Evidence map›Paper›PMID 11704848›Full record

ReviewOncogene2001

Transcriptional regulation in acute promyelocytic leukemia.

R J Lin, T Sternsdorf, M Tini, R M Evans

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
–field-weighted citation impact
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

55 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. The Role of HDACs as Leukemia Therapy Targets using HDI.International journal of hematology-oncology and stem cell research · 2015
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Nuclear receptor corepressor complexes in cancer: mechanism, function and regulation.American journal of clinical and experimental urology · 2014
    Review
  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

4 authors.

R J LinHoward Hughes Medical Institute, Gene Expression Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California, CA 92037, USA.
T Sternsdorf
M Tini
R M Evans

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been 10 years since the seminal discovery that a mutant form of a retinoid acid receptor (RARalpha) is associated with acute promyelocytic leukemia (APL). This finding, coupled with the remarkable success of retinoic acid (RA), the natural ligand of RARalpha, in the treatment of APL, has made APL a unique model system in the study of oncogenic conversion of transcription factors in hematological malignancies. Indeed, subsequent basic and clinical studies showed that chromosomal translocation involving the RARalpha gene is the cytogenetic hallmark of APL and that these mutant forms of RARs are the oncogenes in APL that interfere with the proliferation and differentiation pathways controlled by both RAR and their fusion partners. However, it was not until recently that the role of aberrant transcriptional regulation in the pathogenesis of APL was revealed. In this review, we summarize the biochemical and biological mechanisms of transcriptional regulation by mutant RARs and their corresponding wild-type fusion partner PML and PLZF. These studies have been instrumental in our understanding of the process of leukemogenesis in general and have laid the scientific foundation for the novel concept of transcription therapy in the treatment of human cancer.

Indexed as

Gene Expression Regulation, LeukemicNuclear ProteinsCell DifferentiationCell DivisionCell Nucleus StructuresDNA-Binding ProteinsGene SilencingHumansKruppel-Like Transcription FactorsLeukemia, Promyelocytic, AcuteMacromolecular SubstancesMutationNeoplasm ProteinsOncogene Proteins, FusionOrganellesPromyelocytic Leukemia ProteinDNA-Binding ProteinsKruppel-Like Transcription FactorsMacromolecular SubstancesNeoplasm ProteinsNuclear ProteinsOncogene Proteins, FusionPML protein, humanPromyelocytic Leukemia ProteinPromyelocytic Leukemia Zinc Finger ProteinRARA protein, humanReceptors, Retinoic AcidRetinoic Acid Receptor alphaTranscription FactorsTumor Suppressor ProteinsZBTB16 protein, human

Identifiers

PMID11704848

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.