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1. Park YS: [COX-2 inhibitors in inflammatory bowel disease: friends or foes?]. Korean J Gastroenterol; 2007 Dec;50(6):350-5
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  • COX-2 is frequently overexpressed in colonic adenoma and carcinoma.
  • Specific inhibitors of COX-2 have been shown to induce apoptosis in tumor cells and to inhibit tumor growth in animal models and in humans.
  • In a recent study, powerful chemopreventive ability of selective COX-2 inhibitor was observed in colitis-related colon carcinogenesis in mouse model.
  • But it was reported that even selective COX inhibitors aggravated the DSS-induced colonic inflammation.
  • It is assumed that endogenous PGs are involved in the mucosal defense against DSS-induced colonic ulcerations which are produced by COX-1 at early phase and by COX-2 at late phase.
  • Long-term use of COX-2 inhibitors for the chemoprevention of colitic cancer is needed to define their mechanism of action, that reduce side effects and have specific tumor target.
  • [MeSH-major] Colitis, Ulcerative / drug therapy. Cyclooxygenase 2 Inhibitors / therapeutic use
  • [MeSH-minor] Animals. Colonic Neoplasms / diagnosis. Cyclooxygenase 1 / metabolism. Cyclooxygenase 2 / metabolism. Humans. Mice. Models, Animal

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  • (PMID = 18159171.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2
  • [Number-of-references] 59
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2. Scott PA, Kingsley GH, Smith CM, Choy EH, Scott DL: Non-steroidal anti-inflammatory drugs and myocardial infarctions: comparative systematic review of evidence from observational studies and randomised controlled trials. Ann Rheum Dis; 2007 Oct;66(10):1296-304
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  • [Title] Non-steroidal anti-inflammatory drugs and myocardial infarctions: comparative systematic review of evidence from observational studies and randomised controlled trials.
  • OBJECTIVE: The comparative risk of myocardial infarction (MI) with cyclo-oxygenase-2-specific drugs and traditional non-steroidal anti-inflammatory drugs (NSAIDs) was determined.
  • METHODS: The results of studies of a suitable size in colonic adenoma and arthritis-that had been published in English and from which crude data about MIs could be extracted-were evaluated.
  • Four RCTs of NSAIDs in colonic adenoma (6000 patients) showed an increased risk of MI (RR 2.68; 95% CI 1.43 to 5.01).
  • Fourteen RCTs in arthritis (45 425 patients) showed more MIs with cyclo-oxygenase-2-specific drugs (Peto OR 1.6; 95% CI 1.1 to 2.4), but fewer serious upper gastrointestinal events (Peto OR 0.40; 95% CI 0.31 to 0.53).
  • CONCLUSION: The overall risk of MI with NSAIDs and cyclo-oxygenase-2-specific drugs was small; rofecoxib showed the highest risk.
  • There was an increased MI risk with cyclo-oxygenase-2-specific drugs compared with NSAIDs, but less serious upper gastrointestinal toxicity.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Myocardial Infarction / chemically induced
  • [MeSH-minor] Adenoma / drug therapy. Arthritis / drug therapy. Colonic Neoplasms / drug therapy. Cyclooxygenase 2 Inhibitors / adverse effects. Gastrointestinal Diseases / chemically induced. Humans. Randomized Controlled Trials as Topic. Research Design. Risk Assessment

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  • (PMID = 17344246.001).
  • [ISSN] 0003-4967
  • [Journal-full-title] Annals of the rheumatic diseases
  • [ISO-abbreviation] Ann. Rheum. Dis.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors
  • [Number-of-references] 115
  • [Other-IDs] NLM/ PMC1994282
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3. Wagenaar-Miller RA, Hanley G, Shattuck-Brandt R, DuBois RN, Bell RL, Matrisian LM, Morgan DW: Cooperative effects of matrix metalloproteinase and cyclooxygenase-2 inhibition on intestinal adenoma reduction. Br J Cancer; 2003 May 6;88(9):1445-52
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  • [Title] Cooperative effects of matrix metalloproteinase and cyclooxygenase-2 inhibition on intestinal adenoma reduction.
  • Matrix metalloproteinases (MMPs) and cyclooxygenase-2 (COX-2) are expressed in both sporadic and familial adenomatous colonic polyps and tumours and have been independently shown to play causal roles in intestinal tumour formation in mouse models of colon cancer.
  • The apparent roles of these enzymes in intestinal tumorigenesis led us to examine, in the Min mouse model of colon cancer, if selective COX-2 and MMP inhibitors provide additive or synergistic therapeutic benefits in intestinal tumour prevention.
  • MMPI) and the selective COX-2 inhibitor (A-285969; COX-2I) both showed dose-dependent inhibition of the number of adenomas in Min mice.
  • Apoptosis, proliferation, and angiogenesis were assayed in tumors from each treatment group.

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  • (PMID = 12778076.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA60867; United States / NCI NIH HHS / CA / T32 CA009385; United States / NCI NIH HHS / CA / P30 CA68485; United States / NCI NIH HHS / CA / T32 CA 09385; United States / NCI NIH HHS / CA / P30 CA068485; United States / NCI NIH HHS / CA / R01 CA060867
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / A 177430; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Enzyme Inhibitors; 0 / Isoenzymes; 0 / Matrix Metalloproteinase Inhibitors; 0 / Peptides, Cyclic; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  • [Other-IDs] NLM/ PMC2741031
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4. Serfaty L, De Leusse A, Rosmorduc O, Desaint B, Flejou JF, Chazouilleres O, Poupon RE, Poupon R: Ursodeoxycholic acid therapy and the risk of colorectal adenoma in patients with primary biliary cirrhosis: an observational study. Hepatology; 2003 Jul;38(1):203-9
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  • [Title] Ursodeoxycholic acid therapy and the risk of colorectal adenoma in patients with primary biliary cirrhosis: an observational study.
  • Ursodeoxycholic acid (UDCA) is the first-line treatment for primary biliary cirrhosis (PBC).
  • The long-term administration of UDCA might indirectly favor colon carcinogenesis by increasing the fecal excretion of secondary bile acids or, in contrast, it might inhibit colon carcinogenesis, as demonstrated in animal models.
  • In patients with PBC, we examined the effect of prolonged UDCA administration on the prevalence and recurrence of colorectal adenoma and on the proliferation of colon epithelial cells.
  • The prevalence of colon adenoma was compared in patients already treated with UDCA (mean duration 46 months) at the time of colonoscopy (treated group, n = 52) and in patients undergoing colonoscopy just prior to treatment initiation (untreated group, n = 62).
  • The recurrence of adenoma following removal (mean follow-up, 35 months) was compared between UDCA-treated patients and appropriate age- and gender-matched controls (2/1) selected from a cohort of 205 patients undergoing polypectomy.
  • Epithelial cell proliferation was assessed using anti-Ki67 antibodies on colon biopsies from both treated and untreated patients.
  • The prevalence of colorectal adenomas was 13% in the treated group versus 24% in the untreated group (P =.16).
  • The colon epithelial cell proliferation index was significantly lower in treated patients than in untreated patients (P =.001).
  • Following removal of the adenoma, the probability of recurrence was significantly lower in patients treated with UDCA than in controls (7% vs. 28% at 3 years, P =.04).
  • In conclusion, this study suggests that, in patients with PBC, the prolonged administration of UDCA (1) is not associated with an increased prevalence of colorectal adenomas, and (2) significantly decreases the probability of colorectal adenoma recurrence following removal.
  • These results are strengthened by the significant reduction in colon epithelial cell proliferation seen in patients treated with UDCA.
  • [MeSH-major] Adenoma / epidemiology. Cholagogues and Choleretics / therapeutic use. Colorectal Neoplasms / epidemiology. Liver Cirrhosis, Biliary / drug therapy. Liver Cirrhosis, Biliary / epidemiology. Ursodeoxycholic Acid / therapeutic use
  • [MeSH-minor] Adult. Cell Division / drug effects. Colonoscopy. Female. Humans. Intestinal Mucosa / pathology. Male. Middle Aged. Neoplasm Recurrence, Local. Prevalence. Product Surveillance, Postmarketing. Risk Factors

