From glaucoma to Stargardt disease, age-related macular degeneration (AMD) to retinitis pigmentosa, or a corneal transplant to Bietti’s crystalline dystrophy, the 27th Annual Meeting of the American Society of Gene & Cell Therapy (ASGCT) is working to bring some light to patients with age and congenital diseases that affect vision. From May 7-11, 2024, thousands of scientists are gathering in Baltimore to show their advances against the challenges of delivering genes and cells to the correct place, avoiding immunogenicity and improving diseases.
From glaucoma to Stargardt disease, age-related macular degeneration (AMD) to retinitis pigmentosa, or a corneal transplant to Bietti’s crystalline dystrophy, the 27th Annual Meeting of the American Society of Gene & Cell Therapy (ASGCT) is working to bring some light to patients with age and congenital diseases that affect vision. From May 7-11, 2024, thousands of scientists are gathering in Baltimore to show their advances against the challenges of delivering genes and cells to the correct place, avoiding immunogenicity and improving diseases.
“Prenatal therapies are the next disruptive technologies in health care, which will advance and shape the future of patient care in the 21st century,” said Graça Almeida-Porada, a professor at the Fetal Research and Therapy Center of the Wake Forest Institute for Regenerative Medicine in Winston-Salem, North Carolina. At the American Society of Gene & Cell Therapy (ASGCT) annual meeting in Baltimore on May 5, 2024, Almeida-Porada introduced the first presentation of the scientific symposium “Prospects for Prenatal Gene and Cell Therapy.”
A group of scientists from the French National Center for Scientific Research (CNRS) have overturned a scientific dogma by demonstrating, for the first time, that DNA mutations are not essential for the development of cancer. The researchers temporarily disrupted gene silencing led by Polycomb proteins in fruit flies, and observed that this could produce tumors caused only by epigenetic changes, without permanent changes to the genome.
A protein whose expression decreases during aging could be key to preserving cellular maintenance mechanisms and preventing the progressive loss of muscle mass that occurs during aging. Scientists from the Institute for Research in Biomedicine (IRB) and the University of Barcelona (UB) have revealed the role of the TP53INP2 protein in autophagy and the effects of its reduction on skeletal muscle during aging.
Scientists at Massachusetts General Hospital have linked the risk of heart failure during pregnancy and senescence proteins produced by placental aging, which could clarify how peripartum cardiomyopathy (PPCM) is triggered and opens the door to the development of cardiac function therapies in late pregnancy.
Cross-talk between macrophages and tumor cells could modulate cachexia in pancreatic cancer patients. A group of scientists from the University of Oklahoma has discovered a new pathway that promoted muscle wasting after the recruitment of this immune cell in the tumor microenvironment, activating cachexia-inducing factors.
Cross-talk between macrophages and tumor cells could modulate cachexia in pancreatic cancer patients. A group of scientists from the University of Oklahoma has discovered a new pathway that promoted muscle wasting after the recruitment of this immune cell in the tumor microenvironment, activating cachexia-inducing factors. Macrophage depletion and the inhibition of this signaling could be developed as a therapeutic target for this condition.
The first cellular human and mouse map focused on muscle fibers and their microenvironment has revealed both the mechanisms of deterioration of this tissue over time and its adaptive capacity for regeneration. “We intended to map the skeletal muscle, isolating all the cell types, and characterizing how they change with age,” first author Veronika Kedlian from the Wellcome Sanger Institute in Cambridge told BioWorld.
An enzyme that activates cell death could be targeted to avoid the inflammation and lung lesions caused by influenza A virus (IAV). A collaborative study demonstrated that an inhibitor of receptor-interacting serine/threonine-protein kinase 3 (RIPK3) blocked necroptosis in infected alveolar epithelial cells and prevented the consequences in the lungs of severe disease.
