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

Anand P Chokkalingam1, Catherine Metayer, Ghislaine Scelo

  • 1School of Public Health, University of California Berkeley, Berkeley, CA, USA. anandc@berkeley.edu

Cancer Causes & Control : CCC
|August 11, 2012
PubMed

Insights

Genes regulating fetal growth, particularly the Insulin-like Growth Factor (IGF) axis, are linked to childhood acute lymphoblastic leukemia (ALL) risk. This study highlights the importance of early growth in ALL development.

Area of Science:

  • Genetics
  • Pediatric Oncology
  • Epidemiology

Background:

  • Childhood acute lymphoblastic leukemia (ALL) may originate during fetal development.
  • High birth weight is a known risk factor for ALL, but underlying mechanisms remain unclear.

Purpose of the Study:

  • To investigate the association between genes regulating fetal growth and body size and the risk of childhood ALL.
  • To explore the role of the Insulin-like Growth Factor (IGF) axis in ALL etiology.

Main Methods:

  • A population-based epidemiologic study involving 377 childhood ALL cases and 448 controls.
  • Utilized a haplotype-based approach to analyze eight candidate genes involved in fetal growth and body size regulation.
  • Examined associations for IGF1, IGF2, IGF2R, IGF1R, LEP, LEPR, GHRL, and NPY.

Main Results:

  • Significant haplotype associations with childhood ALL risk were found for IGF1 (overall), IGF2 (Hispanics), and IGF2R (Hispanics and non-Hispanics).
  • No significant associations were observed for IGF1R or genes related to body size regulation (LEP, LEPR, GHRL, NPY).
  • This is the first study to link the IGF axis genes to childhood ALL risk.

Conclusions:

  • The findings suggest that genes within the IGF axis play a role in the risk of childhood ALL.
  • Emphasizes the critical window of fetal development for lymphoid progenitor cell susceptibility to malignant transformation.
  • Further research is needed to validate these genetic associations and pinpoint causal variants.

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