Evidence map›Paper›PMID 26447191›Full record

ReviewBlood2015

From cytopenia to leukemia: the role of Gfi1 and Gfi1b in blood formation.

Tarik Möröy, Lothar Vassen, Brian Wilkes, Cyrus Khandanpour

Open access · bronzeAbstract readReview
In one paragraph

Review in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. CD13 identifies S100A4Biology direct · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

13 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

4 authors at 2 institutions in 2 countries.

Tarik MöröyInstitut de recherches cliniques de Montréal, Montréal, QC, Canada; Department de microbiologie, infectiologie et immunologie, Université de Montréal, Montréal, QC, Canada; Division of Experimental Medicine, McGill University, Montréal, QC, Canada; and.
Lothar VassenInstitut de recherches cliniques de Montréal, Montréal, QC, Canada; Department of Hematology, Universitätsklinikum Essen, Essen, Germany.
Brian WilkesInstitut de recherches cliniques de Montréal, Montréal, QC, Canada;
Cyrus KhandanpourInstitut de recherches cliniques de Montréal, Montréal, QC, Canada; Department of Hematology, Universitätsklinikum Essen, Essen, Germany.ORCID http://orcid.org/0000-0003-4655-6269
Essen University Hospital · DEMontreal Clinical Research Institute · CA

Funding

DEVELOPMENT OF RECEPTOR-SPECIFIC OPIOID PEPTIDE ANALOGSR01DA004443 · NIDA · CLINICAL RESEARCH INSTITUTE OF MONTREAL · PI SCHILLER, PETER W · 1987 to 2016
$2.0M
DEVELOPMENT OF RECEPTOR SPECIFIC OPIOID PEPTIDE ANALOGSR37DA004443 · NIDA · CLINICAL RESEARCH INSTITUTE OF MONTREAL · PI SCHILLER, PETER W · 1997 to 2003
$621k
Canadian Institutes of Health ResearchNIDA NIH HHS DA004443NIDA NIH HHS R01 DA004443NIDA NIH HHS R37 DA004443
6 · The paper itself

Abstract

The DNA-binding zinc finger transcription factors Gfi1 and Gfi1b were discovered more than 20 years ago and are recognized today as major regulators of both early hematopoiesis and hematopoietic stem cells. Both proteins function as transcriptional repressors by recruiting histone-modifying enzymes to promoters and enhancers of target genes. The establishment of Gfi1 and Gfi1b reporter mice made it possible to visualize their cell type-specific expression and to understand their function in hematopoietic lineages. We now know that Gfi1 is primarily important in myeloid and lymphoid differentiation, whereas Gfi1b is crucial for the generation of red blood cells and platelets. Several rare hematologic diseases are associated with acquired or inheritable mutations in the GFI1 and GFI1B genes. Certain patients with severe congenital neutropenia carry mutations in the GFI1 gene that lead to the disruption of the C-terminal zinc finger domains. Other mutations have been found in the GFI1B gene in families with inherited bleeding disorders. In addition, the Gfi1 locus is frequently found to be a proviral integration site in retrovirus-induced lymphomagenesis, and new, emerging data suggest a role of Gfi1 in human leukemia and lymphoma, underlining the role of both factors not only in normal hematopoiesis, but also in a wide spectrum of human blood diseases.

Indexed as

AnimalsBlood CellsCongenital Bone Marrow Failure SyndromesDNA-Binding ProteinsGene Expression RegulationGene Regulatory NetworksGenes, ReporterHematologic DiseasesHematologic NeoplasmsHematopoiesisHematopoietic Stem CellsHistone CodeHumansLeukemia Virus, MurineMiceMice, TransgenicDNA-Binding ProteinsGFI1B protein, humanGFI1 protein, humanGfi1 protein, mouseProto-Oncogene ProteinsRepressor ProteinsTranscription Factors

Identifiers

PMID26447191
PMCPMC4671106
OpenAlexW2233438852

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.