ArticleExperimental hematology2020
Human pediatric B-cell acute lymphoblastic leukemias can be classified as B-1 or B-2-like based on a minimal transcriptional signature.
Article in Experimental hematology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Functional and molecular single-cell analyses implicate PRDM14 in the initiation of B cell leukemia in mice.Scientific reports · 2025Article
- Variant to function mapping at single-cell resolution through network propagation.Nature biotechnology · 2022Article
- Increasing Complexity of Molecular Landscapes in Human Hematopoietic Stem and Progenitor Cells during Development and Aging.International journal of molecular sciences · 2022Review
- Variant to function mapping at single-cell resolution through network propagation.bioRxiv : the preprint server for biology · 2022Article
- Ikaros deficiency is associated with aggressive BCR-ABL1 B-cell precursor acute lymphoblastic leukemia independent of the lineage and developmental origin.Haematologica · 2022Article
- Does lineage plasticity enable escape from CAR-T cell therapy? Lessons from MLL-r leukemia.Experimental hematology · 2021Review
- The Origin of B-cells: Human Fetal B Cell Development and Implications for the Pathogenesis of Childhood Acute Lymphoblastic Leukemia.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
The finding that transformed mouse B-1 and B-2 progenitors give rise to B-cell acute lymphoblastic leukemias (B-ALLs) with varied aggressiveness suggests that B-cell lineage might also be a factor in the initiation and progression of pediatric B-ALLs in humans. If this is the case, we hypothesized that human pediatric B-ALLs would share gene expression patterns with mouse B-1 or B-2 progenitors. We tested this premise by deriving a distinct 30-gene B-1 and B-2 progenitor signature that was applied to a microarray data set of human pediatric ALLs. Cluster analysis revealed that CRLF2, E2A-PBX1, ERG, and ETV6-RUNX1 leukemias were B-1-like, whereas BCR-ABL1, hyperdiploid, and MLL leukemias were B-2-like. Examination of the 30-gene signature in two independent data sets of pediatric ALLs supported this result. Our data suggest that common genetic subtypes of human ALL have their origin in the B-1 or B-2 lineage.
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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.