涝渍胁迫对转多基因库安托杨生长及生理性状的影响

以库安托杨转多基因株系(D5-9、D5-18、D5-19、D5-20、D5-21、D5-24、D5-26)和未转化株系(对照CK)为试材,研究不同水分处理(水涝胁迫、浸渍胁迫、正常供水)对其生长及生理性状的影响。结果表明:随着胁迫的加剧,各株系株高、根系生长和生物量累积呈下降趋势,而地径生长有所增加。浸渍、水涝胁迫下对照株系的净光合速率均最低,分别为11.99、10.37μmol.m-2.s-1,比正常供水分别减少了14.0%和25.6%;浸渍胁迫下D5-26的净光合速率最高,为13.95μmol.m-2.s-1;水涝胁迫下D5-19的净光合速率最高为12.01μmol.m-2.s-1。蒸腾速率、水分利用效率、气孔限制值、叶绿素a、叶绿素b和总叶绿素含量均下降,叶绿素a的降幅小于叶绿素b,叶绿素a/b值先降后升,而气孔导度和细胞间隙CO2浓度增大。PSⅡ的实际光化学效率、电子传递速率、潜在光化学活性和最大光化学效率均降低,初始荧光产量和最大荧光产量增加。涝渍胁迫对所有供试材料的生长及光合、叶绿素荧光等生理性状均有影响,但对转多基因株系的影响明显较对照小,且株系间存在差异。以生长、光合参数和叶绿素荧光参数为指标对供试材料进行综合评价,各株系的抗涝能力从高到低的排序为:D5-26>D5-19>D5-18>D5-21>D5-9>D5-20>D5-24>CK。

转多基因库安托杨对土壤微生物群落功能的影响

【目的】研究转基因库安托杨和非转基因库安托杨根际土壤微生物的碳源利用水平,为揭示转多基因库安托杨对土壤微生物系统的影响提供科学依据。【方法】在北京市房山区韩村河东营苗圃,取转基因库安托杨5个无性系（D5-9,D5-19,D5-20,D5-21和D5-24）、非转基因库安托杨（CK）根际土壤以及无植物种植土壤（NP）。通过Biolog生态板培养土壤微生物,用多功能酶标仪读数,计算碳源利用能力、丰富度指数、优势度指数和均匀度指数。【结果】温育24 h后,土壤微生物逐渐适应了Biolog微平板基质环境,随后进入对数增长期,平均颜色变化率（AWCD）快速增加直至96 h,此时微生物活性旺盛,碳源开始被明显利用,随后缓慢增长,直至趋于稳定。各培养阶段的AWCD均为D5-24的根际土最高,表明其微生物群落碳源利用量最多,代谢活性最强,CK根际土次之,而NP土微生物代谢最慢,活性最弱。说明栽植杨树的根际土壤丰富了碳源,从而促进微生物的代谢活性。土壤微生物对胺类、酚酸类、羧酸类、多聚物、氨基酸和碳水化合物的利用强度存在差异,微生物对碳水化合物和氨基酸的代谢比较旺盛而对酚酸类和胺类的代谢较弱。对72 h的数据进行主成分（PCA）分析,31个主成分因子中前20个的方差贡献率达100%,其中主成分1的方差贡献率为42.31%,主成分2为13.57%,第3-20主成分贡献率较小,为1.32%-11.64%。PC1和PC2的累积贡献率高达55.88%,相关性分析表明,与PC1正相关程度最高的碳源为D-纤维二糖（0.900）,负相关的碳源为衣康酸（-0.266）;与PC2正相关程度最高的碳源为苯乙胺（0.668）,负相关的碳源为α-丁酮酸（-0.631）。NP和CK分别分布在最小和最大两端。在PC2轴上NP和D5-9分布在正向,D5-20和D5-24分布在负向,CK、D5-19和D5-21两边均有分布,NP与其他无性系之间的分布区域有明显差异。【结论】转多基因库安托杨对土壤微生物系统没有明显的影响。不同转基因无性系之间的差别可能是由于外源基因插入位置、拷贝数等差异导致植株的生理生化及代谢特性发生变化,而非基因表达产物本身的影响。不论栽植非转基因杨树还是转基因杨树都会增加根际土壤微生物的代谢活性。

