ArticleCancer research communications2026
Cell State Transitions Drive the Evolution of Disease Progression in B-Lymphoblastic Leukemia.
Article in Cancer research communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
2 citing papers in PubMed.
- Mechanistic learning to predict and understand minimal residual disease.bioRxiv : the preprint server for biology · 2026Article
- Modeling the evolutionary dynamics of clonal hematopoiesis.Nature genetics · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
Cancer stem cells (CSC) are hypothesized to promote tumor progression through innate chemoresistance and self-renewal. CSCs reside in the CD34+/CD38- immunophenotypic subpopulation of acute myeloid leukemia (AML). Isolation of CSCs from B-lymphoblastic leukemia (B-ALL) has proven difficult, and the cells of interest apparently are not isolated to the CD34+/CD38- compartment. This may be explained, in part, by temporal variations of CD34 and CD38 expression which result in stochastic cell state transitions (e.g., from CD34+/CD38+ to CD34+/CD38-). We present a mathematical model of these transitions and correlate salient findings with BCR::ABL1 status, minimal residual disease (MRD), and relapse in adult B-ALL. As the CSC hypothesis is well supported in AML, we focus on transitions to and from the hematopoietic stem cell compartment (CD34+/CD38-). Our analysis suggests the presence of dedifferentiating transitions to a CD34+/CD38- stem cell-like immunophenotype, especially in B-ALL with BCR::ABL1. In contrast, BCR::ABL1-negative patient samples have low CD34+/CD38- self-renewal rates and either high CD34+/CD38+ or CD34-/CD38+ incoming rates. High CD34+/CD38- self-renewal is also associated with positive MRD following induction chemotherapy. We find a lack of observable changes in cell state transitions between diagnosis and relapse specimens. Furthermore, simulated therapies targeting the stem cell-like compartment indicate that blocking transitions to the CD34+/CD38- state (i.e., blocking dedifferentiation) is more effective than promoting transitions from the CD34+/CD38- state toward other states (i.e., promoting differentiation) to reduce the proportion of CD34+/CD38- cells. The modeling framework used here is a novel, useful tool to infer prognosis and genotype from routine flow cytometry. SIGNIFICANCE: Flow cytometry characterization of B-ALL samples (diagnosis, remission, and relapse) is used to parameterize a mathematical model of cell state transition rates and stratify patients for post-induction chemotherapy MRD.
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