Evidence map›Paper›PMID 7759992›Full record

ArticleThe Journal of experimental medicine1995

PML suppresses oncogenic transformation of NIH/3T3 cells by activated neu.

J H Liu, Z M Mu, K S Chang

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

31 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
  2. Article
  3. The nuclear bodies inside out: PML conquers the cytoplasm.Current opinion in cell biology · 2011
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Role of promyelocytic leukemia (PML) protein in tumor suppression.The Journal of experimental medicine · 2001
    Article
  16. A bcr-3 isoform of RARalpha-PML potentiates the development of PML-RARalpha-driven acute promyelocytic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 1999
    Article
  17. Article
  18. Article
  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

3 authors at 1 institution in 1 country.

J H LiuDivision of Laboratory Medicine, University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.
Z M Mu
K S Chang
The University of Texas MD Anderson Cancer Center · 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 chromosomal translocation t(15;17)(q22;q12) is a consistent feature of acute promyelocytic leukemia (APL) that results in the disruption of genes for the zinc finger transcription factor PML and the retinoic acid receptor alpha (RAR alpha). We have previously shown that PML is a growth suppressor and is able to suppress transformation of NIH/3T3 by activated neu oncogene. In the study presented here, the full-length PML cDNA was transfected into B104-1-1 cells (NIH/3T3 cells transformed by the activated neu oncogene) by retrovirally mediated gene transfer. We found that expression of PML could reverse phenotypes of B104-1-1 including morphology, contact-limiting properties, and growth rate in both transient-expression and stable transfectants. We also demonstrated that PML is able to suppress clonogenicity of B104-1-1 in soft agar assay and tumorigenicity in nude mice. These results strongly support our previous finding that PML is a transformation or growth suppressor. Our results further demonstrate that expression of PML in B104-1-1 cells has little effect on cell cycle distribution. Western blot analysis demonstrated that suppression of neu expression in B104-1-1 by PML was insignificant in the transient transfection experiment but significant in the PML stable transfectants. This study suggests that PML may suppress neu expression and block signaling events associated with activated neu. This study supports our hypothesis that disruption of the normal function of PML, a growth or transformation suppressor, is a critical event in APL leukomogenesis.

Indexed as

Cell Transformation, NeoplasticGenes, erbB-2Neoplasm ProteinsNuclear Proteins3T3 CellsAnimalsCell CycleChromosome MappingChromosomes, Human, Pair 15Chromosomes, Human, Pair 17Clone CellsErb-b2 Receptor Tyrosine KinasesFluorescent Antibody TechniqueGene ExpressionHumansLeukemia, Promyelocytic, AcuteErb-b2 Receptor Tyrosine KinasesNeoplasm ProteinsNuclear ProteinsPML protein, humanPml protein, mousePromyelocytic Leukemia ProteinRecombinant ProteinsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID7759992
PMCPMC2192078
OpenAlexW2103764985

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.