Evidence map›Paper›PMID 27419633›Full record

ArticleOncotarget2016

COBL is a novel hotspot for IKZF1 deletions in childhood acute lymphoblastic leukemia.

Bruno Almeida Lopes, Claus Meyer, Thayana Conceição Barbosa, Udo Zur Stadt, Martin Horstmann, Nicola C Venn, Susan Heatley, Deborah L White, Rosemary Sutton, Maria S Pombo-de-Oliveira and 2 more

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

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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

5 citing papers in PubMed.

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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.

Bruno Almeida LopesPediatric Hematology-Oncology Program, Research Center, Instituto Nacional de Câncer, Rio de Janeiro, RJ, Brazil.
Claus MeyerDiagnostic Center of Acute Leukemia/Institute of Pharmaceutical Biology/ZAFES, Goethe-University of Frankfurt, Biocenter, Germany.
Thayana Conceição BarbosaPediatric Hematology-Oncology Program, Research Center, Instituto Nacional de Câncer, Rio de Janeiro, RJ, Brazil.
Udo Zur StadtCenter for Diagnostics, University Medical Center Hamburg Eppendorf, Hamburg, Germany.
Martin HorstmannCenter for Diagnostics, University Medical Center Hamburg Eppendorf, Hamburg, Germany.
Nicola C VennChildren's Cancer Institute, Lowy Cancer Research Centre UNSW, Sydney, New South Wales, Australia.
Susan HeatleySouth Australian Health and Medical Research Institute (SAHMRI), Adelaide, South Australia, Australia.
Deborah L WhiteSouth Australian Health and Medical Research Institute (SAHMRI), Adelaide, South Australia, Australia.
Rosemary SuttonChildren's Cancer Institute, Lowy Cancer Research Centre UNSW, Sydney, New South Wales, Australia.
Maria S Pombo-de-OliveiraPediatric Hematology-Oncology Program, Research Center, Instituto Nacional de Câncer, Rio de Janeiro, RJ, Brazil.
Rolf MarschalekDiagnostic Center of Acute Leukemia/Institute of Pharmaceutical Biology/ZAFES, Goethe-University of Frankfurt, Biocenter, Germany.
Mariana EmerencianoPediatric Hematology-Oncology Program, Research Center, Instituto Nacional de Câncer, Rio de Janeiro, RJ, Brazil.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IKZF1 deletion (ΔIKZF1) is an important predictor of relapse in childhood B-cell precursor acute lymphoblastic leukemia. Because of its clinical importance, we previously mapped breakpoints of intragenic deletions and developed a multiplex PCR assay to detect recurrent intragenic ΔIKZF1. Since the multiplex PCR was not able to detect complete deletions (IKZF1 Δ1-8), which account for ~30% of all ΔIKZF1, we aimed at investigating the genomic scenery of IKZF1 Δ1-8. Six samples of cases with IKZF1 Δ1-8 were analyzed by microarray assay, which identified monosomy 7, isochromosome 7q, and large interstitial deletions presenting breakpoints within COBL gene. Then, we established a multiplex ligation-probe amplification (MLPA) assay and screened copy number alterations within chromosome 7 in 43 diagnostic samples with IKZF1 Δ1-8. Our results revealed that monosomy and large interstitial deletions within chromosome 7 are the main causes of IKZF1 Δ1-8. Detailed analysis using long distance inverse PCR showed that six patients (16%) had large interstitial deletions starting within intronic regions of COBL at diagnosis, which is ~611 Kb downstream of IKZF1, suggesting that COBL is a hotspot for ΔIKZF1. We also investigated a series of 25 intragenic deletions (Δ2-8, Δ3-8 or Δ4-8) and 24 relapsed samples, and found one IKZF1-COBL tail-to-tail fusion, thus supporting that COBL is a novel hotspot for ΔIKZF1. Finally, using RIC score methodology, we show that breakpoint sequences of IKZF1 Δ1-8 are not analog to RAG-recognition sites, suggesting a different mechanism of error promotion than that suggested for intragenic ΔIKZF1.

Indexed as

Gene DeletionAdolescentAmino Acid SequenceBase SequenceChild, PreschoolChromosome BreakpointsChromosome DeletionChromosomes, Human, Pair 7DNA Copy Number VariationsFemaleHumansIkaros Transcription FactorInfantIsochromosomesMaleMicrofilament ProteinsCobl protein, humanIkaros Transcription FactorIKZF1 protein, humanMicrofilament Proteinsacute lymphoblastic leukemiaCOBLIKZF1RAGrelapse

Identifiers

PMID27419633
PMCPMC5288169

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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.