转多基因抗病番茄及试种示范

国家生物工程中心利用现代生物技术,率先获得了世界首例转多基因高抗烟草花叶病毒(TMV)、黄瓜花叶病毒(CMV)、马铃薯 X 病毒(PVX)和抗青枯病、晚疫病二种真菌番茄植株。培育出了'DRD8012'、'DRD8013'、'DRD8018'早、中、晚熟,抗病番茄新品种。通过在病素易发区的两广、海南和吉林等省区多点试种示范表明,该抗病番茄不仅抗病毒、抗真菌效果突出,而且高产、优质,适应性广。

转多基因抗病番茄及试种示范

国家生物工程中心利用现代生物技术率先获得了世界首例转多基因高抗烟草花叶病毒（TMV）、黄瓜花叶病毒（CMV）、马铃薯X病毒（PXV）和抗斑枯病、晚疫病二种真菌的番茄植株,培育出了DRD8012、DRD8013、DRD8018早、中、晚熟多抗番茄新品种。通过在病毒易发区多由试种示范表明,该多抗番茄不但抗病毒抗真菌效果突出,而且高产优质,适应性广。有关部门的专家们认为“这是我国番茄育种史上的重大新突破”。目前通过了国家级技术鉴定。 一、工程番茄的抗病性 TMV、CMV、PXV和致使番茄患斑枯病、晚疾病的二种真菌是番茄栽培的大害。其中CMV病毒为害尤烈,被称为“植物癌症”,对800多种农作物都有极大危害。农药等常规防治手段对它根本不起作用,人类目前也尚未找到一株能天然带有抗病毒特性的植株。国际上许多研究机构都在着力采用“转基因技术”以期获得生产上的多种品种。

转多基因抗病番茄及其栽培技术

国家生物工程中心利用现代生物技术,成功地将既抗多种病毒又抗真菌的人工合成卫星RNA基因转入同一番茄植株,获得了世界首例转多基因高抗烟草花叶病毒(TMV)、黄瓜花叶病毒(CMV)、马铃薯X病毒(PVX)和抗青枯病、晚疫病二种真菌的番茄植株。且培育出了“DRD8012”、“DBD8013”、“DRD8018”早、中、晚熟、抗病番茄新品种。通过在病毒易发区的两广、海南和吉林等省区多点试种示范表明,该抗病番茄不仅抗病毒、抗真菌效果突出,

转多基因抗病番茄

藜米为藜科一年生草本粮食作物,原产南美洲,具有很高的经济和营养价值,号称“粮中宝藏”,是一种极有发展前途的作物。藜米茎干直立,株高80～150厘米,根系分布在0～40厘米的土层。叶宽卵形,边缘具深波状的锯齿。

8年生转基因库安托杨外源基因转移及对土壤微生物数量影响的检测

[目的]评价转基因库安托杨可能引起的生态风险。[方法]利用PCR扩增研究外源基因水平转移情况,利用稀释平板法研究土壤中细菌、真菌和放线菌数量。[结果]电泳结果显示:林下杂草混合样品和土壤微生物DNA样品中均未出现目的基因片段。转基因株系和非转基因株系的非根际土壤中可培养的细菌、真菌和放线菌数量在杨树的不同生长期出现一定的变化,但是这种变化没有明显的规律。[结论]8年生转基因库安托杨未出现外源基因水平转移,也未对土壤微生物的数量产生显著影响。

