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1. Vandrovcova J, Lagerstedt-Robinsson K, Påhlman L, Lindblom A: Somatic BRAF-V600E mutations in familial colorectal cancer. Cancer Epidemiol Biomarkers Prev; 2006 Nov;15(11):2270-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The BRAF gene is mutated in 4% to 12% of unselected colorectal cancers, particularly those with high microsatellite instability and in premalignant lesions, such as serrated adenomas and hyperplastic polyps.
  • To evaluate the role of oncogenic BRAF mutations in non-hereditary nonpolyposis colorectal cancer/non-familial adenomatous polyposis familial colorectal cancer, we did a mutation screening of the most common BRAF mutation, the V600E mutation, in 194 colorectal tumors from patients with a positive family history of the disease.
  • Interestingly, families with extracolonic tumors showed a much higher mutation frequency (17.5%) compared with families with colonic cancer only (3.5%; P = 0.009).
  • Subjects from families where the V600E mutation was identified had less adenomas compared with those from families where no BRAF mutation had been found (odds ratio, 8.5; 95% confidence interval, 1.1-64.6).
  • These findings indicate that adenomas might be less important in the cancer development in the group of families with BRAF-V600E mutations and indirectly support a previous hypothesis that tumors might develop through the hyperplastic polyp-serrated adenoma pathway.

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  • (PMID = 17119056.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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2. Dubé C, Rostom A, Lewin G, Tsertsvadze A, Barrowman N, Code C, Sampson M, Moher D, U.S. Preventive Services Task Force: The use of aspirin for primary prevention of colorectal cancer: a systematic review prepared for the U.S. Preventive Services Task Force. Ann Intern Med; 2007 Mar 6;146(5):365-75
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  • DATA SYNTHESIS: Regular use of aspirin reduced the incidence of colonic adenomas in RCTs (relative risk [RR], 0.82 [95% CI, 0.7 to 0.95]), case-control studies (RR, 0.87 [CI, 0.77 to 0.98]), and cohort studies (RR, 0.72 [CI, 0.61 to 0.85]).
  • CONCLUSIONS: Aspirin appears to be effective at reducing the incidence of colonic adenoma and colorectal cancer, especially if used in high doses for more than 10 years.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Colorectal Neoplasms / prevention & control. Primary Prevention
  • [MeSH-minor] Adenoma / prevention & control. Adult. Cardiovascular Diseases / chemically induced. Colonic Polyps / prevention & control. Female. Gastrointestinal Diseases / chemically induced. Humans. Incidence. Male. United States / epidemiology

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  • [CommentIn] ACP J Club. 2007 Jul-Aug;147(1):15-6 [17608380.001]
  • [CommentIn] Gastroenterology. 2007 Aug;133(2):717-8 [17681190.001]
  • [CommentIn] Ann Intern Med. 2007 Nov 6;147(9):674; author reply 674-5 [17975195.001]
  • [SummaryForPatientsIn] Ann Intern Med. 2007 Mar 6;146(5):I35 [17339615.001]
  • (PMID = 17339622.001).
  • [ISSN] 1539-3704
  • [Journal-full-title] Annals of internal medicine
  • [ISO-abbreviation] Ann. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; R16CO5Y76E / Aspirin
  • [Number-of-references] 61
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3. 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).
  • Similar patterns were found for adenomas and ibuprofen.
  • Overall protection was consistent in both the descending colon or sigmoid and the rectum, but more evident in males.
  • 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

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  • (PMID = 20808298.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / N01 CN25522; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; R16CO5Y76E / Aspirin; WK2XYI10QM / Ibuprofen
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4. Poshkus T, Samalavichus NE, Dracutene G: [Flat adenomas of the colon]. Ter Arkh; 2007;79(2):77-81
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  • [Title] [Flat adenomas of the colon].
  • [MeSH-major] Adenoma / pathology. Adenomatous Polyps / pathology. Colonic Neoplasms / pathology

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  • (PMID = 17460974.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Number-of-references] 79
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5. Fujita K, Mondal AM, Horikawa I, Nguyen GH, Kumamoto K, Sohn JJ, Bowman ED, Mathe EA, Schetter AJ, Pine SR, Ji H, Vojtesek B, Bourdon JC, Lane DP, Harris CC: p53 isoforms Delta133p53 and p53beta are endogenous regulators of replicative cellular senescence. Nat Cell Biol; 2009 Sep;11(9):1135-42
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  • The senescence-associated signature of p53 isoform expression (that is, elevated p53beta and reduced Delta133p53) was observed in vivo in colon adenomas with senescent phenotypes.
  • The increased Delta133p53 and decreased p53beta isoform expression found in colon carcinoma may signal an escape from the senescence barrier during the progression from adenoma to carcinoma.

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  • (PMID = 19701195.001).
  • [ISSN] 1476-4679
  • [Journal-full-title] Nature cell biology
  • [ISO-abbreviation] Nat. Cell Biol.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / / Z01 BC005480-22; United States / Intramural NIH HHS / / ZIA BC010878-02; United Kingdom / Cancer Research UK / / ; United States / Intramural NIH HHS / / Z01 BC005795-13; United States / Intramural NIH HHS / / Z01 BC005795-14; United States / Intramural NIH HHS / / ZIA BC005795-15; United States / Intramural NIH HHS / / Z01 BC010878-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MIRN34 microRNA, human; 0 / MicroRNAs; 0 / Protein Isoforms; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ NIHMS161529; NLM/ PMC2802853
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6. Perçinel S, Savaş B, Ensari A, Kuzu I, Kuzu MA, Bektaş M, Cetinkaya H, Kurşun N: Mucins in the colorectal neoplastic spectrum with reference to conventional and serrated adenomas. Turk J Gastroenterol; 2007 Dec;18(4):230-8
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  • [Title] Mucins in the colorectal neoplastic spectrum with reference to conventional and serrated adenomas.
  • BACKGROUND/AIMS: Alterations in expression of mucins and aberrant expression of various types of mucin genes were observed in colorectal adenomas and carcinomas, though their significance in neoplastic transformation of colorectal epithelium is yet to be determined.
  • The aim of this study was to determine expression of MUC1, MUC2, MUC5AC, and MUC6 through conventional adenoma-carcinoma sequence and polyps involved in the "serrated" pathway of the colorectum using tissue array technique.
  • METHODS: In this study, a total of 172 cases including 100 colorectal polyps [8 hyperplastic polyps, 10 sessile serrated adenomas, 19 tubular, 37 tubulovillous, and 26 villous adenomas], 16 adenomas with intramucosal carcinoma, 28 conventional colorectal cancers, and 28 normal mucosae were examined.
  • Sessile serrated adenomas exhibited the highest MUC5AC expression while adenomatous polyps showed an increase in MUC5AC expression in parallel with neoplastic progression (p<0.001).
  • Hyperplastic polyps seemed to lie between normal mucosa and sessile serrated adenomas in terms of mucin expression, suggesting that they are morphologically and histogenetically linked.
  • CONCLUSIONS: Upregulation of MUC1 and MUC6 through the adenoma-carcinoma sequence together with downregulation of MUC2 and MUC5AC at the neoplastic end of the spectrum seem to follow the steps of malignant transformation.
  • [MeSH-major] Adenoma / metabolism. Colonic Polyps / metabolism. Colorectal Neoplasms / metabolism. Mucins / metabolism


7. Schrier JC, Ouwehand F, Aronson DC, Booij KA, Benninga MA, Verbeek PC: [A colo-colic invagination on the basis of MutYH-associated polyposis in a boy aged 14]. Ned Tijdschr Geneeskd; 2007 Jul 14;151(28):1589-92
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  • Colo-colic intussusception was diagnosed by means of a colonic contrast X-ray.
  • Hundreds of polyps were seen throughout the entire colon.
  • The pathology specimen showed an intramucosal carcinoma and multiple adenomas.
  • [MeSH-major] Adenomatous Polyposis Coli / diagnosis. Colonic Diseases / diagnosis. DNA Glycosylases / genetics. Intussusception / diagnosis

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  • [CommentIn] Ned Tijdschr Geneeskd. 2008 Jan 5;152(1):56-7; author reply 57 [18240762.001]
  • (PMID = 17715770.001).
  • [ISSN] 0028-2162
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
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8. Woerner SM, Kloor M, Mueller A, Rueschoff J, Friedrichs N, Buettner R, Buzello M, Kienle P, Knaebel HP, Kunstmann E, Pagenstecher C, Schackert HK, Möslein G, Vogelsang H, von Knebel Doeberitz M, Gebert JF, German HNPCC Consortium: Microsatellite instability of selective target genes in HNPCC-associated colon adenomas. Oncogene; 2005 Apr 7;24(15):2525-35
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  • [Title] Microsatellite instability of selective target genes in HNPCC-associated colon adenomas.
  • Instability at coding microsatellites (cMS) in specific target genes causes frameshift mutations and functional inactivation of affected proteins, thereby providing a selective growth advantage to MMR deficient cells.
  • In this study, we examined 30 HNPCC-associated MSI-H colorectal adenomas of different grades of dysplasia for frameshift mutations in 26 cMS-bearing genes, which, according to our previous model, represent Selective Target genes of MSI.
  • About 30% (8/26) of these genes showed a high mutation frequency (> or =50%) in colorectal adenomas, similar to the frequencies reported for colorectal carcinomas.
  • Mutations in one gene (PTHL3) occurred significantly less frequently in MSI adenomas compared to published mutation rates in MSI carcinomas (36.0 vs 85.7%, P=0.023).
  • [MeSH-major] Adenoma / genetics. Adenoma / physiopathology. Cell Transformation, Neoplastic / genetics. Chromosomal Instability. Colonic Neoplasms / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Microsatellite Repeats

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  • (PMID = 15735733.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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9. Lee SE, Park NH, Park IA, Kang SB, Lee HP: Tubulo-villous adenoma of the vagina. Gynecol Oncol; 2005 Feb;96(2):556-8
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  • [Title] Tubulo-villous adenoma of the vagina.
  • BACKGROUND: Tubulo-villous adenomas are common in the colon and rectum, but extremely rare in the vagina.
  • As far as we know, only two cases of tubulo-villous adenoma have ever been reported.
  • We report the third case of enteric-type tubulo-villous adenoma of the vagina.
  • The tumor was excised and pathologically confirmed as a tubulo-villous adenoma.
  • CONCLUSION: Because some tubulo-villous adenomas in the colon and rectum can progress to the cancer, this case requires long-term follow-up to detect recurrence and malignant transformation.
  • [MeSH-major] Adenoma, Villous / pathology. Vaginal Neoplasms / pathology

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  • (PMID = 15661252.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 17
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10. Harewood GC, Rathore O, Patchett S, Murray F: Assessment of adherence to published surveillance guidelines--opportunity to enhance efficiency of endoscopic practice. Ir Med J; 2008 Sep;101(8):248-50
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  • Surveillance procedures were classified as: a) Barrett's oesophagus, b) chronic IBD, c) prior adenomatous colorectal polyps and, d) prior surgical resection of colorectal cancer.
  • Of these, 50 of 133 (37.6%) Barrett's patients, 92 of 213 (43.2%) patients with prior colonic polyps, 36 of 48 (75.0%) patients with prior colonic malignancy and 17 of 47 (36.2%) patients for IBD surveillance were scheduled prematurely.
  • [MeSH-minor] Adenomatous Polyposis Coli / diagnosis. Barrett Esophagus / diagnosis. Colorectal Neoplasms / diagnosis. Databases as Topic. Great Britain. Humans. Inflammatory Bowel Diseases / diagnosis. Ireland

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  • (PMID = 18990956.001).
  • [ISSN] 0332-3102
  • [Journal-full-title] Irish medical journal
  • [ISO-abbreviation] Ir Med J
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Ireland
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11. Winawer SJ, Zauber AG, Fletcher RH, Stillman JS, O'brien MJ, Levin B, Smith RA, Lieberman DA, Burt RW, Levin TR, Bond JH, Brooks D, Byers T, Hyman N, Kirk L, Thorson A, Simmang C, Johnson D, Rex DK: Guidelines for colonoscopy surveillance after polypectomy: a consensus update by the US Multi-Society Task Force on Colorectal Cancer and the American Cancer Society. CA Cancer J Clin; 2006 May-Jun;56(3):143-59; quiz 184-5
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  • Adenomatous polyps are the most common neoplastic findings uncovered in people who undergo colorectal screening or have a diagnostic workup for symptoms.
  • It was common practice in the 1970s for these patients to have annual follow-up surveillance examinations to detect additional new adenomas as well as missed synchronous adenomas.
  • As a result of the National Polyp Study report in 1993, which demonstrated clearly in a randomized design that the first postpolypectomy examination could be deferred for 3 years, guidelines published by a gastrointestinal consortium in 1997 recommended that the first follow-up surveillance be 3 years after polypectomy for most patients.
  • In 2003, these guidelines were updated, colonoscopy was recommended as the only follow-up examination, and stratification at baseline into lower and higher risk for subsequent adenomas was suggested.
  • In the present paper, a careful analytic approach was designed addressing all evidence available in the literature to delineate predictors of advanced pathology, both cancer and advanced adenomas, so that patients can be more definitely stratified at their baseline colonoscopy into those at lower or increased risk for a subsequent advanced neoplasia.
  • People at increased risk have either three or more adenomas, or high-grade dysplasia, or villous features, or an adenoma > or =1 cm in size.
  • People at lower risk who have one or two small (< 1 cm) tubular adenomas with no high-grade dysplasia can have a follow-up in 5 to 10 years, whereas people with hyperplastic polyps only should have a 10-year follow-up as average-risk people.
  • It has been shown that the first screening colonoscopy and polypectomy produces the greatest effects on reducing the incidence of colorectal cancer in patients with adenomatous polyps.
  • [MeSH-minor] Adenomatous Polyps / epidemiology. Adenomatous Polyps / prevention & control. Adenomatous Polyps / surgery. American Cancer Society. Colonic Polyps / epidemiology. Colonic Polyps / prevention & control. Colonic Polyps / surgery. Humans. Societies, Medical. United States / epidemiology


12. Siddiqui AA, Patel A, Huerta S: Determinants of compliance with colonoscopy in patients with adenomatous colon polyps in a veteran population. Aliment Pharmacol Ther; 2006 Dec;24(11-12):1623-30
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  • [Title] Determinants of compliance with colonoscopy in patients with adenomatous colon polyps in a veteran population.
  • AIM: To determine factors affecting compliance of a follow-up colonoscopy in patients with previously diagnosed adenomatous colon polyps.
  • METHODS: A retrospective review was performed on patients with adenomatous polyps excised between January and December 1998.
  • RESULTS: One hundred and nineteen patients with adenomatous colon polyps were identified.
  • In a univariate analysis, greater number of polyps (P = 0.04), NSAID use (P = 0.02), statin use (P = 0.005), first-degree relatives with colon cancer (P = 0.05) and compliance with out-patient clinic follow-up (P < 0.001) were significantly associated with patient compliance.
  • Multivariate analysis revealed statin use (P = 0.05), first-degree relatives with colon cancer (P = 0.06) and compliance with out-patient clinic follow-up (P < 0.001) were independent predictors of compliance.
  • CONCLUSIONS: History of statin use and family history of colon cancer are good predictors of compliance.
  • Strong efforts should be directed at improving patient education about colon cancer by the physician and facilitating patient compliance.
  • [MeSH-major] Adenomatous Polyps / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Colonoscopy. Patient Compliance

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  • (PMID = 17206950.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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13. Bafandeh Y, Khoshbaten M, Eftekhar-Sadat AT, Farhang S: Colorectal neoplasms in symptomatic patients without evidence of bleeding: a prospective study in an Iranian population. Asian Pac J Cancer Prev; 2007 Oct-Dec;8(4):485-8
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  • Data on its prevalence are lacking in Iran, as well as for adenomatous polyps.
  • This study was conducted to estimate prevalence of CRC in patients with long lasting colonic symptoms (except for known risk factors for cancer and those with rectal bleeding) who underwent total colonoscopy.
  • RESULTS: Thirty four subjects (14.9%) were found to have colorectal neoplasia and 112 (49.1%) had a completely normal colon.
  • Adenomatous polyps were detected in 27 patients, which included 15.6% of men and 7.0% of women.
  • Mean age of patients with a polyp (51.1+/-12.5 years) was not significantly different compared to others (p=0.381) nor mean duration of symptoms (21.1 months, p=0.435).
  • None of the symptoms were predictors of cancer or polyps.
  • CONCLUSION: The low prevalence of colorectal neoplasms as well as the less advanced pattern of adenomas in Iran are compatible with other data from Asia and the Middle East, contrasting with western countries.
  • [MeSH-major] Adenoma / diagnosis. Colonic Polyps / diagnosis. Colorectal Neoplasms / diagnosis

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  • (PMID = 18260716.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
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14. Matusiak D, Benya RV: CYP27A1 and CYP24 expression as a function of malignant transformation in the colon. J Histochem Cytochem; 2007 Dec;55(12):1257-64
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  • [Title] CYP27A1 and CYP24 expression as a function of malignant transformation in the colon.
  • However, vitamin D precursors do not present toxicity concerns and may be sufficient for CRC chemoprevention or chemotherapy, providing the appropriate enzymes are present in colonic epithelia.
  • We previously showed that CYP27B1 is present at equally high levels in the colon and CRC irrespective of differentiation but was not present in metastases.
  • In this study we used quantitative immunohistochemistry to show that CYP27A1, converting D3 to 25-hydroxycholecalciferol, is present in increasing concentrations in the nuclei of normal colonic epithelia, aberrant crypt foci (ACF), and adenomatous polyps.
  • Similarly, increasing amounts of the deactivating enzyme CYP24 are present in the nuclei of normal colonic epithelia, ACFs, and adenomatous polyps.
  • These data indicate that non-toxic vitamin D precursors should be sufficient for CRC chemoprevention, but that neither vitamin D nor its precursors may be sufficient for CRC chemotherapy.
  • [MeSH-minor] Adenomatous Polyps / enzymology. Adenomatous Polyps / ultrastructure. Colon / enzymology. Colon / pathology. Colon / ultrastructure. Humans. Immunohistochemistry. Intestinal Mucosa / enzymology. Intestinal Mucosa / ultrastructure. Lymphatic Metastasis. Vitamin D3 24-Hydroxylase

