{"type":"rich","version":"1.0","provider_name":"Transistor","provider_url":"https://transistor.fm","author_name":"Blood Podcast","title":"Mutations in AMBRA1 aggravate β-thalassemia; targeting MYD88 mutations in lymphomas; air pollution and incident VTE risk","html":"<iframe width=\"100%\" height=\"180\" frameborder=\"no\" scrolling=\"no\" seamless src=\"https://share.transistor.fm/e/e5ad1753\"></iframe>","width":"100%","height":180,"duration":1068,"description":"In this week's podcast, a potential new therapeutic target in beta-thalassemia. The E3 ubiquitin ligase AMBRA1 promotes autophagic clearance of free alpha-globin. Researchers describe mutations in the AMBRA1 gene that impair this clearance, exacerbating ineffective erythropoiesis and disease severity. After that: targeting MYD88 mutations. Lasalocid-A is a compound that selectively binds to the MYD88 L265P mutant protein, which is found in a range of B-cell lymphomas. New research shows its potential to inhibit tumor growth, overcome ibrutinib resistance, and synergize with venetoclax. Finally: air pollution is linked to an increased risk of venous thromboembolism in a prospective, community-based cohort study. The findings highlight the harms of pollution, and support the case for global efforts to improve public health.Featured Articles:Mutations in AMBRA1 aggravate β-thalassemia by impairing autophagy-mediated clearance of free α-globinLasalocid A selectively induces the degradation of MYD88 in lymphomas harboring the MYD88 L265P mutationAir pollution is associated with increased risk of venous thromboembolism: the Multi-Ethnic Study of Atherosclerosis","thumbnail_url":"https://img.transistorcdn.com/v7MGyoJEM-ebFBYi5VpSwDRF3QY3zbinfCyyOAH1TGk/rs:fill:0:0:1/w:400/h:400/q:60/mb:500000/aHR0cHM6Ly9pbWct/dXBsb2FkLXByb2R1/Y3Rpb24udHJhbnNp/c3Rvci5mbS9kY2Q4/YzJhZmMwODBjOWRi/YTNhN2Y1NWJkMzMw/NTBjZi5qcGc.webp","thumbnail_width":300,"thumbnail_height":300}