BACKGROUND. The etiology of most pediatric neoplasms remains elusive. Examination of population-based incidence data provides insight regarding etiology among various demographic groups and may result in new hypotheses. The objective of the current study was to present updated information regarding childhood cancer incidence and trends in the U.S. overall and among demographic subgroups, including Asian/Pacific Islanders and Hispanics, for whom to the authors' knowledge trends have not been previously examined. RESULTS. Between 1992 and 2004, a modest, nonsignificant increase in the averageannual incidence rate (APC, 0.4%; 95% CI, 20.1%-0.8%) was observed for all pediatric cancer diagnoses combined. There was a suggestion of an increase in leukemia (APC, 0.7%; 95% CI, 20.1%-1.5%), and acute lymphoblastic leukemia in particular (APC, 0.8%; 95% CI, 20.4%-1.9%), whereas rates for central nervous system tumors overall were stable (APC, 20.1%; 95% CI, 21.1%-1.0%); 2 joinpoints were observed for astrocytoma. Rate increases were noted for hepatoblastoma (APC, 4.3%; 95% CI, 0.2%-8.7%) and melanoma (APC, 2.8%; 95% CI, 0.5%-5.1%).Differences by demographic group (sex, age, and race/ethnicity) are also described.CONCLUSIONS. The observed trends reinforce an ongoing need for populationbased surveillance and further etiologic studies.

BACKGROUND: Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma in children and adolescents aged <20 years; its etiology remains largely unknown. It is believed that embryonal (ERMS) and alveolar rhabdomyosarcoma (ARMS), the most common subtypes, arise through distinct biologic mechanisms. The authors of this report evaluated incidence and survival trends by RMS demographic subgroups to inform future etiologic hypotheses. METHODS: Incidence and survival trends in RMS among children and adolescents aged <20 years were analyzed using data from the Surveillance, Epidemiology, and End Results Program. Frequencies, age‐adjusted incidence and survival rates, and joinpoint regression results, including annual percentage change (APC) and 95% confidence interval (CI), were calculated. RESULTS: Between 1975 and 2005, the incidence of ERMS was stable, whereas a significant increase in the incidence of ARMS was observed (APC, 4.20%; 95%CI, 2.60%‐5.82%). This trend may have been attributable in part to shifts in diagnosis, because a significant negative trend in RMS, not otherwise specified was observed concurrently. A bimodal age peak for ERMS was observed, with the second, smaller peak in adolescence noted for males only; ARMS incidence did not vary by age or sex. Five‐year survival rates for RMS and ERMS increased during the period from 1976 to 1980 (52.7% and 60.9%, respectively) to the period from 1996 to 2000 (61.8% and 73.4%, respectively), whereas there was little improvement for ARMS (40.1% and 47.8%, respectively). CONCLUSIONS: Observed differences in incidence and survival for 2 major RMS subtypes across sex and age subgroups further supported the hypothesis that there are unique underlying etiologies for these tumors. Exploration of these differences presents an opportunity to increase current knowledge of RMS. Cancer 2009. © 2009 American Cancer Society.

