Matching-adjusted indirect comparison of isatuximab plus carfilzomib and dexamethasone with daratumumab plus lenalidomide and dexamethasone in relapsed multiple myeloma.

Backgound: Lenalidomide-based regimens are commonly used for early relapse in patients with relapsed and/or refractory multiple myeloma (RRMM) receiving at least one prior line of therapy. In the absence of head-to-head comparison, matching-adjusted indirect comparison (MAIC) was conducted to demonstrate efficacy and safety of isatuximab+carfilzomib+dexamethasone (Isa-Kd) versus daratumumab + lenalidomide + dexamethasone (Dara-Rd) in RRMM.

Methods: Patient-level data from IKEMA trial (Isa-Kd, n = 179) were matched to aggregate data from POLLUX (Dara-Rd, n = 286).

Real-World Treatment Patterns and Outcomes Among Multiple Myeloma Patients with Asthma and COPD in the United States.

Introduction: Multiple myeloma (MM) is the second most frequent hematologic malignancy after lymphoma, contributing to approximately 10% of all hematologic malignancies. The prognosis of patients with MM is impacted by the heterogeneity of the disease, with worse outcomes reported in patients classified as International Staging System stage III, those with high-risk cytogenetics and elevated serum lactate dehydrogenase, and among patients who are elderly and have comorbidities. Previous studies have demonstrated an association between the presence of lung disease and worse outcomes; however, this impact in a real-world setting is not well understood.

The long non-coding RNA NEAT1 is responsive to neuronal activity and is associated with hyperexcitability states.

Despite their abundance, the molecular functions of long non-coding RNAs in mammalian nervous systems remain poorly understood. Here we show that the long non-coding RNA, NEAT1, directly modulates neuronal excitability and is associated with pathological seizure states. Specifically, NEAT1 is dynamically regulated by neuronal activity in vitro and in vivo, binds epilepsy-associated potassium channel-interacting proteins including KCNAB2 and KCNIP1, and induces a neuronal hyper-potentiation phenotype in iPSC-derived human cortical neurons following antisense oligonucleotide knockdown.