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1. [Tuberculosis in compromised hosts]. Kekkaku; 2003 Nov;78(11):717-22
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  • Many new findings and useful reports for practical medical treatment are submitted; why these compromised hosts are predisposed to tuberculosis, tuberculosis diagnostic and remedial notes of those compromised hosts etc.
  • 1. Tuberculosis in diabetes mellitus: aggravation and its immunological mechanism: Kazuyoshi KAWAKAMI (Department of Internal Medicine, Division of Infectious Diseases, Graduate School and Faculty of Medicine, University of the Ryukyus).
  • The onset of this disease is more frequent in DM patients than in individuals with any underlying diseases.
  • However, the precise mechanism of this finding remains to be fully understood.
  • In 1980, Saiki and co-workers reported that host defense and delayed-type hypersensitivity response to M. tuberculosis was hampered in a mouse DM model established by injecting streptozotocin (Infect Immun.
  • In our preliminary study, the production of these cytokines by PBMC from DM patients and healthy subjects was not affected under a high glucose condition.
  • Thus, it is not likely that the increased level of glucose directly suppresses the cell-mediated immune responses.
  • 2. A study of gastrectomy cases in pulmonary tuberculosis patients: Takenori YAGI (Division of Thoracic Disease, National Chiba-Higashi Hospital).
  • Gastrectomy was done due to carcinoma of the stomach in 31 cases, gastric and/or duodenal ulcer in 21 cases, adenomatous polyp in two cases, and accidental injury in one case.
  • 3. Immunodefficiency and tuberculosis in dialysis patients: Hajime INAMOTO (Division of Dialysis, Keio University School of Medicine).
  • The patients who have renal insufficiency is fatal, but they can live much longer by dialysis.
  • The morbidity rate, the mortality rate and the prevalence of tuberculosis was much higher than the general population.
  • Most of those tuberculosis patients appear the disease from the period immediately before the beginning of dialysis to one year after that.
  • Due to the decrease in the cell immunity, cavities are not formed easily.
  • It is easy to stay in the leaching lesion so that anti-tuberculosis drugs are much effective, and the patients recover easily.
  • With AIDS patients with tuberculosis, there are the following problems on the treatment. (1) The adverse reactions by antituberculosis drugs tend to occur in AIDS patients.
  • Eleven of 33 AIDS patients with tuberculosis had the adverse reactions (skin rash, fever, liver dysfunction) considered to be due to antituberculosis drugs.
  • It is a very large burden for the HIV infected persons to take simultaneously antituberculosis drugs, medicines for opportunistic infections, and anti-HIV medicines.
  • Since many medicines are taken, it is difficult to determine which drug is the cause once an adverse reaction occurs and all medicines should be often stopped. (2) The combined use with rifampicin (RFP) is difficult for the protease inhibitors and nonnuclear acid reverse transcriptase inhibitors.
  • RFP induces cytochrome P-450 in liver, accelerates the metabolism of some concomitant drug agents, and reduces blood concentration them remarkably.
  • When starting the two above-mentioned medicines during tuberculosis treatment, RFP should be changed to rifabutin (RFB) which has less induction of P-450 than RFP.

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  • (PMID = 14672050.001).
  • [ISSN] 0022-9776
  • [Journal-full-title] Kekkaku : [Tuberculosis]
  • [ISO-abbreviation] Kekkaku
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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2. Petrick N, Haider M, Summers RM, Yeshwant SC, Brown L, Iuliano EM, Louie A, Choi JR, Pickhardt PJ: CT colonography with computer-aided detection as a second reader: observer performance study. Radiology; 2008 Jan;246(1):148-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: To evaluate the effect of computer-aided detection (CAD) as second reader on radiologists' diagnostic performance in interpreting computed tomographic (CT) colonographic examinations by using a primary two-dimensional (2D) approach, with segmental, unblinded optical colonoscopy as the reference standard.
  • Two-dimensional transverse views were used for initial polyp detection, while three-dimensional (3D) endoluminal and 2D multiplanar views were available for problem solving.
  • After initial review without CAD, the reader was shown CAD-identified polyp candidates.
  • Polyp location, CT Colonography Reporting and Data System categorization, and reader confidence as to the likelihood of a candidate being a polyp were recorded before and after CAD reading.
  • RESULTS: Use of CAD led to nonsignificant average reader AUC increases of 0.03, 0.03, and 0.04 for patients with adenomatous polyps 6 mm or larger, 6-9 mm, and 10 mm or larger, respectively (P > or = .25); likewise, CAD increased average reader sensitivity by 0.15, 0.16, and 0.14 for those respective groups, with a corresponding decrease in specificity of 0.14.
  • These changes achieved significance for the 6 mm or larger group (P < .01), 6-9 mm group (P < .02), and for specificity (P < .01), but not for the 10 mm or larger group (P > .16).
  • CONCLUSION: Use of CAD led to a significant increase in sensitivity for detecting polyps in the 6 mm or larger and 6-9 mm groups at the expense of a similar significant reduction in specificity.
  • [MeSH-major] Colonic Polyps / radiography. Colonography, Computed Tomographic / methods. Diagnosis, Computer-Assisted

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  • [Copyright] RSNA, 2007
  • [ErratumIn] Radiology. 2008 Aug;248(2):704
  • (PMID = 18096536.001).
  • [ISSN] 1527-1315
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
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3. Herszényi L, Juhász M, Prónai L, Tulassay Z: [Chemoprevention of colorectal cancer]. Orv Hetil; 2004 Mar 21;145(12):603-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Most colorectal cancers are believed to arise from adenomatous polyps.
  • Aspirin and other nonsteroidal anti-inflammatory drugs are the most widely studied agents, their use has been consistently associated with reduction in the risk of mortality and the incidence of colorectal adenomas and cancers.
  • The selective cyclooxygenase-2 (COX-2) inhibitors (coxibs) have been demonstrated to decrease the number and the size of polyps in patients with familial adenomatous polyposis syndrome.
  • Because the gastrointestinal toxicity of coxibs is lower, it might be safer than aspirin or other non-selective nonsteroidal anti-inflammatory drugs for long-term use.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Anticarcinogenic Agents / therapeutic use. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Animals. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Antineoplastic Agents / therapeutic use. Aspirin / therapeutic use. Cyclooxygenase Inhibitors / therapeutic use. Humans. Incidence

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  • (PMID = 15119114.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents; 0 / Cyclooxygenase Inhibitors; R16CO5Y76E / Aspirin
  • [Number-of-references] 50
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4. Gill S, Sinicrope FA: Colorectal cancer prevention: is an ounce of prevention worth a pound of cure? Semin Oncol; 2005 Feb;32(1):24-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Colorectal carcinogenesis is a multistep process characterized by molecular and cellular alterations that result in an identifiable precursor lesion, ie, the adenomatous polyp.
  • The transition from normal mucosa to adenoma and its subsequent progression to carcinoma are protracted events that offer opportunities for preventive interventions.
  • Suppression or reversal of the carcinogenic process in the colorectum with nonpharmacologic or pharmacologic agents, ie, chemoprevention, is an area of considerable research interest and activity.
  • Interest in this field derives from multiple epidemiologic studies showing that regular and continued use of nonsteroidal anti-inflammatory drugs (NSAIDs), predominantly aspirin, is associated with significant reductions in both colorectal adenoma and carcinoma incidence.
  • NSAIDs were first shown to be effective in patients with familial adenomatous polyposis (FAP).
  • Subsequent randomized trials in FAP demonstrated that sulindac and the selective cyclooxygenase-2 (COX-2) inhibitor, celecoxib, can significantly regress existing adenomas, and resulted in Food and Drug Administration (FDA) approval of celecoxib for adjunctive management of these patients.
  • Based on the aforementioned data, aspirin and coxibs have been or are currently being evaluated for the prevention of sporadic adenoma recurrence in high-risk patient populations.
  • Evidence indicates that aspirin can reduce adenoma recurrence rates in patients with prior colorectal neoplasia; however, questions remain, including the optimal dosage, timing of initiation and duration of treatment, and clinical benefit versus potential harm to patients.
  • These same issues apply to the nonpharmacologic agents such as calcium, folic acid, and selenium given as dietary supplements.
  • Apart from aspirin, calcium carbonate is the only other agent that has been shown to modestly reduce sporadic adenoma recurrence rates in a randomized trial.
  • In addition to demonstrating efficacy, chemopreventive agents must also be safe for long-term use, be well accepted by patients, and be cost-effective.
  • In this review, the current status of CRC chemoprevention will be discussed, including the available evidence for selected pharmacologic and nonpharmacologic agents, particularly among high-risk populations.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Adenoma / pathology. Animals. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Calcium / therapeutic use. Clinical Trials as Topic. Cyclooxygenase Inhibitors / therapeutic use. Eflornithine / therapeutic use. Folic Acid / therapeutic use. Humans. Intestinal Mucosa / pathology. Selenium / therapeutic use. Ursodeoxycholic Acid / therapeutic use

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  • (PMID = 15726503.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents; 0 / Cyclooxygenase Inhibitors; 724L30Y2QR / Ursodeoxycholic Acid; 935E97BOY8 / Folic Acid; H6241UJ22B / Selenium; R16CO5Y76E / Aspirin; SY7Q814VUP / Calcium; ZQN1G5V6SR / Eflornithine
  • [Number-of-references] 122
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5. North GL: Celecoxib as adjunctive therapy for treatment of colorectal cancer. Ann Pharmacother; 2001 Dec;35(12):1638-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To describe the role of celecoxib as adjunctive therapy in the treatment of familial adenomatous polyposis (FAP), an inherited autosomal dominant predisposition syndrome for colorectal cancer.
  • DATA SOURCES: Literature was evaluated through MEDLINE search (1995-March 2000) and through secondary sources, using the search terms celecoxib, cyclooxygenase-2 inhibitors, and familial adenomatous polyps.
  • DATA SYNTHESIS: Observational studies have found a decreased rate of colorectal cancer in people who regularly took aspirin or other nonsteroidal antiinflammatory drugs (NSAIDs).
  • The Food and Drug Administration granted accelerated approval in December 1999 for the NSAID celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, for adjunctive therapy in patients with FAP, based on a six-month, randomized, controlled clinical trial.
  • CONCLUSIONS: Aspirin and other NSAIDs reduce the incidence of colorectal cancer in the general population.
  • Limited clinical studies in patients with FAP using nonaspirin NSAIDs have shown a reduction in polyp burden.
  • A current clinical trial using celecoxib has also shown a reduction in polyp burden in patients with FAP.
  • The long-term clinical impact of using a selective COX-2 inhibitor is not known, since celecoxib has not been studied beyond six months in patients with FAP.
  • By reducing the polyp burden in FAP patients, celecoxib may be useful as adjunctive chemotherapy, in addition to routine endoscopic surveillance and surgery.
  • [MeSH-major] Adenomatous Polyposis Coli. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Colorectal Neoplasms. Cyclooxygenase Inhibitors / therapeutic use. Sulfonamides / therapeutic use

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  • (PMID = 11793634.001).
  • [ISSN] 1060-0280
  • [Journal-full-title] The Annals of pharmacotherapy
  • [ISO-abbreviation] Ann Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; JCX84Q7J1L / Celecoxib; R16CO5Y76E / Aspirin
  • [Number-of-references] 17
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6. Palozza P, Serini S, Maggiano N, Tringali G, Navarra P, Ranelletti FO, Calviello G: beta-Carotene downregulates the steady-state and heregulin-alpha-induced COX-2 pathways in colon cancer cells. J Nutr; 2005 Jan;135(1):129-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Experimental studies have shown that beta-carotene inhibited the growth of colon cancer cells, and human trials have demonstrated that the carotenoid reduces colon cell proliferation of adenomatous polyps; however, molecular mechanisms underlying this chemopreventive activity remain unclear.
  • We evaluated the effects of beta-carotene on the growth of human colon adenocarcinoma cells overexpressing (LS-174, HT-29, WiDr) or not expressing (HCT116) COX-2.
  • This effect was not observed in cells treated with retinoic acid or retinol.
  • Moreover, cells not expressing COX-2 were insensitive to the growth-inhibitory and proapoptotic effects of the carotenoid.
  • Here, we report that the suppression of COX-2 by beta-carotene may represent a molecular mechanism by which this compound acts as an antitumor agent in colon carcinogenesis.
  • [MeSH-minor] Caspase 3. Caspases / metabolism. Cell Cycle / physiology. Cell Line, Tumor. Colonic Neoplasms. Cyclooxygenase 1. Cyclooxygenase 2. Dinoprostone / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Membrane Proteins. Reactive Oxygen Species / metabolism

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  • (PMID = 15623844.001).
  • [ISSN] 0022-3166
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Neuregulin-1; 0 / Reactive Oxygen Species; 0 / heregulin alpha; 01YAE03M7J / beta Carotene; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS1 protein, human; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; K7Q1JQR04M / Dinoprostone
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7. Bigler J, Whitton J, Lampe JW, Fosdick L, Bostick RM, Potter JD: CYP2C9 and UGT1A6 genotypes modulate the protective effect of aspirin on colon adenoma risk. Cancer Res; 2001 May 1;61(9):3566-9
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  • [Title] CYP2C9 and UGT1A6 genotypes modulate the protective effect of aspirin on colon adenoma risk.
  • Regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) has a protective effect on the incidence of colon neoplasia.
  • We tested the hypothesis that the slow alleles of these enzymes can modify the inverse association between NSAIDs and colon neoplasia in the Minnesota Cancer Prevention Research Unit (CPRU) adenomatous polyp case-control study.
  • CYP2C9 and UGT1A6 genotypes were determined for 474 adenoma cases and 563 controls.
  • NSAID use was inversely associated with adenoma risk [odds ratio (OR), 0.63; 95% confidence interval (CI), 0.44-0.90 for aspirin; and OR, 0.50; 95% CI, 0.31-0.82 for nonaspirin NSAID].
  • However, this association was absent in aspirin users who carried the CYP2C9 variant alleles (OR, 0.88; 95% CI, 0.51-1.53) or who were homozygous wild-type UGT1A6 (OR, 0.86; 95% CI, 0.50-1.50).
  • Carriers of both of these alleles who use aspirin were also not at reduced risk of adenomatous polyps (OR, 1.59; 95% CI, 0.68-3.73).
  • The variants of these enzymes did not influence the association between nonaspirin NSAIDs and adenoma risk.
  • These data indicate that the effectiveness of chemopreventive drugs can be modulated by the genotype of metabolizing enzymes.
  • [MeSH-major] Adenoma / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Anticarcinogenic Agents / therapeutic use. Aryl Hydrocarbon Hydroxylases. Aspirin / therapeutic use. Colonic Neoplasms / prevention & control. Cytochrome P-450 Enzyme System / genetics. Glucuronosyltransferase / genetics. Steroid 16-alpha-Hydroxylase. Steroid Hydroxylases / genetics
  • [MeSH-minor] Adenomatous Polyps / enzymology. Adenomatous Polyps / genetics. Adult. Aged. Case-Control Studies. Cytochrome P-450 CYP2C9. Female. Genotype. Humans. Male. Middle Aged

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  • (PMID = 11325819.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA59045
  • [Publication-type] Journal Article; Multicenter Study; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.- / Steroid Hydroxylases; EC 1.14.13.- / CYP2C9 protein, human; EC 1.14.13.- / Cytochrome P-450 CYP2C9; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / Steroid 16-alpha-Hydroxylase; EC 2.4.1.- / UDP-glucuronosyltransferase, UGT1A6; EC 2.4.1.17 / Glucuronosyltransferase; R16CO5Y76E / Aspirin
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8. Shen R, Tao L, Xu Y, Chang S, Van Brocklyn J, Gao JX: Reversibility of aberrant global DNA and estrogen receptor-alpha gene methylation distinguishes colorectal precancer from cancer. Int J Clin Exp Pathol; 2009;2(1):21-33
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  • However, the significance of epigenetic changes for diagnosis and/or prognosis of colorectal cancer have not been established, although it has been extensively investigated.
  • Recently we have identified a new type of cancer cell called precancerous stem cells (pCSCs) and proposed that cancer may arise from a lengthy development process of tumor initiating cells (TICs) --> pCSCs --> cancer stem cells (CSCs) --> cancer, which is in parallel to histological changes of hyperplasia (TICs) --> precancer (pCSCs) --> carcinoma (CSCs/cancer cells), accompanied by clonal evolutionary epigenetic and genetic alterations.
  • The profile of global DNA and estrogen receptor (ER)-alpha gene methylation during cancer development was determined by analysis of 5-methylcytosine (5-MeC) using immunohistochemical (IHC) staining, dot blot analysis or a quantitative gene methylation assay (QGMA).
  • Herein we show that global DNA hypomethylation and ER-alpha gene hypermethylation are progressively enhanced from hyperplastic polyps (HPs) --> adenomatous polyps (APs) --> adenomatous carcinoma (AdCa).
  • The aberrant methylation can be completely reversed in APs, but not in AdCa by a nonsteroidal anti-inflammatory drug (NSAID) celecoxib, which is a selective inhibitor of cyclooxygenase-2 (Cox-2), suggesting that the epigenetic alterations between colorectal precancer (AP) and cancer (AdCa) are fundamentally different in response to anti-cancer therapy.
  • In normal colorectal mucosa, while global DNA methylation was not affected by aging, ER-alpha gene methylation was significantly increased with aging.
  • However, this increase did not reach the level observed in colorectal APs.

