Childhood cancer risk in those with chromosomal and non-chromosomal congenital anomalies in Washington State: 1984-2013.

BACKGROUND: The presence of a congenital anomaly is associated with increased childhood cancer risk, likely due to large effects of Down syndrome and chromosomal anomalies for leukemia. Less is known about associations with presence of non-chromosomal anomalies. METHODS: Records of children diagnosed with cancer at <20 years of age during 1984-2013 in Washington State cancer registries were linked to their birth certificates (N = 4,105). A comparison group of children born in the same years was identified. Congenital anomalies were assessed from birth records and diagnosis codes in linked hospital discharge data. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) for cancer, and for specific cancer types in relation to the presence of any anomaly and specific anomalies. RESULTS: Having any congenital anomaly was associated with an increased risk of childhood cancer (OR: 1.46, 95% CI 1.28-1.65). Non-chromosomal anomalies were also associated with increased childhood cancer risk overall (OR: 1.35; 95% CI: 1.18-1.54), and with increased risk of several cancer types, including neuroblastoma, renal, hepatoblastoma, soft-tissue sarcoma, and germ cell tumors. Increasing number of non-chromosomal anomalies was associated with a stronger risk of childhood cancer (OR for 3+ anomalies: 3.11, 95% CI: 1.54-6.11). Although central nervous system (CNS) anomalies were associated with CNS tumors (OR: 6.05, 95% CI 2.75-13.27), there was no strong evidence of other non-chromosomal anomalies being specifically associated with cancer occurring in the same organ system or anatomic location. CONCLUSIONS: Non-chromosomal anomalies increased risk of several cancer types. Additionally, we found that increasing number of non-chromosomal anomalies was associated with a stronger risk of cancer. Pooling similar data from many regions would increase power to identify specific associations in order to inform molecular studies examining possible common developmental pathways in the etiologies of birth defects and cancer.

The validity of self-reported behaviors: methods for estimating underreporting of risk behaviors.

PURPOSE: When individuals underreport risk behaviors, data gathered from public health research and practice will underestimate risk. To date, there is little guidance on if or how reports can be adjusted to better reflect true levels of a risk behavior in a given cohort, sample or, by extension, population. METHODS: We develop the underreporting correction factor (UCF), which can be used to correct estimates of the prevalence of a risk behavior using self-report of the behavior and a specific (but not necessarily sensitive) biomarker. The UCF rests on three assumptions: (1) there is no overreporting of the behavior, (2) the biomarker can only be acquired if the person engages in the behavior, and (3) the presence of the biomarker does not affect reporting of the behavior. We investigate the sensitivity of the UCF to violation of these assumptions and develop confidence intervals for the UCF and the corrected prevalence of the behavior. RESULTS: The UCF is most sensitive to the second assumption (biomarker perfectly specific). We apply the UCF to estimates of sexual risk behaviors in various settings using a variety of biomarkers. CONCLUSIONS: Implementation of the UCF corrects for underreporting and more accurately quantifies risk in cohorts.