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Healthcare utilization disparities among children with high-risk neuroblastoma treated on Children's Oncology Group
Jamie Shoag1, Yimei Li2, Kelly D Getz2,3
1Division of Pediatric Hematology and Oncology, Department of Pediatrics, Cleveland Clinic, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA.
Insights
Hispanic children with high-risk neuroblastoma (HRNBL) experienced more intensive care unit (ICU) admissions, suggesting treatment toxicity may drive survival disparities. Further research is needed to address these inequities.
Area of Science:
- Pediatric Oncology
- Health Disparities Research
- Clinical Toxicology
Background:
- Persistent survival and relapse disparities exist for high-risk neuroblastoma (HRNBL) in marginalized populations.
- Differential treatment toxicity is a potential driver of these disparities in other cancers.
- Understanding racial and ethnic differences in HRNBL treatment toxicity is crucial.
Purpose of the Study:
- To investigate racial and ethnic disparities in treatment-associated toxicity among children with HRNBL.
- To examine intensive care unit (ICU)-level care utilization as a proxy for toxicity.
- To identify potential mechanisms underlying outcome disparities in HRNBL.
Main Methods:
- Retrospective analysis of a merged cohort from Children's Oncology Group (COG) trials ANBL0032 and ANBL0931 (2005-2014).
- Categorization of race-ethnicity: Hispanic, non-Hispanic Black (NHB), non-Hispanic Other (NHO), and non-Hispanic White (NHW).
- Log binomial regression used to assess associations between race-ethnicity and ICU-level care, reporting risk ratios (RR) and 95% confidence intervals (CI).
Main Results:
- The study included 370 children with HRNBL.
- Hispanic children showed a significantly higher risk of ICU-level care (aRR 2.5, 95% CI: 1.6-3.7) compared to non-Hispanic White (NHW) children.
- Hispanic children had the highest incidence of cardiovascular-driven ICU-level care.
Conclusions:
- Hispanic children with HRNBL receiving clinical trial therapy were more likely to require ICU-level care.
- These findings highlight the need to investigate treatment-related toxicity as a factor in outcome disparities.
- Further research into modifiable mechanisms is warranted to address HRNBL survival inequities.
Introduction:
Disparities in relapse and survival from high-risk neuroblastoma (HRNBL) persist among children from historically marginalized groups even in highly standardized clinical trial settings. Research in other cancers has identified differential treatment toxicity as one potential underlying mechanism. Whether racial and ethnic disparities in treatment-associated toxicity exist in HRNBL is poorly understood.
Methods:
This is a retrospective study utilizing a previously assembled merged cohort of children with HRNBL on Children's Oncology Group (COG) post-consolidation immunotherapy trials ANBL0032 and ANBL0931 at Pediatric Health Information System (PHIS) centers from 2005 to 2014. Race and ethnicity were categorized to reflect historically marginalized populations as Hispanic, non-Hispanic Black (NHB), non-Hispanic other (NHO), and non-Hispanic White (NHW). Associations between race-ethnicity and intensive care unit (ICU)-level care utilization as a proxy for treatment-associated toxicity were examined with log binomial regression and summarized as risk ratio (RR) and corresponding 95% confidence interval (CI).
Results:
The analytic cohort included 370 children. Overall, 88 (23.8%) patients required ICU-level care for a median of 3.0 days (interquartile range [IQR]: 1.0-6.5 days). Hispanic children had nearly three times the risk of ICU-level care (RR 3.1, 95% CI: 2.1-4.5; fully adjusted RR [aRR] 2.5, 95% CI: 1.6-3.7) compared to NHW children and the highest percentage of children requiring cardiovascular-driven ICU-level care.
Conclusion:
Children of Hispanic ethnicity with HRNBL receiving clinical trial-delivered therapy were more likely to experience ICU-level care compared to NHW children. These data suggest that further investigation of treatment-related toxicity as a modifiable mechanism underlying outcome disparities is warranted.
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