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A Review of Clonal Relationships in Myeloproliferative Neoplasms With Co-Mutations of JAK2, CALR or MPL and BCR::ABL1.
Clin Lymphoma Myeloma Leuk
December 2024
Vali-E-Asr Reproductive Health Research Center, Family Health Research Institute, Tehran University of Medical Sciences, Tehran, Iran.
BCR::ABL1-negative myelo-proliferative neoplasms (MPNs) are characterized by mutations in JAK2, CALR, or MPL. Usually these mutations are co-exclusive of each other and of BCR::ABL1. We reviewed clonal interactions in 177 subjects with mutations in JAK2, CALR, or MPL and BCR::ABL1 including JAK2/BCR::ABL1 (N = 142), CALR/BCR::ABL1 (N = 31), MPL/BCR::ABL1 (N = 3).
View Article and Find Full Text PDFNodal mature plasmacytoid dendritic cell proliferation mimicking lymphoma in a patient with CALR-mutated myelofibrosis.
Int J Hematol
December 2024
Unit of Pathology, Department of Medicine and Technological Innovation, University of Insubria, Via Ottorino Rossi, 9, 21100, Varese, Italy.
CALR frameshift mutation detection in myeloproliferative neoplasms by microfluidic chip analysis.
Lab Med
December 2024
Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, TX, United States.
Background: CALR mutation analysis is routinely used to diagnose BCR/ABL1-negative myeloproliferative neoplasms. The 2 most common CALR mutations are a 52-base pair (bp) deletion and a 5-bp insertion, which account for approximately 85% of cases.
Methods: To evaluate our new microfluidic chip assay, we tested CALR mutant and wild-type specimens that were previously analyzed using conventional methods at a reference laboratory.
HMGA2 overexpression with specific chromosomal abnormalities predominate in CALR and ASXL1 mutated myelofibrosis.
Leukemia
December 2024
Division of Hematology/Oncology, Department of Medicine, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Although multiple genetic events are thought to play a role in promoting progression of the myeloproliferative neoplasms (MPN), the individual events that are associated with the development of more aggressive disease phenotypes remain poorly defined. Here, we report that novel genomic deletions at chromosome 12q14.3, as detected by a high-resolution array comparative genomic hybridization plus single nucleotide polymorphisms platform, occur in 11% of MPN patients with myelofibrosis (MF) and MPN-accelerated/blast phase (AP/BP) but was not detected in patients with polycythemia vera or essential thrombocythemia.
View Article and Find Full Text PDFMolecular and Clinical Risk Factors Associated with Thrombosis and Bleeding in Myelofibrosis Patients.
Hamostaseologie
December 2024
Klinik für Innere Medizin II, Abteilung Hämatologie und Internistische Onkologie, Universitätsklinikum Jena, Jena, Germany.
Background: The risk of thrombosis and bleeding in myelofibrosis (MF) has been historically underappreciated. We sought to investigate potential molecular and clinical risk factors for venous (VTE) and arterial (ATE) thrombotic events as well as bleeding episodes.
Methods: Data from 246 consecutive MF patients were analyzed.
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