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31. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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 frequency of CDKN2A/p16 promoter methylation was very rare in normal colorectal tissue with a frequency of approximately 2%.
  • 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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32. Jenkins PJ: Cancers associated with acromegaly. Neuroendocrinology; 2006;83(3-4):218-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • More recently, it has become apparent that patients with acromegaly may also have an increased prevalence of colorectal adenomas and cancer.
  • This may be due to elevated IGF-I, which is implicated in the development of sporadic colorectal cancer, and environmental factors, such as the bile acid deoxycholic acid, the levels of which are also increased in acromegaly.
  • Large-scale epidemiological studies are required to clarify this issue.
  • [MeSH-major] Acromegaly / complications. Breast Neoplasms / etiology. Colorectal Neoplasms / etiology. Prostatic Neoplasms / etiology
  • [MeSH-minor] Adenoma / blood. Adenoma / epidemiology. Adenoma / etiology. Carcinoma / blood. Carcinoma / epidemiology. Carcinoma / etiology. Female. Human Growth Hormone / blood. Humans. Male


33. Moslehi R, Chatterjee N, Church TR, Chen J, Yeager M, Weissfeld J, Hein DW, Hayes RB: Cigarette smoking, N-acetyltransferase genes and the risk of advanced colorectal adenoma. Pharmacogenomics; 2006 Sep;7(6):819-29
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cigarette smoking, N-acetyltransferase genes and the risk of advanced colorectal adenoma.
  • BACKGROUND: Cigarette use is associated with greater risk for colorectal adenoma, a colorectal cancer precursor.
  • Our interest is in the polymorphisms within the NAT1 and NAT2 genes that influence the tobacco-colorectal tumor relationship by impacting on the metabolic activation and detoxification of tobacco smoke-derived carcinogens.
  • METHODS: In the Prostate, Lung, Colorectal and Ovarian (PLCO) cancer screening trial, we compared NAT1 and NAT2 gene variant distributions for 772 cases with left-sided advanced adenoma and 777 gender and age-matched controls.
  • RESULTS: Risks for advanced colorectal adenoma were significantly increased among recent smokers (current smokers or those who quit less than 10 years ago) (odds ratio [OR] = 2.3, 95% confidence interval [CI]: 1.7-3.1) and among those who smoked more than 20 cigarettes per day (OR = 1.7, 95% CI: 1.3-2.2), compared with nonsmokers.
  • CONCLUSIONS: Our study indicated that NAT2 gene variants associated with a slow acetylator phenotype were more susceptible to the effects of tobacco smoking with respect to adenoma risk, providing leads for disease prevention.

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  • (PMID = 16981843.001).
  • [ISSN] 1462-2416
  • [Journal-full-title] Pharmacogenomics
  • [ISO-abbreviation] Pharmacogenomics
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-34627; United States / NCI NIH HHS / CA / CA034627-21; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R01 CA034627; United States / NCI NIH HHS / CA / R01 CA034627-21
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Isoenzymes; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / N-acetyltransferase 1; EC 2.3.1.5 / NAT2 protein, human
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4. Hassan C, Zullo A, Winn S, Eramo A, Tomao S, Rossini FP, Morini S: The colorectal malignant polyp: scoping a dilemma. Dig Liver Dis; 2007 Jan;39(1):92-100
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The colorectal malignant polyp: scoping a dilemma.
  • Colorectal adenomas containing invasive carcinoma represent the majority of early colorectal cancers.
  • [MeSH-major] Adenomatous Polyps / pathology. Colonic Polyps / pathology. Colorectal Neoplasms / pathology

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  • (PMID = 17113842.001).
  • [ISSN] 1590-8658
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 80
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35. Ayanian JZ, Sequist TD, Zaslavsky AM, Johannes RS: Physician reminders to promote surveillance colonoscopy for colorectal adenomas: a randomized controlled trial. J Gen Intern Med; 2008 Jun;23(6):762-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Physician reminders to promote surveillance colonoscopy for colorectal adenomas: a randomized controlled trial.
  • BACKGROUND: Most colorectal cancers develop from adenomatous polyps.
  • PATIENTS: Seven hundred seventeen patients who had colorectal adenomas removed during 1995 through 2000 and no follow-up colonoscopy identified via automated review of electronic records through March, 2006.
  • MEASUREMENTS AND MAIN RESULTS: The use of colonoscopy and detection of new adenomas or cancer were assessed at 6 months by a blinded medical record review in all patients.
  • New adenomas or cancer were detected in 14 (3.9%) intervention patients and 6 (1.7%) control patients (P = 0.06), representing 42.4% and 37.5% of patients who underwent colonoscopy in each group, respectively.
  • CONCLUSIONS: Among patients with prior colorectal adenomas, physician reminders increased the use of surveillance colonoscopy, but better systems are needed to identify eligible patients (ClinicalTrials.gov ID number NCT00397969).
  • [MeSH-major] Adenomatous Polyps / diagnosis. Appointments and Schedules. Colonic Polyps / diagnosis. Colonoscopy / utilization. Colorectal Neoplasms / diagnosis. Reminder Systems

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  • (PMID = 18386103.001).
  • [ISSN] 1525-1497
  • [Journal-full-title] Journal of general internal medicine
  • [ISO-abbreviation] J Gen Intern Med
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00397969
  • [Grant] United States / NCI NIH HHS / CA / R21 CA112365; United States / NCI NIH HHS / CA / R21-CA112365
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2517870
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36. Hariri LP, Tumlinson AR, Besselsen DG, Utzinger U, Gerner EW, Barton JK: Endoscopic optical coherence tomography and laser-induced fluorescence spectroscopy in a murine colon cancer model. Lasers Surg Med; 2006 Apr;38(4):305-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND AND OBJECTIVES: The diagnostic feasibility of optical coherence tomography (OCT) and laser-induced fluorescence (LIF) have been evaluated for human colorectal cancer.
  • This study applies these technologies to a murine model of colorectal adenoma.
  • One adenoma was histologically identified; OCT visualized mucosal thickening/abnormal mass development over the imaging timepoints.
  • CONCLUSIONS: These preliminary data indicate endoscopic OCT-LIF has the potential to identify colorectal adenomas in murine models.

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16596657.001).
  • [ISSN] 0196-8092
  • [Journal-full-title] Lasers in surgery and medicine
  • [ISO-abbreviation] Lasers Surg Med
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109385; United States / NCI NIH HHS / CA / CA083148; United States / NCI NIH HHS / CA / CA095060; United States / NCI NIH HHS / CA / CA109385
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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37. Noffsinger AE, Hart J: Serrated adenoma: a distinct form of non-polypoid colorectal neoplasia? Gastrointest Endosc Clin N Am; 2010 Jul;20(3):543-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serrated adenoma: a distinct form of non-polypoid colorectal neoplasia?
  • Until recently, 2 major forms of colorectal polyp were recognized: the adenoma and the hyperplastic polyp.
  • Adenomas were known to represent a precursor to colorectal cancer, whereas hyperplastic polyps were viewed as nonneoplastic, having no potential for progression to malignancy.
  • We now recognize, however, that the lesions diagnosed as hyperplastic polyps in the past represent a heterogeneous group of polyps, some of which truly are hyperplastic, and others that truly have a significant risk for transformation to colorectal cancer.
  • These polyps have a characteristic serrated architecture, and include not only hyperplastic polyps but also the recently recognized serrated adenomas.
  • Serrated adenomas occur in 2 forms: the traditional serrated adenoma, which is usually a polypoid lesion endoscopically, and the sessile serrated adenoma, a flat or slightly raised, usually right-sided lesion.
  • Serrated adenomas of both types show characteristic molecular alterations not commonly seen in traditional colorectal adenomas, and probably progress to colorectal cancer by means of a different pathway, the so-called serrated neoplasia pathway.
  • The morphologic features of serrated colorectal lesions, the molecular alterations that characterize them, and their role in colorectal cancer development are discussed.
  • [MeSH-major] Adenoma / diagnosis. Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis
  • [MeSH-minor] Apoptosis. Colonic Polyps / diagnosis. Colonic Polyps / genetics. Colonic Polyps / pathology. CpG Islands / genetics. DNA Methylation. Disease Progression. Humans. Microsatellite Instability. Mutation. Phenotype. Polymorphism, Genetic. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics. Receptor, EphB2 / genetics. Risk Assessment. ras Proteins / genetics