盐胁迫下转复合多基因欧美杨107杨幼苗生长及生理响应

【目的】通过观测转复合多基因欧美杨107杨(转基因107杨)幼苗在不同浓度盐胁迫下生长性状,质膜透性、光合作用等各项指标,以及外源基因表达产物积累量的变化,综合评价转复合多基因杨树在盐胁迫下的适应能力。【方法】以转化成功且已经过验证的转基因107杨为试验材料,未转基因107杨为对照(CK),进行组培扩繁,在幼苗株高10 cm时定植在花盆中,置于人工气候室中培养。分别用0、3、6 g·L^(-1)的Na Cl溶液进行盐胁迫处理,胁迫25天后观测2个株系幼苗的生长指标、生理参数变化,以及甜菜碱与Bt毒蛋白的积累量。【结果】2个株系的生长指标观测结果表明:在低盐浓度处理下,转基因107杨幼苗株高增长量显著高于非转基因对照,转基因株系幼苗地径增长量与对照差异不显著;高盐浓度处理下,2个株系幼苗株高与地径均受到盐胁迫的显著影响。2个株系的生理参数观测结果表明:在低盐浓度处理下,转基因107杨幼苗质膜透性显著低于对照107杨,叶绿素含量有一定程度的增加,净光合速率与蒸腾速率显著高于对照,光系统Ⅱ实际光合效率Y(Ⅱ)小幅度降低但显著高于对照,光系统Ⅱ能够保持较高的电子传递速率;F_v/F_m增幅较高,具有较大光合作用潜力。在高盐浓度下,转基因株系幼苗叶绿素含量降幅较小,而质膜透性、净光合速率均显著降低,F_v/F_m、Y(Ⅱ)均呈现较大幅度下降,光系统Ⅱ电子传递速率受到较大影响,光合能力下降,变化趋势与对照相同,2个株系幼苗均受到较大程度的盐害。转基因株系中外源基因表达产物积累量的ELISA研究结果表明,随盐浓度的增加,Cry1Ac毒蛋白、Cry3A毒蛋白及甜菜碱含量都呈现增加趋势;在高盐浓度胁迫下外源基因产物积累量均显著增加。【结论】转基因107杨在低浓度盐胁迫下表现出良好的适应性,耐盐性优于对照107杨。在高浓度盐胁迫下转基因株系与对照107杨均受到较大影响,转基因株系并未显示其优势。盐胁迫可以诱导外源Bt基因、BADH基因表达加强,盐胁迫下转基因107杨表现出良好的耐盐和抗虫潜力。

Impact of Copy Number on Transgene Expression In Tobacco

对农杆菌介导法获得的转 β_葡糖醛酸酶 (β_glucuronidase ,GUS)基因 (uidA)烟草 (NicotianatabacumL .)进行GUS表达分析 ,发现部分转基因植株无GUS活性。进一步Southern杂交结果发现 ,GUS基因失活植株的基因组中整合了多个uidA拷贝 ,而GUS活性高的转基因植株多为uidA单拷贝整合 ,表明uidA基因失活与基因多拷贝整合有关。Northern杂交结果显示 ,失活植株无特异uidARNA杂交带 ,而GUS活性高的植株可检测到明显的杂交信号 ,说明多拷贝引起的基因失活发生在RNA水平。

Establishment of a Multiplex PCR System for Detecting Transgenic Ingredients from Citrus

