Evidence map›Paper›PMID 18185524›Full record

ArticleLeukemia2008

Cooperative genetic defects in TLX3 rearranged pediatric T-ALL.

P Van Vlierberghe, I Homminga, L Zuurbier, J Gladdines-Buijs, E R van Wering, M Horstmann, H B Beverloo, R Pieters, J P P Meijerink

Abstract read
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In one paragraph

Article in Leukemia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.8field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
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  8. Enhancer Hijacking Drives OncogenicCancer discovery · 2021
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  10. Bcl11b/Ctip2 in Skin, Tooth, and Craniofacial System.Frontiers in cell and developmental biology · 2020
    Review
  11. Haematologica · 2018
    Article
  12. Article
  13. FBXW7 negatively regulates ENO1 expression and function in colorectal cancer.Laboratory investigation; a journal of technical methods and pathology · 2015
    Article
  14. Acute lymphoblastic leukaemia.Lancet (London, England) · 2013
    Review
  15. Article
  16. Review
  17. Genomic profiling of B-progenitor acute lymphoblastic leukemia.Best practice & research. Clinical haematology · 2011
    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

9 authors at 3 institutions in 1 country.

P Van VlierbergheDepartment of Pediatric Oncology/Hematology, Erasmus MC/Sophia Children's Hospital, Rotterdam, The Netherlands.
I Homminga
L Zuurbier
J Gladdines-Buijs
E R van Wering
M Horstmann
H B Beverloo
R Pieters
J P P Meijerink
Erasmus MC - Sophia Children’s Hospital · NLErasmus MC · NLStichting Kinderoncologie Nederland · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes. About 20% of pediatric T-ALL cases are characterized by TLX3 expression due to a cryptic translocation t(5;14)(q35;q32). Although a number of collaborating genetic events have been identified in TLX3 rearranged T-ALL patients (NOTCH1 mutations, p15/p16 deletions, NUP214-ABL1 amplifications), further elucidation of additional genetic lesions could provide a better understanding of the pathogenesis of this specific T-ALL subtype. In this study, we used array-CGH to screen TLX3 rearranged T-ALL patients for new chromosomal imbalances. Array-CGH analysis revealed five recurrent genomic deletions in TLX3 rearranged T-ALL, including del(1)(p36.31), del(5)(q35), del(13)(q14.3), del(16)(q22.1) and del(19)(p13.2). From these, the cryptic deletion, del(5)(q35), was exclusively identified in about 25% of TLX3 rearranged T-ALL cases. In addition, 19 other genetic lesions were detected once in TLX3 rearranged T-ALL cases, including a cryptic WT1 deletion and a deletion covering the FBXW7 gene, an U3-ubiquitin ligase that mediates the degradation of NOTCH1, MYC, JUN and CyclinE. This study provides a genome-wide overview of copy number changes in TLX3 rearranged T-ALL and offers great new challenges for the identification of new target genes that may play a role in the pathogenesis of T-ALL.

Indexed as

Chromosome AberrationsSequence DeletionCell Cycle ProteinsChildDNA Mutational AnalysisF-Box ProteinsF-Box-WD Repeat-Containing Protein 7Gene DosageGene RearrangementGenome, HumanHomeodomain ProteinsHumansIn Situ Hybridization, FluorescenceLeukemia-Lymphoma, Adult T-CellUbiquitin-Protein LigasesWT1 ProteinsCell Cycle ProteinsF-Box ProteinsF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanHomeodomain ProteinsTLX3 protein, humanUbiquitin-Protein LigasesWT1 Proteins

Identifiers

PMID18185524
OpenAlexW1981915151

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.