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20656251.001).
  • [ISSN] 1558-1950
  • [Journal-full-title] Gastrointestinal endoscopy clinics of North America
  • [ISO-abbreviation] Gastrointest. Endosc. Clin. N. Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Receptor, EphB2; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / ras Proteins
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38. Yamaji Y, Okamoto M, Yoshida H, Kawabe T, Wada R, Mitsushima T, Omata M: The effect of body weight reduction on the incidence of colorectal adenoma. Am J Gastroenterol; 2008 Aug;103(8):2061-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effect of body weight reduction on the incidence of colorectal adenoma.
  • OBJECTIVES: Obesity is thought to be associated with colorectal cancer and adenoma.
  • We aimed to investigate the effect of body weight on the risk of colorectal adenoma both in cross-sectional and longitudinal analyses.
  • METHODS: This is a retrospective cohort study in a large-scale health appraisal institution in Japan.
  • The association with the prevalence of colorectal adenoma was evaluated according to the body mass index (BMI) at the initial examination.
  • The incidence of colorectal adenoma at the second colonoscopy was investigated according to the initial BMI and body weight changes during the year.
  • RESULTS: The prevalence of colorectal adenoma increased in relation to increases in the BMI: 15.4%, 20.6%, 22.7%, and 24.2%, respectively, in the first (BMI < 21.350), second (21.350 < or = BMI < 23.199), third (23.199 < or = BMI < 25.156), and fourth (25.156 < or = BMI) quartiles.
  • The incidence rates of colorectal adenoma after 1 yr also increased proportionally according to the initial BMI: Group Q1 (12.9%), Group Q2 (15.7%), Group Q3 (18.3%), and Group Q4 (19.0%).
  • CONCLUSIONS: Obesity was associated with the risk for colorectal adenoma, and body weight reduction was suggested to decrease this risk.
  • [MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Obesity / complications. Weight Loss

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  • (PMID = 18796100.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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39. Hisamuddin IM, Wehbi MA, Yang VW: Pharmacogenetics and diseases of the colon. Curr Opin Gastroenterol; 2007 Jan;23(1):60-6
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  • They affect the management of inflammatory bowel disease, colorectal cancer and the chemoprevention of colorectal adenoma by influencing the metabolism of their respective substrates, azathioprine/6-mercaptopurine, 5-fluorouracil and sulindac.

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  • (PMID = 17133087.001).
  • [ISSN] 0267-1379
  • [Journal-full-title] Current opinion in gastroenterology
  • [ISO-abbreviation] Curr. Opin. Gastroenterol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK052230; United States / NIDDK NIH HHS / DK / DK064399-05; United States / NCI NIH HHS / CA / R01 CA084197-09; United States / NIDDK NIH HHS / DK / R24 DK064399-05; United States / NCI NIH HHS / CA / CA084197-09; United States / NIDDK NIH HHS / DK / R01 DK052230-11; United States / NCI NIH HHS / CA / R01 CA084197; United States / NIDDK NIH HHS / DK / R24 DK064399; United States / NIDDK NIH HHS / DK / DK52230; United States / NIDDK NIH HHS / DK / DK052230-11; United States / NCI NIH HHS / CA / CA84197
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 57
  • [Other-IDs] NLM/ NIHMS37179; NLM/ PMC2213557
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40. Speake D, Biyani D, Frizelle FA, Watson AJ: Flat adenomas. ANZ J Surg; 2007 Jan-Feb;77(1-2):4-8
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  • [Title] Flat adenomas.
  • This article was presented at the conjoint CSSA and RACS (colorectal section) spring meeting Queensland, Australia, September 2004.
  • The adenoma-carcinoma sequence describes a succession of events from polypoid adenoma to colorectal cancer.
  • However, this model only accounts for up to two-thirds of colorectal cancers.
  • There is growing evidence that flat adenomas are precursor lesions to a flat type of colorectal cancer and certain subtypes of these polyps are at greater risk of malignant transformation.
  • If confirmed, the implications for screening, endoscopic recognition and management will become of increasing importance if we are to decrease the incidence of colorectal cancer.
  • [MeSH-major] Adenocarcinoma / physiopathology. Adenoma / physiopathology. Colonic Neoplasms / physiopathology. Colonic Polyps / physiopathology

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  • (PMID = 17295810.001).
  • [ISSN] 1445-1433
  • [Journal-full-title] ANZ journal of surgery
  • [ISO-abbreviation] ANZ J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Number-of-references] 72
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41. Alberts DS, Martínez ME, Hess LM, Einspahr JG, Green SB, Bhattacharyya AK, Guillen J, Krutzsch M, Batta AK, Salen G, Fales L, Koonce K, Parish D, Clouser M, Roe D, Lance P, Phoenix and Tucson Gastroenterologist Networks: Phase III trial of ursodeoxycholic acid to prevent colorectal adenoma recurrence. J Natl Cancer Inst; 2005 Jun 1;97(11):846-53
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  • [Title] Phase III trial of ursodeoxycholic acid to prevent colorectal adenoma recurrence.
  • We conducted a phase III, double-blind placebo-controlled trial of UDCA to evaluate its ability to prevent colorectal adenoma recurrence.
  • METHODS: We randomly assigned 1285 individuals who had undergone removal of a colorectal adenoma within the past 6 months to daily treatment with UDCA (8-10 mg/kg of body weight; 661 participants) or with placebo (624 participants) for 3 years or until follow-up colonoscopy.
  • Recurrence rates (number of recurrent adenomas per unit time) were compared by use of a Huber-White variance estimator.
  • Proportions of participants with one or more recurrent adenomas were compared with a Pearson chi-square statistic; adjusted odds ratios (ORs) were obtained by logistic regression.
  • RESULTS: We observed a non-statistically significant 12% reduction in the adenoma recurrence rate associated with UDCA treatment, compared with placebo treatment.
  • However, UDCA treatment was associated with a statistically significant reduction (P = .03) in the recurrence of adenomas with high-grade dysplasia (adjusted OR = 0.61, 95% confidence interval = 0.39 to 0.96).
  • We observed no statistically significant differences between UDCA and placebo groups in recurrence with regard to adenoma size, villous histology, or location.
  • CONCLUSIONS: UDCA treatment was associated with a non-statistically significant reduction in total colorectal adenoma recurrence but with a statistically significant 39% reduction in recurrence of adenomas with high-grade dysplasia.
  • Because severely dysplastic lesions have a high risk of progression to invasive colorectal carcinoma, this finding indicates that future chemoprevention trials of UDCA in individuals with such lesions should be considered.
  • [MeSH-major] Adenoma / prevention & control. Antineoplastic Agents / therapeutic use. Colorectal Neoplasms / prevention & control. Neoplasm Recurrence, Local / prevention & control. Ursodeoxycholic Acid / therapeutic use

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  • (PMID = 15928305.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-23074; United States / NCI NIH HHS / CA / P01-CA-41108
  • [Publication-type] Clinical Trial; Clinical Trial, Phase III; 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
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 724L30Y2QR / Ursodeoxycholic Acid
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42. Wang JY, Wang YH, Jao SW, Lu CY, Kuo CH, Hu HM, Hsieh JS, Chong IW, Cheng TL, Lin SR: Molecular mechanisms underlying the tumorigenesis of colorectal adenomas: correlation to activated K-ras oncogene. Oncol Rep; 2006 Dec;16(6):1245-52
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  • [Title] Molecular mechanisms underlying the tumorigenesis of colorectal adenomas: correlation to activated K-ras oncogene.
  • Mutations of K-ras gene have been demonstrated in 40-50% of colorectal cancer and large adenoma (>1 cm).
  • This study was intended to clarify the correlation between the existence of K-ras oncogene and the pathological features of colorectal adenomas using our recently developed membrane arrays.
  • Moreover, the downstream genes regulated by K-ras oncogene were explored to serve as potential biomarkers in the early diagnosis and risk assessment of patients with colorectal adenoma.
  • Specimens were collected from 70 patients with colorectal adenoma.
  • Furthermore, activated K-ras oncogene was identified in 18 of 70 (25.7%) adenoma by membrane arrays.
  • The analysis of the correlation between the experimental data and pathological characteristics of adenoma showed that activated K-ras oncogenes were significantly associated with the size, number and histology of adenomas (all P<0.001).
  • Finally, we found the downstream genes activated by K-ras oncogene, including B-cell CLL/lymphoma 2 (BCL2), Homo sapiens H2A histone family, member Z (H2AFZ), Homo sapiens RAP1B, member of RAS oncogene family (RAP1B), Homo sapiens T-box 19 (TBX19), Homo sapiens E2F transcription factor 4, p107/p130-binding (E2F4) and matrix metallopeptidase 1 (MMP1), of which were overexpressed in most of all examined adenomas.
  • Therefore, we propose that activated K-ras oncogene in colorectal adenomas may play an important role in the subsequent colorectal carcinogenesis through a group of K-ras-related molecular targets.
  • [MeSH-major] Adenoma / genetics. Adenoma / pathology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Genes, ras

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  • (PMID = 17089045.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA Primers
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43. Vinikoor LC, Schroeder JC, Millikan RC, Satia JA, Martin CF, Ibrahim J, Galanko JA, Sandler RS: Consumption of trans-fatty acid and its association with colorectal adenomas. Am J Epidemiol; 2008 Aug 1;168(3):289-97
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  • [Title] Consumption of trans-fatty acid and its association with colorectal adenomas.
  • To investigate the association between colorectal adenomas and trans-fatty acid consumption, the authors utilized data from a cross-sectional study of 622 individuals who underwent complete colonoscopy between 2001 and 2002 at the University of North Carolina Hospitals.
  • Participants were interviewed about demographic, lifestyle, and dietary factors thought to be related to colorectal cancer. trans-Fatty acid consumption, energy adjusted by the residual method, was categorized into quartiles based on its distribution in controls.
  • Compared with participants in the lowest quartile of consumption, those in the highest quartile had an increased prevalence of colorectal adenomas, with an adjusted prevalence odds ratio of 1.86 (95% confidence interval: 1.04, 3.33).
  • The authors further investigated the relation between trans-fatty acid consumption and colorectal neoplasia by examining the adenoma characteristics, with the adjusted prevalence odds ratios showing little or no difference by adenoma location, size, or number.
  • These results suggest that consumption of high amounts of trans-fatty acid may increase the risk of colorectal neoplasia, and they provide additional support to recommendations to limit trans-fatty acid consumption.

