[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 15 of about 15
1. Gupta M, Eisen GM: NSAIDs and the gastrointestinal tract. Curr Gastroenterol Rep; 2009 Oct;11(5):345-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] BMJ. 1988 Oct 22;297(6655):1017-21 [3142593.001]
  • [Cites] Lancet. 2002 Jan 5;359(9300):14-22 [11809181.001]
  • [Cites] Am J Gastroenterol. 2000 Sep;95(9):2218-24 [11007221.001]
  • [Cites] Inflamm Bowel Dis. 2004 Jul;10(4):352-6 [15475742.001]
  • [Cites] Cancer Prev Res (Phila). 2009 Apr;2(4):310-21 [19336730.001]
  • [Cites] Arch Intern Med. 2002 Jan 28;162(2):169-75 [11802750.001]
  • [Cites] Ann Intern Med. 1991 Feb 15;114(4):257-63 [1987872.001]
  • [Cites] Lancet. 2002 Jan 5;359(9300):9-13 [11809180.001]
  • [Cites] N Engl J Med. 1998 Mar 12;338(11):727-34 [9494149.001]
  • [Cites] Ann Intern Med. 1991 Nov 15;115(10):787-96 [1834002.001]
  • [Cites] JAMA. 2000 Sep 13;284(10):1247-55 [10979111.001]
  • [Cites] N Engl J Med. 1998 Mar 12;338(11):719-26 [9494148.001]
  • [Cites] N Engl J Med. 2003 Mar 6;348(10):891-9 [12621133.001]
  • [Cites] Gut. 1992 Jul;33(7):887-9 [1644327.001]
  • [Cites] Clin Gastroenterol Hepatol. 2007 Jul;5(7):818-28, 828.e1-5; quiz 768 [17556027.001]
  • [Cites] Am J Gastroenterol. 2000 Aug;95(8):1949-54 [10950041.001]
  • [Cites] Aliment Pharmacol Ther. 2004 Apr 1;19(7):755-64 [15043516.001]
  • [Cites] Am J Gastroenterol. 2008 Apr;103(4):872-82 [18371130.001]
  • [Cites] Aliment Pharmacol Ther. 2005 Jun 15;21(12):1411-8 [15948807.001]
  • [Cites] Health Technol Assess. 2007 Dec;11(51):iii-iv, 1-164 [18021578.001]
  • [Cites] Clin Gastroenterol Hepatol. 2003 May;1(3):160-9 [15017486.001]
  • [Cites] J Rheumatol Suppl. 1999 Apr;56:18-24 [10225536.001]
  • [Cites] Lancet. 2007 Feb 10;369(9560):465-73 [17292766.001]
  • [Cites] Aliment Pharmacol Ther. 2008 Jul;28(1):97-106 [18397385.001]
  • [Cites] N Engl J Med. 1996 May 30;334(22):1435-9 [8618582.001]
  • [Cites] Arch Intern Med. 1993 Jul 26;153(14):1665-70 [8333804.001]
  • [Cites] Clin Gastroenterol Hepatol. 2006 Feb;4(2):203-11 [16469681.001]
  • [Cites] N Engl J Med. 2001 Mar 29;344(13):967-73 [11274623.001]
  • [Cites] Gastroenterology. 2008 Jan;134(1):29-38 [18022173.001]
  • [Cites] N Engl J Med. 2003 Mar 6;348(10):883-90 [12621132.001]
  • [Cites] N Engl J Med. 2006 Aug 31;355(9):885-95 [16943401.001]
  • [Cites] Clin Gastroenterol Hepatol. 2005 Jan;3(1):55-9 [15645405.001]
  • [Cites] BMJ. 2003 May 24;326(7399):1118 [12763982.001]
  • [Cites] Lancet. 2007 May 12;369(9573):1621-6 [17499604.001]
  • [Cites] N Engl J Med. 2006 Aug 31;355(9):873-84 [16943400.001]
  • [Cites] Aliment Pharmacol Ther. 2008 Sep 1;28(5):629-37 [18616644.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2001 Oct;15(5):723-38 [11566037.001]