[Objective] This study aimed to establish a multiplex PCR system for de- tecting transgenic ingredients from Citrus. [Method] Based on the pBI121 plasmid sequences published in GenBank and actin gene sequence of Citrus, the primers specific to CaMV35S promoter, NOS promoter, NOS terminator and actin gene were designed, to establish a multiple PCR system which could detect four types of sequences. In addition, orthogonal tests were performed to determine the optimal concentrations of all the components in PCR reaction system, as well as the optimal PCR cycle parameters. [Result] The optimal PCR reaction system should contain 2.5μl of 10xPCR buffer, 2.0μl of MgCI2 （25 mmol/L）, 2.0 μl of dNTP mixture （2.5 mmol/L of each dNTP）, 1.0 μl of actin gene primers （10μmol/L）, 1.0μl of 35S promoter primers （10 μmol/L）, 1.5 μl of NOS promoter primers （10 μmol/L） and 0.5 μl of NOS terminator primers （10μmol/L）, 0.1 μg of template DNA, 1.25 U of Taq DNA polymerase; ddH20 was added to the total reaction system of 25μl. The PCR reaction program consisted of pre-denaturing at 94℃ for 5 min; 31 cycles of denaturing at 94℃ for 30 s, annealing at 64.1℃ for 45 s and extension at 72℃ for 50 s; final extension at 72℃ for 10 min. The reaction system optimized with the orthogonal tests could detect as less as 0.1% transgenic component in the tested samples. [Conclusion] The MPCR detection system established in this study can meet the requirements in theory for detecting the genetically modified ingredients in Citrus or the deep-processed products.

Single nucleotide polymorphism in DNA methyltransferase 3B promoter and its association with gastric cardiac adenocarcinoma in North China

AIM:To investigate the association between single nucleotide polymorphism (SNP) in promoter of the DNA methyltrans-ferase 3B(DNMT3B) gene and risk for development and lymphatic metastasis of gastric cardiac adenocarcinoma (GCA). METHODS: The hospital based case-control study included 212 GCA patients and 294 control subjects without overt cancer. The DNMT3B SNP was genotyped by PCR and restriction fragment length polymorphism (RFLP) analysis. RESULTS: The C/C genotype was not detected in both GCA patients and controls. In control subjects, the frequency of T/T and C/T genotypes was 94.9% and 5.1% respectively, and that of T and C alleles was 97.4% and 2.6%, respectively. The genotype and allelotype distribution in the GCA patients was not significantly different from that in controls (P=0.34 and 0.33, respectively). When stratified by smoking status and family history of upper gastrointestinal cancer, significant difference in the genotype distribution was not observed between GCA patients and controls. The distribution of DNMT3B genotypes in GCA patents with or without lymphatic metastasis did not show significant difference (P= 0.42). CONCLUSION: The distribution of DNMT3B SNP in North China is distinct from that in Caucasians. Although this SNP has been associated with susceptibility to lung, head, neck and breast cancer, it may not be used as a stratification marker to predict susceptibility and lymphatic metastasis of GCA, at least in the population of North China.

DNA methyltransferase 3B promoter polymorphism and its susceptibility to primary hepatocellular carcinoma in the Chinese Han nationality population:A case-control study

AIM： To investigate the correlation between C/T single nucleotide polymorphism （SNP） in the promoter of the DNA methyltransferase 3B （D/VMT3B） gene and risk for development and progression of primary hepatocellular carcinoma （HCC）. METHODS： One hundred case subjects were selected consecutively from Tongji Hospital （Wuhan, China）. from March to November 2006. They did not receive radiotherapy or chemotherapy for newly diagnosed and histopathologically confirmed HCC. One hundred and forty control subjects having no history of cancerous or genetic diseases were healthy volunteers to Wuhan Blood Center in the same period. Frequency was matched for sex, age, alcohol consumption and cigarette smoking status of the case subjects. C/T polymorphism of the DNMT3B promoter was analyzed using polymerase chain reaction-restriction fragment length polymorphism （PCR-RFLP） and sequencing analysis. The association between genotypes of DNMT3B and clinicopathological parameters among cases was also studied. RESULTS： The CC genotype HCC patients and controls. was not detected in both In control subjects, the frequency of TT and CT genotypes was 99.3% and 0.7% respectively, and that of T and C alleles was 99.6% and 0.4% respectively. The frequency of CT genotype was higher in HCC （3.0%）. The frequency of T and C alleles was 98.5% and 1.5% respectively. However, the genotype and allelotype distribution in HCC patients was not significantly different from that in controls. CONCLUSION： C/T polymorphism is not associated with the increased risk of HCC. DNMT3B genetic polymorphism is variable in different races, ethnic groups or geographic areas. Further study is needed to clarify the role of DNMT3B SNP in the development of HCCamong other populations.

