Acute Myeloid Leukemia (AML)
Vijaya Bhatt, MD
Pinkal Desai, MD, MPH
Carlos E. Vigil, MD
FDA Grants Aspacytarabine Fast Track Status for Older Patients With AML
Safety and activity of selinexor in patients with myelodysplastic syndromes or oligoblastic acute myeloid leukaemia refractory to hypomethylating agents: a single-centre, single-arm, phase 2 trial
Background: The median overall survival of patients with high-risk myelodysplastic syndromes myelodysplastic syndromes:
TP53 mutations in myelodysplastic syndromes and secondary AML confer an immunosuppressive phenotype
Somatic gene mutations are key determinants of outcome in patients with myelodysplastic syndromes myelodysplastic syndromes:
Glasdegib as maintenance therapy for patients with AML and MDS patients at high risk for postallogeneic stem cell transplant relapse
Posttransplantation, glasdegib maintenance therapy in patients at high risk for relapse did not meaningfully reduce relapse incidence.Use of glasdegib in the posttransplantation setting was complicated by adverse events requiring drug holds and occasional discontinuation.
Prognostic significance of serial molecular annotation in myelodysplastic syndromes (MDS) and secondary acute myeloid leukemia (sAML)
The implementation of next-generation sequencing (NGS) has influenced diagnostic, prognostic, and therapeutic decisions in myeloid malignancies. However, the clinical relevance of serial molecular annotation in patients with myelodysplastic syndrome (MDS) undergoing active treatment is unknown.
HDAC4 inhibition disrupts TET2 function in high-risk MDS and AML
Aberrant DNA methylation often silences transcription of tumor-suppressor genes and is considered a hallmark of myeloid neoplasms. Similarly, histone deacetylation represses transcription of genes responsible for cell differentiation/death. A previous clinical study suggested potential pharmacodynamic antagonism between histone deacetylase inhibitors (HDACi) and DNA hypomethylating agents (HMA).
