sc-236 and Adenoma

sc-236 has been researched along with Adenoma* in 2 studies

Other Studies

2 other study(ies) available for sc-236 and Adenoma

Article	Year
Interaction of cigarette smoking with cyclooxygenase-2 on ulcerative colitis-associated neoplasia in mice. Cancer investigation, 2007, Volume: 25, Issue:8 The interactions of cigarette smoking with COX-2 on colitis and colitis-associated adenoma formation were studied. Mice were induced with colitis and exposed to cigarette smoke (CS) and/or SC236 (a COX-2 inhibitor). Results indicated that CS did not alter acute colonic inflammation. Addition of SC236 abolished the induction of proliferation and oxidative damage by colitis. Chronic SC236 treatment abolished the promoting effect of CS on colonic adenoma formation, via suppression of COX-2- and VEGF-mediated proliferation and angiogenesis, and reversed bcl-2-mediated inhibition of apoptosis by CS. To conclude, COX-2 inhibitor could be an implication on cancer prevention in smokers with chronic colitis. Topics: Adenoma; Animals; Apoptosis; Cell Proliferation; Colitis, Ulcerative; Colonic Neoplasms; Cyclooxygenase 2; Dextran Sulfate; Male; Mice; Mice, Inbred BALB C; Pyrazoles; Smoking; Sulfonamides	2007
Ubiquinol and the papaverine derivative caroverine prevent the expression of tumour- promoting factors in adenoma and carcinoma colon cancer cells induced by dietary fat. BioFactors (Oxford, England), 2005, Volume: 25, Issue:1-4 High consumption of dietary fat promotes colon carcinogenesis. While this effect is well known the underlying mechanism is not understood. Fatty acid hydroperoxides (LOOH) arise from unsaturated fatty acids in the presence of oxygen and elevated temperature during food processing. An approach was made starting from the assumption that LOOH are present in dietary fats as a result of boiling. LOOH undergoes homolytic cleavage in the presence of iron. We studied their effects on gene expression in colorectal tumour cells using linoleic acid hydroperoxide (LOOH) as model compound. Addition to the medium of LT97 adenoma and SW480 carcinoma cells enhanced the production of hydrogen peroxide. Both cell lines were observed to increase VEGF and COX-II expression based on mRNA. Expression of VEGF was inhibited by caroverine and ubiquinon. Topics: Adenoma; Carcinoma; Colonic Neoplasms; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase Inhibitors; Dietary Fats; Gene Expression Regulation, Neoplastic; Humans; Linoleic Acids; Lipid Peroxides; Organic Chemicals; Pyrazoles; Quinoxalines; Sulfonamides; Tumor Cells, Cultured; Ubiquinone; Vascular Endothelial Growth Factor A	2005

Article

Year

Interaction of cigarette smoking with cyclooxygenase-2 on ulcerative colitis-associated neoplasia in mice.

Cancer investigation, 2007, Volume: 25, Issue:8

The interactions of cigarette smoking with COX-2 on colitis and colitis-associated adenoma formation were studied. Mice were induced with colitis and exposed to cigarette smoke (CS) and/or SC236 (a COX-2 inhibitor). Results indicated that CS did not alter acute colonic inflammation. Addition of SC236 abolished the induction of proliferation and oxidative damage by colitis. Chronic SC236 treatment abolished the promoting effect of CS on colonic adenoma formation, via suppression of COX-2- and VEGF-mediated proliferation and angiogenesis, and reversed bcl-2-mediated inhibition of apoptosis by CS. To conclude, COX-2 inhibitor could be an implication on cancer prevention in smokers with chronic colitis.

Topics: Adenoma; Animals; Apoptosis; Cell Proliferation; Colitis, Ulcerative; Colonic Neoplasms; Cyclooxygenase 2; Dextran Sulfate; Male; Mice; Mice, Inbred BALB C; Pyrazoles; Smoking; Sulfonamides

2007

Ubiquinol and the papaverine derivative caroverine prevent the expression of tumour- promoting factors in adenoma and carcinoma colon cancer cells induced by dietary fat.

BioFactors (Oxford, England), 2005, Volume: 25, Issue:1-4

High consumption of dietary fat promotes colon carcinogenesis. While this effect is well known the underlying mechanism is not understood. Fatty acid hydroperoxides (LOOH) arise from unsaturated fatty acids in the presence of oxygen and elevated temperature during food processing. An approach was made starting from the assumption that LOOH are present in dietary fats as a result of boiling. LOOH undergoes homolytic cleavage in the presence of iron. We studied their effects on gene expression in colorectal tumour cells using linoleic acid hydroperoxide (LOOH) as model compound. Addition to the medium of LT97 adenoma and SW480 carcinoma cells enhanced the production of hydrogen peroxide. Both cell lines were observed to increase VEGF and COX-II expression based on mRNA. Expression of VEGF was inhibited by caroverine and ubiquinon.

Topics: Adenoma; Carcinoma; Colonic Neoplasms; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase Inhibitors; Dietary Fats; Gene Expression Regulation, Neoplastic; Humans; Linoleic Acids; Lipid Peroxides; Organic Chemicals; Pyrazoles; Quinoxalines; Sulfonamides; Tumor Cells, Cultured; Ubiquinone; Vascular Endothelial Growth Factor A

2005