Tracking leukemic residuals: dissecting the inverse relationship between CD26+ stem cells and extracellular BCR::ABL1 transcript in Chronic Myeloid Leukemia (CML).
1/5 보강
Chronic myeloid leukemia (CML) persists due to leukemic stem cells, notably the CD26+ subset.
APA
Mutti S, Cavalleri A, et al. (2025). Tracking leukemic residuals: dissecting the inverse relationship between CD26+ stem cells and extracellular BCR::ABL1 transcript in Chronic Myeloid Leukemia (CML).. Stem cells translational medicine, 14(12). https://doi.org/10.1093/stcltm/szaf062
MLA
Mutti S, et al.. "Tracking leukemic residuals: dissecting the inverse relationship between CD26+ stem cells and extracellular BCR::ABL1 transcript in Chronic Myeloid Leukemia (CML).." Stem cells translational medicine, vol. 14, no. 12, 2025.
PMID
41277535 ↗
Abstract 한글 요약
Chronic myeloid leukemia (CML) persists due to leukemic stem cells, notably the CD26+ subset. We investigated correlations between circulating CD26+ leukemic stem cells (LSCs) and BCR::ABL1 transcripts in an extracellular vesicle-enriched secretome (EVES) from plasma samples of 44 CML patients. EVES were characterized and BCR::ABL1 quantified via digital PCR. We observed an inverse correlation between CD26+LSC counts and EVES BCR::ABL1 levels, especially in deep molecular responders (DMR). CD26+LSCs were elevated in patients in treatment-free remission (TFR), while EVES BCR::ABL1 levels were higher in those receiving therapy. These findings suggest distinct dynamics between LSC populations and vesicle-mediated transcript release, with potential implications for CML monitoring and prognosis.
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