Evidence map›Paper›PMID 11704847›Full record

ReviewOncogene2001

Translocations of the RARalpha gene in acute promyelocytic leukemia.

A Zelent, F Guidez, A Melnick, S Waxman, J D Licht

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 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
–field-weighted citation impact, top 98% 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

76 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. [Involvement of PML proteins in treatment of acute promyelocytic leukemia with arsenic trioxide].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018
    Review
  12. Review
  13. Article
  14. Article
  15. Eya2, a Target Activated by Plzf, Is Critical forMolecular and cellular biology · 2017
    Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

16 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 1 institution in 1 country.

A ZelentLeukemia Research Fund Centre at the Institute of Cancer Research, Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB, UK. a.zelent@icr.ac.uk
F Guidez
A Melnick
S Waxman
J D Licht
Institute of Cancer Research · GB

Funding

The PLZF Protein of t(11;17)-Promyelocytic LeukemiaR01CA059936 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LICHT, JONATHAN · 1993 to 2007
$2.9M
TRANSCRIPTIONAL REGULATION BY THE PLZF PROTEINK08CA073762 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI MELNICK, ARI M. · 1997 to 2001
$181k
NCI NIH HHS CA59936NCI NIH HHS KO8 CA73762
6 · The paper itself

Abstract

Acute promyelocytic leukemia (APL) has been recognized as a distinct clinical entity for over 40 years. Although relatively rare among hematopoietic malignancies (approximately 10% of AML cases), this disease has attracted a particularly good share of attention by becoming the first human cancer in which all-trans-retinoic acid (ATRA), a physiologically active derivative of vitamin A, was able to induce complete remission (CR). ATRA induced remission is not associated with rapid cell death, as in the case of conventional chemotherapy, but with a restoration of the 'normal' granulocytic differentiation pathway. With this remarkable medical success story APL has overnight become a paradigm for the differentiation therapy of cancer. A few years later, excitement with APL was further enhanced by the discovery that a cytogenetic marker for this disease, the t(15:17) reciprocal chromosomal translocation, involves a fusion between the retinoic acid receptor alpha (RARalpha) gene and a previously unknown locus named promyelocytic leukemia (PML). Consequence of this gene rearrangement is expression of the PML-RARalpha chimeric oncoprotein, which is responsible for the cellular transformation as well as ATRA response that is observed in APL. Since this initial discovery, a number of different translocation partner genes of RARalpha have been reported in rarer cases of APL, strongly suggesting that disruption of RARalpha underlies its pathogenesis. This article reviews various rearrangements of the RARalpha gene that have so far been described in literature, functions of the proteins encoded by the different RARalpha partner loci, and implications that these may have for the molecular pathogenesis of APL.

Indexed as

Milk ProteinsAntigens, NuclearCell Cycle ProteinsDNA-Binding ProteinsHumansLeukemia, Promyelocytic, AcuteNeoplasm ProteinsNuclear Matrix-Associated ProteinsNuclear ProteinsNucleophosminOncogene Proteins, FusionReceptors, Retinoic AcidRetinoic Acid Receptor alphaSTAT5 Transcription FactorTrans-ActivatorsTranslocation, GeneticAntigens, NuclearCell Cycle ProteinsDNA-Binding ProteinsMilk ProteinsNeoplasm ProteinsNPM-RARalpha protein, humanNuclear Matrix-Associated ProteinsNuclear ProteinsNucleophosminNUMA1 protein, humanNuMa-RARalpha protein, humanOncogene Proteins, FusionPLZF-RARalpha fusion protein, humanpromyelocytic leukemia-retinoic acid receptor alpha fusion oncoproteinRARA protein, humanReceptors, Retinoic AcidRetinoic Acid Receptor alphaSTAT5 Transcription FactorTrans-ActivatorsTretinoin

Identifiers

PMID11704847
OpenAlexW569821447

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.