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  • (PMID = 12830003.001).
  • [ISSN] 0270-9139
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cholagogues and Choleretics; 724L30Y2QR / Ursodeoxycholic Acid
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5. Hsu HH, Cheng SF, Chen LM, Liu JY, Chu CH, Weng YJ, Li ZY, Lin CS, Lee SD, Kuo WW, Huang CY: Over-expressed estrogen receptor-alpha up-regulates hTNF-alpha gene expression and down-regulates beta-catenin signaling activity to induce the apoptosis and inhibit proliferation of LoVo colon cancer cells. Mol Cell Biochem; 2006 Sep;289(1-2):101-9
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  • [Title] Over-expressed estrogen receptor-alpha up-regulates hTNF-alpha gene expression and down-regulates beta-catenin signaling activity to induce the apoptosis and inhibit proliferation of LoVo colon cancer cells.
  • Epidemiologic studies reported that the prevalence of hereditary non-polyposis colon cancer (HNPCC) in male is about 1.5-fold higher than that in female.
  • Patients that received E(2) replacement therapy were found to have a reduction in the incidence of colon adenoma and carcinoma.
  • The results clearly demonstrated that overexpressed ERalpha with or without E(2) (10(-8) M) treatment could activate caspase -8, -9, and 3 and induce DNA fragmentation in LoVo cell.
  • At the same time, overexpressed ERalpha plus E(2) significantly increases the expression and promoter activity of hTNF-alpha, and the DNA fragmentation effect induced by E(2) plus ERalpha were reduced by the addition of hTNF antibody (0.1 ng(ml).
  • Efforts aiming at enhancing ERalpha expression and(or activity may be proved to be an alternative therapy against colorectal cancer.
  • [MeSH-major] Apoptosis. Colonic Neoplasms / pathology. Estrogen Receptor alpha / metabolism. Gene Expression Regulation. Signal Transduction. Tumor Necrosis Factor-alpha / genetics. beta Catenin / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / metabolism. Caspases / metabolism. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Proliferation. DNA Fragmentation. Down-Regulation / genetics. Estrogens / pharmacology. Female. Humans. Male. Middle Aged. Promoter Regions, Genetic / drug effects. Transfection. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / metabolism. Up-Regulation / genetics. Wnt Proteins / metabolism

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  • (PMID = 16628468.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cell Cycle Proteins; 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / TNF protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; 0 / Wnt Proteins; 0 / beta Catenin; EC 3.4.22.- / Caspases
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6. Burn J, Bishop DT, Mecklin JP, Macrae F, Möslein G, Olschwang S, Bisgaard ML, Ramesar R, Eccles D, Maher ER, Bertario L, Jarvinen HJ, Lindblom A, Evans DG, Lubinski J, Morrison PJ, Ho JW, Vasen HF, Side L, Thomas HJ, Scott RJ, Dunlop M, Barker G, Elliott F, Jass JR, Fodde R, Lynch HT, Mathers JC, CAPP2 Investigators: Effect of aspirin or resistant starch on colorectal neoplasia in the Lynch syndrome. N Engl J Med; 2008 Dec 11;359(24):2567-78
Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .

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  • BACKGROUND: Observational and epidemiologic data indicate that the use of aspirin reduces the risk of colorectal neoplasia; however, the effects of aspirin in the Lynch syndrome (hereditary nonpolyposis colon cancer) are not known.
  • Resistant starch has been associated with an antineoplastic effect on the colon.
  • METHODS: In a randomized, placebo-controlled trial, we used a two-by-two design to investigate the effects of aspirin, at a dose of 600 mg per day, and resistant starch (Novelose), at a dose of 30 g per day, in reducing the risk of adenoma and carcinoma among persons with the Lynch syndrome.
  • Over a mean period of 29 months (range, 7 to 74), colonic adenoma or carcinoma developed in 141 participants.
  • Of 693 participants randomly assigned to receive aspirin or placebo, neoplasia developed in 66 participants receiving aspirin (18.9%), as compared with 65 receiving placebo (19.0%) (relative risk, 1.0; 95% confidence interval [CI], 0.7 to 1.4).
  • Among the 727 participants receiving resistant starch or placebo, neoplasia developed in 67 participants receiving starch (18.7%), as compared with 68 receiving placebo (18.4%) (relative risk, 1.0; 95% CI, 0.7 to 1.4).
  • Advanced adenomas and colorectal cancers were evenly distributed in the two groups.
  • CONCLUSIONS: The use of aspirin, resistant starch, or both for up to 4 years has no effect on the incidence of colorectal adenoma or carcinoma among carriers of the Lynch syndrome. (Current Controlled Trials number, ISRCTN59521990. )
  • [MeSH-major] Adenoma / prevention & control. Aspirin / therapeutic use. Carcinoma / prevention & control. Colorectal Neoplasms / prevention & control. Colorectal Neoplasms, Hereditary Nonpolyposis / drug therapy. Starch / therapeutic use
  • [MeSH-minor] Adult. Aged. DNA Mismatch Repair / genetics. Drug Therapy, Combination. Female. Humans. Incidence. Male. Middle Aged. Proportional Hazards Models. Risk. Treatment Failure

