suppressed GBM growth (21). Similarly, magnetic field mobilization of mitochondria-targeting magnetic nanoparticle chains demonstrated efficacy in inhibiting GBM growth in mice (22). While these studies showed that magnetic field–controlled nanomaterials can be used in cancer treatment, the utility of magnetic nanomaterials in treating chemoresistant tumors, the root cause of tumor relapse and patient death, remains unexplored.
GBM displays an extreme level of heterogeneity at genomic, epigenetic, biochemical signaling, and cellular composition levels (23). The heterogeneous nature of GBM confers treatment resilience to tumors and leads to a unifying therapy resistance mechanism; i.e., suppressing selected proteins or biochemical pathways provides a fertile ground for alternative signaling mechanisms, which are not targeted by the given therapy, to fuel GBM growth (24). In other words, the “whack-a-mole” approach failed to benefit patients with GBM for decades. For this reason, we hypothesized that nanomaterial-based mechanical treatment of cancer cells, rather than specific targeting of signaling pathways, can overcome the therapy resistance of this biologically plastic disease. To this end, we engineered a mechanical nanosurgery approach using magnetic CNTs (mCNTs; nanotubes with carbon surface and a cavity filled with iron particles) based on the following reasons.
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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