N-Acetyltransferase 2 genetic polymorphisms and risk of colorectal cancer

AIM:To investigate the possible association between meat intake,cigarette smoking and N-acetyltransferase 2 (NAT2) genetic polymorphisms on colorectal cancer (CRC) risk.METHODS:Patients with CRC were matched for gender and age to healthy controls.Meat intake and cigarette smoking were assessed using a specific frequency questionnaire.DNA was extracted from peripheral blood and the genotypes of the polymorphism were assessed by polymerase chain reaction-restriction fragment length polymorphism.Five NAT2 alleles were studied (WT,M1,M2,M3 and M4) using specific digestion enzymes.RESULTS:A total of 147 patients with colorectal cancer (76 women and 90 men with colon cancer) and 212 controls were studied.The mean age of the two groups was 62 years.More than half the subjects (59.8% in the case group and 51.9% in the control group) were NAT2 slow acetylators.The odds ratio for colorectal cancer was 1.38 (95% CI:0.90-2.12) in slow acetylators.Although the number of women was small (n=76 in the case group),the cancer risk was found to be lower in intermediate (W/Mx) acetylators [odds ratio (OR):0.55,95% confidence interval (95% CI):0.29-1.02].This difference was not observed in men (OR:0.56,95% CI:0.16-2.00).Among NAT2 fast acetylators (W/W or W/Mx),meat consumption more than 3 times a week increased the risk of colorectal cancer (OR:2.05,95% CI:1.01-4.16).In contrast,cigarette smoking increased the risk of CRC among slow acetylators (OR:1.97,95% CI:1.02-3.79).CONCLUSION:The risk of CRC was higher among fast acetylators who reported a higher meat intake.Slow NAT2 acetylation was associated with an increased risk of CRC.

Polymorphisms in sulfotransferase 1A1 and glutathione 5-transferase P1 genes in relation to colorectal cancer risk and patients' survival

AIM： To examine whether polymorphisms in SULTIA1 and GSTP1 genes contribute to colorectal cancer development and whether they are associated with clinicopathological variables are not well identified. METHODS： We examined the genotypes of 125 colorectal cancer patients and 666 healthy controls in a Swedish population by using PCR-restriction fragment length polymorphism （RFLP）. RESULTS： SULTIA1 ＊2/＊2 genotype （OR = 2.49, 95%CI = 1.48-4.19, P = 0.0002） and ＊2 allele （OR = 1.56, 95%CI =1.16-2.10, P = 0.002） had an effect on colorectal cancer susceptibility, while GSTP1 genotype was without effect. However, GSTP1 G-type predicted a worse prognosis in the patients independently of gender, age, Dukes＇ stage, growth pattern, and differentiation （P = 0.03）.CONCLUSION： Polymorphism in SULTIA1 may predispose to colorectal cancer and GSTP1 may be a biological indicator of prognosis in the patients.

Vegetable/fruit, smoking, glutathione S-transferase polymorphisms and risk for colorectal cancer in Taiwan