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  • (PMID = 17875655.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-094346
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.14.- / Steroid Hydroxylases; EC 1.14.13.126 / Vitamin D3 24-Hydroxylase; EC 1.14.13.15 / CYP27A1 protein, human; EC 1.14.13.15 / Cholestanetriol 26-Monooxygenase
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15. Srivastava A, Redston M, Farraye FA, Yantiss RK, Odze RD: Hyperplastic/serrated polyposis in inflammatory bowel disease: a case series of a previously undescribed entity. Am J Surg Pathol; 2008 Feb;32(2):296-303
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  • Herein, we describe the clinical, pathologic, immunohistochemical, and molecular features of 3 unique patients with long standing inflammatory bowel disease, all of whom developed numerous discrete hyperplastic/serrated colonic polyps similar to those described in the hyperplastic/serrated polyposis syndrome.
  • The 3 patients (2 with ulcerative colitis and 1 with Crohn ileo-colitis) were evaluated for a variety of clinical, histologic (including the type, location and number of polyps in the colon), and immunohistochemical features [MLH-1, MSH-2, MGMT (O(6)-methylguanine-DNA methyltransferase), beta-catenin, and p53].
  • KRAS and BRAF mutation analysis was also performed on a subset of polyps from 2 patients.
  • All patients had moderate-severe pancolitis of more than 10 years duration and had >20 colonic polyps.
  • None had polyps in the upper gastrointestinal tract.
  • Pathologically, a combination of conventional hyperplastic polyps and sessile serrated polyps (adenomas) were present in the 3 cases.
  • In addition, serrated adenomas were present in 2 and conventional adenomas in 1.
  • However, 2 cases showed loss of MGMT in several serrated polyps, and one also in adjacent colitic mucosa.
  • KRAS mutations were detected in 5/11 serrated polyps.
  • However, BRAF mutations were not present in any of the polyps tested.
  • [MeSH-major] Adenomatous Polyps / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Inflammatory Bowel Diseases / pathology. Precancerous Conditions / pathology

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  • (PMID = 18223333.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Biomarkers, Tumor; 0 / MLH1 protein, human; 0 / MLH2 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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16. Zhao C, Ivanov I, Dougherty ER, Hartman TJ, Lanza E, Bobe G, Colburn NH, Lupton JR, Davidson LA, Chapkin RS: Noninvasive detection of candidate molecular biomarkers in subjects with a history of insulin resistance and colorectal adenomas. Cancer Prev Res (Phila); 2009 Jun;2(6):590-7
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  • [Title] Noninvasive detection of candidate molecular biomarkers in subjects with a history of insulin resistance and colorectal adenomas.
  • We have developed novel molecular methods using a stool sample, which contains intact sloughed colon cells, to quantify colonic gene expression profiles.
  • For this purpose, the effects of a legume-enriched, low glycemic index, high fermentable fiber diet was evaluated in subjects with four possible combinations of risk factors, including insulin resistance and a history of adenomatous polyps.
  • Linear discriminant analysis was successfully used to identify the best single genes and two- to three-gene combinations for distinguishing subjects with insulin resistance, a history of polyps, or exposure to a chemoprotective legume-rich diet.
  • These results support our premise that gene products (RNA) isolated from stool have diagnostic value in terms of assessing colon cancer risk.

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  • (PMID = 19470793.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK071707-02; United States / NCI NIH HHS / CA / R01 CA129444-01; United States / NIDDK NIH HHS / DK / R01 DK071707-01A2; United States / NIDDK NIH HHS / DK / R01 DK071707-01A2S1; United States / NCI NIH HHS / CA / R01 CA059034-05; United States / NCI NIH HHS / CA / CA059034-12; United States / NCI NIH HHS / CA / CA059034-08; United States / NIEHS NIH HHS / ES / P30ES09106; United States / NCI NIH HHS / CA / R01 CA059034-07; United States / NCI NIH HHS / CA / CA059034-13; United States / NCI NIH HHS / CA / R01 CA059034; United States / NIDDK NIH HHS / DK / DK071707; United States / NCI NIH HHS / CA / R01 CA059034-15; United States / NCI NIH HHS / CA / R01 CA059034-11; United States / NCI NIH HHS / CA / CA059034-06; United States / NCI NIH HHS / CA / R01 CA059034-09; United States / NIDDK NIH HHS / DK / R01 DK071707-03; United States / NCI NIH HHS / CA / CA059034-09; United States / NIDDK NIH HHS / DK / DK071707-03; United States / NCI NIH HHS / CA / R01 CA129444-02; United States / NCI NIH HHS / CA / R01 CA059034-08; United States / NCI NIH HHS / CA / CA59034; United States / NCI NIH HHS / CA / CA059034-05; United States / NCI NIH HHS / CA / R01 CA059034-10; United States / NCI NIH HHS / CA / CA129444-01; United States / NCI NIH HHS / CA / CA059034-10; United States / NCI NIH HHS / CA / R01 CA059034-14; United States / NCI NIH HHS / CA / R01 CA059034-12; United States / NIDDK NIH HHS / DK / DK071707-01A2S1; United States / NIDDK NIH HHS / DK / DK071707-01A2; United States / NCI NIH HHS / CA / CA129444-02; United States / NCI NIH HHS / CA / CA059034-15; United States / NIDDK NIH HHS / DK / DK071707-02; United States / NCI NIH HHS / CA / CA059034-11; United States / NCI NIH HHS / CA / CA129444; United States / NCI NIH HHS / CA / CA059034-14; United States / NIDDK NIH HHS / DK / R01 DK071707; United States / NIEHS NIH HHS / ES / P30 ES009106; United States / NCI NIH HHS / CA / CA059034-07; United States / NCI NIH HHS / CA / R01 CA059034-06; United States / NCI NIH HHS / CA / R01 CA059034-13; United States / NCI NIH HHS / CA / R01 CA129444
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger
  • [Other-IDs] NLM/ NIHMS120536; NLM/ PMC2745241
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17. Barreda B F, Combe G J, Valdez P LA, Sánchez L J: [Clinical aspects in polyps of the colon]. Rev Gastroenterol Peru; 2007 Apr-Jun;27(2):131-47
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  • [Title] [Clinical aspects in polyps of the colon].
  • [Transliterated title] Aspectos clínicos de los pólipos colónicos.
  • INTRODUCTION: The colonics polyps according to their number, size, location, age of presentation and mainly, according to their histology, have the potentiality of malignant degeneration, which makes of a continuous study and pursuit susceptible.
  • OBJECTIVES: To evaluate the relation between the histologic type of the colon polyps, its location, the degree of dysplasia, the size, its possible commitment by carcinoma, the age, sex and the handling that has occurred them, in a series of 684 patients of the National Institute of Enfermedades Neoplásicas (INEN) between the 1 of January from 1974 to the 31 of March of the 2004.
  • MATERIAL AND METHODS: The revision of clinical histories of 840 patients with the diagnosis of colon polyp was made who attended the service of Gastroenterology of the INEN between the 1 of January from 1974 to the 31 of March of 2004 and a card predesigned for each clinical history filled.
  • 1162 resecteds polyps evaluated themselves in this period.
  • The final sample was of 684 patients, in whom it was 1057 polyps.
  • Other endoscopic findings were: internal hemorrhoids (172), colonic diverticulosis (50), anal fissure (4), and nonspecific ulcerative colitis (2).
  • RESULTS: 1057 polyps extirpated, by means of the endoscopy polipectomy were 1016, with colectomy were 32 and with transanal resection without colectomy they 9.
  • Within the histology of the 1057 polyps, 331 was briefed (31.3%) that were hyperplasic, 448 (42.4%) adenomas, 278 (26.3%) others and 35 (8.2%) adenocarcinomas on adenomas.
  • The location but frequence of the adenomas was in the left colon (76.6%).
  • Adenocarcinoma (carcinomas on adenomas), was present mainly in polyps villous type, with dysplasia severe and greater to 10 mm.
  • Nevertheless, in smaller polyps of 5mm with dysplasia severe, was a polyp invaded by cancer, that represents the 0,8% of millimetric polyps.
  • The made handling was mainly endoscopic, with 96% of the resected polyps this way, also slogan transanal resection and segmental colonic resection.
  • The colectomy was necessary in 3% of all the made interventions, dysplasia severe or carcinoma was made in adenomatous polyps with, and in greater percentage in greater polyps of 20 mm (53%).
  • On the other hand, in polyps with level of invasion Haggitt 3 and 4, the colectomy was the election treatment.
  • CONCLUSIONS: The Evaluation of colonic polyps in INEN is predominantly by endoscopy.
  • The polyps are more frequent over the 50 years and have preferred location in the left colon.
  • The carcinoma is more probable with severe dysplasia and greater size of the adenoma.
  • All polyps, from the millimetric ones, including the hyperplasic, must be considered marks of neoplasia and extirpated in its totality.
  • [MeSH-major] Colonic Polyps / pathology. Colonic Polyps / surgery

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  • (PMID = 17712391.001).
  • [ISSN] 1022-5129
  • [Journal-full-title] Revista de gastroenterología del Perú : órgano oficial de la Sociedad de Gastroenterología del Perú
  • [ISO-abbreviation] Rev Gastroenterol Peru
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Peru
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18. Landau D, Garrett C, Chodkiewicz C: A case of primary squamous cell colon cancer. J Oncol Pharm Pract; 2007 Mar;13(1):47-8
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  • [Title] A case of primary squamous cell colon cancer.
  • Carcinomas of the colon are a common cancer seen in both inpatient and outpatient settings with approximately 145,000 new cases being diagnosed every year in the USA.
  • Despite the frequency of these cancers being seen, it continues to be a rarity to see a primary squamous cell cancer of the colon.
  • While the exact aetiology of this rare tumour is currently still not completely understood, various aetiologies include chronic irritation leading to squamous differentiation, embryonic migration of ectodermal cells to the colon, or adenomas undergoing squamous transformation.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Colonic Neoplasms / pathology

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  • (PMID = 17621567.001).
  • [ISSN] 1078-1552
  • [Journal-full-title] Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners
  • [ISO-abbreviation] J Oncol Pharm Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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19. Pranesh N, Haboubi NY, O'Dwyer ST: Pigmented mesenteric lymphadenopathy in familial adenomatous polyposis - an unusual cause of intraoperative abandonment of ileo-anal pouch. Ann R Coll Surg Engl; 2005 Jul;87(4):W1-4
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  • [Title] Pigmented mesenteric lymphadenopathy in familial adenomatous polyposis - an unusual cause of intraoperative abandonment of ileo-anal pouch.
  • Familial adenomatous polyposis (FAP) is an autosomal dominant condition with near complete penetrance, characterised by the presence of numerous adenomatous polyps of the colon and rectum.
  • Melanosis coli describes the brownish-black discolouration of the colon resulting from the accumulation of a granular pigment in the phagosomes of macrophages in the colonic lamina propria.
  • The presence of melanosis pigment in pericolonic lymph nodes has been reported in patients with coincidental melanosis coli, following segmental colonic resection.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Lymphatic Diseases / complications. Melanosis / complications. Mesentery. Peritoneal Diseases / complications
  • [MeSH-minor] Adolescent. Colonic Pouches. Female. Humans. Intraoperative Complications / etiology. Proctocolectomy, Restorative. Reoperation


20. Juhn E, Khachemoune A: Gardner syndrome: skin manifestations, differential diagnosis and management. Am J Clin Dermatol; 2010;11(2):117-22
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  • Gardner syndrome is a variant of familial adenomatous polyposis (FAP) and results in the manifestation of numerous external and internal symptoms including gastrointestinal polyps, osteomas, tumors, and epidermoid cysts.
  • Stemming from a mutation in the adenomatous polyposis coli (APC) gene, Gardner syndrome shares genetic correlations with the FAP phenotype; as a result, it becomes all the more crucial for physicians to be able to discern Gardner syndrome from other differential diagnoses such as Turcot syndrome, FAP, and other attenuated forms of familial polyposis.
  • Fortunately, Gardner syndrome has characteristic polyps in the colon, osteomas, and also exhibits abnormalities in the retinal epithelium that discern it from others.
  • Surgery is the most effective method of management for Gardner syndrome; restorative proctocolectomy with ileal pouch anal anastomosis with mucosectomy is the top choice for colonic malignancies, and skin manifestations can be treated through a variety of excisions and therapy depending on location, size, and number of malignancies.
  • Currently, there are no specific screening recommendations for Gardner syndrome, but testing following general screening recommendations for extra-colonic malignancies, genetic counseling, and endoscopy are encouraged.
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis. Colorectal Neoplasms, Hereditary Nonpolyposis / pathology. Colorectal Neoplasms, Hereditary Nonpolyposis / therapy. Diagnosis, Differential. Genetic Counseling / methods. Humans. Mutation

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  • (PMID = 20141232.001).
  • [ISSN] 1175-0561
  • [Journal-full-title] American journal of clinical dermatology
  • [ISO-abbreviation] Am J Clin Dermatol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Number-of-references] 29
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21. Herbst A, Bommer GT, Kriegl L, Jung A, Behrens A, Csanadi E, Gerhard M, Bolz C, Riesenberg R, Zimmermann W, Dietmaier W, Wolf I, Brabletz T, Göke B, Kolligs FT: ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition. Gastroenterology; 2009 Aug;137(2):639-48, 648.e1-9
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  • [Title] ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition.
  • RESULTS: ITF-2B is strongly expressed in colon adenomas but frequently down-regulated in carcinomas because of LOH at 18q21.
  • Loss of ITF-2B expression correlates with loss of p21(Cip1) expression in primary colon carcinomas.
  • ITF-2B, which is up-regulated during early colorectal carcinogenesis because of loss of adenomatous polyposis coli, is a target for LOH on chromosome 18q, along with deleted in colorectal carcinoma and Smad4.
  • This finding, along with the fact that ITF-2B is a regulator of the key cell cycle inhibitor p21(Cip1), indicates that ITF-2B is a tumor suppressor that has an important function at the adenoma to carcinoma transition.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyposis Coli / genetics. Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 18 / genetics. Colorectal Neoplasms / genetics. DNA-Binding Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 19394332.001).
  • [ISSN] 1528-0012
  • [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 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / TCF3 protein, human; 0 / TCF4 protein, human; 0 / Transcription Factors
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22. Ye C, Shrubsole MJ, Cai Q, Ness R, Grady WM, Smalley W, Cai H, Washington K, Zheng W: Promoter methylation status of the MGMT, hMLH1, and CDKN2A/p16 genes in non-neoplastic mucosa of patients with and without colorectal adenomas. Oncol Rep; 2006 Aug;16(2):429-35
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  • [Title] Promoter methylation status of the MGMT, hMLH1, and CDKN2A/p16 genes in non-neoplastic mucosa of patients with and without colorectal adenomas.
  • CpG island methylation has been observed in aberrant crypt foci (ACF) and adenomas in the colon, implicating it in the earliest aspects of colon cancer formation.
  • In addition, some investigators have identified an age-related increase in DNA methylation of the ESR1 locus in the colon mucosa, suggesting that DNA methylation may be a pre-neoplastic change that increases the risk of colon adenomas and colon cancer.
  • We investigated the methylation status in the promoter regions of the CDKN2A/p16, hMLH1, and MGMT genes in human non-neoplastic rectal mucosa and evaluated whether these methylation markers may predict the presence of adenomatous polyps in the colon.
  • The promoter methylation patterns of these genes were examined in rectal biopsies (mucosa samples) of 97 colorectal adenoma cases and 94 healthy controls using methylation-specific PCR (MSP) assays.
  • The methylation status of these genes in rectal mucosa biopsies detected by MSP assays may not distinguish between patients with and without adenomas in the colon.

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  • (PMID = 16820927.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / P50 CA95103; United States / NCI NIH HHS / CA / R01CA97386
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / MLH1 protein, human; 0 / Nuclear Proteins; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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23. Glazer E, Golla V, Forman R, Zhu H, Levi G, Bodenheimer HC Jr: Serrated adenoma is a risk factor for subsequent adenomatous polyps. Dig Dis Sci; 2008 Aug;53(8):2204-7
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  • [Title] Serrated adenoma is a risk factor for subsequent adenomatous polyps.
  • BACKGROUND: Serrated adenomas (SA) are histologically defined by the presence of both hyperplastic and adenomatous features.
  • These uncommon polyps are thought to play an important role in the development of sporadic colorectal cancers (CRC) with microsatellite instability (MSI).
  • This study was undertaken to define the relationship between SA and the future development of adenomatous polyps.
  • These were matched to controls by age, sex, indication for colonoscopy, polyp type and number and duration of follow-up.
  • Of these, 80 patients (0.5%) with SA were found, and of these SA, 80% were found in the left colon.
  • On follow-up examination four patients (24%) and no controls had adenomatous polyps (P = 0.01).
  • Serrated adenomas appear to be found more commonly in the left colon and in older patients.
  • This study found a significant association between SA and the subsequent development of adenomatous polyps.
  • [MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Precancerous Conditions / pathology

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  • [ISSN] 0163-2116
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24. Jones LE Jr, Ying L, Hofseth AB, Jelezcova E, Sobol RW, Ambs S, Harris CC, Espey MG, Hofseth LJ, Wyatt MD: Differential effects of reactive nitrogen species on DNA base excision repair initiated by the alkyladenine DNA glycosylase. Carcinogenesis; 2009 Dec;30(12):2123-9
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  • To understand the effects of RNS on BER in vivo, we examined intestinal adenomas for levels of inducible nitric oxide synthase (iNOS) and AAG.
  • We found AAG to be nitrated in human adenomas, suggesting that this RNS modification is relevant in the human disease.
  • POLbeta protein was increased in nearly all adenomas compared with adjacent non-tumor tissues, whereas APE1 expression was only increased in approximately half of the adenomas and also was relocalized to the cytoplasm in adenomas.
  • Collectively, the results suggest that BER is dysregulated in colon adenomas.

