Publications by authors named "Amelia Barnett"
Article Synopsis
- The study examined whether having low platelet counts (thrombocytopenia) increases the risk of bleeding in patients with atrial fibrillation (AF) on anticoagulants, comparing two groups: those with low platelets (<100,000/μL) and those with normal counts (>150,000/μL).
- Results showed that patients with AF and thrombocytopenia had significantly higher rates of major bleeding (13.3% vs 5.7%) and clinically relevant bleeding (24.5% vs 16.7%) after one year.
- Thrombocytopenia was confirmed as an independent risk factor for major bleeding, with the risk increasing as the severity of low platelet counts worsened, highlighting
The metabolic enzyme methionine adenosyltransferase 2A (MAT2A) was recently implicated as a synthetic lethal target in cancers with deletion of the methylthioadenosine phosphorylase () gene, which is adjacent to the tumor suppressor and codeleted with in approximately 15% of all cancers. Previous attempts to target MAT2A with small-molecule inhibitors identified cellular adaptations that blunted their efficacy. Here, we report the discovery of highly potent, selective, orally bioavailable MAT2A inhibitors that overcome these challenges.
View Article and Find Full Text PDFThe methylthioadenosine phosphorylase (MTAP) gene is located adjacent to the cyclin-dependent kinase inhibitor 2A (CDKN2A) tumor-suppressor gene and is co-deleted with CDKN2A in approximately 15% of all cancers. This co-deletion leads to aggressive tumors with poor prognosis that lack effective, molecularly targeted therapies. The metabolic enzyme methionine adenosyltransferase 2α (MAT2A) was identified as a synthetic lethal target in MTAP-deleted cancers.
View Article and Find Full Text PDFArticle Synopsis
- The study focuses on how the mTORC1 pathway plays a crucial role in cancer cell growth by regulating polyamine dynamics, which are vital for tumor development.
- Researchers used metabolomics on mouse models and human prostate cancer biopsies, discovering that mTORC1 alters the production of key metabolites like dcSAM and affects the stability of the enzyme AMD1.
- Findings show that high AMD1 levels correlate with active mTORC1 in human prostate cancer, while patients treated with the mTORC1 inhibitor everolimus experienced reduced AMD1 levels and cell proliferation, highlighting mTORC1's role in oncogenic metabolism.