Evidence map›Paper›PMID 14729970›Full record

ArticleMolecular and cellular biology2004

E2a/Pbx1 induces the rapid proliferation of stem cell factor-dependent murine pro-T cells that cause acute T-lymphoid or myeloid leukemias in mice.

David B Sykes, Mark P Kamps

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Comprehensive summary: the role of PBX1 in development and cancers.Frontiers in cell and developmental biology · 2024
    Review
  7. Underexpression ofFrontiers in oncology · 2022
    Article
  8. PBX1: a key character of the hallmarks of cancer.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
  9. Article
  10. Molecular processes involved in B cell acute lymphoblastic leukaemia.Cellular and molecular life sciences : CMLS · 2018
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

David B SykesDepartment of Pathology, University of California-San Diego, La Jolla, California 92093-0612, USA.
Mark P Kamps
University of San Diego · US

Funding

Hoxa9, Meis1, and Pbx in Self-renewal and LeukemogenesisR01CA056876 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KAMPS, MARK P · 1992 to 2012
$4.1M
NCI NIH HHS CA56876NCI NIH HHS R01 CA056876
6 · The paper itself

Abstract

Oncoprotein E2a/Pbx1 is produced by the t(1;19) chromosomal translocation of human pre-B acute lymphoblastic leukemia. E2a/Pbx1 blocks differentiation of primary myeloid progenitors but, paradoxically, induces apoptosis in established pre-B-cell lines, and no transforming function of E2a/Pbx1 has been reported in cultured lymphoid progenitors. Here, we demonstrate that E2a/Pbx1 induces immortal proliferation of stem cell factor (SCF)-dependent pro-T thymocytes by a mechanism dependent upon both its transactivation and DNA-binding functions. E2a-Pbx1 cooperated with cytokines or activated signaling oncoproteins to induce cell division, as inactivation of conditional E2a/Pbx1 in either factor-dependent pro-T cells or pro-T cells made factor independent by expression of Bcr/Abl resulted in pro-T-cell quiescence, while reactivation of E2a/Pbx1 restored cell division. Infusion of E2a/Pbx1 pro-T cells in mice caused T lymphoblastic leukemia and, unexpectedly, acute myeloid leukemia. The acute lymphoblastic leukemia did not evidence further maturation, suggesting that E2a/Pbx1 establishes an early block in pro-T-cell development that cannot be overcome by marrow or thymic microenvironments. In an E2a/Pbx1 pro-T thymocyte clone that induced only pro-T acute lymphoblastic leukemia, coexpression of Bcr/Abl expanded its leukemic phenotype to include acute myeloid leukemia, suggesting that unique functions of cooperating signaling oncoproteins can influence the lymphoid versus myeloid character of E2a/Pbx1 leukemia and may cooperate with E2a/Pbx1 to dictate the pre-B-cell phenotype of human leukemia containing t(1;19).

Indexed as

Repressor ProteinsAnimalsCell DivisionCo-Repressor ProteinsDNA-Binding ProteinsHematopoietic Stem CellsHomeodomain ProteinsLeukemia, MyeloidLymphoid Enhancer-Binding Factor 1Membrane ProteinsMiceNuclear ProteinsPre-B-Cell Leukemia Transcription Factor 1Proto-Oncogene ProteinsReceptors, NotchStem Cell FactorCo-Repressor ProteinsDNA-Binding ProteinsHomeodomain ProteinsLymphoid Enhancer-Binding Factor 1Membrane ProteinsNuclear ProteinsPBX1 protein, humanPbx1 protein, mousePre-B-Cell Leukemia Transcription Factor 1Proto-Oncogene ProteinsReceptors, NotchRepressor ProteinsStem Cell FactorTle1 protein, mouseTranscription Factors

Identifiers

PMID14729970
PMCPMC321418
OpenAlexW2114332522

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.