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  • (PMID = 18587137.001).
  • [ISSN] 1476-6256
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA044684; United States / NIDDK NIH HHS / DK / P30 DK034987; United States / NCI NIH HHS / CA / R01CA44684; United States / NIDDK NIH HHS / DK / P30DK34987; United States / NIDDK NIH HHS / DK / T32 DK007634; United States / NIDDK NIH HHS / DK / T32DK07634
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Trans Fatty Acids
  • [Other-IDs] NLM/ NIHMS64890; NLM/ PMC2533637
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44. Otani T, Iwasaki M, Ikeda S, Kozu T, Saito H, Mutoh M, Wakabayashi K, Tsugane S: Serum triglycerides and colorectal adenoma in a case-control study among cancer screening examinees (Japan). Cancer Causes Control; 2006 Dec;17(10):1245-52
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  • [Title] Serum triglycerides and colorectal adenoma in a case-control study among cancer screening examinees (Japan).
  • OBJECTIVE: Most epidemiologic studies have shown serum triglycerides to be associated with colorectal adenoma.
  • We cross-sectionally investigated the association of serum triglycerides with the risk of adenoma by smoking status.
  • METHODS: We identified 782 newly diagnosed adenoma cases from the examinees of a colorectal cancer screening program.
  • We determined 738 controls without present illness or past history of adenoma from among the examinees.
  • We calculated odds ratios (OR) and 95% confidence intervals (CI) of colorectal adenoma for serum triglycerides.
  • RESULTS: High serum triglycerides were associated with colorectal adenoma (OR 1.5; 95% CI 1.1-2.0 for the highest versus the lowest quartile, P (trend, )0.030).
  • A stronger association was observed between three or more adenoma cases and study controls (OR 2.3; 95% CI 1.3-4.2, P (trend,) < 0.0010).
  • CONCLUSIONS: Our results suggested that a higher serum triglyceride level may be related to a larger number of adenomas.
  • Adenoma development involving an elevated serum triglyceride level may be modified by smoking.
  • [MeSH-major] Adenoma / blood. Adenoma / diagnosis. Colorectal Neoplasms / blood. Colorectal Neoplasms / diagnosis. Mass Screening. Triglycerides / blood

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  • (PMID = 17111255.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Triglycerides
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45. Caswell S, Anderson AS, Steele RJ: Diet and physical activity in patients with colorectal adenomas: directions for intervention programmes. J Hum Nutr Diet; 2008 Oct;21(5):494-501
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  • [Title] Diet and physical activity in patients with colorectal adenomas: directions for intervention programmes.
  • The aim of the current exploratory research was to identify diet and activity habits in adults diagnosed with colorectal adenomas on screening colonoscopy in order to inform the development of an intervention study in this patient group.
  • [MeSH-major] Adenoma / prevention & control. Colorectal Neoplasms / prevention & control. Diet. Exercise

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  • (PMID = 18631284.001).
  • [ISSN] 1365-277X
  • [Journal-full-title] Journal of human nutrition and dietetics : the official journal of the British Dietetic Association
  • [ISO-abbreviation] J Hum Nutr Diet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dietary Carbohydrates; 0 / Dietary Fats; 0 / Dietary Proteins
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46. Fujimoto T, Yoshimatsu K, Watanabe K, Yokomizo H, Otani T, Matsumoto A, Osawa G, Onda M, Ogawa K: Overexpression of human X-box binding protein 1 (XBP-1) in colorectal adenomas and adenocarcinomas. Anticancer Res; 2007 Jan-Feb;27(1A):127-31
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  • [Title] Overexpression of human X-box binding protein 1 (XBP-1) in colorectal adenomas and adenocarcinomas.
  • To investigate the involvement of XBP-1 in colorectal tumorigenecity, the expression of XBP-1 was examined in four colon cancer cell lines, six colorectal polyps and five colorectal carcinomas.
  • MATERIALS AND METHODS: The study population consisted of eleven patients who had undergone resection for colorectal cancer or adenoma from 2000 to 2002.
  • RESULTS: The XBP-1 gene was overexpressed in four cases out of five primary colorectal carcinomas and in four cases out of six colorectal adenomas.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenoma / metabolism. Colorectal Neoplasms / metabolism. DNA-Binding Proteins / biosynthesis. Nuclear Proteins / biosynthesis

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  • (PMID = 17352224.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / regulatory factor X transcription factors
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47. Greenhough A, Wallam CA, Hicks DJ, Moorghen M, Williams AC, Paraskeva C: The proapoptotic BH3-only protein Bim is downregulated in a subset of colorectal cancers and is repressed by antiapoptotic COX-2/PGE(2) signalling in colorectal adenoma cells. Oncogene; 2010 Jun 10;29(23):3398-410
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  • [Title] The proapoptotic BH3-only protein Bim is downregulated in a subset of colorectal cancers and is repressed by antiapoptotic COX-2/PGE(2) signalling in colorectal adenoma cells.
  • Overexpression of cyclooxygenase-2 (COX-2) and elevated levels of its enzymatic product prostaglandin E2 (PGE(2)) occur in the majority of colorectal cancers and have important roles in colorectal tumorigenesis.
  • Here, we have shown that PGE(2) suppresses apoptosis via repression of the proapoptotic BH3-only protein Bim in human colorectal adenoma cells.
  • Reduction of Bim expression using RNA interference reduced spontaneous apoptosis in adenoma cells and abrogated PGE(2)-dependent apoptosis suppression.
  • Treatment of COX-2-expressing colorectal carcinoma cells with COX-2-selective NSAIDs-induced Bim expression, suggesting that Bim repression via PGE(2) signalling may be opposed by COX-2 inhibition.
  • Examination of Bim expression in two established in vitro models of the adenoma-carcinoma sequence revealed that downregulation of Bim expression was associated with tumour progression towards an anchorage-independent phenotype.
  • Finally, immunohistochemical analyses revealed that Bim expression is markedly reduced in approximately 40% of human colorectal carcinomas in vivo.
  • These observations highlight the COX-2/PGE(2) pathway as an important negative regulator of Bim expression in colorectal tumours and suggest that Bim repression may be an important step during colorectal cancer tumorigenesis.
  • [MeSH-major] Adenoma / etiology. Apoptosis Regulatory Proteins / physiology. Colorectal Neoplasms / etiology. Cyclooxygenase 2 / physiology. Dinoprostone / physiology. Membrane Proteins / physiology. Proto-Oncogene Proteins / physiology. Signal Transduction / physiology

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  • (PMID = 20348947.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A5301; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BAD protein, human; 0 / BCL2L11 protein, human; 0 / Bcl-2-Like Protein 11; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / bcl-Associated Death Protein; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.25.1 / Proteasome Endopeptidase Complex; K7Q1JQR04M / Dinoprostone
  • [Other-IDs] NLM/ PMC2883743; NLM/ UKMS28872
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48. Hsu CH, Taylor JM, Long Q, Alberts DS: Analysis of colorectal adenoma recurrence data subject to informative censoring. Cancer Epidemiol Biomarkers Prev; 2009 Mar;18(3):712-7
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  • [Title] Analysis of colorectal adenoma recurrence data subject to informative censoring.
  • The treatment effect of a colorectal polyp prevention trial is often evaluated from the colorectal adenoma recurrence status at the end of the trial.