BACKGROUND. Survival trends provide a measure of improvement in detection and treatment over time. In the current study, updated childhood and adolescent cancer survival statistics are presented, overall and among demographic subgroups, including Hispanics, for whom to the authors' knowledge national rates have not been previously reported. These results extend those provided by the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) program in their detail and interpretation. METHODS. Survival trends of primary cancers in children and adolescents (ages birth to 19 years) were evaluated using SEER 9 data. Five‐year and 10‐year relative survival rates across 5‐year (1975‐1979, 1985‐1989, and 1995‐1999) and 10‐year (1975‐1984 and 1985‐1994) cohorts were compared via Z‐tests. Annual percent change (APC) in survival was computed via weighted least‐squares regression. Rates in Hispanic children and adolescents were compared with those in non‐Hispanic whites and blacks (SEER 13, 1995‐1999). RESULTS. Five‐year survival rates increased significantly overall (1975‐1979: 63% vs 1995‐1999: 79%; P < .0001) and for nearly all histologic types examined; increases were greatest for ependymoma (+37%; P < .0001) and non‐Hodgkin lymphoma (+34%; P < .0001). Hispanic children and adolescents had somewhat poorer 5‐year rates than non‐Hispanic whites overall (74% vs 81%; P < .0001) and for Ewing sarcoma, leukemia, central nervous system tumors, and melanoma. Ten‐year rates also increased significantly overall (1975‐1984: 61% vs 1985‐1994: 72%; P < .0001) and for a majority of cancer types. The largest improvements were noted for acute lymphoblastic leukemia (+19%; P < .0001) and non‐Hodgkin lymphoma (+19%; P < .0001). CONCLUSIONS. Observed trends reinforce the need for resources devoted to advancing treatment modalities, reducing disparities among racial/ethnic groups and adolescents, and providing long‐term care of survivors. Cancer 2008. © 2008 American Cancer Society.

Background/Objective Parental obesity influences infant body size. To fully characterize their relative effects on infant adiposity, associations between maternal and paternal body mass index (BMI) category (normal: ≤25 kg/m2, overweight: 25–<30 kg/m2, obese: ≥30 kg/m2) and infant BMI were compared in Fels Longitudinal Study participants. Methods A median of 9 serial weight and length measures from birth-3.5 years were obtained from 912 European American children born in 1928–2008. Using multivariable mixed effects regression, contributions of maternal versus paternal BMI status to infant BMI growth curves were evaluated. Cubic spline models also included parental covariates, infant sex, age, and birth variables, and interactions with child’s age. Results Infant BMI curves were significantly different across the three maternal BMI categories (POverall<0.0001), and offspring of obese mothers had greater mean BMI at birth and between 1.5–3.5 years than those of over- and normal weight mothers (P≤0.02). Average differences between offspring of obese and normal weight mothers were similar at birth (0.8 kg/m2, P=0.0009) and between 2–3.5 years (0.7–0.8 kg/m2, P<0.0001). Infants of obese fathers also had BMI growth curves distinct from those of normal weight fathers (P=0.02). Infant BMI was more strongly associated with maternal than paternal obesity overall (P<0.0001); significant differences were observed at birth (1.11 kg/m2, P=0.006) and from 2–3 years (0.62 kg/m2, P3years=0.02). Conclusion At birth and in later infancy, maternal BMI has a stronger influence on BMI growth than paternal BMI, suggesting weight control in reproductive age women may be of particular benefit for preventing excess infant BMI.

Atopic disease is hypothesized to be protective against several malignancies, including childhood/adolescent leukemia. To summarize the available epidemiologic evidence, the authors performed a meta-analysis of associations between atopy/allergies, asthma, eczema, hay fever, and hives and childhood/adolescent leukemia, acute lymphoblastic leukemia (ALL), and acute myeloid leukemia (AML). They searched MEDLINE literature (1952-March 2009) and queried international experts to identify eligible studies. Ten case-control studies were included. Summary odds ratios and 95% confidence intervals were computed via random-effects models. Odds ratios for atopy/allergies were 1.42 (95% confidence interval (CI): 0.60, 3.35) for 3 studies of leukemia overall, 0.69 (95% CI: 0.54, 0.89) for 6 studies of ALL, and 0.87 (95% CI: 0.62, 1.22) for 2 studies of AML, with high levels of heterogeneity detected for leukemia overall and ALL. Inverse associations were observed for ALL and asthma (odds ratio (OR) = 0.79, 95% CI: 0.61, 1.02), eczema (OR = 0.74, 95% CI: 0.58, 0.96), and hay fever (OR = 0.55, 95% CI: 0.46, 0.66) examined separately. Odds ratios for ALL differed by study design, exposure data source, and latency period, indicating that these factors affect study results. These results should be interpreted cautiously given the modest number of studies, substantial heterogeneity, and potential exposure misclassification but are useful in designing future research.