Yamada Ikuhiro, Matsuyama Masato, Ozaka Masato, Inoue Dai, Muramatsu Yusuke, Ishii Hiroshi, Junko Ueda, Ueno Makoto, Egawa Naoto, Nakao Haruhisa, Mori Mitsuru, Matsuo Keitaro, Nishiyama Takeshi, Ohkawa Shinichi, Hosono Satoyo, Wakai Kenji, Nakamura Kozue, Tamakoshi Akiko, Kuruma Sawako, Nojima Masanori, Takahashi Mami, Shimada Kazuaki, Yagyu Kiyoko, Kikuchi Shogo, Lin Yingsong
Hepatobiliary and Pancreatic Section, Gastroenterological Division, Cancer Institute Hospital, Tokyo, Japan E-mail :
Asian Pac J Cancer Prev. 2014;15(1):391-5. doi: 10.7314/apjcp.2014.15.1.391.
We aimed to evaluate the role of genetic polymorphisms in tobacco carcinogen-metabolizing genes and their interactions with smoking in a hospital-based case-control study of Japanese subjects.
We examine the associations of pancreatic cancer risk with genetic polymorphisms in GSTM1, GSTT1 and GSTP1, phase II enzymes that catalyze the conjugation of toxic and carcinogenic electrophilic molecules. The study population consisted of 360 patients and 400 control subjects, who were recruited from several medical facilities in Japan. Unconditional logistic regression methods were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the associations between genotypes and pancreatic cancer risk.
Among the control subjects, the prevalence of the GSTM1-null genotype and the GSTT1-null genotype was approximately 56% and 48%, respectively. Cases and controls were comparable in terms of GSTM1 and GSTT1 genotype distributions. Neither of the deleted polymorphisms in GSTM1 and GSTT1 was associated with the risk of pancreatic cancer, with an age- and sex-adjusted OR of 0.99 (95%CI: 0.74-1.32) for the GSTM1-null genotype, and 0.98 (95%CI: 0.73-1.31) for the GSTT1-null genotype. The OR was 0.97 (95%CI: 0.64-1.47) for individuals with the GSTM1 and GSTT1-null genotypes compared with those with the GSTM1 and GSTT1- present genotypes. No synergistic effects of smoking or GST genotypes were observed.
Our results indicate no overall association between the GSTM1 and GSTT1 deletion polymorphisms and pancreatic cancer risk in the Japanese subjects in our study.
在一项针对日本受试者的基于医院的病例对照研究中,我们旨在评估烟草致癌物代谢基因中的基因多态性及其与吸烟的相互作用的作用。
我们研究了胰腺癌风险与GSTM1、GSTT1和GSTP1基因多态性之间的关联,这些基因是催化有毒和致癌亲电分子共轭的II期酶。研究人群包括360例患者和400例对照受试者,他们来自日本的几家医疗机构。采用无条件逻辑回归方法估计基因型与胰腺癌风险之间关联的比值比(OR)和95%置信区间(CI)。
在对照受试者中,GSTM1缺失基因型和GSTT1缺失基因型的患病率分别约为56%和48%。病例组和对照组在GSTM1和GSTT1基因型分布方面具有可比性。GSTM1和GSTT1中的缺失多态性均与胰腺癌风险无关,GSTM1缺失基因型的年龄和性别调整OR为0.99(95%CI:0.74-1.32),GSTT1缺失基因型的年龄和性别调整OR为0.98(95%CI:0.73-1.31)。与同时具有GSTM1和GSTT1基因型的个体相比,同时具有GSTM1和GSTT1缺失基因型的个体的OR为0.97(95%CI:0.64-1.47)。未观察到吸烟或GST基因型的协同效应。
我们的结果表明,在我们研究的日本受试者中,GSTM1和GSTT1缺失多态性与胰腺癌风险之间没有总体关联。