HMGB1 Polymorphisms in Acute Lymphoblastic Leukemia

Elham Rayzan; Saeed Farajzadeh Valilou; Sara Hemmati; Amin Sadeghi; Hamid Farajifard; Sepideh Shahkarami; Nima Rezaei

doi:10.18502/igj.v8i1.17994

Elham Rayzan Research Center for Immunodeficiencies (RCID), Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran
Saeed Farajzadeh Valilou Medical Genetics Network (Megene), Universal Scientific Education and Research Network (USERN), Tehran, Iran
Sara Hemmati Molecular Medicine Interest Group (MMIG), Universal Scientific Education and Research Network (USERN), Tehran, Iran
Amin Sadeghi Molecular Medicine Interest Group (MMIG), Universal Scientific Education and Research Network (USERN), Tehran, Iran
Hamid Farajifard Immunology and Microbiology Department, School of Medicine, Qom University of Medical Sciences
Sepideh Shahkarami Research Center for Immunodeficiencies (RCID), Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran
Nima Rezaei Research Center for Immunodeficiencies (RCID), Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran

DOI: https://doi.org/10.18502/igj.v8i1.17994

Keywords: Acute lymphoblastic leukemia (ALL); HMGB1; Polymorphism; Sanger Sequencing

Abstract

Acute lymphoblastic leukemia (ALL) is the most common pediatric malignancy and the leading cause of childhood death in contrast to the 90% cure rate. ALL includes different subtypes described by interrupt collections of somatic chromosomal alterations and sequence mutations that disrupt normal body functions such as lymphoid maturation, cell-cycle regulation, and tumor suppression. Having a significant role in several cancers, the high mobility group box-1 (HMGB1) gene is considered an important gene in the development of tumors. Herein, the genetic role of HMGB1 was studied in the 49 Iranian patients with newly diagnosed ALL using Sanger sequencing of HMGB1 coding regions (exons 2 to 5). The results showed that none of the subjects in the study had any promising variants in the coding sequences of the HMGB1. These findings suggest that HMGB1 is not directly associated with ALL incidence and behavior. Further investigations using a large group of patients with different races and ethnicities are required to analyze the possible role of HMGB1 gene polymorphisms in ALL patients.