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  • (PMID = 19864471.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR017698; United States / NCRR NIH HHS / RR / P20 RR17698; United States / NCI NIH HHS / CA / R01 CA100450; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Reactive Nitrogen Species; EC 2.7.7.- / DNA Polymerase beta; EC 3.2.2.- / 3-methyladenine-DNA glycosylase; EC 3.2.2.- / DNA Glycosylases; EC 4.2.99.18 / APEX1 protein, human; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase
  • [Other-IDs] NLM/ PMC2792317
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25. García Sánchez Mdel V, González R, Iglesias Flores E, Gómez Camacho F, Casais Juanena L, Cerezo Ruiz A, Montero Pérez-Barquero M, Muntané J, de Dios Vega JF: [Diagnostic value of fecal calprotectin in predicting an abnormal colonoscopy]. Med Clin (Barc); 2006 Jun 10;127(2):41-6
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  • [Transliterated title] Precisión diagnóstica de la calprotectina fecal para predecir una colonoscopia patológica.
  • The colonoscopy is the gold standard method of detecting an organic pathology in the colon.
  • Fecal calprotectin (FCP) is a marker that may detect organic pathologies of the colon.
  • People were divided in: normal colonoscopy: 117 people, and 28 colon adenomas, 20 colorectal cancer (CRC) and 25 IBD.
  • 217 mg/kg was the best cut-off for discriminating patients with organic colon disorders.
  • The measurement of FCP is a non-invasive, inexpensive, reliable and easily measured test.
  • [MeSH-major] Colonic Diseases / diagnosis. Colonic Neoplasms / diagnosis. Colonoscopy. Feces / chemistry. Inflammatory Bowel Diseases / diagnosis. Leukocyte L1 Antigen Complex / analysis

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  • (PMID = 16801001.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] spa
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Leukocyte L1 Antigen Complex
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26. Yuan B, Jin X, Zhu R, Zhang X, Liu J, Wan H, Lu H, Shen Y, Wang F: Cronkhite-Canada syndrome associated with rib fractures: a case report. BMC Gastroenterol; 2010;10:121
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  • Esophagogastroduodenoscopy, video capsule endoscopy and colonoscopy revealed various sizes of generalized gastrointestinal polyps.
  • Histological examination of the biopsy specimens obtained from the stomach and the colon showed adenomatous polyp and inflammatory polyp respectively.

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  • (PMID = 20955587.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2972238
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27. 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.
  • The aim of our study was to investigate if exisulind induces regression of sporadic colonic adenomas.
  • 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).
  • 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

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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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28. Lee SS, Park SH, Choi EK, Kim SY, Kim MJ, Lee KH, Kim YH: Colorectal polyps on portal phase contrast-enhanced CT colonography: lesion attenuation and distinction from tagged feces. AJR Am J Roentgenol; 2007 Jul;189(1):35-40
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  • [Title] Colorectal polyps on portal phase contrast-enhanced CT colonography: lesion attenuation and distinction from tagged feces.
  • OBJECTIVE: The purpose of our study was to determine the attenuation of colorectal polyps on portal phase contrast-enhanced CT colonography (CTC) and evaluate whether enhanced polyps can be clearly distinguished from tagged feces during CTC review.
  • Forty-eight colonoscopy-proven polyps (6-20 mm) and 41 polypoid tagged feces (6-19 mm) were selected from contrast-enhanced CTC performed without (n = 37 examinations) and with (n = 10 examinations) fecal tagging, respectively.
  • Attenuation of the polyps and tagged feces was measured.
  • Four independent blinded radiologists reviewed the polyps and tagged feces at both wide (width, 1,500 H; level -400 H) and soft-tissue (width, 400 H; level, 20 H) window settings to distinguish them by using subjective visual assessment.
  • RESULTS: Polyp attenuation on the portal phase was not correlated with size (R = -0.003; p = 0.99) and was not different between histologic types (p = 0.884).
  • Enhanced polyps (mean +/- SD, 119.9 +/- 25.3 H; range, 50-173 H) showed significantly lower attenuation than did tagged feces (1,521.4 +/- 683.6 H; range, 495-2,683 H) without any overlap (p < 0.0005).
  • An 8-mm sessile adenomatous polyp was misinterpreted as tagged feces by one reviewer.
  • CONCLUSION: Polyp attenuation on portal phase contrast-enhanced CTC ranges from 50 to 173 H.
  • Contrast-enhanced polyps are clearly and consistently distinguished from barium-tagged polypoid feces.
  • [MeSH-major] Colonic Polyps / radiography. Colonography, Computed Tomographic / methods. Contrast Media / administration & dosage. Feces. Radiographic Image Enhancement / methods. Rectal Diseases / radiography

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  • (PMID = 17579149.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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29. Kim MS, Jung HK, Jung HS, Choi JY, Na YJ, Pyun GW, Ryu JH, Moon IH, Jo MS: [A Case of Cronkhite-Canada syndrome showing resolution with Helicobacter pylori eradication and omeprazole]. Korean J Gastroenterol; 2006 Jan;47(1):59-64
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  • We describe a 58-year-old woman who was incidentally found to have gastric and colonic polyposis, hypoalbuminemia, cutaneous hyperpigmentation and onychodystrophy (Cronkhite-Canada syndrome).
  • Histology of polyps from the stomach showed features of juvenile or retention type (hamartomatous) polyps with Helicobacter pylori (H. pylori) infection.
  • The large pedunculated colonic polyps showed hamartomatous polyps with adenomatous component and polypectomy was performed.
  • After the treatment with H. pylori eradication and omeprazole, the gastric polyposis, hypoalbuminemia and anemia regressed, and endoscopic polypectomy of gastric polyps were performed.
  • [MeSH-major] Anti-Ulcer Agents / therapeutic use. Helicobacter Infections / drug therapy. Helicobacter pylori. Omeprazole / therapeutic use. Polyps / complications. Stomach Neoplasms / complications
  • [MeSH-minor] Colonic Polyps / complications. Colonic Polyps / microbiology. Colonic Polyps / pathology. Female. Humans. Hyperpigmentation / pathology. Middle Aged. Nails, Malformed / pathology. Proton Pump Inhibitors. Syndrome

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  • (PMID = 16434870.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Proton Pump Inhibitors; KG60484QX9 / Omeprazole
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30. Scott RH, Mansour S, Pritchard-Jones K, Kumar D, MacSweeney F, Rahman N: Medulloblastoma, acute myelocytic leukemia and colonic carcinomas in a child with biallelic MSH6 mutations. Nat Clin Pract Oncol; 2007 Feb;4(2):130-4
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  • [Title] Medulloblastoma, acute myelocytic leukemia and colonic carcinomas in a child with biallelic MSH6 mutations.
  • Background A 13-year-old girl presented with rectal bleeding and was found to have two colonic carcinomas (stage Dukes' C) and multiple colonic polyps.
  • A three-generation family history identified no relatives with colonic carcinomas or polyposis.
  • Investigations Immunohistochemical analysis was performed on a sample of colonic adenoma.
  • [MeSH-major] Cerebellar Neoplasms / genetics. Colonic Neoplasms / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Medulloblastoma / genetics


31. Stergiou N, Frenz MB, Menke D, Riphaus A, Wehrmann T: Reduction of miss rates of colonic adenomas by zoom chromoendoscopy. Int J Colorectal Dis; 2006 Sep;21(6):560-5
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  • [Title] Reduction of miss rates of colonic adenomas by zoom chromoendoscopy.
  • BACKGROUND AND AIMS: The aim of this study was to determine the detection rate of polyps using zoom chromoendoscopy (ZE) compared with standard video colonoscopy.
  • The second colonoscopy (C2) was done with a zoom colonoscope spraying the whole colon with indigocarmine (0.4%).
  • During C1, 56 lesions were detected in 26 of 50 patients (34 hyperplastic and 22 adenomatous).
  • During C2, 19 additional polyps were documented prior to ZE (15% tandem miss rate), and 20 further lesions were detected with ZE (21% additional polyp detection rate compared to C1 and C2 without ZE).
  • Of the 39 additional lesions removed during C2 after ZE, 29 were hyperplastic and 10 were adenomatous.
  • Most adenomas detected during the second investigation were found in patients in whom adenomatous polyps had already been removed during the initial colonoscopy (9 of 26 patients vs 1 of 24 patients, p<0.02).
  • The pit pattern classification allowed a correct differentiation between hyperplastic and adenomatous polyps (accuracy 93%, sensitivity 90%, specificity 97%).
  • CONCLUSION: Using zoom chromoendoscopy, the rate of detecting colonic polyps can be increased at the cost of a longer retrieval time.
  • [MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology. Colonoscopy / methods. Coloring Agents. Diagnostic Errors / prevention & control. Indigo Carmine

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  • (PMID = 16283340.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Coloring Agents; D3741U8K7L / Indigo Carmine
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32. Bretthauer M, Hoff G: [Prevention and early diagnosis of colorectal cancer]. Tidsskr Nor Laegeforen; 2007 Oct 18;127(20):2688-91
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  • CRC develops from benign adenomas in the colon over a long time.
  • RESULTS AND INTERPRETATION: Acetylsalicylic-acid, non-steroidal anti-inflammatory drugs and COX-2 inhibitors are shown to reduce adenoma growth, but it remains uncertain whether these drugs reduce the incidence of CRC.
  • [MeSH-minor] Colon / radiography. Colonoscopy. Early Diagnosis. Evidence-Based Medicine. Humans. Mass Screening. Occult Blood. Prognosis. Randomized Controlled Trials as Topic. Sigmoidoscopy

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  • (PMID = 17952153.001).
  • [ISSN] 0807-7096
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Norway
  • [Number-of-references] 35
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33. Kim DK, Myung SJ, Yang SK, Hong SS, Kim KJ, Byeon JS, Lee GH, Kim JH, Min YI, Lee SM, Jeong JY, Song K, Jung SA: Analysis of PTEN gene mutations in Korean patients with Cowden syndrome and polyposis syndrome. Dis Colon Rectum; 2005 Sep;48(9):1714-22
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  • We analyzed the DNA of various organs and lesions in Korean patients with Cowden syndrome, their family members, and patients with familial adenomatous polyposis for germline or somatic PTEN mutations.
  • METHODS: The 11 patients included in this study were 5 patients with Cowden syndrome, 4 of their family members, and 2 patients with familial adenomatous polyposis.
  • Deletions and mutations in exons 1 to 9 of the PTEN gene were evaluated by polymerase chain reaction-single strand conformation polymorphism and sequencing analysis in esophageal acanthosis, gastric polyps, colonic polyps, skin lesions, and peripheral blood mononuclear cells.
  • RESULTS: All patients with Cowden syndrome showed several to numerous polyps in the gastrointestinal tract.
  • Identical mutations were found in all tissue samples, including colonic polyps, from each patient.
  • No PTEN mutations were found in their family members or in any patient with familial adenomatous polyposis.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Chromosomes, Human, Pair 10. Germ-Line Mutation. Hamartoma Syndrome, Multiple / genetics. Phosphoric Monoester Hydrolases / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 16007494.001).
  • [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 / Tumor Suppressor Proteins; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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34. Glei M, Hovhannisyan G, Pool-Zobel BL: Use of Comet-FISH in the study of DNA damage and repair: review. Mutat Res; 2009 Jan-Feb;681(1):33-43
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  • The Comet-FISH technique is a useful tool to detect overall and region-specific DNA damage and repair in individual cells.
  • Whereas the Comet assay allows separating fragmented from non-fragmented DNA, FISH helps to detect specifically labelled DNA sequences of interest, including whole chromosomes.
  • Thus the combination of both techniques has been applied in particular for detection of site-specific breaks in DNA regions which are relevant for development of different diseases.
  • This paper reviews the relevant literature and presents three examples on how Comet-FISH was used for studying the induction of DNA damage by genotoxic compounds related to oxidative stress in colon cancer-relevant genes (TP53, APC, KRAS) of a colon adenoma cell line.
  • A third example relates to measuring repair of specific gene regions using Comet-FISH, a method that can be developed to biomarker application.
  • Taken together, available data suggests that Comet-FISH helps to get further insights into sensitivity of specific DNA regions and consequently in mechanisms of carcinogenesis.
  • Although the nature of the measured Comet-FISH endpoint precludes us from stating basically that damage and repair are occurring within the specific gene, it is at least possible to evaluate whether the damage and repair are occurring within the vicinity of the gene of interest.
  • [MeSH-minor] Cell Line, Tumor. Colonic Neoplasms / genetics. Colonic Neoplasms / metabolism. Genes, APC / drug effects. Genes, p53 / drug effects. Genes, ras / drug effects. Genetic Markers. Humans. Mutagens / toxicity. Oxidative Stress / genetics. Telomere / drug effects. Telomere / genetics

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  • (PMID = 18304859.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Genetic Markers; 0 / Mutagens
  • [Number-of-references] 88
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35. Bastos P, Cardoso H, Ferreira F, Pimentel-Nunes P, Bartosch C, Souto-Moura C, Ribeiro A, Macedo G: Adenocarcinoma of the colon associated with hyperplastic polyposis. Gastroenterol Hepatol; 2010 Jun-Jul;33(6):470-1
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  • [Title] Adenocarcinoma of the colon associated with hyperplastic polyposis.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Adenomatous Polyps / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Neoplasms, Multiple Primary / pathology. Neoplastic Syndromes, Hereditary / diagnosis
  • [MeSH-minor] Adenoma, Villous / pathology. Adenoma, Villous / surgery. Adenomatous Polyposis Coli / diagnosis. Adult. Colectomy. Colonoscopy. CpG Islands. DNA Methylation / genetics. Diagnosis, Differential. Female. Humans. Hyperplasia. Proto-Oncogene Proteins B-raf / genetics

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  • (PMID = 20363055.001).
  • [ISSN] 0210-5705
  • [Journal-full-title] Gastroenterología y hepatología
  • [ISO-abbreviation] Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Spain
  • [Chemical-registry-number] EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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36. Ashktorab H, Belgrave K, Hosseinkhah F, Brim H, Nouraie M, Takkikto M, Hewitt S, Lee EL, Dashwood RH, Smoot D: Global histone H4 acetylation and HDAC2 expression in colon adenoma and carcinoma. Dig Dis Sci; 2009 Oct;54(10):2109-17
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  • [Title] Global histone H4 acetylation and HDAC2 expression in colon adenoma and carcinoma.
  • Chromatin remodeling and activation of transcription are important aspects of gene regulation, but these often go awry in disease progression, including during colon cancer development.
  • We investigated the status of global histone acetylation (by measuring H3, H4 acetylation of lysine residues, which also occur over large regions of chromatin including coding regions and non-promoter sequences) and expression of histone deacetylase 2 (HDAC2) in colorectal cancer (CRC) tissue microarrays using immunohistochemical staining.
  • Specifically, HDAC2 and the acetylation of histones H4K12 and H3K18 were evaluated in 134 colonic adenomas, 55 moderate to well differentiated carcinomas, and 4 poorly differentiated carcinomas compared to matched normal tissue.
  • HDAC2 nuclear expression was detected at high levels in 81.9%, 62.1%, and 53.1% of CRC, adenomas, and normal tissue, respectively (P = 0.002).
  • HDAC2 expression was correlated significantly with progression of adenoma to carcinoma (P = 0.002), with a discriminative power of 0.74, when comparing cancer and non-cancer cases.

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  • (PMID = 19057998.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA122959; United States / NCI NIH HHS / CA / CA122959-02; United States / NCI NIH HHS / CA / R01 CA122959-02; United States / PHS HHS / / A102681; United States / NCI NIH HHS / CA / R01 CA122959
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Histones; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ NIHMS118762; NLM/ PMC2737733
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37. Rennert G, Almog R, Tomsho LP, Low M, Pinchev M, Chaiter Y, Bonner JD, Rennert HS, Greenson JK, Gruber SB: Colorectal polyps in carriers of the APC I1307K polymorphism. Dis Colon Rectum; 2005 Dec;48(12):2317-21
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  • [Title] Colorectal polyps in carriers of the APC I1307K polymorphism.
  • The prevalence of polyps and adenomas in specimens of colorectal cancer who are carriers and noncarriers of the APC I1307K polymorphism is compared.
  • METHOD: Prevalence of adenomatous polyps in the pathology specimens of the study participants, stratified by their APC I1307K polymorphism status, was studied in 900 consecutive cases of colorectal cancer diagnosed in northern Israel between 1998 and 2002, within the framework of a population-based, case-controlled study (MECC Study).
  • Prevalence was higher among Ashkenazi Jews (11.2 percent) than among non-Ashkenazi Jews (2.7 percent) or Arabs (3.1 percent).
  • After adjustment for age, APC I1307K carriers were significantly more likely than noncarriers to have polyps in their surgical specimen (51.3 percent vs. 32.6 percent, P = 0.002).
  • Adenomas with a tubular component (either tubular adenomas or tubulovillous adenomas), but not villous adenomas, were significantly more frequent among carriers (37.2 percent vs. 23.6 percent, P = 0.005).
  • CONCLUSION: Together with former evidence of I1307K being a risk factor for colorectal cancer, these data suggest that colonoscopic surveillance for colorectal adenomas and cancer may be warranted in I1307K carriers, even in the absence of other identifiable risk factors.
  • [MeSH-major] Adenoma / genetics. Colonic Polyps / genetics. Colorectal Neoplasms / genetics. Genes, APC. Polymorphism, Genetic

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  • (PMID = 16228836.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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38. Suzuki R, Kohno H, Sugie S, Tanaka T: Dose-dependent promoting effect of dextran sodium sulfate on mouse colon carcinogenesis initiated with azoxymethane. Histol Histopathol; 2005 04;20(2):483-92
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  • [Title] Dose-dependent promoting effect of dextran sodium sulfate on mouse colon carcinogenesis initiated with azoxymethane.
  • We previously reported a powerful tumor-promoting ability of dextran sodium sulfate (DSS) in a novel mouse model for colitis-related colon carcinogenesis initiated with azoxymethane (AOM).
  • All animals were sacrificed at week 14 and histological alterations in their colon and nitrotyrosine immunohistochemistry were examined to evaluate the nitrosative stress.
  • In the mice which received AOM and 2% DSS, the incidences (multiplicity) of colonic tubular adenoma and adenocarcinoma were 75% (1.25+/-1.26/mouse) and 100% (2.75+/-2.22/mouse), respectively.
  • Mice given AOM and 1% DSS had 80% incidence of adenoma (1.00+/-0.71/mouse) and 60% incidence of adenocarcinoma (1.40+/-2.07/mouse) in the colon.
  • In a mouse treated with AOM and 0.5% DSS, only one colonic adenoma (20% incidence with 0.20+/-0.45 multiplicity) developed.
  • Higher frequency of high-grade colonic dysplasia was noted in mice given AOM and 2% or 1% DSS when compared with mice treated with AOM and lower doses of DSS.
  • Also, scoring of inflammation and nitrotyrosine immunoreactivity suggested that severe inflammation and nitrosation stress caused by high-doses (2% and 1%) of DSS contribute its tumor-promoting effects in mouse colon carcinogenesis initiated with a low dose of AOM.
  • [MeSH-major] Carcinogens / toxicity. Colonic Neoplasms / chemically induced. Dextran Sulfate / toxicity. Tyrosine / analogs & derivatives
  • [MeSH-minor] Animals. Azoxymethane / administration & dosage. Azoxymethane / toxicity. Cocarcinogenesis. Colitis / chemically induced. Colitis / pathology. Colonic Diseases / chemically induced. Colonic Diseases / pathology. Dose-Response Relationship, Drug. Intestinal Mucosa / drug effects. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Male. Mice. Mice, Inbred ICR. Ulcer / chemically induced. Ulcer / pathology

