OBJECTIVE Health disparities in access to care, early detection, and survival exist among adult patients with cancer. However, there have been few reports assessing how health disparities impact pediatric patients with malignancies. The objective in this study was to examine the impact of racial/ethnic and social factors on disease presentation and outcome for children with primary CNS solid tumors. METHODS The authors examined all children (age ≤ 18 years) in whom CNS solid tumors were diagnosed and who were enrolled in the Texas Cancer Registry between 1995 and 2009 (n = 2421). Geocoded information was used to calculate the driving distance between a patient's home and the nearest pediatric cancer treatment center. Socioeconomic status (SES) was determined using the Agency for Healthcare Research and Quality formula and 2007–2011 US Census block group data. Logistic regression was used to determine factors associated with advanced-stage disease. Survival probability and hazard ratios were calculated using life table methods and Cox regression. RESULTS Children with advanced-stage CNS solid tumors were more likely to be < 1 year old, Hispanic, and in the lowest SES quartile (all p < 0.05). The adjusted odds ratios of presenting with advanced-stage disease were higher in children < 1 year old compared with children > 10 years old (OR 1.71, 95% CI 1.06–2.75), and in Hispanic patients compared with non-Hispanic white patients (OR 1.56, 95% CI 1.19–2.04). Distance to treatment and SES did not impact disease stage at presentation in the adjusted analysis. Furthermore, 1- and 5-year survival probability were worst in children 1–10 years old, Hispanic patients, non-Hispanic black patients, and those in the lowest SES quartile (p < 0.05). In the adjusted survival model, only advanced disease and malignant behavior were predictive of mortality. CONCLUSIONS Racial/ethnic disparities are associated with advanced-stage disease presentation for children with CNS solid tumors. Disease stage at presentation and tumor behavior are the most important predictors of survival.

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Ninety-six parents in a preschool and pediatric clinic participated in a randomized study of a brief parenting intervention. The Attitudes Toward Spanking (ATS) scale was measured at baseline, and, on average, 4 months postintervention. Higher ATS scores are correlated with increased use of physical punishment. In the intervention group, there was a 2.7-point decrease in the ATS score at follow-up compared with baseline (P = 0.01). There was no decrease in the ATS in the control group. Brief interventions may shift parental attitudes toward using less physical punishment and have implications for improving anticipatory guidance within primary care and early education.

The purpose of this review is to outline recent advancements in diagnosis, treatment, and prevention of pediatric melanoma. Despite the recent decline in incidence, it continues to be the deadliest form of skin cancer in children and adolescents. Pediatric melanoma presents differently from adult melanoma; thus, the traditional asymmetry, border irregularity, color variegation, diameter >6 mm, and evolution (ABCDE) criteria have been modified to include features unique to pediatric melanoma (amelanotic, bleeding/bump, color uniformity, de novo/any diameter, evolution of mole). Surgical and medical management of pediatric melanoma continues to derive guidelines from adult melanoma treatment. However, more drug trials are being conducted to determine the specific impact of drug combinations on pediatric patients. Alongside medical and surgical treatment, prevention is a central component of battling the incidence, as ultraviolet (UV)-related mutations play a central role in the vast majority of pediatric melanoma cases. Aggressive prevention measures targeting sun safety and tanning bed usage have shown positive sun-safety behavior trends, as well as the potential to decrease melanomas that manifest later in life. As research into the field of pediatric melanoma continues to expand, a prevention paradigm needs to continue on a community-wide level.

Summary Interactions in the tumour microenvironment can promote chronic lymphocytic leukaemia (CLL) cell survival, proliferation and drug resistance. A detailed comparison of three co‐culture systems designed to mimic the CLL lymph node and vascular microenvironments were performed; two were mouse fibroblast cell lines transfected with human CD40LG or CD31 and the third was a human microvascular endothelial cell line, HMEC‐1. All three co‐culture systems markedly enhanced CLL cell survival and induced a consistent change in CLL cell phenotype, characterized by increased expression of CD38, CD69, CD44 and ITGA4 (CD49d); this phenotype was absent following co‐culture on untransfected mouse fibroblasts. In contrast to HMEC‐1 cells, the CD40LG and CD31‐expressing fibroblasts also induced ZAP70 expression and marked CLL cell proliferation as evidenced by carboxyfluorescein succinimidyl ester labelling and increased Ki‐67 expression. Taken together, our data show that co‐culture on different stroma induced a remarkably similar activation phenotype in CLL cells but only the CD40LG and CD31‐expressing fibroblasts increased ZAP70 expression and CLL cell proliferation, indicating that ZAP70 may play a critical role in this process. This comparative study reveals a number of striking similarities between the co‐culture systems tested but also highlights important differences that should be considered when selecting which system to use for in‐vitro investigations.

Prognostic and epidemiology study, level III.

Background: Colorectal cancer is the second most common cause of cancer related death in the developed world. To date, no blood or stool biomarkers with both high sensitivity and specificity for potentially curable early stage disease have been validated for clinical use. SELDI and MALDI profiling are being used increasingly to search for biomarkers in both blood and urine. Both techniques provide information predominantly on the low molecular weight proteome (<15 kDa). There have been several reports that colorectal cancer is associated with changes in the serum proteome that are detectable by SELDI and we hypothesised that proteomic changes would also be detectable in urine.

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