Abstract 665: Association between early life factors and childhood rhabdomyosarcoma

Abstract

Abstract Background: Rhabdomyosarcoma (RMS) is the most common type of soft-tissue sarcoma among 0-19 year olds, with the incidence rate highest among children of ages 0-4. Since, childhood cancers tend to have relatively shorter lag time between exposure and disease, early childhood cancer such as RMS could be due to exposures during pregnancy or early infancy. Very little is known about environmental factors that may increase the susceptibility to RMS. Two major subtypes_embryonal and alveolar_have been linked with overexpression of the gene encoding insulin-like growth factor 2 (IFG2), which is also associated with fetal overgrowth syndrome. A couple of studies have suggested accelerated fetal growth as a risk factor, but needs to be confirmed. We examined associations between fetal growth measures and all RMS, and separately for the two major subtypes. We also examined other prenatal/perinatal factors including prenatal care, parental age, and parity. Methods: We conducted a population based case-control study in California by linking California Cancer registry and birth certificate data. Incident cases in children 0-5 ages (overall n=359, embryonal RMS=218, alveolar RMS=81) diagnosed in 1988-2008 and controls, frequency matched on birth year (1986-2007, n=205,230) were included. Logistic regression was applied to examine the associations of interest in crude and adjusted models. Results: The point estimates in adjusted models suggested an increased risk for embryonal RMS for all fetal growth measures employed, i.e., high birthweight (4000-5250 gms) at term births only, for high birth weight (4000-5250 gms) adjusted for gestational age, and large for gestational age births (OR (95%CI): 1.28 (0.85, 1.92); 1.21 (0.81, 1.81); 1.13 (0.73, 1.75) respectively), but not for alveolar RMS or overall RMS cases. We found increased risk for alveolar RMS among those with prenatal care starting after the first trimester or no care at all compared to prenatal care in the first trimester (OR(95%CI): 1.68 (1.01, 2.80)). Findings for other factors including higher risk among male and higher parental age at child birth were consistent with findings from existing studies. Conclusion: We did not find a convincingly positive association between fetal growth and RMS, although our data suggested small risk increases particularly for embryonal RMS. However, our findings on starting time of prenatal care and parental age at childbirth further support the notion that the early fetal/embryonic environment may be important for developing RMS in early childhood. Larger studies examining well-measured early life environment that may cause genetic and epigenetic alteration observed in RMS cases are needed to improve our understanding of the RMS etiology. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 665. doi:1538-7445.AM2012-665