Chronic leukemias account for fewer than 5 per cent of childhood hematologic malignancies. The various subtypes are chronic mylocytic leukemia (adult, juvenile, and familial), chronic myelomonocytic leukemia chronic monocytic leukemia, and chronic lymphocytic leukemia. The most common of these, adult-type chronic myelocytic leukemia, is characterized by specific cytogenetic alterations; recent advances in molecular biology are linking these genetic events to the pathophysiology and course of this fascinating neoplasm.
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Extracellular vesicles from chronic lymphocytic leukemia cells promote leukemia aggressiveness by inducing the differentiation of monocytes into nurse-like cells via an RNA-dependent mechanism.
Hemasphere
January 2025
Laboratory of Clinical Cell Therapy Université Libre de Bruxelles (ULB), Jules Bordet Institute Brussels Belgium.
Chronic lymphocytic leukemia (CLL) cells receive several stimuli from surrounding cells, such as B-cell receptor (BCR) stimulation, and can manipulate their microenvironment via extracellular vesicle (EV) release. Here, we investigated the small RNA content (microRNA and YRNA) of CLL-EVs from leukemic cells cultured with/without BCR stimulation. We highlight an increase of miR-155-5p, miR-146a-5p, and miR-132-3p in EVs and in cells after BCR stimulation ( < 0.
View Article and Find Full Text PDFBosutinib for the Treatment of CML-Using it Safely: a Podcast.
Target Oncol
January 2025
Division of Hematology and SCT, Georgia Cancer Centre, Augusta, GA, USA.
Bosutinib is a second-generation tyrosine kinase inhibitor (TKI) approved for use in patients with newly diagnosed Philadelphia chromosome (Ph)-positive chronic phase (CP) chronic myeloid leukemia (CML), as well as Ph-positive CP, accelerated phase, or blast phase (with chemotherapy) CML resistant or intolerant to prior therapy. Clinical trials have shown bosutinib is effective as first-line therapy for patients with CML as well as in later lines of therapy after prior TKI failure. Bosutinib has an established safety profile; however, as with all TKIs approved for the treatment of CML, there are adverse events (AEs) that require management.
View Article and Find Full Text PDFComprehensive analysis of clinical, pathological, and molecular features in chronic myelomonocytic leukemia: frequent and mutations and higher mutation burden in myeloproliferative CMML compared to myelodysplastic CMML.
Leuk Lymphoma
January 2025
Department of Laboratory Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Various aspects of myeloproliferative chronic myelomonocytic leukemia (MP-CMML) and myelodysplastic CMML (MD-CMML) have been reported but inconsistencies remain. This study conducted a comprehensive retrospective analysis of clinical, pathological, and molecular data from a cohort of CMML. The results revealed a higher frequency of and mutations and a greater mutation burden in MP-CMML, characterized by more tier 1 or 2 variants and dominant mutations.
View Article and Find Full Text PDFTyrosine Kinase Inhibitor Treatment Patterns in Patients With Chronic-Phase Chronic Myeloid Leukemia: A Single Center Data From China.
Clin Lymphoma Myeloma Leuk
December 2024
Peking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation, Beijing, China; Hematology Center, Peking University People's Hospital, Qingdao, China. Electronic address:
Aim: To describe tyrosine kinase inhibitor (TKI) treatment patterns and analyze co-variates of TKI switch for chronic myeloid leukemia (CML) patients in a center from China.
Methods: A retrospectively study was designed to analyze TKI switching patterns, reasons and associated covariates in patients with CP-CML.
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A triad of somatic mutagenesis converges in self-reactive B cells to cause a virus-induced autoimmune disease.
Immunity
January 2025
Garvan Institute of Medical Research, Darlinghurst, NSW, Australia; St Vincent's Clinical School, UNSW Sydney, Sydney, NSW, Australia. Electronic address:
The unexplained association between infection and autoimmune disease is strongest for hepatitis C virus-induced cryoglobulinemic vasculitis (HCV-cryovas). To analyze its origins, we traced the evolution of pathogenic rheumatoid factor (RF) autoantibodies in four HCV-cryovas patients by deep single-cell multi-omic analysis, revealing three sources of B cell somatic mutation converged to drive the accumulation of a large disease-causing clone. A method for quantifying low-affinity binding revealed recurring antibody variable domain combinations created by V(D)J recombination that bound self-immunoglobulin G (IgG) but not viral E2 antigen.
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