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Minimal residual disease (MRD) detection using rearrangement of immunoglobulin/T cell receptor genes in adult patients with acute lymphoblastic leukemia (ALL).利用免疫球蛋白/T细胞受体基因重排检测成年急性淋巴细胞白血病(ALL)患者的微小残留病(MRD)
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本文引用的文献

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Concordance between glucose-6-phosphate dehydrogenase (G6PD) genotype and phenotype and rasburicase use in patients with hematologic malignancies.葡萄糖-6-磷酸脱氢酶(G6PD)基因型与表型在血液系统恶性肿瘤患者中与拉布立酶使用的一致性。
Pharmacogenomics J. 2019 Jun;19(3):305-314. doi: 10.1038/s41397-018-0043-3. Epub 2018 Sep 12.
2
Genome-Wide Study Links PNPLA3 Variant With Elevated Hepatic Transaminase After Acute Lymphoblastic Leukemia Therapy.全基因组研究将 PNPLA3 变异与急性淋巴细胞白血病治疗后肝转氨酶升高联系起来。
Clin Pharmacol Ther. 2017 Jul;102(1):131-140. doi: 10.1002/cpt.629. Epub 2017 Apr 4.
3
Clinical and Genetic Risk Factors for Acute Pancreatitis in Patients With Acute Lymphoblastic Leukemia.急性淋巴细胞白血病患者急性胰腺炎的临床和遗传危险因素
J Clin Oncol. 2016 Jun 20;34(18):2133-40. doi: 10.1200/JCO.2015.64.5812. Epub 2016 Apr 25.
4
Prognostic significance of minimal residual disease in high risk B-ALL: a report from Children's Oncology Group study AALL0232.高危B淋巴细胞白血病微小残留病的预后意义:儿童肿瘤协作组AALL0232研究报告
Blood. 2015 Aug 20;126(8):964-71. doi: 10.1182/blood-2015-03-633685. Epub 2015 Jun 29.
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Genome-wide analysis links NFATC2 with asparaginase hypersensitivity.全基因组分析将NFATC2与天冬酰胺酶超敏反应联系起来。
Blood. 2015 Jul 2;126(1):69-75. doi: 10.1182/blood-2015-02-628800. Epub 2015 May 18.
6
Clinical Pharmacogenetics Implementation Consortium (CPIC) guidelines for rasburicase therapy in the context of G6PD deficiency genotype.临床药物遗传学实施联盟(CPIC)关于 G6PD 缺乏基因型下尿酸酶治疗的指南。
Clin Pharmacol Ther. 2014 Aug;96(2):169-74. doi: 10.1038/clpt.2014.97. Epub 2014 May 2.
7
Safe chemotherapy and hormone therapy for treating early breast cancer in a glucose 6-phosphate dehydrogenase-deficient patient: case report.葡萄糖-6-磷酸脱氢酶缺乏症患者的早期乳腺癌的安全化疗和激素治疗:病例报告。
Anticancer Drugs. 2012 Aug;23(7):758-60. doi: 10.1097/CAD.0b013e3283556bbe.
8
PharmGKB summary: very important pharmacogene information for G6PD.药物基因组知识库总结:关于葡萄糖-6-磷酸脱氢酶(G6PD)的非常重要的药物基因信息。
Pharmacogenet Genomics. 2012 Mar;22(3):219-28. doi: 10.1097/FPC.0b013e32834eb313.
9
Medications and glucose-6-phosphate dehydrogenase deficiency: an evidence-based review.药物与葡萄糖-6-磷酸脱氢酶缺乏:循证综述。
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10
Treating childhood acute lymphoblastic leukemia without cranial irradiation.不进行颅脑照射治疗儿童急性淋巴细胞白血病。
N Engl J Med. 2009 Jun 25;360(26):2730-41. doi: 10.1056/NEJMoa0900386.

没有证据表明 G6PD 缺乏症会影响柔红霉素在急性淋巴细胞白血病诱导治疗中的疗效或安全性。

No evidence that G6PD deficiency affects the efficacy or safety of daunorubicin in acute lymphoblastic leukemia induction therapy.

机构信息

Department of Pharmaceutical Sciences, St. Jude Children's Research Hospital, Memphis, Tennessee.

Department of Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee.

出版信息

Pediatr Blood Cancer. 2019 Jun;66(6):e27681. doi: 10.1002/pbc.27681. Epub 2019 Mar 7.

DOI:10.1002/pbc.27681
PMID:30848065
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6518412/
Abstract

BACKGROUND/OBJECTIVES: Anthracyclines are used in induction therapy of pediatric acute lymphoblastic leukemia (ALL) and are known to generate oxidative stress; whether this translates into enhanced antileukemic activity or hemolytic effects in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency is unknown.

DESIGN/METHODS: Among 726 pediatric patients with newly diagnosed ALL treated at St. Jude Children's Research Hospital, 22 had deficient G6PD activity. We compared the prevalence of positive minimal residual disease (MRD) ≥1% at Day 15/Day 19 of induction or ≥0.01% at Day 42/Day 46 (end of induction) and the number of red blood cell (RBC) transfusions after daunorubicin in induction between patients with or without G6PD deficiency, adjusting for ALL risk group, treatment protocol, age, and gender.

RESULTS

There was no difference in Day 15/19 (P = 1) or end of induction MRD (P = 0.76) nor in the number of RBC transfusions (P = 0.73); the lack of association with MRD was confirmed in a dataset of 1192 newly diagnosed male patients enrolled in a Children's Oncology Group trial (P = 0.78).

CONCLUSION

We found no evidence that G6PD deficiency affects daunorubicin activity during induction treatment for ALL.

摘要

背景/目的:蒽环类药物用于儿童急性淋巴细胞白血病(ALL)的诱导治疗,已知其会产生氧化应激;然而,在葡萄糖-6-磷酸脱氢酶(G6PD)缺乏症患者中,这种氧化应激是否会转化为增强的抗白血病活性或溶血作用尚不清楚。

方法/设计:在圣裘德儿童研究医院接受新诊断的 ALL 治疗的 726 名儿科患者中,有 22 名患者的 G6PD 活性不足。我们比较了诱导治疗第 15/19 天(Day 15/19)或第 42/46 天(诱导结束时)微小残留病(MRD)阳性≥1%的患者比例,以及在诱导治疗中使用柔红霉素后红细胞(RBC)输注的数量,在 G6PD 缺乏症患者和非 G6PD 缺乏症患者之间,同时调整 ALL 风险组、治疗方案、年龄和性别。

结果

Day 15/19 时(P=1)或诱导结束时(P=0.76)MRD 没有差异,也没有 RBC 输注数量的差异(P=0.73);在儿童肿瘤组一项纳入 1192 名新诊断男性患者的临床试验数据集(Children's Oncology Group trial)中,这种与 MRD 缺乏的关联也得到了确认(P=0.78)。

结论

我们没有发现证据表明 G6PD 缺乏会影响 ALL 诱导治疗期间柔红霉素的活性。