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  • (PMID = 15736053.001).
  • [ISSN] 0213-3911
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Carcinogens; 3604-79-3 / 3-nitrotyrosine; 42HK56048U / Tyrosine; 9042-14-2 / Dextran Sulfate; MO0N1J0SEN / Azoxymethane
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39. Martínez Torrente F, Orts Castro A, García-Montoto F, Pérez-Cerdá F: [Patient with right ventricular arrhythmogenic dysplasia, ascites and ulcerative colitis: anesthetic management during major abdominal surgery]. Rev Esp Anestesiol Reanim; 2005 Dec;52(10):631-3
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  • [Transliterated title] Manejo anestésico de un paciente con displasia arritmogénica de ventrículo derecho, ascitis y colitis ulcerosa para una cirugía abdominal mayor.
  • A 43-year-old man with ulcerative colitis was scheduled for pancolectomy owing to adenomatous transformation of polyps.
  • [MeSH-minor] Adenomatous Polyps / surgery. Adult. Analgesia, Epidural / methods. Atracurium / analogs & derivatives. Catheter Ablation. Colonic Neoplasms / surgery. Colonic Polyps / surgery. Defibrillators, Implantable. Equipment Failure. Fentanyl. Humans. Isoflurane. Male. Monitoring, Intraoperative. Pain, Postoperative / drug therapy. Postoperative Care. Postoperative Complications / surgery. Preanesthetic Medication. Respiration, Artificial. Thiopental

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  • (PMID = 16435619.001).
  • [ISSN] 0034-9356
  • [Journal-full-title] Revista española de anestesiología y reanimación
  • [ISO-abbreviation] Rev Esp Anestesiol Reanim
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 64228-79-1 / Atracurium; 76-75-5 / Thiopental; CYS9AKD70P / Isoflurane; QX62KLI41N / cisatracurium; UF599785JZ / Fentanyl
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40. Hoffman A, Sar F, Goetz M, Tresch A, Mudter J, Biesterfeld S, Galle PR, Neurath MF, Kiesslich R: High definition colonoscopy combined with i-Scan is superior in the detection of colorectal neoplasias compared with standard video colonoscopy: a prospective randomized controlled trial. Endoscopy; 2010 Oct;42(10):827-33
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  • The primary endpoint was the detection of patients having colon cancer or at least one adenoma.
  • Significantly more neoplastic (adenomatous and cancerous) lesions and more flat adenomas could be detected using high definition endoscopy with surface enhancement.
  • [MeSH-major] Adenoma / diagnosis. Colonic Polyps / diagnosis. Colonoscopy / methods. Colorectal Neoplasms / diagnosis. Image Enhancement / instrumentation. Image Enhancement / methods


41. Jurek D, Fleckl E, Marian B: Bile acid induced gene expression in LT97 colonic adenoma cells. Food Chem Toxicol; 2005 Jan;43(1):87-93
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  • [Title] Bile acid induced gene expression in LT97 colonic adenoma cells.
  • LT97 human colonic adenoma cells reflecting early premalignant genotype and growth characteristics have been posed to tumor promoting bile acids in order to identify marker genes that permit identification of tumor promoters in vitro.
  • Physiologically relevant concentrations of desoxycholate (DOC) and chenodesoxycholate (CDC) upregulated expression of c-fos and COX-2 in a concentration- and time-dependent manner.
  • Transient induction of c-fos was seen with the non-promoting taurodesoxycholate (TDOC) as well as DOC, however extended induction at 3 h was only achieved by DOC and CDC reaching 3-6-fold as compared to the control.
  • Stimulation of COX-2 expression was completely specific for the tumor promoting analogs DOC and CDC.
  • Expression of VEGF was stimulated 4-5-fold in the tumor promoter (DOC and CDC) groups and about 2-fold in the non-promoting controls TDOC and GCDC.
  • At later times the tumor promoter specific difference was lost.
  • Our results show that all three genes are modulated in a tumor promoter dependent way and that their upregulation in LT97 adenoma cells can be used for in vitro testing of colon tumor promoters and chemopreventive compounds.
  • [MeSH-major] Adenoma / metabolism. Bile Acids and Salts / pharmacology. Biomarkers, Tumor / metabolism. Colonic Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / drug effects

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  • (PMID = 15582199.001).
  • [ISSN] 0278-6915
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / Biomarkers, Tumor; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins c-fos; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 005990WHZZ / Deoxycholic Acid; 0GEI24LG0J / Chenodeoxycholic Acid; 516-50-7 / Taurodeoxycholic Acid; 63231-63-0 / RNA; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases
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42. Buecher B, Bezieau S, Dufilhol C, Cauchin E, Heymann MF, Mosnier JF: [Emerging concepts in colorectal serrated polyps]. Gastroenterol Clin Biol; 2007 Jan;31(1):39-54
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  • [Title] [Emerging concepts in colorectal serrated polyps].
  • Colorectal serrated polyps are heterogeneous epithelial lesions characterized by a serrated architecture.
  • They include the classical hyperplastic polyps and the much rarer serrated adenomas and mixed polyps.
  • Whereas serrated adenomas are composed of an unequivocal adenomatous epithelium with architectural serrated, mixed polyps include two separate hyperplastic and adenomatous components.
  • During the past few years, another type of serrated polyp with only very subtle proliferation abnormalities has been described.
  • These atypical serrated polyps may occur either sporadically or in the context of colorectal polyposis.
  • Despite their close resemblance to traditional hyperplastic polyps, some authors argued that they should be regarded as authentically neoplastic lesions and have proposed to call them "sessile serrated adenomas".
  • This article reviews the histological features, the endoscopic appearance, the natural history and the molecular phenotype of the different categories of serrated polyps and introduces the concept of "serrated neoplastic pathway" in the development of colorectal cancer.
  • [MeSH-major] Adenoma / pathology. Colonic Polyps / pathology. Colorectal Neoplasms / pathology

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  • (PMID = 17273130.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 90
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43. van Kouwen MC, Laverman P, van Krieken JH, Oyen WJ, Nagengast FM, Drenth JP: Noninvasive monitoring of colonic carcinogenesis: feasibility of [(18)F]FDG-PET in the azoxymethane model. Nucl Med Biol; 2006 Feb;33(2):245-8
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  • [Title] Noninvasive monitoring of colonic carcinogenesis: feasibility of [(18)F]FDG-PET in the azoxymethane model.
  • BACKGROUND: Azoxymethane (AOM) is a potent carcinogen that induces colorectal cancer and adenomas in rats.
  • At present, it is unknown at which stage FDG accumulation occurs during the adenoma carcinoma sequence.
  • RESULTS: Macroscopic examination revealed 21 tumors (7 located in the small bowel and 14 in the colon) in 19 rats.
  • On histological examination, we found 10 colonic adenocarcinomas (the first being observed at Week 22) and 7 adenocarcinoma in the small bowel.
  • In total, seven colon adenomas were found in five rats, six of which expressed high-grade dysplasia.
  • [(18)F]FDG uptake was lower in adenomas than in carcinomas.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / radionuclide imaging. Colonic Neoplasms / metabolism. Colonic Neoplasms / radionuclide imaging. Disease Models, Animal. Fluorodeoxyglucose F18 / pharmacokinetics

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  • (PMID = 16546679.001).
  • [ISSN] 0969-8051
  • [Journal-full-title] Nuclear medicine and biology
  • [ISO-abbreviation] Nucl. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; MO0N1J0SEN / Azoxymethane
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44. Goldstein NS: Serrated pathway and APC (conventional)-type colorectal polyps: molecular-morphologic correlations, genetic pathways, and implications for classification. Am J Clin Pathol; 2006 Jan;125(1):146-53
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  • [Title] Serrated pathway and APC (conventional)-type colorectal polyps: molecular-morphologic correlations, genetic pathways, and implications for classification.
  • This review addresses the genetic mutations and cell signaling pathway alterations in colorectal premalignant polyps, focusing on the link between molecular changes and morphologic features.
  • Biallelic APC (adenomatous polyposis coli) mutations are directly responsible for the specific and characteristic cytologic features of dysplastic cells in conventional tubular adenomas.
  • Sessile serrated adenomas (SSAs) are the precursor lesions of the serrated neoplasia pathway.
  • Intracellular butyrate inhibits histone deacetylase, allowing histone hyperacetylation and, eventually, transcriptional activation of specific genes.
  • Progressive loss of cell cycle control and decreased and altered cytoplasmic differentiation produce the characteristic constellation of morphologic changes of SSAs and traditional serrated adenomas.
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Colonic Polyps / pathology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenomatous Polyposis Coli Protein / physiology. Carrier Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Nuclear Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics

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  • (PMID = 16483003.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / CDKN1A protein, human; 0 / Carrier Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / MLH1 protein, human; 0 / Nuclear Proteins; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
  • [Number-of-references] 123
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45. Tobi M, Kam M, Ullah N, Qureshi K, Yordanova V, Hatfield J, Fligiel SE, Sochacki P, McGarrity T, Cole C, Lawson M, Jacoby R: An anti-adenoma antibody, Adnab-9, may reflect the risk for neoplastic progression in familial hamartomatous polyposis syndromes. Dig Dis Sci; 2008 Mar;53(3):723-9
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  • [Title] An anti-adenoma antibody, Adnab-9, may reflect the risk for neoplastic progression in familial hamartomatous polyposis syndromes.
  • Patients with the hamartomatous polyposis Peutz-Jeghers and familial juvenile polyposis syndromes are predisposed to colorectal cancer but lack early genetic alterations found in adenomatous premalignant lesions.
  • We studied hamartomatous polyps for the expression of an early preneoplastic colorectal neoplasia risk marker also found in familial adenomatous polyposis patients.
  • Retrospective, genetic, and hospital archival tissue immunohistochemistry using Adnab-9, a premalignant marker often found in Paneth-like cells (PCs), was performed on sections of polyps from eight patients with Peutz-Jeghers syndrome, eight patients with familial juvenile polyposis, and 36 hyperplastic polyp control sections.
  • Hamartomatous polyposis patients also underwent specific genetic analysis.
  • Eighty-nine percent of Peutz-Jeghers syndrome polyps labeled with Adnab-9 compared with 63% for AD5; 88% of familial juvenile polyposis sections also labeled with Adnab-9.
  • Of the 36 hyperplastic polyp sections, only four (11%) labeled with Adnab-9 and one (3%) with AD5.
  • Adnab-9 labeling of PCs in the epithelial elements of hamartomatous colonic lesions of hereditary hamartomatous syndrome patients reflects the predisposition to colorectal cancer, further justifying early intervention strategies.
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Antibodies, Monoclonal. Biomarkers, Tumor. Colon / pathology. Colonic Polyps / pathology. Peutz-Jeghers Syndrome / pathology

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  • (PMID = 17934846.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [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 / Adnab-9; 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / alpha-Defensins; 0 / alpha-defensin 5, human; EC 2.7.1.- / STK11 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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46. Lee HL, Son BK, Lee OY, Jeon YC, Han DS, Sohn JH, Yoon BC, Choi HS, Hahm JS, Lee MH, Lee DH, Kee CS: [Abdominal obesity, insulin resistance, and the risk of colonic adenoma]. Korean J Gastroenterol; 2007 Mar;49(3):147-51
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  • [Title] [Abdominal obesity, insulin resistance, and the risk of colonic adenoma].
  • BACKGROUND/AIMS: Abdominal obesity and hyperinsulinemia or insulin resistance are of interest in connection with colon carcinogenesis.
  • We conducted a prospective case controlled study for the evaluation of relationship between abdominal obesity, insulin resistance, and colorectal adenoma.
  • METHODS: Fifty patients with colorectal adenoma and fifty healthy subjects were included in this study.
  • RESULTS: There were no differences in sex, serum insulin, FBS, HOMA-IR, TG, CROL between adenoma and control group.
  • Subjects with high BMI, WHR, percent body fat, and obesity were more likely to have colonic adenoma.
  • Multiple logistic regression analysis after adjusting confounding factors, had revealed that WHR was the most important independent risk factor for colon adenoma.
  • CONCLUSIONS: Abdominal obesity was most closely related to colonic adenoma.
  • However, insulin resistance was not related to colonic adenoma.
  • [MeSH-major] Abdominal Fat. Adenoma / etiology. Colonic Neoplasms / etiology. Insulin Resistance. Obesity / complications

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  • [CommentIn] Korean J Gastroenterol. 2007 Mar;49(3):192-5 [18172350.001]
  • (PMID = 18172342.001).
  • [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. Park JG, Kim IJ: [Hereditary colorectal cancer]. Korean J Gastroenterol; 2005 Feb;45(2):78-87
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  • Hereditary CRC is conventionally divided into two major categories: hereditary non-polyposis colorectal cancer (HNPCC) and those related to polyposis syndromes including familial adenomatous polyposis (FAP), Peutz-Jegher syndrome (PJS), and juvenile polyposis (JP).
  • Germ-line mutation of the APC gene induces FAP, an autosomal dominant disorder, characterized by the development of hundreds to thousands of colonic adenomas.
  • Recently, a mutation on the MYH gene is increasingly being investigated in patients with multiple polyps, and autosomal recessive MYH polyposis is considered to be a new category of polyposis.
  • Although there is no polyposis, polyps seem to be more villous and dysplastic and appear to grow rapidly into CRCs.
  • PJS and JP are reported to be characterized by hamartomatous polyps throughout the GI tract and germ-line mutations in the STK11 gene (PJS) and the DPC4/BMPR1A gene (JP).
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Intestinal Polyposis / genetics. Peutz-Jeghers Syndrome / genetics

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  • (PMID = 15725711.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Number-of-references] 40
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48. Knoll N, Weise A, Claussen U, Sendt W, Marian B, Glei M, Pool-Zobel BL: 2-Dodecylcyclobutanone, a radiolytic product of palmitic acid, is genotoxic in primary human colon cells and in cells from preneoplastic lesions. Mutat Res; 2006 Feb 22;594(1-2):10-9
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  • [Title] 2-Dodecylcyclobutanone, a radiolytic product of palmitic acid, is genotoxic in primary human colon cells and in cells from preneoplastic lesions.
  • Results of previous in vitro studies with primary human colon cells and in vivo experiments with rats fed with 2-alkylcyclobutanones indicated that these radiolytic derivatives may be genotoxic and enhance the progression of colon tumors.
  • In particular, we explored the relative sensitivities of human colon cells, representing different stages of tumor development and healthy colon tissues, respectively.
  • HT29clone19A cells, LT97 adenoma cells and primary human epithelial cells were exposed to 2dDCB (150-2097 microM).
  • Genotoxicity, reflected as strand breaks, was assessed using the alkaline version of the comet assay and chromosomal abnormalities were investigated by 24-color fluorescence-in-situ-hybridization.
  • 2dDCB was cytotoxic in a time- and dose-dependent manner in LT97 adenoma cells and in freshly isolated primary cells but not in the human colon tumor cell line.
  • Associated with this was a marked induction of DNA damage by 2dDCB in LT97 adenoma cells and in freshly isolated colonocytes, whereas in the HT29clone19A cells no strand breaks were detectable.
  • A long-term incubation of LT97 adenoma cells with lower concentrations of 2dDCB revealed cytogenetic effects.
  • In summary, 2dDCB was clearly genotoxic in healthy human colon epithelial cells and in cells representing preneoplastic colon adenoma.
  • These findings provide additional evidence that this compound may be regarded as a possible risk factor for processes in colon carcinogenesis related to initiation and progression.
  • [MeSH-major] Colon / drug effects. Cyclobutanes / toxicity. Mutagens / toxicity. Palmitic Acid / metabolism. Precancerous Conditions / genetics

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  • (PMID = 16153665.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cyclobutanes; 0 / Mutagens; 2V16EO95H1 / Palmitic Acid; 35493-46-0 / 2-dodecylcyclobutanone
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49. Folker MB, Bernstein IT, Holck S: [Serrated, hyperplastic and hyperplasia-like colorectal polyps]. Ugeskr Laeger; 2006 Nov 13;168(46):4005-9
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  • [Title] [Serrated, hyperplastic and hyperplasia-like colorectal polyps].
  • The colorectal hyperplastic polyp has generally been considered a finding of no clinical significance.
  • Recent research has, however, called attention to the existence of some variants of hyperplastic polyp which are potentially malignant.
  • The term "advanced serrated polyp" has been coined for such cases, which comprise mixed hyperplastic/adenomatous tissue, serrated adenoma, and sessile serrated polyp, in contrast to the traditional hyperplastic polyp.
  • Since epithelial dysplasia is an integrated component of mixed hyperplastic/adenomatous polyp and of the serrated adenoma, such a diagnosis would dictate control colonoscopy comparable to the guidelines for subjects with conventional adenomas.
  • The cytology of the sessile serrated polyp is, however, closer to that of the traditional hyperplastic polyp, whereas the architecture mimics that of the serrated adenoma.
  • For this reason, a consensus regarding the optimal management of such patients has not been obtained, but if the polyp is sizeable and located in the right colon, control should be considered.
  • The small, usually left-sided traditional polyp as a rule needs no follow-up, but the context in which such a lesion is found and its morphology may influence the clinical decision.
  • Future large-scale investigations of serrated colorectal polyps, including interobserver studies, will be required to identify histological details of clinical utility which can be adopted in daily routine practice.
  • [MeSH-major] Adenoma / pathology. Colonic Polyps / pathology. Colorectal Neoplasms / pathology

