Background/Aims: Monitoring overweight prevalence and its trends in Dutch youth is frequently based on self-reported data. The validity of self-reported data especially in young adolescents is not sufficiently known. The purpose of this study is to study the validity of self-reported height and weight in 12- to 13-year-olds, to identify sociodemographic correlates and to explore whether correction factors can be developed to estimate the prevalence of overweight in youth. Methods: 5,525 12- to 13-year-old pupils in the Rotterdam area filled in a confidential questionnaire on health topics, including their height and weight. In a sub-sample of 499 pupils both self-reported and measured height and weight were available. Results: Self-reported data led to a considerable underestimation of Body Mass Index and consequently the prevalence of overweight. Underestimation was higher in pupils who regarded themselves as more fat, were of non-Dutch origin and in lower education levels. Conclusion: Self-reported height and weight appeared to be inappropriate to estimate the overweight prevalence in 12- to 13-year-olds, unless the figures were adjusted. Using adjusted self-reported BMI on an individual level is questionable. Actual measurements of height and weight are necessary to draw up valid correction formulas in new samples.

Purpose: Developing strategies to overcome resistance to sunitinib is a major challenge in human renal cell carcinoma (RCC). We hypothesized that sunitinib-induced tumor necrosis-associated hypoxia could interact with renal cancer stem cells in patients with metastatic RCC.Experimental Design: We studied tissue samples from 7 patients with primary metastatic RCC, before and after sunitinib treatment, and from six xenograft models derived from human RCC. Two xenograft models were responders to sunitinib, the four others were nonresponders. CD133/CXCR4-coexpressing cells derived from the two responder xenograft models were used for in vitro studies.Results: In the seven primary RCCs, we identified a significantly larger number of CD133/CXCR4-coexpressing cells in perinecrotic versus perivascular areas. Their numbers also significantly increased after treatment, in perinecrotic areas. We reproduced these clinical and pathologic results in all six RCC xenograft models with again a preferential perinecrotic distribution of CD133-expressing cells. Necrosis occurred at day 7 in the two responder models treated with sunitinib, whereas it occurred at day 21 in the untreated controls and in the four nonresponder models. Strikingly, when we studied the six RCC xenograft models at the time necrosis, whether spontaneous or sunitinib-induced, occurred, necrosis area correlated with stem-cell number in all 120 xenografted RCCs. When studied under experimental hypoxia, the number of CD133/CXCR4-coexpressing cells and their tumorigenic potency increased whereas their sensitivity to sunitinib decreased.Conclusions: In human RCC, sunitinib was able to generate resistance to its own therapeutic effect via induced hypoxia in perinecrotic areas where cancer stem cells were found in increased numbers.