Idris Hadeil Me, Elderdery Abozer Y, Khalil Hiba B, Mills Jeremy
Department of Hematology, Faculty of Medical Laboratory Sciences, Al Neelain University, Sudan.
Clinical Laboratory Sciences, Faculty of Applied Medical Sciences, Shaqra University, Saudi Arabia.
Asian Pac J Cancer Prev. 2020 Feb 1;21(2):499-503. doi: 10.31557/APJCP.2020.21.2.499.
The development of cancer results from an imbalance between exposure to carcinogens and the capacity of various enzyme systems engaged in activation or in the detoxification of xenobiotics. The aim of the present study is to investigate the association of GSTP1, GSTM1 and GSTT1 gene polymorphisms in susceptibility to Chronic Myeloid Leukaemia (CML).
A total of 200 CML patients and 100 controls were enrolled in a case-control study with GSTM1 and GSTT1 analysis with PCR and GSTP1 analysis with PCR-RFLP.
The GSTT1 null genotype was significantly higher among CML patients suggesting that this genotype is associated with an increased risk of CML. It was found in 42% of cases as compared with 21% of the controls, (OR =2.78, 95% CI: 1.59 - 4.85; p-value =0.000). The presence of the GSTT1 genotype may thus be considered a protective factor for CML. The frequency of individuals carrying GSTM1 null genotype was slightly higher in the control group but this difference was not statistically significant. The GSTM1 null genotype was present in 35% of control cases and 34% of the CML patients, (OR=0.975, 95%CI: 0.58-1.58;p-value=0.863). Individuals with a combined GSTM1 null/GSTT1null genotype had an estimated 2.85-fold increased risk of CML, but no associated risk between GSTP1 Ile 105 Val polymorphism and CML was found (OR=1.99, 95% CI: 0.40 - 9.32; p-value = 0.417).
No association between GSTP1 and GSTM1 with susceptibility to CML was found. GSTT1 genotype may be a protective factor for CML, while the null genotype shows association with developing CML.
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癌症的发生是由于接触致癌物与参与外源性物质活化或解毒的各种酶系统能力之间的失衡所致。本研究的目的是调查谷胱甘肽S-转移酶P1（GSTP1）、谷胱甘肽S-转移酶M1（GSTM1）和谷胱甘肽S-转移酶T1（GSTT1）基因多态性与慢性髓性白血病（CML）易感性之间的关联。
共有200例CML患者和100例对照纳入一项病例对照研究，采用聚合酶链反应（PCR）分析GSTM1和GSTT1，采用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）分析GSTP1。
CML患者中GSTT1缺失基因型显著更高，提示该基因型与CML风险增加相关。在42%的病例中发现该基因型，而对照组为21%，（比值比[OR]=2.78，95%可信区间[CI]：1.59 - 4.85；P值=0.000）。因此，GSTT1基因型的存在可能被认为是CML的一个保护因素。携带GSTM1缺失基因型个体的频率在对照组中略高，但这种差异无统计学意义。GSTM1缺失基因型在35%的对照病例和34%的CML患者中存在，（OR=0.975，95%CI：0.58 - 1.58；P值=0.863）。GSTM1缺失/GSTT1缺失联合基因型个体患CML的风险估计增加2.85倍，但未发现GSTP1第105位异亮氨酸（Ile）/缬氨酸（Val）多态性与CML之间存在相关风险（OR=1.99，95%CI：0.40 - 9.32；P值=0.417）。
未发现GSTP1和GSTM1与CML易感性之间存在关联。GSTT1基因型可能是CML的一个保护因素，而缺失基因型与CML的发生相关。
