Evidence map›Paper›PMID 28481918›Full record

ArticlePloS one2017

Confirmation of involvement of new variants at CDKN2A/B in pediatric acute lymphoblastic leukemia susceptibility in the Spanish population.

Angela Gutierrez-Camino, Idoia Martin-Guerrero, Nagore Garcia de Andoin, Ana Sastre, Ana Carbone Bañeres, Itziar Astigarraga, Aurora Navajas, Africa Garcia-Orad

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. The Role ofCancers · 2020
    Review
  10. Article
  11. Article
  12. Genetic susceptibility in childhood acute lymphoblastic leukemia.Medical oncology (Northwood, London, England) · 2017
    Review
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

8 authors at 5 institutions in 1 country.

Angela Gutierrez-CaminoDepartment of Genetics, Physic Anthropology and Animal Physiology, University of the Basque Country, UPV/EHU, Leioa, Spain.
Idoia Martin-GuerreroDepartment of Genetics, Physic Anthropology and Animal Physiology, University of the Basque Country, UPV/EHU, Leioa, Spain.
Nagore Garcia de AndoinDepartment of Pediatrics, University Hospital Donostia, San Sebastian, Spain.
Ana SastreDepartment of Oncohematology, University Hospital La Paz, Madrid, Spain.
Ana Carbone BañeresDepartment of Pediatrics, University Hospital Miguel Servet, Zaragoza, Spain.
Itziar AstigarragaDepartment of Pediatrics, University Hospital Cruces, Barakaldo, Spain.
Aurora NavajasBioCruces Health Research Institute, Barakaldo, Spain.
Africa Garcia-OradDepartment of Genetics, Physic Anthropology and Animal Physiology, University of the Basque Country, UPV/EHU, Leioa, Spain.ORCID http://orcid.org/0000-0002-5575-3080
University of the Basque Country · ESBioCruces Health research Institute · ESBiogipuzkoa Health Research Institute · ESHospital Universitario La Paz · ESHospital Universitario Miguel Servet · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The locus CDKN2A/B (9p21.3), which comprises the tumor suppressors genes CDKN2A and CDKN2B and the long noncoding RNA (lncRNA) known as ANRIL (or CDKN2B-AS), was associated with childhood acute lymphoblastic leukemia (ALL) susceptibility in several genome wide association studies (GWAS). However, the variants associated in the diverse studies were different. Recently, new and independent SNPs deregulating the locus function were also identified in association with ALL risk. This diversity in the results may be explained because different variants in each population could alter CDKN2A/B locus function through diverse mechanisms. Therefore, the aim of this study was to determine whether the annotated risk variants in the CDKN2A/B locus affect the susceptibility of B cell precursor ALL (B-ALL) in our Spanish population and explore if other SNPs altering additional regulatory mechanisms could be also involved. We analyzed the four SNPs proposed by GWAs and two additional SNPs in miRNA binding sites in 217 pediatric patients with B-ALL and 330 healthy controls. The SNPs rs2811712, rs3731249, rs3217992 and rs2811709 were associated with B-ALL susceptibility in our Spanish population. ALL subtypes analyses showed that rs2811712 was associated with B-hyperdiploid ALL. These results provide evidence for the influence of genetic variants at CDKN2A/B locus with the risk of developing B-ALL.

Indexed as

MutationAdolescentChildChild, PreschoolCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18FemaleGenotypeHumansInfantLeukemia, B-CellMalePrecursor Cell Lymphoblastic Leukemia-LymphomaSpainCDKN2A protein, humanCDKN2B protein, humanCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18

Identifiers

PMID28481918
PMCPMC5421813
OpenAlexW2613913182

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.