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  • (PMID = 17125655.001).
  • [ISSN] 1603-6824
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Denmark
  • [Number-of-references] 40
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50. Brouland JP, Gélébart P, Kovàcs T, Enouf J, Grossmann J, Papp B: The loss of sarco/endoplasmic reticulum calcium transport ATPase 3 expression is an early event during the multistep process of colon carcinogenesis. Am J Pathol; 2005 Jul;167(1):233-42
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  • [Title] The loss of sarco/endoplasmic reticulum calcium transport ATPase 3 expression is an early event during the multistep process of colon carcinogenesis.
  • To better characterize the role of SERCA3 in colon carcinogenesis, its expression has been investigated in colonic epithelium, benign lesions, adenomas, and adenocarcinomas.
  • In addition, the regulation of SERCA3 expression was analyzed in the context of the adenomatous polyposis coli/beta-catenin/T-cell factor 4 (TCF4) pathway and of specificity protein 1 (Sp1)-like factor-dependent transcription.
  • We report that SERCA3 expression increased along the crypts as cells differentiated in normal colonic mucosa and in hyperplastic polyps, was moderately and heterogeneously expressed in colonic adenomas with expression levels inversely correlated with the degree of dysplasia, was barely detectable in well and moderately differentiated adenocarcinomas, and was absent in poorly differentiated tumors.
  • Inhibition of Sp1-like factor-dependent transcription blocked SERCA3 expression during cell differentiation, and SERCA3 expression was induced by the expression of dominant-negative TCF4 in colon cancer cells.
  • These data link SERCA3 expression to the state of differentiation of colonic epithelial cells, and relate SERCA3 expression, already decreased in adenomas, to enhanced adenomatous polyposis coli/beta-catenin/TCF4-dependent signaling and deficient Sp1-like factor-dependent transcription.
  • In conclusion, intracellular calcium homeostasis becomes progressively anomalous during colon carcinogenesis as reflected by deficient SERCA3 expression.
  • [MeSH-major] Biomarkers, Tumor / analysis. Calcium / metabolism. Calcium-Transporting ATPases / biosynthesis. Colonic Neoplasms / enzymology. Intestinal Mucosa / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / genetics. Blotting, Western. Cell Line, Tumor. Cell Transformation, Neoplastic. Colonic Polyps / enzymology. Cytoskeletal Proteins / genetics. DNA-Binding Proteins. Endoplasmic Reticulum / metabolism. Humans. Immunohistochemistry. Sarcoplasmic Reticulum Calcium-Transporting ATPases. TCF Transcription Factors. Trans-Activators / genetics. Transcription Factor 7-Like 2 Protein. Transcription Factors. Transfection. Transgenes. beta Catenin

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  • (PMID = 15972967.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Trans-Activators; 0 / Transcription Factor 7-Like 2 Protein; 0 / Transcription Factors; 0 / beta Catenin; EC 3.6.3.8 / ATP2A3 protein, human; EC 3.6.3.8 / Calcium-Transporting ATPases; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC1603437
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51. Hawk ET, Levin B: Colorectal cancer prevention. J Clin Oncol; 2005 Jan 10;23(2):378-91
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  • Four classes of chemopreventive compounds have demonstrated efficacy in reducing recurrent colorectal adenomas and/or cancer in randomized, controlled trials.
  • Considerable effort is being expended to define chemopreventive activity, optimal dose, administration schedule, and toxicity for the coxibs in adenoma recurrence prevention trials.
  • [MeSH-minor] Adenomatous Polyps / complications. Adenomatous Polyps / diagnosis. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Clinical Trials as Topic. Colonic Polyps / diagnosis. Cyclooxygenase Inhibitors / therapeutic use. Female. Forecasting. Humans. Male. Patient Selection. Precancerous Conditions / diagnosis. Precancerous Conditions / therapy. Risk

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  • (PMID = 15637400.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA131378; United States / NCI NIH HHS / CA / R01 CA148817; United States / NCI NIH HHS / CA / R01 CA155638
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase Inhibitors; R16CO5Y76E / Aspirin
  • [Number-of-references] 167
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52. Murff HJ, Shrubsole MJ, Smalley WE, Wu H, Shyr Y, Ness RM, Zheng W: The interaction of age and hormone replacement therapy on colon adenoma risk. Cancer Detect Prev; 2007;31(2):161-5
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  • [Title] The interaction of age and hormone replacement therapy on colon adenoma risk.
  • BACKGROUND: Several studies have identified a possible interaction between age and hormone replacement therapy on colon neoplasm risk.
  • RESULTS: There was a significant interaction between age and hormone replacement therapy use (P=0.03) with current estrogen users who were over 56 years of age having a reduced odds of colon adenoma (OR, 0.40; 95% CI, 0.16-0.98) when compared to never users.
  • Both older women who had used hormone replacement therapy for 3 or less years (OR, 0.07; 95% CI, 0.006-0.81) and those reporting greater than 10 years of use (OR, 0.27; 95% CI, 0.09-0.80) had a reduced adjusted odds for adenomas when compared to non-users.
  • CONCLUSIONS: Duration of use is not likely to explain the stronger association of hormone replacement therapy use with colon neoplasm in older women.

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  • (PMID = 17433566.001).
  • [ISSN] 0361-090X
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / K07 CA114029; United States / NCI NIH HHS / CA / R01 CA097386-01; United States / NCI NIH HHS / CA / K07 CA114029-01A2; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / P50 CA095103-01; United States / NCI NIH HHS / CA / CA95103; United States / NCI NIH HHS / CA / CA097386-01; United States / NCI NIH HHS / CA / R01 CA97386
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS24075; NLM/ PMC1949417
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53. Knöbel Y, Glei M, Weise A, Osswald K, Schäferhenrich A, Richter KK, Claussen U, Pool-Zobel BL: Uranyl nitrilotriacetate, a stabilized salt of uranium, is genotoxic in nontransformed human colon cells and in the human colon adenoma cell line LT97. Toxicol Sci; 2006 Oct;93(2):286-97
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  • [Title] Uranyl nitrilotriacetate, a stabilized salt of uranium, is genotoxic in nontransformed human colon cells and in the human colon adenoma cell line LT97.
  • To assess possible hazards, we investigated the genotoxic effects of uranyl nitrilotriacetate (U-NTA) in human colon tumor cells (HT29 clone 19A), adenoma cells (LT97), and nontransformed primary colon cells.
  • Colon cells were incubated with U-NTA.
  • Cell survival, cytotoxicity, cellular glutathione (GSH) levels, genotoxicity, and DNA repair capacity (comet assay), as well as gene- and chromosome-specific damage combination of comet assay and fluorescence in situ hybridization [FISH], 24-color FISH) were determined.
  • U-NTA was also genotoxic in LT97 cells and primary colon cells, where it additionally increased migration of TP53 into the comet tail.
  • [MeSH-major] Colon / drug effects. Uranium / toxicity
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Cell Line, Tumor. Cell Survival / drug effects. Chromosome Aberrations. Colonic Neoplasms / genetics. Colonic Neoplasms / pathology. DNA Damage. Glutathione / analysis. Humans. In Situ Hybridization, Fluorescence. Reactive Oxygen Species. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 16840563.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 0 / Tumor Suppressor Protein p53; 4OC371KSTK / Uranium; GAN16C9B8O / Glutathione
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54. Varey AH, Rennel ES, Qiu Y, Bevan HS, Perrin RM, Raffy S, Dixon AR, Paraskeva C, Zaccheo O, Hassan AB, Harper SJ, Bates DO: VEGF 165 b, an antiangiogenic VEGF-A isoform, binds and inhibits bevacizumab treatment in experimental colorectal carcinoma: balance of pro- and antiangiogenic VEGF-A isoforms has implications for therapy. Br J Cancer; 2008 Apr 22;98(8):1366-79
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  • Using isoform-specific enzyme-linked immunosorbent assay and quantitative polymerase chain reaction, we found that over 90% of the VEGF in normal colonic tissue was VEGF(xxx)b, but there was a variable upregulation of VEGF(xxx) and downregulation of VEGF(xxx)b in paired human CRC samples.
  • Furthermore, cultured colonic adenoma cells expressed predominantly VEGF(xxx)b, whereas colonic carcinoma cells expressed predominantly VEGF(xxx).
  • However, adenoma cells exposed to hypoxia switched their expression from predominantly VEGF(xxx)b to predominantly VEGF(xxx).
  • VEGF(165)b overexpression in LS174t colon cancer cells inhibited colon carcinoma growth in mouse xenograft models.
  • However, although bevacizumab effectively inhibited the rapid growth of colon carcinomas expressing VEGF(165), it did not affect the slower growth of tumours from colonic carcinoma cells expressing VEGF(165)b.
  • Both bevacizumab and anti-VEGF(165)b-specific antibodies were cytotoxic to colonic epithelial cells, but less so to colonic carcinoma cells.
  • Together with the identification of an autocrine cytoprotective role for VEGF(165)b in colonic epithelial cells, these results indicate that bevacizumab treatment of human CRC may depend upon this balance of VEGF isoforms.
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Bevacizumab. Cell Line, Tumor. Cell Proliferation. Colon / metabolism. Humans. Mice. Protein Isoforms. RNA Splicing. RNA, Messenger / analysis

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  • (PMID = 18349829.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / British Heart Foundation / / FS/06/038; United Kingdom / British Heart Foundation / / BS/06/005/20340; United Kingdom / British Heart Foundation / / FS/04/22; United Kingdom / Cancer Research UK / / A8451; United Kingdom / Cancer Research UK / / ; United Kingdom / British Heart Foundation / / BS/2001003/12790; United Kingdom / British Heart Foundation / / BB2000003
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 2S9ZZM9Q9V / Bevacizumab
  • [Other-IDs] NLM/ PMC2361696; NLM/ UKMS2582
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55. Knöbel Y, Weise A, Glei M, Sendt W, Claussen U, Pool-Zobel BL: Ferric iron is genotoxic in non-transformed and preneoplastic human colon cells. Food Chem Toxicol; 2007 May;45(5):804-11
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  • [Title] Ferric iron is genotoxic in non-transformed and preneoplastic human colon cells.
  • We previously demonstrated genotoxic effects by ferric iron using the human colon cancer cell line HT29.
  • Here we investigated ferric iron in primary non-transformed colon cells and in a preneoplastic colon adenoma cell line (LT97), which both are suitable models to study effects of carcinogens during early stages of cell transformation.
  • Comet FISH (fluorescence in situ hybridization) was used to assess specific effects on TP53.
  • Fe-NTA (0-1000 microM, 30 min, 37 degrees C) significantly induced single strand breaks in primary colon cells (500 microM Fe-NTA: Tail intensity [TI] 22.6%+/-5.0% versus RPMI control: TI 10.6%+/-3.9%, p<0.01) and in LT97 cells (1000 microM Fe-NTA: TI 26.8%+/-7.3% versus RPMI control: TI 11.1%+/-3.7%, p<0.01).
  • With the Comet FISH protocol lower concentrations of Fe-NTA significantly increased DNA damage already at 100 and 250 microM Fe-NTA in primary colon and LT97 adenoma cells, respectively.
  • In conclusion, Fe-NTA acts genotoxic in non-transformed and in preneoplastic human colon cells, in which it also enhances migration of TP53 at relatively low concentrations.
  • Translated to the in vivo situation these results suggest that iron overload putatively contributes to a genotoxic risk during early stages of colorectal carcinogenesis on account of its genotoxic potential in non-tumorigenic human colon cells.
  • [MeSH-major] Colon / drug effects. DNA Damage / drug effects. Ferric Compounds / toxicity. Nitrates / toxicity
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Cell Line, Tumor. Chromosome Aberrations. Colonic Neoplasms / genetics. Colonic Neoplasms / pathology. Comet Assay. Dose-Response Relationship, Drug. Humans. In Situ Hybridization, Fluorescence. Reactive Oxygen Species / metabolism. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 17157427.001).
  • [ISSN] 0278-6915
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ferric Compounds; 0 / Nitrates; 0 / Reactive Oxygen Species; 0 / Tumor Suppressor Protein p53; N8H8402XOB / ferric nitrate
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56. Paskett ED, Reeves KW, Pineau B, Albert PS, Caan B, Hasson M, Iber F, Kikendall JW, Lance P, Shike M, Slattery ML, Weissfeld J, Kahle L, Schatzkin A, Lanza E, Polyp Prevention Trial Study Group: The association between cigarette smoking and colorectal polyp recurrence (United States). Cancer Causes Control; 2005 Nov;16(9):1021-33
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  • [Title] The association between cigarette smoking and colorectal polyp recurrence (United States).
  • OBJECTIVE: Although evidence exists linking smoking to precancerous colorectal adenomatous polyps, few studies have examined the association between cigarette smoking and recurrence of colorectal polyps.
  • This association was investigated prospectively with data from the Polyp Prevention Trial.
  • The study was completed by 1872 men and women with presence of adenomas at baseline colonoscopy.
  • Multiple logistic regression analysis was used to examine the association between cigarette smoking and polyp recurrence (adenomatous and hyperplastic) up to four years from baseline.
  • RESULTS: Adenoma recurrence was not related to cigarette smoking.
  • Current smokers had increased odds of hyperplastic polyps at follow-up compared to never smokers (OR 2.88, 95% CI 2.06-4.01).
  • Current smoking was associated with subsequent distal (OR 3.44, 95% CI 2.38-4.95) and rectal (OR 3.53, 95% CI 2.15-5.78) hyperplastic polyps, but not subsequent proximal hyperplastic polyps.
  • Cigarette smoking was associated with subsequent multiple and small size (4 mm) hyperplastic polyps.
  • Significant linear trends were observed between development of subsequent hyperplastic polyps and all smoking variables.
  • CONCLUSIONS: Although no association with recurrent adenomas was observed, cigarette smoking was significantly associated with hyperplastic polyp development, except for those in the proximal colon.
  • This prospective study confirms that cigarette smoking has a significant effect on the development of hyperplastic colorectal polyps.
  • [MeSH-major] Colonic Polyps / pathology. Precancerous Conditions. Smoking / epidemiology
  • [MeSH-minor] Adenoma / epidemiology. Adenoma / pathology. Aged. Colonoscopy. Epidemiologic Studies. Female. Humans. Hyperplasia / epidemiology. Hyperplasia / pathology. Male. Middle Aged. Recurrence. Risk Assessment. Risk Factors. Surveys and Questionnaires. Time Factors. United States

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  • (PMID = 16184467.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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57. Roberts ML, Drosopoulos KG, Vasileiou I, Stricker M, Taoufik E, Maercker C, Guialis A, Alexis MN, Pintzas A: Microarray analysis of the differential transformation mediated by Kirsten and Harvey Ras oncogenes in a human colorectal adenocarcinoma cell line. Int J Cancer; 2006 Feb 1;118(3):616-27
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  • Colorectal cancer arises after a series of mutational events in the colon epithelia and is often used as a model of the multistep progression of tumorigenesis.
  • In order to examine the distinctive function that Ki-Ras plays in cancer development in the colon, we introduced constitutively active mutant Ki- and Ha-Ras genes into an intermediate-stage colon adenoma cell line (Caco-2).
  • We found that mutant active Ha-RasV12 was more efficient at transforming these colon epithelial cells as assessed by anchorage-independent growth, tumor formation in SCID mice and the development of mesenchymal morphology compared to transformation by Ki-RasV12.
  • Specifically, we found that Ki-RasV12 regulated genes involved in cytokine signaling, cell adhesion and colon development, whereas Ha-RasV12 mainly regulated genes involved in controlling cell morphology, correlating to an epithelial-mesenchymal transition only observed in these cells.
  • Our results demonstrate how 2 Ras isoforms regulate disparate biologic processes, revealing a number of genes whose deregulated expression may influence colon carcinogenesis (supplementary material for this article can be found on the International Journal of Cancer website at http://www.interscience.wiley.com/jpages/0020-7136/suppmat/index.html).

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16152623.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Protein Isoforms
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58. Tajika M, Nakamura T, Nakahara O, Kawai H, Komori K, Hirai T, Kato T, Bhatia V, Baba H, Yamao K: Prevalence of adenomas and carcinomas in the ileal pouch after proctocolectomy in patients with familial adenomatous polyposis. J Gastrointest Surg; 2009 Jul;13(7):1266-73
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  • [Title] Prevalence of adenomas and carcinomas in the ileal pouch after proctocolectomy in patients with familial adenomatous polyposis.
  • PURPOSE: Restorative proctocolectomy has become the most common surgical option for patients with familial adenomatous polyposis (FAP).
  • However, adenomas may develop in the ileal pouch mucosa over time, and even carcinoma in the pouch has been reported.
  • Our aim was to evaluate the prevalence, nature, and etiology of ileal pouch and nonpouch adenomas and carcinoma in patients with FAP.
  • All patients were followed with a standardized protocol including chromoendoscopy and biopsies of visible polyps in the ileal pouch and nonpouch mucosa.
  • RESULTS: Sixteen of 24 pouch patients (Kock and IPAA) developed adenomas in the ileal pouch mucosa, and all patients with IRA developed adenomas in the rectal mucosa.
  • The prevalence of ileal adenomas was significantly higher in pouch patients than in IRA patients (P = 0.002).
  • Only one patient with Kock showed adenoma in the prepouch area.
  • Two cases of adenocarcinomas and one case of advanced adenoma were found in the ileal pouch mucosa.
  • CONCLUSION: Our results show a high frequency of adenomas in the ileal pouch mucosa, with evolution into carcinoma in some patients.
  • [MeSH-major] Adenoma / epidemiology. Adenomatous Polyposis Coli / surgery. Carcinoma / epidemiology. Colonic Neoplasms / surgery. Colonic Pouches / pathology. Neoplasm Recurrence, Local / pathology

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  • (PMID = 19333660.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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59. Shin JE, Jung SA, Kim SE, Joo YH, Shim KN, Kim TH, Yoo K, Moon IH: [Expression of MMP-2, HIF-1alpha and VEGF in colon adenoma and colon cancer]. Korean J Gastroenterol; 2007 Jul;50(1):9-18
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  • [Title] [Expression of MMP-2, HIF-1alpha and VEGF in colon adenoma and colon cancer].
  • BACKGROUND/AIMS: This study was aimed to investigate the expression of matrix metalloproteinase-2 (MMP-2), hypoxia-inducible factor (HIF)-1alpha, and vascular endothelial growth factor (VEGF) in colonic adenoma-carcinoma sequence.
  • METHODS: Thirty-two tissue samples of colon adenoma, 11 of early colon cancer and 36 of advanced colon cancer were collected by colonoscopic biopsy.
  • Normal colonic tissues were also collected from the same subjects.
  • RESULTS: The expression level of MMP-2 mRNA showed a progressive increase in the advance of the colorectal adenoma-carcinoma sequence (p<0.05).
  • In colon cancer tissues, the expression level of MMP-2 mRNA showed an increasing trend according to differentiation, lymphatic invasion and Dukes' stage (p<0.05).
  • The mRNA expression levels of HIF-1alpha and VEGF were greater in tissues of early and advanced colon cancer compared with colon adenoma (p<0.05; p<0.001).
  • CONCLUSIONS: MMP-2, HIF-1alpha, and VEGF may be useful in detecting early carcinogenesis and progression of colon cancer.
  • [MeSH-major] Adenoma / metabolism. Colonic Neoplasms / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Matrix Metalloproteinase 2 / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 18172354.001).
  • [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)
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; EC 3.4.24.24 / Matrix Metalloproteinase 2
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60. Herszényi L, Lakatos G, Tulassay Z: [Quality colonoscopy: assumptions and expectations]. Orv Hetil; 2010 Aug 15;151(33):1331-9
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  • Colonoscopy has become accepted as the most effective method of screening of the colon for neoplasia.
  • [MeSH-minor] Adenomatous Polyposis Coli / diagnosis. Adenomatous Polyposis Coli / surgery. Analgesics / administration & dosage. Colonic Polyps / diagnosis. Colonic Polyps / surgery. Computer Simulation. Gastroenterology / education. Gastrointestinal Hemorrhage / etiology. Humans. Medical Records / standards. Preoperative Care / methods


