Evidence map›Paper›PMID 22923493›Full record

ArticleBlood2012

HLA-DP genetic variation, proxies for early life immune modulation and childhood acute lymphoblastic leukemia risk.

Kevin Y Urayama, Anand P Chokkalingam, Catherine Metayer, Xiaomei Ma, Steve Selvin, Lisa F Barcellos, Joseph L Wiemels, John K Wiencke, Malcolm Taylor, Paul Brennan and 5 more

Open access · bronzeAbstract readComparative StudyMulticenter Study
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
3.5field-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

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Infant milk-feeding practices and childhood leukemia: a systematic review.The American journal of clinical nutrition · 2019
    Pooled it
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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

15 authors at 7 institutions in 4 countries.

Kevin Y UrayamaSchool of Public Health, University of California, Berkeley, CA 94704, USA. kurayama@luke.or.jp
Anand P Chokkalingam
Catherine Metayer
Xiaomei Ma
Steve Selvin
Lisa F Barcellos
Joseph L Wiemels
John K Wiencke
Malcolm Taylor
Paul Brennan
Gary V Dahl
Priscilla Moonsamy
Henry A Erlich
Elizabeth Trachtenberg
Patricia A Buffler
University of California, Berkeley · USUniversity of California, San Francisco · USCentre international de recherche sur le cancer · FRLife Science Institute · JPStanford University · USUniversity of Manchester · GBYale University · US

Funding

Training CoreP42ES004705 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI MCHALE, CLIONA · 1987 to 2025
$74.6M
Environmental and Molecular Epidemiology of Childhood LeukemiaR01ES009137 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI METAYER, CATHERINE · 1999 to 2013
$21.1M
MHC Genetic Variation, Exposure to Infections and Risk of Childhood LeukemiaR03CA125823 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI BUFFLER, PATRICIA A · 2007 to 2008
$123k
NCI NIH HHS R03 CA125823NCI NIH HHS R03CA125823NIEHS NIH HHS P42ES0470518NIEHS NIH HHS R01 ES009137NIEHS NIH HHS R01ES09137
6 · The paper itself

Abstract

The human leukocyte antigen (HLA) genes are candidate genetic susceptibility loci for childhood acute lymphoblastic leukemia (ALL). We examined the effect of HLA-DP genetic variation on risk and evaluated its potential interaction with 4 proxies for early immune modulation, including measures of infectious exposures in infancy (presence of older siblings, daycare attendance, ear infections) and breastfeeding. A total of 585 ALL cases and 848 controls were genotyped at the HLA-DPA1 and DPB1 loci. Because of potential heterogeneity in effect by race/ethnicity, we included only non-Hispanic white (47%) and Hispanic (53%) children and considered these 2 groups separately in the analysis. Logistic regression analyses showed an increased risk of ALL associated with HLA-DPB1*01:01 (odds ratio [OR] = 1.43, 95% CI, 1.01-2.04) with no heterogeneity by Hispanic ethnicity (P = .969). Analyses of DPB1 supertypes showed a marked childhood ALL association with DP1, particularly for high-hyperdiploid ALL (OR = 1.83; 95% CI, 1.20-2.78). Evidence of interaction was found between DP1 and older sibling (P = .036), and between DP1 and breastfeeding (P = .094), with both showing statistically significant DP1 associations within the lower exposure categories only. These findings support an immune mechanism in the etiology of childhood ALL involving the HLA-DPB1 gene in the context of an insufficiently modulated immune system.

Indexed as

Immunologic FactorsAdolescentAdultCase-Control StudiesChildChild, PreschoolFemaleGenetic Predisposition to DiseaseGenetic VariationGenotypeHispanic or LatinoHLA-DP alpha-ChainsHLA-DP beta-ChainsHumansInfantMaleHLA-DPA1 antigenHLA-DP alpha-ChainsHLA-DPB1 antigenHLA-DP beta-ChainsImmunologic Factors

Identifiers

PMID22923493
PMCPMC3471514
OpenAlexW2076640961

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.