Despite the major success obtained by the use of tyrosine kinase inhibitors (TKI) in chronic myeloid leukemia (CML), resistances to therapies occur due to mutations in the ABL-kinase domain of the BCR-ABL oncogene. Amongst these mutations, the "gatekeeper" T315I is a major concern as it renders leukemic cells resistant to all licenced TKI except Ponatinib. We report here that Fourier transform infrared (FTIR) microspectroscopy is a powerful methodology allowing rapid and direct identification of a spectral signature in single cells expressing T315I-mutated BCR-ABL. The specificity of this spectral signature is confirmed using a Dox-inducible T315I-mutated BCR-ABL-expressing human UT-7 cells as well as in murine embryonic stem cells. Transcriptome analysis of UT-7 cells expressing BCR-ABL as compared to BCR-ABL T315I clearly identified a molecular signature which could be at the origin of the generation of metabolic changes giving rise to the spectral signature. Thus, these results suggest that this new methodology can be applied to the identification of leukemic cells harbouring the T315I mutation at the single cell level and could represent a novel early detection tool of mutant clones. It could also be applied to drug screening strategies to target T315I-mutated leukemic cells.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.bbrc.2018.07.127 | DOI Listing |
Clin Epigenetics
January 2025
School of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW, 2308, Australia.
Background: Hypomethylating agents (HMA), such as azacytidine (AZA) and decitabine (DAC), are epigenetic therapies used to treat some patients with acute myeloid leukaemia (AML) and myelodysplastic syndrome. HMAs act in a replication-dependent manner to remove DNA methylation from the genome. However, AML cells targeted by HMA therapy are often quiescent within the bone marrow, where oxygen levels are low.
View Article and Find Full Text PDFDrug Resist Updat
January 2025
Loma Linda University Cancer Center, Loma Linda, CA 92354, United States; Department of Basic Sciences, Loma Linda University, Loma Linda, CA 92354, United States. Electronic address:
Chromosomal rearrangements (CR) initiate leukemogenesis in approximately 50 % of acute myeloid leukemia (AML) patients; however, limited targeted therapies exist due to a lack of accurate molecular and genetic biomarkers of refractory mechanisms during treatment. Here, we investigated the pathological landscape of treatment resistance and relapse in 16 CR-AML patients by monitoring cytogenetic, RNAseq, and genome-wide changes among newly diagnosed, refractory, and relapsed AML. First, in FISH-diagnosed KMT2A (MLL gene, 11q23)/AFDN (AF6, 6q27)-rearrangement, RNA-sequencing identified an unknown CCDC32 (15q15.
View Article and Find Full Text PDFHemasphere
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 PDFR Soc Open Sci
January 2025
Department of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa 9200293, Japan.
Acute myeloid leukaemia (AML) is a haematologic malignancy with high relapse rates in both adults and children. Leukaemic stem cells (LSCs) are central to leukaemopoiesis, treatment response and relapse and frequently associated with measurable residual disease (MRD). However, the dynamics of LSCs within the AML microenvironment is not fully understood.
View Article and Find Full Text PDFEcancermedicalscience
November 2024
Internal Medicine Service, Sanatorio Sagrado Corazón, Buenos Aires, CP 1039, Argentina.
Plasmacytoid blast dendritic cell neoplasm is a rare subtype of acute leukaemia that represents less than 1% of haematologic neoplasms. It is characterised by skin involvement and leukaemic dissemination in the rest of the body. The immunophenotype is represented by the expression of CD4, CD56 and CD123.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!