61. Subramaniam MM, Chan JY, Soong R, Ito K, Yeoh KG, Wong R, Guenther T, Will O, Chen CL, Kumarasinghe MP, Ito Y, Salto-Tellez M: RUNX3 inactivation in colorectal polyps arising through different pathways of colonic carcinogenesis. Am J Gastroenterol; 2009 Feb;104(2):426-36
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  • [Title] RUNX3 inactivation in colorectal polyps arising through different pathways of colonic carcinogenesis.
  • OBJECTIVES: We hypothesized that RUNX3 inactivation by promoter hypermethylation in colorectal polyps is an early molecular event in colorectal carcinogenesis.
  • METHODS: RUNX3 protein expression was analyzed immunohistochemically in 50 sporadic colorectal polyps comprising 19 hyperplastic polyps (HPs), 14 traditional serrated adenomas (TSAs), and 17 sporadic traditional adenomas (sTAs) as well as in 19 familial adenomatous polyposis (FAP) samples from 10 patients showing aberrant crypt foci (ACF) (n=91), small adenomas (SmAds) (n=40), and large adenomas (LAds) (n=13).
  • In addition, we assessed the frequency of promoter hypermethylation of RUNX3 by methylation-specific PCR (MSP) in all the 50 sporadic polyps as well as 38 microdissected FAP polyps comprising ACF, SmAds, and LAds obtained from 7 FAP samples.
  • A total of 12 normal colon samples were also included for RUNX3 MSP analysis.
  • RESULTS: Compared to normal colon (2 of 12, 16%) and sTAs (3 of 17, 18%), HPs (15 of 19, 79%) and TSAs (8 of 14, 57%) displayed significant inactivation of RUNX3 (P<0.05).
  • Promoter hypermethylation of RUNX3 was significantly higher in colorectal polyps (64 of 87, 74%) compared to normal colon (2 of 12, 16%) (P=0.001).
  • Serrated polyps such as HPs (17 of 19, 89%) and TSAs (12 of 14, 86%) were significantly more methylated than sTAs (7 of 17, 44%) (P=0.004).
  • RUNX3 hypermethylation was observed in 28 of the total 38 (74%) FAP polyps.
  • Overall, RUNX3 promoter methylation correlated with inactivation of RUNX3 expression in sporadic (27 of 36, 75%) (P=0.022) and FAP (21 of 28, 75%) (P=0.021) polyps.
  • CONCLUSIONS: Our data suggest that RUNX3 inactivation due to promoter hypermethylation in colorectal polyps represents an early event in colorectal cancer (CRC) progression.
  • In addition, epigenetic RUNX3 inactivation is a frequent event in the serrated colonic polyps as well as in the ACF of FAP polyps.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Colonic Neoplasms / genetics. Colonic Neoplasms / pathology. Colonic Polyps / genetics. Colonic Polyps / pathology. Core Binding Factor Alpha 3 Subunit / genetics

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  • (PMID = 19174785.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 3 Subunit; 0 / Runx3 protein, human
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62. Aust DE, Baretton GB, Members of the Working Group GI-Pathology of the German Society of Pathology: Serrated polyps of the colon and rectum (hyperplastic polyps, sessile serrated adenomas, traditional serrated adenomas, and mixed polyps)-proposal for diagnostic criteria. Virchows Arch; 2010 Sep;457(3):291-7
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  • [Title] Serrated polyps of the colon and rectum (hyperplastic polyps, sessile serrated adenomas, traditional serrated adenomas, and mixed polyps)-proposal for diagnostic criteria.
  • Until recently, two major types of colorectal epithelial polyps were distinguished: the adenoma and the hyperplastic polyp.
  • While adenomas-because of their cytological atypia-were recognized as the precursor lesions for colorectal carcinoma, hyperplastic polyps were perceived as harmless lesions without any potential for malignant progression mainly because hyperplastic polyps are missing cytological atypia.
  • Meanwhile, it is recognized that the lesions, formerly classified as hyperplastic, represent a heterogeneous group of polyps with characteristic serrated morphology some of which exhibit a significant risk of neoplastic progression.
  • These serrated lesions show characteristic epigenetic alterations not commonly seen in colorectal adenomas and progress to colorectal carcinoma via the so-called serrated pathway (CpG-island-methylation-phenotype pathway).
  • This group of polyps is comprised not only of hyperplastic polyps, but also of sessile serrated adenomas, traditional serrated adenomas and mixed polyps, showing serrated and "classical" adenomatous features.
  • In a consensus conference of the Working Group of Gastroenterological Pathology of the German Society of Pathology, standardization of nomenclature and diagnostic criteria as well as recommendations for clinical management of these serrated polyps were formulated and are presented herein.
  • [MeSH-major] Colonic Polyps / diagnosis. Precancerous Conditions / diagnosis
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Humans. Rectum / pathology

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  • (PMID = 20617338.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Consensus Development Conference; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 36
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63. Li SR, Wang HH, Hu JC, Li N, Liu YL, Wu ZT, Zheng Y, Wang HH, Wu K, Ye H: [Comparison of three FOBT protocols for colorectal cancer screening in Chinese--a multicenter study]. Zhonghua Yi Xue Za Zhi; 2005 Mar 16;85(10):697-700
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  • RESULTS: 323 eligible patients including 49 colorectal cancers, 60 colon adenomas, 60 chronic colitis, 15 hemorrhoids and 139 normal colon were observed.
  • 41.6% approximately 48.3% of adenomas was found by the 3 protocols, and 87.5% of adenomas over 2 cm in diameter were detected by any one of FOBT.
  • The majority of adenomas in that advanced lesion existed might be detected by FOBT.
  • [MeSH-minor] Adenoma / prevention & control. Colonoscopy. Cost-Benefit Analysis. Female. Humans. Male


64. Mukhopadhyay S, Marhaba A, Sidhu JS: Small advanced neuroendocrine carcinoma of rectum discovered in an adenomatous polyp. Endoscopy; 2005 Dec;37(12):1256-7
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  • [Title] Small advanced neuroendocrine carcinoma of rectum discovered in an adenomatous polyp.
  • [MeSH-major] Carcinoma, Neuroendocrine / secondary. Colonic Polyps / pathology. Liver Neoplasms / secondary. Rectal Neoplasms / pathology

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  • (PMID = 16329031.001).
  • [ISSN] 0013-726X
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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65. Alferez DG, Ryan AJ, Goodlad RA, Wright NA, Wilkinson RW: Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model. Int J Oncol; 2010 Oct;37(4):767-72
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  • [Title] Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model.
  • The Apc(MIN/+) mouse is a well-characterised model of intestinal tumourigenesis in which animals develop macroscopically detectable adenomas.
  • However, most of the adenomas are formed in the small intestine and resolution of events in the colon, the most relevant site for human disease, is limited.
  • Inducing colitis with dextran sodium sulphate (DSS) can selectively enhance the development of lesions in the colon.
  • We demonstrated that a DSS pre-treatment is well tolerated and effective at inducing colon adenomas in an Apc(MIN/+) mouse model.
  • We then investigated the effect of inhibiting vascular endothelial growth factor (VEGFR)- and epidermal growth factor receptor (EGFR)-dependent signalling pathways on the development of adenomas induced in DSS-pretreated (DSS/Apc(MIN/+)) or non-DSS-pretreated (Apc(MIN/+)) mice using vandetanib (ZD6474), a potent and selective inhibitor of VEGFR and EGFR tyrosine kinase activity.
  • Eight-week old Apc(MIN/+) mice were given either drinking water or 1.8% DSS and then vandetanib (ZD6474) (50 mg/kg/day) or vehicle by oral gavage for 28 days and sacrificed 24 h after the last dose and assessed for adenoma formation in the intestines.
  • DSS pre-treatment was well tolerated and significantly enhanced formation of adenomas in the colon of control Apc(MIN/+) mice.
  • Vandetanib treatment significantly reduced adenoma formation in the small intestine by 68% (P=0.001) and the colon by 77% (from 13.8 to 3.1, P=0.01) of DSS-pretreated Apc(MIN/+) mice.
  • In the Apc(MIN/+) group, vandetanib also reduced the mean number of adenomas in the small intestine by 76% (P<0.001) and in the colon by 60% (from 3.9 to 1.5, P=0.1).
  • DSS-pre-treatment increased the resolution of the model, allowing us to confirm statistically significant effects of vandetanib on the development and growth of colon adenomas in the Apc(MIN/+) mouse.
  • [MeSH-major] Adenoma / prevention & control. Antineoplastic Agents / pharmacology. Colitis / chemically induced. Colonic Neoplasms / prevention & control. Dextran Sulfate. Genes, APC. Piperidines / pharmacology. Protein Kinase Inhibitors / pharmacology. Quinazolines / pharmacology

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  • (PMID = 20811697.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CTNNB1 protein, mouse; 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Piperidines; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / beta Catenin; 9042-14-2 / Dextran Sulfate; EC 2.7.10.1 / EGFR protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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66. Yamaguchi T, Yamamoto S, Fujita S, Akasu T, Moriya Y: Long-term outcome of metachronous rectal cancer following ileorectal anastomosis for familial adenomatous polyposis. J Gastrointest Surg; 2010 Mar;14(3):500-5
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  • [Title] Long-term outcome of metachronous rectal cancer following ileorectal anastomosis for familial adenomatous polyposis.
  • BACKGROUND: Total colectomy with ileorectal anastomosis (IRA) for familial adenomatous polyposis (FAP) carries a potential risk of metachronous cancer in the residual rectum.
  • The incidence of dense-type rectal polyps (4/17, 24%) was significantly higher in patients who developed metachronous rectal cancer following IRA compared to that in patients who did not (1/39, 3%).
  • Moreover, 60% of patients with dense-type colon polyps developed metachronous rectal cancer compared to 24% in patients without and 80% of those with dense type rectal polyps developed metachronous rectal cancer compared to 25% without.
  • CONCLUSIONS: Effective IRA requires selection of patients without invasive rectal cancer and without dense rectal polyps in whom long-term postoperative follow-up of the residual rectum is possible.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Anastomosis, Surgical / adverse effects. Ileum / surgery. Neoplasms, Second Primary / etiology. Rectal Neoplasms / etiology. Rectum / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Cohort Studies. Colectomy / adverse effects. Colectomy / methods. Colonic Pouches. Comorbidity. Female. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Risk Assessment. Statistics, Nonparametric. Survival Analysis. Treatment Outcome. Young Adult

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  • (PMID = 19937474.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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67. Kenney BC, Jain D: Identification of lymphatics within the colonic lamina propria in inflammation and neoplasia using the monoclonal antibody D2-40. Yale J Biol Med; 2008 Sep;81(3):103-13
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  • [Title] Identification of lymphatics within the colonic lamina propria in inflammation and neoplasia using the monoclonal antibody D2-40.
  • CONTEXT: Lymphatic vessels are believed to be absent in the colon above the level of the mucularis mucosae.
  • OBJECTIVE: We sought to assess the presence of lymphatics within the colonic lamina propria in neoplastic and inflammatory conditions using the lymphatic endothelium-specific immunohistochemical marker D2-40.
  • DESIGN: Representative sections of normal colon, inflamed colon, hyperplastic polyps, inflammatory polyps, adenomatous polyps, adenomatous polyps containing intramucosal carcinoma, and invasive colonic adenocarcinomas were subjected to immunohistochemical staining with D2-40.
  • RESULTS: Lymphatics were not identified within the lamina propria of normal colon.
  • Additionally, there was a non-significant trend toward higher lymphatic vessel density in cases with increasing inflammation.
  • CONCLUSIONS: Lymphatic vessels are present within the lamina propria of colon in pathologic states, including cases of intramucosal carcinoma.
  • [MeSH-major] Antibodies, Monoclonal / analysis. Biomarkers, Tumor / analysis. Colitis / pathology. Colonic Neoplasms / chemistry. Colonic Neoplasms / pathology. Lymphatic Vessels / pathology. Mucous Membrane / pathology

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  • (PMID = 18827885.001).
  • [ISSN] 1551-4056
  • [Journal-full-title] The Yale journal of biology and medicine
  • [ISO-abbreviation] Yale J Biol Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / monoclonal antibody D2-40
  • [Other-IDs] NLM/ PMC2553648
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68. Konda A, Duffy MC: Surveillance of patients at increased risk of colon cancer: inflammatory bowel disease and other conditions. Gastroenterol Clin North Am; 2008 Mar;37(1):191-213, viii
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  • [Title] Surveillance of patients at increased risk of colon cancer: inflammatory bowel disease and other conditions.
  • Colonoscopic screening with removal of adenomatous polyps in individuals at average risk is known to decrease the incidence and associated mortality from colon cancer.
  • Certain conditions, notably inflammatory bowel disease involving the colon, a family history of polyps or cancer, a personal history of colon cancer or polyps, and other conditions such as acromegaly, ureterosigmoidostomy, and Streptococcus bovis bacteremia are associated with an increased risk of colonic neoplasia.

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  • (PMID = 18313546.001).
  • [ISSN] 0889-8553
  • [Journal-full-title] Gastroenterology clinics of North America
  • [ISO-abbreviation] Gastroenterol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 157
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69. Habermann N, Lund EK, Pool-Zobel BL, Glei M: Modulation of gene expression in eicosapentaenoic acid and docosahexaenoic acid treated human colon adenoma cells. Genes Nutr; 2009 Mar;4(1):73-6
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  • [Title] Modulation of gene expression in eicosapentaenoic acid and docosahexaenoic acid treated human colon adenoma cells.
  • The aim of the study was to compare the modulation of gene expression in LT97 colon adenoma cells in response to EPA and DHA treatment.
  • In our approach, we used preneoplastic adenoma cells which are a relevant model for target cells of chemoprevention.
  • If verified with real time PCR, these results identify genes and targets for chemoprevention of colon cancer.

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  • (PMID = 19234733.001).
  • [ISSN] 1555-8932
  • [Journal-full-title] Genes & nutrition
  • [ISO-abbreviation] Genes Nutr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2654050
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70. Emmons KM, McBride CM, Puleo E, Pollak KI, Clipp E, Kuntz K, Marcus BH, Napolitano M, Onken J, Farraye F, Fletcher R: Project PREVENT: a randomized trial to reduce multiple behavioral risk factors for colon cancer. Cancer Epidemiol Biomarkers Prev; 2005 Jun;14(6):1453-9
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  • [Title] Project PREVENT: a randomized trial to reduce multiple behavioral risk factors for colon cancer.
  • BACKGROUND: This report examines the outcome data for Project PREVENT, a two-site randomized control trial designed to reduce behavioral risk factors for colorectal cancer among individuals who have been diagnosed with adenomatous colon polyps.
  • METHODS: The study sample included 1,247 patients with recent diagnosis of adenomatous colorectal polyps.
  • [MeSH-major] Colonic Neoplasms / prevention & control. Diet. Health Behavior
  • [MeSH-minor] Adenomatous Polyposis Coli / complications. Adult. Aged. Alcohol Drinking. Exercise. Female. Humans. Male. Middle Aged. Risk Factors. Smoking. Telephone

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  • (PMID = 15941955.001).
  • [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 R01 CA74000-04
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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71. Phelps RA, Broadbent TJ, Stafforini DM, Jones DA: New perspectives on APC control of cell fate and proliferation in colorectal cancer. Cell Cycle; 2009 Aug 15;8(16):2549-56
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  • Aberrant Wnt/beta-catenin signaling following loss of the tumor suppressor adenomatous polyposis coli (APC) is thought to initiate colon adenoma formation.
  • However, examination of tumors from familial adenomatous polyposis coli (FAP) patients has failed to confirm the presence of nuclear beta-catenin in early lesions following APC loss despite robust staining in later lesions.
  • This observation presents the possibility that colon adenomas arise through a beta-catenin-independent function of APC.
  • Though there are currently contrasting models to explain colon tumorigenesis, our goal is to begin to reconcile data from multiple different model systems and provide a functional view into the initiation and progression of colon cancer.
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Cell Differentiation / physiology. Colorectal Neoplasms / pathology

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  • (PMID = 19597346.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 94
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72. Young J, Jass JR: The case for a genetic predisposition to serrated neoplasia in the colorectum: hypothesis and review of the literature. Cancer Epidemiol Biomarkers Prev; 2006 Oct;15(10):1778-84
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  • In recent years, an alternative pathway of colorectal cancer development has been described in which serrated polyps replace the traditional adenoma as the precursor lesion.
  • Importantly, serrated polyps and a subset of colorectal cancer show largely nonoverlapping mutation profiles to those found in adenomas and the majority of colorectal cancer.
  • The two most well-characterized syndromes, familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer (Lynch syndrome), both develop via the adenoma-carcinoma pathway and together account for approximately one third of familial colorectal cancer.
  • Further, CIMP is observed in the normal colonic mucosa of individuals with hyperplastic polyposis consistent with a field defect in epigenetic regulation.