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  • (PMID = 18830381.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; DNA methylation / Precancer / cancer progression / colorectal cancer / epigenetic / estrogen receptor-α / nonsteroidal anti-inflammatory drugs / tumor initiation
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9. Pignone M, Levin B: Recent developments in colorectal cancer screening and prevention. Am Fam Physician; 2002 Jul 15;66(2):297-302
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  • Randomized trials show that calcium is effective but fiber is not effective in preventing reoccurrence of adenomatous polyps.
  • Preliminary data suggest that nonsteroidal anti-inflammatory drugs may prevent adenomatous polyps and that DNA stool tests and virtual colonoscopy may show promise as screening tools.
  • [MeSH-minor] Adenoma / prevention & control. Barium Sulfate. Calcium / therapeutic use. Colonic Polyps / prevention & control. Colonoscopy. Evidence-Based Medicine. Humans. Occult Blood. Sensitivity and Specificity. Sigmoidoscopy

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  • [CommentIn] Am Fam Physician. 2003 Mar 15;67(6):1188 [12674445.001]
  • [CommentIn] Am Fam Physician. 2003 Feb 1;67(3):465 [12588066.001]
  • (PMID = 12152966.001).
  • [ISSN] 0002-838X
  • [Journal-full-title] American family physician
  • [ISO-abbreviation] Am Fam Physician
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 25BB7EKE2E / Barium Sulfate; SY7Q814VUP / Calcium
  • [Number-of-references] 26
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10. Nair S, Norkus EP, Hertan H, Pitchumoni CS: Serum and colon mucosa micronutrient antioxidants: differences between adenomatous polyp patients and controls. Am J Gastroenterol; 2001 Dec;96(12):3400-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum and colon mucosa micronutrient antioxidants: differences between adenomatous polyp patients and controls.
  • OBJECTIVES: Micronutrient antioxidants, by virtue of their free radical scavenging properties, are potential chemopreventive agents against colon cancer.
  • It is also not known whether a relationship exists between serum and mucosal tissue antioxidant levels.
  • Previous studies evaluating the occurrence of polyps after supplementation with vitamin E and beta-carotene have yielded mixed results.
  • The aim of this study was to determine the concentrations of seven micronutrient antioxidants (alpha- and gamma-tocopherol, lutein, beta-cryptoxanthin, lycopene, and alpha- and beta-carotene) in colonic mucosa and to determine whether serum levels of each antioxidant could predict levels of that antioxidant in the right and left colon of patients with normal mucosa or in those with adenomatous polyps.
  • METHODS: Mucosal tissue concentrations and serum levels of antioxidants were determined in 10 patients with adenomatous polyps and 15 control subjects (GI patients with normal colonic mucosa).
  • RESULTS: Patients with polyps similar serum antioxidant status similar to that of control.
  • However, polyp patients had significantly lower concentrations of all seven antioxidants in both the right (p < 0.0070) and left colon (p < 0.0026) than did controls.
  • Finally, serum antioxidant levels predict right and left colon antioxidant levels in controls but not in patients with polyps.
  • CONCLUSIONS: Patients with adenomatous polyps have low levels of micronutrient antioxidants in their colon mucosa.
  • Because the serum levels of these antioxidants were similar in controls and polyp patients, our findings suggest an increased level of free radical activity in patients with polyps compared to normal subjects.
  • [MeSH-major] Adenomatous Polyps / metabolism. Antioxidants / metabolism. Colon / metabolism. Colonic Neoplasms / metabolism. Intestinal Mucosa / metabolism. Micronutrients / chemistry

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  • (PMID = 11774956.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Micronutrients
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11. Ferrández A, DiSario JA: Hereditary colorectal cancer: screening and management. Curr Treat Options Oncol; 2002 Dec;3(6):459-74
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  • Detection and removal of its precursor lesions, the adenomatous polyps, is the foundation of preventive strategies.
  • Chemoprevention with nonsteroidal anti-inflammatory drugs may have a role in high-risk populations.
  • [MeSH-major] Colorectal Neoplasms / diagnosis. Colorectal Neoplasms / therapy. Genetic Predisposition to Disease / genetics. Mass Screening / methods
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Colectomy. Genetic Testing. Health Behavior. Hormone Replacement Therapy. Humans. Intestinal Polyps / diagnosis


12. Cooper K, Squires H, Carroll C, Papaioannou D, Booth A, Logan RF, Maguire C, Hind D, Tappenden P: Chemoprevention of colorectal cancer: systematic review and economic evaluation. Health Technol Assess; 2010 Jun;14(32):1-206
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  • Approximately 25% of cases occur in individuals with a family history of CRC, including 5% caused by familial adenomatous polyposis (FAP) or hereditary non-polyposis CRC (HNPCC).
  • Most develop from adenomatous polyps arising from the intestine lining.
  • Individuals with these polyps undergo polypectomy and are invited for endoscopic surveillance.
  • OBJECTIVES: To evaluate the clinical effectiveness and cost-effectiveness of drug and micronutrient interventions for the prevention of CRC and/or adenomatous polyps.
  • Interventions considered include: non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin and cyclo-oxygenase-2 (COX-2) inhibitors; folic acid; calcium; vitamin D and antioxidants (including vitamin A, vitamin C, vitamin E, selenium and beta-carotene).
  • Chemoprevention was assessed in the general population, in individuals at increased risk of CRC, and in individuals with FAP or HNPCC.
  • DATA SOURCES: A systematic review identified randomised controlled trials (RCTs) assessing drug and nutritional agents for the prevention of CRC or adenomatous polyps.
  • A health economic model was developed to assess the cost-effectiveness of chemoprevention for two populations with different levels of risk of developing CRC: the general population and an intermediate-risk population.
  • A small study of aspirin in FAP patients produced no statistically significant reduction in polyp number but a possible reduction in polyp size.
  • There was a statistically significant 21% reduction in risk of adenoma recurrence [relative risk (RR) 0.79, 95% confidence interval (CI) 0.68 to 0.92] in an analysis of aspirin versus no aspirin in individuals with a history of adenomas or CRC.
  • In the general population, a significant 26% reduction in CRC incidence was demonstrated in studies with a 23-year follow-up (RR 0.74, 95% CI 0.57 to 0.97).
  • Non-aspirin NSAID use in FAP individuals produced a non-statistically significant reduction in adenoma incidence after 4 years of treatment and follow-up and reductions in polyp number and size.
  • In individuals with a history of adenomas there was a statistically significant 34% reduction in adenoma recurrence risk (RR 0.66, 95% CI 0.60 to 0.72) and a statistically significant 55% reduction in advanced adenoma incidence (RR 0.45, 95% CI 0.35 to 0.58).
  • No studies assessed the effect of non-aspirin NSAIDs in the general population.
  • There was no significant effect of folic acid versus placebo on adenoma recurrence (RR 1.16, 95% CI 0.97 to 1.39) or advanced adenoma incidence in individuals with a history of adenomas.
  • In the general population there was no significant effect of folic acid on risk of CRC (RR 1.13, 95% CI 0.77 to 1.64), although studies were of relatively short duration.
  • Calcium use by FAP patients produced no significant reduction in polyp number or disease progression.
  • In individuals with a history of adenomas there was a statistically significant 18% reduction in risk of adenoma recurrence (RR 0.82, 95% CI 0.69 to 0.98) and a non-significant reduction in risk of advanced adenomas (RR 0.77, 95% CI 0.50 to 1.17).
  • In the general population there was no significant effect of calcium on risk of CRC (RR 1.08, 95% CI 0.87 to 1.34), although studies were of relatively short duration.
  • There were no studies of antioxidant use in individuals with FAP or HNPCC, and in individuals with a history of adenomas no statistically significant differences in relative risk of adenoma recurrence were found.
  • In the general population there was no difference in incidence of CRC (RR 1.00, 95% CI 0.88 to 1.13) with antioxidant use compared with no antioxidant use.
  • People have fewer concerns about using antioxidants or other supplements, but their perception of the benefits of these agents is less well-defined.
  • The model analysis suggested that the most cost-effective age-range policy in the general population would be to provide chemoprevention to all individuals within the general population from age 50 to 60 years.
  • The use of aspirin in addition to screening within the general population is likely to result in a discounted cost per life-year gained of around 10,000 pounds and a discounted cost per quality-adjusted life-year (QALY) gained of around 23,000 pounds compared with screening alone.
  • COX-2 inhibitors may decrease polyp number in patients with FAP.
  • There is some evidence for aspirin reducing the incidence of CRC in the general population.
  • Both aspirin and NSAIDs are associated with adverse effects so it will be important to consider the risk-benefit ratio before recommending these agents for chemoprevention.
  • [MeSH-minor] Adenomatous Polyposis Coli / economics. Adenomatous Polyposis Coli / epidemiology. Adenomatous Polyposis Coli / prevention & control. Anti-Inflammatory Agents / therapeutic use. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Antioxidants / therapeutic use. Calcium / therapeutic use. Colorectal Neoplasms, Hereditary Nonpolyposis / economics. Colorectal Neoplasms, Hereditary Nonpolyposis / epidemiology. Colorectal Neoplasms, Hereditary Nonpolyposis / prevention & control. Cyclooxygenase 2 Inhibitors / therapeutic use. Folic Acid / therapeutic use. Great Britain / epidemiology. Humans. Incidence. Models, Economic. Prognosis. Risk Assessment. Selenium / therapeutic use. beta Carotene / therapeutic use

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  • (PMID = 20594533.001).
  • [ISSN] 2046-4924
  • [Journal-full-title] Health technology assessment (Winchester, England)
  • [ISO-abbreviation] Health Technol Assess
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antioxidants; 0 / Cyclooxygenase 2 Inhibitors; 01YAE03M7J / beta Carotene; 935E97BOY8 / Folic Acid; H6241UJ22B / Selenium; SY7Q814VUP / Calcium
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13. Augoff K, Rabczynski J, Tabola R, Czapla L, Ratajczak K, Grabowski K: Immunohistochemical study of decorin expression in polyps and carcinomas of the colon. Med Sci Monit; 2008 Oct;14(10):CR530-5
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  • [Title] Immunohistochemical study of decorin expression in polyps and carcinomas of the colon.
  • BACKGROUND: Recent studies showed that a small leucine-rich proteoglycan, decorin, may suppress tumor progression as a natural anticancer agent negatively controlling cellular growth.
  • It was hypothesized that physiological expression of decorin may be associated with cellular senescence of the colorectal mucosa and that its down-regulation, promoting an increase in cellular proliferation, could participate in the progression of adenoma to adenocarcinoma.
  • Therefore the expression of decorin in hyperplastic and neoplastic polyps of the colorectum was examined and compared with normal colonic mucosa and colon cancer tissues.
  • MATERIAL/METHODS: Tissue samples were obtained from 41 patients with different types of colonic polyps (6 hyperplastic adenomas, 34 neoplastic adenomas, and 1 adenomatous polyp with focal carcinoma) and 12 patients with colon cancer.
  • The decrease in decorin reactivity in tubulo-villous adenomas was significant as compared with other polyps and controls.
  • Weak decorin immunoreactivity in stroma adjacent to clusters of cancerous cells was also found in most cases of common types of adenocarcinoma, but not in adenocarcinoma mucinosum.
  • CONCLUSIONS: The expression of decorin may be involved in the differentiation of colonic polyps and reduced expression of decorin may abrogate the defensive potential of stromal tissue and promote the development of common types of colon carcinoma.
  • [MeSH-major] Colon / pathology. Colonic Polyps / metabolism. Colorectal Neoplasms / metabolism. Extracellular Matrix Proteins / metabolism. Proteoglycans / metabolism

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  • (PMID = 18830193.001).
  • [ISSN] 1643-3750
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / DCN protein, human; 0 / Decorin; 0 / Extracellular Matrix Proteins; 0 / Proteoglycans
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14. Keku TO, Lund PK, Galanko J, Simmons JG, Woosley JT, Sandler RS: Insulin resistance, apoptosis, and colorectal adenoma risk. Cancer Epidemiol Biomarkers Prev; 2005 Sep;14(9):2076-81
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  • [Title] Insulin resistance, apoptosis, and colorectal adenoma risk.
  • Compelling evidence from epidemiologic studies indicates that elevated circulating insulin-like growth factor (IGF)-I, insulin resistance, and associated complications, such as elevated fasting plasma insulin, glucose and free fatty acids, glucose intolerance, increased body mass index, and visceral adiposity, are linked with increased risk of colorectal cancer.
  • However, the role of insulin and markers of glucose control in the development of adenomas, precursors to colorectal cancer, has not been fully explored.
  • Participants were classified as cases or controls based on whether they had one or more colorectal adenomatous polyps.
  • Logistic regression was used to examine the association between adenoma status and insulin-IGF markers.
  • Adenoma cases (n = 239) and adenoma-free controls (n = 517) provided rectal biopsies and/or blood samples and interview data.
  • Consistent with prior findings, cases were more likely to be males, older, have higher waist-to-hip ratio, lower calcium intake, lower apoptosis, and less likely to report nonsteroidal anti-inflammatory drug use.
  • Those in the highest quartile of insulin (adjusted odds ratio, 2.2; 95% confidence interval, 1.1-4.2) and glucose (adjusted odds ratio, 1.8; 95% confidence interval, 0.9-3.6) were more likely to have an adenoma compared with the lowest quartile.
  • The results provide novel evidence that elevated insulin and glucose are associated with increased adenoma risk and decreased apoptosis in normal rectal mucosa.
  • These findings suggest that insulin may act early in the adenoma-carcinoma sequence to promote the development of colorectal adenoma by decreasing apoptosis in the normal mucosa.
  • [MeSH-minor] Adenoma / epidemiology. Adenoma / etiology. Adenoma / physiopathology. Blood Glucose / analysis. Case-Control Studies. Cell Transformation, Neoplastic. Diet. Female. Humans. Life Style. Male. Middle Aged. Risk Assessment. Somatomedins / analysis

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  • (PMID = 16172212.001).
  • [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 / NIDDK NIH HHS / DK / P30 DK34987; United States / NCI NIH HHS / CA / R01 CA 44684; United States / NCI NIH HHS / CA / R01 CA93654-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 0 / Somatomedins
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15. Marshall JR: Nutrition and colon cancer prevention. Curr Opin Clin Nutr Metab Care; 2009 Sep;12(5):539-43
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  • Although screening is direct and effective, dietary modification or low-risk chemopreventive agents might prevent colon cancer development.
  • An exciting recent discovery is that the combination of diflouromethylornithine and sulindac substantially decreases adenomatous polyp recurrence.
  • Screening has an important role, although it will probably not eliminate all colon cancer.
  • Nutritional modification remains potentially valuable, although research has not yet identified the objects of nutritional intervention.
  • NSAIDs hold promise as chemopreventive agents.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Colonic Neoplasms / prevention & control. Diet. Nutritional Physiological Phenomena
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Dietary Fiber / therapeutic use. Eflornithine / therapeutic use. Epidemiologic Studies. Humans. Primary Prevention. Risk Factors. Smoking / adverse effects. Sulindac / therapeutic use

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  • (PMID = 19512917.001).
  • [ISSN] 1473-6519
  • [Journal-full-title] Current opinion in clinical nutrition and metabolic care
  • [ISO-abbreviation] Curr Opin Clin Nutr Metab Care
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents; 184SNS8VUH / Sulindac; R16CO5Y76E / Aspirin; ZQN1G5V6SR / Eflornithine
  • [Number-of-references] 41
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16. Hawk E, Viner JL: The adenoma prevention with celecoxib and prevention of colorectal sporadic adenomatous polyps trials: stepping stones to progress. Cancer Epidemiol Biomarkers Prev; 2007 Feb;16(2):185-7
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  • [Title] The adenoma prevention with celecoxib and prevention of colorectal sporadic adenomatous polyps trials: stepping stones to progress.
  • [MeSH-major] Adenomatous Polyps / prevention & control. Colorectal Neoplasms / prevention & control. Cyclooxygenase Inhibitors / therapeutic use. Pyrazoles / therapeutic use. Sulfonamides / therapeutic use
  • [MeSH-minor] Celecoxib. Dose-Response Relationship, Drug. Humans. Outcome Assessment (Health Care). Randomized Controlled Trials as Topic. Secondary Prevention

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  • (PMID = 17301246.001).
  • [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
  • [Publication-type] Editorial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; JCX84Q7J1L / Celecoxib
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17. van den Broek I, Sparidans RW, Engwegen JY, Cats A, Depla AC, Schellens JH, Beijnen JH: Evaluation of human neutrophil peptide-1, -2 and -3 as serum markers for colorectal cancer. Cancer Biomark; 2010;7(2):109-15
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  • Serum was obtained from patients with indications for colonoscopy, subsequently diagnosed as normal colon or hyperplastic polyp (CON; n= 368), adenomatous polyp (AP; n = 179) or colorectal cancer (CRC; n = 69).


