Vincent Gagné1, Pascal St-Onge1, Patrick Beaulieu1, Caroline Laverdière1,2, Jean-Marie Leclerc1,2, Thai H Tran1,2, Stephen E Sallan3,4, Donna Neuberg5, Lewis B Silverman3,4, Daniel Sinnett1,2, Maja Krajinovic1,2,6. 1. Charles-Bruneau Cancer Center, CHU Sainte-Justine Research Center, University of Montreal, Montreal, Quebec, H3T 1C5, Canada. 2. Department of Pediatrics, Faculty of Medicine, University of Montreal, Montreal, Quebec, H3T 1J4, Canada. 3. Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA. 4. Division of Hematology/Oncology, Children's Hospital, Boston, MA 02115, USA. 5. Department of Biostatistics & Computational Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. 6. Department of Pharmacology & physiology, Faculty of Medicine, University of Montreal, Montreal, Quebec, H3T 1J4, Canada.
Abstract
Aim: To evaluate the association between human leukocyte antigen (HLA) alleles and native Escherichia coli asparaginase hypersensitivity (AH) in children with acute lymphoblastic leukemia (ALL) who received Dana-Farber Cancer Institute treatment protocols. Patients & methods: HLA-DQA1, HLA-DRB1 and HLA-DQB1 alleles were retrieved from available whole exome sequencing data of a subset of childhood ALL patients from Quebec ALL cohort and analyzed for an association with AH. PCR assay was developed to analyze associated alleles in the entire discovery and replication cohorts. Results: Two alleles in linkage disequilibrium (HLA-DRB1*07:01 and DQA1*02:01) were associated with AH. Additional analyses, performed to distinguish between HLA-DRB1*07:01 haplotypes with and without DQB1*02:02 allele, showed that the association was dependent on the presence of DQB1*02:02. Conclusion: This study confirms the implication of HLA-DRB1*07:01, DQA1*02:01 and DQB1*02:02 alleles in developing AH in childhood ALL.
Aim: To evaluate the association between human leukocyte antigen (HLA) alleles and native Escherichia coli asparaginase hypersensitivity (AH) in children with acute lymphoblastic leukemia (ALL) who received Dana-Farber Cancer Institute treatment protocols. Patients & methods: HLA-DQA1, HLA-DRB1 and HLA-DQB1 alleles were retrieved from available whole exome sequencing data of a subset of childhood ALL patients from Quebec ALL cohort and analyzed for an association with AH. PCR assay was developed to analyze associated alleles in the entire discovery and replication cohorts. Results: Two alleles in linkage disequilibrium (HLA-DRB1*07:01 and DQA1*02:01) were associated with AH. Additional analyses, performed to distinguish between HLA-DRB1*07:01 haplotypes with and without DQB1*02:02 allele, showed that the association was dependent on the presence of DQB1*02:02. Conclusion: This study confirms the implication of HLA-DRB1*07:01, DQA1*02:01 and DQB1*02:02 alleles in developing AH in childhood ALL.
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