Evidence map›Paper›PMID 27279837›Full record

ArticleArchives of medical science : AMS2016

Analysis of possible genetic risk factors contributing to development of childhood acute lymphoblastic leukaemia in the Latvian population.

Madara Kreile, Linda Piekuse, Dmitrijs Rots, Zane Dobele, Zhanna Kovalova, Baiba Lace

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Archives of medical science : AMS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 6 pooled it
3.3field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 6 syntheses or guidelines pooled it, 26 citations in OpenAlex.

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  14. Is There Etiologic Heterogeneity between Subtypes of Childhood Acute Lymphoblastic Leukemia? A Review of Variation in Risk by Subtype.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019
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  16. Genetic susceptibility in childhood acute lymphoblastic leukemia.Medical oncology (Northwood, London, England) · 2017
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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

6 authors at 3 institutions in 1 country.

Madara KreileScientific Laboratory of Molecular Genetics, Riga Stradiņš University, Riga, Latvia; Institute of Oncology, Riga Stradiņš University, Riga, Latvia.
Linda PiekuseScientific Laboratory of Molecular Genetics, Riga Stradiņš University, Riga, Latvia.
Dmitrijs RotsScientific Laboratory of Molecular Genetics, Riga Stradiņš University, Riga, Latvia.
Zane DobeleScientific Laboratory of Molecular Genetics, Riga Stradiņš University, Riga, Latvia.
Zhanna KovalovaDepartment of Hematology and Oncology, Children's Clinical University Hospital, Riga, Latvia.
Baiba LaceLatvian Biomedical Research and Study Centre, Riga, Latvia.
Riga Stradiņš University · LVChildren's Clinical University Hospital · LVLatvian Biomedical Research and Study Centre · LV

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionChildhood acute lymphoblastic leukaemia (ALL) is a complex disease caused by a combination of genetic susceptibility and environmental exposure. Previous genome-wide association studies have reported several single nucleotide polymorphisms (SNPs) associated with the incidence of ALL. Several variations in genes encoding enzymes involved in carcinogenesis are suggested as being associated with an increased risk of ALL development. MATERIAL AND

methodsWe enrolled 77 paediatric ALL patients and 122 healthy controls, and in addition parental DNA was also available for 45 probands. SNPs rs10821936 (ARID5B), rs4132601 (IKZF1), rs2239633 (CEBPE), rs3731217 (CDKN2A) and rs1800566 (NQO1) and the presence of GSTT1 and GSTM1 null variants were detected. For statistical analysis the hybrid method of two designs 'Haplin' was used as well as linkage disequilibrium for family-based association studies.

resultsWe identified the SNP rs10821936 in the ARID5B gene as being statistically significantly associated with childhood ALL, especially if the C allele is in a homozygous state, relative risk (RR) 4.65, 95% CI: 2.03-10.6, p = 0.0006. Statistically significant differences were not found in other SNPs. We found risk combinations including all five variations, the strongest association being found in a combination where all five genetic variants are in a homozygous state, CCTTTTTTCC, p = 0.032.

conclusionsThe identified SNP rs10821936 could serve as a potential risk marker for childhood ALL development. Further studies in an independent population are needed for verification.

Indexed as

ARID5Bchildhood acute lymphoblastic leukaemiaIKZF1single nucleotide polymorphisms

Identifiers

PMID27279837
PMCPMC4889682
OpenAlexW2408312993

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.