18. Webendörfer S, Messerer P, Eberle F, Zober A: [Precautions for intestinal cancer in the workplace. An initiative for secondary prevention in the BASF joint-stock company]. Dtsch Med Wochenschr; 2004 Feb 6;129(6):239-43
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  • Against this background the department of occupational medicine and health protection of the BASF Aktiengesellschaft initiated a study on the potential prevention of colorectal cancer among the staff at its Ludwigshafen site.
  • If the test was positive and/or a positive answer was given to the question on blood in the stool or on a positive family history, coloscopy - to be arranged via the general practitioner - was advised, in line with the recommendations of the German Society of Digestive and Metabolic diseases (Deutsche Gesellschaft für Verdauungs- und Stoffwechselerkrankungen).
  • Adenomatous polyps were found in an additional 61 and subsequently excised.
  • Health care within a company is a valuable complementation in Germany of medical care provided by general practitioners or specialist, if close cooperation between practitioners in the given region is assured.
  • [MeSH-minor] Adenomatous Polyps / diagnosis. Adenomatous Polyps / surgery. Colonic Polyps / diagnosis. Colonic Polyps / surgery. Colonoscopy. Cost-Benefit Analysis. Female. Germany. Humans. Male. Middle Aged. Occult Blood. Surveys and Questionnaires


19. Parker-Ray N, Barakat J, Roy PK, White RE, Schrader RM, Hoffman RM: Statin use does not prevent recurrent adenomatous polyp formation in a VA population. Indian J Gastroenterol; 2010 Jun;29(3):106-11
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  • [Title] Statin use does not prevent recurrent adenomatous polyp formation in a VA population.
  • PURPOSE: To evaluate whether statin use was associated with recurrent adenomatous polyps.
  • We obtained data on pathology, demographics, body mass index, comorbidity, habits, family history, and medications.
  • During follow-up, 88 (47%) of patients received statins, but use was not protective against recurrent adenomas (hazard ratio = 1.36, 95% CI 0.35-8.27).
  • Only number of polyps at initial colonoscopy predicted recurrent adenomas (1.98, 95% CI 1.27-3.08).
  • CONCLUSIONS: The use of statins was not protective against the recurrence of adenomatous polyps.
  • [MeSH-major] Adenomatous Polyposis Coli / prevention & control. Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use. Neoplasm Recurrence, Local / prevention & control. Veterans

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  • (PMID = 20658327.001).
  • [ISSN] 0975-0711
  • [Journal-full-title] Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology
  • [ISO-abbreviation] Indian J Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors
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20. 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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  • [Title] Influence of proton pump inhibitor use in gastrointestinal polyps.
  • Proton pump inhibitors (PPIs) are the most potent anti-acid agents and are extensively used worldwide.
  • 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.
  • 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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21. Simone F, Pappalardo G, Maiani G, Guadalaxara A, Bugianesi R, Conte AM, Azzini E, Mobarhan S: Accumulation and interactions of beta-carotene and alpha-tocopherol in patients with adenomatous polyps. Eur J Clin Nutr; 2002 Jun;56(6):546-50
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  • [Title] Accumulation and interactions of beta-carotene and alpha-tocopherol in patients with adenomatous polyps.
  • (1) to determine whether short-term supplementation of beta-carotene (BC) or vitamin E (VE; alpha-tocopherol) would result in their respective accumulation in normal colonic mucosa and in adenomatous polyps;.
  • SUBJECTS: Eighteen volunteers with colonic adenomatous polyps were enrolled into this study.
  • In placebo subjects after supplementation, the plasma concentrations of BC and VE remained unchanged, however only two patients were recruited in this group and therefore we did not include this group in our final analysis.
  • In VE group, VE concentrations increased (P<0.01) and BC did not change, and in BC/VE group both BC (P<0.001) and VE levels (P<0.01) increased significantly.
  • After supplementation, the tissue concentration of BC in normal colonic mucosa in BC group increased significantly (P<0.01) while the VE concentration did not change.
  • In VE group, the concentration of VE in normal colonic mucosa increased slightly but did not reach statistical significance.
  • However, VE concentration increased significantly (P<0.05) in the polyps of this group.
  • Interestingly in the polyps, although the BC concentration increased (P<0.01), the concentration of VE was reduced moderately but did not reach statistical significance.
  • [MeSH-major] Adenomatous Polyps / metabolism. Antioxidants / administration & dosage. Colon / metabolism. Colonic Neoplasms / metabolism. alpha-Tocopherol / administration & dosage. beta Carotene / administration & dosage
  • [MeSH-minor] Adult. Aged. Biopsy. Dietary Supplements. Drug Interactions. Female. Humans. Intestinal Mucosa / chemistry. Intestinal Mucosa / metabolism. Male. Middle Aged. Tissue Distribution

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  • (PMID = 12032655.001).
  • [ISSN] 0954-3007
  • [Journal-full-title] European journal of clinical nutrition
  • [ISO-abbreviation] Eur J Clin Nutr
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 01YAE03M7J / beta Carotene; H4N855PNZ1 / alpha-Tocopherol
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22. Levi Z, Rozen P, Hazazi R, Vilkin A, Waked A, Maoz E, Birkenfeld S, Lieberman N, Klang S, Niv Y: Sensitivity, but not specificity, of a quantitative immunochemical fecal occult blood test for neoplasia is slightly increased by the use of low-dose aspirin, NSAIDs, and anticoagulants. Am J Gastroenterol; 2009 Apr;104(4):933-8
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  • [Title] Sensitivity, but not specificity, of a quantitative immunochemical fecal occult blood test for neoplasia is slightly increased by the use of low-dose aspirin, NSAIDs, and anticoagulants.
  • OBJECTIVES: We evaluated the effect of the use of aspirin, nonsteroidal anti-inflammatory drugs (NSAIDS), and anticoagulants on the performance of immunochemical fecal occult blood test (I-FOBT).
  • Information regarding the use of medications was collected from the health medical organization (HMO) database.
  • RESULTS: Colorectal cancer (CRC) was found in 17 and advanced adenomatous polyp (AAP) in 97 patients.
  • The specificity, however, was not affected by the use of aspirin/NSAIDS.
  • This study suggests that there is no need to stop these agents before I-FOBT testing.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Anticoagulants / adverse effects. Aspirin / adverse effects. Colonic Polyps / diagnosis. Colorectal Neoplasms / diagnosis. Gastrointestinal Hemorrhage / diagnosis. Occult Blood


23. Rice PL, Goldberg RJ, Ray EC, Driggers LJ, Ahnen DJ: Inhibition of extracellular signal-regulated kinase 1/2 phosphorylation and induction of apoptosis by sulindac metabolites. Cancer Res; 2001 Feb 15;61(4):1541-7
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  • Regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin and sulindac is associated with a decreased mortality from colorectal cancer.
  • Sulindac causes regression of precancerous adenomatous polyps and inhibits the growth of cultured colon cell lines.
  • Both the sulfide and sulfone metabolites of sulindac as well as more potent cyclic GMP-dependent phosphodiesterase inhibitors were shown to cause inhibition of extracellular signal-regulated kinase (ERK)1/2 phosphorylation at doses (40-600 microM) and times (1-5 days) consistent with the induction of apoptosis by the drugs.
  • Inhibition of ERK1/2 activity may, therefore, be a useful biochemical target for the development of chemopreventive and chemotherapeutic drugs for human colon cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. MAP Kinase Kinase Kinase 1. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinases / metabolism. Sulindac / pharmacology
  • [MeSH-minor] 3',5'-Cyclic-GMP Phosphodiesterases / antagonists & inhibitors. 3',5'-Cyclic-GMP Phosphodiesterases / metabolism. Anti-Inflammatory Agents, Non-Steroidal / metabolism. Butadienes / pharmacology. Caspase 3. Caspase 7. Caspases / metabolism. Colonic Neoplasms / enzymology. Colonic Neoplasms / pathology. Down-Regulation. Enzyme Activation. Enzyme Inhibitors / pharmacology. Humans. MAP Kinase Signaling System / drug effects. MAP Kinase Signaling System / physiology. Mitogen-Activated Protein Kinase 3. Nitriles / pharmacology. Phosphorylation / drug effects. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases / metabolism. Tumor Cells, Cultured / drug effects

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  • (PMID = 11245463.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 5T32DK07038
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents; 0 / Butadienes; 0 / Enzyme Inhibitors; 0 / Nitriles; 0 / U 0126; 184SNS8VUH / Sulindac; 6UVA8S2DEY / sulindac sulfide; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinase 1; EC 2.7.11.25 / MAP3K1 protein, human; EC 3.1.4.35 / 3',5'-Cyclic-GMP Phosphodiesterases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP7 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7; EC 3.4.22.- / Caspases; K619IIG2R9 / sulindac sulfone
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24. Half EE, Arber N: Chemoprevention of colorectal cancer: two steps forward, one step back? Future Oncol; 2006 Dec;2(6):697-704
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  • The poor survival rate has prompted the emphasis on prevention of this disease.
  • Progress has been remarkable because of the availability of reliable animal models and clinical studies using colonic adenomas as a reliable and economic target for testing chemopreventive agents.
  • Nonsteroidal anti-inflammatory drugs have drawn the most attention.
  • Sulindac and celecoxib were shown to be effective in promoting polyp regression in high-risk individuals with familial adenomatous polyposis.
  • In the more common sporadic setting, the Adenomatous Polyp PRevention On Vioxx (rofecoxib), Adenoma Prevention with Celecoxib and Prevention of Sporadic Adenomatous Polyps (celecoxib) trials have demonstrated a significant reduction in adenoma recurrence, but important concerns were raised regarding cardiovascular toxicity associated with selective cyclo-oxygenase-2 inhibitors.
  • Potential advantage versus risk for a given chemopreventive agent will have to be assessed on an individual basis.
  • Currently, the only approved agent for chemoprevention is celecoxib in high-risk individuals with familial adenomatous polyposis.
  • [MeSH-major] Adenoma / prevention & control. Adenomatous Polyps / drug therapy. Anticarcinogenic Agents / therapeutic use. Colonic Polyps / drug therapy. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Cyclooxygenase 2 Inhibitors / adverse effects. Cyclooxygenase 2 Inhibitors / therapeutic use. Drug Therapy, Combination. Hormone Replacement Therapy. Humans

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  • (PMID = 17155896.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents; 0 / Cyclooxygenase 2 Inhibitors
  • [Number-of-references] 59
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25. Hartman TJ, Albert PS, Snyder K, Slattery ML, Caan B, Paskett E, Iber F, Kikendall JW, Marshall J, Shike M, Weissfeld J, Brewer B, Schatzkin A, Lanza E, Polyp Prevention Study Group: The association of calcium and vitamin D with risk of colorectal adenomas. J Nutr; 2005 Feb;135(2):252-9
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  • The Polyp Prevention Trial (PPT) was a multicenter randomized clinical trial designed to determine the effects of a high-fiber, high-fruit and vegetable, low-fat diet on the recurrence of adenomatous polyps in the large bowel.
  • Adenoma recurrence was ascertained by complete colonoscopy at baseline and after 1 and 4 y.
  • We evaluated the association between calcium and vitamin D intake and adenomatous polyp recurrence after adjusting for intervention group, age, gender, nonsteroidal anti-inflammatory drug use, total energy intake, and the interaction of gender and intervention group.
  • There were no overall significant associations between adenoma recurrence and dietary calcium intake [odds ratio (OR) for the 5th compared with the lowest quintile = 0.91; 95% CI = 0.67-1.23; P-trend = 0.68], total calcium intake (OR = 0.86; 95% CI = 0.62-1.18; P-trend = 0.20), or dietary vitamin D intake (OR = 0.93; 95% CI = 0.69-1.25; P-trend = 0.43) averaged over follow-up.
  • Total vitamin D intake was weakly inversely associated with adenoma recurrence (OR = 0.84; 95% CI = 0.62-1.13; P-trend = 0.03).
  • Supplemental calcium and vitamin D use during follow-up also were inversely associated with adenoma recurrence (OR for any compared with no use = 0.82; 95% CI = 0.68-0.99; and OR = 0.82; 95% CI = 0.68-0.99; for calcium and vitamin D, respectively).
  • Our analyses did not suggest a significant effect modification between total calcium and total vitamin D intake (P = 0.14) on risk for adenoma recurrence.
  • This trial cohort provides some evidence that calcium and vitamin D may be inversely associated with adenoma recurrence.
  • [MeSH-major] Adenoma / epidemiology. Calcium. Colonic Neoplasms / epidemiology. Diet. Rectal Neoplasms / epidemiology. Vitamin D
  • [MeSH-minor] Body Mass Index. Colonic Polyps / prevention & control. Diet Records. Dietary Supplements. Educational Status. Female. Humans. Male. Middle Aged. Recurrence. Risk Factors. United States / epidemiology

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  • (PMID = 15671222.001).
  • [ISSN] 0022-3166
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 1406-16-2 / Vitamin D; SY7Q814VUP / Calcium
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26. Summers RM, Handwerker LR, Pickhardt PJ, Van Uitert RL, Deshpande KK, Yeshwant S, Yao J, Franaszek M: Performance of a previously validated CT colonography computer-aided detection system in a new patient population. AJR Am J Roentgenol; 2008 Jul;191(1):168-74
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  • OBJECTIVE: A computer-aided detection (CAD) system with high sensitivity in the detection of adenomatous polyps in varied CT colonography (CTC) data sets increases the utility of CAD in the clinical setting.
  • Most of the patients were at average risk, had CTC findings suggestive of polyps, and underwent colonoscopy.
  • Patients underwent cathartic bowel preparation, were given an oral contrast agent, and underwent imaging in the prone and supine positions.
  • In a previous non-polyp-enriched screening cohort, the standalone performance of the CAD system was 93.3% (28/30) sensitivity for adenomatous polyps 10 mm or larger, 51.1% (47/92) sensitivity for adenomas 6-9 mm, and a mean false-positive rate of 8.6 per patient.
  • RESULTS: The CAD system had per-polyp sensitivities of 91.5% (43/47; 95% CI, 78.7-97.2%; p = 1.0) for adenomas 10 mm or larger and 82.1% (32/39; 65.9-91.9%; p = 0.0009) for adenomas 6-9 mm.
  • CONCLUSION: The CAD system evaluated has a high level of performance in the detection of adenomatous polyps with CTC data from a polyp-enriched cohort different from that used to train the system.
  • [MeSH-major] Artificial Intelligence. Colonic Polyps / radiography. Colonography, Computed Tomographic / methods. Colorectal Neoplasms / radiography. Pattern Recognition, Automated / methods. Radiographic Image Interpretation, Computer-Assisted / methods

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  • (PMID = 18562741.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural; Validation Studies
  • [Publication-country] United States
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27. Hoensch HP, Kirch W: Potential role of flavonoids in the prevention of intestinal neoplasia: a review of their mode of action and their clinical perspectives. Int J Gastrointest Cancer; 2005;35(3):187-95
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  • Intestinal neoplasia (adenomas and carcinomas) can possibly be prevented by a diet rich in vegetables and fruits, treatment with aspirin and other nonsteroidal antiinflammatory drugs, and early colonoscopic removal of adenomas.
  • Ballast, fiber, and secondary plant products could play a major role in colon cancer prevention.
  • Flavonoids are secondary plant products with a wide variety of beneficial biological properties, and they possess anticarcinogenic, antimutagenic, and antioxidative modes of actions.
  • We will focus this review on flavonoids which are derived from tea products such as proanthocyanidins (green tea) and flavons (camomille tea).
  • Oral supplementation with bioflavonoids derived from tea could be used in humans to prevent growth of intestinal neoplasia such as adenomatous polyps of the colon.
  • In models of intestinal polyposis, flavonoids suppress polyp formation.
  • [MeSH-minor] Animals. Chemoprevention. Disease Models, Animal. Humans. Plants / chemistry. Tea

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  • (PMID = 16110120.001).
  • [ISSN] 1537-3649
  • [Journal-full-title] International journal of gastrointestinal cancer
  • [ISO-abbreviation] Int J Gastrointest Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Tea
  • [Number-of-references] 58
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28. Shin A, Shrubsole MJ, Rice JM, Cai Q, Doll MA, Long J, Smalley WE, Shyr Y, Sinha R, Ness RM, Hein DW, Zheng W: Meat intake, heterocyclic amine exposure, and metabolizing enzyme polymorphisms in relation to colorectal polyp risk. Cancer Epidemiol Biomarkers Prev; 2008 Feb;17(2):320-9
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  • [Title] Meat intake, heterocyclic amine exposure, and metabolizing enzyme polymorphisms in relation to colorectal polyp risk.
  • Most colorectal cancers arise from adenomatous polyps or certain hyperplastic polyps.
  • Only a few studies have investigated potential genetic modifiers of the associations between meat intake and polyp risk, and results are inconsistent.
  • Using data from the Tennessee Colorectal Polyp Study, a large colonoscopy-based study, including 1,002 polyp cases (557 adenoma only, 250 hyperplastic polyp only, 195 both polyps) and 1,493 polyp-free patients, we evaluated the association of colorectal polyp risk with carcinogen exposure from meat and genetic polymorphisms in enzymes involved in heterocyclic amine (HCA) metabolism, including N-acetyltransferase 1 (NAT1) and N-acetyltransferase 2 (NAT2), cytochrome P450 1A2 (CYP1A2), and aryl hydrocarbon receptor (AhR).
  • Data on intake levels of meats by preparation methods, doneness preferences, and other lifestyle factors were obtained.
  • No clear association was found for any polymorphisms with polyp risk.
  • However, apparent interactions were found for intake of meat and HCAs with AhR, NAT1, and NAT2 genotypes, and the interactions were statistically significant for the group with both adenomatous and hyperplastic polyps.
  • Dose-response relationships with meat or HCA intake were found only among those with the AhR GA/AA (rs2066853) genotype, NAT1 rapid, or NAT2 rapid/intermediate acetylators but not among those with other genotypes of these genes.
  • These results provide strong evidence for a modifying effect of metabolizing genes on the association of meat intake and HCA exposure with colorectal polyp risk.

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  • (PMID = 18268115.001).
  • [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 / P50 CA950103; United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / CA095103-010005; United States / NCI NIH HHS / CA / R01 CA097386-01; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / R01 CA034627; United States / NCI NIH HHS / CA / CA097386-01; United States / NCI NIH HHS / CA / R01 CA34627; United States / NCI NIH HHS / CA / R01 CA034627-15; United States / NCI NIH HHS / CA / P50 CA095103-010005
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Aryl Hydrocarbon; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 2.3.1.- / Acetyltransferases
  • [Other-IDs] NLM/ NIHMS72769; NLM/ PMC2572782
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29. Xu HX: Contrast-enhanced ultrasound in the biliary system: Potential uses and indications. World J Radiol; 2009 Dec 31;1(1):37-44
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  • The use of contrast-enhanced US (CEUS) has reached the field of bile duct disease in recent years and promising results have been achieved.
  • (4) To detect malignant change in Caroli's disease;.
  • (6) To make a distinction between gallbladder cholesterol polyp, adenoma and polypoid cancer;.
  • (9) For differentiation diagnosis between common bile duct cancer and sludge or stone without acoustic shadowing; and (10) In patients who are suspected of having a drop of their percutaneous transhepatic cholangiodrainage tube, US contrast agent can be administered to through the tube detect the site of the tube.

