Evidence map›Paper›PMID 27229005›Full record

ArticleBlood2016

Integration of genetic and clinical risk factors improves prognostication in relapsed childhood B-cell precursor acute lymphoblastic leukemia.

Julie A E Irving, Amir Enshaei, Catriona A Parker, Rosemary Sutton, Roland P Kuiper, Amy Erhorn, Lynne Minto, Nicola C Venn, Tamara Law, Jiangyan Yu and 12 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
14.2field-weighted citation impact, top 1% 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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.

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  5. Genotype-Specific Minimal Residual Disease Interpretation Improves Stratification in Pediatric Acute Lymphoblastic Leukemia.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2018
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21 more citing papers are in PubMed but not listed here.

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

22 authors at 7 institutions in 4 countries.

Julie A E IrvingNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, United Kingdom;
Amir EnshaeiNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, United Kingdom;
Catriona A ParkerChildren's Cancer Group, Institute of Cancer, Faculty of Medical & Human Sciences, The University of Manchester, Manchester, United Kingdom; Royal Manchester Children's Hospital, Central Manchester University Hospitals Foundation Trust, Manchester Academic Health Science Centre, Manchester, United Kingdom;
Rosemary SuttonChildren's Cancer Institute Australia, Lowy Cancer Research Centre, University of New South Wales, Sydney, Australia;
Roland P KuiperDepartment of Human Genetics, Radboud University Medical Center, Nijmegen, The Netherlands;
Amy ErhornNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, United Kingdom;
Lynne MintoNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, United Kingdom;
Nicola C VennChildren's Cancer Institute Australia, Lowy Cancer Research Centre, University of New South Wales, Sydney, Australia;
Tamara LawChildren's Cancer Institute Australia, Lowy Cancer Research Centre, University of New South Wales, Sydney, Australia;
Jiangyan YuDepartment of Human Genetics, Radboud University Medical Center, Nijmegen, The Netherlands;
Claire SchwabNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, United Kingdom;
Rosanna DaviesNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, United Kingdom;
Elizabeth MathesonNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, United Kingdom;
Alysia DaviesNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, United Kingdom;
Edwin SonneveldDutch Childhood Oncology Group, The Hague, The Netherlands;
Monique L den BoerDutch Childhood Oncology Group, The Hague, The Netherlands; Department of Paediatric Oncology and Haematology, Erasmus MC-Sophia Children's Hospital, University Medical Centre, Rotterdam, The Netherlands;
Sharon B LoveCentre for Statistics in Medicine, University of Oxford, Oxford, United Kingdom;
Christine J HarrisonNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, United Kingdom;
Peter M HoogerbruggeDutch Childhood Oncology Group, The Hague, The Netherlands; Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands;
Tamas ReveszDepartment of Haematology-Oncology, SA Pathology at Women's and Children's Hospital and University of Adelaide, Adelaide, Australia; and.
Vaskar SahaChildren's Cancer Group, Institute of Cancer, Faculty of Medical & Human Sciences, The University of Manchester, Manchester, United Kingdom; Royal Manchester Children's Hospital, Central Manchester University Hospitals Foundation Trust, Manchester Academic Health Science Centre, Manchester, United Kingdom; Tata Translational Cancer Research Centre, Tata Medical Center, New Town, Kolkata, India.
Anthony V MoormanNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, United Kingdom;ORCID 0000-0002-9781-6107
Newcastle University · GBStichting Kinderoncologie Nederland · NLUNSW Sydney · AUManchester Academic Health Science Centre · GBRadboud University Nijmegen · NLSouth Australia Pathology · AUUniversity of Oxford · GB

Funding

Cancer Research UK 14840Cancer Research UK 16895Medical Research Council MC_PC_14101
6 · The paper itself

Abstract

Somatic genetic abnormalities are initiators and drivers of disease and have proven clinical utility at initial diagnosis. However, the genetic landscape and its clinical utility at relapse are less well understood and have not been studied comprehensively. We analyzed cytogenetic data from 427 children with relapsed B-cell precursor ALL treated on the international trial, ALLR3. Also we screened 238 patients with a marrow relapse for selected copy number alterations (CNAs) and mutations. Cytogenetic risk groups were predictive of outcome postrelapse and survival rates at 5 years for patients with good, intermediate-, and high-risk cytogenetics were 68%, 47%, and 26%, respectively (P < .001). TP53 alterations and NR3C1/BTG1 deletions were associated with a higher risk of progression: hazard ratio 2.36 (95% confidence interval, 1.51-3.70, P < .001) and 2.15 (1.32-3.48, P = .002). NRAS mutations were associated with an increased risk of progression among standard-risk patients with high hyperdiploidy: 3.17 (1.15-8.71, P = .026). Patients classified clinically as standard and high risk had distinct genetic profiles. The outcome of clinical standard-risk patients with high-risk cytogenetics was equivalent to clinical high-risk patients. Screening patients at relapse for key genetic abnormalities will enable the integration of genetic and clinical risk factors to improve patient stratification and outcome. This study is registered at www.clinicaltrials.org as #ISCRTN45724312.

Indexed as

Genetic Predisposition to DiseaseAdolescentChildChild, PreschoolChromosome AberrationsCohort StudiesCytogenetic AnalysisDemographyDisease-Free SurvivalDNA Copy Number VariationsFemaleHumansInfantMaleMutationPrecursor B-Cell Lymphoblastic Leukemia-Lymphoma

Identifiers

PMID27229005
PMCPMC5026463
OpenAlexW2405220018

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.