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 ris...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.展开更多
The objective of this study was to investigate the pantoprazole and rebamipide efficiency on NSAIDs （nonsteroidal anti-inflammatory drugs）-gastropathy restoring and healing in patients with coronary heart disease, s...The objective of this study was to investigate the pantoprazole and rebamipide efficiency on NSAIDs （nonsteroidal anti-inflammatory drugs）-gastropathy restoring and healing in patients with coronary heart disease, stable angina, who have been taking aspirin for a long time period. The study included three groups of patients according to the treatment they have got： ASA （acetylsalicylic acid） in the first group; ASA and pantoprazole in the second; ASA, pantoprazole and rebamipide in the third one. To obtain the results, endoscopic method and proinflammatory cytokines LTB4 and protective prostaglandin E2 determination in the blood were used. The research demonstrated no ulcer effects in the group of patients who were treated by rebamipide, and significantly fewer gastroduodenal erosions, in comparison to the group, where treatment contained ASA and pantoprazole. The LTB4 （leukotriene B4） level decreased in pantoprazole and rebamipide treatment groups, but the PGE2 （prostaglandin E2） level increased only after rebamipide therapy. Therefore, rebamipide should be included to the therapy for the better NSAIDs-gastropathy treatment, in reason of its good reparative and gastroprotective properties.展开更多
基金Supported by A Damon Runyon Cancer Research Foundation Clinical Investigator Award,CI-8An R25 training grant from the National Cancer Institute,R25T CA094186+1 种基金The Case Center for Transdisciplinary Research on Energetics and Cancer,1U54 CA-116867-01A National Cancer Institute K22 Award,1K22 CA120545-01
文摘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.
文摘The objective of this study was to investigate the pantoprazole and rebamipide efficiency on NSAIDs （nonsteroidal anti-inflammatory drugs）-gastropathy restoring and healing in patients with coronary heart disease, stable angina, who have been taking aspirin for a long time period. The study included three groups of patients according to the treatment they have got： ASA （acetylsalicylic acid） in the first group; ASA and pantoprazole in the second; ASA, pantoprazole and rebamipide in the third one. To obtain the results, endoscopic method and proinflammatory cytokines LTB4 and protective prostaglandin E2 determination in the blood were used. The research demonstrated no ulcer effects in the group of patients who were treated by rebamipide, and significantly fewer gastroduodenal erosions, in comparison to the group, where treatment contained ASA and pantoprazole. The LTB4 （leukotriene B4） level decreased in pantoprazole and rebamipide treatment groups, but the PGE2 （prostaglandin E2） level increased only after rebamipide therapy. Therefore, rebamipide should be included to the therapy for the better NSAIDs-gastropathy treatment, in reason of its good reparative and gastroprotective properties.
