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A child initially treated for neuroblastoma developed treatment-related acute myeloid leukemia (tAML) six years later, with emphasis on how EVI1 disruption accelerates secondary tumor progression. Genetic analysis highlights variations in PTPN11 and KMT2C and suggests interplay between inherited susceptibility and chemotherapy-induced mutagenesis. Discusses relevance of topoisomerase II inhibitors to inform future therapeutic strategies and underscores the importance of early detection and individualized diagnosis to improve long-term prognosis.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/evi1-disruption-post-neuroblastoma-treatment-a-case-analysis-of-treatment-associated-acute-myeloid-leukemia-in-a-pediatric-patient/380564/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/evi1-disruption-post-neuroblastoma-treatment-a-case-analysis-of-treatment-associated-acute-myeloid-leukemia-in-a-pediatric-patient/380564.png","ImageObject",300,407,{"name":92,"@type":93},"Grenda","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-30","2026-09-24",true,{"@type":102,"interactionType":103,"userInteractionCount":44},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What secondary malignancy developed in the pediatric patient after neuroblastoma treatment?","Question",{"text":112,"@type":113},"The patient developed treatment-related acute myeloid leukemia (tAML) six years after completing neuroblastoma therapy.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"Why is EVI1 disruption considered important in this case?",{"text":117,"@type":113},"The study emphasizes that EVI1 disruption plays a crucial role in accelerating the progression of secondary tumors in this patient.",{"name":119,"@type":110,"acceptedAnswer":120},"Which genetic alterations were reported in the case analysis?",{"text":121,"@type":113},"Genetic anomalies included variations in the PTPN11 and KMT2C genes, suggesting a combined effect of genetic susceptibility and chemotherapy-induced mutagenesis.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},380564,1790575282,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":44,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":34,"language":139,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":67,"update_tm":143,"read_time":144},7971474921005,"https://ap-avatar.wpscdn.com/davatar_29158cc5080c5b710cf443261637dec0","Case Reports in Oncology  \n\n| Case Rep Oncol 2023;16:893–899 |  |\n| --- | --- |\n| DOI: 10.1159/000533571\u003Cbr>Received: June 30, 2023\u003Cbr>Accepted: August 8, 2023\u003Cbr>Published online: September 12, 2023 | © 2023 The Author(s) .\u003Cbr>Published by S. Karger AG, Basel [www.karger.com/cro](www.karger.com/cro) |\n\nThis article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC) ([http://www.karger.com/Services/OpenAccessLicense](http://www.karger.com/Services/OpenAccessLicense)). Usage and distribution for commercial purposes requires written permission.  \nCase Report  \nEVI1 Disruption Post Neuroblastoma Treatment: A Case Analysis of Treatment-Associated Acute Myeloid Leukemia in a Pediatric Patient  \nXin Zhang  \nDepartment of Pediatric Hematology and Oncology, Xinhua Hospital Affilliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China  \nKeywords  \nSecond malignant neoplasms · Neuroblastoma · Mutation · Leukemia · Child  \nAbstract  \nIn recent years, there has been an increasing focus on understanding the long-term consequences of pediatric cancer treatments, particularly the emergence of secondary malignant neoplasms (SMNs) . Here, we present a case study highlighting the aftermath of treatment, where a pediatric patient, initially treated for neuroblastoma, developed treatment-related acute myeloid leukemia (tAML) 6 years later. Our investigation emphasizes the crucial role of EVI1 disruption in accelerating the progression of secondary tumors. This case underscores the significant risk of SMNs following pediatric cancer therapy. By analyzing genetic anomalies, weidentified variations in the PTPN11 and KMT2C genes, suggesting a complex interplay between genetic susceptibility and chemotherapy-induced mutagenesis in tAML development. Furthermore, our exploration of the involvement of topoisomerase II inhibitors in tAML provides insights into potential future therapeutic approaches. Reporting this case is vital for deepening our understanding of the mechanisms driving SMNs after pediatric cancer treatments. Through a comprehensive analysis of genetic anomalies and treatment variables, we can offer more precise clinical diagnoses and treatment strategies. This approach holds the potential to reduce the occurrence of secondary tumors and improve the long-term prognosis for pediatric patients.  \n© 2023 The Author(s) .  \nPublished by S. KargerAG, Basel  \nCorrespondence to:  \nXin Zhang, [zxcongufo](zxcongufo@ 163.com)[@](zxcongufo@ 163.com)[ 163.com](zxcongufo@ 163.com)  \nCase Reports in Oncology  \nCase Rep Oncol 2023;16:893–899 894  \n\n| DOI: 10.1159/000533571 | © 2023 The Author(s) . Published by S. Karger AG, Basel [www.karger.com/cro](www.karger.com/cro) |\n| --- | --- |\n\nZhang: tAML after NB Treatment  \nIntroduction  \nWhile the adverse effects of cancer treatment, such as nausea, alopecia, and myelosuppression, are well-known, the emergence of late-term toxicities in long-term cancer survivors poses a more intricate challenge in detection and management. Among these complexities, the emergence of secondary malignant neoplasms (SMNs) stands as a formidable complication. SMNs denote novel malignancies that arise autonomously from the primary ailment, distinct from metastatic tumors [1, 2] . In the cohort of individuals diagnosed with primary malignant neoplasms, SMNs constitute a prominent contributor to non-relapserelated late-stage mortality, accounting for approximately 50% of non-relapse-related deaths in cancer survivors at the 5-year mark [3] . The most robust correlation between chemotherapy and the incidence of SMNs is observed in cases of treatment-related acute myeloid leukemia (tAML) . According to the World Health Organization (WHO), tAML is characterized as a belated consequence of cytotoxic chemotherapy employed for either neoplastic or nonneoplastic conditions. Almost universally, alkylating agents and topoisomerase II inhibitors administered in this therapeuti","cbCaipsQH7Y2INR6","https://ap.wps.com/l/cbCaipsQH7Y2INR6","pdf",415503,"English","# Introduction\n# Case Report\n# Discussion\n# Conclusion","[{\"question\":\"What secondary malignancy developed in the pediatric patient after neuroblastoma treatment?\",\"answer\":\"The patient developed treatment-related acute myeloid leukemia (tAML) six years after completing neuroblastoma therapy.\"},{\"question\":\"Why is EVI1 disruption considered important in this case?\",\"answer\":\"The study emphasizes that EVI1 disruption plays a crucial role in accelerating the progression of secondary tumors in this patient.\"},{\"question\":\"Which genetic alterations were reported in the case analysis?\",\"answer\":\"Genetic anomalies included variations in the PTPN11 and KMT2C genes, suggesting a combined effect of genetic susceptibility and chemotherapy-induced mutagenesis.\"}]","EVI1 Disruption Post Neuroblastoma Treatment - A Case Analysis of Treatment-Associated Acute Myeloid Leukemia in a Pediatric Patient | PDF",1790240692,18]