Evidence map›Paper›PMID 20376082›Full record

ArticleLeukemia2010

POU4F1 is associated with t(8;21) acute myeloid leukemia and contributes directly to its unique transcriptional signature.

J M Fortier, J E Payton, P Cahan, T J Ley, M J Walter, T A Graubert

Open access · greenAbstract read
In one paragraph

Article in Leukemia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

21 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Activation of Bivalent Gene POU4F1 Promotes and Maintains Basal-like Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  5. Article
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  7. Review
  8. Article
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  10. Article
  11. Elucidation of Novel Therapeutic Targets for Acute Myeloid Leukemias withInternational journal of molecular sciences · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
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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

6 authors at 1 institution in 1 country.

J M FortierDepartment of Internal Medicine, Division of Oncology, Stem Cell Biology Section, Washington University, St Louis, MO 63110, USA.
J E Payton
P Cahan
T J Ley
M J Walter
T A Graubert
Washington University in St. Louis · US

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
Specimen Acquistition and Expression ProfilingP01CA101937 · NCI · WASHINGTON UNIVERSITY · PI LEY, TIMOTHY J. · 2003 to 2023
$58.8M
NCI NIH HHS P01 CA101937NCI NIH HHS P30 CA091842NCI NIH HHS P30 CA91842
6 · The paper itself

Abstract

The t(8;21)(q22;q22) translocation, present in approximately 5% of adult acute myeloid leukemia (AML) cases, produces the AML1/ETO (AE) fusion protein. Dysregulation of the Pit/Oct/Unc (POU) domain-containing transcription factor POU4F1 is a recurring abnormality in t(8;21) AML. In this study, we showed that POU4F1 overexpression is highly correlated with, but not caused by, AE. We observed that AE markedly increases the self-renewal capacity of myeloid progenitors from murine bone marrow or fetal liver and drives the expansion of these cells in liquid culture. POU4F1 is neither necessary nor sufficient for these AE-dependent properties, suggesting that it contributes to leukemia through novel mechanisms. To identify targets of POU4F1, we performed gene expression profiling in primary mouse cells with genetically defined levels of POU4F1 and identified 140 differentially expressed genes. This expression signature was significantly enriched in human t(8;21) AML samples and was sufficient to cluster t(8;21) AML samples in an unsupervised hierarchical analysis. Among the most highly differentially expressed genes, half are known AML1/ETO targets, implying that the unique transcriptional signature of t(8;21) AML is, in part, attributable to POU4F1 and not AML1/ETO itself. These genes provide novel candidates for understanding the biology and developing therapeutic approaches for t(8;21) AML.

Indexed as

Gene Expression ProfilingAnimalsBiomarkers, TumorBone Marrow CellsChromosomes, Human, Pair 21Chromosomes, Human, Pair 8Core Binding Factor Alpha 2 SubunitFetusHumansLeukemia, Myeloid, AcuteLiverMiceMice, KnockoutOligonucleotide Array Sequence AnalysisOncogene Proteins, FusionReverse Transcriptase Polymerase Chain ReactionAML1-ETO fusion protein, humanBiomarkers, TumorCore Binding Factor Alpha 2 SubunitOncogene Proteins, FusionPOU4F1 protein, humanPou4f1 protein, mouseRNA, MessengerRUNX1 Translocation Partner 1 ProteinTranscription Factor Brn-3A

Identifiers

PMID20376082
PMCPMC2868953
OpenAlexW1977933501

What OpenQuestion holds

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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.