Editorial: Multidisciplinary aspects and performance in racket sports-volume III.

Neuroblastoma is the most common extracranial solid tumor of childhood and one of the most biologically heterogeneous pediatric malignancies. It develops from primitive sympathoadrenal progenitor cells derived from the neural crest and encompasses a wide spectrum of clinical presentations, from spontaneous regression and differentiation to benign ganglioneuroma to rapidly progressive metastatic disease with poor survival (, ). Despite significant progress in multimodal therapeutic approaches, high-risk neuroblastoma remains responsible for a disproportionate share of global pediatric cancer mortality, with almost half of all cases classified as high-risk (, ). Neuroblastoma represents approximately 8–10% of all pediatric malignancies and accounts for nearly 15% of pediatric cancer-related fatalities, underscoring its considerable clinical and public health significance (, ). The disease affects mainly infants and young children, with a median age at diagnosis of approximately 17 months; more than 90% of cases are diagnosed before age 5, and it carries a slight male preponderance (, ). Epidemiological analyses reveal significant geographic and socioeconomic variations in incidence, mortality, and disability-adjusted life years (DALYs), highlighting inequalities in diagnostic infrastructure, access to specialist oncology care, and therapeutic outcomes across regions (). The clinical behavior of neuroblastoma is highly heterogeneous and is modulated by complex interactions between developmental biology, genomic instability, epigenetic dysregulation, and tumor microenvironment remodeling (). Historically, prognostication has been driven largely by clinicopathological parameters such as age at diagnosis, disease stage, histopathological classification, and MYCN amplification status (). Increasing knowledge of molecular heterogeneity, however, has fundamentally reshaped the understanding of neuroblastoma biology. Diverse oncogenic drivers and prognostic biomarkers have been identified — including ALK mutations, ATRX alterations, TERT rearrangements, segmental chromosomal aberrations, epigenetic signatures, and immune microenvironment-associated pathways — which collectively influence tumor progression, therapeutic resistance, and survival outcomes (, , ). Contemporary therapeutic regimens incorporating intensive chemotherapy, surgery, radiotherapy, autologous stem cell transplantation, differentiation therapy, and anti-GD2 immunotherapy have improved survival in selected patient subsets; however, outcomes for children with high-risk and relapsed disease remain unsatisfactory (). Treatment resistance, relapse, treatment-related toxicities, and intratumoral heterogeneity remain important clinical challenges (, ). Furthermore, conventional diagnostic techniques relying primarily on histopathology and imaging are increasingly recognized as insufficient to fully characterize the dynamic molecular complexity and evolutionary behavior of neuroblastoma.