  • [Cites] Gastroenterology. 2008 Nov;135(5):1517-25 [18823986.001]
  • [Cites] N Engl J Med. 2000 Jun 29;342(26):1946-52 [10874062.001]
  • [Cites] Scand J Gastroenterol. 2008;43(4):490-6 [18365915.001]
  • [Cites] Lancet. 1999 Dec 18-25;354(9196):2106-11 [10609815.001]
  • [Cites] Gastroenterology. 2001 Feb;120(3):594-606 [11179238.001]
  • [Cites] Gut. 1997 May;40(5):619-22 [9203940.001]
  • [Cites] Ann Intern Med. 1991 May 1;114(9):735-40 [2012355.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2001 Oct;15(5):739-53 [11566038.001]
  • [Cites] Lancet. 2006 Nov 18;368(9549):1771-81 [17113426.001]
  • [Cites] Am J Med. 2006 Aug;119(8):624-38 [16887404.001]
  • [Cites] Gastroenterology. 2003 Aug;125(2):328-36 [12891533.001]
  • [Cites] Gut. 1999 Sep;45(3):362-6 [10446103.001]
  • [Cites] Fam Med. 1996 Mar;28(3):204-10 [8900554.001]
  • [Cites] Arch Intern Med. 2002 Oct 14;162(18):2105-10 [12374519.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2006 Sep;18(9):965-7 [16894309.001]
  • [Cites] Lancet. 2000 Aug 5;356(9228):455-60 [10981888.001]
  • [Cites] Ann Intern Med. 1995 Aug 15;123(4):241-9 [7611589.001]
  • [Cites] Clin Gastroenterol Hepatol. 2006 Feb;4(2):130-42 [16469671.001]
  • [Cites] Ann Intern Med. 2007 Mar 6;146(5):365-75 [17339622.001]
  • [Cites] Gastroenterology. 1987 Sep;93(3):480-9 [3609658.001]
  • [Cites] J Am Coll Surg. 1997 Sep;185(3):250-4 [9291402.001]
  • [Cites] Gastroenterology. 2005 May;128(5):1172-8 [15887101.001]
  • [Cites] Dig Dis Sci. 1989 Mar;34(3):424-8 [2646087.001]
  • [Cites] Aliment Pharmacol Ther. 2007 May 15;25(10):1211-22 [17451567.001]
  • [Cites] JAMA. 1999 Nov 24;282(20):1921-8 [10580457.001]
  • [Cites] Gastroenterology. 2003 Feb;124(2):288-92 [12557133.001]
  • [Cites] Clin Gastroenterol Hepatol. 2006 Feb;4(2):196-202 [16469680.001]
  • [Cites] Gastroenterology. 1989 Feb;96(2 Pt 2 Suppl):626-31 [2642448.001]
  • [Cites] Lancet. 2004 Aug 21-27;364(9435):665-74 [15325831.001]
  • [Cites] Ann Rheum Dis. 2004 Jul;63(7):759-66 [15194568.001]
  • [Cites] Arch Intern Med. 2003 Jul 14;163(13):1606-12 [12860586.001]
  • [Cites] Gastroenterology. 2006 Dec;131(6):1674-82 [17087947.001]
  • [Cites] J Gastroenterol. 2009;44 Suppl 19:23-9 [19148789.001]
  • [Cites] N Engl J Med. 2002 Dec 26;347(26):2104-10 [12501222.001]
  • [Cites] Am J Gastroenterol. 2009 Mar;104(3):728-38 [19240698.001]
  • [Cites] N Engl J Med. 2000 Nov 23;343 (21):1520-8, 2 p following 1528 [11087881.001]
  • [Cites] Clin Gastroenterol Hepatol. 2009 May;7(5):524-9 [19249402.001]
  • [Cites] Clin Gastroenterol Hepatol. 2005 Feb;3(2):133-41 [15704047.001]
  • (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
  •  go-up   go-down


