ArticleJournal of cellular and molecular medicine2025
Assessment of Chronic Myeloid Leukaemia In Vitro Models Variability: Insights Into Extracellular Vesicles.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Time-resolved Hippo-YAP transcript and microRNA responses to imatinib in K562 chronic myeloid leukemia cells with exploratory analysis of CD34⁺ progenitor transcriptomes.Molecular biology reports · 2026Article
- Caffeic acid phenethyl ester induced apoptosis in chronic myeloid leukemia cells by inhibiting mitochondrial complex I.Scientific reports · 2026Article
- Differentially expressed proteins in plasma-derived extracellular vesicles from chronic myeloid leukemia patients.Frontiers in genetics · 2026Article
- Assessment of Chronic Myeloid Leukaemia In Vitro Models Variability: Insights Into Extracellular Vesicles.Journal of cellular and molecular medicine · 2025Article
Corrections and comments
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Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic Myeloid Leukaemia is driven by the BCR::ABL1 fusion gene. Although Tyrosine Kinase Inhibitors have significantly improved patient outcomes, drug resistance and disease persistence remain challenges, highlighting the need for effective preclinical models. We observed cellular heterogeneity among CML models in response to TKIs, influencing viability, metabolism, and molecular markers. With growing interest in extracellular vesicles as mediators of leukaemia progression via oncogenic cargo like BCR::ABL1, we explored whether EVs from different CML cell lines exhibit distinct features. EVs from K562 and KCL22 cells were characterised under basal conditions using Fourier Transform Infrared spectroscopy, Atomic Force Microscopy, dot blotting, and Nanoparticle Tracking Analysis. We assessed EV release and BCR::ABL1 content before and after treatment with imatinib, nilotinib, or dasatinib, alongside Ki67 expression to gauge proliferation. Fourier Transform Infrared Spectroscopy with Principal Component Analysis revealed distinct clustering of EVs by cell line. While untreated K562 and KCL22 cells showed similar EV output and BCR::ABL1 content, post-treatment K562 cells released more EVs with elevated BCR::ABL1 transcripts. KCL22 cells showed earlier reduction in Ki67 expression. These findings highlight model-dependent EV behaviour, reflecting patient heterogeneity and reinforcing the need for careful model selection in CML research.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.