AIM: To investigate the colorectal cancer risk associated with polymorphic GSTM1, GSTT1 and GSTP1 and the effect of diet and smoking.METHODS: With consents, genotypes of the genes were determined using PCR methods for 727 cases and 736sex and age-matched healthy controls recruited at a medical center in the Northern Taiwan. Nurses who were blind to the study hypothesis conducted interviews with study participants for the information of socio-demographic variables, diet and smoking.RESULTS: There was no significant association between GSTM1 genotypes and the disease. Men, not women, with GSTT1 null genotype were at significant risk of colorectal cancer, but limited to rectal tumor, and in men aged 60 years and less. The corresponding association with the GSTP1 with G allele compared to GSTP1 A/A genotype was at borderline significance. Compared to men with GSTT1 present and GSTP1 A/A combined, men with both GSTT1 null and GSTP1 with G allele genotypes were at significant risk (odds ratio (OR) = 1.91, 95% confidence interval (CI) = 1.21-3.02), also limited to the rectal tumor and younger men. The beneficial effects of vegetable/fruit intake on colorectal cancer were much higher for men with GSTT1 present (OR = 0.32, 95%CI = 0.20-0.50) or GSTP1 A/A genotypes (OR = 0.40, 95%CI = 0.25-0.64).These effects remained significant for women. But, the greatest protective effect from vegetable/fruit intake for women was observed in those with GSTT1 null or GSTP1 with G allele genotypes. In addition, non-smoking men benefitted significantly from combined effect of higher vegetable/fruit intake and GSTT1 present or GSTP1 A/A genotypes with OR = 0.17 and 0.21 respectively.CONCLUSION: This study suggests that the GSTT1 gene can modulate the colorectal cancer risk and vegetable/fruit-related colorectal cancer risk, particularly in men of no smoking history.

ASSOCIATION ANALYSIS OF POLYMORPHISMS OF ACE GENE AND AGT GENE WITH ESSENTIAL HYPERTENSION IN CHINESE HAN'S POPULATION

Objective. To investigate whether the polymorphisms in the angiotensin converting enzyme (ACE) gene and angiotensinogen (AGT) gene are associated with essential hypertension. Methods. A case-control study was carried out using 103 hypertensive (HT) and 131 normotensive (NT) subjects. The insertion/deletion(I / D ) polymorphism of the ACE gene and the methionine→threo- nine variant at position 235 (M235T) of the AGT gene were determined by the polymerase chain reaction (PCR) technique and PCR/restriction fragment length polymorphism (PCR/RFLP) analysis, respective- ly. Results. The differences of D allele frequency and genotype distribution of the ACE gene between NT and HT groups were statistically significant (X^2=18.12, P<0. 005 ). The T235 allele frequency of the AGT gene was 69% in NT Chinese group (approximately 1. 38 to l. 64 fold that in Caucasians), and was greater in female HT than in NT (0. 82 vs 0. 72, X^2= 8. l, P<0. 025). A correlation between M235T molecular variant of the AGT gene and I/D molecular variant of ACE gene to hypertension was found. Cbeclusions. The possession of D allele of the ACE gene might be a marker for predisposition to hyper- tension. The T235 allele of the AGT gene was more common in Chinese than in Caucasians, and might contribute to the risk for hypertension in female Chinese.

Glutathione-S-transferase M1 polymorphisms on the susceptibility to esophageal cancer among three Chinese minorities:Kazakh,Tajik and Uygur

AIM： To investigate the glutathione-S-transferase M1 （GSTM1） polymorphisms in three Chinese minorities, Kazakh, Uygur, and Tajik; and the pathological significance of GSTM1 polymorphisms in esophageal carcinogenesis in Kazakh.METHODS： A total of 1121 blood samples （442 males and 679 females） were obtained from healthy Kazakh （654）, Uygur （412） and Tajik （55）. Primary esophageal squamous cell cancer （ESCC） tissues from Kazakh were obtained from 116 patients who underwent surgery. GSTM1 polymorphisms were analyzed by a combined approach of PCR and electrophoresis techniques.RESULTS： GSTM1 null genotype was found in 62.63% Uygur, 50.91% Tajik and 47.40% Kazakh. A significantly higher frequency of GSTM1 null genotype in Uygur was observed compared with Kazakh （OR： 1.859, 95% CI： 1.445 -2.391, χ^2 = 23.71, P = 0.000）. In addition, GSTM1 null genotype was found in 23.53% of welldifferentiated ESCC in Kazakh, in 49.23% of poorly differentiated ESCC, with a significant difference （OR： 3.152, 95% CI： 1.403-7.080, χ^2 = 8.018, P = 0.007）.CONCLUSION： There is a marked difference in the frequency of common GSTM1 null genotype between Uygur and Kazakh. GSTM1 null genotype is associated with differentiation of ESCC in Kazakh.

