Review Series On Acute Myeloid Leukemia
New drugs before, during, and after hematopoietic stem cell transplantation for patients with acute myeloid leukemia
Update on current treatments for adult acute myeloid leukemia: to treat acute myeloid leukemia intensively or non-intensively? That is the question
ARTICLES IN THREE SENTENCES
Early expression of CD94 and loss of CD96 on CD8+ T cells after allogeneic stem cell tranplantation is predictive of subsequent relapse and survival
Relapse of malignant disease is the primary cause of treatment failure after allogeneic stem cell transplantation and reflects loss of the immunological graft-versus-leukemia effect. Verma and colleagues studied the transcriptional and phenotypic profile of CD8+ T cells in the first month following transplantation and its correlation with the risk of subsequent relapse. They found that the relative expression of CD94 and CD96 on CD8+ T cells both act as strong determinants of disease relapse, providing novel insights into T-cell differentiation in the early post-transplant period and identifying new opportunities for immunotherapy.
Since SUMOylation is activated in cancer cells with high MYC levels, targeting MYC-induced SUMOylation as a therapeutic vulnerability seems highly attractive. Demel and colleagues investigated SUMOylation as a MYC-induced molecular vulnerability in aggressive B-cell lymphoma. Their findings identify SUMO inhibition as a powerful therapy in a subset of MYC-driven B-cell lymphoma.
Serum vascular endothelial growth factor is associated with cardiovascular involvement and response to therapy in Erdheim-Chester disease
Erdheim-Chester disease (ECD) is a rare histiocytosis, considered to be an inflammatory myeloid neoplasm. Starting from the hypothesis that that vascular endothelial growth factor-A (VEGF) might play a role in ECD pathophysiology, Roeser and colleagues conducted a study to assess serum VEGF concentrations in ECD patients, and their association with patients’ characteristics. Their findings suggest that serum level of this molecule may reflect cardiovascular involvement, and its determination could potentially help to improve the detection and follow-up of such involvement in patients with ECD.
Mutations in the RACGAP1 gene cause autosomal recessive congenital dyserythropoietic anemia type III
Congenital dyserythropoietic anemia type III (CDA III) is characterized by macrocytic anemia, signs of intravascular hemolysis, and giant multinucleated erythroblasts in the bone marrow. Using next-generation sequencing Hernández and colleagues identified two pathogenic missense mutations in the RACGAP1 gene in three unrelated families affected by the recessive form of CDA III. They demonstrated, by ex vivo experiments, that these mutations cause alterations in erythroid differentiation due to a GTPase imbalance that leads to blockage of cytokinesis.
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