Evidence map›Paper›PMID 21972289›Full record

ArticleBlood2011

ATF5 polymorphisms influence ATF function and response to treatment in children with childhood acute lymphoblastic leukemia.

Julie Rousseau, Vincent Gagné, Malgorzata Labuda, Cyrielle Beaubois, Daniel Sinnett, Caroline Laverdière, Albert Moghrabi, Stephen E Sallan, Lewis B Silverman, Donna Neuberg and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Trial
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Pharmacogenetics of asparaginase in acute lymphoblastic leukemia.Cancer drug resistance (Alhambra, Calif.) · 2019
    Review
  17. Inhibition of GCN2 sensitizes ASNS-low cancer cells to asparaginase by disrupting the amino acid response.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  18. Review
  19. Novel Gene and Network Associations Found for Acute Lymphoblastic Leukemia Using Case-Control and Family-Based Studies in Multiethnic Populations.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2017
    Article
  20. Review
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

12 authors at 5 institutions in 2 countries.

Julie RousseauResearch Center, Centre Hospitalier Universitaire Sainte-Justine, Montreal, QC.
Vincent Gagné
Malgorzata Labuda
Cyrielle Beaubois
Daniel Sinnett
Caroline Laverdière
Albert Moghrabi
Stephen E Sallan
Lewis B Silverman
Donna Neuberg
Jeffery L Kutok
Maja Krajinovic
Centre Hospitalier Universitaire Sainte-Justine · CAUniversité de Montréal · CADana-Farber Cancer Institute · USBoston Children's Hospital · USBrigham and Women's Hospital · US

Funding

Zebrafish Screens for Genetic Modifiers and Human Application in T-ALLP01CA068484 · NCI · DANA-FARBER CANCER INSTITUTE · PI SALLAN, STEPHEN E · 1995 to 2010
$31.9M
CIHRNCI NIH HHS P01 CA068484NCI NIH HHS P01 CA 68484
6 · The paper itself

Abstract

Asparaginase is a standard and critical component in the therapy of childhood acute lymphoblastic leukemia. Asparagine synthetase (ASNS) and the basic region leucine zipper activating transcription factor 5 (ATF5) and arginosuccinate synthase 1 (ASS1) have been shown to mediate the antileukemic effect of asparaginase and to display variable expression between leukemia cells that are resistant and sensitive to treatment. Fourteen polymorphisms in the regulatory and coding regions of these genes were investigated for an association with acute lymphoblastic leukemia outcome. Lower event-free survival (EFS) was associated with ATF5 T1562C, tandem-repeat ASNS polymorphism, derived haplotype, and ASS1 G1343T and G34T substitutions (P ≤ .03). Associations were limited to patients who received Escherichia coli asparaginase. Variations that sustained correction for multiple testing (ATF5 T1562C, P = .005; ASNS tandem-repeat and related haplotype, P ≤ .01) were subsequently analyzed in the replication cohort. The E coli-dependent association of the ATF5 T1562 allele with reduced EFS was confirmed (P = .01). A gene-reporter assay showed that the haplotype tagged by T1562 had higher promoter activity (P ≤ .01). The remaining regulatory polymorphisms also appeared to affect ATF5 function; 2 additional high-activity haplotypes were identified (P ≤ .02) and were further corroborated by quantitative mRNA analysis in lymphoblastoid cell lines. The ATF5-regulated increase in ASNS expression in response to more efficacious E coli-induced asparagine depletion may explain our observed results.

Indexed as

Polymorphism, GeneticActivating Transcription FactorsAspartate-Ammonia LigaseBase SequenceBiomarkers, TumorChildChild, PreschoolFemaleGene Expression Regulation, EnzymologicGene Expression Regulation, LeukemicGenotypeHumansInfantInfant, NewbornLinkage DisequilibriumMaleActivating Transcription FactorsAspartate-Ammonia LigaseATF5 protein, humanBiomarkers, Tumor

Identifiers

PMID21972289
PMCPMC3342855
OpenAlexW2073512501

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.