Transforming growth factor-β1 gene polymorphisms are associated with progression of liver fibrosis in Caucasians with chronic hepatitis C infection

AIM: Considerable attention is focused on polymorphisms in the gene encoding transforming growth factor-pi (TGF-β1), a multifunctional cytokine that is in turn a potent growth inhibitor involved in wound healing and differentiation. In humans, it promotes the pathogenesis of organ fibrosis, atherosclerosis, cancer, autoimmune and inflammatory diseases, keloid disease, and hypertrophic scarring. For this reason, much emphasis has been placed on studies elucidating the impact of TGF-β1 and its gene variations for the susceptibility and pathogenesis of these diseases. Unfortunately, some studies have serious limitations. METHODS: We have recently described a high-throughput method for investigation the Arg25Pro polymorphism of human TGF-β1 gene and showed that the frequency of the Pro25 allele is significantly associated with hepatic fibrogenesis. In this report, we describe two novel LightCyder (LC) techniques that facilitate the examination of the two other known alterations in the coding region of TGF-β1. We investigated whether these polymorphisms contribute to hepatitis-induced progression of fibrogenesis in Chinese and Caucasians. RESULTS: In the Chinese ancestry, the gene polymorphisms at codons 25 and 263 were not found and the genetic variant at codon 10 is unlikely to confer susceptibility to hepatic fibrosis. Contrarily, in Caucasians TGF-β1 allelic variations are more frequent and the presence of prolines either in codon 25 or 10 is associated with the interindividual variability in developing more severe fibrosis during chronic hepatitis C infection. CONCLUSION: In summary, these results confirm the hypothesis that TGF-β1 polymorphisms are associated with fibrosis progression in Caucasians chronically infected with hepatitis C.

No association between cyclooxygenase-2 and uridine diphosphate glucuronosyltransferase 1A6 genetic polymorphisms and colon cancer risk

AIM：To investigate the association of variations in the cyclooxygenase-2 （COX2） and uridine diphosphate glucuronosyltransferase 1A6 （UGTIA6） genes and non-steroidal anti-inflammatory drugs （NSAIDs） use with risk of colon cancer.METHODS： NSAIDs, which are known to reduce the risk of colon cancer, act directly on COX2 and reduce its activity. Epidemiological studies have associated variations in the COX2 gene with colon cancer risk, but others were unable to replicate this finding. Similarly,enzymes in the UGT1A6 gene have been demonstrated to modify the therapeutic effect of NSAIDs on colon adenomas. Polymorphisms in the UGTIA6 gene have been statistically shown to interact with NSAID intake to influence risk of developing colon adenomas, but not colon cancer. Here we examined the association of tagging single nucleotide polymorphisms （SNPs） in the COX2 and UGTIA6 genes, and their interaction with NSAID consumption, on risk of colon cancer in a population of 422 colon cancer cases and 481 population controls.RESULTS： No SNP in either gene was individually statistically significantly associated with colon cancer, nor did they statistically significantly change the protective effect of NSAID consumption in our sample. Like others, we were unable to replicate the association of variants in the COX2 gene with colon cancer risk （P 〉 0.05）,and we did not observe that these variants modify the protective effect of NSAIDs （P 〉 0.05）. We were able to confirm the lack of association of variants in UGT1A6 with colon cancer risk, although further studies will have to be conducted to confirm the association of these variants with colon adenomas.CONCLUSION： Our study does not support a role of COX2 and UGTIA6 genetic variations in the development of colon cancer.