In 1,083 core biopsies of the bone marrow with myeloproliferative diseases 454 cases or 42% were found to have neoplastic megakaryopoiesis. Neoplasia of megakaryocytes was assumed from the conspicuous cytological atypicality revealed by light microscopy, extending and confirming earlier ultrastructural findings. Histopathology of the bone marrow in these patients was described as chronic megakaryocytic-granulocytic myelosis - CMGM - since neutrophilic granulopoiesis is also apparently neoplastic and both cell lineages showed a complete differentiation to mature forms. CMGM should be separated from the chronic granulocytic leukemia - CGL - which consists of only a single line proliferation. The incidence of CGL in our total of 1,083 patients was 25%. Both entities are included in chronic myeloid leukemia - CML - because of the demonstration of the Philadelphia chromosome in the hematopoietic cells of these two groups of patients. Primary or idiopathic thrombocythemia has to be differentiated from CMGM since there is no evidence for malignancy of the granulocytic series.
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http://dx.doi.org/10.1007/BF00430654 | DOI Listing |
Circ Res
January 2025
Division of Cardiovascular Medicine, Department of Medicine (J.B.H., J.D.B., A.C.D.), Vanderbilt University Medical Center, Nashville, TN.
Cardiovascular and cardiometabolic diseases are leading causes of morbidity and mortality worldwide, driven in part by chronic inflammation. Emerging research suggests that the bone marrow microenvironment, or marrow niche, plays a critical role in both immune system regulation and disease progression. The bone marrow niche is essential for maintaining hematopoietic stem cells (HSCs) and orchestrating hematopoiesis.
View Article and Find Full Text PDFR Soc Open Sci
January 2025
WestCHEM, Department of Pure and Applied Chemistry, University of Strathclyde, 295 Cathedral Street, Glasgow G1 1XL, UK.
Chronic myeloid leukaemia (CML) is primarily treated using imatinib mesylate, a tyrosine kinase inhibitor (TKI) targeting the BCR::ABL1 oncoprotein. However, the development of drug resistance and adverse side effects necessitate the exploration of alternative therapeutic agents. This study presents the synthesis and characterization of a novel imatinib analogue, 3-chloro--(2-methyl-5-((4-(pyridin-2-yl)pyrimidin-2-yl)amino)phenyl)benzamide (PAPP1).
View Article and Find Full Text PDFFarm Hosp
January 2025
Servicio de Farmacia, Complejo Hospitalario Universitario de Canarias, Santa Cruz de Tenerife, España; Unidad de Investigación, Complejo Hospitalario Universitario de Canarias, Santa Cruz de Tenerife, España. Electronic address:
Aims: Tyrosine kinase inhibitors (TKIs) have been successful in changing the course of chronic myeloid leukaemia (CML) due to their high efficacy. However, their effectiveness is conditioned by adherence to treatment. The aim of this study was to analyse the adherence of CML patients treated with TKIs and to evaluate the impact of pharmaceutical care on adherence in a prospective and interventional manner.
View Article and Find Full Text PDFArch Pathol Lab Med
January 2025
the Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis (Stohler, Vance).
Context.—: Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by proliferation of the granulocytic cell line. The incidence of CML in Kenya is estimated at near 2000 cases annually.
View Article and Find Full Text PDFImmunity
January 2025
Institute for Stroke and Dementia Research (ISD), University Hospital, Ludwig-Maximilian-University (LMU), Munich, Germany; Deutsches Zentrum für Neurodegenerative Erkrankungen e. V. (DZNE), Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance (MHA), Munich, Germany. Electronic address:
Common genetic variants in a conserved cis-regulatory element (CRE) at histone deacetylase (HDAC)9 are a major risk factor for cardiovascular disease, including stroke and coronary artery disease. Given the consistency of this association and its proinflammatory properties, we examined the mechanisms whereby HDAC9 regulates vascular inflammation. HDAC9 bound and mediated deacetylation of NLRP3 in the NACHT and LRR domains leading to inflammasome activation and lytic cell death.
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