Evidence map›Paper›PMID 19996307›Full record

ReviewMolecular cancer research : MCR2009

Emerging roles of the EBF family of transcription factors in tumor suppression.

Daiqing Liao

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular cancer research : MCR, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

  1. Pooled it
  2. Article
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  8. Article
  9. Mutations Upstream of ppp2ca Affect Body Weight in Asian Seabass.Marine biotechnology (New York, N.Y.) · 2025
    Article
  10. Review
  11. EBF3 Gene-Related Fetal Phenotypes.Maternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
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4 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Daiqing LiaoDepartment of Anatomy and Cell Biology, UF Shands Cancer Center, University of Florida, Gainesville, FL 32611-3633, USA. dliao@ufl.edu
University of Florida Health · US

Funding

Deregulation of Cell Pathways by Ad E1B 55K OncoproteinsR01CA092236 · NCI · UNIVERSITY OF FLORIDA · PI LIAO, DAIQING · 2001 to 2005
$1.4M
NCI NIH HHS R01 CA092236
6 · The paper itself

Abstract

Alterations in various developmental pathways are common themes in cancer. The early B-cell factors (EBF) are a family of four highly conserved DNA-binding transcription factors with an atypical zinc-finger and helix-loop-helix motif. They are involved in the differentiation and maturation of several cell lineages including B-progenitor lymphoblasts, neuronal precursors, and osteoblast progenitors. During B-cell development, EBF1 is required for the expression of Pax5, an essential factor for the production of antibody-secreting cells. Accumulating evidence indicates that genomic deletion of the EBF1 gene contributes to the pathogenesis, drug resistance, and relapse of B-progenitor acute lymphoblastic leukemia (ALL). Epigenetic silencing and genomic deletion of the EBF3 locus in chromosome 10q are very frequent in glioblastoma (GBM). Strikingly, the frequency of EBF3 loss in GBM is similar to that of the loss of Pten, a key suppressor of gliomagenesis. Cancer-specific somatic mutations were detected in EBF3 in GBM and in both EBF1 and EBF3 in pancreatic ductal adenocarcinoma. These missense mutations occur in the DNA-binding domain or the conserved IPT/TIG domain, suggesting that they might disrupt the functions of these two proteins. Functional studies revealed that EBF3 represses the expression of genes required for cell proliferation [e.g., cyclins and cyclin-dependent kinases (CDK)] and survival (e.g., Mcl-1 and Daxx) but activates those involved in cell cycle arrest (e.g., p21 and p27), leading to growth suppression and apoptosis. Therefore, EBFs represent new tumor suppressors whose inactivation blocks normal development and contributes to tumorigenesis of diverse types of human cancer.

Indexed as

AnimalsGrowth and DevelopmentHumansNeoplasmsProtein BindingTranscription FactorsTumor Suppressor ProteinsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID19996307
PMCPMC5545892
OpenAlexW2112412205

What OpenQuestion holds

Textmetadata
LicenceTDM
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.