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  • (PMID = 21160719.001).
  • [ISSN] 1949-8470
  • [Journal-full-title] World journal of radiology
  • [ISO-abbreviation] World J Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2999303
  • [Keywords] NOTNLM ; Bile duct / Cholangiocarcinoma / Contrast-enhanced ultrasound / Gallbladder / Polypoid lesion / Ultrasound contrast agent
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30. Peek RM Jr: Prevention of colorectal cancer through the use of COX-2 selective inhibitors. Cancer Chemother Pharmacol; 2004 Sep;54 Suppl 1:S50-6
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  • Colonic neoplasia develops in a stepwise fashion progressing from normal mucosa to adenomatous polyps to carcinoma, a process that takes years, thereby providing a prime opportunity for intervention.
  • Population-based studies have previously determined that long-term ingestion of aspirin or other nonsteroidal antiinflammatory drugs (NSAIDs) leads to a 40-50% reduction in mortality. from colorectal cancer.
  • Experimental studies in mice have revealed that genetic ablation or pharmacologic inhibition of COX-2 attenuates the number and size of intestinal polyps that develop in animals harboring a mutation in Apc, which confers an increased risk for intestinal neoplasia.
  • (1) reduce intestinal polyp burden in patients with familial adenomatous polyposis;.
  • These findings indicate that a widely used and relatively safe class of drugs may represent a viable and effective anticancer strategy for a disease that causes over a half-million deaths per year.
  • [MeSH-minor] Animals. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Cyclooxygenase 2. Enzyme Inhibitors / therapeutic use. Humans. Intestinal Polyps / drug therapy. Membrane Proteins. Mice. Prostaglandin-Endoperoxide Synthases / metabolism. Risk

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  • (PMID = 15309515.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Enzyme Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 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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31. Jin XF, Tong JL, Ran ZH: [Selective cyclooxygenase-2 inhibitors for the prevention of colorectal adenomas: a meta-analysis]. Zhonghua Yi Xue Za Zhi; 2007 Jul 24;87(28):1958-61
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  • METHODS: The relevant data were retrieved from Medline (1966 to 2006), OVID (1996 to January 2007), EMBASE (1980 to January 2007), Chinese Cochrane Centre databases (up to January 2007) and Chinese Biological Medicine Disk (CBM disk, 1997 to 2007).
  • CONCLUSION: Selective COX-2 inhibitors can induce sufficient regression of colorectal adenomatous polyps and thus be used for chemoprevention of colorectal neoplasms.
  • However, because of the potential cardiovascular events, it is not routinely recommended for this indication.
  • [MeSH-major] Adenoma / drug therapy. Colorectal Neoplasms / drug therapy. Cyclooxygenase 2 Inhibitors / therapeutic use

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  • (PMID = 17923032.001).
  • [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; Meta-Analysis
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors
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32. Heher EC, Thier SO, Rennke H, Humphreys BD: Adverse renal and metabolic effects associated with oral sodium phosphate bowel preparation. Clin J Am Soc Nephrol; 2008 Sep;3(5):1494-503
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  • [Title] Adverse renal and metabolic effects associated with oral sodium phosphate bowel preparation.
  • Colorectal cancer can be prevented by the removal of adenomatous polyps during screening colonoscopy, but adequate bowel preparation is required.
  • Oral sodium phosphate (OSP), an effective bowel purgative, is available over the counter and requires a substantially lower volume than polyethylene glycol-based preparative agents.
  • Several recent observational studies have provided new information on these important issues while supporting a link between OSP and acute phosphate nephropathy as well as the development of chronic kidney disease in elderly patients, many of whom had a normal serum creatinine at the time of OSP ingestion.
  • [MeSH-major] Adenoma / surgery. Cathartics / adverse effects. Colonic Polyps / surgery. Colonoscopy. Colorectal Neoplasms / prevention & control. Kidney Diseases / chemically induced. Metabolic Diseases / chemically induced. Phosphates / adverse effects
  • [MeSH-minor] Administration, Oral. Biopsy. Dose-Response Relationship, Drug. Evidence-Based Medicine. Humans. Hypophosphatemia, Familial / complications. Nephrocalcinosis / chemically induced. Preoperative Care / adverse effects. Risk Factors. Time Factors


33. Głuszko P, Bielińska A: Non-steroidal anti-inflammatory drugs and the risk of cardiovascular diseases: are we going to see the revival of cyclooxygenase-2 selective inhibitors? Pol Arch Med Wewn; 2009 Apr;119(4):231-5
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  • [Title] Non-steroidal anti-inflammatory drugs and the risk of cardiovascular diseases: are we going to see the revival of cyclooxygenase-2 selective inhibitors?
  • The use of non-steroidal anti-inflammatory drugs (NSAID) is associated with a number of gastrointestinal and other adverse effects.
  • Introduction of selective cyclooxygenase-2 (COX-2) inhibitors at the end of the 20th century raised hopes for a substantial reduction in the rate of serious events such as upper gastrointestinal ulcers, bleeding and perforations.
  • In 2004 and 2005, predictions of some pharmacologists were confirmed when the Adenomatous Polyp Prevention on VIOXX trial (APPROVE) and other randomized, double-blind, placebo-controlled trials with COX-2 inhibitors showed an increased rate of thrombotic vascular events, including myocardial infarction, in patients treated with coxibs.
  • For patients at high cardiovascular risk, contradictory warnings and recommendations have been published recently by the American Heart Association, Food and Drug Administration, and by independent experts.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Cardiovascular Diseases / chemically induced. Cyclooxygenase 2 Inhibitors / therapeutic use
  • [MeSH-minor] Arthritis, Rheumatoid / drug therapy. Drug Eruptions / etiology. Gastrointestinal Diseases / chemically induced. Humans. Inflammation / drug therapy. Kidney Diseases / chemically induced. Risk Assessment

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  • (PMID = 19413182.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors
  • [Number-of-references] 23
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34. Ligresti A, Bisogno T, Matias I, De Petrocellis L, Cascio MG, Cosenza V, D'argenio G, Scaglione G, Bifulco M, Sorrentini I, Di Marzo V: Possible endocannabinoid control of colorectal cancer growth. Gastroenterology; 2003 Sep;125(3):677-87
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  • the levels of endocannabinoids, cannabinoid CB(1) and CB(2) receptors, and fatty acid amide hydrolase (FAAH, which catalyzes endocannabinoid hydrolysis) in colorectal carcinomas (CRC), adenomatous polyps, and neighboring healthy mucosa; and (2).
  • This effect is blocked by the CB(1) antagonist SR141716A, but not by the CB(2) antagonist SR144528, and is mimicked by CB(1)-selective, but not CB(2)-selective, agonists.
  • Inhibitors of endocannabinoid inactivation may prove useful anticancer agents.
  • [MeSH-major] Colorectal Neoplasms / pathology. Fatty Acids, Unsaturated / physiology
  • [MeSH-minor] Amidohydrolases / metabolism. Caco-2 Cells. Cannabinoid Receptor Modulators. Cell Differentiation. Cell Division. Cyclooxygenase 2. Endocannabinoids. Humans. Isoenzymes / analysis. Isoenzymes / antagonists & inhibitors. Membrane Proteins. Prostaglandin-Endoperoxide Synthases / analysis. Receptors, Cannabinoid. Receptors, Drug / analysis

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  • [CommentIn] Gastroenterology. 2003 Sep;125(3):973-5 [12949741.001]
  • (PMID = 12949714.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cannabinoid Receptor Modulators; 0 / Endocannabinoids; 0 / Fatty Acids, Unsaturated; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Receptors, Cannabinoid; 0 / Receptors, Drug; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 3.5.- / Amidohydrolases; EC 3.5.1.- / fatty-acid amide hydrolase
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35. Jaszewski R, Misra S, Tobi M, Ullah N, Naumoff JA, Kucuk O, Levi E, Axelrod BN, Patel BB, Majumdar AP: Folic acid supplementation inhibits recurrence of colorectal adenomas: a randomized chemoprevention trial. World J Gastroenterol; 2008 Jul 28;14(28):4492-8
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  • AIM: To determine whether folic acid supplementation will reduce the recurrence of colorectal adenomas, the precursors of colorectal cancer, we performed a double-blind placebo-controlled trial in patients with adenomatous polyps.
  • METHODS: In the current double-blind, placebo-controlled trial at this VA Medical Center, patients with colorectal adenomas were randomly assigned to receive either a daily 5 mg dose of folic acid or a matched identical placebo for 3 years.
  • All polyps were removed at baseline colonoscopy and each patient had a follow up colonoscopy at 3 years.
  • RESULTS: Of 137 subjects, who were eligible after confirmation of polyp histology and run-in period to conform compliance, 94 completed the study; 49 in folic acid group and 45 in placebo group.
  • The mean number of recurrent polyps at 3-year was 0.36 (SD, 0.69) for folic acid treated patients compared to 0.82 (SD, 1.17) for placebo treated subjects, resulting in a 3-fold increase in polyp recurrence in the placebo group.
  • CONCLUSION: High dose folic acid supplementation is associated with a significant reduction in the recurrence of colonic adenomas suggesting that folic acid may be an effective chemopreventive agent for colorectal neoplasia.
  • [MeSH-major] Adenoma / prevention & control. Colorectal Neoplasms / prevention & control. Dietary Supplements. Folic Acid / therapeutic use. Neoplasm Recurrence, Local / prevention & control
  • [MeSH-minor] Aged. Colonoscopy. Dose-Response Relationship, Drug. Double-Blind Method. Female. Follow-Up Studies. Humans. Longitudinal Studies. Male. Middle Aged. Risk Factors. Treatment Outcome

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  • (PMID = 18680228.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R01 AG014343
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] China
  • [Chemical-registry-number] 935E97BOY8 / Folic Acid
  • [Other-IDs] NLM/ PMC2731275
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36. Herendeen JM, Lindley C: Use of NSAIDs for the chemoprevention of colorectal cancer. Ann Pharmacother; 2003 Nov;37(11):1664-74
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  • OBJECTIVE: To discuss the role of nonsteroidal antiinflammatory drugs (NSAIDs) in the chemoprevention of colorectal cancer.
  • Search items included, but were not limited to, NSAIDs, colorectal cancer, chemoprevention, cyclooxygenase-2 (COX-2)-specific inhibitors, and familial adenomatous polyposis (FAP).
  • DATA SYNTHESIS: Numerous experimental, epidemiologic, and clinical studies suggest that NSAIDs have promise as anticancer agents.
  • The mechanism by which NSAIDs lead to decreased colon carcinogenesis is not fully understood, but may involve restoration of apoptosis and inhibition of prostaglandin-mediated angiogenesis.
  • Compelling evidence from many observational studies has consistently documented a 40-50% reduction in the risk of adenomatous polyps, colorectal cancer incidence, and mortality in patients using NSAIDs.
  • In addition, randomized studies using sulindac and celecoxib in patients with FAP have documented significant regression of existing adenomatous polyps.
  • However, controversy exists about the safety, efficacy, and optimal treatment regimen of NSAIDs as long-term chemopreventive agents in the general population.
  • Ongoing studies in high-risk patients with both selective and nonselective COX inhibitors will provide important information in the area of colorectal chemoprevention, but clinical trials' use of adenomas as surrogate markers for chemoprevention trials makes their application to the general population limited.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Animals. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Cyclooxygenase Inhibitors / adverse effects. Cyclooxygenase Inhibitors / pharmacology. Cyclooxygenase Inhibitors / therapeutic use. Epidemiologic Studies. Humans. Isoenzymes / antagonists & inhibitors. Membrane Proteins. Prostaglandin-Endoperoxide Synthases. Randomized Controlled Trials as Topic

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  • (PMID = 14565811.001).
  • [ISSN] 1060-0280
  • [Journal-full-title] The Annals of pharmacotherapy
  • [ISO-abbreviation] Ann Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 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] 123
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37. Robb-Nicholson C: By the way, doctor. I keep hearing that aspirin can help prevent colon cancer, but I have no idea how much I should take. Can you help? I've had adenomatous polyps in the past. Harv Womens Health Watch; 2010 Dec;18(4):8
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  • [Title] By the way, doctor. I keep hearing that aspirin can help prevent colon cancer, but I have no idea how much I should take. Can you help? I've had adenomatous polyps in the past.
  • [MeSH-major] Adenomatous Polyposis Coli / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Aspirin / administration & dosage. Colonic Neoplasms / prevention & control. Health Knowledge, Attitudes, Practice
  • [MeSH-minor] Anticarcinogenic Agents / therapeutic use. Dose-Response Relationship, Drug. Humans. Patient Education as Topic

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  • (PMID = 21268798.001).
  • [ISSN] 1070-910X
  • [Journal-full-title] Harvard women's health watch
  • [ISO-abbreviation] Harv Womens Health Watch
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents; R16CO5Y76E / Aspirin
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38. Calaluce R, Earnest DL, Heddens D, Einspahr JG, Roe D, Bogert CL, Marshall JR, Alberts DS: Effects of piroxicam on prostaglandin E2 levels in rectal mucosa of adenomatous polyp patients: a randomized phase IIb trial. Cancer Epidemiol Biomarkers Prev; 2000 Dec;9(12):1287-92
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  • [Title] Effects of piroxicam on prostaglandin E2 levels in rectal mucosa of adenomatous polyp patients: a randomized phase IIb trial.
  • Our dose-finding study on piroxicam, a nonsteroidal anti-inflammatory drug with chemopreventive effects in preclinical colon carcinoma models, suggested that 7.5 mg/day was well tolerated and associated with significant depression of rectal mucosa PGE2 concentrations in comparison with baseline values.
  • We therefore conducted a randomized Phase IIb cancer prevention clinical trial to investigate the chemopreventive properties of piroxicam in patients with a history of resected colorectal adenomatous polyps.
  • Consequently, the gastrointestinal toxicities appear to override the potential benefit that piroxicam may offer as a long-term colon cancer chemopreventive agent.
  • [MeSH-major] Adenomatous Polyps / surgery. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Anticarcinogenic Agents / therapeutic use. Colorectal Neoplasms / surgery. Dinoprostone / analysis. Intestinal Mucosa / drug effects. Piroxicam / therapeutic use. Rectum / drug effects

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  • (PMID = 11142413.001).
  • [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 / CA-23074; United States / NCI NIH HHS / CA / CA-41108
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents; 13T4O6VMAM / Piroxicam; K7Q1JQR04M / Dinoprostone
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39. Kuehle CA, Langhorst J, Ladd SC, Zoepf T, Nuefer M, Grabellus F, Barkhausen J, Gerken G, Lauenstein TC: Magnetic resonance colonography without bowel cleansing: a prospective cross sectional study in a screening population. Gut; 2007 Aug;56(8):1079-85
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  • BACKGROUND AND AIMS: To evaluate the diagnostic accuracy of magnetic resonance colonography (MRC) without bowel cleansing in a screening population and compare the results to colonoscopy as a standard of reference.
  • For MRC, a tagging agent (5.0% Gastrografin, 1.0% barium sulphate, 0.2% locust bean gum) was ingested with each main meal within 2 days prior to MRC.
  • Adenomatous polyps >5 mm were detected by means of MRC, with a sensitivity of 83.0%.
  • However, only 16 of 153 lesions <5 mm and 9 of 127 hyperplastic polyps could be visualised on magnetic resonance images.
  • It provides good accuracy for the detection of relevant (ie, adenomatous) colorectal lesions >5 mm in a screening population.
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / pathology. Aged. Aged, 80 and over. Colonoscopy / methods. Contrast Media. Cross-Sectional Studies. Diatrizoate Meglumine. Feces. Female. Humans. Hyperplasia / diagnosis. Hyperplasia / pathology. Intestinal Polyposis / diagnosis. Intestinal Polyposis / pathology. Male. Mass Screening / methods. Middle Aged. Prospective Studies. Reference Standards. Sensitivity and Specificity

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  • (PMID = 17341542.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Contrast Media; 3X9MR4N98U / Diatrizoate Meglumine
  • [Other-IDs] NLM/ PMC1955492
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40. Telang N, Katdare M: Cell culture model for colon cancer prevention and therapy: an alternative approach to animal experimentation. ALTEX; 2007;24(1):16-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Mouse models for colon cancer that harbor a germ line mutation in the tumor suppressor gene Adenomatous polyposis coli (Apc) exhibit a primary genetic defect that predisposes to a high incidence of adenomatous polyps in the small intestine rather than in the colon.
  • The newly developed colon epithelial cell lines 1638N COL-Cl(1) (clonal derivative of the parental Apc mutant cell line 1638N COL) and 1638N COL-Pr(1) (tumor derivative of the clone), established from an Apc1638N [+/-] mutant mouse, exhibit aberrant cell cycle progression, downregulated apoptosis, enhanced carcinogenic risk and tumor formation, indicating that aberrantly proliferative preneoplastic1638N COL-Cl(1) cells exhibit a quantifiable risk for carcinogenesis.
  • Treatment of these preneoplastic Apc mutant cells with a combination of celecoxib and 5-fluorouracil at clinically achievable low concentrations produced a 2.1 fold to 5.5 fold higher efficacy for cytostatic growth arrest and a 40.2% to 52.4% higher efficacy for inhibition of carcinogenic risk, relative to that obtained by these agents used individually.
  • Thus, a low dose combination of mechanistically distinct agents resulted in enhanced efficacy.
  • These data validate a novel cell culture model and a rapid mechanism-based approach to prioritize efficacious drug combinations for animal studies and clinical trials on cancer prevention and, thereby, support the 3R concept by refining and/or reducing the use of animals in biomedical research relevant to prevention/therapy of colon cancer.
  • [MeSH-major] Animal Testing Alternatives. Colonic Neoplasms / drug therapy. Colonic Neoplasms / prevention & control. Genes, APC. Precancerous Conditions / prevention & control
  • [MeSH-minor] Animals. Anticarcinogenic Agents / pharmacology. Antineoplastic Agents / pharmacology. Cell Cycle / drug effects. Cell Line, Tumor. Cell Transformation, Neoplastic. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical. Humans. Mice. Mice, Inbred C57BL. Tumor Cells, Cultured

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  • (PMID = 17361317.001).
  • [ISSN] 1868-596X
  • [Journal-full-title] ALTEX
  • [ISO-abbreviation] ALTEX
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-29502-20; United States / NCI NIH HHS / CA / CA-29502-S1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents
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41. Huls G, Koornstra JJ, Kleibeuker JH: Non-steroidal anti-inflammatory drugs and molecular carcinogenesis of colorectal carcinomas. Lancet; 2003 Jul 19;362(9379):230-2
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  • [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 molecular carcinogenesis of colorectal carcinomas.
  • Non-steroidal anti-inflammatory drugs (NSAIDs) can inhibit colorectal carcinogenesis and are among the few agents known to be chemopreventive.
  • Randomised trials have shown that sulindac and celecoxib suppress the development of adenomatous polyps and cause regression of existing polyps in patients with familial adenomatous polyposis (FAP), who have a high risk for developing colorectal cancer.
  • The mechanisms by which NSAIDs inhibit neoplastic growth are not fully known.
  • After a follow-up of around 31 months, the mean number of adenomas was lower in the aspirin group than in the placebo group, corresponding to a relative risk of any recurrent adenoma in the aspirin group of 0.65.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Antineoplastic Agents / therapeutic use. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Apoptosis / drug effects. Aspirin / pharmacology. Aspirin / therapeutic use. Cell Cycle / drug effects. Chemoprevention. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / metabolism. Humans. Molecular Biology

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  • (PMID = 12885487.001).
  • [ISSN] 1474-547X
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; R16CO5Y76E / Aspirin
  • [Number-of-references] 26
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42. McLaren CE, Fujikawa-Brooks S, Chen WP, Gillen DL, Pelot D, Gerner EW, Meyskens FL Jr: Longitudinal assessment of air conduction audiograms in a phase III clinical trial of difluoromethylornithine and sulindac for prevention of sporadic colorectal adenomas. Cancer Prev Res (Phila); 2008 Dec;1(7):514-21
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  • A phase III clinical trial assessed the recurrence of adenomatous polyps after treatment for 36 months with difluoromethylornithine (DFMO) plus sulindac or matched placebos.
  • Dose intensity did not add information to models.
  • The estimated attributable risk of ototoxicity from exposure to the drug is 8.4% (95% confidence interval, -2.0% to 18.8%; P = 0.12).

