Evidence map›Paper›PMID 24909161›Full record

ReviewOncogene2015

The ets transcription factor Fli-1 in development, cancer and disease.

Y Li, H Luo, T Liu, E Zacksenhaus, Y Ben-David

Abstract readReview
In one paragraph

Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.

  1. Pooled it
  2. International journal of molecular medicine · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Characterization of a novelHaematologica · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. iScience · 2024
    Article
  17. Review
  18. Acute Erythroid Leukemia: From Molecular Biology to Clinical Outcomes.International journal of molecular sciences · 2024
    Review
  19. Article
  20. Article

21 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

5 authors at 2 institutions in 2 countries.

Y LiDepartment of Anatomy, Norman Bethune College of Medicine, Jilin University, Changchun, China.
H LuoDivision of Biology, the Key Laboratory of Chemistry for Natural Products of Guizhou Province and Chinese Academy of Sciences, Guiyang, China.
T LiuDivision of Biology, the Key Laboratory of Chemistry for Natural Products of Guizhou Province and Chinese Academy of Sciences, Guiyang, China.
E Zacksenhaus1] Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada [2] Division of Advanced Diagnostics, Toronto General Research Institute-University Health Network, Toronto, Ontario, Canada.
Y Ben-David1] Division of Biology, the Key Laboratory of Chemistry for Natural Products of Guizhou Province and Chinese Academy of Sciences, Guiyang, China [2] Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
Key Laboratory of Chemistry for Natural Products of Guizhou Province and Chinese Academy of Sciences · CNUniversity of Toronto · CA

Funding

CIHR 110952-1CIHR 84460-1CIHR MOP-110952
6 · The paper itself

Abstract

Friend leukemia virus-induced erythroleukemia-1 (Fli-1), an E26 transformation specific (ETS) transcription factor, was isolated a quarter century ago through a retrovirus mutagenesis screen. Fli-1 has since been recognized to play critical roles in normal development and homeostasis. For example, it transcriptionally regulates genes that drive normal hematopoiesis and vasculogenesis. Indeed, Fli-1 is one of 10 key regulators of hematopoietic stem/progenitor cell maintenance and differentiation. Aberrant expression of Fli-1 also underlies a number of virally induced leukemias, including Friend virus-induced erythroleukemia and various types of human cancers, and it is the target of chromosomal translocations in childhood Ewing's sarcoma. Abnormal expression of Fli-1 is important in the etiology of autoimmune diseases such as systemic lupus erythematosus and systemic sclerosis. These studies establish Fli-1 as a strong candidate for drug development. Despite difficulties in targeting transcription factors, recent studies identified small-molecule inhibitors for Fli-1. Here we review past and ongoing research on Fli-1 with emphasis on its mechanistic function in autoimmune disease and malignant transformation. The significance of identifying Fli-1 inhibitors and their clinical applications for treatment of disease and cancer with deregulated Fli-1 expression are discussed.

Indexed as

AnimalsCell Transformation, NeoplasticHematopoiesisHematopoietic Stem CellsHumansLeukemiaLupus Erythematosus, SystemicMiceNeovascularization, PathologicProto-Oncogene Protein c-fli-1Sarcoma, EwingScleroderma, SystemicProto-Oncogene Protein c-fli-1

Identifiers

PMID24909161
PMCPMC5028196
OpenAlexW2028130619

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.