Fetal growth and risk of childhood acute lymphoblastic leukemia: results from an Australian case-control study

E Milne1, J A Royle, N H de Klerk

  • 1Centre for Child Health Research, Telethon Institute for Child Health Research, University of Western Australia, Perth, Western Australia, Australia. lizm@ichr.uwa.edu.au

Insights

Faster fetal growth, measured by optimal birth weight, is linked to increased risk of childhood acute lymphoblastic leukemia. This finding suggests accelerated growth, not just high birth weight, plays a role.

Area of Science:

  • Pediatric Oncology
  • Reproductive Epidemiology
  • Growth Factor Biology

Background:

  • Childhood acute lymphoblastic leukemia (ALL) is the most common childhood cancer.
  • Intrauterine growth patterns may influence childhood cancer risk.
  • The role of fetal growth in ALL etiology requires further investigation.

Purpose of the Study:

  • To investigate the association between intrauterine growth and the risk of childhood acute lymphoblastic leukemia (ALL).
  • To determine if accelerated fetal growth, independent of birth weight, is a risk factor for ALL.

Main Methods:

  • Population-based case-control study in Australia (2003-2006).
  • Included 347 childhood ALL cases and 762 controls (<15 years).
  • Assessed proportion of optimal birth weight via maternal questionnaires and analyzed using logistic regression.

Main Results:

  • A positive association was found between proportion of optimal birth weight and ALL risk (OR=1.18 per SD increase).
  • The association persisted even in children without high birth weight, indicating accelerated growth is key.
  • Similar associations were observed across sexes, age groups, and ALL subtypes.

Conclusions:

  • Accelerated fetal growth, indicated by a higher proportion of optimal birth weight, is associated with an increased risk of childhood ALL.
  • Findings support the hypothesis that insulin-like growth factors may be involved in the causal pathway of ALL.
  • This study confirms previous research linking rapid fetal growth to subsequent ALL risk.