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  • (PMID = 19240239.001).
  • [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 / P30 CA023074; United States / NCI NIH HHS / CA / P30 CA023074-30; United States / NCI NIH HHS / CA / CA041108-22; United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / CA041108-21; United States / NCI NIH HHS / CA / P30 CA023074-28; None / None / / P30 CA023074-30; United States / NCI NIH HHS / CA / P01 CA041108; United States / NCI NIH HHS / CA / CA23074; United States / NCI NIH HHS / CA / P01 CA041108-21; United States / NCI NIH HHS / CA / P01 CA041108-22; United States / NCI NIH HHS / CA / CA41108
  • [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 / Cholagogues and Choleretics; 724L30Y2QR / Ursodeoxycholic Acid
  • [Other-IDs] NLM/ NIHMS104698; NLM/ PMC2668929
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49. Bertagnolli MM: Cox-2 and cancer chemoprevention: picking up the pieces. Recent Results Cancer Res; 2007;174:73-8
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  • The recent reports of cardiovascular adverse events in patients treated with selective Cox-2 inhibitors for colorectal adenoma prevention remind us that all therapies carry risks as well as benefits.
  • This article will discuss the biologic rationale for using selective Cox-2 inhibitors in cancer chemoprevention, and outline new avenues of research necessary to allow their successful use in patients at risk for colorectal cancer.

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  • (PMID = 17302187.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; EC 1.14.99.1 / Cyclooxygenase 2
  • [Number-of-references] 41
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50. Kang HW, Kim D, Kim HJ, Kim CH, Kim YS, Park MJ, Kim JS, Cho SH, Sung MW, Jung HC, Lee HS, Song IS: Visceral obesity and insulin resistance as risk factors for colorectal adenoma: a cross-sectional, case-control study. Am J Gastroenterol; 2010 Jan;105(1):178-87
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  • [Title] Visceral obesity and insulin resistance as risk factors for colorectal adenoma: a cross-sectional, case-control study.
  • OBJECTIVES: Colorectal adenoma is known to be associated with obesity, but the association between colorectal adenoma and visceral adipose tissue (VAT) area measured by abdominal computed tomography (CT) has not been documented clearly.
  • In addition, the relationship between insulin resistance and colorectal adenomas, which underlies the mechanism that links obesity and colorectal adenoma, has not been studied extensively.
  • The aim of this study was to examine VAT area and insulin resistance as risk factors of colorectal adenoma.
  • VAT, subcutaneous adipose tissue (SAT), and homeostatic metabolic assessment (HOMA) index were evaluated as potential risk factors of colorectal adenoma in 2,244 age- and sex-matched subjects.
  • RESULTS: According to univariate analysis, the prevalences of smoking, hypertension, metabolic syndrome, and family history of colorectal cancer were higher in the adenoma group than in the normal control group.
  • According to the multivariate analysis adjusted for multiple confounders, VAT area was independently associated with the risk of colorectal adenoma (odds ratio (OR)=3.09, 95% confidence interval (CI): 2.19-4.36, highest quintile vs. lowest quintile).
  • Mean HOMA index was higher in the adenoma group than in the control group (OR=1.99, 95% CI: 1.35-2.92, highest vs. lowest quintile).
  • CONCLUSIONS: Visceral obesity was found to be an independent risk factor of colorectal adenoma, and insulin resistance was associated with the presence of colorectal adenoma.
  • [MeSH-major] Adenoma / etiology. Colorectal Neoplasms / etiology. Insulin Resistance. Intra-Abdominal Fat / pathology. Obesity / complications

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  • [CommentIn] Am J Gastroenterol. 2010 Jul;105(7):1677 [20606672.001]
  • (PMID = 19755965.001).
  • [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 / Lipids
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51. Bresalier RS, Sandler RS, Quan H, Bolognese JA, Oxenius B, Horgan K, Lines C, Riddell R, Morton D, Lanas A, Konstam MA, Baron JA, Adenomatous Polyp Prevention on Vioxx (APPROVe) Trial Investigators: Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial. N Engl J Med; 2005 Mar 17;352(11):1092-102
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  • [Title] Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial.
  • We report on the cardiovascular outcomes associated with the use of the selective COX-2 inhibitor rofecoxib in a long-term, multicenter, randomized, placebo-controlled, double-blind trial designed to determine the effect of three years of treatment with rofecoxib on the risk of recurrent neoplastic polyps of the large bowel in patients with a history of colorectal adenomas.
  • METHODS: A total of 2586 patients with a history of colorectal adenomas underwent randomization: 1287 were assigned to receive 25 mg of rofecoxib daily, and 1299 to receive placebo.
  • CONCLUSIONS: Among patients with a history of colorectal adenomas, the use of rofecoxib was associated with an increased cardiovascular risk.
  • [MeSH-major] Adenomatous Polyps / prevention & control. Cardiovascular Diseases / chemically induced. Colorectal Neoplasms / prevention & control. Cyclooxygenase Inhibitors / adverse effects. Lactones / adverse effects. Sulfones / adverse effects. Thrombosis / chemically induced


52. Bresalier RS: Chemoprevention of colorectal cancer: why all the confusion? Curr Opin Gastroenterol; 2008 Jan;24(1):48-50
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  • [Title] Chemoprevention of colorectal cancer: why all the confusion?
  • PURPOSE OF REVIEW: Chemoprevention provides an opportunity to complement screening for the prevention of colorectal neoplasia.
  • RECENT FINDINGS: A recent prospective randomized trial demonstrates that folic acid supplementation in patients with a previous history of colorectal adenomas does not reduce future colorectal adenoma risk, and may possibly increase the risk of colorectal neoplasia.
  • [MeSH-major] Colorectal Neoplasms / prevention & control. Diet. Folic Acid / pharmacology

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  • (PMID = 18043232.001).
  • [ISSN] 1531-7056
  • [Journal-full-title] Current opinion in gastroenterology
  • [ISO-abbreviation] Curr. Opin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 935E97BOY8 / Folic Acid; SY7Q814VUP / Calcium
  • [Number-of-references] 13
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53. Taylor JC, Kendall CA, Stone N, Cook TA: Optical adjuncts for enhanced colonoscopic diagnosis. Br J Surg; 2007 Jan;94(1):6-16
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  • [Title] Optical adjuncts for enhanced colonoscopic diagnosis.
  • BACKGROUND: Optical techniques using previously unexploited properties of light interaction with tissue may be valuable in the detection, diagnosis and staging of colorectal neoplasia.
  • METHODS: A Medline search (1990 to present) was conducted on optical diagnostics in the detection of colorectal neoplasia.
  • RESULTS AND CONCLUSION: Chromoendoscopy is the only optical adjunct to colonoscopy that has been tested in large randomized clinical trials.
  • It improves the detection of small and flat colorectal adenomas, and of neoplasia in chronic ulcerative colitis and hereditary non-polyposis colorectal cancer.
  • Optical techniques may, however, permit immediate clinical diagnosis, removing the need for histological analysis.
  • They may also improve the diagnosis of early colonic neoplasia.
  • [MeSH-major] Colonoscopy / methods. Colorectal Neoplasms / diagnosis

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  • [Copyright] Copyright 2007 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.
  • (PMID = 17205497.001).
  • [ISSN] 0007-1323
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Grant] United Kingdom / Department of Health / / CSA/03/07/017
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 87
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54. Wang J, Wang X, Gong W, Mi B, Liu S, Jiang B: Increased expression of beta-catenin, phosphorylated glycogen synthase kinase 3beta, cyclin D1, and c-myc in laterally spreading colorectal tumors. J Histochem Cytochem; 2009 Apr;57(4):363-71
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  • [Title] Increased expression of beta-catenin, phosphorylated glycogen synthase kinase 3beta, cyclin D1, and c-myc in laterally spreading colorectal tumors.
  • Laterally spreading tumors (LSTs) are considered a special subtype of superficial colorectal tumor.
  • This study was performed to characterize the clinicopathological features and examine activation of the Wnt/beta-catenin pathway in LSTs and protruded-type colorectal adenomas (PAs).
  • [MeSH-major] Colorectal Neoplasms / metabolism. Cyclin D1 / biosynthesis. Glycogen Synthase Kinase 3 / biosynthesis. Proto-Oncogene Proteins c-myc / biosynthesis. beta Catenin / biosynthesis
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Biomarkers, Tumor / biosynthesis. Humans. Immunohistochemistry. Phosphorylation

