Evidence map›Paper›PMID 9122233›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

A PMLRARalpha transgene initiates murine acute promyelocytic leukemia.

D Brown, S Kogan, E Lagasse, I Weissman, M Alcalay, P G Pelicci, S Atwater, J M Bishop

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
176citing papers in PubMed, 1 pooled it
11.6field-weighted citation impact, top 1% 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

176 citing papers in PubMed, 1 synthesis or guideline pooled it, 446 citations in OpenAlex.

  1. Therapy-related acute promyelocytic leukemia: a systematic review.Medical oncology (Northwood, London, England) · 2013
    Pooled it
  2. Trial
  3. Article
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  5. Mutation in the UnrearrangedResearch (Washington, D.C.) · 2025
    Article
  6. PML::RARA and GATA2 proteins interact via DNA templates to induce aberrant self-renewal in mouse and human hematopoietic cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  8. Review
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  20. Review

116 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

8 authors at 3 institutions in 2 countries.

D BrownG.W. Hooper Foundation, Department of Biochemistry and Biophysics, University of California, San Francisco 94143-0552, USA.
S Kogan
E Lagasse
I Weissman
M Alcalay
P G Pelicci
S Atwater
J M Bishop
University of California, San Francisco · USStanford University · USEuropean Institute of Oncology · IT

Funding

RETROVIRUSES AND CANCER GENESR35CA044338 · NCI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI BISHOP, J MICHAEL · 1987 to 2000
$1.8M
NCI NIH HHS CA 44338
6 · The paper itself

Abstract

The malignant cells of acute promyelocytic leukemia (APL) contain a reciprocal chromosomal translocation that fuses the promyelocytic leukemia gene (PML) with the retinoic acid receptor alpha gene (RAR alpha). To test the hypothesis that the chimera PMLRAR alpha plays a role in leukemogenesis, we expressed a PMLRAR alpha cDNA in myeloid cells of transgenic mice. PMLRAR alpha transgenic mice exhibited impaired neutrophil maturation early in life, which progressed at a low frequency over the course of several months to overt APL. Both the preleukemic state and the leukemia could be transplanted to nontransgenic mice, and the transplanted preleukemia could progress to APL. The APL recapitulated features of the human disease, including a response to retinoic acid. Retinoic acid caused the leukemic cells to differentiate in vitro and in vivo, eliciting remissions of both the preleukemic state and APL in mice. Our results demonstrate that PMLRAR alpha impairs neutrophil differentiation and initiates the development of APL. The transgenic mice described here provide an apparently accurate model for human APL that includes clear evidence of tumor progression. The model should be useful for exploring the molecular pathogenesis of APL and the mechanisms of the therapeutic response to retinoic acid, as well as for preclinical studies of therapeutic regimens.

Indexed as

Neoplasm ProteinsNuclear ProteinsAnimalsAntineoplastic AgentsBone MarrowCell DifferentiationChromosomes, Human, Pair 15Flow CytometryHumansLeukemia, Promyelocytic, AcuteMiceMice, TransgenicNeutrophilsPromyelocytic Leukemia ProteinReceptors, Retinoic AcidRecombinant Fusion ProteinsAntineoplastic AgentsNeoplasm ProteinsNuclear ProteinsPML protein, humanPml protein, mousePromyelocytic Leukemia ProteinRARA protein, humanRara protein, mouseReceptors, Retinoic AcidRecombinant Fusion ProteinsRetinoic Acid Receptor alphaTranscription FactorsTretinoinTumor Suppressor Proteins

Identifiers

PMID9122233
PMCPMC20126
OpenAlexW2079526924

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.