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  • (PMID = 19139001.001).
  • [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 / R01 CA059024; United States / NCI NIH HHS / CA / R01 CA088078-05; United States / NCI NIH HHS / CA / P30 CA023074; None / None / / R01 CA059024-04; United States / NCI NIH HHS / CA / P30 CA062203-13; United States / NCI NIH HHS / CA / R01 CA059024-04; United States / NCI NIH HHS / CA / CA 23074; United States / NCI NIH HHS / CN / N01 CN 75019; United States / NCI NIH HHS / CA / CA 95060; United States / NCI NIH HHS / CN / N01 CN075019; United States / NCI NIH HHS / CA / P50 CA095060-07; United States / NCI NIH HHS / CA / CA 88078; United States / NCI NIH HHS / CA / P50 CA095060; United States / NCI NIH HHS / CA / CA 59024; United States / NCI NIH HHS / CA / CA095060-07; United States / NCI NIH HHS / CA / P30 CA062203; United States / NCI NIH HHS / CA / R01 CA088078; United States / NCI NIH HHS / CN / N01 CN085182; United States / NCI NIH HHS / CA / CA088078-05; United States / NCI NIH HHS / CA / R01 CA063640; United States / NCI NIH HHS / CA / CA062203-13
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 184SNS8VUH / Sulindac; ZQN1G5V6SR / Eflornithine
  • [Other-IDs] NLM/ NIHMS91693; NLM/ PMC2702261
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43. Selgrad M, Koornstra JJ, Fini L, Blom M, Huang R, Devol EB, Boersma-van Ek W, Dijkstra G, Verdonk RC, de Jong S, Goel A, Williams SL, Meyer RL, Haagsma EB, Ricciardiello L, Boland CR: JC virus infection in colorectal neoplasia that develops after liver transplantation. Clin Cancer Res; 2008 Oct 15;14(20):6717-21
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  • EXPERIMENTAL DESIGN: JCV TAg DNA and protein expression were determined in normal colonic epithelium (n = 15) and adenomatous polyps (n = 26) from LTRs and compared with tissue samples from control patients (normal colon, n = 21; adenomas, n = 40).
  • CONCLUSIONS: The presence of JCV in the colorectal mucosa and adenomas from LTRs, in concert with the use of immunosuppressive agents, suggests that JCV may undergo reactivation, and the subsequent TAg protein expression might explain the increased risk of colorectal neoplasia in LTRs.

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  • (PMID = 18927316.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / CA098572-05; United States / NCI NIH HHS / CA / R01 CA098572; United States / NCI NIH HHS / CA / R01 CA098572-05; United States / NCI NIH HHS / CA / R01 CA98572
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / DNA, Viral
  • [Other-IDs] NLM/ NIHMS187522; NLM/ PMC2846598
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44. Half E, Arber N: Colon cancer: preventive agents and the present status of chemoprevention. Expert Opin Pharmacother; 2009 Feb;10(2):211-9
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  • [Title] Colon cancer: preventive agents and the present status of chemoprevention.
  • CRC has a natural history of transition from a precursor lesion, ie adenomatous polyp to cancer, that spans over 10 to 15 years providing an extended opportunity for intervention and cancer prevention.
  • Suppression of the carcinogenic process by use of pharmacological or natural agents is the cornerstone of chemoprevention.
  • OBJECTIVES: The aim of this review was to give an up-to-date overview on the different agents that had been studied, over the last decade, as chemopreventive agents and the current status of chemoprevention.
  • All articles and other referenced materials were retrieved using the keywords "colon cancer", "adenoma", "chemoprevention", "non steroidal anti-inflammatory drugs", "aspirin", "HMG-CoA reductase inhibitors", "bile acids", "Difluoromethylornithine", "hormone replacement therapy", "mesalamine", "curcumin", and "calcium".
  • RESULTS: Recent preclinical as well as clinical trials have provided data on the potential benefit of a number of drugs and nutritional elements in the field of CRC prevention.
  • Currently, only celecoxib is FDA approved for chemoprevention of CRC and only for high-risk patients with Familial Adenomatous Polyposis (FAP).
  • Combination therapy, using lower doses of each medication, is drawing a great deal of attention and many studies utilizing a variety of chemopreventive agents are presently under study.
  • CONCLUSION: Many agents have shown positive results in the field of chemoprevention however, the ideal chemopreventive agent remains to be discovered with great emphasis on need not to harm.
  • Combining different agents may maximize effectiveness while limiting drug toxicity.
  • [MeSH-major] Adenomatous Polyps / prevention & control. Anticarcinogenic Agents. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Animals. Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Bile Acids and Salts / therapeutic use. Cyclooxygenase 2 Inhibitors / adverse effects. Cyclooxygenase 2 Inhibitors / therapeutic use. Drug Therapy, Combination. Hormone Replacement Therapy. Humans. Hydroxymethylglutaryl-CoA Reductase Inhibitors / adverse effects. Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use

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  • (PMID = 19236194.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents; 0 / Bile Acids and Salts; 0 / Cyclooxygenase 2 Inhibitors; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • [Number-of-references] 87
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45. Haile RW, Yochim JM, Cortessis VK, Lin J, Levine AJ, Diep A, Danenberg K, Danenberg P: A molecular/epidemiologic analysis of expression of cyclooxygenases 1 and 2, use of nonsteroidal antiinflammatory drugs, and risk of colorectal adenoma. Clin Colorectal Cancer; 2005 Mar;4(6):390-5
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  • [Title] A molecular/epidemiologic analysis of expression of cyclooxygenases 1 and 2, use of nonsteroidal antiinflammatory drugs, and risk of colorectal adenoma.
  • Nonsteroidal antiinflammatory drugs (NSAIDs) are postulated to protect against colorectal cancer and adenomas at least in part by a cyclooxygenase (COX-mediated mechanism.
  • Paraffin-embedded tissue samples and data describing selected risk factors were obtained from cases enrolled in a case-control study of colorectal adenomatous polyps.
  • Results suggest that use of NSAIDs is associated with lower levels of COX-2 expression and that the protective effect of NSAIDs on polyp occurrence is stronger in the subgroup of cases with higher expression of COX-2 and a higher COX-2/COX-1 ratio.
  • The results suggest that at least part of the protective effect of NSAIDs on the risk of colorectal adenoma involves a COX-mediated pathway.
  • [MeSH-major] Adenoma / chemically induced. Adenoma / genetics. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms / genetics. Gene Expression Profiling. Prostaglandin-Endoperoxide Synthases / biosynthesis
  • [MeSH-minor] Aged. Case-Control Studies. Colonic Polyps / epidemiology. Colonic Polyps / genetics. Cyclooxygenase 1. Cyclooxygenase 2. Female. Humans. Incidence. Male. Membrane Proteins. Middle Aged. Odds Ratio. RNA, Messenger / analysis. RNA, Messenger / biosynthesis. Risk Factors

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  • (PMID = 15807932.001).
  • [ISSN] 1533-0028
  • [Journal-full-title] Clinical colorectal cancer
  • [ISO-abbreviation] Clin Colorectal Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Membrane Proteins; 0 / RNA, Messenger; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS1 protein, human; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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46. Nam JH, Yang CH: [Clinical characteristics and risk factors of colon polyps in gyeongju and pohang area]. Korean J Gastroenterol; 2008 Sep;52(3):142-9
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  • [Title] [Clinical characteristics and risk factors of colon polyps in gyeongju and pohang area].
  • BACKGROUND/AIMS: The purposes of this study were to investigate various environmental factors for colon polyps and to analyze locoregional clinical characteristics of colon polyps in Gyeongju and Pohang area.
  • METHODS: From October 2005 to September 2006, patients who underwent colonoscopy were analyzed based on their ages, genders, body mass indices (BMI), dietary habits, smoking behaviors, accompaying diseases, and medications as risk factors for the occurrence of colon polyps.
  • Then clinical manifestations, gross appearances and pathologic findings of polyps were investigated.
  • RESULTS: Among 253 patients enrolled, a total of 296 colon polyps were found in 108 patients.
  • The incidence of colon polyps in more than 50-year old patients was 3.2-fold greater compared to less than 50-year old patients.
  • Smoking habits were also significantly associated with the occurence of colon polyps.
  • Among adenomatous polyps, tubulovillous type and moderate to severe dysplasia were frequently observed as the size increased, yet the location of polyps was not significantly associated.
  • CONCLUSIONS: Older age and smoking habit increase the risk of colon polyps.
  • Rectal polyps have less chance to be adenomatous type.
  • The larger the polyp grows, the more likely it to be tubulovillous and dysplastic.
  • [MeSH-major] Colonic Polyps / diagnosis. Colorectal Neoplasms / diagnosis
  • [MeSH-minor] Adenomatous Polyps / pathology. Adult. Aged. Aged, 80 and over. Female. Humans. Korea. Male. Middle Aged. Multivariate Analysis. Odds Ratio. Risk Factors. Rural Population. Surveys and Questionnaires

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  • (PMID = 19077510.001).
  • [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
  • [Publication-country] Korea (South)
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47. Siddiqui A, Nazario HE, Patel M, Mahgoub A, Spechler SJ: Reduction in low-density lipoprotein cholesterol levels during statin therapy is associated with a reduced incidence of advanced colon polyps. Am J Med Sci; 2009 Nov;338(5):378-81
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  • [Title] Reduction in low-density lipoprotein cholesterol levels during statin therapy is associated with a reduced incidence of advanced colon polyps.
  • BACKGROUND: Elevated serum cholesterol levels may stimulate proliferation in adenomatous polyps (AP).
  • These findings remained significant even when adjusted for nonsteroidal antiinflammatory drug use, age, family history of APs, and body mass index.
  • CONCLUSIONS: A reduction in LDL levels of > or=30% during a 3- to 5-year period of statin therapy was associated with a 53% reduction in the incidence of advanced APs, even after adjustment for other known polyp risk factors.
  • [MeSH-major] Cholesterol, LDL / blood. Colonic Polyps / blood. Hydroxymethylglutaryl-CoA Reductase Inhibitors / blood

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  • (PMID = 19794305.001).
  • [ISSN] 1538-2990
  • [Journal-full-title] The American journal of the medical sciences
  • [ISO-abbreviation] Am. J. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cholesterol, LDL; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors
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48. 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
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  • 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.
  • Over the duration of the supplementation period, LI in the control group did not alter significantly (9.3 (7.8, 10.3) v 9.6 (8.9, 10.4)).
  • [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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49. Holt PR, Bresalier RS, Ma CK, Liu KF, Lipkin M, Byrd JC, Yang K: Calcium plus vitamin D alters preneoplastic features of colorectal adenomas and rectal mucosa. Cancer; 2006 Jan 15;106(2):287-96
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  • BACKGROUND: Calcium and vitamin D are chemopreventive agents for colorectal neoplasia.
  • Biologic changes that may occur in colorectal adenomas after chemopreventive regimens have not been reported.
  • METHODS: In the current study, adenomatous polyps were transected, approximately 50% were removed for histologic examination, and the remnants tattooed before the administration of either calcium carbonate (1500 mg 3 times daily) plus vitamin D(3) 400 IU or a placebo for 6 months.
  • At study end, polyp remnants were resected completely and were used for histologic examination.
  • Immunohistochemical staining was performed in both flat mucosa and in polyp tissue.
  • Proliferative indices fell both in flat mucosa and in polyps in the treatment group, and there were no significant changes in the control group.
  • Apoptosis and Bcl-2 immunostaining were unchanged in both groups, but the frequency of BAK-immunostained cells in the interior of polyps rose significantly.
  • There were no significant changes in galectin-3 staining, but a striking reduction in MUC5AC mucin staining in polyps was observed after treatment with calcium plus vitamin D.
  • CONCLUSIONS: The administration of a calcium plus vitamin D chemopreventive regimen resulted in several changes in adenomatous tissue that may have contributed to reduced polyp formation.
  • [MeSH-major] Adenoma / drug therapy. Adenomatous Polyps / drug therapy. Calcium / administration & dosage. Colorectal Neoplasms / prevention & control. Precancerous Conditions / drug therapy. Vitamin D / administration & dosage
  • [MeSH-minor] Apoptosis. Biomarkers, Tumor / analysis. Cell Proliferation. Female. Humans. Intestinal Mucosa / drug effects. Intestinal Mucosa / pathology. Male. Middle Aged. Rectum / pathology

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  • (PMID = 16353199.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CN / N01CN25439-1; United States / NCI NIH HHS / CA / R01CA69480
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 1406-16-2 / Vitamin D; SY7Q814VUP / Calcium
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50. Niv Y, Delpre G, Sperber AD, Sandbank J, Zirkin H: Hyperplastic gastric polyposis, hypergastrinaemia and colorectal neoplasia: a description of four cases. Eur J Gastroenterol Hepatol; 2003 Dec;15(12):1361-6
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  • Increased gastrin may be the link between these two conditions insofar as gastrin has been reported to be a growth-promoting tumoural agent.
  • METHODS: Four male patients with no family history of cancer, who were found to have multiple gastric hyperplastic polyps, hypergastrinaemia and colorectal cancers or an adenomatous polyp, were evaluated.
  • Assessment included clinical evaluation, biochemical and haematological profiles, fasting gastrin levels, Helicobacter pylori serology, cobalamin, parietal cell antibodies, gastroscopy with biopsies of polyps and gastric mucosa, urease tests, and colonoscopy with biopsies of colorectal neoplasms.
  • Immunohistochemistry of specimens from gastric polyps and colonic carcinomas was performed for chromogranin A, synaptophysin, Leu 7, neuron-specific enolase and gastrin.
  • RESULTS: The mean age at diagnosis of gastric polyps was 71.2 years and at removal of colorectal neoplasm was 70.0 years.
  • Immunohistochemistry failed to identify neuroendocrine cells in the hyperplastic gastric polyps and three of the colonic carcinomas.
  • Gastrin is not secreted by the gastric polyps or colonic carcinomas and may be related to gastric mucosal changes and H. pylori colonization.
  • [MeSH-major] Colorectal Neoplasms / pathology. Gastrins / blood. Polyps / pathology. Stomach Neoplasms / pathology

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  • (PMID = 14624161.001).
  • [ISSN] 0954-691X
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gastrins
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51. Schmid K, Nair J, Winde G, Velic I, Bartsch H: Increased levels of promutagenic etheno-DNA adducts in colonic polyps of FAP patients. Int J Cancer; 2000 Jul 1;87(1):1-4
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  • [Title] Increased levels of promutagenic etheno-DNA adducts in colonic polyps of FAP patients.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) can regress adenomas in patients with familial adenomatous polyposis (FAP), and the mechanism involves inhibition of cyclooxygenases (COX).
  • Reactive intermediates formed during the arachidonic acid cascade, notably by COX-2, which is upregulated in polyps of FAP patients, may promote various stages of the polyp --> adenoma --> carcinoma sequence.
  • We tested this hypothesis in colonic polyps from FAP patients and colorectal tissue from cancer patients to see whether increased formation of etheno-DNA adducts occurs.
  • Using an ultra-sensitive and specific immunoaffinity/(32)P-postlabelling method, 1, N(6)-ethenodeoxyadenosine (straightepsilondA) and 3, N(4)-ethenodeoxycytidine (straightepsilondC) were quantitated in epithelial cell DNA from asymptomatic colon, FAP polyps and colon tumor tissues.
  • Mean adduct levels in FAP polyps were 65 straightepsilondA/10(9) and 59 straightepsilondC/10(9) parent nucleotides, being 2 to 3 times higher than in unaffected colon tissue (p < 0.02 for straightepsilondA; p < 0.05 for straightepsilondC).
  • Adduct levels in colonic epithelia decreased in the order: FAP polyps > tumor-adjacent tissue > tumor, normal and tumor-distal tissue.
  • Based on this study, requiring confirmation in a larger number of patients and in experimental models, we have demonstrated the formation of promutagenic etheno-DNA adducts in adenomatous polyps of FAP patients that may contribute to genetic instability and cancer progression.
  • [MeSH-major] Adenoma / genetics. Adenoma / metabolism. Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Colonic Polyps / genetics. Colonic Polyps / metabolism. Colorectal Neoplasms / genetics. Colorectal Neoplasms / metabolism. DNA Adducts / biosynthesis

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  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 10861445.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / DNA Adducts; 0 / Deoxyadenosines; 0W860991D6 / Deoxycytidine; 68498-25-9 / 1,N(6)-ethenodeoxyadenosine; 68498-26-0 / 3,N(4)-ethenodeoxycytidine
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52. Rex DK: Screening for colon cancer and evaluation of chemoprevention with coxibs. J Pain Symptom Manage; 2002 Apr;23(4 Suppl):S41-50
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  • Most colorectal cancers are believed to arise from adenomatous polyps, premalignant mucosal masses that account for up to two thirds of colorectal polyps.
  • Colonoscopy has emerged as the dominant method for evaluating symptomatic patients with colorectal cancer and for surveillance of patients with previous colon polyps or cancer.
  • For both screening and surveillance, the type of screening test used and the intervals at which it is performed are based on risk stratification, which also serves as the basis for selecting potential candidates for chemoprevention.
  • A variety of agents with potential chemopreventive benefits have been identified, including cyclooxygenase (COX)-2-specific inhibitors (coxibs) even though these agents have not been approved for this use in the United States.
  • COX-2 is overexpressed in colonic adenomas and cancers, and its inhibition has been shown to produce regression of polyps in familial adenomatous polyposis.
  • Nonselective COX inhibition with nonsteroidal anti-inflammatory drugs (NSAIDs) has been consistently associated with reductions in the risk of mortality and the incidence of colorectal adenomas and cancers in case-control studies.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Colonic Neoplasms / diagnosis. Colonic Neoplasms / prevention & control. Cyclooxygenase Inhibitors / therapeutic use. Isoenzymes / physiology. Prostaglandin-Endoperoxide Synthases / physiology
  • [MeSH-minor] Adenomatous Polyposis Coli / drug therapy. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Humans. Membrane Proteins