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  • (PMID = 19064714.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ PMC2664982
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55. Arslan N, Dehdashti F, Siegel BA: FDG uptake in colonic villous adenomas. Ann Nucl Med; 2005 Jun;19(4):331-4
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  • [Title] FDG uptake in colonic villous adenomas.
  • Colonic adenomas constitute 70-80% of all colorectal polyps, and their clinical significance relates primarily to their relationship with colorectal cancer.
  • The malignant potential of the polyps detected by FDG-PET is unknown, as not all the colonic lesions identified by FDG-PET represent colorectal malignancies.
  • The purpose of this study was to investigate the rate of FDG-PET positivity within colonic villous adenomas.
  • A pathology database search was performed to identify all patients diagnosed with colonic villous adenoma between June 1, 1996 and December 1, 2000.
  • Patients with a pathologic diagnosis of colonic villous adenoma and who also had a FDG-PET study up to 1 month before colonoscopy were included in this study.
  • Of more than 4,000 patients, six patients were diagnosed with colonic adenoma on subsequent colonoscopy following FDG-PET study.
  • Based on the pathological findings, these 6 patients had a total of 2 villous and 9 tubulovillous adenomas.
  • Five of the 6 patients showed foci of increased FDG uptake in the region of the colon that corresponded to the villous adenoma(s) detected on colonoscopy, which accounted for a true-positive rate of 83.3% (5/6 subjects).
  • Focal lesions in the colon seen on FDG-PET examinations need to be investigated further, even though some of these will prove to be villous adenomas rather than colorectal carcinomas.
  • [MeSH-major] Adenoma, Villous / radionuclide imaging. Colorectal Neoplasms / radionuclide imaging. Fluorodeoxyglucose F18 / pharmacokinetics. Positron-Emission Tomography / methods

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  • (PMID = 16097645.001).
  • [ISSN] 0914-7187
  • [Journal-full-title] Annals of nuclear medicine
  • [ISO-abbreviation] Ann Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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56. Li ZX, Zeng SD, Liu YD, Liao YJ, Hua WF, Lin F, Xie D: [Clinicopathological significance of expression and amplification of P21-activated kinase 1 gene in colorectal carcinoma]. Zhonghua Wei Chang Wai Ke Za Zhi; 2009 Mar;12(2):185-8
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  • [Title] [Clinicopathological significance of expression and amplification of P21-activated kinase 1 gene in colorectal carcinoma].
  • OBJECTIVE: To investigate the clinicopathological value of the expression and amplification of P21-activated kinase 1 gene (PAK1) in colorectal carcinoma(CRC).
  • METHODS: Immunohistochemistry (IHC), fluorescence in situ hybridization (FISH) and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling(TUNEL) methods were used to examine the protein expression, amplification of PAK1 and cell apoptosis in 80 cases of CRC and 30 cases of colorectal adenoma by tissue microarray.
  • RESULTS: IHC showed an overexpression of PAK1 protein in 26% of colorectal adenomas and 62% of CRCs.
  • CONCLUSIONS: Overexpression of PAK1 protein may play an important role in development and progression of colorectal neoplasms and it is closely associated with the malignant histological and invasive phenotype of CRCs.
  • [MeSH-major] Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. p21-Activated Kinases / genetics

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  • (PMID = 19296259.001).
  • [ISSN] 1671-0274
  • [Journal-full-title] Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery
  • [ISO-abbreviation] Zhonghua Wei Chang Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.11.1 / PAK1 protein, human; EC 2.7.11.1 / p21-Activated Kinases
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57. Boutron-Ruault MC, Marteau P, Lavergne-Slove A, Myara A, Gerhardt MF, Franchisseur C, Bornet F, Eripolyp Study Group: Effects of a 3-mo consumption of short-chain fructo-oligosaccharides on parameters of colorectal carcinogenesis in patients with or without small or large colorectal adenomas. Nutr Cancer; 2005;53(2):160-8
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  • [Title] Effects of a 3-mo consumption of short-chain fructo-oligosaccharides on parameters of colorectal carcinogenesis in patients with or without small or large colorectal adenomas.
  • Intervention studies of colorectal adenoma recurrence have demonstrated the need for surrogate markers of the cancer risk.
  • We investigated differences in biological markers between adenoma and adenoma-free subjects, before and after 3 mo of daily intake of 10 g sc-FOS, within a multicenter study.
  • After a full colonoscopy, 3 groups were studied at baseline and after 3 mo: 26 subjects with small colorectal adenoma(s), 18 with large adenoma(s), and 30 with no adenoma.
  • At baseline, the mean fecal butyrate concentration was significantly lower in the adenoma groups than in the adenoma-free group (12.01 +/- 5.08 vs. 17.28 +/- 7.34 mmol/g dry weight) but was significantly increased in that group after 3-mo ingestion of sc-FOS (15.7 +/- 8.0 mmol/g; P = 0.02).
  • In subjects without adenoma, sc-FOS ingestion was associated with a decrease in fecal lithocholic acid (P = 0.02) and an increase in cholic acid (P = 0.02), chenodeoxycholic acid (P = 0.04), total primary bile acids (P = 0.03), and ursodeoxycholic acid (P = 0.05).
  • In subjects with and without adenoma, sc-FOS affects some aspects of the colonic environment, which may be involved in prevention of colorectal neoplasia.
  • [MeSH-major] Adenoma / drug therapy. Colorectal Neoplasms / drug therapy. Feces / chemistry. Oligosaccharides / pharmacology

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  • (PMID = 16573377.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / Biomarkers; 0 / Butyrates; 0 / Oligosaccharides; 0 / fructooligosaccharide; 724L30Y2QR / Ursodeoxycholic Acid
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58. Mroczko B, Groblewska M, Wereszczynska-Siemiatkowska U, Kedra B, Konopko M, Szmitkowski M: The diagnostic value of G-CSF measurement in the sera of colorectal cancer and adenoma patients. Clin Chim Acta; 2006 Sep;371(1-2):143-7
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  • [Title] The diagnostic value of G-CSF measurement in the sera of colorectal cancer and adenoma patients.
  • Cancer cells, including colorectal cancer, can produce this cytokine.
  • The aim of this study was to compare the diagnostic value of measurement of G-CSF and classic tumor markers--carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA 19-9) in the sera of colorectal cancer with adenoma patients and to determine its usefulness in the diagnosis of colorectal cancer and polyps.
  • PATIENTS AND METHODS: The serum levels of G-CSF and tumor markers were assayed in 76 colorectal cancer, 35 colorectal adenoma patients and in 65 healthy subjects.
  • RESULTS: Median values of G-CSF and tumor markers were significantly higher in colorectal cancer patients than those in healthy subjects.
  • There were significant differences in the serum levels of G-CSF between adenoma patients and healthy subjects.
  • The concentrations of tumor markers in colorectal cancer patients were higher than those in polyps.
  • Combined use of G-CSF with CEA improved their diagnostic sensitivity in colorectal cancer.
  • CONCLUSIONS: Measurement of G-CSF might be useful in the diagnosis of colorectal cancer patients, but not in the differentiation between colorectal cancer and polyps.
  • [MeSH-major] Adenoma / diagnosis. Biomarkers, Tumor / blood. Colorectal Neoplasms / diagnosis. Granulocyte Colony-Stimulating Factor / blood

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  • (PMID = 16603145.001).
  • [ISSN] 0009-8981
  • [Journal-full-title] Clinica chimica acta; international journal of clinical chemistry
  • [ISO-abbreviation] Clin. Chim. Acta
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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59. Baron JA: Statins and the colorectum: hope for chemoprevention? Cancer Prev Res (Phila); 2010 May;3(5):573-5
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  • This perspective on Bertagnolli et al. (beginning on p. 588 in this issue of the journal) and Lipkin et al. (beginning on p. 597) considers the likelihood that statins have chemopreventive efficacy in the large bowel.
  • An observational analysis within a clinical trial of celecoxib found no benefit of statin use on the risk of colorectal adenomas (and some suggestions of an adverse effect).
  • On the other hand, variation in the 3-hydroxy-3-methylglutaryl coenzyme A reductase gene modified the association of statins with risk of colorectal cancer.
  • [MeSH-major] Chemoprevention / methods. Colorectal Neoplasms / prevention & control. Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use

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  • [CommentOn] Cancer Prev Res (Phila). 2010 May;3(5):588-96 [20403998.001]
  • [CommentOn] Cancer Prev Res (Phila). 2010 May;3(5):597-603 [20403997.001]
  • (PMID = 20403999.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] eng
  • [Publication-type] Comment; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticholesteremic Agents; 0 / Antineoplastic Agents; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • [Number-of-references] 27
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60. Kloor M, Michel S, Buckowitz B, Rüschoff J, Büttner R, Holinski-Feder E, Dippold W, Wagner R, Tariverdian M, Benner A, Schwitalle Y, Kuchenbuch B, von Knebel Doeberitz M: Beta2-microglobulin mutations in microsatellite unstable colorectal tumors. Int J Cancer; 2007 Jul 15;121(2):454-8
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  • [Title] Beta2-microglobulin mutations in microsatellite unstable colorectal tumors.
  • MSI-H cancers may develop either sporadically or in the context of the hereditary nonpolyposis colorectal cancer (HNPCC) syndrome that is caused by germline mutations of MMR genes.
  • In colorectal cancer (CRC), MSI-H is characterized by a dense lymphocytic infiltration, reflecting a high immunogenicity of these cancers.
  • To examine the implications of beta2m mutations during MSI-H colorectal tumor development, we analyzed the prevalence of beta2m mutations in MSI-H colorectal adenomas (n=38) and carcinomas (n=104) of different stages.
  • Mutations were observed in 6/38 (15.8%) MSI-H adenomas and 29/104 (27.9%) MSI-H CRCs.
  • The high frequency of beta2m mutations in HNPCC-associated MSI-H CRCs is in line with the hypothesis that immunoselection may be particularly pronounced in HNPCC patients with inherited predisposition to develop MSI-H cancers. beta2m mutations were positively related to stage in tumors without distant metastases (UICC I-III), suggesting that loss of beta2m expression may promote local progression of colorectal MSI-H tumors.
  • [MeSH-major] Colorectal Neoplasms / pathology. Microsatellite Repeats / genetics. Mutation. beta 2-Microglobulin / genetics

