EVI1 Disruption Post Neuroblastoma Treatment: A Case Analysis of Treatment-Associated Acute Myeloid Leukemia in a Pediatric Patient.
EVI1 Disruption Post Neuroblastoma Treatment: A Case Analysis of Treatment-Associated Acute Myeloid Leukemia in a Pediatric Patient.
复制标题
DOI：
10.1159/000533571
复制
发表时间：
2023-01
影响因子：
0.8
通讯作者：
Zhang, Xin
中科院分区：
文献类型：
--
作者：
Zhang, Xin
近年来，人们越来越关注了解儿科癌症治疗的长期后果，特别是继发性恶性肿瘤（SMN）的出现。在这里，我们提出了一个病例研究，强调治疗的后果，其中一个儿科患者，最初治疗神经母细胞瘤，发展治疗相关的急性髓性白血病（tAML）6年后。我们的研究强调了EVI1破坏在加速继发性肿瘤进展中的关键作用。该病例强调了儿科癌症治疗后SMN的显著风险。通过分析遗传异常，我们确定了PTPN11和KMT2C基因的变异，表明在tAML发展中遗传易感性和化疗诱导的诱变之间存在复杂的相互作用。此外，我们对拓扑异构酶II抑制剂参与tAML的探索为未来潜在的治疗方法提供了见解。报告这一病例对于加深我们对儿科癌症治疗后驱动SMN的机制的理解至关重要。通过对遗传异常和治疗变量的综合分析，我们可以提供更精确的临床诊断和治疗策略。这种方法有可能减少继发性肿瘤的发生，改善儿科患者的长期预后。
In 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, we identified 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.
登录
查看更多内容
DOI：
10.1001/jama.2017.0693
发表时间：
2017-02-28
期刊：
JAMA
影响因子：
--
作者：
Turcotte LM;Liu Q;Yasui Y;Arnold MA;Hammond S;Howell RM;Smith SA;Weathers RE;Henderson TO;Gibson TM;Leisenring W;Armstrong GT;Robison LL;Neglia JP
通讯作者：
Neglia JP
影响因子：
64.8
作者：
Ma X;Liu Y;Liu Y;Alexandrov LB;Edmonson MN;Gawad C;Zhou X;Li Y;Rusch MC;Easton J;Huether R;Gonzalez-Pena V;Wilkinson MR;Hermida LC;Davis S;Sioson E;Pounds S;Cao X;Ries RE;Wang Z;Chen X;Dong L;Diskin SJ;Smith MA;Guidry Auvil JM;Meltzer PS;Lau CC;Perlman EJ;Maris JM;Meshinchi S;Hunger SP;Gerhard DS;Zhang J
通讯作者：
Zhang J
DOI：
10.1186/s13014-021-01943-x
发表时间：
2021-11-27
期刊：
Radiation oncology (London, England)
影响因子：
--
作者：
Zhen H;Guan H;Ma J;Wang W;Jing S;Miao Z;Zhang F;Liu Z
通讯作者：
Liu Z
影响因子：
8.8
作者：
Chen R;Okeyo-Owuor T;Patel RM;Casey EB;Cluster AS;Yang W;Magee JA
通讯作者：
Magee JA
影响因子：
14.9
作者：
Szlachta, Karol;Manukyan, Arkadi;Wang, Yuh-Hwa
通讯作者：
Wang, Yuh-Hwa