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  • [Copyright] 2008 Massachusetts Medical Society
  • [CommentIn] N Engl J Med. 2009 Apr 2;360(14):1462; author reply 1462-3 [19348022.001]
  • [CommentIn] Gastroenterology. 2009 Aug;137(2):730-2 [19563844.001]
  • [CommentIn] N Engl J Med. 2009 Apr 2;360(14):1461-2; author reply 1462-3 [19339729.001]
  • [ErratumIn] N Engl J Med. 2009 Apr 2;360(14):1470
  • (PMID = 19073976.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ISRCTN/ ISRCTN59521990
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / D20173; United Kingdom / Medical Research Council / / G0100496; United Kingdom / Medical Research Council / / MC/ U127527198; United Kingdom / Cancer Research UK / / A4994; United Kingdom / Cancer Research UK / / C1297/A5013; United Kingdom / Cancer Research UK / / C588/A4994
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9005-25-8 / Starch; R16CO5Y76E / Aspirin
  • [Investigator] Adamson P; Armstrong O; Ball J; Baxter L; Birkett A; Boussioutas A; Bradshaw N; Brewer C; Broughton M; Bulman B; Castiglione M; Clarke S; Ching R; Chu C; Coaker J; Cina S; Cook J; Coxhead J; Crawford G; Cummings C; Davies R; Debniak T; de Moncuit C; Drummond S; Ellis T; Farthing K; Fidalgo P; Gallinger S; Gascoyne J; Gilroy J; Goff S; Goldberg P; Goodman S; Harocopos C; Hodgson S; Jeffcoat R; Jeffers L; Jordan S; Killick P; Krauss C; Kristensen J; Langman C; Leite J; Liljegren A; Lindgren G; Lynagh L; Oliani C; Marks C; Miller J; Miles T; Murday V; Perez Segura P; Pietersen E; Platten U; Reed L; Rossi G; Sala P; Sampson J; Schmocker B; Shaw J; Spigelman A; Tempesta A; Toes R; Velthuizen M; Wakelen P; Walpole I; Lynch H; Burn J; Mathers J; Bishop DT; Fodde R; Mecklin JP; Macrae F; Vasen H; Möslein G; Ramesar R; Kerr D; Perkins S; Cuzick J; Faulds Wood L; Steele R; Altman D; Paraskeva C; Atkin W; Hull M
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7. Singh M, Dhindsa G, Friedland S, Triadafilopoulos G: Long-term use of proton pump inhibitors does not affect the frequency, growth, or histologic characteristics of colon adenomas. Aliment Pharmacol Ther; 2007 Oct 1;26(7):1051-61
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  • [Title] Long-term use of proton pump inhibitors does not affect the frequency, growth, or histologic characteristics of colon adenomas.
  • BACKGROUND: The clinical significance of the trophic effects of long-term proton pump inhibitors (PPI)-related hypergastrinemia on colon polyps remains unknown.
  • AIM: To study the frequency, growth, and histology of colon polyps in patients on chronic PPI therapy (cases), compared to those not receiving acid suppression (controls).
  • RESULTS: Demographics and risk factors for colon cancer were comparable between the two groups.
  • At baseline the mean frequency and size of adenomatous polyps were similar in cases and controls (P > 0.05) and at follow-up, these were 0.89 and 1.18 (P > 0.05; 95% CI of -0.08 to 0.66) and 4.09 mm and 4.00 mm (P > 0.05; 95% CI -2.29 to 2.11), respectively with no significant change.
  • However, control group had a higher mean frequency and size of hyperplastic polyps at baseline as well as at follow-up colonoscopy (P < 0.05).
  • CONCLUSIONS: The long-term use of PPI does not influence the frequency, growth, or histology of adenomatous polyps, but is associated with a reduction in both baseline and interval development of hyperplastic polyps.
  • [MeSH-major] Adenomatous Polyps / drug therapy. Colonic Polyps / drug therapy. Proton Pump Inhibitors / therapeutic use
  • [MeSH-minor] Colonoscopy. Female. Humans. Male. Middle Aged. Retrospective Studies. Treatment Outcome

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  • (PMID = 17877512.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK063624
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proton Pump Inhibitors
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8. Ju J, Hao X, Lee MJ, Lambert JD, Lu G, Xiao H, Newmark HL, Yang CS: A gamma-tocopherol-rich mixture of tocopherols inhibits colon inflammation and carcinogenesis in azoxymethane and dextran sulfate sodium-treated mice. Cancer Prev Res (Phila); 2009 Feb;2(2):143-52
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  • [Title] A gamma-tocopherol-rich mixture of tocopherols inhibits colon inflammation and carcinogenesis in azoxymethane and dextran sulfate sodium-treated mice.
  • We investigated the effects of a gamma-tocopherol-rich mixture of tocopherols (gamma-TmT, containing 57% gamma-T, 24% delta-T, and 13% alpha-T) on colon carcinogenesis in azoxymethane (AOM)/dextran sulfate sodium (DSS)-treated mice.
  • In the AOM/DSS-treated mice, dietary gamma-TmT treatment resulted in a significantly lower colon inflammation index (52% of the control) on day 7 and number of colon adenomas (9% of the control) on week 7. gamma-TmT treatment also resulted in higher apoptotic index in adenomas, lower prostaglandin E2, leukotriene B4, and nitrotyrosine levels in the colon, and lower prostaglandin E2, leukotriene B4, and 8-isoprostane levels in the plasma on week 7.
  • In experiment 2 with AOM/DSS- treated mice sacrificed on week 21, dietary 0.17% or 0.3% gamma-TmT treatment, starting 1 week before the AOM injection, significantly inhibited adenocarcinoma and adenoma formation in the colon (to 17-33% of the control).
  • Dietary 0.3% gamma-TmT that was initiated after DSS treatment also exhibited a similar inhibitory activity.
  • The present study showed that gamma-TmT effectively inhibited colon carcinogenesis in AOM/DSS-treated mice, and the inhibition may be due to the apoptosis-inducing, anti-inflammatory, antioxidative, and reactive nitrogen species-trapping activities of tocopherols.

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  • (PMID = 19155443.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA072720; United States / NIEHS NIH HHS / ES / ES05022; United States / NIEHS NIH HHS / ES / P30 ES005022; United States / NCI NIH HHS / CA / P30 CA072720-12; United States / NIEHS NIH HHS / ES / ES005022-109003; United States / NIEHS NIH HHS / ES / P30 ES005022-109003; United States / NCI NIH HHS / CA / CA72720; United States / NCI NIH HHS / CA / CA072720-12
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Carcinogens; 1HGW4DR56D / Leukotriene B4; 27415-26-5 / 8-epi-prostaglandin F2alpha; 3604-79-3 / 3-nitrotyrosine; 42HK56048U / Tyrosine; 8EF1Z1238F / gamma-Tocopherol; 9042-14-2 / Dextran Sulfate; B7IN85G1HY / Dinoprost; K7Q1JQR04M / Dinoprostone; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ NIHMS172441; NLM/ PMC2821738
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9. Doyle KJ, McLaren CE, Shanks JE, Galus CM, Meyskens FL: Effects of difluoromethylornithine chemoprevention on audiometry thresholds and otoacoustic emissions. Arch Otolaryngol Head Neck Surg; 2001 May;127(5):553-8
eScholarship, California Digital Library, University of California. Full text from University of California eScholarship .

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  • DESIGN: A prospective, randomized, placebo-controlled phase 2 clinical trial of DFMO in participants with a prior adenomatous colonic polyp.
  • PARTICIPANTS: One hundred twenty-three volunteer subjects with colorectal polyps and normal hearing for the frequencies 250 through 2000 Hz.
  • OUTCOME MEASURES: Pure-tone audiometric thresholds for the frequencies 250, 500, 1000, 2000, 3000, 4000, 6000, and 8000 Hz and DPOAE levels were measured at baseline and 1, 3, 6, 9, and 12 months after starting treatment with DFMO or placebo and 3 months after cessation of treatment if there was a suggestion of possible changes at the 12-month measurement.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Audiometry, Pure-Tone. Auditory Threshold / drug effects. Deafness / prevention & control. Eflornithine / administration & dosage. Ornithine Decarboxylase Inhibitors. Otoacoustic Emissions, Spontaneous / drug effects
  • [MeSH-minor] Colonic Polyps / drug therapy. Colorectal Neoplasms / diet therapy. Enzyme Inhibitors / administration & dosage. Humans. Prospective Studies

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  • (PMID = 11346432.001).
  • [ISSN] 0886-4470
  • [Journal-full-title] Archives of otolaryngology--head & neck surgery
  • [ISO-abbreviation] Arch. Otolaryngol. Head Neck Surg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 59024
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Ornithine Decarboxylase Inhibitors; ZQN1G5V6SR / Eflornithine
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10. Scott RH, Mansour S, Pritchard-Jones K, Kumar D, MacSweeney F, Rahman N: Medulloblastoma, acute myelocytic leukemia and colonic carcinomas in a child with biallelic MSH6 mutations. Nat Clin Pract Oncol; 2007 Feb;4(2):130-4
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  • [Title] Medulloblastoma, acute myelocytic leukemia and colonic carcinomas in a child with biallelic MSH6 mutations.
  • Background A 13-year-old girl presented with rectal bleeding and was found to have two colonic carcinomas (stage Dukes' C) and multiple colonic polyps.
  • At the age of 7 years she had widespread hyperpigmented and hypopigmented skin lesions, and had developed medulloblastoma, which was treated with chemotherapy and craniospinal irradiation.
  • At the age of 10 years she had developed acute myelocytic leukemia, M5.
  • She was treated with chemotherapy including sibling bone marrow transplant with busulfan/cyclophosphamide conditioning.
  • A three-generation family history identified no relatives with colonic carcinomas or polyposis.
  • Investigations Immunohistochemical analysis was performed on a sample of colonic adenoma.
  • [MeSH-major] Cerebellar Neoplasms / genetics. Colonic Neoplasms / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Medulloblastoma / genetics