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  • (PMID = 17035382.001).
  • [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 / U01 CA097735; United States / PHS HHS / / U-01-74778
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
  • [Number-of-references] 93
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73. Boissan M, De Wever O, Lizarraga F, Wendum D, Poincloux R, Chignard N, Desbois-Mouthon C, Dufour S, Nawrocki-Raby B, Birembaut P, Bracke M, Chavrier P, Gespach C, Lacombe ML: Implication of metastasis suppressor NM23-H1 in maintaining adherens junctions and limiting the invasive potential of human cancer cells. Cancer Res; 2010 Oct 1;70(19):7710-22
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  • We silenced NM23-H1 expression in human hepatoma and colon carcinoma cells and methodologically investigated effects on cell-cell adhesion, migration, invasion, and signaling linked to cancer progression.
  • Analysis of NM23-H1 expression in clinical specimens revealed high expression in premalignant lesions (liver cirrhosis and colon adenoma) and the central body of primary liver or colon tumors, but downregulation at the invasive front of tumors.
  • [MeSH-minor] Actins / metabolism. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cell Line, Tumor. Cell Movement / genetics. Colonic Neoplasms / genetics. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Cytoskeleton / metabolism. Cytoskeleton / pathology. Gene Silencing. Humans. Liver Neoplasms / genetics. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Matrix Metalloproteinase 14 / metabolism. Neoplasm Invasiveness. Wnt Proteins / metabolism


74. Dworakowska D, Gueorguiev M, Kelly P, Monson JP, Besser GM, Chew SL, Akker SA, Drake WM, Fairclough PD, Grossman AB, Jenkins PJ: Repeated colonoscopic screening of patients with acromegaly: 15-year experience identifies those at risk of new colonic neoplasia and allows for effective screening guidelines. Eur J Endocrinol; 2010 Jul;163(1):21-8
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  • [Title] Repeated colonoscopic screening of patients with acromegaly: 15-year experience identifies those at risk of new colonic neoplasia and allows for effective screening guidelines.
  • OBJECTIVE: It is suggested that patients with acromegaly have an increased risk of colorectal cancer and pre-malignant adenomatous polyps.
  • RESULTS: The presence of hyperplastic or adenomatous polyps was assessed in all patients, while one cancer was detected at the second surveillance.
  • At the third surveillance, mean (+/-s.d.) serum IGF1 levels (ng/ml) in patients with hyperplastic polyps were significantly higher than those with normal colons (P<0.05).
  • The presence of an adenoma rather than a normal colon at the first colonoscopy was associated with a significantly increased risk of adenoma at the second (odds ratio (OR) 4.4, 95% confidence interval (CI) 1.9-10.4) and at the third (OR 8.8, 95% CI 2.9-26.5) screens.
  • Conversely, a normal colon at the first surveillance gave a high chance of normal findings at the second (78%) or third surveillance (78%), and a normal colon at the second colonoscopy was associated with normality at the third colonoscopy (81%).
  • CONCLUSIONS: Repeated colonoscopic screening of patients with acromegaly demonstrated a high prevalence of new adenomatous and hyperplastic colonic polyps, dependent on both the occurrence of previous polyps and elevated IGF1 levels.


75. Loffeld SM, Loffeld RJ: Colorectal cancer and adenomas are rare in individuals of Turkish descent living in the Zaanstreek region in the Netherlands. J Cancer Res Clin Oncol; 2010 Sep;136(9):1439-43
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  • [Title] Colorectal cancer and adenomas are rare in individuals of Turkish descent living in the Zaanstreek region in the Netherlands.
  • Screening and detection of its precursor lesion, the adenoma could prevent development of colorectal cancer.
  • AIM: To evaluate the prevalence of colorectal cancer and adenoma in patients living in the Zaanstreek region, the Netherlands, and correlate these findings with ethnicity.
  • MATERIALS AND METHODS: All patients undergoing endoscopy of the colon and rectum during a period of 16 consecutive years in whom colorectal cancer and/or a polyp were diagnosed, were included in this study.
  • A total of 2,744 patients had one or more polyp(s) during endoscopy.
  • CONCLUSION: Colorectal cancer and colonic adenoma are rare in patients of Turkish descent living in the Zaanstreek region, the Netherlands.
  • [MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology

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  • (PMID = 20140623.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2908754
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76. Al-Thihli K, Palma L, Marcus V, Cesari M, Kushner YB, Barkun A, Foulkes WD: A case of Cowden's syndrome presenting with gastric carcinomas and gastrointestinal polyposis. Nat Clin Pract Gastroenterol Hepatol; 2009 Mar;6(3):184-9
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  • BACKGROUND: A 73-year-old white man was referred to a cancer genetics clinic for evaluation of a approximately 20-year history of mixed upper and lower gastrointestinal polyposis, including hyperplastic, inflammatory and adenomatous polyps, colonic ganglioneuromas, and associated diffuse, esophageal glycogenic acanthosis.
  • Multiple hyperplastic polyps and small, sessile polyps were also observed in the gastrectomy specimen.
  • [MeSH-major] Carcinoma / etiology. Gastrointestinal Diseases / etiology. Hamartoma Syndrome, Multiple / complications. Polyps / etiology. Stomach Neoplasms / etiology

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  • (PMID = 19190598.001).
  • [ISSN] 1743-4386
  • [Journal-full-title] Nature clinical practice. Gastroenterology & hepatology
  • [ISO-abbreviation] Nat Clin Pract Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] P6YC3EG204 / Vitamin B 12
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77. Cirocchi R, Coccetta M, De Sol A, Morelli U, Spizzirri A, Cattorini L, Farinella E, Giustozzi G, Sciannameo F: [Minimally invasive treatment of synchronous colorectal tumours]. Chir Ital; 2008 Mar-Apr;60(2):237-41
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  • [Transliterated title] Trattamento mini-invasivo delle neoplasie sincrone del colon-retto.
  • In patients with colorectal cancers synchronous neoplastic lesions are an increasingly frequent finding at preoperative staging; 3% of the cases are other cancers while 33-35% of the synchronous lesions are villous adenomas.
  • The treatment of most colorectal adenomas can be performed by endoscopic poplypectomy.
  • Surgical timing involved performing a sequential exeresis characterised by a cancer resection, followed by resection of the voluminous adenoma: TEM for rectal cancer followed by a laparoscopic right hemicolectomy with an extracorporeal anastomosis for a voluminous villous adenoma (1 patient) and laparoscopic right hemicolectomy with an extracorporeal anastomosis for cancer followed by TEM for a voluminous villous adenoma (2 patients).
  • One patient with left colon cancer associated with a voluminous villous rectal adenoma first underwent TEM for the rectal adenoma and then a left laparoscopic hemicolectomy with an extracorporeal anastomosis in order to ease the transit of the circular mechanical stapler.
  • Another patient with rectal and right colon adenomas first underwent TEM for a voluminous rectal sessile adenoma and later a right hemicolectomy.
  • [MeSH-major] Adenoma / surgery. Colectomy / methods. Colorectal Neoplasms / surgery. Laparoscopy. Microsurgery

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  • (PMID = 18689172.001).
  • [ISSN] 0009-4773
  • [Journal-full-title] Chirurgia italiana
  • [ISO-abbreviation] Chir Ital
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
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78. Tony J, Harish K, Ramachandran TM, Sunilkumar K, Thomas V: Profile of colonic polyps in a southern Indian population. Indian J Gastroenterol; 2007 May-Jun;26(3):127-9
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  • [Title] Profile of colonic polyps in a southern Indian population.
  • BACKGROUND: In Western countries, colonic polyps are usually adenomatous in nature, are evenly distributed along the entire colon in asymptomatic per-sons and show a left-sided predominance in symptomatic patients.
  • Clinical features, colonoscopic description and histologic findings of all patients with polyps were noted.
  • Association of the degree of dysplasia with the size, site and type of polyps and the person's age was assessed.
  • RESULTS: Polyps were seen in 124 (5.1%) of 2412 complete colonoscopies.
  • Mean age of patients with polyps was 58.1 (SD 19.9) years; ninety were men.
  • A majority of polyps (92%) were located in the left colon.
  • They were adenomatous in 99 (79.8%), juvenile in 12 (9.8%), hyperplastic in 11 (8.8 %), inflammatory in 1 (0.8%) and Peutz-Jegher's polyp in 1 (0.8%).
  • Dysplasia was severe in large (>2 cm) polyps compared to small (< 1 cm) ones (p< 0.001).
  • Age of patient and location of polyp had no association with degree of dysplasia.
  • CONCLUSIONS: In southern Indian adults, most colonic polyps are adenomatous and are in the left colon.
  • Large polyps are associated with severe dysplasia.
  • [MeSH-major] Colonic Polyps / epidemiology

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  • (PMID = 17704579.001).
  • [ISSN] 0254-8860
  • [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
  • [Publication-country] India
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79. Lee H, Kim JH, Yang SY, Kong J, Oh M, Jeong DH, Chung JI, Bae KB, Shin JY, Hong KH, Choi I: Peripheral blood gene expression of B7 and CD28 family members associated with tumor progression and microscopic lymphovascular invasion in colon cancer patients. J Cancer Res Clin Oncol; 2010 Sep;136(9):1445-52
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  • [Title] Peripheral blood gene expression of B7 and CD28 family members associated with tumor progression and microscopic lymphovascular invasion in colon cancer patients.
  • PURPOSE: To associate the global gene expression of B7/CD28 family transcripts with pathologic features of colon cancer, we determined the B7/CD28 family transcripts in peripheral blood mononuclear cells (PBMCs) from normal subjects and patients with adenomatous polyps and colon cancer, and correlated the results with pathologic features of colon cancer.
  • METHODS: PBMCs from age-matched normal subjects and patients with adenomatous polyps and colon cancer were analyzed for peripheral blood transcripts (PBTs) of B7/CD28 family using real-time PCR.
  • Differences in expression levels of B7/CD28 PBTs across all cancer stages and between colon cancer patients with or without microscopic lymphovascular invasion (LVI) were analyzed.
  • RESULTS: The results showed a significant upregulation of PBTs of co-inhibitory molecules such as B7-H3 and PD-1 and a significant PBT downregulation of co-stimulatory molecules including CD28 and ICOS in colon cancer patients.
  • In addition, the ratios of PBT expression of CD28 family to B7 family such as CTLA-4 to B7-H2 and PD-1 to B7-H2 were significantly higher in colon cancer patients with microscopic LVI than in those without LVI (P = 0.001 and P = 0.016, respectively).
  • CONCLUSIONS: Our results suggest that B7/CD28 family PBTs may serve as valuable markers reflecting the pathological features of colon cancer.
  • [MeSH-major] Antigens, CD28 / genetics. Antigens, CD80 / genetics. Colonic Neoplasms / genetics. Colonic Neoplasms / pathology. Gene Expression Regulation, Neoplastic. Leukocytes, Mononuclear / pathology

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  • (PMID = 20140740.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD28; 0 / Antigens, CD80
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80. Coppola D, Parikh V, Boulware D, Blanck G: Substantially reduced expression of PIAS1 is associated with colon cancer development. J Cancer Res Clin Oncol; 2009 Sep;135(9):1287-91
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  • [Title] Substantially reduced expression of PIAS1 is associated with colon cancer development.
  • This project was designed to assess PIAS1 expression in colon cancer.
  • METHODS: To determine whether PIAS1, one of the PIAS family members, or IFN-gamma signaling pathway components could be used to stratify colon tumors, we stained tissue microarrays for PIAS1, interferon regulatory factor-1 (IRF-1) and STAT1alpha.
  • RESULTS: PIAS1 staining of the colon cancer tissue microarrays indicated a strong correlation of normal colon cells, and adenomas, with high expression of both PIAS1 and IRF-1.
  • CONCLUSION: The PIAS1 results in particular may represent a basis for new approaches for efficiently distinguishing adenomas from colon cancer.
  • [MeSH-major] Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Disease Progression. Down-Regulation. Protein Inhibitors of Activated STAT / biosynthesis. Protein Inhibitors of Activated STAT / deficiency. Small Ubiquitin-Related Modifier Proteins / biosynthesis. Small Ubiquitin-Related Modifier Proteins / deficiency

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  • (PMID = 19288270.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Interferon Regulatory Factor-1; 0 / PIAS1 protein, human; 0 / Protein Inhibitors of Activated STAT; 0 / Small Ubiquitin-Related Modifier Proteins
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81. Li FE, Ye HJ, Li J, Wang JP, Liu YG, Yu GY, Yin WH: [Clinical, enteroscopic, and pathological characteristics of 796 cases of colorectal polyps]. Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2005 Aug;30(4):463-6
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  • [Title] [Clinical, enteroscopic, and pathological characteristics of 796 cases of colorectal polyps].
  • OBJECTIVE: To study the age, clinical, enteroscopic and pathological characteristics of colorectal polyps and factors affected polyp-carcinoma.
  • METHODS: We analyzed the clinical, enteroscopic and pathological characteristics of 7276 cases of colorectal polyps.
  • RESULTS: The incidence of colorectal polyps was 10.94%, including 521 men and 275 women.
  • The rate of colorectal polyp was 82.29% in 30-69 year olds.
  • The adenomatous, inflammatory, hyperplastic and juvenile polyps were 43.84%, 42.09%, 11.06% and 1.51%, respectively.
  • The canceration rates in villous, mixed and tubular adenomas were 29.73%, 11.11%, and 4.86%.
  • Conclusion The ages between 30-69 tend to suffer from colorectal polyps.
  • Colorectal polyps are more likely to locate in left colon.
  • The common pathological types were adenomatous and inflammatory polyps.
  • There is a high canceration of polyps in the left colon, villous adenomas and > or = 2.0 cm polyps.
  • The broader the pedicles and the larger the diameters of polyps are, the higher the canceration rate.
  • All of the colon polyps should be excised and undergo the pathological examination.
  • [MeSH-major] Colonic Polyps / pathology. Colonoscopy. Colorectal Neoplasms / pathology. Intestinal Polyps / pathology
  • [MeSH-minor] Adenoma / pathology. Adolescent. Adult. Aged. Aged, 80 and over. Cell Transformation, Neoplastic / pathology. Child. Child, Preschool. Female. Humans. Male

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  • (PMID = 16190400.001).
  • [ISSN] 1672-7347
  • [Journal-full-title] Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
  • [ISO-abbreviation] Zhong Nan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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82. Nilbert M, Kristoffersson U, Ericsson M, Johannsson O, Rambech E, Mangell P: Broad phenotypic spectrum in familial adenomatous polyposis; from early onset and severe phenotypes to late onset of attenuated polyposis with the first manifestation at age 72. BMC Med Genet; 2008;9:101
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  • [Title] Broad phenotypic spectrum in familial adenomatous polyposis; from early onset and severe phenotypes to late onset of attenuated polyposis with the first manifestation at age 72.
  • BACKGROUND: Familial adenomatous polyposis (FAP) is typically characterized by multiple colonic polyps and frequent extracolonic features.
  • Whereas the number of colonic polyps has been linked to the APC gene mutation, possible genotype-phenotype correlations largely remain to be defined for the extracolonic manifestations.
  • Two sisters with an insertion in codon 528 (c.1582_1583insGC) both showed severe phenotypes with classical polyposis, upper gastrointestinal polyps and thyroid cancer.
  • A woman with a 3'APC mutation (c.5030_5031insAA) developed colon cancer at age 72 as the first manifestation of attenuated FAP.
  • We report novel APC mutations and present two FAP cases that suggest familial aggregation of thyroid cancer and demonstrate the need to consider attenuated FAP also among elderly patients with colon cancer.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC. Mutation. Phenotype


83. Chimenos-Küstner E, Pascual M, Blanco I, Finestres F: Hereditary familial polyposis and Gardner's syndrome: contribution of the odonto-stomatology examination in its diagnosis and a case description. Med Oral Patol Oral Cir Bucal; 2005 Nov-Dec;10(5):402-9
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  • Familial Adenomatous Polyposis (FAP) and its phenotype variant, Gardner's syndrome, constitute a rare autosomal dominant inherited disorder.
  • They are characterised by the development, generally during the second and third decades of life, of multiple adenomatous polyps in the colon and rectum.
  • These polyps have a high risk of subsequently becoming malignant, which normally occurs in the third and fourth decades of life.
  • As well as colorectal polyps, these individuals can present with extra-colonic symptoms, among which are particularly: gastro-duodenal polyps, dermoid and epidermoid cysts, desmoid tumours, congenital hypertrophy of the retinal pigment epithelium, disorders of the maxillary and skeletal bones and dental anomalies.
  • [MeSH-major] Adenomatous Polyposis Coli / diagnosis. Jaw Neoplasms / etiology. Osteoma / etiology
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / genetics. Adult. Cementoma / diagnosis. Cementoma / etiology. Codon, Nonsense. Diagnosis, Differential. Early Diagnosis. Epidermal Cyst / diagnosis. Epidermal Cyst / etiology. Female. Fibroma / diagnosis. Fibroma / etiology. Gardner Syndrome / complications. Gardner Syndrome / diagnosis. Gardner Syndrome / genetics. Genes, APC. Humans. Hypertrophy. Pedigree. Pigment Epithelium of Eye / abnormalities. Prognosis

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  • (PMID = 16264375.001).
  • [ISSN] 1698-6946
  • [Journal-full-title] Medicina oral, patología oral y cirugía bucal
  • [ISO-abbreviation] Med Oral Patol Oral Cir Bucal
  • [Language] eng; spa
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Codon, Nonsense
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84. Ferrández A, Navarro M, Díez M, Sopena F, Roncalés P, Polo-Tomas M, Sáinz R, Lanas A: Risk factors for advanced lesions undetected at prior colonoscopy: not always poor preparation. Endoscopy; 2010 Dec;42(12):1071-6
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  • BACKGROUND AND STUDY AIM: Colonoscopy is regarded as the gold standard for diagnosis of colonic lesions.
  • However, adenoma miss rates in tandem colonoscopy studies vary from 2 % to 26 %.
  • Undetected lesions were defined as advanced adenoma or colorectal cancer (CRC) not reported in a colonoscopy performed in the previous 2 or 3 years, respectively.
  • Patients with hereditary nonpolyposis CRC (HNPCC) and familial adenomatous polyposis (FAP) were excluded.
  • RESULTS: Between 2002 and 2005, 795 patients were diagnosed with at least one advanced adenoma and 386 with CRC.
  • Among these, 107/795 patients (13.5 %) had advanced adenoma that had been undetected in a previous colonoscopy (39 % [53/135 lesions] in the right colon); 92/107 (86 %) had an undetected advanced adenoma ≥ 10 mm.
  • Previously undetected CRCs were found in 27/386 patients (6.7 %), located in the left colon in 21/27 (78 %); in 7 the area had not been reached in the previous colonoscopy.
  • Risk factors for undetected advanced adenoma were advanced age, male gender, the presence of another advanced adenoma at first colonoscopy, and history of advanced neoplasia.
  • Previously undetected advanced lesions are more frequently found in the left colon and rectum.
  • Risk factors for non-detection of advanced adenoma are similar to those for advanced neoplasia recurrence.
  • Lowering non-detection rates is crucial for correct follow-up recommendations.
  • [MeSH-major] Adenoma / diagnosis. Colonic Polyps / diagnosis. Colonoscopy. Colorectal Neoplasms / diagnosis
  • [MeSH-minor] Adenomatous Polyposis Coli / complications. Age Factors. Aged. Colonic Neoplasms / diagnosis. Colonic Neoplasms / epidemiology. Colonic Neoplasms / pathology. Colorectal Neoplasms, Hereditary Nonpolyposis / complications. False Negative Reactions. Female. Humans. Logistic Models. Male. Middle Aged. Rectal Neoplasms / diagnosis. Rectal Neoplasms / epidemiology. Rectal Neoplasms / pathology. Retrospective Studies. Risk Factors. Sex Factors