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  • (PMID = 11992750.001).
  • [ISSN] 0885-3924
  • [Journal-full-title] Journal of pain and symptom management
  • [ISO-abbreviation] J Pain Symptom Manage
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 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] 72
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53. Giardiello FM, Hylind LM, Trimbath JD, Hamilton SR, Romans KE, Cruz-Correa M, Corretti MC, Offerhaus GJ, Yang VW: Oral contraceptives and polyp regression in familial adenomatous polyposis. Gastroenterology; 2005 Apr;128(4):1077-80
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  • [Title] Oral contraceptives and polyp regression in familial adenomatous polyposis.
  • We describe a patient in the placebo arm of a 4-year primary chemoprevention trial who developed adenomatous polyps and then had eradication of polyps after the administration of oral contraceptives.
  • No change in the prostaglandin levels in the colonic mucosa was noted after polyp elimination, making nonsteroidal anti-inflammatory drug ingestion unlikely as a cause.
  • [MeSH-major] Adenomatous Polyposis Coli / physiopathology. Contraceptives, Oral / therapeutic use
  • [MeSH-minor] Child. Colon / metabolism. Female. Humans. Intestinal Mucosa / metabolism. Menstruation Disturbances / drug therapy. Prostaglandins / metabolism. Remission Induction

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  • (PMID = 15825088.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 51085; United States / NCI NIH HHS / CA / CA 53801; United States / NCI NIH HHS / CA / CA 63721; United States / NCI NIH HHS / CA / P50 CA 9316
  • [Publication-type] Case Reports; 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 / Contraceptives, Oral; 0 / Prostaglandins
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54. Misikangas M, Tanayama H, Rajakangas J, Lindén J, Pajari AM, Mutanen M: Inulin results in increased levels of beta-catenin and cyclin D1 as the adenomas increase in size from small to large in the Min/+ mouse. Br J Nutr; 2008 May;99(5):963-70
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  • To address this issue we fed Min/+ mice with two diets known to lead to different adenoma outcomes: a high-fat control diet (n 15) or a high-fat inulin-enriched (10 % w/w) diet (n 13).
  • To study the effect of diet on cell signalling during adenoma growth, the adenomas of each Min/+ mouse were divided into three size-categories, and the levels of beta-catenin, E-cadherin, cyclin D1 and matrix metalloproteinase-9, which are known to be involved in colon tumorigenesis, were determined.
  • Neither phenomenon was seen in the control group during adenoma growth.
  • Our results suggest that in addition to the number, size, and growth rate of adenomatous polyps, the signalling pattern of the adenomas should also be considered when evaluating preventive dietary strategies.
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Cyclin D1 / metabolism. Diet. Inulin / pharmacology. beta Catenin / metabolism
  • [MeSH-minor] Animals. Cadherins / metabolism. Dietary Fats / administration & dosage. Disease Models, Animal. Disease Progression. Mice. Mice, Inbred C57BL. Neoplasm Proteins / metabolism. Signal Transduction / drug effects


55. Lauenstein TC, Goehde SC, Debatin JF: Fecal tagging: MR colonography without colonic cleansing. Abdom Imaging; 2002 Jul-Aug;27(4):410-7
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  • Colorectal cancer, mostly arising (>90%) from preexisting adenomatous polyps, continues to be the second leading cause of cancer death.
  • Magnetic resonance colonography (MRC) permits accurate detection of colonic polyps with a diameter larger than 10 mm.
  • Because residual colonic stool cannot be differentiated from polyps, MRC requires a clean colon.
  • The need for colonic cleansing could be eliminated, if stool were to acquire a signal intensity different from polyps and identical to the enema used to fill and distend the colon.
  • In principle, there are two approaches to this concept of fecal tagging: dark polyps surrounded by bright stool and a bright enema, and bright polyps surrounded by dark stool and a dark enema.
  • Gadolinium (Gd)-DOTA was administered as an oral contrast agent with meals preceding MRC based on the administration of a Gd-based enema.
  • In the second approach patients are provided with barium as an oral fecal tagging agent to render stool dark, and barium for the enema is used to distend the colon during MRC.
  • The colonic wall and polyps arising from it can be made visible after intravenous administration of Gd-based extracellular contrast.
  • Barium as the tagging agent is promising because it is inexpensive, commercially available, and characterized by an excellent safety profile.
  • [MeSH-minor] Barium Sulfate. Colonic Polyps / diagnosis. Colonoscopy. Colorectal Neoplasms / diagnosis. Enema. Feasibility Studies. Feces. Gadolinium. Humans. Patient Compliance

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  • (PMID = 12066239.001).
  • [ISSN] 0942-8925
  • [Journal-full-title] Abdominal imaging
  • [ISO-abbreviation] Abdom Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 25BB7EKE2E / Barium Sulfate; AU0V1LM3JT / Gadolinium
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56. Guadagni F, Ferroni P, Palmirotta R, Del Monte G, Formica V, Roselli M: Non-steroidal anti-inflammatory drugs in cancer prevention and therapy. Anticancer Res; 2007 Sep-Oct;27(5A):3147-62
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  • [Title] Non-steroidal anti-inflammatory drugs in cancer prevention and therapy.
  • Long-term use of non-steroidal anti-inflammatory drugs (NSAIDs) can be regarded as an effective approach for cancer chemoprevention, as demonstrated by a bulk of clinical and experimental evidence.
  • However, the clinical use of these drugs as chemopreventive agents is limited by many open questions about the optimal drug, dose, duration of therapy and knowledge about the mechanism(s) by which these drugs act.
  • In particular, the recent data on cardiovascular toxicity of coxibs has posed some limitations on the use of NSAIDs for cancer chemoprevention in the general population.
  • The situation is different in certain genetically susceptible subgroups, such as in individuals with genetic mutations associated with hereditary nonpolyposis colon cancer (HNPCC) or familiar adenomatous polyps (FAP) in whom lifetime risk increases up to 70-90% and in whom the benefit of a chemopreventive drug might justify its use even in the presence of adverse effects.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Anticarcinogenic Agents / pharmacology. Neoplasms / prevention & control
  • [MeSH-minor] Animals. Humans

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  • (PMID = 17970056.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents
  • [Number-of-references] 142
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57. Luebeck EG, Moolgavkar SH: Multistage carcinogenesis and the incidence of colorectal cancer. Proc Natl Acad Sci U S A; 2002 Nov 12;99(23):15095-100
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  • We use general multistage models to fit the age-specific incidence of colorectal cancers in the Surveillance, Epidemiology, and End Results registry, which covers approximately 10% of the U.S. population, while simultaneously adjusting for birth cohort and calendar year effects.
  • The incidence of colorectal cancers in the Surveillance, Epidemiology, and End Results registry is most consistent with a model positing two rare events followed by a high-frequency event in the conversion of a normal stem cell into an initiated cell that expands clonally to give rise to an adenomatous polyp.
  • The two rare events involved in initiation are interpreted to represent the homozygous loss of adenomatous polyposis coli gene function.
  • The subsequent transition of a preinitiated stem cell into an initiated cell capable of clonal expansion via symmetric division is predicted to occur with a frequency too high for a mutational event but may reflect a positional effect in colonic crypts.
  • Our results suggest it is not necessary to invoke genomic instability to explain colorectal cancer incidence rates in human populations.
  • The model also predicts that interventions, such as administration of nonsteroidal anti-inflammatory drugs, designed to decrease the growth rate of adenomatous polyps, are very efficient at lowering colon cancer risk substantially, even when begun later in life.
  • By contrast, interventions that decrease the rate of mutations at the adenomatous polyposis coli locus are much less effective in reducing the risk of colon cancer.

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  • (PMID = 12415112.001).
  • [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 / R01 CA047658; United States / NCI NIH HHS / CA / P01 CA76466; United States / NCI NIH HHS / CA / R01 CA47658
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC137549
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58. Thun MJ, Henley SJ, Patrono C: Nonsteroidal anti-inflammatory drugs as anticancer agents: mechanistic, pharmacologic, and clinical issues. J Natl Cancer Inst; 2002 Feb 20;94(4):252-66
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  • [Title] Nonsteroidal anti-inflammatory drugs as anticancer agents: mechanistic, pharmacologic, and clinical issues.
  • Numerous experimental, epidemiologic, and clinical studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDs), particularly the highly selective cyclooxygenase (COX)-2 inhibitors, have promise as anticancer agents.
  • NSAIDs restore normal apoptosis in human adenomatous colorectal polyps and in various cancer cell lines that have lost adenomatous polyposis coli gene function.
  • Many epidemiologic studies have found that long-term use of NSAIDs is associated with a lower risk of colorectal cancer, adenomatous polyps, and, to some extent, other cancers.
  • Two NSAIDs, sulindac and celecoxib, have been found to inhibit the growth of adenomatous polyps and cause regression of existing polyps in randomized trials of patients with familial adenomatous polyposis (FAP).
  • Moreover, the development of safe and effective drugs for chemoprevention is complicated by the potential of even rare, serious toxicity to offset the benefit of treatment, particularly when the drug is administered to healthy people who have low annual risk of developing the disease for which treatment is intended.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Anticarcinogenic Agents / therapeutic use. Antineoplastic Agents / therapeutic use
  • [MeSH-minor] Adenomatous Polyposis Coli / drug therapy. Angiogenesis Inhibitors / therapeutic use. Animals. Apoptosis / drug effects. Aspirin / therapeutic use. Clinical Trials as Topic. Colorectal Neoplasms / prevention & control. Humans

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  • (PMID = 11854387.001).
  • [ISSN] 0027-8874
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents; R16CO5Y76E / Aspirin
  • [Number-of-references] 218
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59. Attene-Ramos MS, Wagner ED, Plewa MJ, Gaskins HR: Evidence that hydrogen sulfide is a genotoxic agent. Mol Cancer Res; 2006 Jan;4(1):9-14
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  • [Title] Evidence that hydrogen sulfide is a genotoxic agent.
  • However, a mechanistic model that explains the connection between H2S and ulcerative colitis or colorectal cancer development has not been completely formulated.
  • Sulfide was not genotoxic in the standard SCGE assay.
  • These data indicate that given a predisposing genetic background that compromises DNA repair, H2S may lead to genomic instability or the cumulative mutations found in adenomatous polyps leading to colorectal cancer.
  • [MeSH-minor] Animals. CHO Cells. Cell Nucleus / drug effects. Comet Assay. Cricetinae. DNA Damage. Genome / drug effects. HT29 Cells. Humans. Hydroxyurea / pharmacology

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  • (PMID = 16446402.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mutagens; X6Q56QN5QC / Hydroxyurea; YY9FVM7NSN / Hydrogen Sulfide
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60. Martin C, Connelly A, Keku TO, Mountcastle SB, Galanko J, Woosley JT, Schliebe B, Lund PK, Sandler RS: Nonsteroidal anti-inflammatory drugs, apoptosis, and colorectal adenomas. Gastroenterology; 2002 Dec;123(6):1770-7
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  • [Title] Nonsteroidal anti-inflammatory drugs, apoptosis, and colorectal adenomas.
  • BACKGROUND & AIMS: Observational studies indicate that nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the risk of colorectal neoplasia.
  • We examined grossly normal rectal mucosa in patients with adenomas and adenoma-free controls to assess the associations between NSAID use, adenomatous polyps, and apoptosis.
  • Apoptosis was scored from coded, H&E-stained sections using morphologic methods.
  • RESULTS: There were 226 patients with adenomas and 493 adenoma-free controls.
  • NSAID use and apoptotic activity were not correlated (r = 0.10).
  • Mucosal proliferation was not related to adenomas or NSAID use.
  • [MeSH-major] Adenoma / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Apoptosis / drug effects. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Cell Division / drug effects. Control Groups. Cytoprotection. Female. Humans. Intestinal Mucosa / pathology. Intestinal Mucosa / physiopathology. Male. Middle Aged. Prevalence. Prospective Studies. Rectum / pathology. Rectum / physiopathology. Regression Analysis

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  • (PMID = 12454832.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK34987; United States / NCI NIH HHS / CA / R01 CA 44684; United States / NIDDK NIH HHS / DK / T32 DK07634
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
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61. Kline CL, Jackson R, Engelman R, Pledger WJ, Yeatman TJ, Irby RB: Src kinase induces tumor formation in the c-SRC C57BL/6 mouse. Int J Cancer; 2008 Jun 15;122(12):2665-73
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  • Src kinase has been linked as a causative agent in the progression of a number of cancers including colon, breast, lung and melanoma.
  • However, although Src protein is increased in colon cancer as early as the adenomatous polyp stage, a role for Src in carcinogenesis has not been established.
  • No additional carcinogenic agent was administered.
  • Of the mice with the transgene, 15% developed tumors in the liver while no tumors were detected in wild type C57BL/6 mice.
  • [MeSH-minor] Animals. Base Sequence. DNA Primers. Humans. Metallothionein / genetics. Mice. Mice, Inbred C57BL. Mice, Transgenic. Promoter Regions, Genetic. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18351644.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 9038-94-2 / Metallothionein; EC 2.7.10.2 / src-Family Kinases
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62. Mayne ST, Cartmel B: Chemoprevention of second cancers. Cancer Epidemiol Biomarkers Prev; 2006 Nov;15(11):2033-7
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  • BACKGROUND: "Second cancers" can be thought of in two general categories: (a) those occurring as a consequence of cancer treatment and (b) primary cancers that are thought to develop largely as a consequence of prior lifestyle habits (e.g., chronic smoking, drinking, sun exposures), genetic susceptibility, or interactions of the two.
  • METHODS/RESULTS: Trials aimed at preventing second cancers in patients with tobacco-related cancers (head and neck, lung), skin cancers, breast cancer, and colorectal adenomatous polyps have been completed with some success.
  • However, one finding that has emerged is that, across several cancer sites, subgroups are found with differential response to the chemopreventive agent.
  • Stratum-specific (subgroup) findings may occur by chance, requiring a need for supportive evidence from observational epidemiologic studies of the agent (where available), mechanistic studies, or results of other related trials.
  • CONCLUSIONS: Although chemoprevention of second cancers has been realized, it has become increasingly apparent that not all benefit equally.
  • The finding of subgroup effects in completed trials results in the need to consider such subgroup effects in the design of future trials, by either restricting enrollment to particular subgroups (e.g., never or former smokers), or by increasing sample size requirements to allow for variation in response in subgroups in a statistically powerful way.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Genetic Predisposition to Disease. Neoplasms / prevention & control. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / prevention & control
  • [MeSH-minor] Alcohol Drinking. Breast Neoplasms / drug therapy. Breast Neoplasms / prevention & control. Clinical Trials as Topic. Female. Humans. Nutritional Status. Smoking. beta Carotene / pharmacology

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  • (PMID = 17057027.001).
  • [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
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 01YAE03M7J / beta Carotene
  • [Number-of-references] 38
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63. Asano TK, McLeod RS: Nonsteroidal anti-inflammatory drugs and aspirin for the prevention of colorectal adenomas and cancer: a systematic review. Dis Colon Rectum; 2004 May;47(5):665-73
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  • [Title] Nonsteroidal anti-inflammatory drugs and aspirin for the prevention of colorectal adenomas and cancer: a systematic review.
  • PURPOSE: A systematic review was conducted to determine the effect of nonsteroidal anti-inflammatory drugs for the prevention or regression of colorectal adenomas and cancer.
  • Nonsteroidal anti-inflammatory drugs were the interventions.
  • The primary outcomes were the number of patients with at least one colorectal adenoma, a change in polyp burden, or colorectal cancer.
  • RESULTS: Nine trials with 150 familial adenomatous polyposis and 24,143 population patients met the inclusion criteria.
  • In another three trials, patients with familial adenomatous polyposis who received nonsteroidal anti-inflammatory drugs had a greater proportional reduction (range, 11.9-44 percent) in the number of colorectal adenomas compared with those in the control group (range, 4.5-10 percent).
  • CONCLUSIONS: There is combined evidence from three randomized trials that aspirin significantly reduced the recurrence of sporadic adenomatous polyps.
  • There was evidence from short-term trials to support regression, but not elimination or prevention, of colorectal polyps in familial adenomatous polyposis.
  • [MeSH-major] Adenoma / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Colorectal Neoplasms / prevention & control. Neoplastic Syndromes, Hereditary / prevention & control

