Publications by authors named "A R Branagan"
Multiple myeloma (MM) remains incurable despite novel therapeutics. A major contributor to the development of relapsed/refractory and resistant MM is extraosseous extramedullary disease (EMD), whose molecular biology is still not fully understood. We analyzed 528 MM patients who presented to our institution between 2014 and 2021 and who had undergone molecular testing.
View Article and Find Full Text PDFElotuzumab is an approved monoclonal antibody targeting SLAMF7 on plasma and NK cells that enhances the activity of lenalidomide, pomalidomide, and bortezomib in multiple myeloma (MM). The OPTIMISMM study showed improved outcomes with the combination of pomalidomide, bortezomib, and dexamethasone (PVd) in relapsed/refractory MM. We therefore studied adding elotuzumab to PVd (elo-PVd) in relapsed/refractory MM in a multicenter phase 2 trial.
View Article and Find Full Text PDFArticle Synopsis
- - Neonatal encephalopathy (NE) leads to multiorgan injury in newborns, with therapeutic hypothermia being the common treatment; this study aims to identify effective scoring systems for assessing organ dysfunction in NE.
- - A systematic review of 628 articles was conducted, identifying 12 relevant studies, which showed a correlation between the severity of NE and multiorgan dysfunction, but highlighted significant differences across scoring systems used.
- - For a comprehensive scoring system, the study suggests including assessments of various organ systems (renal, hepatic, respiratory, neurological, hematological, and cardiovascular), while noting that further validation and standardization are necessary for effective use, especially considering the impact of therapeutic hypothermia.
Article Synopsis
- Covalent Bruton's tyrosine kinase-inhibitors (cBTK-i) are effective in treating MYD88-mutated Waldenstrom's macroglobulinaemia by inhibiting key signaling pathways that promote tumor growth.* -
- BTK mutations can lead to treatment resistance by reactivating ERK1/2, which causes increased inflammatory cytokine production and helps BTK wild-type tumor cells survive.* -
- Pirtobrutinib, a non-covalent BTK-inhibitor, has been shown to successfully block damaging ERK1/2 activity and can overcome resistance in MYD88 lymphoma cells with mutated BTK.*