Evidence map›Paper›PMID 10611345›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

A bcr-3 isoform of RARalpha-PML potentiates the development of PML-RARalpha-driven acute promyelocytic leukemia.

J L Pollock, P Westervelt, A K Kurichety, P G Pelicci, J L Grisolano, T J Ley

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 112 citations in OpenAlex.

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  5. Blood · 2019
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  17. Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha.Proceedings of the National Academy of Sciences of the United States of America · 2005
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  18. Review
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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

6 authors at 1 institution in 1 country.

J L PollockWashington University School of Medicine, Division of Bone Marrow Transplantation, Department of Internal Medicine, St. Louis, MO 63110, USA.
P Westervelt
A K Kurichety
P G Pelicci
J L Grisolano
T J Ley
European Institute of Oncology · IT

Funding

TRANSCRIPTIONAL REGULATION AND ROLE OF BCL-2 IN DEVELOPMENT AND NEOPLASIAP01CA049712 · NCI · WASHINGTON UNIVERSITY · PI LEY, TIMOTHY J · 1989 to 1999
–
NCI NIH HHS CA49712
6 · The paper itself

Abstract

Acute promyelocytic leukemia (APML) most often is associated with the balanced reciprocal translocation t(15;17) (q22;q11.2) and the expression of both the PML-RARalpha and RARalpha-PML fusion cDNAs that are formed by this translocation. In this report, we investigated the biological role of a bcr-3 isoform of RARalpha-PML for the development of APML in a transgenic mouse model. Expression of RARalpha-PML alone in the early myeloid cells of transgenic mice did not alter myeloid development or cause APML, but its expression significantly increased the penetrance of APML in mice expressing a bcr-1 isoform of PML-RARalpha (15% of animals developed APML with PML-RARalpha alone vs. 57% with both transgenes, P < 0.001). The latency of APML development was not altered substantially by the expression of RARalpha-PML, suggesting that it does not behave as a classical "second hit" for development of the disease. Leukemias that arose from doubly transgenic mice were less mature than those from PML-RARalpha transgenic mice, but they both responded to all-trans retinoic acid in vitro. These findings suggest that PML-RARalpha drives the development of APML and defines its basic phenotype, whereas RARalpha-PML potentiates this phenotype via mechanisms that are not yet understood.

Indexed as

Translocation, GeneticAnimalsBone Marrow CellsCathepsinsCrosses, GeneticGene ExpressionHumansLeukemia, Promyelocytic, AcuteMiceMice, TransgenicNeoplasm ProteinsOncogene Proteins, FusionPenetrancePhenotypeProtein IsoformsSpleenCathepsinsNeoplasm ProteinsOncogene Proteins, Fusionpromyelocytic leukemia-retinoic acid receptor alpha fusion oncoproteinProtein IsoformsTretinoin

Identifiers

PMID10611345
PMCPMC24780
OpenAlexW2066789082

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.