Evidence map›Paper›PMID 23823658›Full record

ArticleLeukemia2014

Deletions of IKZF1 and SPRED1 are associated with poor prognosis in a population-based series of pediatric B-cell precursor acute lymphoblastic leukemia diagnosed between 1992 and 2011.

L Olsson, A Castor, M Behrendtz, A Biloglav, E Forestier, K Paulsson, B Johansson

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In one paragraph

Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
9.8field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. IKAROS in Acute Leukemia: A Positive Influencer or a Mean Hater?International journal of molecular sciences · 2023
    Review
  7. Impact ofCancers · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Progress in experimental research on SPRED protein family.The Journal of international medical research · 2020
    Review
  14. Article
  15. Article
  16. Frontiers in oncology · 2020
    Article
  17. Article
  18. Review
  19. Review
  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 4 institutions in 1 country.

L OlssonDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.
A CastorDepartment of Pediatrics, Skåne University Hospital, Lund, Sweden.
M BehrendtzDepartment of Pediatrics, Linköping University Hospital, Linköping, Sweden.
A BiloglavDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.
E ForestierDepartment of Medical Bioscience, University of Umeå, Umeå, Sweden.
K PaulssonDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.
B Johansson1] Division of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden [2] Department of Clinical Genetics, University and Regional Laboratories Region Skåne, Lund, Sweden.
Lund University · SELinköping University Hospital · SESkåne University Hospital · SEUmeå University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the favorable prognosis of childhood acute lymphoblastic leukemia (ALL), a substantial subset of patients relapses. As this occurs not only in the high risk but also in the standard/intermediate groups, the presently used risk stratification is suboptimal. The underlying mechanisms for treatment failure include the presence of genetic changes causing insensitivity to the therapy administered. To identify relapse-associated aberrations, we performed single-nucleotide polymorphism array analyses of 307 uniformly treated, consecutive pediatric ALL cases accrued during 1992-2011. Recurrent aberrations of 14 genes in patients who subsequently relapsed or had induction failure were detected. Of these, deletions/uniparental isodisomies of ADD3, ATP10A, EBF1, IKZF1, PAN3, RAG1, SPRED1 and TBL1XR1 were significantly more common in B-cell precursor ALL patients who relapsed compared with those remaining in complete remission. In univariate analyses, age (≥10 years), white blood cell counts (>100 × 10(9)/l), t(9;22)(q34;q11), MLL rearrangements, near-haploidy and deletions of ATP10A, IKZF1, SPRED1 and the pseudoautosomal 1 regions on Xp/Yp were significantly associated with decreased 10-year event-free survival, with IKZF1 abnormalities being an independent risk factor in multivariate analysis irrespective of the risk group. Older age and deletions of IKZF1 and SPRED1 were also associated with poor overall survival. Thus, analyses of these genes provide clinically important information.

Indexed as

Gene DeletionAdaptor Proteins, Signal TransducingAdolescentChildChild, PreschoolChromosome AberrationsFemaleGene FrequencyHumansIkaros Transcription FactorInfantInfant, NewbornIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsPolymorphism, Single NucleotideAdaptor Proteins, Signal TransducingIkaros Transcription FactorIKZF1 protein, humanIntracellular Signaling Peptides and ProteinsMembrane ProteinsSPRED1 protein, human

Identifiers

PMID23823658
OpenAlexW2138439953

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.