Evidence map›Paper›PMID 23091296›Full record

ArticleBlood2012

Small sizes and indolent evolutionary dynamics challenge the potential role of P2RY8-CRLF2-harboring clones as main relapse-driving force in childhood ALL.

Maria Morak, Andishe Attarbaschi, Susanna Fischer, Christine Nassimbeni, Reinhard Grausenburger, Stephan Bastelberger, Stefanie Krentz, Gunnar Cario, David Kasper, Klaus Schmitt and 7 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Journal for immunotherapy of cancer · 2024
    Article
  4. Article
  5. Article
  6. Comprehensive detection ofFrontiers in molecular biosciences · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. The enigmatic role(s) ofOncotarget · 2017
    Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

17 authors at 7 institutions in 3 countries.

Maria MorakChildren's Cancer Research Institute, St Anna Kinderkrebsforschung, Vienna, Austria.
Andishe Attarbaschi
Susanna Fischer
Christine Nassimbeni
Reinhard Grausenburger
Stephan Bastelberger
Stefanie Krentz
Gunnar Cario
David Kasper
Klaus Schmitt
Lisa J Russell
Ulrike Pötschger
Martin Stanulla
Conny Eckert
Georg Mann
Oskar A Haas
Renate Panzer-Grümayer
St Anna Children's Hospital · ATCharité - Universitätsmedizin Berlin · DESt. Anna Children's Cancer Research InstituteUniversity Hospital Schleswig-Holstein · DEMedical University of Vienna · ATNewcastle University · GBWomen's General Hospital · AT

Funding

Austrian Science Fund FWF P 22073
6 · The paper itself

Abstract

The P2RY8-CRLF2 fusion defines a particular relapse-prone subset of childhood acute lymphoblastic leukemia (ALL) in Italian Association of Pediatric Hematology and Oncology Berlin-Frankfurt-Münster (AIEOP-BFM) 2000 protocols. To investigate whether and to what extent different clone sizes influence disease and relapse development, we quantified the genomic P2RY8-CRLF2 fusion product and correlated it with the corresponding CRLF2 expression levels in patients enrolled in the BFM-ALL 2000 protocol in Austria. Of 268 cases without recurrent chromosomal translocations and high hyperdiploidy, representing approximately 50% of all cases, 67 (25%) were P2RY8-CRLF2 positive. The respective clone sizes were ≥ 20% in 27% and < 20% in 73% of them. The cumulative incidence of relapse of the entire fusion-positive group was clone size independent and significantly higher than that of the fusion-negative group (35% ± 8% vs 13% ± 3%, P = .008) and primarily confined to the non-high-risk group. Of 22 P2RY8-CRLF2-positive diagnosis/relapse pairs, only 4/8 had the fusion-positive dominant clone conserved at relapse, whereas none of the original 14 fusion-positive small clones reappeared as the dominant relapse clone. We conclude that the majority of P2RY8-CRLF2-positive clones are small at diagnosis and virtually never generate a dominant relapse clone. Our findings therefore suggest that P2RY8-CRLF2-positive clones do not have the necessary proliferative or selective advantage to evolve into a disease-relevant relapse clone.

Indexed as

AdolescentCell SizeChildChild, PreschoolClonal EvolutionClone CellsCohort StudiesDisease ProgressionFemaleGene Expression Regulation, LeukemicHumansInfantMaleOncogene Proteins, FusionPrecursor Cell Lymphoblastic Leukemia-LymphomaReceptors, CytokineCRLF2 protein, humanOncogene Proteins, FusionP2RY8 protein, humanReceptors, CytokineReceptors, Purinergic P2Y

Identifiers

PMID23091296
PMCPMC4194314
OpenAlexW2034920499

What OpenQuestion holds

Textmetadata
LicenceTDM
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.