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  • (PMID = 15054679.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; R16CO5Y76E / Aspirin
  • [Number-of-references] 45
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64. Rial NS, Lazennec G, Prasad AR, Krouse RS, Lance P, Gerner EW: Regulation of deoxycholate induction of CXCL8 by the adenomatous polyposis coli gene in colorectal cancer. Int J Cancer; 2009 May 15;124(10):2270-80
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  • [Title] Regulation of deoxycholate induction of CXCL8 by the adenomatous polyposis coli gene in colorectal cancer.
  • Elevated deoxycholic acid (DCA), mutations in the adenomatous polyposis coli (APC) gene and chronic inflammation are associated with increased risk of colorectal cancer.
  • DCA increased steady state mRNA and protein levels of CXCL8 in cells which do not express wild-type APC.
  • Steady-state CXCL8 mRNA and protein were suppressed when cells with conditional expression of wild-type APC were exposed to DCA.
  • Immunostaining did not detect CXCL8 in normal human colonic mucosa.
  • CXCL8 was expressed in adenomatous polyps and adenocarcinomas.
  • Wild-type APC suppressed this effect.
  • Phenotypic assays determined that DCA-mediated invasion was blocked by antibody-directed against CXCL8 or wild-type APC.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
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  • (PMID = 19173296.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA023074; United States / NCI NIH HHS / CA / P01 CA072008-08; United States / NCI NIH HHS / CA / CA95060; United States / NCI NIH HHS / CA / CA123065-02; United States / NCI NIH HHS / CA / R01 CA123065-02; United States / NCI NIH HHS / CA / P01 CA072008-01A10001; United States / NCI NIH HHS / CA / P50 CA095060-07; United States / NCI NIH HHS / CA / CA072008-01A10001; United States / NCI NIH HHS / CA / P01 CA041108; United States / NCI NIH HHS / CA / P50 CA095060; United States / NCI NIH HHS / CA / R01 CA123065; United States / NCI NIH HHS / CA / CA095060-08; United States / NCI NIH HHS / CA / CA023074; United States / NCI NIH HHS / CA / P01 CA072008; United States / NCI NIH HHS / CA / CA095060-07; United States / NCI NIH HHS / CA / P50 CA095060-08; United States / NCI NIH HHS / CA / 2P01 CA041108; United States / NCI NIH HHS / CA / 2P30CA023074
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / IL8 protein, human; 0 / Interleukin-8; 0 / RNA, Messenger; 005990WHZZ / Deoxycholic Acid
  • [Other-IDs] NLM/ NIHMS98402; NLM/ PMC2669776
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65. Ponz D: Prevention and chemoprevention of colorectal neoplasms. Dig Liver Dis; 2002 Jan;34(1):59-69
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  • Available evidence does not support the contention that a more appropriate diet can be of great help in the prevention of these neoplasms, either because the scientific evidence is poor and highly controversial, or because changes in diet are difficult to implement, at least in many Western countries.
  • Secondary prevention--i.e., the systematic removal of adenomatous polyps--can hardly be applied in the general population, with the exception of individuals at risk because members of families with Adenomatosis coli or Lynch syndrome, or affected by inflammatory bowel diseases.
  • Finally, chemoprevention (i.e., the attempt to prevent tumour development through the administration of drugs or natural compounds that interfere with various phases of carcinogenesis) is still in its infancy Though attractive, this approach requires well-designed studies which should be carried out for years before being evaluated and interpreted; so far most of these investigations gave inconsistent or controversial results.
  • In conclusion, both primary and secondary prevention of colorectal malignancies appear difficult to apply in the general population, and chemoprevention is still at the beginning of a (presumably] long story.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Colorectal Neoplasms / prevention & control. Diet. Exercise. Sulindac / therapeutic use

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  • (PMID = 11926575.001).
  • [ISSN] 1590-8658
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antioxidants; 0 / Vitamins; 184SNS8VUH / Sulindac; 935E97BOY8 / Folic Acid
  • [Number-of-references] 128
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66. Ferrís I Tortajada J, Ortega García JA, Garcia I Castell J, López Andreu JA, Ribes Koninckx C, Berbel Tornero O: [Risks factors for pediatric malignant liver tumors]. An Pediatr (Barc); 2008 Apr;68(4):377-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Factores de riesgo para los tumores hepáticos malignos pediátricos.
  • c) adenomatous polyps of the colon;.
  • e) Hereditary Tyrosinemia Type 1;.
  • Also systematic monitoring of HBV and HCV in blood, hemoderivates, donated organs and drug addicts, are very useful.

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  • (PMID = 18394385.001).
  • [ISSN] 1695-4033
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 56
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67. Serrano D, Lazzeroni M, Decensi A: Chemoprevention of colorectal cancer: an update. Tech Coloproctol; 2004 Dec;8 Suppl 2:s248-52
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  • Adjuvant treatment does not seem to be highly effective and recurrent or metastatic disease occurs in half of the new cases within one year of diagnosis and median survival does not exceed 18 months.
  • Colon cancer is supposed to arise as the result of a series of genetic mutations, which parallel histopathologic and molecular changes, from normal colonic epithelium to invasive carcinoma, with adenomatous polyps as an intermediate step.
  • The more studied agents are the non-steroidal anti-inflammatory drugs.
  • Among those, aspirin has been shown, in two recent randomised trials, to lower the incidence on polyps vs. placebo.
  • Intervention studies on diet showed disappointing results, but diet micronutrients are promising agents in CRC prevention.
  • [MeSH-major] Chemoprevention / methods. Colorectal Neoplasms / drug therapy

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  • (PMID = 15666100.001).
  • [ISSN] 1123-6337
  • [Journal-full-title] Techniques in coloproctology
  • [ISO-abbreviation] Tech Coloproctol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 44
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68. Meyskens FL Jr, McLaren CE, Pelot D, Fujikawa-Brooks S, Carpenter PM, Hawk E, Kelloff G, Lawson MJ, Kidao J, McCracken J, Albers CG, Ahnen DJ, Turgeon DK, Goldschmid S, Lance P, Hagedorn CH, Gillen DL, Gerner EW: Difluoromethylornithine plus sulindac for the prevention of sporadic colorectal adenomas: a randomized placebo-controlled, double-blind trial. Cancer Prev Res (Phila); 2008 Jun;1(1):32-8
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  • Preclinical studies of chemoprevention drugs given in combination at low doses show remarkable efficacy in preventing adenomas with little additional toxicities, suggesting a strategy to improve risk to benefit ratios for preventing recurrent adenomas.
  • Colorectal adenoma recurrence was compared among the groups with log-binomial regression.
  • Recurrent adenomatous polyps can be markedly reduced by a combination of low oral doses of DFMO and sulindac and with few side effects.

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  • (PMID = 18841250.001).
  • [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 / R01 CA059024; United States / NCI NIH HHS / CA / CA72008; United States / NCI NIH HHS / CA / P30 CA023074; None / None / / R01 CA123065-01A2; United States / NCI NIH HHS / CA / CA95060; United States / NCI NIH HHS / CA / P30 CA023074-209010; United States / NCI NIH HHS / CA / CA47396; United States / NCI NIH HHS / CN / N01 CN075019; United States / NCI NIH HHS / CA / R01 CA123065-01A2; None / None / / P30 CA023074-209010; United States / NCI NIH HHS / CA / CA88078; United States / NCI NIH HHS / CN / N01-CN75019; United States / NCI NIH HHS / CA / P50 CA095060; United States / NCI NIH HHS / CA / R01 CA123065; None / None / / P50 CA095060-05; United States / NCI NIH HHS / CA / CA59024; United States / NCI NIH HHS / CA / P01 CA072008; United States / NCI NIH HHS / CA / CA63640; United States / NCI NIH HHS / CA / P30 CA062203; United States / NCI NIH HHS / CA / R01 CA088078; United States / NCI NIH HHS / CA / P50 CA095060-05; United States / NCI NIH HHS / CA / R01 CA063640
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Placebos; 184SNS8VUH / Sulindac; ZQN1G5V6SR / Eflornithine
  • [Other-IDs] NLM/ NIHMS58572; NLM/ PMC2562024
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69. Morimoto LM, Newcomb PA, Ulrich CM, Bostick RM, Lais CJ, Potter JD: Risk factors for hyperplastic and adenomatous polyps: evidence for malignant potential? Cancer Epidemiol Biomarkers Prev; 2002 Oct;11(10 Pt 1):1012-8
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  • [Title] Risk factors for hyperplastic and adenomatous polyps: evidence for malignant potential?
  • Recent studies have suggested that hyperplastic polyps may be benign precursor lesions for a distinct subset of colorectal tumors.
  • We conducted a clinic-based case-control study to evaluate risk factors for hyperplastic polyps.
  • Cases with hyperplastic polyps (n = 219), adenomas (n = 437), and both types of polyps (n = 138), along with colonoscopy-negative controls (n = 708), were identified at a gastroenterology practice in the Minneapolis area during 1991-1994.
  • Risk factors for hyperplastic and adenomatous polyps were generally similar to those for colorectal cancer.
  • Male sex, smoking, and alcohol consumption were associated with increased risk of all polyp groups; nonsteroidal anti-inflammatory drug use, hormone replacement therapy use, and calcium intake were associated with reduced risk.
  • There was no apparent association between increasing age and hyperplastic polyp risk (P = 0.21) in this analysis, although it was a strong risk factor for adenoma (P < 0.001).
  • The odds ratio (OR) for hyperplastic polyps associated with >25 pack-years of smoking was 4.1 [95% confidence interval (CI), 2.2-7.6], whereas the OR for adenoma alone was 1.3 (95% CI, 0.8-2.3).
  • The OR estimate for individuals diagnosed with both polyp types was 4.2 (95% CI, 1.9-9.3).
  • These results suggest, as one possibility, that the consistent association of adenoma and smoking observed in previous studies may be partially attributable to the inclusion of individuals with both adenomas and hyperplastic polyps in the adenoma case group.
  • To the contrary, individuals with both polyp types may be expressing a phenotype distinct from those who have only adenomas and should be considered separately.
  • Further studies are necessary to establish which polyp phenotypes are related to smoking.
  • Overall, the similarity of the risk profiles of colorectal hyperplastic polyps, adenoma, and cancer provides additional support for the growing body of evidence that some hyperplastic polyps may have neoplastic potential.
  • [MeSH-major] Adenomatous Polyps / etiology. Colonic Neoplasms / etiology. Colonic Polyps / etiology. Smoking / adverse effects
  • [MeSH-minor] Adult. Aged. Alcohol Drinking / adverse effects. Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Case-Control Studies. Female. Hormone Replacement Therapy / adverse effects. Humans. Hyperplasia. Male. Middle Aged. Phenotype. Risk Factors. Sex Factors

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  • (PMID = 12376501.001).
  • [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 / 5-T32-CA09168; United States / NIEHS NIH HHS / ES / ES-07033; United States / NCI NIH HHS / CA / P01 CA 50405; United States / NCI NIH HHS / CA / T32 CA09661
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
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70. Bukin YUV, Draudin-Krylenko VA, Levchuk AA, Poddubniy BK, Mazurov ST: The effect of high doses of folic acid on the overexpression of ornithine decarboxylase and S-adenosylmethionine content in human colon adenomatous polyps. Ann N Y Acad Sci; 2001 Dec;952:175-6
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  • [Title] The effect of high doses of folic acid on the overexpression of ornithine decarboxylase and S-adenosylmethionine content in human colon adenomatous polyps.
  • It was shown that the 3-month supplementation of patients having colon polyps with folic acid (5 mg/day) led to a 35% decrease in abnormally high ornithine decarboxylase activity in polyps that was accompanied by a 43% increase of S-adenosylmethionine content in polyps.
  • [MeSH-major] Adenomatous Polyps / metabolism. Colonic Polyps / metabolism. Folic Acid / pharmacology. Neoplasm Proteins / biosynthesis. Ornithine Decarboxylase / biosynthesis. S-Adenosylmethionine / metabolism
  • [MeSH-minor] Disease Progression. Double-Blind Method. Enzyme Induction / drug effects. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male

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  • (PMID = 11795438.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 7LP2MPO46S / S-Adenosylmethionine; 935E97BOY8 / Folic Acid; EC 4.1.1.17 / Ornithine Decarboxylase
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71. Powers HJ, Hill MH, Welfare M, Spiers A, Bal W, Russell J, Duckworth Y, Gibney E, Williams EA, Mathers JC: Responses of biomarkers of folate and riboflavin status to folate and riboflavin supplementation in healthy and colorectal polyp patients (the FAB2 Study). Cancer Epidemiol Biomarkers Prev; 2007 Oct;16(10):2128-35
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  • [Title] Responses of biomarkers of folate and riboflavin status to folate and riboflavin supplementation in healthy and colorectal polyp patients (the FAB2 Study).
  • A double-blind randomized placebo-controlled intervention study (the FAB2 Study) was carried out in healthy controls and patients with colorectal polyps (adenomatous and hyperplastic) to examine effects of folic acid and riboflavin supplements on biomarkers of nutrient status and on putative biomarkers of colorectal cancer risk (DNA methylation and DNA damage; to be reported elsewhere).
  • Ninety-eight healthy controls and 106 patients with colorectal polyps were stratified for the thermolabile variant of methylene tetrahydrofolate reductase, MTHFR C677T, and were randomized to receive 400 microg of folic acid, 1,200 microg of folic acid, or 400 microg of folic acid plus 5 mg of riboflavin or placebo for 6 to 8 weeks.
  • Riboflavin supplement enhanced the response to low-dose folate in people carrying at least one T allele and having polyps.
  • The magnitude of the response in mucosal folate was positively related to the increase in plasma 5-methyl tetrahydrofolate but was not different between the healthy group and polyp patients.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Biomarkers, Tumor / blood. Folic Acid / administration & dosage. Folic Acid / blood. Riboflavin / administration & dosage. Riboflavin / blood
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Alleles. Biopsy. Colonoscopy. Dose-Response Relationship, Drug. Double-Blind Method. Drug Therapy, Combination. Erythrocytes / drug effects. Erythrocytes / metabolism. Female. Follow-Up Studies. Genetic Variation / genetics. Genotype. Heterozygote Detection. Homocysteine / blood. Humans. Intestinal Mucosa / pathology. Male. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Middle Aged. Polymorphism, Single Nucleotide. Sigmoidoscopy. Tetrahydrofolates / blood

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  • (PMID = 17932361.001).
  • [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
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tetrahydrofolates; 0LVT1QZ0BA / Homocysteine; 134-35-0 / 5-methyltetrahydrofolate; 935E97BOY8 / Folic Acid; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2); TLM2976OFR / Riboflavin
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72. Half E, Bercovich D, Rozen P: Familial adenomatous polyposis. Orphanet J Rare Dis; 2009;4:22
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  • [Title] Familial adenomatous polyposis.
  • Familial adenomatous polyposis (FAP) is characterized by the development of many tens to thousands of adenomas in the rectum and colon during the second decade of life.
  • Generally, cancers start to develop a decade after the appearance of the polyps.
  • A less aggressive variant of FAP, attenuated FAP (AFAP), is characterized by fewer colorectal adenomatous polyps (usually 10 to 100), later age of adenoma appearance and a lower cancer risk.
  • Classic FAP is inherited in an autosomal dominant manner and results from a germline mutation in the adenomatous polyposis (APC) gene.
  • Most patients (~70%) have a family history of colorectal polyps and cancer.
  • In a subset of individuals, a MUTYH mutation causes a recessively inherited polyposis condition, MUTYH-associated polyposis (MAP), which is characterized by a slightly increased risk of developing CRC and polyps/adenomas in both the upper and lower gastrointestinal tract.
  • Differential diagnoses include other disorders causing multiple polyps (such as Peutz-Jeghers syndrome, familial juvenile polyps or hyperplastic polyposis, hereditary mixed polyposis syndromes, and Lynch syndrome).
  • Patients with progressive tumors and unresectable disease may respond or stabilize with a combination of cytotoxic chemotherapy and surgery (when possible to perform).
  • Adjunctive therapy with celecoxib has been approved by the US Food and Drug Administration and the European Medicines Agency in patients with FAP.
  • [MeSH-major] Adenomatous Polyposis Coli / diagnosis. Adenomatous Polyposis Coli / pathology
  • [MeSH-minor] Animals. Female. Humans. Male

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  • (PMID = 19822006.001).
  • [ISSN] 1750-1172
  • [Journal-full-title] Orphanet journal of rare diseases
  • [ISO-abbreviation] Orphanet J Rare Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 114
  • [Other-IDs] NLM/ PMC2772987
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73. Mulcahy HE, O'Donoghue D: Nonsteroidal anti-inflammatory drugs and their colonic effects: more interesting than irritating? Eur J Gastroenterol Hepatol; 2002 Nov;14(11):1177-8
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  • [Title] Nonsteroidal anti-inflammatory drugs and their colonic effects: more interesting than irritating?
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) have both beneficial and deleterious effects on the colon.
  • Long-term use is associated with a substantial decrease in colorectal cancer incidence and regression of adenomatous polyps.
  • In contrast, significant adverse effects are also interesting, but rare, and include mucosal inflammation and ulceration, exacerbation of inflammatory bowel disease, diverticular bleeding, and diaphragm-like stricturing of the proximal colon.
  • Discontinuation of the offending drug results in symptom resolution in the majority of cases, but some require endoscopic balloon dilation or surgical resection of strictures.
  • [MeSH-major] Adenomatous Polyps / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Colonic Diseases / chemically induced. Colonic Neoplasms / prevention & control. Rectal Diseases / chemically induced

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  • [CommentOn] Eur J Gastroenterol Hepatol. 2002 Nov;14(11):1265-9 [12439124.001]
  • (PMID = 12439110.001).
  • [ISSN] 0954-691X
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
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74. Florie J, Jensch S, Nievelstein RA, Bartelsman JF, Baak LC, van Gelder RE, Haberkorn B, van Randen A, van der Ham MM, Snel P, van der Hulst VP, Bossuyt PM, Stoker J: MR colonography with limited bowel preparation compared with optical colonoscopy in patients at increased risk for colorectal cancer. Radiology; 2007 Apr;243(1):122-31
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  • [Title] MR colonography with limited bowel preparation compared with optical colonoscopy in patients at increased risk for colorectal cancer.
  • PURPOSE: To prospectively evaluate the diagnostic performance of magnetic resonance (MR) colonography by using limited bowel preparation in patients with polyps of 10 mm or larger in diameter in a population at increased risk for colorectal cancer, with optical colonoscopy as the reference standard.
  • In this multicenter study, patients undergoing colonoscopy because of a personal or family history of colorectal cancer or adenomatous polyps were included.
  • Two blinded observers independently evaluated T1- and T2-weighted MR colonographic images obtained with limited bowel preparation (bright-lumen fecal tagging) for the presence of polyps.
  • The limited bowel preparation consisted of a low-fiber diet, with ingestion of lactulose and an oral gadolinium-based contrast agent (with all three major meals) starting 48 hours prior to imaging.
  • Patient sensitivity, patient specificity, polyp sensitivity, and interobserver agreement for lesions of 10 mm or larger were calculated for both observers individually and combined.
  • At colonoscopy, 12 patients had 22 polyps of 10 mm or larger.
  • Per-patient sensitivity was 58% (seven of 12) for observer 1, 67% (eight of 12) for observer 2, and 75% (nine of 12) for both observers combined for polyps of 10 mm or larger.
  • Per-polyp sensitivity was 55% (12 of 22) for observer 1, 50% (11 of 22) for observer 2, and 77% (17 of 22) for both observers combined.
  • CONCLUSION: In patients at increased risk for colorectal cancer, specificity of MR colonography by using limited bowel preparation was high, but sensitivity was modest.
  • [MeSH-major] Colonic Polyps / diagnosis. Colorectal Neoplasms / diagnosis. Magnetic Resonance Imaging


75. Allison JE, Sakoda LC, Levin TR, Tucker JP, Tekawa IS, Cuff T, Pauly MP, Shlager L, Palitz AM, Zhao WK, Schwartz JS, Ransohoff DF, Selby JV: Screening for colorectal neoplasms with new fecal occult blood tests: update on performance characteristics. J Natl Cancer Inst; 2007 Oct 3;99(19):1462-70
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  • BACKGROUND: One type of fecal occult blood test (FOBT), the unrehydrated guaiac fecal occult blood test (GT), is recommended by the United States Preventive Services Task Force and the Institute of Medicine for use in screening programs, but it has relatively low sensitivity as a single test for detecting advanced colonic neoplasms (cancer and adenomatous polyps > or = 1 cm in diameter).
  • [MeSH-minor] Aged. Colonoscopy. Female. Humans. Indicators and Reagents. Male. Middle Aged. Predictive Value of Tests. Sensitivity and Specificity. Sigmoidoscopy. United States

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  • [CommentIn] J Natl Cancer Inst. 2007 Oct 3;99(19):1424-5 [17895471.001]
  • (PMID = 17895475.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA074562-01
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Indicators and Reagents; 9000-29-7 / Guaiac
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76. Tanaka T: Colorectal carcinogenesis: Review of human and experimental animal studies. J Carcinog; 2009;8:5
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  • The large majority of colorectal malignancies develop from an adenomatous polyp (adenoma).
  • Carcinomas usually originate from pre-existing adenomas, but this does not imply that all polyps undergo malignant changes and does not exclude de novo oncogenesis.
  • Besides adenomas, there are other types of pre-neoplasia, which include hyperplastic polyps, serrated adenomas, flat adenomas and dysplasia that occurs in the inflamed colon in associated with inflammatory bowel disease.