11. Scott IS, Morris LS, Bird K, Davies RJ, Vowler SL, Rushbrook SM, Marshall AE, Laskey RA, Miller R, Arends MJ, Coleman N: A novel immunohistochemical method to estimate cell-cycle phase distribution in archival tissue: implications for the prediction of outcome in colorectal cancer. J Pathol; 2003 Oct;201(2):187-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel immunohistochemical method to estimate cell-cycle phase distribution in archival tissue: implications for the prediction of outcome in colorectal cancer.
  • An immunohistochemical method for assessing cell-cycle phase distribution in colorectal resection specimens would enable phase data to be incorporated into diagnostic algorithms for the estimation of prognosis and response to adjuvant chemotherapy in colorectal cancer.
  • Paraffin sections of normal colon (n = 25), colonic adenoma (n = 15), and colonic adenocarcinoma (n = 30) were analysed by immunohistochemistry using antibodies against markers of cell-cycle entry, Mcm-2 and Ki67, and putative markers of the cell-cycle phase, cyclins D1 and E (putative markers of G1 phase), cyclin A (S phase), cytoplasmic cyclin B1 (G2 phase), and phosphohistone H3 (M phase).
  • The phase specificity of each marker was assessed by examining the degree of co-expression of adjacent phase markers using double-antibody fluorescence confocal microscopy and by comparison with flow cytometric analysis performed on adjacent tissue sections.
  • The S-phase specificity of detectable cyclin A was also assessed in combination with in situ DNA replication using fluorescence confocal microscopy.
  • Adjacent phase markers were not significantly co-expressed, confirming the relative specificity of these markers in tissue sections of colon.
  • The S-phase labelling index, as defined by detectable cyclin A expression, showed a positive correlation with the Mcm-2 labelling index and increased in the progression from normal colon to adenocarcinoma.
  • In conclusion, a combination of these cell-cycle phase markers can be used to calculate the distribution of cells throughout each phase of the cell cycle in colorectal tissue sections.
  • Detectable cyclin A can be used as a surrogate marker of S phase and may be of value in predicting prognosis and response to adjuvant therapy.
  • [MeSH-major] Adenocarcinoma / pathology. Cell Cycle Proteins / analysis. Colonic Neoplasms / pathology
  • [MeSH-minor] Adenoma / chemistry. Adenoma / pathology. Biomarkers / analysis. Cell Cycle. Cyclin A / analysis. Cyclin B / analysis. Cyclin B1. Cyclin D1 / analysis. Cyclin E / analysis. Flow Cytometry. Histones / analysis. Humans. Immunohistochemistry / methods. Ki-67 Antigen / analysis. Microscopy, Confocal. Minichromosome Maintenance Complex Component 2. Nuclear Proteins / analysis. Predictive Value of Tests. Prognosis. Sensitivity and Specificity. Statistics, Nonparametric

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  • [Copyright] Copyright 2003 John Wiley & Sons, Ltd.
  • (PMID = 14517835.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / CCNB1 protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin A; 0 / Cyclin B; 0 / Cyclin B1; 0 / Cyclin E; 0 / Histones; 0 / Ki-67 Antigen; 0 / Nuclear Proteins; 136601-57-5 / Cyclin D1; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 2
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12. Hillson JL, Furst DE: Rofecoxib. Expert Opin Pharmacother; 2000 Jul;1(5):1053-66
SciCrunch. DrugBank: Data: Chemical .

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  • Rofecoxib (Vioxx, Merck & Co., Inc.) is a new orally-effective non-steroidal anti-inflammatory drug (NSAID) approved for treatment of acute pain, fever, primary dysmenorrhea and pain and inflammation in osteoarthritis (OA).
  • It is also being evaluated for treatment of rheumatoid arthritis and adenomatous polyps of the colon.
  • Rofecoxib is a specific inhibitor of cyclooxygenase-2 (COX-2), thereby inhibiting prostanoid synthesis in cells that express COX-2, including inflammatory cells.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Cyclooxygenase Inhibitors / therapeutic use. Isoenzymes / drug effects. Lactones / therapeutic use. Prostaglandin-Endoperoxide Synthases / drug effects
  • [MeSH-minor] Animals. Arthritis / drug therapy. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Drug Approval. Humans. Membrane Proteins. Pain / drug therapy. Sulfones

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  • (PMID = 11249495.001).
  • [ISSN] 1465-6566
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Lactones; 0 / Membrane Proteins; 0 / Sulfones; 0QTW8Z7MCR / rofecoxib; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  • [Number-of-references] 63
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13. Yu MK, Wade M, Fitzpatrick FA: Evaluating 2-chlorodeoxycytidine for its novel mechanism as a DNA methylation inhibitor. J Clin Oncol; 2004 Jul 15;22(14_suppl):3125

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although the adenomatous polyposis coli gene is frequently somatically mutated in colon carcinoma, methylation of the adenomatous polyposis coli gene is seen in early colon adenomas.
  • Thus, epigenetic silencing of tumor suppressor genes may play a role in the progression of colon polyps to carcinomas.
  • Further, reactivation of critical tumor suppressor genes in carcinomas may decrease chemotherapy resistance.
  • This drug has problems of DNA mutagenesis.
  • We are evaluating 2-chlorodeoxycytidine for its inhibitory properties of s-adenosylhomocysteine hydrolase.
  • This time point is then used for future experiments.
  • Methylation sensitive endonuclease digested DNA will be amplified by real time polymerase chain reaction to assess for promoter methylation.

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  • (PMID = 28014866.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Nobuoka A, Takayama T, Miyanishi K, Sato T, Takanashi K, Hayashi T, Kukitsu T, Sato Y, Takahashi M, Okamoto T, Matsunaga T, Kato J, Oda M, Azuma T, Niitsu Y: Glutathione-S-transferase P1-1 protects aberrant crypt foci from apoptosis induced by deoxycholic acid. Gastroenterology; 2004 Aug;127(2):428-43
Hazardous Substances Data Bank. DEOXYCHOLIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND & AIMS: Aberrant crypt foci, precursors of colonic adenoma, are frequently positive for glutathione-S-transferase P1-1.
  • Because deoxycholic acid is an apoptosis-inducing xenobiotic in the colon, we examined the possibility that aberrant crypt foci, through the cytoprotecting function of glutathione-S-transferase P1-1, resist deoxycholic acid-induced apoptosis, thereby surviving to become adenomas and subsequently cancer.
  • Glutathione-S-transferase P1-1 was transfected into colon cancer cells (M7609) and human lung fibroblasts, and deoxycholic acid-induced apoptosis was evaluated by a dye-uptake assay and flow cytometry.
  • The percentage of apoptotic cells in aberrant crypt foci was significantly lower than in healthy epithelium, and the difference became more apparent with deoxycholic acid treatment.
  • The impaired sensitivity of aberrant crypt foci to deoxycholic acid was restored by the glutathione-S-transferase P1-1-specific inhibitor gamma-glutamyl-S-(benzyl)cysteinyl-R-phenylglycine diethylester.
  • The aberrant crypt foci in adenoma patients treated with sulindac, which was shown to bind to glutathione-S-transferase P1-1, underwent apoptosis in 4 days and mostly regressed in 2-3 months.
  • CONCLUSIONS: Glutathione-S-transferase P1-1 protects aberrant crypt foci from deoxycholic acid-induced apoptosis and may play a pivotal role in early colon carcinogenesis.
  • [MeSH-major] Adenoma / drug therapy. Apoptosis / physiology. Colonic Neoplasms / drug therapy. Deoxycholic Acid / toxicity. Detergents / toxicity. Glutathione / analogs & derivatives. Glutathione Transferase / metabolism. Sulindac / analogs & derivatives
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Cell Line, Tumor. Cyclooxygenase 2. Enzyme Inhibitors / pharmacology. Fibroblasts / cytology. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Intestinal Mucosa / drug effects. Intestinal Mucosa / pathology. Isoenzymes / genetics. Lung / cytology. Membrane Proteins. Prostaglandin-Endoperoxide Synthases / genetics. RNA, Messenger / analysis. Transfection

