ARTICLES IN THREE SENTENCES
Characteristics and clinical outcomes of patients with acute myeloid leukemia with inv(3)(q21q26.2) or t(3;3)(q21;q26.2)
Acute myeloid leukemia (AML) with inv(3)(q21q26.2)/t(3;3)(q21;q26.2) is a rare subtype of AML. Richard-Carpentier et al. retrospectively reviewed the largest cohort of patients with AML with inv(3)/t(3;3) and evaluated the clinicopathological characteristics, including mutation analyses, and their association with clinical outcomes. They confirm the very poor prognosis with similar results provided by intensive chemotherapy and hypomethylating agents and the benefit from hematopoietic stem cell transplantation only in first CR.
Myeloid cells from Langerhans cell histiocytosis patients exhibit increased vesicle trafficking and an altered secretome capable of activating NK cells
Langerhans cell histiocytosis (LCH) is a potentially life-threatening inflammatory myeloid neoplasia. Hagey et al. used an in vitro differentiation system and RNA-sequencing to compare monocyte-derived dendritic cells from LCH patients to those derived from healthy controls or patients with Crohn’s disease. Their results indicated that increased proliferation, endocytosis and exocytosis are amongst the most pronounced phenotypes in LCH cells and, for the first time, implicate extracellular vesicles in the pathology of this disorder.
IL-18 and VEGF-A trigger type 2 innate lymphoid cell accumulation and pro-tumoral function in chronic myeloid leukemia
Different subsets of innate lymphoid cells (ILC) are involved in different physiological processes and can be phenotypically or functionally altered in solid tumors and hematologic malignancies. Fiordi et al. investigated whether ILC are altered in the leukemic niche of chronic myeloid leukemia (CML), where the cytokine dysregulation has a role in the survival of leukemic stem cells. Overall, their study uncovers the involvement of the subset 2 of ILC in CML progression, mediated by VEGF-A and IL-18.
Inhibition of menin, BCL-2, and FLT3 combined with a hypomethylating agent cures NPM1/FLT3-ITD/-TKD mutant acute myeloid leukemia in a patient-derived xenograft model
Combination of targeted therapy is a promising therapeutic strategy for acute myeloid leukemia (AML). Menin inhibition has antileukemia activity in both MLL-rearranged and NPM1-mutant AML. Carter et al. here report that combined inhibition of menin, BCL-2, and FLT3 had superior antileukemia activities in NPM1/FLT3-mutated AML in vitro and in vivo, and that the combination effectively reduced BCL-2 and HOX9/MEIS expression. This treatment is potentially curative in an NPM1/FLT3-mutated AML mouse model, and its efficacy is further enhanced in combination with 5-azacitidine.
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