2. Farraye FA, Wallace M: Clinical significance of small polyps found during screening with flexible sigmoidoscopy. Gastrointest Endosc Clin N Am; 2002 Jan;12(1):41-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical significance of small polyps found during screening with flexible sigmoidoscopy.
  • In deciding how to interpret the significance and management of small distal adenomatous polyps found on FS, one must first decide on the goal of a screening program.
  • Multiple studies support the recommendation that villous polyps regardless of size and adenomatous polyps greater than 1 cm found on FS are important markers for the presence of advanced polyps and cancer in the proximal colon.
  • If one assumes that a sigmoidoscopy-based approach is reasonable, and accepts that such an approach always misses a small number of proximal lesions, how should one manage patients with a small adenomatous polyp on FS?
  • In aggregate, the studies discussed previously suggest that patients with no distal polyps, distal hyperplastic polyps, or a single small distal tubular adenoma have a similar and low risk of advanced proximal adenomas of the colon.
  • The study by Read et al also included patients with distal villous adenomas in their low-risk group.
  • Given these caveats, what can one conclude about the predictive value of a small tubular adenoma found on FS?
  • These studies suggest that the risk of proximal advanced polyps is similar or slightly increased in patients with a distal adenoma than those with a negative FS.
  • The risk of finding an advanced adenoma seems to be 0% to 4% regardless of the findings of no polyps, hyperplastic polyps, or small tubular adenomatous polyps on FS in low-risk patients.
  • A small portion of patients with hyperplastic polyps found on FS have advanced proximal adenomas.
  • If a hyperplastic polyp on FS is not an indication for colonoscopy and the risk of proximal advanced adenomas is similar in patients with only a small distal adenoma, it is inconsistent to recommend colonoscopy for a small distal tubular adenoma and not a hyperplastic polyp.
  • Based on the studies of asymptomatic patients with no family history and negative FOBT, the authors believe it is reasonable to defer colonoscopy if no polyp, a hyperplastic, or a small tubular adenoma is found at sigmoidoscopy in low-risk patients.
  • It remains to be seen if the increase in costs and risks justifies the improved detection rate of colonic polyps.
  • Given manpower issues that face us today, and examining the question from a population perspective, reserving colonoscopy for only those patients with an advanced distal polyp on FS gives the biggest yield.
  • [MeSH-major] Colonic Polyps / diagnosis. Sigmoidoscopy