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  • (PMID = 15300575.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Detergents; 0 / Enzyme Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / gamma-Glu-S-BzCys-PhGly diethyl ester; 005990WHZZ / Deoxycholic Acid; 184SNS8VUH / Sulindac; 6UVA8S2DEY / sulindac sulfide; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 2.5.1.18 / Glutathione Transferase; GAN16C9B8O / Glutathione; K619IIG2R9 / sulindac sulfone
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15. Iwama T: NSAIDs and colorectal cancer prevention. J Gastroenterol; 2009;44 Suppl 19:72-6
MedlinePlus Health Information. consumer health - Colorectal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This article discusses the merits and limits of nonsteroidal antiinflammatory drugs (NSAIDs), including cyclooxygenase (COX)-2 inhibitors, for colorectal cancer prevention.
  • Then, the results of a randomized double-blind clinical test that examined the regressive effect of a COX-2-specific inhibitor on adenoma of familial adenomatous polyposis (FAP) are presented.
  • These results suggest that a higher dose of COX-2 inhibitors has a suppressive effect on adenoma of the colon and rectum, although a moderate clinical dose of COX-2 inhibitors does not induce clinically effective suppression of adenoma.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Colorectal Neoplasms / prevention & control. Cyclooxygenase 2 Inhibitors / therapeutic use
  • [MeSH-minor] Adenoma / pathology. Adenoma / prevention & control. Adenomatous Polyposis Coli / drug therapy. Adenomatous Polyposis Coli / pathology. Clinical Trials as Topic. Dose-Response Relationship, Drug. Humans. Practice Guidelines as Topic

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  • (PMID = 19148797.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors
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16. van Gorkom BA, Karrenbeld A, van der Sluis T, Zwart N, van der Meer R, de Vries EG, Kleibeuker JH: Calcium or resistant starch does not affect colonic epithelial cell proliferation throughout the colon in adenoma patients: a randomized controlled trial. Nutr Cancer; 2002;43(1):31-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Calcium or resistant starch does not affect colonic epithelial cell proliferation throughout the colon in adenoma patients: a randomized controlled trial.
  • Patients with a history of sporadic adenomas have increased epithelial cell proliferative activity, an intermediate risk marker for colorectal cancer.
  • To evaluate whether calcium or resistant starch could reduce proliferative activity throughout the colon, we performed a randomized controlled trial in 111 sporadic adenoma patients.
  • After 2 mo, biopsies were collected from the cecum, transverse and sigmoid colon, and rectum during colonoscopy.
  • Colonic epithelial cell proliferative activity throughout the colon of sporadic adenoma patients is not affected by supplementation with 1 g of calcium or 19 g of resistant starch.
  • [MeSH-major] Adenoma / diet therapy. Calcium, Dietary / administration & dosage. Colon / drug effects. Colon / pathology. Colorectal Neoplasms / diet therapy. Epithelial Cells / drug effects. Epithelial Cells / pathology. Starch / administration & dosage
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Division / drug effects. Female. Humans. Male. Middle Aged

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  • (PMID = 12467132.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium, Dietary; 9005-25-8 / Starch
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17. Vilaichone RK, Mahachai V, Kullavanijaya P, Nunthapisud P: Spontaneous bacterial peritonitis caused by Streptococcus bovis: case series and review of the literature. Am J Gastroenterol; 2002 Jun;97(6):1476-9
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  • Streptococcus bovis is the rare cause of spontaneous bacterial peritonitis in decompensated cirrhosis. S. bovis bacteremia has long been known to be associated with colon cancer.
  • We describe seven patients and review the seven previous reports of spontaneous bacterial peritonitis patients with S. bovis infection.
  • Colonic adenomatous polyps with dysplastic change were found in 18.2% of the patients.
  • The approach to this group of patients requires diagnostic paracentesis, blood cultures, ascitic fluid culture, and treatment with antimicrobial agents.
  • The physician could make a case that colonoscopy is not needed because the patient is very sick and the possibility of GI pathology, especially colonic lesions, has been low.
  • [MeSH-major] Peritonitis / microbiology. Streptococcal Infections / diagnosis. Streptococcal Infections / drug therapy. Streptococcus bovis
  • [MeSH-minor] Aged. Anti-Bacterial Agents / therapeutic use. Female. Humans. Injections, Intravenous. Male. Middle Aged. Penicillins / administration & dosage. Penicillins / therapeutic use

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  • (PMID = 12094869.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Penicillins
  • [Number-of-references] 16
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18. Graefe T, Wollina U, Schulz H, Burgdorf W: Muir-Torre syndrome - treatment with isotretinoin and interferon alpha-2a can prevent tumour development. Dermatology; 2000;200(4):331-3
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Muir-Torre syndrome - treatment with isotretinoin and interferon alpha-2a can prevent tumour development.
  • A 57-year-old man presented with multiple sebaceous tumours, kerato-acanthomas, verrucous carcinoma of the nose, renal cell and transitional cell carcinomas of the left kidney, adenoma of the colon and a positive family history of colon carcinoma.
  • 3 x 10(6) U three times a week along with 50 mg isotretinoin daily as well as topical isotretinoin gel.
  • During a follow-up of 29 months, only 1 sebaceous skin tumour developed and was removed, whereas more than 30 such skin tumours had been surgically removed during the last 3 years.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasms, Multiple Primary / drug therapy. Sebaceous Gland Neoplasms / drug therapy
  • [MeSH-minor] Humans. Interferon-alpha / administration & dosage. Isotretinoin / administration & dosage. Male. Middle Aged. Recombinant Proteins. Skin / drug effects. Skin / pathology. Syndrome

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  • [Copyright] Copyright 2000 S. Karger AG, Basel
  • (PMID = 10894967.001).
  • [ISSN] 1018-8665
  • [Journal-full-title] Dermatology (Basel, Switzerland)
  • [ISO-abbreviation] Dermatology (Basel)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Recombinant Proteins; 47RRR83SK7 / interferon alfa-2a; EH28UP18IF / Isotretinoin
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19. Pan YL, Zheng S, Xiao ZX, Cao J, Yao HP: [Subcutaneous transplantation of microencapsulated Chinese hamster ovary (CHO) cells/pcDNA 3.1/mIL-12 and subcutaneous transplantation of microencapsulated CHO/pcDNA3.1/mIL-12 combined with 5-fluoro-uracil in treatment of tumor-burdened mice]. Zhonghua Yi Xue Za Zhi; 2003 Jan 10;83(1):51-4
Hazardous Substances Data Bank. FLUOROURACIL .

