Evidence map›Paper›PMID 17008535›Full record

ArticleBlood2007

Commonly dysregulated genes in murine APL cells.

Wenlin Yuan, Jacqueline E Payton, Matthew S Holt, Daniel C Link, Mark A Watson, John F DiPersio, Timothy J Ley

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Clara cells attenuate the inflammatory response through regulation of macrophage behavior.American journal of respiratory cell and molecular biology · 2010
    Article
  15. Article
  16. Article
  17. Review
  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

7 authors at 1 institution in 1 country.

Wenlin YuanDepartment of Medicine, Siteman Cancer Center, and Department of Pathology and Immunology, Washington University, St Louis, MO 63110, USA.
Jacqueline E Payton
Matthew S Holt
Daniel C Link
Mark A Watson
John F DiPersio
Timothy J Ley
Washington University in St. Louis · US

Funding

Specimen Acquistition and Expression ProfilingP01CA101937 · NCI · WASHINGTON UNIVERSITY · PI LINK, DANIEL C · 2003 to 2023
$58.8M
THE BIOLOGY OF PROMYELOCYTIC LEUKEMIA IN A MOUSE MODEL.R01CA083962 · NCI · WASHINGTON UNIVERSITY · PI LEY, TIMOTHY J. · 2000 to 2014
$6.0M
NCI NIH HHS P01 CA0101937NCI NIH HHS P01 CA101937NCI NIH HHS R01 CA083962
6 · The paper itself

Abstract

To identify genes that are commonly dysregulated in a murine model of acute promyelocytic leukemia (APL), we first defined gene expression patterns during normal murine myeloid development; serial gene expression profiling studies were performed with primary murine hematopoietic progenitors that were induced to undergo myeloid maturation in vitro with G-CSF. Many genes were reproducibly expressed in restricted developmental "windows," suggesting a structured hierarchy of expression that is relevant for the induction of developmental fates and/or differentiated cell functions. We compared the normal myeloid developmental transcriptome with that of APL cells derived from mice expressing PML-RARalpha under control of the murine cathepsin G locus. While many promyelocyte-specific genes were highly expressed in all APL samples, 116 genes were reproducibly dysregulated in many independent APL samples, including Fos, Jun, Egr1, Tnf, and Vcam1. However, this set of commonly dysregulated genes was expressed normally in preleukemic, early myeloid cells from the same mouse model, suggesting that dysregulation occurs as a "downstream" event during disease progression. These studies suggest that the genetic events that lead to APL progression may converge on common pathways that are important for leukemia pathogenesis.

Indexed as

Gene Expression Regulation, NeoplasticGenes, NeoplasmAnimalsCathepsin GCathepsinsCell DifferentiationDisease ProgressionGene Expression ProfilingHematopoietic Stem CellsLeukemia, Promyelocytic, AcuteMiceMice, Inbred C57BLMyeloid CellsOncogene Proteins, FusionSerine EndopeptidasesCathepsin GCathepsinsCtsg protein, mouseOncogene Proteins, Fusionpromyelocytic leukemia-retinoic acid receptor alpha fusion oncoproteinSerine Endopeptidases

Identifiers

PMID17008535
PMCPMC1785140
OpenAlexW2010410555

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.