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11916160.001).
  • [ISSN] 1052-5157
  • [Journal-full-title] Gastrointestinal endoscopy clinics of North America
  • [ISO-abbreviation] Gastrointest. Endosc. Clin. N. Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 45
  •  go-up   go-down


3. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Putrescine .
  • Hazardous Substances Data Bank. Eflornithine .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Breast Cancer Res Treat. 2000 Sep;63(2):147-52 [11097090.001]
  • [Cites] Am J Clin Nutr. 1997 Mar;65(3):766-70 [9062527.001]
  • [Cites] Nucleic Acids Res. 1997 May 15;25(10):2012-9 [9115370.001]
  • [Cites] J Pediatr Gastroenterol Nutr. 1997 Mar;24(3):285-8 [9138174.001]
  • [Cites] J Pediatr Gastroenterol Nutr. 1997 Apr;24(4):389-92 [9144120.001]
  • [Cites] Cancer Res. 1997 Jun 1;57(11):2104-8 [9187103.001]
  • [Cites] Cancer Res. 1997 Jul 1;57(13):2630-7 [9205069.001]
  • [Cites] Cancer Res. 1997 Jul 15;57(14):3016-25 [9230217.001]
  • [Cites] Proc Soc Exp Biol Med. 1997 Nov;216(2):246-52 [9349693.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Oct 29;239(3):729-33 [9367837.001]
  • [Cites] Digestion. 1998;59(1):47-52 [9468098.001]
  • [Cites] J Cell Biochem Suppl. 1997;28-29:111-6 [9589355.001]
  • [Cites] Cancer Res. 1990 Aug 15;50(16):5077-83 [2116224.001]
  • [Cites] Biochem Pharmacol. 1990 Oct 15;40(8):1893-900 [2242022.001]
  • [Cites] Int J Cancer. 1991 Feb 20;47(4):633-8 [1847359.001]
  • [Cites] Anal Biochem. 1990 Nov 1;190(2):360-5 [2291479.001]
  • [Cites] Cancer Res. 1991 May 1;51(9):2362-5 [1901761.001]
  • [Cites] Biochem J. 1991 Nov 15;280 ( Pt 1):193-8 [1741747.001]
  • [Cites] Pharmacol Ther. 1991;50(3):443-72 [1754606.001]
  • [Cites] Nucleic Acids Res. 1992 May 25;20(10):2581-90 [1598217.001]
  • [Cites] Jpn J Cancer Res. 1992 Aug;83(8):835-42 [1399821.001]
  • [Cites] Nature. 1992 Nov 26;360(6402):355-8 [1280331.001]
  • [Cites] Biochem J. 1993 Jan 15;289 ( Pt 2):581-6 [8424799.001]
  • [Cites] Biochem Pharmacol. 1993 Mar 9;45(5):1129-36 [8384853.001]
  • [Cites] Biochem J. 1993 May 15;292 ( Pt 1):13-8 [8503840.001]
  • [Cites] Eur J Biochem. 1993 Oct 1;217(1):89-96 [8223591.001]
  • [Cites] Cancer Res. 1994 May 1;54(9):2313-6 [8162572.001]
  • [Cites] Jpn J Cancer Res. 1994 Jun;85(6):578-83 [8063610.001]
  • [Cites] Drug Metab Dispos. 1994 May-Jun;22(3):383-91 [8070314.001]
  • [Cites] Drug Metab Dispos. 1994 May-Jun;22(3):392-9 [8070315.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1994 Oct-Nov;3(7):591-5 [7827590.001]
  • [Cites] Biochem Soc Trans. 1994 Nov;22(4):846-52 [7698473.001]
  • [Cites] Br J Nutr. 1995 Jun;73(6):819-28 [7632663.001]
  • [Cites] Anticancer Res. 1995 May-Jun;15(3):709-16 [7645947.001]
  • [Cites] Nucleic Acids Res. 1996 Mar 15;24(6):1149-57 [8604351.001]
  • [Cites] Mol Cell Endocrinol. 1996 Mar 25;117(2):211-8 [8737382.001]
  • [Cites] Biochem J. 1996 Oct 15;319 ( Pt 2):641-8 [8912706.001]
  • [Cites] Cancer Res. 1996 Dec 15;56(24):5624-30 [8971167.001]
  • [Cites] Cancer Res. 1997 Jan 15;57(2):199-201 [9000553.001]
  • [Cites] Otolaryngol Head Neck Surg. 1998 Jun;118(6):810-5 [9627242.001]
  • [Cites] J Natl Cancer Inst. 1998 Aug 19;90(16):1212-8 [9719082.001]
  • [Cites] Biomed Chromatogr. 1998 Sep-Oct;12(5):291-3 [9787901.001]
  • [Cites] Carcinogenesis. 1998 Oct;19(10):1829-36 [9806166.001]
  • [Cites] Clin Cancer Res. 1996 Nov;2(11):1901-6 [9816147.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Nov;7(11):989-92 [9829706.001]
  • [Cites] Clin Cancer Res. 1999 Jan;5(1):143-7 [9918212.001]
  • [Cites] Exp Cell Res. 1999 Feb 25;247(1):257-66 [10047468.001]
  • [Cites] Am J Physiol. 1999 Mar;276(3 Pt 1):C684-91 [10069996.001]
  • [Cites] Clin Cancer Res. 1999 May;5(5):945-51 [10353725.001]
  • [Cites] Cancer Lett. 1998 Dec 11;134(1):91-5 [10381134.001]
  • [Cites] Oncogene. 1999 Oct 28;18(44):6013-20 [10557090.001]
  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3438-44 [10589756.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2000 Nov;9(11):1163-70 [11097223.001]
  • [Cites] Oncogene. 2000 Nov 23;19(50):5764-71 [11126363.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Jan 26;280(3):848-54 [11162600.001]
  • [Cites] Carcinogenesis. 2001 Feb;22(2):309-14 [11181453.001]
  • [Cites] Urology. 2001 Apr;57(4 Suppl 1):4-27 [11295590.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2001 Jul;281(1):G37-43 [11408253.001]
  • [Cites] Cancer Res. 2001 Aug 15;61(16):6120-30 [11507062.001]
  • [Cites] Clin Cancer Res. 2002 Jan;8(1):149-55 [11801552.001]
  • [Cites] Carcinogenesis. 2002 Feb;23(2):265-72 [11872631.001]
  • [Cites] Clin Cancer Res. 2002 Oct;8(10):3105-17 [12374678.001]
  • [Cites] Mol Cancer Ther. 2002 Nov;1(13):1161-72 [12479697.001]
  • [Cites] Carcinogenesis. 1986 Dec;7(12):2025-31 [3096588.001]
  • [Cites] J Natl Cancer Inst. 1987 May;78(5):931-4 [3106695.001]
  • [Cites] Cancer Res. 1988 Feb 15;48(4):759-74 [3123052.001]
  • [Cites] Carcinogenesis. 1988 Mar;9(3):427-32 [3125995.001]
  • [Cites] Carcinogenesis. 1989 Jan;10(1):175-81 [2491968.001]
  • [Cites] Cancer Res. 1989 Jun 1;49(11):2959-64 [2720656.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Jan 7;267(1):1-6 [10623564.001]
  • [Cites] Anticancer Res. 1999 Jul-Aug;19(4B):3199-203 [10652612.001]
  • [Cites] Food Chem Toxicol. 2000 Jan;38(1):15-23 [10685010.001]
  • [Cites] J Nutr. 2000 May;130(5):1225-31 [10801923.001]
  • [Cites] Cell Biol Toxicol. 2000;16(2):117-30 [10917567.001]
  • [Cites] Gynecol Oncol. 2000 Aug;78(2):123-9 [10926790.001]
  • [Cites] Cancer Res. 2000 Sep 15;60(18):5125-33 [11016639.001]
  • (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
  •  go-up   go-down