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  • [Title] [Subcutaneous transplantation of microencapsulated Chinese hamster ovary (CHO) cells/pcDNA 3.1/mIL-12 and subcutaneous transplantation of microencapsulated CHO/pcDNA3.1/mIL-12 combined with 5-fluoro-uracil in treatment of tumor-burdened mice].
  • OBJECTIVE: To investigate the effect of subcutaneous transplantation of microencapsulated Chinese hamster ovary cells (CHO)/pcDNA3.1/mIL-12 and subcutaneous transplantation of microencapsulated CHO/pcDNA3.1/mIL-12 combined with 5-fluoro-uracilum (5-FU) in treatment of tumor-burdened mice.
  • (1) IL-12 group, microencapsulated CHO/pcDNA3.1/mIL-12 was injected subcutaneously, (2) combined treatment group: CHO/pcDN with 5-FU, (3) 5-FU group: 5-FU was injected intraperitoneally, (4) blank vector group: CHO/pcDNA3.1 was injected subcutaneously, (5) tumor-burdened group: without any treatment, and (6) blank control group: normal mice without any treatment.
  • Except the mice of the blank control group, all mice were injected subcutaneously into the inner side of right thigh with mice colonic adenoma cells.
  • 20 days after the treatment, 5 mice in each group were killed to examine the serum Th1 type cytokines: interferon (IFN)-gamma, IL-12, and Th2 type cytokins: IL-4, IL-10 by double antibody sandwich ELISA.
  • The activity of NK was significantly much more in combined treatment group than in the tumor-burdened group.
  • The levels of Th1 type cytokines were the lowest in the tumor-burdened group.
  • There was no difference in the levels of Th1 type cytokine between the tumor-burdened group and 5-FU group.
  • However, the levels of Th1 type cytokine were significantly higher in the IL-12 group than in other groups.
  • The levels of Th2 type cytokines were rather high in the tumor-burdened group.
  • There was no difference in the levels of Th2 type cytokine between the tumor-burdened group and 5-FU group.
  • However, the levels of Th2 type cytokine were the lowest in the IL-12 group than in other groups.
  • The mean diameters of tumor in the IL-12 group and combined treatment group were significantly smaller than in the 5-FU, tumor-burdened, and blank vector groups (P < 0.05), however, without a difference between the IL-12 group and combined treatment group.
  • The survival periods of the IL-12 group and combined treatment group were significantly longer than those in the blank vector, tumor-burdened and 5-FU groups (P < 0.05).
  • CONCLUSION: Microencapsulated CHO/pcDNA3.1/mIL-12 transplanted subcutaneously significantly improves the immune function of tumor-burdened mice and partially overcomes immune suppression caused by chemotherapy, and is effective in slowing the growth of tumor and lengthening the survival period of tumor-burdened ice.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Fluorouracil / therapeutic use. Interleukin-12 / therapeutic use. Neoplasms, Experimental / drug therapy. Organ Transplantation
  • [MeSH-minor] Animals. CHO Cells. Cricetinae. Disease Models, Animal. Drug Compounding. Female. Mice. Neoplasm Transplantation. Transfection

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  • (PMID = 12757646.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 187348-17-0 / Interleukin-12; U3P01618RT / Fluorouracil
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20. Gupta M, Eisen GM: NSAIDs and the gastrointestinal tract. Curr Gastroenterol Rep; 2009 Oct;11(5):345-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Aspirin and COX-2 inhibitors are associated with reduced colon adenoma risk, but higher dose and longer duration of treatment with aspirin appears effective.
  • Hence, patients at high risk of colorectal cancer (with significant family or personal history of premalignant adenoma) must be identified, and cardiovascular and GI risk must be assessed before using these agents as chemopreventive drugs.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Gastrointestinal Diseases / prevention & control. Gastrointestinal Tract / drug effects
  • [MeSH-minor] Adenoma / prevention & control. Arthritis, Rheumatoid / drug therapy. Colonic Neoplasms / prevention & control. Cyclooxygenase Inhibitors / therapeutic use. Drug Therapy, Combination. Duodenal Ulcer / prevention & control. Humans. Proton Pump Inhibitors / therapeutic use. Risk Assessment. Stomach Ulcer / prevention & control

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  • (PMID = 19765361.001).
  • [ISSN] 1534-312X
  • [Journal-full-title] Current gastroenterology reports
  • [ISO-abbreviation] Curr Gastroenterol Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase Inhibitors; 0 / Proton Pump Inhibitors
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21. Martinez ME, O'Brien TG, Fultz KE, Babbar N, Yerushalmi H, Qu N, Guo Y, Boorman D, Einspahr J, Alberts DS, Gerner EW: Pronounced reduction in adenoma recurrence associated with aspirin use and a polymorphism in the ornithine decarboxylase gene. Proc Natl Acad Sci U S A; 2003 Jun 24;100(13):7859-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pronounced reduction in adenoma recurrence associated with aspirin use and a polymorphism in the ornithine decarboxylase gene.
  • Most sporadic colon adenomas acquire mutations in the adenomatous polyposis coli gene (APC) and show defects in APC-dependent signaling.
  • APC influences the expression of several genes, including the c-myc oncogene and its antagonist Mad1.
  • Ornithine decarboxylase (ODC), the first enzyme in polyamine synthesis, is a transcriptional target of c-myc and a modifier of APC-dependent tumorigenesis.
  • We show that individuals homozygous for the minor ODC A-allele who reported using aspirin are approximately 0.10 times as likely to have an adenoma recurrence as non-aspirin users homozygous for the major G-allele.
  • Mad1 selectively suppressed the activity of the ODC promoter containing the A-allele, but not the G-allele, in a human colon cancer-derived cell line (HT29).
  • Aspirin (>or=10 microM) did not affect ODC allele-specific promoter activity but did activate polyamine catabolism and lower polyamine content in HT29 cells.
  • We propose that the ODC polymorphism and aspirin act independently to reduce the risk of adenoma recurrence by suppressing synthesis and activating catabolism, respectively, of colonic mucosal polyamines.
  • These findings confirm the hypothesis that the ODC polymorphism is a genetic marker for colon cancer risk, and support the use of ODC inhibitors and aspirin, or other nonsteroidal antiinflammatory drugs (NSAIDs), in combination as a strategy for colon cancer prevention.

