ArticleBlood2010
Immature B-cell progenitors survive oncogenic stress and efficiently initiate Ph+ B-acute lymphoblastic leukemia.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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
11 citing papers in PubMed, 17 citations in OpenAlex.
- Asciminib antagonizes transplantable BCR::ABL1-positive lymphoid blast crisis in vivo by targeting malignant stem cells.Leukemia · 2024Article
- Layered immunity and layered leukemogenicity: Developmentally restricted mechanisms of pediatric leukemia initiation.Immunological reviews · 2023Review
- ZNF384 Fusion Oncoproteins Drive Lineage Aberrancy in Acute Leukemia.Blood cancer discovery · 2022Article
- Review
- The Earliest T-Precursors in the Mouse Embryo Are Susceptible to Leukemic Transformation.Frontiers in cell and developmental biology · 2021Article
- B-1 progenitor acute lymphoid leukemia.Blood · 2019Article
- Constitutive Ras signaling andBlood advances · 2017Article
- Article
- Murine B-1 B cell progenitors initiate B-acute lymphoblastic leukemia with features of high-risk disease.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Pbx1 restrains myeloid maturation while preserving lymphoid potential in hematopoietic progenitors.Journal of cell science · 2013Article
- Essential role for Stat5a/b in myeloproliferative neoplasms induced by BCR-ABL1 and JAK2(V617F) in mice.Blood · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Philadelphia chromosome-positive (Ph(+)) B-acute lymphoblastic leukemia (B-ALL) can initiate in committed B-cell progenitors. However, the stages of B-cell differentiation in which disease can initiate and the efficiency with which this occurs are unclear. We now demonstrate that B-cell progenitors, up to and including the pro-B cell, efficiently initiate Ph(+) B-ALL. However, cells at the pre-B-cell stage of development did not initiate disease. We show that this difference in leukemia initiating potential is due to the level at which the Arf tumor suppressor gene is induced in specific stages of B lymphopoiesis. Whereas immature B-cell progenitors survive the relatively low levels of Arf that are induced after oncogene expression, pre-B cells express the tumor suppressor gene at high levels and undergo massive apoptosis. These data demonstrate that the molecular events that control Ph(+) B-ALL initiation and tumor suppression in the B-cell lineage are developmentally regulated.
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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.