ArticleFrontiers in immunology2025
Single-cell multi-omics analysis reveals cellular subpopulations associated with relapse in high-risk B-ALL following intensified chemotherapy.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Acute lymphoblastic leukemia (ALL) is the most prevalent malignant tumor in children, with B-cell ALL (B-ALL) accounting for 85% of cases. Despite advancements in chemotherapy and supportive care, a subset of high-risk B-ALL patients still experience relapse post-treatment. The molecular mechanisms underlying the relapses after intensified chemotherapy remain poorly understood. Methods: We performed an integrated single-cell multi-omics analysis combining single-cell RNA sequencing (scRNA-seq) and single-cell ATAC sequencing (scATAC-seq) on peripheral blood mononuclear cells (PBMCs) from pediatric high-risk B-ALL patients following early intensified chemotherapy, as well as from healthy controls. Bioinformatic pipelines were applied to assess cellular composition, chromatin accessibility, gene ontology enrichment, spectral clustering, and copy number variation. Results: Significant differences in cellular composition were observed between the remission and non-remission groups, with the non-remission group exhibiting a notable increase in HSC/MPP and Pro-B cells. Copy number variation (CNV) analysis also revealed that the CNV levels in HSC/MPP and Pro-B cells were higher in the non-remission group compared to other cell types. We subsequently identified a subcluster associated with resistance to intensified therapy within both the HSC/MPP and Pro-B cell groups. The drug-resistant subcluster of HSC/MPP cells was characterized by high expression of TCF4, EBF1, ERG, AL589693.1, and CRIM1, as well as enrichment of the allograft rejection pathway and the Notch signaling pathway. The drug-resistant subcluster of Pro-B cells was characterized by high expression of RPS29, B2M, RPL41, RPS21, NEIL1, AC007384.1, and CRIM1, as well as enrichment of the B cell receptor signaling pathway. Discussion: Our study identified distinct cellular subpopulations associated with treatment failure, provide insights into the molecular mechanisms underlying treatment resistance in B-ALL and may inform the development of targeted therapies for high-risk patients.
Indexed as
Identifiers
What OpenQuestion holds
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.