Methylation Status of SOCS1 and SOCS3 Genes in Patients with Acute Lymphoid Leukemia

Immunology and Genetics Journal Pub Date : 2024-03-11 DOI:10.18502/igj.v5i2.15097

Mahsima Shabani, Hanieh Mojtahedi, M. Sadr, A. Rezaei, Parivash Afradiasbagharani, G. Sanati, Z. Aryan, F. Kompani, Nima Rezaei

{"title":"Methylation Status of SOCS1 and SOCS3 Genes in Patients with Acute Lymphoid Leukemia","authors":"Mahsima Shabani, Hanieh Mojtahedi, M. Sadr, A. Rezaei, Parivash Afradiasbagharani, G. Sanati, Z. Aryan, F. Kompani, Nima Rezaei","doi":"10.18502/igj.v5i2.15097","DOIUrl":null,"url":null,"abstract":"Background: Acute Lymphoid Leukemia (ALL) is the leading childhood cancer with a high mortality and morbidity. Studies have suggested an association of epigenetic transformations with prognosis, recurrence and immunophenotypes of ALL. SOCS1 and SOCS3 are tumor suppressors inhibiting JAK/STAT signaling pathway and the resultant aberrant cell proliferation. \nMethod: We aimed to assess the association between methylation status and ALL, using bone marrow and peripheral blood samples. 18 patients with ALL and 13 children with no malignancies were included. Using Bisulfite conversion, quantitative multiplex methylation-specific PCR and 2^(-∆∆Ct) formula, the methylated DNA in the promoters of SOCS1 and SOCS3 were measured. \nResults: ALL patients had higher mean methylation in SOCS1 promoter and lower mean methylation in SOCS3 promoter, compared to the control group. However, neither of these mean differences were statistically significant. \nConclusion: This finding can set the foundation for further large-sample studies with the use of healthy children as a control group to strengthen the hypothetical association of the methylation status of SOCS1 and SOCS3 with ALL.","PeriodicalId":406184,"journal":{"name":"Immunology and Genetics Journal","volume":"92 2","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunology and Genetics Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.18502/igj.v5i2.15097","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}

引用次数: 0

Abstract

Background: Acute Lymphoid Leukemia (ALL) is the leading childhood cancer with a high mortality and morbidity. Studies have suggested an association of epigenetic transformations with prognosis, recurrence and immunophenotypes of ALL. SOCS1 and SOCS3 are tumor suppressors inhibiting JAK/STAT signaling pathway and the resultant aberrant cell proliferation. Method: We aimed to assess the association between methylation status and ALL, using bone marrow and peripheral blood samples. 18 patients with ALL and 13 children with no malignancies were included. Using Bisulfite conversion, quantitative multiplex methylation-specific PCR and 2^(-∆∆Ct) formula, the methylated DNA in the promoters of SOCS1 and SOCS3 were measured. Results: ALL patients had higher mean methylation in SOCS1 promoter and lower mean methylation in SOCS3 promoter, compared to the control group. However, neither of these mean differences were statistically significant. Conclusion: This finding can set the foundation for further large-sample studies with the use of healthy children as a control group to strengthen the hypothetical association of the methylation status of SOCS1 and SOCS3 with ALL.

查看原文本刊更多论文

急性淋巴细胞白血病患者 SOCS1 和 SOCS3 基因的甲基化状态

背景：急性淋巴细胞白血病（ALL）是死亡率和发病率都很高的主要儿童癌症。研究表明，表观遗传转化与急性淋巴细胞白血病的预后、复发和免疫表型有关。SOCS1 和 SOCS3 是抑制 JAK/STAT 信号通路的肿瘤抑制因子，可抑制由此导致的细胞异常增殖。方法：我们利用骨髓和外周血样本评估甲基化状态与 ALL 之间的关联。共纳入 18 名 ALL 患者和 13 名无恶性肿瘤的儿童。使用亚硫酸氢盐转换、定量多重甲基化特异性 PCR 和 2^(-∆∆Ct) 公式测量 SOCS1 和 SOCS3 启动子中的甲基化 DNA。结果发现与对照组相比，ALL 患者 SOCS1 启动子的平均甲基化程度较高，而 SOCS3 启动子的平均甲基化程度较低。然而，这两个平均值的差异均无统计学意义。结论这一发现为进一步开展以健康儿童为对照组的大样本研究奠定了基础，从而加强了 SOCS1 和 SOCS3 甲基化状态与 ALL 的假定关联。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Immunology and Genetics Journal

自引率

0.00%

发文量