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17373663.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / MLH1 protein, human; 0 / Nuclear Proteins; 0 / beta 2-Microglobulin; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein
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61. Ulrich CM, Whitton J, Yu JH, Sibert J, Sparks R, Potter JD, Bigler J: PTGS2 (COX-2) -765G &gt; C promoter variant reduces risk of colorectal adenoma among nonusers of nonsteroidal anti-inflammatory drugs. Cancer Epidemiol Biomarkers Prev; 2005 Mar;14(3):616-9
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  • [Title] PTGS2 (COX-2) -765G > C promoter variant reduces risk of colorectal adenoma among nonusers of nonsteroidal anti-inflammatory drugs.
  • For colorectal adenoma, odds ratios (OR) compared with PTGS2 -765GG as reference were GC 1.00 [95% confidence interval (95% CI), 0.74-1.35] and CC 0.53 (95% CI, 0.22-1.28).
  • Among nonusers of aspirin or other NSAIDs, the CC genotype conferred a significant decrease in risk of adenoma (OR, 0.26; 95% CI, 0.07-0.89).
  • Use of aspirin or other NSAIDs reduced risk of adenoma only among those with the -765GG (wild type) and possibly -765CG genotypes (OR, 0.66; 95% CI, 0.48-0.92 and OR, 0.64; 95% CI, 0.40-1.02, respectively).
  • These data suggest that COX-2 expression or activity may be beneficially suppressed, and risk of colorectal polyps reduced, by aspirin or other NSAIDs in PTGS2 -765GG (wild type) individuals and by the -765 CC variant genotype in nonusers of NSAIDs.
  • [MeSH-major] Adenoma / genetics. Adenoma / prevention & control. Colorectal Neoplasms / genetics. Colorectal Neoplasms / prevention & control. Peroxidases / genetics. Polymorphism, Genetic. Prostaglandin-Endoperoxide Synthases / genetics

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  • [ErratumIn] Cancer Epidemiol Biomarkers Prev. 2005 Dec;14(12):3020
  • (PMID = 15767339.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA59045; United States / NCI NIH HHS / CA / R01CA89445
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Membrane Proteins; EC 1.11.1.- / Peroxidases; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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62. Moreira LR, Schenka AA, Filho PL, Lima CS, Trevisan MA, Vassallo J: Comparison of blood neoangiogenesis and lymphatic vascularization in colorectal adenomas from patients with and without concomitant colorectal cancer. Braz J Med Biol Res; 2009 Jul;42(7):593-8
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  • [Title] Comparison of blood neoangiogenesis and lymphatic vascularization in colorectal adenomas from patients with and without concomitant colorectal cancer.
  • Most colorectal carcinomas develop from adenomas (adenoma-carcinoma sequence) in a process due to accumulation of molecular genetic alterations.
  • Adenomas from patients with carcinoma showed significantly higher values of total vascular area determined by immunostaining for CD105 (cutoff value = 4386 microm(2); P = 0.019) and of lymphatic microvessel density determined by immunostaining with D2-40 (cutoff value = 11.5; P = 0.041) when compared with those from patients without cancer.
  • The present data indicate a significant increase in blood microvascular area and in lymphatic microvascular counts in adenomas removed from patients with cancer.

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  • (PMID = 19466284.001).
  • [ISSN] 1414-431X
  • [Journal-full-title] Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • [ISO-abbreviation] Braz. J. Med. Biol. Res.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD; 0 / Biomarkers; 0 / ENG protein, human; 0 / Receptors, Cell Surface; 0 / monoclonal antibody D2-40
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63. Rowan A, Halford S, Gaasenbeek M, Kemp Z, Sieber O, Volikos E, Douglas E, Fiegler H, Carter N, Talbot I, Silver A, Tomlinson I: Refining molecular analysis in the pathways of colorectal carcinogenesis. Clin Gastroenterol Hepatol; 2005 Nov;3(11):1115-23
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  • [Title] Refining molecular analysis in the pathways of colorectal carcinogenesis.
  • BACKGROUND & AIMS: In the stepwise model, specific genetic and epigenetic changes accumulate as colorectal adenomas progress to carcinomas (CRCs).
  • [MeSH-major] Carcinoma / genetics. Colorectal Neoplasms / genetics

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  • (PMID = 16271343.001).
  • [ISSN] 1542-3565
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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64. Martínez ME, Jacobs ET, Ashbeck EL, Sinha R, Lance P, Alberts DS, Thompson PA: Meat intake, preparation methods, mutagens and colorectal adenoma recurrence. Carcinogenesis; 2007 Sep;28(9):2019-27
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  • [Title] Meat intake, preparation methods, mutagens and colorectal adenoma recurrence.
  • Red meat intake has been shown to be associated with higher risk of colorectal cancer.
  • We prospectively assessed the relation between type of meat, meat preparation method, doneness, a metric of HCAs and other mutagens and colorectal adenoma recurrence among 869 participants in a chemoprevention trial of ursodeoxycholic acid.
  • Most meat variables assessed were positively but weakly associated with recurrence of any adenoma.
  • In contrast, recurrence of advanced or multiple adenomas was more strongly associated with a number of the meat exposure variables evaluated.
  • Significant positive associations were shown for recurrence of multiple adenomas and the following variables: processed meat (OR = 1.83; 95% CI = 1.10-3.04), pan-fried red meat (OR = 1.63; 95% CI = 1.01-2.61), well/very well done red meat (OR = 1.68; 95% CI = 1.03-2.74), 2-amino-3,4,8-trimethylimidazo[4,5,-f]quinoxaline (OR = 1.74; 95% CI = 1.07-2.82) and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (OR = 1.68; 95% CI = 1.03-2.75).
  • [MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Cooking / methods. Meat / analysis. Mutagens / analysis

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  • (PMID = 17690112.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-23074; United States / NCI NIH HHS / CA / CA-41108; United States / NCI NIH HHS / CA / CA106269; United States / NCI NIH HHS / CA / CA95060
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Mutagens; 724L30Y2QR / Ursodeoxycholic Acid
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65. Heitman SJ, Ronksley PE, Hilsden RJ, Manns BJ, Rostom A, Hemmelgarn BR: Prevalence of adenomas and colorectal cancer in average risk individuals: a systematic review and meta-analysis. Clin Gastroenterol Hepatol; 2009 Dec;7(12):1272-8
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  • [Title] Prevalence of adenomas and colorectal cancer in average risk individuals: a systematic review and meta-analysis.
  • BACKGROUND & AIMS: There is an extensive yet inconsistent body of literature reporting on the prevalence of adenomatous polyps (adenomas) and colorectal cancer among average risk individuals.
  • The objectives of our study were to determine the pooled prevalence of adenomas and colorectal cancer, as well as nonadvanced and advanced adenomas, among average risk North Americans.
  • Two reviewers independently selected cross-sectional studies reporting adenoma and colorectal cancer prevalence rates in average risk individuals and assessed studies for inclusion and quality, and extracted the data for analysis.
  • Pooled adenoma and colorectal cancer prevalence rates were estimated using fixed and random effects models.
  • RESULTS: Based on 18 included studies, the pooled prevalence of adenomas, colorectal cancer, nonadvanced adenomas, and advanced adenomas was 30.2%, 0.3%, 17.7%, and 5.7%, respectively.
  • Heterogeneity was observed in the pooled prevalence rates for overall adenomas, advanced adenomas, and colorectal cancer and was explained by the mean age (> or = 65 years vs < 65 years) with older cohorts reporting higher prevalence rates.
  • CONCLUSIONS: The high prevalence of advanced adenomas and colorectal cancer, especially among older screen-eligible individuals, provides impetus for expanding colorectal cancer screening programs.
  • [MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology

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  • (PMID = 19523536.001).
  • [ISSN] 1542-7714
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 40
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66. Cao J, Chen XP, Li WL, Xia J, Du H, Tang WB, Wang H, Chen XW, Xiao HQ, Li YY: Decreased fragile histidine triad expression in colorectal cancer and its association with apoptosis inhibition. World J Gastroenterol; 2007 Feb 21;13(7):1018-26
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  • [Title] Decreased fragile histidine triad expression in colorectal cancer and its association with apoptosis inhibition.
  • AIM: To detect the expression of fragile histidine triad (FHIT) in normal colorectal tissue, colorectal adenoma and colorectal cancer (CRC) tissue, and to analyze its relationship with the clinicopathological features of CRC, and apoptosis-associated proteins (Bcl-2, Bax, survivin) and apoptosis in colorectal cancer.
  • Tissue microarray (TMA) was established to detect the expression of FHIT, Bcl-2, Bax and survivin genes in 80 CRC tissue specimens, 16 colorectal adenoma tissue specimens and 16 hemorrhoid (PPH) tissue specimens during the same period of time as the control.
  • RESULTS: Ten out of 26 (38.5%) CRC tissue specimens expressed aberrant FHIT transcripts, none of the aberrant FHIT transcripts was observed in the matched normal tissue and colorectal adenoma tissue by nested RT-PCR assay.
  • The positive rate of FHIT gene expression in normal colorectal tissue, colorectal adenoma and carcinoma tissue was 93.75%, 68.75% and 46.25%, respectively.
  • CONCLUSION: The FHIT gene plays an important role in the regulation of apoptosis and decreased FHIT expression plays a key role in the initiation and progression of colorectal carcinoma.
  • [MeSH-major] Acid Anhydride Hydrolases / metabolism. Adenocarcinoma / metabolism. Adenoma / metabolism. Apoptosis / physiology. Colorectal Neoplasms / metabolism. Neoplasm Proteins / metabolism

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  • (PMID = 17373735.001).
  • [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
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; 0 / fragile histidine triad protein; EC 3.6.- / Acid Anhydride Hydrolases
  • [Other-IDs] NLM/ PMC4146863
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67. Sun Y, Tian H, Xiao FM, Xie XY, Song YG: [PI3K p85alpha expression and its role in the progression of colorectal cancer]. Nan Fang Yi Ke Da Xue Xue Bao; 2009 Mar;29(3):416-8
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  • [Title] [PI3K p85alpha expression and its role in the progression of colorectal cancer].
  • OBJECTIVE: To investigate the expression of PI3K p85alpha in normal colorectal tissue, colorectal adenoma and primary colorectal carcinoma and explore its significance in the progression of colorectal cancer.
  • METHODS: The expression of PI3K p85alpha was detected in 116 normal colorectal tissue, colorectal adenoma and primary colorectal carcinoma specimens using immunohistochemical staining, and the relationship between the expression of PI3K p85alpha protein and the clinicopathological factors was analyzed.
  • RESULTS: The positivity rates of the expression of PI3K p85alpha protein increased gradually in the progression of colorectal cancer and showed significant differences between the tissues (P<0.05).
  • A significant difference was also noted in the positivity rates of the PI3K p85alpha expression in colorectal carcinoma tissues at different Dukes' stages (P<0.05).
  • CONCLUSIONS: Abnormal PI3K p85alpha expression occurs in the progression of colorectal cancer in close relation to the clinical stage, and the PI3K/AKT pathway plays an important role in the progression of colorectal cancer.
  • [MeSH-major] Carcinoma / enzymology. Colorectal Neoplasms / enzymology. Disease Progression. Phosphatidylinositol 3-Kinases / metabolism
  • [MeSH-minor] Adenoma / enzymology. Adenoma / pathology. Adult. Aged. Humans. Immunohistochemistry. Middle Aged. Signal Transduction. Young Adult

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  • (PMID = 19304514.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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68. Ramadas A, Kandiah M: Food intake and colorectal adenomas: a case-control study in Malaysia. Asian Pac J Cancer Prev; 2009;10(5):925-32
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  • [Title] Food intake and colorectal adenomas: a case-control study in Malaysia.
  • It is well established that almost all colorectal cancers arise from benign, neoplastic adenomatous polyps.
  • In previous studies, intake of fruits, vegetables and legumes were found to decrease the risk for colorectal adenomas (CRA) and colorectal cancer.
  • In conclusion, our data support protective roles for soy, fruits and vegetables in the aetiology of colorectal adenomas and increase in risk in those with high intakes of red meat and tubers.
  • [MeSH-major] Adenoma / etiology. Adenoma / prevention & control. Colorectal Neoplasms / etiology. Colorectal Neoplasms / prevention & control. Diet. Eating

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  • (PMID = 20104992.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Thailand
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69. Bobe G, Sansbury LB, Albert PS, Cross AJ, Kahle L, Ashby J, Slattery ML, Caan B, Paskett E, Iber F, Kikendall JW, Lance P, Daston C, Marshall JR, Schatzkin A, Lanza E: Dietary flavonoids and colorectal adenoma recurrence in the Polyp Prevention Trial. Cancer Epidemiol Biomarkers Prev; 2008 Jun;17(6):1344-53
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  • [Title] Dietary flavonoids and colorectal adenoma recurrence in the Polyp Prevention Trial.
  • Two recent case-control studies suggested that some flavonoid subgroups may play a role in preventing colorectal cancer.
  • The Polyp Prevention Trial was a randomized dietary intervention trial, which examined the effectiveness of a low-fat, high-fiber, high-fruit, and high-vegetable diet on adenoma recurrence.
  • Multivariate logistic regression models (adjusted for age, body mass index, sex, regular non-steroidal anti-inflammatory use, and dietary fiber intake) were used to estimate odds ratios and 95% confidence intervals for both any and advanced adenoma recurrence within quartiles of energy-adjusted flavonoid intake (baseline, during the trial, and change during the trial).
  • Total flavonoid intake was not associated with any or advanced adenoma recurrence.
  • However, high intake of flavonols, which are at greater concentrations in beans, onions, apples, and tea, was associated with decreased risk of advanced adenoma recurrence (4th versus 1st quartile during the trial; odds ratio, 0.24; 95% confidence interval, 0.11, 0.53; P(trend) = 0.0006).
  • Our data suggest that a flavonol-rich diet may decrease the risk of advanced adenoma recurrence.
  • [MeSH-major] Adenoma / prevention & control. Colorectal Neoplasms / prevention & control. Flavonoids / administration & dosage. Neoplasm Recurrence, Local / prevention & control

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  • (PMID = 18559549.001).
  • [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 / Intramural NIH HHS / / Z01 BC010025-12
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Flavonoids
  • [Other-IDs] NLM/ NIHMS56510; NLM/ PMC2517243
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70. Wu H, Dai Q, Shrubsole MJ, Ness RM, Schlundt D, Smalley WE, Chen H, Li M, Shyr Y, Zheng W: Fruit and vegetable intakes are associated with lower risk of colorectal adenomas. J Nutr; 2009 Feb;139(2):340-4
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  • [Title] Fruit and vegetable intakes are associated with lower risk of colorectal adenomas.
  • Participants were part of the Tennessee Colorectal Polyp Study.
  • Cases had at least one adenoma and controls were polyp free.
  • Associations between dietary intakes and adenoma risk were evaluated using unconditional logistic regression with restricted cubic function spline.
  • In multivariate analyses of 764 cases and 1517 controls, increased intakes of total fruits, berries, fruit juice, and green leafy vegetables were associated with reduced adenoma risk.
  • This study provides additional evidence that high total fruit intake and certain fruit and vegetable intakes may be associated with a reduced risk of colorectal adenomas.

