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1. Shailubhai K, Yu HH, Karunanandaa K, Wang JY, Eber SL, Wang Y, Joo NS, Kim HD, Miedema BW, Abbas SZ, Boddupalli SS, Currie MG, Forte LR: Uroguanylin treatment suppresses polyp formation in the Apc(Min/+) mouse and induces apoptosis in human colon adenocarcinoma cells via cyclic GMP. Cancer Res; 2000 Sep 15;60(18):5151-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Uroguanylin treatment suppresses polyp formation in the Apc(Min/+) mouse and induces apoptosis in human colon adenocarcinoma cells via cyclic GMP.
  • The enteric peptides, guanylin and uroguanylin, are local regulators of intestinal secretion by activation of receptor-guanylate cyclase (R-GC) signaling molecules that produce cyclic GMP (cGMP) and stimulate the cystic fibrosis transmembrane conductance regulator-dependent secretion of Cl- and HCO3-.
  • [MeSH-major] Adenocarcinoma / pathology. Adenomatous Polyposis Coli / prevention & control. Apoptosis / drug effects. Colonic Neoplasms / pathology. Cyclic GMP / physiology. Gastrointestinal Hormones. Peptides / pharmacology
  • [MeSH-minor] Aged. Aged, 80 and over. Amino Acid Sequence. Animals. Caco-2 Cells / drug effects. Down-Regulation / drug effects. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Mice. Mice, Inbred C57BL. Middle Aged. Molecular Sequence Data. Natriuretic Peptides. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptors, Cell Surface / biosynthesis. Receptors, Cell Surface / genetics. Receptors, Cell Surface / physiology. Tumor Cells, Cultured

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  • (PMID = 11016642.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Gastrointestinal Hormones; 0 / Natriuretic Peptides; 0 / Peptides; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 140653-38-9 / guanylin; 152175-68-3 / uroguanylin; H2D2X058MU / Cyclic GMP
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2. Bobe G, Albert PS, Sansbury LB, Lanza E, Schatzkin A, Colburn NH, Cross AJ: Interleukin-6 as a potential indicator for prevention of high-risk adenoma recurrence by dietary flavonols in the polyp prevention trial. Cancer Prev Res (Phila); 2010 Jun;3(6):764-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-6 as a potential indicator for prevention of high-risk adenoma recurrence by dietary flavonols in the polyp prevention trial.
  • We estimated odds ratios and 95% confidence intervals (95% CI) to determine whether serum IL-6 was associated with colorectal adenoma recurrence and flavonol intake and thus may serve as a risk indicator and as a response indicator to dietary flavonols.
  • Serum IL-6 concentrations at baseline, year 1, and year 3 were measured in 872 participants from the intervention arm of the Polyp Prevention Trial, a 4-year trial that examined the effectiveness of a low-fat, high-fiber, high-fruit and vegetable diet on adenoma recurrence.
  • Intake of flavonols, especially of isorhamnetin, kaempferol, and quercetin, was inversely associated with serum IL-6 concentrations (highest versus lowest flavonol intake quartile, 1.80 versus 2.20 pg/mL) and high-risk (OR, 0.51; 95% CI, 0.26-0.98) and advanced adenoma recurrence (OR, 0.17; 95% CI, 0.06-0.50).
  • A decrease in IL-6 concentration during the trial was inversely associated with high-risk (OR, 0.44; 95% CI, 0.23-0.84) and advanced adenoma recurrence (OR, 0.47; 95% CI, 0.19-1.18).
  • Individuals with above median flavonol intake and equal or below median IL-6 change after baseline had the lowest risk of recurrence of high-risk and advanced adenoma.

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  • [Copyright] 2010 AACR.
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  • (PMID = 20484173.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NIH HHS / OD / OD08-007; United States / Intramural NIH HHS / / Z99 CA999999; United States / Intramural NIH HHS / / Z99 HD999999; United States / PHS HHS / / 8-007
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antioxidants; 0 / Biomarkers; 0 / Flavonols; 0 / IL6 protein, human; 0 / Interleukin-6
  • [Other-IDs] NLM/ NIHMS170216; NLM/ PMC2881177
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3. Ulrich CM, Bigler J, Sparks R, Whitton J, Sibert JG, Goode EL, Yasui Y, Potter JD: Polymorphisms in PTGS1 (=COX-1) and risk of colorectal polyps. Cancer Epidemiol Biomarkers Prev; 2004 May;13(5):889-93
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  • Two isoforms of prostaglandin H synthase (PTGS = COX) are key enzymes in prostaglandin synthesis and primary targets for aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs).
  • Use of aspirin or other NSAIDs is associated with a lower risk and reduced recurrence of colorectal adenomas, established precursors of adenocarcinoma.
  • This study investigated risk of colorectal adenomatous and hyperplastic polyps associated with several polymorphisms in the coding region of PTGS1.
  • Within the Minnesota polyp case-control study, patients with colorectal adenomatous (n = 521) or hyperplastic (n = 194) polyps and n = 621 polyp-free controls were genotyped for four PTGS1 polymorphisms (R8W, L15-L16del, P17L, L237M); these had been predicted to affect protein function based on sequence-homology software.
  • Whereas there was no appreciable difference in adenoma or hyperplastic polyp risk associated with R8W, P17L, and L237M, an increased risk was observed for individuals heterozygous for the L15-L16del polymorphism (OR = 3.6, 95% CI 1.2-11.2).
  • The variant L15-L16del allele appeared to be associated with a stronger increase in adenoma risk among nonusers of aspirin/other NSAIDs.
  • The reduced risk observed with aspirin/other NSAID use was limited to those wild type for P17L [PP users: OR = 0.6 (0.5-0.8) versus PP nonusers: 1.0 (referent) (P interaction = 0.03)].
  • [MeSH-major] Adenomatous Polyps / genetics. Colonic Polyps / genetics. Colorectal Neoplasms / genetics. Genetic Predisposition to Disease. Polymorphism, Genetic. Prostaglandin-Endoperoxide Synthases / genetics

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  • (PMID = 15159324.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA59045; United States / NCI NIH HHS / CA / R01CA89445
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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