- Inherited genetic susceptibility to acute lymphoblastic leukemia in Down syndrome
- Lentiviral and genome-editing strategies for the treatment of β-hemoglobinopathies
- The α-emitter astatine-211 targeted to CD38 can eradicate multiple myeloma in a disseminated disease model
- Prospective isolation of nonhematopoietic cells of the niche and their differential molecular interactions with HSCs
- Five-year follow-up of SWOG S0816: limitations and values of a PET-adapted approach with stage III/IV Hodgkin lymphoma
Prospective isolation of nonhematopoietic cells of the niche and their differential molecular interactions with HSCs
The bone marrow niche environment is essential for the control and maintenance of hematopoietic stem cells (HSCs). The investigators present the first global analysis of the communication between distinct niche cell types and HSCs.
The authors report the interaction between Down syndrome, a major genetic leukemia predisposition condition, and inherited genetic alleles associated with increased susceptibility to childhood acute lymphoblastic leukemia.
This review article summarizes the clinical outcomes and genotoxicity issues of gene therapy for hemoglobinopathies based on lentiviral vectors carrying a b-globin–like gene or genome editing to correct the erythropoietic defect.
Five-year follow-up of SWOG S0816: limitations and values of a PET-adapted approach for stage III/IVHodgkin lymphoma
The investigators present results on the long-term value and limitations of early interim positron emission tomography (PET) scanning in advanced Hodgkin lymphoma.
The α-emitter astatine-211 targeted to CD38 can eradicate multiple myeloma in a disseminated disease model
Minimal residual disease (MRD) has become an increasingly prevalent and important entity in multiple myeloma (MM). Despite deepening responses to frontline therapy, roughly 75% of MM patients never become MRD-negative to ≤10−5, which is concerning because MRD-negative status predicts significantly longer survival.
Targeting PRMT1-mediated FLT3 methylation disrupts maintenance of MLL-rearranged acute lymphoblastic leukemia
Relapse remains the main cause of MLL-rearranged (MLL-r) acute lymphoblastic leukemia (ALL) treatment failure resulting from persistence of drug-resistant clones after conventional chemotherapy treatment or targeted therapy.