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  • [Copyright] © Georg Thieme Verlag KG Stuttgart · New York.
  • (PMID = 20960390.001).
  • [ISSN] 1438-8812
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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85. Fernández-Suárez A, Cordero Fernández C, García Lozano R, Pizarro A, Garzón M, Núñez Roldán A: Clinical and ethical implications of genetic counselling in familial adenomatous polyposis. Rev Esp Enferm Dig; 2005 Sep;97(9):654-65
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  • [Title] Clinical and ethical implications of genetic counselling in familial adenomatous polyposis.
  • The association of specific genetic disturbances with the development of hereditary cancer helps us to understand the risk of suffering from it, the possibility of an earlier diagnosis, and the treatment and prevention of this disease.
  • Familial adenomatous polyposis (FAP) is a pre-neoplastic syndrome characterized by the presence of hundreds of adenomatous polyps in the colon, which develop into a carcinoma.
  • FAP can be diagnosed using sequencing techniques to detect mutations in the germinal line of the APC (adenomatous polyposis coli) gene.
  • [MeSH-major] Adenomatous Polyposis Coli / prevention & control. Genetic Counseling


86. Galamb O, Gyorffy B, Sipos F, Spisák S, Németh AM, Miheller P, Dinya E, Molnár B, Tulassay Z: [Identification of colorectal cancer, adenoma, and inflammatory bowel disease specific gene expression patterns using whole genomic oligonucleotide microarray system]. Orv Hetil; 2007 Nov 4;148(44):2067-79
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  • [Title] [Identification of colorectal cancer, adenoma, and inflammatory bowel disease specific gene expression patterns using whole genomic oligonucleotide microarray system].
  • [Transliterated title] Vastagbél-adenoma, vastagbélrák és IBD-specifikus génexpressziós mintázatok meghatározása teljes genomszintu oligonukleotid microarray-rendszerrel.
  • BACKGROUND: Discrimination and classification of colorectal diseases (adenoma, colorectal cancer, inflammatory bowel disease) using biopsy samples and expression microarrays, has not been solved yet, nevertheless, it can contribute to the understanding of the colonic diseases.
  • METHODS: Total ribonucleic acid was extracted, amplified and biotinylated from frozen colonic biopsies of 15 patients with colorectal cancer, 15 with adenoma, 14 with inflammatory bowel disease and 8 normal controls.
  • RESULTS: Top validated genes included CD44 antigen, met proto-oncogene, chemokine ligand-12, ADAM-like decysin-1 and ATP-binding casette-A8 genes in adenoma; collagen IValpha1, lipocalin-2, calumenin, aquaporin-8 genes in colorectal cancer; and lipocalin-2, ubiquitin D and interferon induced transmembrane protein 2 genes in inflammatory bowel disease.
  • The expression of 94% of the 52 genes measured by Taqman real-time polymerase chain reaction correlated with the results obtained using Affymetrix microarrays at a significance of p < 0.05.
  • [MeSH-major] Adenoma / diagnosis. Colorectal Neoplasms / diagnosis. Gene Expression Profiling. Inflammatory Bowel Diseases / diagnosis. Oligonucleotide Array Sequence Analysis


87. Oset P, Jasińska A, Szcześniak P, Orszulak-Michalak D, Talar-Wojnarowska R, Małecka-Panas E: [Analysis of serum gastrin levels in patients with adenomatous polyps of the colon]. Pol Merkur Lekarski; 2009 May;26(155):458-61
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  • [Title] [Analysis of serum gastrin levels in patients with adenomatous polyps of the colon].
  • Adenomatous polyps are known risk factor of colon cancer.
  • Gastrin is a peptide hormone involved in the growth of both normal and malignant intestinal tissue, which probably may promote progression through the adenoma-carcinoma sequence.
  • AIM OF OUR STUDY: To assess the association between serum gastrin levels and size, type and localization of colonic adenomas.
  • MATERIAL AND METHODS: The study included 60 patients with adenomatous polyps of the colon and 30 healthy volunteers.
  • RESULTS: We observed higher serum gastrin levels in patients with colonic adenomas compared to control group (59.65 pg/ml vs. 46.89 pg/ml; p < 0.05).
  • There was no association between gastrin levels and size, number, localisation and histologic type of polyps (p > 0.05).
  • CONCLUSION: Despite of elevated serum levels in patients with colonic adenomas we did not observe the association between gastrin levels and size, grade of dysplasia and histologic type of polyps.
  • The exact role of hipergastrinemia in process of colon carcinogenesis remains to be determined.
  • [MeSH-major] Adenomatous Polyps / blood. Gastrins / blood

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  • (PMID = 19606697.001).
  • [ISSN] 1426-9686
  • [Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
  • [ISO-abbreviation] Pol. Merkur. Lekarski
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Gastrins
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88. Fujiya M, Moriichi K, Saitoh Y, Watari J, Kohgo Y: Endoscopic piecemeal resection is a practical option to cure colorectal tumors. Dig Endosc; 2009 Jul;21 Suppl 1:S28-30
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  • Endoscopic mucosal resection (EMR) and endoscopic piecemeal resection (EPMR) are therapeutic options widely accepted for the treatment of colon adenoma, intramucosal cancer and minimally invasive submucosal cancer.
  • [MeSH-major] Adenoma / surgery. Colonoscopy / methods. Colorectal Neoplasms / surgery. Intestinal Mucosa / surgery

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  • (PMID = 19691729.001).
  • [ISSN] 1443-1661
  • [Journal-full-title] Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society
  • [ISO-abbreviation] Dig Endosc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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89. Anupindi S, Perumpillichira J, Jaramillo D, Zalis ME, Israel EJ: Low-dose CT colonography in children: initial experience, technical feasibility, and utility. Pediatr Radiol; 2005 May;35(5):518-24
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  • BACKGROUND: CT colonography (CTC) is utilized as a diagnostic tool in the detection of colon polyps and early colorectal cancer in adults.
  • Large studies in the literature, although focused on adult populations, have shown CTC to be a safe, accurate, non-invasive technique.
  • MATERIALS AND METHODS: From November 2001 to April 2004 we evaluated eight patients (3-17 years) with non-contrast CTC.
  • Sensitivity for polyps 5-10 mm was 100%, and sensitivity for polyps 10 mm and larger was 66.7%.
  • [MeSH-minor] Adenomatous Polyposis Coli / diagnostic imaging. Adolescent. Barium Sulfate. Child. Child, Preschool. Colonic Polyps / diagnostic imaging. Colonoscopy. Contrast Media. Enema. Feasibility Studies. Female. Gastrointestinal Hemorrhage / diagnostic imaging. Humans. Image Processing, Computer-Assisted. Imaging, Three-Dimensional. Male. Radiation Dosage. Rectum. Safety. Sensitivity and Specificity

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  • [ErratumIn] Pediatr Radiol. 2005 Jul;35(7):733
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  • (PMID = 15789249.001).
  • [ISSN] 0301-0449
  • [Journal-full-title] Pediatric radiology
  • [ISO-abbreviation] Pediatr Radiol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Contrast Media; 25BB7EKE2E / Barium Sulfate
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90. Ye YN, Wu WK, Shin VY, Bruce IC, Wong BC, Cho CH: Dual inhibition of 5-LOX and COX-2 suppresses colon cancer formation promoted by cigarette smoke. Carcinogenesis; 2005 Apr;26(4):827-34
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  • [Title] Dual inhibition of 5-LOX and COX-2 suppresses colon cancer formation promoted by cigarette smoke.
  • Previous studies indicate that the arachidonic acid-metabolizing enzymes COX-2 and 5-LOX are overexpressed during the process of colonic adenoma formation promoted by cigarette smoke.
  • The aims of the present study were to investigate whether there exists a relationship between COX-2 and 5-LOX, and whether dual inhibition of COX-2 and 5-LOX has an anticarcinogenic effect in the colonic tumorigenesis promoted by cigarette smoke.
  • Results showed that pretreating colon cancer cells with cigarette smoke extract (CSE) promoted colon cancer growth in the nude mouse xenograft model.
  • In an in vitro study, we found that the action of CSE on colon cancer cells was mediated by 5-LOX DNA demethylation.
  • In summary, these results indicate that inhibition of COX-2 may lead to a shunt of arachidonic acid metabolism towards the leukotriene pathway during colonic tumorigenesis promoted by CSE.
  • [MeSH-major] Adenocarcinoma / prevention & control. Colonic Neoplasms / prevention & control. Cyclooxygenase Inhibitors / therapeutic use. Lipoxygenase Inhibitors / therapeutic use. Prostaglandin-Endoperoxide Synthases / drug effects

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  • (PMID = 15637091.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Lipoxygenase Inhibitors; 0 / RNA, Messenger; 0 / Smoke; 1HGW4DR56D / Leukotriene B4; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; K7Q1JQR04M / Dinoprostone
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91. Qasim A, Muldoon C, McKiernan S: Colonic adenoma patients have higher incidence of hyperplastic polyps on surveillance colonoscopy. Eur J Gastroenterol Hepatol; 2009 Aug;21(8):877-81
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  • [Title] Colonic adenoma patients have higher incidence of hyperplastic polyps on surveillance colonoscopy.
  • OBJECTIVES: To determine the incidence of hyperplastic polyps in patients undergoing surveillance colonoscopy and to compare with the prevalence in individuals undergoing index colonoscopy.
  • PATIENTS AND METHODS: This prospective observational study included patients with index colonoscopy findings of adenomas, adenoma with concomitant hyperplastic polyps and advanced neoplasia who subsequently underwent surveillance colonoscopy.
  • On index colonoscopy, adenomas, adenoma with concomitant hyperplastic polyps and advanced neoplasia were present in 61, 35 and 12 patients, respectively.
  • Findings on surveillance examination included hyperplastic polyps in 35 and 57% of patients with past adenomas and adenoma with concomitant hyperplastic polyps, respectively.
  • Hyperplastic polyps, adenomas and advanced neoplasia were found in 155 (4%), 388 (10%) and 60 (1.5%) of patients, respectively.
  • Hyperplastic polyps and adenoma were significantly higher in study group as compared with control group (P >0.5).
  • CONCLUSION: Incidence of hyperplastic polyps is significantly higher on surveillance colonoscopy as compared with the prevalence on index colonoscopy.
  • This may signify a continuous spectrum of biological evolution between hyperplastic polyps and adenomas.
  • [MeSH-major] Adenoma / pathology. Colonic Polyps / pathology. Colonoscopy / methods. Colorectal Neoplasms / pathology


92. du Toit J, Hamilton W, Barraclough K: Risk in primary care of colorectal cancer from new onset rectal bleeding: 10 year prospective study. BMJ; 2006 Jul 8;333(7558):69-70
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  • OBJECTIVE: To measure the risk of colorectal cancer and adenoma with new onset rectal bleeding reported to primary care.
  • MAIN OUTCOME MEASURES: Percentage of participants in whom colorectal cancer or colonic adenoma was identified after investigation of the bowel.
  • Of these, 15 (5.7%, 95% confidence interval 3.2% to 9.2%) had colorectal cancer, and 13 (4.9%, 2.6% to 8.4%) had colonic adenoma.
  • CONCLUSIONS: One in 10 patients aged 45 or more with new onset rectal bleeding had colonic neoplasia, so investigation of the bowel should be offered to all such patients, whether or not they have other symptoms.
  • [MeSH-major] Adenoma / etiology. Colorectal Neoplasms / etiology. Gastrointestinal Hemorrhage / etiology. Rectal Diseases / etiology


93. Durno CA: Colonic polyps in children and adolescents. Can J Gastroenterol; 2007 Apr;21(4):233-9
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  • [Title] Colonic polyps in children and adolescents.
  • Colonic polyps most commonly present with rectal bleeding in children.
  • The isolated juvenile polyp is the most frequent kind of polyp identified in children.
  • 'Juvenile' refers to the histological type of polyp and not the age of onset of the polyp.
  • Adolescents and adults with multiple juvenile polyps are at a significant risk of intestinal cancer.
  • Attenuated familial adenamatous polyposis (AFAP) can occur either by a mutation at the extreme ends of the adenomatous polyposis coli gene or by biallelic mutations in the mutY homologue (MYH) gene.
  • Colonic polyps, including isolated juvenile polyps, juvenile polyposis syndrome, FAP, AFAP and MYH-associated polyposis, are discussed in the present review.
  • [MeSH-major] Colonic Polyps
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / pathology. Adolescent. Child. DNA Glycosylases / genetics. Genes, APC. Genetic Counseling. Genetic Predisposition to Disease. Genetic Testing. Humans. Mutation

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  • (PMID = 17431512.001).
  • [ISSN] 0835-7900
  • [Journal-full-title] Canadian journal of gastroenterology = Journal canadien de gastroenterologie
  • [ISO-abbreviation] Can. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Canada
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
  • [Number-of-references] 47
  • [Other-IDs] NLM/ PMC2657698
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94. Tan KL, Wilson S, O'Neill C, Gordon D, Napier S: Something not quite right: Gardner syndrome diagnosed by multiple cutaneous lesions and genetic testing. Surgeon; 2005 Dec;3(6):412-5
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  • Gardner syndrome is a variant of familial adenomatous polyposis characterized by intestinal adenomatous polyps, which can progress to adenocarcinoma, and a variety of extraintestinal manifestations, including skin cysts, osteomas, soft tissue fibrous tumours and a characteristic ocular lesion.
  • Gardner syndrome was considered only after excision of subcutaneous fibrous tumours from the mastoid region and paraspinal area and was confirmed by genetic testing in spite of the patient's refusal to undergo colonic endoscopic examination.
  • Subsequent resection revealed approximately 70 adenomatous colonic polyps in the colon and rectum but no invasive tumour, highlighting the benefits of genetic testing in treatment planning.

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  • (PMID = 16353862.001).
  • [ISSN] 1479-666X
  • [Journal-full-title] The surgeon : journal of the Royal Colleges of Surgeons of Edinburgh and Ireland
  • [ISO-abbreviation] Surgeon
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
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95. García-Faroldi G, Sánchez-Jiménez F, Fajardo I: The polyamine and histamine metabolic interplay in cancer and chronic inflammation. Curr Opin Clin Nutr Metab Care; 2009 Jan;12(1):59-65
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  • RECENT FINDINGS: The most recent and relevant findings that might reflect a link between the polyamines/histamine metabolic interplay and the development of cancer and chronic inflammation-related diseases include: the observation that histamine catabolism is downregulated in the colonic mucosa of patients with colonic adenoma; the finding that some polyamine and histamine-related metabolites are different between a breast cancer cell line and a reference mammary epithelial cell line; and the demonstration of the critical role that mast cells (a cell type in which the polyamine/histamine metabolic interplay has been confirmed) play in the development of pancreatic tumors.
  • There is still, however, a lack of specific studies elucidating the exact contribution of the polyamine/histamine metabolic interplay in these clinical settings.

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  • (PMID = 19057189.001).
  • [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; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Polyamines; 7LP2MPO46S / S-Adenosylmethionine; 820484N8I3 / Histamine
  • [Number-of-references] 64
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96. Tabuchi M, Kitayama J, Nagawa H: Hypertriglyceridemia is positively correlated with the development of colorectal tubular adenoma in Japanese men. World J Gastroenterol; 2006 Feb 28;12(8):1261-4
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  • [Title] Hypertriglyceridemia is positively correlated with the development of colorectal tubular adenoma in Japanese men.
  • AIM: To determine the real association between serum lipid levels and colonic polyp formation.
  • METHODS: We performed a large scale retrospective study to analyze the correlation between the incidence of colorectal adenoma or carcinoma and the fasting serum levels of total cholesterol (TC) and triglycerides (TG) in patients who underwent total colonoscopy for screening for colon cancer.
  • RESULTS: Both levels were significantly elevated in patients with adenomas as compared with patients without any neoplastic lesion (TC 207.6+/-29.5 vs 199.5+/-34.3, n=4883, P<0.001; TG 135.0+/-82.2 vs 108.7+/-71.5, n=4874, P<0.001).
  • The difference was significant in patients with tubular adenoma but not in those with villous or serrated adenoma.
  • The level of TG in patients with invasive carcinoma did not show a significant elevation from that in patients with adenoma.
  • These findings suggest that hypertriglyceridemia is an independent risk factor for colonic adenoma in men.
  • [MeSH-major] Adenoma / blood. Adenoma / etiology. Colorectal Neoplasms / blood. Colorectal Neoplasms / etiology. Hypertriglyceridemia / complications

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  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
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97. Phelps RA, Chidester S, Dehghanizadeh S, Phelps J, Sandoval IT, Rai K, Broadbent T, Sarkar S, Burt RW, Jones DA: A two-step model for colon adenoma initiation and progression caused by APC loss. Cell; 2009 May 15;137(4):623-34
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  • [Title] A two-step model for colon adenoma initiation and progression caused by APC loss.
  • Aberrant Wnt/beta-catenin signaling following loss of the tumor suppressor adenomatous polyposis coli (APC) is thought to initiate colon adenoma formation.
  • These findings suggest that, following APC loss, CtBP1 contributes to adenoma initiation as a first step, whereas KRAS activation and beta-catenin nuclear localization promote adenoma progression to carcinomas as a second step.
  • Consistent with this model, human FAP adenomas showed robust upregulation of CtBP1 in the absence of detectable nuclear beta-catenin, whereas nuclear beta-catenin was detected in carcinomas.

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  • (PMID = 19450512.001).
  • [ISSN] 1097-4172
  • [Journal-full-title] Cell
  • [ISO-abbreviation] Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA073992; United States / NCI NIH HHS / CA / CA116468-03; United States / NCI NIH HHS / CA / CA073992-06A10003; United States / NCI NIH HHS / CA / R01 CA116468-03; United States / NCI NIH HHS / CA / CA96934; United States / NCI NIH HHS / CA / P01 CA073992-06A10003; United States / NCI NIH HHS / CA / R01 CA116468; United States / NCI NIH HHS / CA / P01 CA073992; United States / NCI NIH HHS / CA / CA116468-04; United States / NCI NIH HHS / CA / CA042014; United States / NCI NIH HHS / CA / P30 CA042014; United States / NCI NIH HHS / CA / R01 CA116468-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / DNA-Binding Proteins; 0 / Peptide Fragments; 0 / Rac1 GTP-binding protein (17-32); 0 / beta Catenin; EC 1.1.- / Alcohol Oxidoreductases; EC 1.1.1.- / C-terminal binding protein; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf; EC 3.6.5.2 / rac1 GTP-Binding Protein; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS102940; NLM/ PMC2706149
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98. Peeters M: Cardiovascular risk status can influence the colorectal cancer screening strategy. Digestion; 2010;81(1):18-9
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