Gregory A Yanik1, Marguerite T Parisi2,3, Arlene Naranjo4, Helen Nadel5, Michael J Gelfand6, Julie R Park3, Ruth L Ladenstein7, Ulrike Poetschger8, Ariane Boubaker9, Dominique Valteau-Couanet10, Bieke Lambert11, Maria-Rita Castellani12, Zvi Bar-Sever13, Aurore Oudoux14, Anna Kaminska15, Susan G Kreissman16, Barry L Shulkin17, Katherine K Matthay18. 1. Department of Pediatrics and Communicable Diseases, University of Michigan Medical Center, Ann Arbor, Michigan gyanik@umich.edu. 2. Department of Radiology, University of Washington School of Medicine/Seattle Children's Hospital, Seattle, Washington. 3. Department of Pediatrics, University of Washington School of Medicine/Seattle Children's Hospital, Seattle, Washington. 4. Children's Oncology Group Statistics and Data Center, University of Florida, Gainesville, Florida. 5. Department of Radiology, BC Children's Hospital, Vancouver, British Columbia, Canada. 6. Department of Radiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. 7. Department of Pediatrics, St. Anna Children's Hospital, Vienna, Austria. 8. Department of Statistics, St. Anna Children's Cancer Research Institute, Vienna, Austria. 9. Institute of Radiology, Clinique de La Source, Lausanne, Switzerland. 10. Department of Pediatric and Adolescent Oncology, Gustave Roussy Institute, Universite Paris-Sud, Villejuif, France. 11. Radiology and Nuclear Medicine, Ghent University, Ghent, Belgium. 12. Nuclear Medicine Division, Istituto Nazionale Tumori di Milano, Milan, Italy. 13. Schneider Children's Medical Center of Israel, Petah-Tivka, Israel. 14. Centre Oscar-Lambret, Lille, France. 15. Children's Memorial Health Institute, Warsaw, Poland. 16. Department of Pediatrics, Duke University Medical Center, Durham, North Carolina. 17. Department of Diagnostic Imaging, St. Jude Children's Research Hospital, Memphis, Tennessee; and. 18. Department of Pediatrics, University of California San Francisco School of Medicine, San Francisco, California.
Abstract
A semiquantitative 123I-metaiodobenzylguanidine (123I-MIBG) scoring method (the Curie score, or CS) was previously examined in the Children's Oncology Group (COG) high-risk neuroblastoma trial, COG A3973, with a postinduction CS of more than 2 being associated with poor event-free survival (EFS). The validation of the CS in an independent dataset, International Society of Paediatric Oncology European Neuroblastoma/High-Risk Neuroblastoma 1 (SIOPEN/HR-NBL1), is now reported. Methods: A retrospective analysis of 123I-MIBG scans obtained from patients who had been prospectively enrolled in SIOPEN/HR-NBL1 was performed. All patients exhibited 123I-MIBG-avid, International Neuroblastoma Staging System stage 4 neuroblastoma. 123I-MIBG scans were evaluated at 2 time points, diagnosis (n = 345) and postinduction (n = 330), before consolidation myeloablative therapy. Scans of 10 anatomic regions were evaluated, with each region being scored 0-3 on the basis of disease extent and a cumulative CS generated. Cut points for outcome analysis were identified by Youden methodology. CSs from patients enrolled in COG A3973 were used for comparison. Results: The optimal cut point for CS at diagnosis was 12 in SIOPEN/HR-NBL1, with a significant outcome difference by CS noted (5-y EFS, 43.0% ± 5.7% [CS ≤ 12] vs. 21.4% ± 3.6% [CS > 12], P < 0.0001). The optimal CS cut point after induction was 2 in SIOPEN/HR-NBL1, with a postinduction CS of more than 2 being associated with an inferior outcome (5-y EFS, 39.2% ± 4.7% [CS ≤ 2] vs. 16.4% ± 4.2% [CS > 2], P < 0.0001). The postinduction CS maintained independent statistical significance in Cox models when adjusted for the covariates of age and MYCN gene copy number. Conclusion: The prognostic significance of postinduction CSs has now been validated in an independent cohort of patients (SIOPEN/HR-NBL1), with a postinduction CS of more than 2 being associated with an inferior outcome in 2 independent large, cooperative group trials.
A semiquantitative 123I-metaiodobenzylguanidine (123I-MIBG) scoring method (the Curie score, or CS) was previously examined in the Children's Oncology Group (COG) high-risk neuroblastoma trial, COG A3973, with a postinduction CS of more than 2 being associated with poor event-free survival (EFS). The validation of the CS in an independent dataset, International Society of Paediatric Oncology European Neuroblastoma/High-Risk Neuroblastoma 1 (SIOPEN/HR-NBL1), is now reported. Methods: A retrospective analysis of 123I-MIBG scans obtained from patients who had been prospectively enrolled in SIOPEN/HR-NBL1 was performed. All patients exhibited 123I-MIBG-avid, International Neuroblastoma Staging System stage 4 neuroblastoma. 123I-MIBG scans were evaluated at 2 time points, diagnosis (n = 345) and postinduction (n = 330), before consolidation myeloablative therapy. Scans of 10 anatomic regions were evaluated, with each region being scored 0-3 on the basis of disease extent and a cumulative CS generated. Cut points for outcome analysis were identified by Youden methodology. CSs from patients enrolled in COG A3973 were used for comparison. Results: The optimal cut point for CS at diagnosis was 12 in SIOPEN/HR-NBL1, with a significant outcome difference by CS noted (5-y EFS, 43.0% ± 5.7% [CS ≤ 12] vs. 21.4% ± 3.6% [CS > 12], P < 0.0001). The optimal CS cut point after induction was 2 in SIOPEN/HR-NBL1, with a postinduction CS of more than 2 being associated with an inferior outcome (5-y EFS, 39.2% ± 4.7% [CS ≤ 2] vs. 16.4% ± 4.2% [CS > 2], P < 0.0001). The postinduction CS maintained independent statistical significance in Cox models when adjusted for the covariates of age and MYCN gene copy number. Conclusion: The prognostic significance of postinduction CSs has now been validated in an independent cohort of patients (SIOPEN/HR-NBL1), with a postinduction CS of more than 2 being associated with an inferior outcome in 2 independent large, cooperative group trials.
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