Genetic Markers of Acute Childhood B-Lineage Lymphoblastic Leukemia in the Kazakh Population.

IF 0.7 4区医学 Q4 PATHOLOGY

Fetal and Pediatric Pathology Pub Date : 2024-07-01 Epub Date: 2024-07-11 DOI:10.1080/15513815.2024.2375523

Gulnara Svyatova, Galina Berezina, Aigul Bazarbayeva, Kulyan Omarova, Abay Kussainov

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引用次数: 0

Abstract

Introduction: To investigate the genetic contribution of 24 GWAS-associated polymorphic gene variants on the development of children's B-lineage acute lymphoblastic leukemia (B-ALL) in an ethnically homogeneous population of Kazakhs.

Methods: A study of 205 children with B-ALL and 204 healthy children was conducted. Genotyping of polymorphic loci was carried out using the TaqMan method.

Results: Significant associations (p < 0.05) with the risk of childhood B-ALL were found for twelve variants, including rs6457327 of the HLA gene, rs4251961 of the IL1RN gene, and rs1800630 of the TNF gene. Carriage of the minor allele A of the protective rs1801157 polymorphism A of the CXCL12 gene reduces the risk of B-ALL in the Kazakh population by 40%.

Discussion: The results reveal significant associations of polymorphic genetic variants, which can serve as a basis for the development of effective methods for predicting the risk of B-ALL, early diagnosis, and timely treatment.

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哈萨克人群中急性儿童 B 系淋巴细胞白血病的遗传标记。

引言目的：在一个哈萨克族同质化人群中，研究 24 个 GWAS 相关多态性基因变异对儿童 B 系急性淋巴细胞白血病（B-ALL）发病的遗传贡献：方法：对 205 名 B-ALL 儿童和 204 名健康儿童进行了研究。采用 TaqMan 方法对多态位点进行基因分型：结果：多态性位点之间存在显著关联（P结果显示，多态性基因变异存在明显关联，这可作为开发预测 B-ALL 风险、早期诊断和及时治疗的有效方法的基础。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Fetal and Pediatric Pathology 医学-病理学

CiteScore

3.00

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： Fetal and Pediatric Pathology is an established bimonthly international journal that publishes data on diseases of the developing embryo, newborns, children, and adolescents. The journal publishes original and review articles and reportable case reports. The expanded scope of the journal encompasses molecular basis of genetic disorders; molecular basis of diseases that lead to implantation failures; molecular basis of abnormal placentation; placentology and molecular basis of habitual abortion; intrauterine development and molecular basis of embryonic death; pathogenisis and etiologic factors involved in sudden infant death syndrome; the underlying molecular basis, and pathogenesis of diseases that lead to morbidity and mortality in newborns; prenatal, perinatal, and pediatric diseases and molecular basis of diseases of childhood including solid tumors and tumors of the hematopoietic system; and experimental and molecular pathology.