Nissar S, Sameer A S, Rasool R, Chowdri N A, Rashid F
Department of Biochemistry, University of Kashmir; Department of Immunology and Molecular Medicine, Sher-I-Kashmir Institute of Medical Sciences; Department of Clinical Biochemistry, University of Kashmir, Srinagar, Jammu and Kashmir, India.
Department of Basic Medical Sciences, College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Jeddah, KSA.
Indian J Cancer. 2016 Oct-Dec;53(4):524-528. doi: 10.4103/ijc.IJC_17_17.
Glutathione S.transferases. (GSTs) are known to play a pivotal role in the detoxification of potential carcinogens, and their gene variation may alter susceptibility to colorectal cancer. (CRC). The aim of the study was to evaluate the genetic association of GSTM1 and GSTT1 gene deletion/null polymorphism with disease susceptibility and risk development in CRC patients of ethnic Kashmiri population.
Genotype frequencies of GSTM1 and GSTT1 gene deletion/null polymorphism were compared between 160 CRC patients and 200 healthy controls using polymerase chain reaction multiplex.
The frequency of GSTM1-null was found to be 76.2% in cases and 81.5% in controls and odds ratio. (OR) = 1.37 (95% confidence interval. [CI]: 0.82-2.28). Likewise, the GSTT1-null genotype was found in 75.5% of cases and 77.5% of controls and the OR = 1.14 (95% CI: 0.76-1.8). The overall association between the GSTM1-null and GSTT1-null polymorphism and the CRC cases was found to be insignificant (P < 0.05). However, individuals with double-null genotype (GSTM1-/GSTT1-) were found to have 3.5-fold increased risk for the development of CRC. Further, the risk genotype (null) of GSTT1 was found to be associated with tumor grade (P = 0.001) and GSTM1 (null) genotype was significantly associated with smoking status (P = 0.004), when compared to the (present) genotype in CRC cases.
Our results suggest that GSTM1 and GSTT1 gene deletion/null gene polymorphisms are not a key modulators of the risk of developing CRC in Kashmiri population.
谷胱甘肽S-转移酶（GSTs）在潜在致癌物的解毒过程中起关键作用，其基因变异可能改变患结直肠癌（CRC）的易感性。本研究旨在评估克什米尔族CRC患者中GSTM1和GSTT1基因缺失/无效多态性与疾病易感性及风险发展的遗传关联。
采用聚合酶链反应多重分析法，比较160例CRC患者和200例健康对照中GSTM1和GSTT1基因缺失/无效多态性的基因型频率。
病例组中GSTM1无效基因型频率为76.2%，对照组为81.5%，优势比（OR）=1.37（95%置信区间[CI]：0.82 - 2.28）。同样，病例组中GSTT1无效基因型为75.5%，对照组为77.5%，OR = 1.14（95% CI：0.76 - 1.8）。GSTM1无效和GSTT1无效多态性与CRC病例之间的总体关联不显著（P < 0.05）。然而，发现双无效基因型（GSTM1 - /GSTT1 - ）个体患CRC的风险增加3.5倍。此外，与CRC病例中的（现有）基因型相比，GSTT1的风险基因型（无效）与肿瘤分级相关（P = 0.001），GSTM1（无效）基因型与吸烟状态显著相关（P = 0.004）。
我们的结果表明，GSTM1和GSTT1基因缺失/无效基因多态性不是克什米尔人群患CRC风险的关键调节因素。