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  • (PMID = 12810952.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA023074; United States / NCI NIH HHS / CA / CA-95060; United States / NCI NIH HHS / CA / CA-41108; United States / NCI NIH HHS / CA / KO1 CA79069-10; United States / NCI NIH HHS / CA / P01 CA041108; United States / NCI NIH HHS / CA / P50 CA095060; United States / NCI NIH HHS / CA / CA-23074; United States / NCI NIH HHS / CA / CA-72008; United States / NCI NIH HHS / CA / P01 CA072008
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Polyamines; 63231-63-0 / RNA; EC 4.1.1.17 / Ornithine Decarboxylase; R16CO5Y76E / Aspirin
  • [Other-IDs] NLM/ PMC164678
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22. Melstrom LG, Bentrem DJ, Salabat MR, Kennedy TJ, Ding XZ, Strouch M, Rao SM, Witt RC, Ternent CA, Talamonti MS, Bell RH, Adrian TA: Overexpression of 5-lipoxygenase in colon polyps and cancer and the effect of 5-LOX inhibitors in vitro and in a murine model. Clin Cancer Res; 2008 Oct 15;14(20):6525-30
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  • [Title] Overexpression of 5-lipoxygenase in colon polyps and cancer and the effect of 5-LOX inhibitors in vitro and in a murine model.
  • Many studies have examined the effects of COX inhibitors on human colorectal cancer, but the role of 5-LOX in colonic cancer development has not been well studied.
  • The purpose of this study was to evaluate the expression of 5-LOX in colonic polyps and cancer and the effect of 5-LOX inhibition on colon cancer cell proliferation.
  • EXPERIMENTAL DESIGN: Colonic polyps, cancer, and normal mucosa were evaluated for 5-LOX expression by immunohistochemistry.
  • Reverse transcription-PCR was used to establish 5-LOX expression in colon cancer cells.
  • A heterotopic xenograft model in athymic mice using HT29 and LoVo human colon cancer cells was used to evaluate the effect of the 5-LOX inhibitor zileuton on tumor growth.
  • RESULTS: 5-LOX is overexpressed in adenomatous polyps and cancer compared with that of normal colonic mucosa.
  • LOX inhibition and 5-LOX inhibition decreased DNA synthesis in a concentration- and time-dependent manner in the Lovo cell line (P < 0.05).
  • Inhibition of 5-LOX in an in vivo colon cancer xenograft model inhibited tumor growth compared with that of controls (P < 0.05).
  • CONCLUSIONS: This study showed that 5-LOX is up-regulated in adenomatous colon polyps and cancer compared with normal colonic mucosa.
  • The blockade of 5-LOX inhibits colon cancer cell proliferation both in vitro and in vivo and may prove a beneficial chemopreventive therapy in colon cancer.
  • [MeSH-major] Arachidonate 5-Lipoxygenase / metabolism. Colonic Neoplasms / enzymology. Colonic Polyps / enzymology. Disease Models, Animal. Lipoxygenase Inhibitors / pharmacology
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / enzymology. Adenoma / pathology. Animals. Apoptosis / drug effects. Cell Proliferation / drug effects. Female. Humans. Immunoenzyme Techniques. In Vitro Techniques. Masoprocol / therapeutic use. Mice. Mice, Inbred BALB C. Mice, Nude. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Thymidine / metabolism. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 18927292.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipoxygenase Inhibitors; 0 / RNA, Messenger; 7BO8G1BYQU / Masoprocol; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; VC2W18DGKR / Thymidine
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23. Varey AH, Rennel ES, Qiu Y, Bevan HS, Perrin RM, Raffy S, Dixon AR, Paraskeva C, Zaccheo O, Hassan AB, Harper SJ, Bates DO: VEGF 165 b, an antiangiogenic VEGF-A isoform, binds and inhibits bevacizumab treatment in experimental colorectal carcinoma: balance of pro- and antiangiogenic VEGF-A isoforms has implications for therapy. Br J Cancer; 2008 Apr 22;98(8):1366-79
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  • [Title] VEGF 165 b, an antiangiogenic VEGF-A isoform, binds and inhibits bevacizumab treatment in experimental colorectal carcinoma: balance of pro- and antiangiogenic VEGF-A isoforms has implications for therapy.
  • Bevacizumab, an anti-vascular endothelial growth factor (VEGF-A) antibody, is used in metastatic colorectal carcinoma (CRC) treatment, but responses are unpredictable.
  • Using isoform-specific enzyme-linked immunosorbent assay and quantitative polymerase chain reaction, we found that over 90% of the VEGF in normal colonic tissue was VEGF(xxx)b, but there was a variable upregulation of VEGF(xxx) and downregulation of VEGF(xxx)b in paired human CRC samples.
  • Furthermore, cultured colonic adenoma cells expressed predominantly VEGF(xxx)b, whereas colonic carcinoma cells expressed predominantly VEGF(xxx).
  • However, adenoma cells exposed to hypoxia switched their expression from predominantly VEGF(xxx)b to predominantly VEGF(xxx).
  • VEGF(165)b overexpression in LS174t colon cancer cells inhibited colon carcinoma growth in mouse xenograft models.
  • However, although bevacizumab effectively inhibited the rapid growth of colon carcinomas expressing VEGF(165), it did not affect the slower growth of tumours from colonic carcinoma cells expressing VEGF(165)b.
  • Both bevacizumab and anti-VEGF(165)b-specific antibodies were cytotoxic to colonic epithelial cells, but less so to colonic carcinoma cells.
  • Together with the identification of an autocrine cytoprotective role for VEGF(165)b in colonic epithelial cells, these results indicate that bevacizumab treatment of human CRC may depend upon this balance of VEGF isoforms.
  • [MeSH-major] Angiogenesis Inhibitors / physiology. Antibodies, Monoclonal / therapeutic use. Colorectal Neoplasms / drug therapy. Vascular Endothelial Growth Factor A / physiology
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Bevacizumab. Cell Line, Tumor. Cell Proliferation. Colon / metabolism. Humans. Mice. Protein Isoforms. RNA Splicing. RNA, Messenger / analysis

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  • (PMID = 18349829.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / British Heart Foundation / / FS/06/038; United Kingdom / British Heart Foundation / / BS/06/005/20340; United Kingdom / British Heart Foundation / / FS/04/22; United Kingdom / Cancer Research UK / / A8451; United Kingdom / Cancer Research UK / / ; United Kingdom / British Heart Foundation / / BS/2001003/12790; United Kingdom / British Heart Foundation / / BB2000003
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 2S9ZZM9Q9V / Bevacizumab
  • [Other-IDs] NLM/ PMC2361696; NLM/ UKMS2582
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24. Hsu WH, Wu IC, Kuo CH, Su YC, Lu CY, Kuo FC, Jan CM, Wang WM, Wu DC, Yu FJ: Influence of proton pump inhibitor use in gastrointestinal polyps. Kaohsiung J Med Sci; 2010 Feb;26(2):76-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Influence of proton pump inhibitor use in gastrointestinal polyps.
  • PPI-induced hypergastrinemia is one of the very few side effects associated with these drugs.
  • However, because hypergastrinemia is related to the occurrence of colonic adenomatous polyps, the purpose of this study was to analyze the relationship between the occurrence of gastrointestinal polyps and hypergastrinemia induced by PPIs.
  • Chart records, including medication history and fasting plasma gastrin level, were reviewed and analyzed.
  • Any subtle polypoid lesions in the stomach and colon were sampled by biopsy for histological examination.
  • A total of 122 patients were receiving PPI treatment for either peptic ulcer disease or reflux esophagitis and were included as the study group.
  • The remaining 137 patients were not treated with PPIs and served as the non-PPI group.
  • The mean fasting gastrin level in PPI users versus non-PPI users was 121.8 ng/L versus 56.8 ng/L, respectively (p < 0.001).
  • Although the prevalence of gastric gland polyps was higher in the PPI group (65.6% vs. 37.2%, p < 0.001), there was no difference in the prevalence of colonic adenomatous polyps observed (22.13% vs. 22.62%, p = 0.928).
  • In conclusion, the prevalence of gastric polyps, particularly fundic gland polyps, was higher among PPI users.
  • However, the prevalence of colonic polyps was not affected by PPI use, regardless of past history of colonic adenomatous polyps.
  • [MeSH-major] Anti-Ulcer Agents / adverse effects. Gastrointestinal Diseases / drug therapy. Polyps / drug therapy. Proton Pump Inhibitors / adverse effects

