Acute Lymphoblastic Leukemia and Associated HLA-A, B, DRB1, and DQB1 Molecules: A Moroccan Pediatric Case–Control Study

TL;DR

This study explores the link between specific HLA molecules and acute lymphoblastic leukemia in Moroccan children.

Contribution

The study identifies specific HLA alleles associated with pediatric ALL in a Moroccan population.

Findings

HLA-A*68 and B*14 were significantly more frequent in ALL patients than controls.

HLA-DRB1*01 and DQB1*05 alleles were elevated in ALL and BCP-ALL patients.

These HLA alleles may be predisposing factors for juvenile ALL development.

Abstract

Leukemia constitutes approximately one-third of all pediatric cancers, with acute lymphoblastic leukemia (ALL) comprising roughly 80% of pediatric leukemia instances. This study sought to ascertain the prevalence of HLA A, B, DR, and DQ allele groups linked with pediatric acute leukemia. We recruited 70 Moroccan children diagnosed with acute lymphoblastic leukemia (ALL), 39 of whom had BCP-ALL and were eligible for hematopoietic stem cell transplantation, compared to a control group of 136 healthy children. Patients and controls were subjected to HLA class I and II typing, utilizing either sequence-specific primers (SSPs) or sequence-specific oligonucleotides (SSOs) in polymerase chain reaction-based techniques. The findings indicated significantly elevated frequencies of HLA-A*68 and B*14 in pediatric patients with ALL relative to the control group (p = 0.001 and p = 0.02, respectively). The frequencies of HLA-DRB1*01 and DQB1*05 allele groups were considerably elevated in children with ALL and BCP-ALL compared to the controls (p < 0.01 for both). The findings of our study indicate that HLA-A*68, -B*14, -DRB1*01, and DQB1*05 may serve as potential predisposing immunogenetic variables for the development of juvenile acute lymphoblastic leukemia (ALL). Nonetheless, additional research including a bigger sample considering other regions of Morocco would be beneficial to more accurately delineate the association between the HLA system and ALL.

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