Excellent Survival Outcomes of Pediatric Patients With Acute Myeloid Leukemia Treated With the MASPORE 2006 Protocol

Sutiman, Natalia; Nwe, Mya Soe; Lai, Eunice En Ni; Lee, Denyse Kawai; Chan, Mei Yoke; Yeoh, Allen Eng-Juh; Soh, Shui Yen; Leung, Wing; Tan, Ah Moy

doi:10.1016/j.clml.2020.11.016

Cited by 1 publication

(2 citation statements)

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“… 7 , 8 , 9 , 10 , 11 Cytarabine (Cytosine arabinoside Ara‐c) and anthracyclines are routinely used in front‐line therapy for AML. 12 , 13 , 14 , 15 Resistance development to chemotherapy is a major obstacle in AML treatment and is responsible for relapses and increased toxicity in second‐line therapies. 16 Ara‐C is a pyrimidine analog which is converted into ara‐CMP by deoxycytidine kinase ( DCK ), later on is converted to ara‐CDP and into ara‐CTP by cytidine/uridine monophosphate kinase 1 ( CMPK1 ) and nucleoside diphosphate kinase 1 (NME1), respectively.…”

Section: Introductionmentioning

confidence: 99%

“…The identification of gene variants that participate in the processes of pharmacodynamics and pharmacokinetics (pharmacogenetics), have become relevant in the era of personalized medicine, in terms of the influence they exert on the response to treatment, 4–6 and the incorporation of interindividual genetic differences for the design of more effective diagnostic and therapeutic strategies 7–11 . Cytarabine (Cytosine arabinoside Ara‐c) and anthracyclines are routinely used in front‐line therapy for AML 12–15 . Resistance development to chemotherapy is a major obstacle in AML treatment and is responsible for relapses and increased toxicity in second‐line therapies 16 .…”

Section: Introductionmentioning

confidence: 99%

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Pharmacogenetics of ABCB1, CDA, DCK, GSTT1, GSTM1 and outcomes in a cohort of pediatric acute myeloid leukemia patients from Colombia

et al. 2022

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Background and Aim: Different studies have shown pharmacogenetic variants related to drug toxicity in acute myeloid leukemia (AML) patients. Our aim was to identify the association between ABCB1, CDA, DCK, GSTT1, and GSTM1 variants with clinical outcomes and toxicity in pediatric patients with AML.Methods: Fifty-one confirmed de novo AML pediatric patients were included. A SNaPshot™ assay and conventional PCR were used to evaluate ABCB1, CDA, DCK, GSTT1, and GSTM1 variants. Clinical outcomes and toxicity associations were evaluated using odds ratios and Chi-square analysis.Results: Patients carrying ABCB1 (1236C > T, rs1128503) GG genotype in had a 6.8 OR (CI 95% 1.08-42.73, p = .044) for cardiotoxicity as compared to patients carrying either AA or GA genotypes 0.14 OR (CI 95% 0.023-0.92, p = .044). For ABCB1 (1236G > A rs1128503/2677C > A/T rs2032582/ 3435G > A rs1045642) AA/AA/AA combined genotypes had a strong association with death after HSTC OR 13.73 (CI 95% 1.94-97.17, p = .009). Combined genotypes GG/CC/GG with CDA (79A > C, rs2072671) CA genotype or CDA (-451G > A, rs532545) CT genotype, had a 4.11 OR (CI 95% 2.32-725, p = .007) and 3.8 OR (CI 95% 2.23-6.47, p = .027) with MRD >0.1% after first chemotherapy cycle, respectively. Conclusion:Our results highlight the importance of pharmacogenetic analysis in pediatric AML, particularly in populations with a high degree of admixture, and might be useful as a future tool for patient stratification for treatment.

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