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  • (PMID = 19332896.001).
  • [ISSN] 1477-3163
  • [Journal-full-title] Journal of carcinogenesis
  • [ISO-abbreviation] J Carcinog
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2678864
  •  go-up   go-down


77. Wilkins T, Reynolds PL: Colorectal cancer: a summary of the evidence for screening and prevention. Am Fam Physician; 2008 Dec 15;78(12):1385-92
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  • Colonoscopy does not have a proven colorectal cancer mortality benefit, but it does have the greatest single-test accuracy, and it is the final test in the pathway to evaluate and treat patients with other abnormal screening tests.
  • There is good evidence that fiber and antioxidants are not effective for primary prevention of colorectal cancer; they should not be recommended for chemoprevention.
  • There is good evidence that aspirin, nonsteroidal antiinflammatory drugs, and cyclooxygenase-2 inhibitors are effective for decreasing the risk of colorectal cancer and adenomatous polyps, but increased risks, such as gastrointestinal bleeding, limit their usefulness.

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  • [CommentIn] Am Fam Physician. 2008 Dec 15;78(12):1340 [19119551.001]
  • [CommentIn] Am Fam Physician. 2010 May 1;81(9):1073 [20433120.001]
  • [CommentIn] Am Fam Physician. 2010 May 1;81(9):1073 [20433119.001]
  • (PMID = 19119558.001).
  • [ISSN] 0002-838X
  • [Journal-full-title] American family physician
  • [ISO-abbreviation] Am Fam Physician
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 25BB7EKE2E / Barium Sulfate
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78. Huang L, Ouyang Q, Wei D, Liu X, Hu R: [The growth inhibition of colorectal adenoma cells by sulindac and its mechanisms]. Hua Xi Yi Ke Da Xue Xue Bao; 2002 Jan;33(1):101-3
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  • [Title] [The growth inhibition of colorectal adenoma cells by sulindac and its mechanisms].
  • OBJECTIVE: This study was conducted to assess the growth inhibition of colorectal adenoma cells by sulindac and identify the possible mechanisms.
  • METHODS: The colorectal adenoma cells from human sporadic adenomatous polyps were cultured, and then treated with sulindac.
  • CONCLUSION: These data suggested that sulindac could inhibit the growth of the colorectal adenoma cells, and its mechanisms might be related to suppressing proliferation and inducing apoptosis.

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  • (PMID = 12599442.001).
  • [ISSN] 0257-7712
  • [Journal-full-title] Hua xi yi ke da xue xue bao = Journal of West China University of Medical Sciences = Huaxi yike daxue xuebao
  • [ISO-abbreviation] Hua Xi Yi Ke Da Xue Xue Bao
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 184SNS8VUH / Sulindac; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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79. Slice LW, Chiu T, Rozengurt E: Angiotensin II and epidermal growth factor induce cyclooxygenase-2 expression in intestinal epithelial cells through small GTPases using distinct signaling pathways. J Biol Chem; 2005 Jan 14;280(2):1582-93
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  • Cyclooxygenase-2 (COX-2) is aberrantly expressed in premalignant adenomatous polyps and colorectal carcinomas and is associated with increased epithelial cell proliferation, decreased apoptosis, and increased cell invasiveness.
  • Recently, in a non-transformed rat intestinal epithelial cell line (IEC-18), we showed induction of cell proliferation and DNA synthesis by angiotensin II (Ang II) via the endogenous Ang II type 1 receptor (Chiu, T., Santiskulvong, C., and Rozengurt, E. (2003) Am. J. Physiol.
  • 285, G1-G11). We report that Ang II potently stimulated expression of COX-2 mRNA and protein as an immediate-early gene response through the Ang II type 1 receptor, correlating with an increase in prostaglandin I2 production.
  • Inhibition of ERK activation by U0126 or PD98059 significantly decreased EGF-dependent COX-2 expression, but did not affect Ang II-dependent COX-2 expression.
  • Conversely, inhibition of p38MAPK by SB202190 or PD169316 inhibited COX-2 expression by Ang II, but did not block COX-2 induction by EGF.
  • EGF did not induce Ca2+ mobilization, and 2-aminobiphenyl borate did not inhibit EGF-dependent COX-2 expression.
  • [MeSH-major] Angiotensin II / pharmacology. Epidermal Growth Factor / pharmacology. Epithelial Cells / drug effects. Gene Expression Regulation, Enzymologic / drug effects. Intestines / cytology. Monomeric GTP-Binding Proteins / metabolism. Prostaglandin-Endoperoxide Synthases / genetics
  • [MeSH-minor] Animals. Cell Line. Cyclooxygenase 2. Dose-Response Relationship, Drug. Epoprostenol / biosynthesis. Epoprostenol / metabolism. Mitogen-Activated Protein Kinases / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Receptor, Angiotensin, Type 1 / metabolism. Signal Transduction / drug effects. Time Factors. Transcription, Genetic / drug effects. Transcription, Genetic / genetics. cdc42 GTP-Binding Protein / metabolism

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  • (PMID = 15525649.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK017294; United States / NIDDK NIH HHS / DK / DK055003; United States / NIDDK NIH HHS / DK / DK056930; United States / NIDDK NIH HHS / DK / DK061485; United States / NIDDK NIH HHS / DK / DK063983
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptor, Angiotensin, Type 1; 11128-99-7 / Angiotensin II; 62229-50-9 / Epidermal Growth Factor; DCR9Z582X0 / Epoprostenol; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.2 / Monomeric GTP-Binding Proteins; EC 3.6.5.2 / cdc42 GTP-Binding Protein
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80. Lanza E, Hartman TJ, Albert PS, Shields R, Slattery M, Caan B, Paskett E, Iber F, Kikendall JW, Lance P, Daston C, Schatzkin A: High dry bean intake and reduced risk of advanced colorectal adenoma recurrence among participants in the polyp prevention trial. J Nutr; 2006 Jul;136(7):1896-903
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  • [Title] High dry bean intake and reduced risk of advanced colorectal adenoma recurrence among participants in the polyp prevention trial.
  • We examined the association between fruits and vegetables and adenomatous polyp recurrence in the Polyp Prevention Trial (PPT).
  • The PPT was a low-fat, high-fiber, high-fruit, and vegetable dietary intervention trial of adenoma recurrence, in which there were no differences in the rate of adenoma recurrence in participants in the intervention and control arms of the trial.
  • In this analysis of the entire PPT trial-based cohort, multiple logistic regression analysis was used to estimate the odds ratio (OR) of advanced and nonadvanced adenoma recurrence within quartiles of baseline and change (baseline minus the mean over 3 y) in fruit and vegetable intake, after adjustment for age, total energyy intake, use of nonsteroidal anti-inflammatory drugs, BMI, and gender.
  • There were no significant associations between nonadvanced adenoma recurrence and overall change in fruit and vegetable consumption; however, those in the highest quartile of change in dry bean intake (greatest increase) compared with those in the lowest had a significantly reduced OR for advanced adenoma recurrence (OR = 0.35; 95% CI, 0.18-0.69; P for trend = 0.001).
  • The PPT trial-based cohort provides evidence that dry beans may be inversely associated with advanced adenoma recurrence.

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  • (PMID = 16772456.001).
  • [ISSN] 0022-3166
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CN / Z01 CN000151-17; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS10712; NLM/ PMC1713264
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81. Tsuda H, Kozu T, Iinuma G, Ohashi Y, Saito Y, Saito D, Akasu T, Alexander DB, Futakuchi M, Fukamachi K, Xu J, Kakizoe T, Iigo M: Cancer prevention by bovine lactoferrin: from animal studies to human trial. Biometals; 2010 Jun;23(3):399-409
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  • Administration of bovine lactoferrin (bLF) suppresses carcinogenesis in the colon and other organs of test animals, and recently it was shown that ingestion of bLF inhibits the growth of adenomatous polyps in human patients.
  • Here we review work which established bLF as an anti-carcinogenic agent in laboratory animals and the results of a clinical trial which demonstrated that bLF can reduce the risk of colon carcinogenesis in humans.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Colorectal Neoplasms / prevention & control. Lactoferrin / pharmacology
  • [MeSH-minor] Animals. Cattle. Humans

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  • (PMID = 20407806.001).
  • [ISSN] 1572-8773
  • [Journal-full-title] Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine
  • [ISO-abbreviation] Biometals
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; EC 3.4.21.- / Lactoferrin
  • [Number-of-references] 64
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82. Arber N, Eagle CJ, Spicak J, Rácz I, Dite P, Hajer J, Zavoral M, Lechuga MJ, Gerletti P, Tang J, Rosenstein RB, Macdonald K, Bhadra P, Fowler R, Wittes J, Zauber AG, Solomon SD, Levin B, PreSAP Trial Investigators: Celecoxib for the prevention of colorectal adenomatous polyps. N Engl J Med; 2006 Aug 31;355(9):885-95
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  • [Title] Celecoxib for the prevention of colorectal adenomatous polyps.
  • BACKGROUND: Overexpression of cyclooxygenase 2 (COX-2) has been associated with colorectal adenomatous polyps and cancer, prompting researchers to propose its inhibition as a chemopreventive intervention.
  • METHODS: The Prevention of Colorectal Sporadic Adenomatous Polyps trial was a randomized, placebo-controlled, double-blind study of the COX-2 inhibitor celecoxib given daily in a single 400-mg dose.
  • Of the 557 subjects in the placebo group and the 840 subjects in the celecoxib group who were included in the efficacy analysis, 264 and 270, respectively, were found to have at least one adenoma at year 1, at year 3, or both.
  • [MeSH-major] Adenoma / prevention & control. Adenomatous Polyps / drug therapy. Colorectal Neoplasms / prevention & control. Cyclooxygenase 2 Inhibitors / therapeutic use. Pyrazoles / therapeutic use. Sulfonamides / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Aspirin / administration & dosage. Cardiovascular Diseases / chemically induced. Cardiovascular Diseases / mortality. Celecoxib. Double-Blind Method. Drug Therapy, Combination. Female. Gastrointestinal Diseases / chemically induced. Humans. Kidney Diseases / chemically induced. Male. Middle Aged. Secondary Prevention

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  • [Copyright] Copyright 2006 Massachusetts Medical Society.
  • [CommentIn] N Engl J Med. 2006 Nov 30;355(22):2371; author reply 2371-3 [17135594.001]
  • [CommentIn] N Engl J Med. 2006 Aug 31;355(9):950-2 [16943408.001]
  • (PMID = 16943401.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00141193
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; JCX84Q7J1L / Celecoxib; R16CO5Y76E / Aspirin
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83. Tunca B, Cecener G, Egeli U, Zorluoglu A, Yilmazlar T: The mutation spectrum of the APC gene in Turkish patients with familial adenomatous polyposis. Dis Colon Rectum; 2007 Nov;50(11):1899-904
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  • [Title] The mutation spectrum of the APC gene in Turkish patients with familial adenomatous polyposis.
  • PURPOSE: Familial adenomatous polyposis, an autosomal-dominant disease characterized by the presence of 100 or more colorectal adenomatous polyps, results from mutations in the adenomatous polyposis coli tumor suppressor gene.
  • This study was designed to investigate adenomatous polyposis coli gene mutations in members of Turkish families with familial adenomatous polyposis to constitute an adenomatous polyposis coli mutation spectrum for the Turkish population and to determine specific biomarkers for use in the early diagnosis of familial adenomatous polyposis.
  • METHODS: We investigated adenomatous polyposis coli gene mutations in six unrelated families with familial adenomatous polyposis by using heteroduplex analysis and DNA sequencing.
  • The mutation of a T to C transversion at codon 1018 does not cause an alteration in the meaning of the codon; however, it was determined that this silent mutation does cause the formation of new exonic splicing enhancers (ESEs) motifs on a mutated sequence by using ESEfinder program.
  • CONCLUSIONS: This study contributes to enlarging the adenomatous polyposis coli gene mutations spectrum and to defining new biomarkers for the early diagnosis of Turkish patients with familial adenomatous polyposis.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC / physiology
  • [MeSH-minor] Aspirin. Biomarkers, Tumor / analysis. Caffeine. Diazepam. Dihydroergotamine. Drug Combinations. Gene Deletion. Heteroduplex Analysis. Humans. Pedigree. Sequence Analysis, DNA. Turkey

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  • (PMID = 17882487.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Drug Combinations; 3G6A5W338E / Caffeine; 436O5HM03C / Dihydroergotamine; 79084-81-4 / Silentan; Q3JTX2Q7TU / Diazepam; R16CO5Y76E / Aspirin
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84. Arber N, Kuwada S, Leshno M, Sjodahl R, Hultcrantz R, Rex D, Exisulind Study Group: Sporadic adenomatous polyp regression with exisulind is effective but toxic: a randomised, double blind, placebo controlled, dose-response study. Gut; 2006 Mar;55(3):367-73
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  • [Title] Sporadic adenomatous polyp regression with exisulind is effective but toxic: a randomised, double blind, placebo controlled, dose-response study.
  • At baseline colonoscopy, left sided polyps (3-10 mm) were tattooed, measured, and left in place.
  • Follow up sigmoidoscopy was performed after six months, and removal of any remaining polyps at the 12 month colonoscopy.
  • The primary efficacy variable was change in polyp size from baseline.
  • The decrease in median polyp size was significantly greater (p=0.03) in patients who received exisulind 400 mg (-10 mm2) compared with those who received placebo (-4 mm2).
  • Complete or partial response was significantly higher in the exisulind 400 mg group (54.6%) compared with the placebo group (30.2%), and disease progression was significantly lower (6.1% v 27.9%) (p=0.04 and 0.02, respectively).
  • CONCLUSION: Exisulind caused significant regression of sporadic adenomatous polyps but was associated with more toxicity.
  • This model of polyp regression, short in its term and involving a comparatively small patient sample size, may be the best available tool to assess a therapeutic regimen before launching into large preventive clinical studies.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Antineoplastic Agents / therapeutic use. Sulindac / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Colonoscopy. Combined Modality Therapy. Disease Progression. Dose-Response Relationship, Drug. Double-Blind Method. Female. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 16150858.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 184SNS8VUH / Sulindac; K619IIG2R9 / sulindac sulfone
  • [Other-IDs] NLM/ PMC1856089
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85. Johnson CC, Hayes RB, Schoen RE, Gunter MJ, Huang WY, PLCO Trial Team: Non-steroidal anti-inflammatory drug use and colorectal polyps in the Prostate, Lung, Colorectal, And Ovarian Cancer Screening Trial. Am J Gastroenterol; 2010 Dec;105(12):2646-55
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  • [Title] Non-steroidal anti-inflammatory drug use and colorectal polyps in the Prostate, Lung, Colorectal, And Ovarian Cancer Screening Trial.
  • OBJECTIVES: Non-steroidal anti-inflammatory drugs (NSAIDs) have been documented in animal and human studies to reduce risk for colorectal cancer and adenomatous polyps, but risk modification for subgroups of the population and effects on hyperplastic polyps have been less studied.
  • Follow-up of detected polyps was accomplished outside the Trial setting and relevant records were sought and abstracted.
  • Cases (n=4,017) included subjects with a biopsy-proven polyp in the left side of the colon (descending colon, sigmoid, and rectum) detected as a consequence of PLCO screening; controls (n=38,396) were subjects with no left-sided colon polyp.
  • RESULTS: Regular use of aspirin (≥ 4 times/month) in the past year was inversely associated with hyperplastic polyps (odds ratios (OR)=0.8, 95% confidence interval (CI)=0.7-0.9), adenomatous polyps (OR=0.8, 95% CI=0.8-0.9), and advanced adenomas (OR=0.8, 95% CI=0.7-0.9).
  • As frequency of aspirin use increased, the prevalence of polyps decreased significantly for each histological classification (P for trend ≤ 0.0004).
  • CONCLUSIONS: This study of a large general risk population supports previous work that recent use of aspirin and ibuprofen is associated with a decreased risk of colorectal adenomas and demonstrates that this protective effect may be stronger in certain population subgroups and is also evident for aspirin and hyperplastic polyps.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Colonic Polyps / prevention & control. Ibuprofen / therapeutic use