Personality's voice: how personality traits shape verbal processes in collaborative problem-solving.

Neuroblastoma is the most prevalent extracranial solid tumor in pediatric populations worldwide, representing approximately 8–10% of childhood malignancies and contributing to approximately 15% of pediatric cancer-related fatalities (). Despite intensive multimodal therapy, the disease is characterized by remarkable clinical heterogeneity, with outcomes ranging from spontaneous regression in infants with favorable biology to relentless disease progression. Approximately half of neuroblastoma cases are classified as high risk according to the International Neuroblastoma Risk Group (INRG) classification system, which integrates clinical, histopathological, and molecular parameters for pretreatment risk stratification (). Despite significant advances in multimodal therapeutic approaches, such as induction chemotherapy, surgical resection, myeloablative consolidation with autologous stem cell transplantation, radiotherapy, and maintenance immunotherapy with anti-GD2 monoclonal antibodies, long-term survival for patients with high-risk neuroblastoma remains suboptimal, with contemporary studies reporting a 5-year survival rate of approximately 50% (). Platinum-based compounds, including cisplatin and carboplatin, constitute essential components of all contemporary induction regimens for high-risk neuroblastoma, with alkylator and platinum doublets serving as the therapeutic backbone across multiple international cooperative group protocols (). A recent systematic review of induction regimens published between 1995 and 2024 reported a median study-level end-induction response rate of 84.4%, yet the response rates have not improved substantially over the past three decades despite iterative refinements in dose intensity and schedule (). Furthermore, the end-induction response has been established as a powerful independent predictor of the ultimate outcome, with patients who fail to achieve an objective response to frontline therapy facing a substantially elevated risk of subsequent relapse and death (). While several recurrent genomic alterations, including MYCN amplification and 11q deletion, have been strongly associated with adverse outcomes, the molecular determinants governing differential responses to multiagent induction chemotherapy remain incompletely characterized (). Chromatin remodeling protein alpha-thalassemia/mental retardation syndrome X-linked (ATRX) has emerged as a recurrently altered gene in high-risk neuroblastoma, with mutations occurring in a recognizable patient subgroup characterized by older age at diagnosis, mutual exclusivity with MYCN amplification, and a chemotherapy-resistant, slowly progressive disease course (, ). Critically, recent studies have demonstrated that the ATRX mutational spectrum in neuroblastoma is uniquely enriched for multiexon deletions, with approximately 70% of ATRX aberrations comprising such structural variants, and an estimated 75% of these deletions are predicted to be in-frame alterations that produce internally truncated protein products (, ). This distinctive mutational pattern, which appears nearly exclusive to neuroblastoma compared with other pediatric malignancies, suggests potential functional divergence between mutation subtypes (). Preliminary evidence indicates that patients harboring ATRX missense mutations may exhibit slightly better overall survival than those with other ATRX mutation types and that 11q deletions cooccur more frequently with multiexon deletions than with other ATRX mutation types or wild-type tumors do (, ). Moreover, ATRX aberrations are strongly correlated with alternative lengthening of the telomere pathway, and both ATRX aberrations and TERT rearrangements are enriched in 11q-deleted high-risk tumors ().