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Impact of calreticulin mutations on treatment and survival outcomes in myelofibrosis during ruxolitinib therapy.
Ann Hematol
January 2025
Department of Engineering for Innovation Medicine, Section of Innovation Biomedicine, Hematology Area, University of Verona, Verona, Italy.
Calreticulin (CALR) mutations are detected in around 20% of patients with primary and post-essential thrombocythemia myelofibrosis (MF). Regardless of driver mutations, patients with splenomegaly and symptoms are generally treated with JAK2-inhibitors, most commonly ruxolitinib. Recently, new therapies specifically targeting the CALR mutant clone have entered clinical investigation.
View Article and Find Full Text PDFClearance of Driver Mutations after Transplantation for Myelofibrosis.
N Engl J Med
January 2025
From the Department of Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Background: Allogeneic hematopoietic stem-cell transplantation is the only curative treatment for myelofibrosis. Driver mutations are the pathophysiological hallmark of the disease, but the role of mutation clearance after transplantation is unclear.
Methods: We used highly sensitive polymerase-chain-reaction technology to analyze the dynamics of driver mutations in peripheral-blood samples from 324 patients with myelofibrosis (73% with mutations, 23% with mutations, and 4% with mutations) who were undergoing transplantation after reduced-intensity conditioning.
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 PDFExploratory Research for HIF-1α Overexpression Tumor Antigen in the Activation of Dendritic Cells and the Potent Anti-Tumor Immune Response.
Cancer Manag Res
December 2024
Clinical Laboratory, the First Affiliated Hospital of Xinxiang Medical University, Xinxiang, People's Republic of China.
Background: Tumor-specific antigens play an important role in dendritic cell (DC)-based immunotherapy. The acquisition of tumor-specific antigens, which are essential for DC-based immunotherapy, poses a significant challenge. This study aimed to explore the efficacy of hypoxia inducible factor-1α (HIF-1α) overexpression tumor antigens in DC-based immunotherapy.
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