Myelodysplastic Syndromes (MDS)
Implications of TP53 allelic state for genome stability, clinical presentation and outcomes in myelodysplastic syndromes
Tumor protein p53 (TP53) is the most frequently mutated gene in cancer1,2.
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:
Kinetics of Pre-Myelodysplastic Syndromes Blood Values Correlate with Disease Risk and Survival
We reviewed pre-diagnosis clinical data of 420 patients with pathologically confirmed 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:
Myelodysplastic Syndromes: 2021 update on Diagnosis, Risk-stratification and Management
Disease overview: The myelodysplastic syndromes myelodysplastic syndromes: (my-eh-lo-diss-PLASS-tik SIN
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).