Evidence map›Paper›PMID 22878902›Full record

ArticleCancer causes & control : CCC2012

Fetal growth and body size genes and risk of childhood acute lymphoblastic leukemia.

Anand P Chokkalingam, Catherine Metayer, Ghislaine Scelo, Jeffrey S Chang, Joshua Schiffman, Kevin Y Urayama, Xiaomei Ma, Helen M Hansen, James H Feusner, Lisa F Barcellos and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer causes & control : CCC, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 2 pooled it
2.6field-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

11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 16 citations in OpenAlex.

  1. Pooled it
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  3. Review
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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

13 authors at 8 institutions in 3 countries.

Anand P ChokkalingamSchool of Public Health, University of California Berkeley, Berkeley, CA, USA. anandc@berkeley.edu
Catherine Metayer
Ghislaine Scelo
Jeffrey S Chang
Joshua Schiffman
Kevin Y Urayama
Xiaomei Ma
Helen M Hansen
James H Feusner
Lisa F Barcellos
John K Wiencke
Joseph L Wiemels
Patricia A Buffler
Berkeley Public Health Division · USCentre International de Recherche sur le Cancer · FRUniversity of California, San Francisco · USNational Health Research Institutes · TWNeurological Surgery · USUniversity of California, Berkeley · USUniversity of Utah · USYale University · US

Funding

Training CoreP42ES004705 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI MORELLO-FROSCH, RACHEL ADELE · 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
NIEHS NIH HHS P42 ES004705NIEHS NIH HHS PS42ES04705NIEHS NIH HHS R01 ES009137NIEHS NIH HHS R01ES09137
6 · The paper itself

Abstract

Accumulating evidence suggests that childhood acute lymphoblastic leukemia (ALL) may be initiated in utero or early in the postnatal period. High birth weight (or rapid fetal growth) is associated with risk of ALL, but the mechanisms are not understood. In a population-based epidemiologic study of childhood ALL, we utilized a haplotype-based approach to assess the role of eight genes involved in fetal growth and body size regulation in 377 childhood ALL cases and 448 controls. We found significant haplotype associations with risk of childhood ALL for IGF1 among non-Hispanics and Hispanics together (p = 0.002), for IGF2 among Hispanics (p = 0.040), and for IGF2R among Hispanics and non-Hispanics (p = 0.051 and 0.009, respectively). No haplotype associations were observed for IGF1R or the studied genes involved in body size regulation, including LEP, LEPR, GHRL, and NPY. Our study is the first to identify an association between the genes involved in the IGF axis and risk of childhood ALL. These findings for childhood ALL emphasize the importance of fetal growth, when lymphoid progenitor cells are not yet fully differentiated and therefore more susceptible to malignant transformation. Additional studies are needed to confirm these findings and identify specific causal variants.

Indexed as

AdolescentBirth WeightBody SizeCase-Control StudiesChildChild, PreschoolFemaleFetal DevelopmentHaplotypesHumansInfantInsulin-Like Growth Factor IInsulin-Like Growth Factor IIMalePrecursor Cell Lymphoblastic Leukemia-LymphomaReceptor, IGF Type 1Insulin-Like Growth Factor IInsulin-Like Growth Factor IIReceptor, IGF Type 1

Identifiers

PMID22878902
PMCPMC3415610
OpenAlexW1992811886

What OpenQuestion holds

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LicenceCC BY
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.