Flavonoids comprise the most common group of plant polyphenols and provide much of the flavor and color to fruits and vegetables. More than 5000 different flavonoids have been described. The six major subclasses of flavonoids include the flavones (e.g., apigenin, luteolin), flavonols (e.g., quercetin, myricetin), flavanones (e.g., naringenin, hesperidin), catechins or flavanols (e.g., epicatechin, gallocatechin), anthocyanidins (e.g., cyanidin, pelargonidin), and isoflavones (e.g., genistein, daidzein). Most of the flavonoids present in plants are attached to sugars (glycosides), although occasionally they are found as aglycones. Interest in the possible health benefits of flavonoids has increased owing to their potent antioxidant and free-radical scavenging activities observed in vitro. There is growing evidence from human feeding studies that the absorption and bioavailability of specific flavonoids is much higher than originally believed. However, epidemiologic studies exploring the role of flavonoids in human health have been inconclusive. Some studies support a protective effect of flavonoid consumption in cardiovascular disease and cancer, other studies demonstrate no effect, and a few studies suggest potential harm. Because there are many biological activities attributed to the flavonoids, some of which could be beneficial or detrimental depending on specific circumstances, further studies in both the laboratory and with populations are warranted.

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.

Activation of Wnt signaling through beta-catenin mutations contributes to the development of hepatocellular carcinoma (HCC) and hepatoblastoma (HB). To explore the contribution of additional Wnt pathway molecules to hepatocarcinogenesis, we examined beta-catenin, AXIN1 and AXIN2 mutations in 73 HCCs and 27 HBs. beta-catenin mutations were detected in 19.2% (14 out of 73) HCCs and 70.4% (19 out of 27) HBs. beta-catenin mutations in HCCs were primarily point mutations, whereas more than half of the HBs had deletions. AXIN1 mutations occurred in seven (9.6%) HCCs and two (7.4%) HBs. The AXIN1 mutations included seven missense mutations, a 1 bp deletion, and a 12 bp insertion. The predominance of missense mutations found in the AXIN1 gene is different from the small deletions or nonsense mutations described previously. Loss of heterozygosity at the AXIN1 locus was present in four of five informative HCCs with AXIN1 mutations, suggesting a tumor suppressor function of this gene. AXIN2 mutations were found in two (2.7%) HCCs but not in HBs. Two HCCs had both AXIN1 and beta-catenin mutations, and one HCC had both AXIN2 and beta-catenin mutations. About half the HCCs with AXIN1 or AXIN2 mutations showed beta-catenin accumulation in the nucleus, cytoplasm or membrane. Overall, these data indicate that besides the approximately 20% of HCCs and 80% of HBs with beta-catenin mutations contributing to hepatocarcinogenesis, AXIN1 and AXIN2 mutations appear to be important in an additional 10% of HCCs and HBs.

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-Fruits and vegetables, foods rich in flavonoids and antioxidants, have been associated with lower risk of stroke, coronary heart disease, and markers of inflammation and oxidative stress in adults. Markers of inflammation and oxidative stress are predictors of coronary heart disease risk; however, it is unknown whether these markers are related to dietary flavonoid and antioxidant intake in youth.

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Epidemiologic studies frequently obtain exposure information through subjects' self-report (personal interview or mailed questionnaire). The authors used data from a case-control study of infant leukemia, to assess the validity and reliability of maternally reported information on birth characteristics such as birth weight, reproductive history, and medical procedures. Cases were gathered from the Children's Cancer Group, a United States and Canadian cooperative clinical trails group with approximately 100 member and affiliate institutions, during 1983-1988. Telephone interviews were completed for 302 cases and 558 matched controls. Medical records of the index pregnancy were obtained for 287 cases and 467 controls. Correlations between medical charts and maternal interview were high for birth weight (r = 0.98, kappa = 0.9) and gestational age (r = 0.86, kappa = 0.6). Mean differences between the two sources were small, -10.5 g for birth weight and -0.36 weeks for gestational age. Reproductive history and medical procedures had high to moderate reliability. Problems after delivery and pregnancy complications generally had low validity and reliability. Little evidence of differential misclassification was found. Time between delivery and interview ranged from zero to 8 years and did not greatly affect reliability. This study suggests that validity and reliability of maternally reported pregnancy and delivery information may differ with the nature of the factor of interest, but is affected little by time from birth or case-control status.

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.