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  • (PMID = 20123595.001).
  • [ISSN] 1607-551X
  • [Journal-full-title] The Kaohsiung journal of medical sciences
  • [ISO-abbreviation] Kaohsiung J. Med. Sci.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Proton Pump Inhibitors
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25. Brändlein S, Pohle T, Vollmers C, Wozniak E, Ruoff N, Müller-Hermelink HK, Vollmers HP: CFR-1 receptor as target for tumor-specific apoptosis induced by the natural human monoclonal antibody PAM-1. Oncol Rep; 2004 Apr;11(4):777-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CFR-1 receptor as target for tumor-specific apoptosis induced by the natural human monoclonal antibody PAM-1.
  • This CFR-1/PAM-1 receptor is post-transcriptionally modified and over-expressed on human epithelial tumors and carcinoma pre-cancer lesions such as H. pylori induced gastritis, intestinal metaplasia and dysplasia of the stomach, ulcerative colitis-related dysplasia and adenomas of the colon, Barrett metaplasia and dysplasia of the esophagus, squamous cell metaplasia and dysplasia of the lung and cervical intraepithelial neoplasia.
  • Both, the unique tumor-specific expression of the CFR-1/PAM-1 receptor and the growth inhibitory effect of the PAM-1 antibody makes this combination a good diagnostic and therapeutic tool for all kinds of epithelial cancers and precursor lesions.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Apoptosis. Carcinoma / drug therapy. Receptors, Cell Surface / antagonists & inhibitors. Sialoglycoproteins / antagonists & inhibitors
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Animals. Biological Assay. Cell Line, Tumor. Humans. Immunochemistry. Mice. Mice, Inbred Strains. Neoplasm Transplantation. Pepsin A / chemistry. Receptors, Fibroblast Growth Factor. Stomach Neoplasms / drug therapy. Stomach Neoplasms / pathology

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  • [ErratumIn] Oncol Rep. 2004 Jul;12(1):201
  • (PMID = 15010872.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / PAM-1 monoclonal antibody, human; 0 / Receptors, Cell Surface; 0 / Receptors, Fibroblast Growth Factor; 0 / Sialoglycoproteins; 0 / cysteine-rich fibroblast growth factor receptor; EC 3.4.23.1 / Pepsin A
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26. Khosraviani K, Weir HP, Hamilton P, Moorehead J, Williamson K: Effect of folate supplementation on mucosal cell proliferation in high risk patients for colon cancer. Gut; 2002 Aug;51(2):195-9
Hazardous Substances Data Bank. FOLIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of folate supplementation on mucosal cell proliferation in high risk patients for colon cancer.
  • AIMS: Intracellular folate deficiency has been implicated in colonic carcinogenesis in epidemiological studies and animal and human cancer models.
  • Our aim was to determine the effect of folate supplementation on patients with recurrent adenomatous polyps using rectal mucosal cell proliferation as a biomarker.
  • PATIENTS AND METHODS: Eleven patients with recurrent adenomatous polyps of the colon were randomised into a treatment group (n=6) receiving a dietary supplement of 2 mg folic acid per day for three months and a control group (n=5) receiving a placebo.
  • The S phase cells which incorporated BrdU into their DNA were identified following immunohistochemical staining.
  • Twenty five orientated crypts were identified for each time point and the number and position of BrdU positive and BrdU negative cells were counted.
  • RESULTS: The LI of the treatment group (9.1 (6.7, 12.3)) and the control group (9.3 (7.8, 10.3)) were comparable at the start.
  • CONCLUSION: These data indicate that (a) folate supplementation decreases colonic mucosal cell proliferation in a high risk group for colon cancer and (b) the most significant reduction takes place at the luminal aspect of the crypt.
  • [MeSH-major] Colonic Neoplasms / prevention & control. Colonic Polyps / drug therapy. Dietary Supplements. Folic Acid / administration & dosage. Intestinal Mucosa / cytology
  • [MeSH-minor] Cell Division / drug effects. Erythrocytes / chemistry. Humans. Rectum. Recurrence. Risk. Statistics, Nonparametric

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  • (PMID = 12117879.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 935E97BOY8 / Folic Acid
  • [Other-IDs] NLM/ PMC1773332
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27. Hudson EA, Howells LM, Gallacher-Horley B, Fox LH, Gescher A, Manson MM: Growth-inhibitory effects of the chemopreventive agent indole-3-carbinol are increased in combination with the polyamine putrescine in the SW480 colon tumour cell line. BMC Cancer; 2003 Jan 14;3:2
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Growth-inhibitory effects of the chemopreventive agent indole-3-carbinol are increased in combination with the polyamine putrescine in the SW480 colon tumour cell line.
  • In animal models of colon carcinogenesis, inhibition of ODC activity by difluoromethylornithine (DFMO) has been shown to reduce the number and size of colon adenomas and carcinomas.
  • Indole-3-carbinol (I3C) has shown promising chemopreventive activity against a range of human tumour cell types, but little is known about the effect of this agent on colon cell lines.
  • Here, we investigated whether inhibition of ODC by I3C could contribute to a chemopreventive effect in colon cell lines.
  • RESULTS: I3C inhibited proliferation of the human colon tumour cell lines HT29 and SW480, and of the normal tissue-derived HCEC line, and at higher concentrations induced apoptosis in SW480 cells.
  • While administration of exogenous putrescine reversed the growth-inhibitory effect of DFMO, it did not reverse the growth-inhibition following an I3C treatment, and in the case of the SW480 cell line, the effect was actually enhanced.
  • In this cell line, combination treatment caused a slight increase in the proportion of cells in the G2/M phase of the cell cycle, and increased the proportion of cells undergoing necrosis, but did not predispose cells to apoptosis.
  • CONCLUSION: While indole-3-carbinol decreased ornithine decarboxylase activity in the colon cell lines, it appears unlikely that this constitutes a major mechanism by which the agent exerts its antiproliferative effect, although accumulation of spermine may cause cytotoxicity and contribute to cell death.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Colonic Neoplasms / drug therapy. Indoles / pharmacology. Putrescine / pharmacology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Apoptosis. Biological Transport / drug effects. Cell Cycle / drug effects. Cell Division / drug effects. Dose-Response Relationship, Drug. Drug Therapy, Combination. Eflornithine / pharmacology. Enzyme Inhibitors / pharmacology. Humans. Ornithine Decarboxylase / metabolism. Ornithine Decarboxylase Inhibitors. Polyamines / analysis. Tumor Cells, Cultured

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  • (PMID = 12525265.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Indoles; 0 / Ornithine Decarboxylase Inhibitors; 0 / Polyamines; C11E72455F / indole-3-carbinol; EC 4.1.1.17 / Ornithine Decarboxylase; V10TVZ52E4 / Putrescine; ZQN1G5V6SR / Eflornithine
  • [Other-IDs] NLM/ PMC149232
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28. Sano Y, Kuga R, Fu KI, Yoshino T, Yoshida S, Ochiai A, Fujii T: Superficially elevated colonic adenoma changed to undetectable configuration on ordinary endoscopy during treatment with preferential cyclooxygenase-2 inhibitor. J Gastroenterol; 2003;38(9):909-10

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Superficially elevated colonic adenoma changed to undetectable configuration on ordinary endoscopy during treatment with preferential cyclooxygenase-2 inhibitor.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / pathology. Colonic Neoplasms / drug therapy. Colonic Neoplasms / pathology. Cyclooxygenase Inhibitors / therapeutic use. Etodolac / therapeutic use

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  • (PMID = 14564639.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 2M36281008 / Etodolac
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