Advertisement
4. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


5. Iwama T: NSAIDs and colorectal cancer prevention. J Gastroenterol; 2009;44 Suppl 19:72-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Natl Cancer Inst. 2006 Oct 18;98(20):1494-500 [17047198.001]
  • [Cites] N Engl J Med. 2003 Mar 6;348(10):891-9 [12621133.001]
  • [Cites] Am J Surg. 1989 Jan;157(1):175-9 [2535920.001]
  • [Cites] Clin Cancer Res. 2003 Oct 15;9(13):4756-60 [14581346.001]
  • [Cites] N Engl J Med. 2003 Mar 6;348(10):883-90 [12621132.001]
  • [Cites] N Engl J Med. 2006 Aug 31;355(9):873-84 [16943400.001]
  • [Cites] J Biol Chem. 2005 Apr 15;280(15):15097-102 [15718247.001]
  • [Cites] N Engl J Med. 2000 Jun 29;342(26):1946-52 [10874062.001]
  • [Cites] Gut. 1996 Apr;38(4):578-81 [8707091.001]
  • [Cites] Clin Cancer Res. 1999 May;5(5):945-51 [10353725.001]
  • [Cites] Cancer Res. 1994 Jun 1;54(11):3011-20 [8187091.001]
  • [Cites] Lancet. 2001 Apr 14;357(9263):1191-4 [11323066.001]
  • [Cites] N Engl J Med. 2002 Apr 4;346(14):1054-9 [11932472.001]
  • [Cites] Cell. 1996 Nov 29;87(5):803-9 [8945508.001]
  • [Cites] Br J Pharmacol. 2000 Jun;130(3):641-9 [10821793.001]
  • [Cites] Ann Intern Med. 2007 Mar 6;146(5):365-75 [17339622.001]
  • [Cites] Nat New Biol. 1971 Jun 23;231(25):232-5 [5284360.001]
  • [Cites] Amino Acids. 2007 Aug;33(2):189-95 [17396214.001]
  • [Cites] Int J Clin Oncol. 2006 Apr;11(2):133-9 [16622748.001]
  • [Cites] Gastroenterology. 2006 Dec;131(6):1674-82 [17087947.001]
  • [Cites] Cancer Res. 1981 May;41(5):1954-7 [7214363.001]
  • [Cites] N Engl J Med. 2005 Mar 17;352(11):1071-80 [15713944.001]
  • (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
  •  go-up   go-down


6. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Toxicol Lett. 2001 Mar 31;120(1-3):301-6 [11323188.001]
  • [Cites] Science. 1998 Sep 4;281(5382):1509-12 [9727977.001]
  • [Cites] Oncogene. 1999 May 6;18(18):2883-91 [10362259.001]
  • [Cites] Cancer Treat Rev. 1998 Jun;24(3):221-40 [9767736.001]
  • [Cites] Mol Cell. 2001 May;7(5):915-26 [11389839.001]
  • [Cites] Cancer Res. 2003 Feb 1;63(3):621-6 [12566305.001]
  • [Cites] Eur J Cancer. 2002 May;38(7):867-71 [11978510.001]
  • [Cites] J Gastroenterol. 2001 Sep;36(9):587-94 [11578061.001]
  • [Cites] Cancer. 1998 Mar 15;82(6):1197-207 [9506368.001]
  • [Cites] Genes Dev. 2000 Aug 1;14 (15):1837-51 [10921899.001]
  • [Cites] Trends Biochem Sci. 1997 Aug;22(8):299-306 [9270303.001]
  • [Cites] J Biol Chem. 2001 Oct 5;276(40):36869-72 [11459850.001]
  • [Cites] Nature. 1999 Apr 1;398(6726):422-6 [10201372.001]
  • [Cites] Cancer Causes Control. 1997 Mar;8(2):146-58 [9134238.001]
  • [Cites] Science. 1997 Feb 21;275(5303):1132-6 [9027315.001]
  • [Cites] Genes Dev. 1997 Dec 15;11(24):3286-305 [9407023.001]
  • [Cites] Cancer Cell. 2002 Apr;1(3):289-98 [12086865.001]
  • [Cites] Mol Pathol. 2001 Aug;54(4):206-14 [11477132.001]
  • [Cites] Carcinogenesis. 1999 Aug;20(8):1397-401 [10426783.001]
  • [Cites] J Clin Invest. 1999 Jul;104(2):155-62 [10411544.001]
  • [Cites] Endocrinology. 1997 Mar;138(3):863-70 [9048584.001]
  • [Cites] CA Cancer J Clin. 2000 Jan-Feb;50(1):7-33 [10735013.001]
  • [Cites] EMBO Rep. 2001 Sep;2(9):775-81 [11559590.001]
  • [Cites] Nucleic Acids Res. 1994 Dec 11;22(24):5506-7 [7816645.001]
  • [Cites] Int J Cancer. 1999 Sep 24;83(1):18-29 [10449602.001]
  • [Cites] Gastroenterology. 2002 Mar;122(3):659-66 [11874999.001]
  • [Cites] Nat Cell Biol. 2002 Apr;4(4):E101-8 [11944044.001]
  • [Cites] Anticancer Res. 2002 May-Jun;22(3):1635-9 [12168847.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Cancer Res. 2001 Feb 15;61(4):1645-51 [11245478.001]
  • [Cites] Mol Cell Endocrinol. 2003 Mar 28;201(1-2):165-75 [12706304.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1603-8 [9990071.001]
  • [Cites] Steroids. 1998 May-Jun;63(5-6):335-9 [9618797.001]
  • [Cites] J Biol Chem. 2000 Mar 10;275(10):7337-42 [10702305.001]
  • (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
  •  go-up   go-down


7. Hillson JL, Furst DE: Rofecoxib. Expert Opin Pharmacother; 2000 Jul;1(5):1053-66
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

  • SciCrunch. DrugBank: Data: Chemical .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


8. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


9. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Heart Attack.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Rheumatol. 2004 May;31(5):951-6 [15124256.001]
  • [Cites] BMC Fam Pract. 2002 May 22;3:10 [12033987.001]
  • [Cites] Curr Med Res Opin. 2004 May;20(5):651-8 [15140330.001]
  • [Cites] Circulation. 2004 Jun 22;109(24):3000-6 [15197149.001]
  • [Cites] Aliment Pharmacol Ther. 2004 Jul 1;20(1):51-63 [15225171.001]
  • [Cites] Ann Rheum Dis. 2004 Aug;63(8):931-9 [15082468.001]
  • [Cites] Lancet. 2004 Aug 21-27;364(9435):639-40 [15325809.001]
  • [Cites] Lancet. 2004 Aug 21-27;364(9435):675-84 [15325832.001]
  • [Cites] Arthritis Rheum. 2004 Aug 15;51(4):549-57 [15334426.001]
  • [Cites] Tob Control. 2004 Sep;13(3):244-50 [15333879.001]
  • [Cites] J Rheumatol. 2004 Sep;31(9):1804-10 [15338504.001]
  • [Cites] Ann Rheum Dis. 2004 Nov;63(11):1419-26 [15020310.001]
  • [Cites] Gastroenterology. 2004 Oct;127(4):1038-43 [15480981.001]
  • [Cites] Clin Exp Rheumatol. 2004 Sep-Oct;22(5):589-96 [15485012.001]
  • [Cites] BMJ. 2004 Oct 16;329(7471):868-9 [15485939.001]
  • [Cites] Lancet. 1995 Dec 16;346(8990):1629 [7500770.001]
  • [Cites] Control Clin Trials. 1996 Feb;17(1):1-12 [8721797.001]
  • [Cites] BMJ. 1998 Jan 10;316(7125):140-4 [9462324.001]
  • [Cites] J Pain. 2004 Nov;5(9):511-20 [15556830.001]
  • [Cites] Lancet. 2004 Dec 4-10;364(9450):2021-9 [15582059.001]
  • [Cites] Ann Intern Med. 2005 Feb 1;142(3):157-64 [15684203.001]
  • [Cites] Arthritis Rheum. 2005 Feb;52(2):402-11 [15693010.001]
  • [Cites] Lancet. 2005 Feb 5-11;365(9458):475-81 [15705456.001]
  • [Cites] JAMA. 2006 Oct 4;296(13):1633-44 [16968831.001]
  • [Cites] Lancet. 2006 Nov 18;368(9549):1771-81 [17113426.001]
  • [Cites] Arch Fam Med. 2000 Nov-Dec;9(10):1124-34 [11115219.001]
  • [Cites] Arthritis Rheum. 2001 Jan;44(1):180-5 [11212158.001]
  • [Cites] Scand J Rheumatol. 2001;30(1):11-8 [11252686.001]
  • [Cites] Am J Gastroenterol. 2001 Apr;96(4):1019-27 [11316141.001]
  • [Cites] Am J Manag Care. 2001 Jun;7(6):609-16 [11439734.001]
  • [Cites] Circulation. 2001 Nov 6;104(19):2280-8 [11696466.001]
  • [Cites] J Pharm Pharmacol. 2001 Dec;53(12):1679-85 [11804398.001]
  • [Cites] Lancet. 2002 Jan 12;359(9301):118-23 [11809254.001]
  • [Cites] Osteoarthritis Cartilage. 2002 Apr;10(4):290-6 [11950252.001]
  • [Cites] Curr Med Res Opin. 2002;18(2):49-58 [12017209.001]
  • [Cites] Arch Intern Med. 2002 May 27;162(10):1099-104 [12020178.001]
  • [Cites] Br J Clin Pharmacol. 2002 Sep;54(3):327-32 [12236854.001]
  • [Cites] Arthritis Rheum. 2004 Aug;50(8):2433-40 [15334455.001]
  • [Cites] Arch Intern Med. 2002 May 27;162(10):1105-10 [12020179.001]
  • [Cites] Arch Intern Med. 2002 May 27;162(10):1111-5 [12020180.001]
  • [Cites] BMJ. 2002 Jun 22;324(7352):1488-92 [12077033.001]
  • [Cites] J Fam Pract. 2002 Jun;51(6):530-7 [12100776.001]
  • [Cites] J Rheumatol. 2002 Aug;29(8):1623-30 [12180720.001]
  • [Cites] Rheumatology (Oxford). 2002 Sep;41(9):1008-16 [12209034.001]
  • [Cites] Rheumatology (Oxford). 2002 Sep;41(9):1052-61 [12209041.001]
  • [Cites] BMJ. 2002 Sep 21;325(7365):619 [12242171.001]
  • [Cites] Scand J Rheumatol. 2002;31(4):230-8 [12369656.001]
  • [Cites] Lancet. 2002 Oct 5;360(9339):1071-3 [12383990.001]
  • [Cites] Arch Intern Med. 2003 Feb 24;163(4):481-6 [12588209.001]
  • [Cites] N Engl J Med. 2003 Mar 6;348(10):883-90 [12621132.001]
  • [Cites] Osteoarthritis Cartilage. 2005 Mar;13(3):206-10 [15727886.001]
  • [Cites] Clin Ther. 2005 Jan;27(1):64-77 [15763607.001]
  • [Cites] N Engl J Med. 2005 Mar 17;352(11):1092-102 [15713943.001]
  • [Cites] N Engl J Med. 2005 Mar 17;352(11):1071-80 [15713944.001]
  • [Cites] Ann Intern Med. 2005 Apr 5;142(7):481-9 [15809459.001]
  • [Cites] Mayo Clin Proc. 2005 Apr;80(4):470-9 [15819283.001]
  • [Cites] Arthritis Rheum. 2005 Apr;52(4):1205-15 [15818702.001]
  • [Cites] Am J Gastroenterol. 2005 May;100(5):1043-50 [15842577.001]
