We report a 59-year-old, male, chronic myeloid leukemia patient with a rare variant Philadelphia (Ph) translocation t(9;10;22)(q34;q22;q11). Fluorescence in situ hybridization with whole chromosome paints was used to confirm the cytogenetic findings. With a BCR/ABL-specific probe, the known rearrangement on the derivative chromosome 22 was found. The prognostic implications as well as the relevance of the additional breakpoint region 10q22 are discussed.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/s0165-4608(01)00417-4 | DOI Listing |
Ann Hematol
January 2025
Department of internal medicine, Albert Schweitzer Hospital, Dordrecht, The Netherlands.
Selected chronic myeloid leukemia (CML) patients may discontinue their tyrosine kinase inihibitor (TKI) in an attempt to achieve sustained treatment-free remission (TFR), which mitigates therapy-related side effects and limits treatment costs. TFR has been extensively studied following the discontinuation of adenosine triphosphate (ATP) - competitive TKI. However, there is minimal data concerning TFR after the discontinuation of the novel TKI asciminib.
View Article and Find Full Text PDFBlood
December 2024
UCLA Signaling Systems Laboratory, Los Angeles, California, United States.
Aging and chronic inflammation are associated with overabundant myeloid-primed multipotent progenitors (MPPs) amongst hematopoietic stem and progenitor cells (HSPCs). While HSC differentiation bias has been considered a primary cause of myeloid bias, whether it is sufficient has not been quantitatively evaluated. Here, we analyzed bone marrow data from the IκB- (Nfkbia+/-Nfkbib-/-Nfkbie-/-) mouse model of inflammation with elevated NFκB activity, which shows increased myeloid-biased MPPs.
View Article and Find Full Text PDFAnticancer Agents Med Chem
January 2025
Department of Chemistry, Illinois State University, Normal, Il, USA.
Many oncoproteins are important therapeutic targets because of their critical role in inducing rapid cell proliferation, which represents one of the salient hallmarks of cancer. Chronic Myeloid Leukemia (CML) is a cancer of hematopoietic stem cells that is caused by the oncogene BCR-ABL1. BCR-ABL1 encodes a constitutively active tyrosine kinase protein that leads to the uncontrolled proliferation of myeloid cells, which is a hallmark of CML.
View Article and Find Full Text PDFExp Hematol
January 2025
Department of Medical Genetics Department, Bezmialem Vakif University Faculty of Medicine, Istanbul, Turkey.
Hematological malignancies encompass a diverse array of subtypes, contributing to substantial heterogeneity that poses challenges in predicting clinical outcomes. Leveraging the capabilities of nuclear magnetic resonance holds substantial promise in the detection of serum biomarkers and individual metabolic alterations in patients. The study involved the analysis of the sera from patients with acute myeloid leukemia, chronic lymphocytic leukemia, and non-Hodgkin lymphoma to investigate the impacted metabolites and their associated pathways.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Illinois College of Medicine at Peoria, Peoria, IL, USA.
Background: Many lines of evidence support that systemic inflammation promotes Alzheimer's disease (AD) progression. Amyloid plaques are closely accompanied with neuroinflammation characterized by activated microglia and reactive astrocytes. Aging is the largest known risk factor for AD and is characterized by chronic, systemic, low-grade inflammation (inflamm-aging).
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!