Evidence map›Paper›PMID 7935403›Full record

ArticleMolecular and cellular biology1994

PML, a growth suppressor disrupted in acute promyelocytic leukemia.

Z M Mu, K V Chin, J H Liu, G Lozano, K S Chang

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
9.2field-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

102 citing papers in PubMed, 292 citations in OpenAlex.

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  13. PML3 Orchestrates the Nuclear Dynamics and Function of TIP60.The Journal of biological chemistry · 2009
    Article
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42 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.

Z M MuDivision of Laboratory Medicine, University of Texas M.D. Anderson Cancer Center, Houston 77030.
K V Chin
J H Liu
G Lozano
K S Chang
Rutgers, The State University of New Jersey · US

Funding

MOLECULAR PATHOLOGY OF ACUTE PROMYELOCYTIC LEUKEMIAR01CA055577 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI CHANG, KUN-SANG · 1992 to 2012
$2.5M
NCI NIH HHS CA-55577
6 · The paper itself

Abstract

The nonrandom chromosomal translocation t(15;17)(q22;q21) in acute promyelocytic leukemia (APL) juxtaposes the genes for retinoic acid receptor alpha (RAR alpha) and the putative zinc finger transcription factor PML. The breakpoint site encodes fusion protein PML-RAR alpha, which is able to form a heterodimer with PML. It was hypothesized that PML-RAR alpha is a dominant negative inhibitor of PML. Inactivation of PML function in APL may play a critical role in APL pathogenesis. Our results demonstrated that PML, but not PML-RAR alpha, is a growth suppressor. This is supported by the following findings: (i) PML suppressed anchorage-independent growth of APL-derived NB4 cells on soft agar and tumorigenicity in nude mice, (ii) PML suppressed the oncogenic transformation of rat embryo fibroblasts by cooperative oncogenes, and (iii) PML suppressed transformation of NIH 3T3 cells by the activated neu oncogene. Cotransfection of PML with PML-RAR alpha resulted in a significant reduction in PML's transformation suppressor function in vivo, indicating that the fusion protein can be a dominant negative inhibitor of PML function in APL cells. This observation was further supported by the finding that cotransfection of PML and PML-RAR alpha resulted in altered normal cellular localization of PML. Our results also demonstrated that PML, but not PML-RAR alpha, is a promoter-specific transcription suppressor. Therefore, we hypothesized that disruption of the PML gene, a growth or transformation suppressor, by the t(15;17) translocation in APL is one of the critical events in leukemogenesis.

Indexed as

Neoplasm ProteinsNuclear ProteinsTranslocation, GeneticAnimalsBase SequenceCell DivisionCells, CulturedCell Transformation, NeoplasticClone CellsHumansLeukemia, Promyelocytic, AcuteMiceModels, BiologicalMolecular Sequence DataOncogenesPromyelocytic Leukemia ProteinNeoplasm ProteinsNuclear ProteinsPML protein, humanPml protein, mousePromyelocytic Leukemia ProteinRARA protein, humanRara protein, mouseRara protein, ratReceptors, Retinoic AcidRecombinant Fusion ProteinsRetinoic Acid Receptor alphaTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID7935403
PMCPMC359216
OpenAlexW1779679253

What OpenQuestion holds

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Registered trials

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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.