  • [Cites] Arch Intern Med. 2005 May 9;165(9):978-84 [15883235.001]
  • [Cites] Arthritis Res Ther. 2005;7(3):R644-65 [15899051.001]
  • [Cites] Curr Med Res Opin. 2005 Apr;21(4):517-26 [15899100.001]
  • [Cites] BMJ. 2005 Jun 11;330(7504):1366 [15947398.001]
  • [Cites] N Engl J Med. 2005 Jun 23;352(25):2576-8 [15972862.001]
  • [Cites] N Engl J Med. 2005 Jun 23;352(25):2578-80 [15972863.001]
  • [Cites] Pharmacotherapy. 2005 Apr;25(4):503-10 [15977911.001]
  • [Cites] Drug Saf. 2005;28(9):803-16 [16119973.001]
  • [Cites] Clin Ther. 2005 Aug;27(8):1196-214 [16199245.001]
  • [Cites] J R Soc Med. 2006 Mar;99(3):132-40 [16508052.001]
  • [Cites] Circulation. 2006 Mar 28;113(12):1578-87 [16534006.001]
  • [Cites] Circulation. 2006 Apr 25;113(16):1950-7 [16618816.001]
  • [Cites] Arthritis Rheum. 2006 May;54(5):1378-89 [16645966.001]
  • [Cites] BMJ. 2006 Jun 3;332(7553):1302-8 [16740558.001]
  • [Cites] Eur Heart J. 2006 Jul;27(14):1657-63 [16731535.001]
  • [Cites] JAMA. 2006 Oct 4;296(13):1653-6 [16968830.001]
  • [Cites] Clin Ther. 1999 Oct;21(10):1688-702 [10566565.001]
  • [Cites] JAMA. 1999 Nov 24;282(20):1921-8 [10580457.001]
  • [Cites] Lancet. 1999 Dec 18-25;354(9196):2106-11 [10609815.001]
  • [Cites] Arthritis Rheum. 2000 Feb;43(2):370-7 [10693877.001]
  • [Cites] Arthritis Rheum. 2000 May;43(5):978-87 [10817549.001]
  • [Cites] Epidemiology. 2000 Jul;11(4):382-7 [10874543.001]
  • [Cites] Arch Intern Med. 2000 Jun 26;160(12):1781-7 [10871971.001]
  • [Cites] JAMA. 2000 Sep 13;284(10):1247-55 [10979111.001]
  • [Cites] Rheumatology (Oxford). 2000 Oct;39(10):1095-101 [11035129.001]
  • [Cites] N Engl J Med. 2000 Nov 23;343(21):1520-8, 2 p following 1528 [11087881.001]
  • [Cites] N Engl J Med. 2003 Mar 6;348(10):891-9 [12621133.001]
  • [Cites] Ann Intern Med. 2003 May 20;138(10):795-806 [12755551.001]
  • [Cites] Am J Gastroenterol. 2003 Aug;98(8):1725-33 [12907325.001]
  • [Cites] Am J Cardiol. 2003 Aug 15;92(4):411-8 [12914871.001]
  • [Cites] J Clin Epidemiol. 2003 Aug;56(8):796-801 [12954473.001]
  • [Cites] Rheumatology (Oxford). 2003 Oct;42(10):1207-15 [12810937.001]
  • [Cites] Ann Intern Med. 2003 Oct 7;139(7):539-46 [14530224.001]
  • [Cites] Rheumatology (Oxford). 2003 Nov;42 Suppl 3:iii53-9 [14585918.001]
  • [Cites] Arthritis Rheum. 2003 Nov;48(11):3102-11 [14613272.001]
  • [Cites] Curr Med Res Opin. 2003;19(8):725-36 [14687444.001]
  • [Cites] Arthritis Rheum. 2004 Feb;50(2):598-606 [14872504.001]
  • [Cites] J Am Coll Cardiol. 2004 Mar 17;43(6):985-90 [15028354.001]
  • [Cites] J Am Geriatr Soc. 2004 May;52(5):666-74 [15086644.001]
  • [Cites] Am J Med. 2004 May 1;116(9):621-9 [15093759.001]
  • [Cites] Arch Intern Med. 2004 Apr 26;164(8):852-6 [15111370.001]
  • [Cites] Circulation. 2004 May 4;109(17):2068-73 [15096449.001]
  • [CommentIn] Nat Clin Pract Rheumatol. 2008 Apr;4(4):182-3 [18285763.001]
  • (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
  •  go-up   go-down


10. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

  • MedlinePlus Health Information. consumer health - Hearing Disorders and Deafness.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Eflornithine .
  • The Lens. Cited by Patents in .
  • eScholarship, California Digital Library, University of California. Full text from University of California eScholarship .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


11. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


12. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Organ Transplantation.
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


13. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

  • Genetic Alliance. consumer health - Lynch syndrome.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 827854759 for PMID:19073976 [PharmGKB] .
  • Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


14. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


15. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Primary biliary cirrhosis.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down






Advertisement