引言：急性髓系白血病（AML）是一种具有异常分子多样性的异质性髓系恶性肿瘤。组织卡利克雷因2（KLK2）是一种丝氨酸蛋白酶，与恶性肿瘤的发生和发展密切相关。各种基因的单核苷酸多态性（SNP）与AML的易感性、治疗和生存有关。方法：我们研究了KLK2 SNP rs198977和rs2664155与AML的关联。我们从汉族人口中招募了284名AML患者和280名健康对照者，并利用MassARRAY系统对KLK2 SNP rs198977和rs2664155进行了基因分型。结果：利用AML患者和对照的临床数据，包括AML易感性、血液计数、风险分层、对诱导化疗的反应和生存情况，我们的结果显示，KLK2 rs198977 TT基因型在隐性模型中与AML易感性的风险增加相关。关于AML患者的白细胞计数，结果显示KLK2 rs198977 TT基因型在共显模型中与高白细胞症的风险增加相关。此外，在隐性模型中，具有KLK2 SNP rs198977 TT基因型的AML患者有着高白细胞症的风险增加。KLK2 rs2664155与AML之间没有显著相关性。讨论：本研究表明，KLK2 rs198977可能是AML发生和高白细胞症中的一个重要遗传因素，为疾病进展和新的治疗靶点提供了新的视角。版权所有© 2023 Meng, Li, Li, Wu, Ma, Sun and Ji.

Introduction: Acute myeloid leukemia (AML) is a heterogeneous myeloid malignancy with abnormal molecular diversity. Tissue kallikrein 2 (KLK2) is a kind of serine protease, and has a close relationship with the occurrence and development of malignant tumors. Single nucleotide polymorphism (SNP) of various genes are associated with susceptibility, treatment and survival of AML. Methods: We investigated the association of KLK2 SNPs rs198977 and rs2664155 with AML. We recruited 284 AML patients and 280 healthy controls from the Han population and genotyping KLK2 SNPs rs198977 and rs2664155 by MassARRAY system. Results: Using clinical data from AML patients and controls, including AML susceptibility, blood count, risk stratification, response to induced chemotherapy and survival, our results showed an increased risk of AML susceptibility with KLK2 rs198977 TT genotype in the recessive model. Regarding white blood cell counts in AML patients, the results showed an increased risk of hyperleukocytosis with the TT genotype of KLK2 rs198977 in a codominant model. Moreover, in the recessive model, AML with KLK2 SNPs rs198977 TT genotype had an increased risk of hyperleukocytosis. No significant correlation was found between KLK2 rs2664155 and AML. Discussion: This study suggests that KLK2 rs198977 may be an important genetic factor in the occurrence of AML and hyperleukocytosis in AML, providing a new perspective for disease progression and new therapeutic targets.Copyright © 2023 Meng, Li, Li, Wu, Ma, Sun and Ji.