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  • (PMID = 19091801.001).
  • [ISSN] 1541-6100
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / CA095103-010005; United States / NCI NIH HHS / CA / R01 CA097386-01; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / R01CA97386; United States / NCI NIH HHS / CA / P50CA95103; United States / NCI NIH HHS / CA / CA097386-01; United States / NCI NIH HHS / CA / P50 CA095103-010005
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS92794; NLM/ PMC2646202
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71. Oka S, Tanaka S, Yoshida S, Hiyama T, Ueno Y, Ito M, Kitadai Y, Yoshihara M, Chayama K: A water-soluble extract from culture medium of Ganoderma lucidum mycelia suppresses the development of colorectal adenomas. Hiroshima J Med Sci; 2010 Mar;59(1):1-6
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  • [Title] A water-soluble extract from culture medium of Ganoderma lucidum mycelia suppresses the development of colorectal adenomas.
  • To confirm cancer-preventive effects of MAK, we performed a no-treatment concurrent controlled trial on patients with colorectal adenomas.
  • Patients who were determined to be carrying colorectal adenomas by colonoscopy were enrolled in this study.
  • Follow-up colonoscopy was performed after 12 months, and the colonoscopists recorded the size, site and macroscopic type of all adenomas.
  • The changes in the number of adenomas up to 12 months increased to 0.66 +/- 0.10 (mean +/- SE) in the control group, while decreasing in the MAK group to -0.42 +/- 0.10 (p < 0.01).
  • The total size of adenomas increased to 1.73 +/- 0.28 mm in the control group and decreased to -1.40 +/- 0.64 mm in the MAK group (p < 0.01).
  • The resultssuggest that MAK suppresses the development of colorectal adenomas - precancerous lesions of the large bowel.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents / therapeutic use. Colorectal Neoplasms / drug therapy. Mycelium / metabolism. Precancerous Conditions / drug therapy. Reishi / metabolism

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  • (PMID = 20518254.001).
  • [ISSN] 0018-2052
  • [Journal-full-title] Hiroshima journal of medical sciences
  • [ISO-abbreviation] Hiroshima J. Med. Sci.
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Culture Media, Conditioned; 059QF0KO0R / Water
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72. Skjelbred CF, Saebø M, Wallin H, Nexø BA, Hagen PC, Lothe IM, Aase S, Johnson E, Hansteen IL, Vogel U, Kure EH: Polymorphisms of the XRCC1, XRCC3 and XPD genes and risk of colorectal adenoma and carcinoma, in a Norwegian cohort: a case control study. BMC Cancer; 2006 Mar 16;6:67
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  • [Title] Polymorphisms of the XRCC1, XRCC3 and XPD genes and risk of colorectal adenoma and carcinoma, in a Norwegian cohort: a case control study.
  • For colorectal cancer the importance of mutations in mismatch repair genes has been extensively documented.
  • Less is known about other DNA repair pathways in colorectal carcinogenesis.
  • METHODS: We used a case-control study design (157 carcinomas, 983 adenomas and 399 controls) to test the association between five polymorphisms in these DNA repair genes (XRCC1 Arg194Trp, Arg280His, Arg399Gln, XRCC3 Thr241Met and XPD Lys751Gln), and risk of colorectal adenomas and carcinomas in a Norwegian cohort.
  • RESULTS: The XRCC1 280His allele was associated with an increased risk of adenomas (OR 2.30, 95% CI 1.19-4.46).
  • The XRCC1 399Gln allele was associated with a reduction of risk of high-risk adenomas (OR 0.62, 95% CI 0.41-0.96).
  • Carriers of the variant XPD 751Gln allele had an increased risk of low-risk adenomas (OR 1.40, 95% CI 1.03-1.89), while no association was found with risk of carcinomas.
  • CONCLUSION: Our results suggest an increased risk for advanced colorectal neoplasia in individuals with the XRCC1 Arg280His polymorphism and a reduced risk associated with the XRCC1 Arg399Gln polymorphism.
  • Interestingly, individuals with the XPD Lys751Gln polymorphism had an increased risk of low-risk adenomas.
  • This may suggest a role in regression of adenomas.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. DNA-Binding Proteins / genetics. Polymorphism, Genetic. Xeroderma Pigmentosum Group D Protein / genetics

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  • (PMID = 16542436.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1; 0 / X-ray repair cross complementing protein 3; EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human
  • [Other-IDs] NLM/ PMC1458350
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73. Rubie C, Frick VO, Wagner M, Schuld J, Gräber S, Brittner B, Bohle RM, Schilling MK: ELR+ CXC chemokine expression in benign and malignant colorectal conditions. BMC Cancer; 2008;8:178
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  • [Title] ELR+ CXC chemokine expression in benign and malignant colorectal conditions.
  • Here, we comparatively analyzed their expression profile in resection specimens from patients with colorectal adenoma (CRA) (n = 30) as well as colorectal carcinoma (CRC) (n = 48) and corresponding colorectal liver metastases (CRLM) (n = 16).
  • [MeSH-major] Adenoma / metabolism. Carcinoma / metabolism. Chemokines, CXC / biosynthesis. Colorectal Neoplasms / metabolism

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  • (PMID = 18578857.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CXCL1 protein, human; 0 / CXCL5 protein, human; 0 / CXCL6 protein, human; 0 / Chemokine CXCL1; 0 / Chemokine CXCL5; 0 / Chemokine CXCL6; 0 / Chemokines, CXC; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2459188
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74. Nagel R, le Sage C, Diosdado B, van der Waal M, Oude Vrielink JA, Bolijn A, Meijer GA, Agami R: Regulation of the adenomatous polyposis coli gene by the miR-135 family in colorectal cancer. Cancer Res; 2008 Jul 15;68(14):5795-802
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  • [Title] Regulation of the adenomatous polyposis coli gene by the miR-135 family in colorectal cancer.
  • Inactivation of the adenomatous polyposis coli (APC) gene is a major initiating event in colorectal tumorigenesis.
  • Interestingly, we find a considerable up-regulation of miR-135a&b in colorectal adenomas and carcinomas, which significantly correlated with low APC mRNA levels.
  • Thus, our results uncover a miRNA-mediated mechanism for the control of APC expression and Wnt pathway activity, and suggest its contribution to colorectal cancer pathogenesis.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / physiology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. MicroRNAs / genetics


75. van den Donk M, Visker MH, Harryvan JL, Kok FJ, Kampman E: Dietary intake of B-vitamins, polymorphisms in thymidylate synthase and serine hydroxymethyltransferase 1, and colorectal adenoma risk: a Dutch case-control study. Cancer Lett; 2007 May 18;250(1):146-53
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  • [Title] Dietary intake of B-vitamins, polymorphisms in thymidylate synthase and serine hydroxymethyltransferase 1, and colorectal adenoma risk: a Dutch case-control study.
  • In a case-control study, including 768 cases and 709 controls, we investigated the associations between colorectal adenomas and TS tandem repeat and SHMT1 C1420T polymorphisms, and the interplay with B-vitamins.
  • The polymorphisms were not associated with adenomas, but there was a borderline significant interaction between TS genotype and vitamin B6: the association between vitamin B6 and adenomas seemed positive in TS 3R/3R individuals, but inverse in TS 2R/2R individuals.
  • This study does not provide evidence for a role of SHMT1 genotype in adenoma occurrence.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Diet. Glycine Hydroxymethyltransferase / genetics. Polymorphism, Genetic. Thymidylate Synthase / genetics. Vitamin B Complex

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  • (PMID = 17113224.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 12001-76-2 / Vitamin B Complex; 8059-24-3 / Vitamin B 6; 935E97BOY8 / Folic Acid; EC 2.1.1.45 / Thymidylate Synthase; EC 2.1.2.1 / Glycine Hydroxymethyltransferase; EC 2.1.2.1 / SHMT protein, human; P6YC3EG204 / Vitamin B 12; TLM2976OFR / Riboflavin
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76. Bugni JM, Meira LB, Samson LD: Alkylation-induced colon tumorigenesis in mice deficient in the Mgmt and Msh6 proteins. Oncogene; 2009 Feb 5;28(5):734-41
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  • MGMT expression is lost by epigenetic silencing in a variety of human cancers including nearly half of sporadic colorectal cancers, suggesting that this loss maybe causal.
  • Using mice with a targeted disruption of the Mgmt gene, we tested whether Mgmt protects against azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF), against AOM and dextran sulfate sodium (DSS)-induced colorectal adenomas and against spontaneous intestinal adenomas in Apc(Min) mice.
  • In addition, following AOM+DSS treatment Mgmt protected against adenoma formation to the same degree as it protected against AOM-induced ACF formation.
  • Finally, Mgmt deficiency did not affect spontaneous intestinal adenoma development in Apc(Min/+) mice, suggesting that Mgmt suppresses intestinal cancer associated with exogenous alkylating agents, and that endogenous alkylation does not contribute to the rapid tumor development seen in Apc(Min/+) mice.

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  • (PMID = 19029948.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / ES02109; United States / NCI NIH HHS / CA / P30 CA014051; United States / NIEHS NIH HHS / ES / P30 ES002109; United States / NCI NIH HHS / CA / CA14051; United States / NCI NIH HHS / CA / CA75576; United States / NCI NIH HHS / CA / R01 CA075576
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Carcinogens; 0 / DNA-Binding Proteins; 0 / Msh6 protein, mouse; 0 / Tumor Suppressor Proteins; 9042-14-2 / Dextran Sulfate; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, mouse; EC 6.5.1.- / DNA Repair Enzymes; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ NIHMS74471; NLM/ PMC3557788
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77. Pequin P, Manfredi S, Quentin V, Heresbach D, Boyer J, Siproudhis L, Bretagne JF: Patients with sporadic duodenal adenoma are a high-risk group for advanced colorectal neoplasia: results of a case-control study. Aliment Pharmacol Ther; 2007 Jul 15;26(2):277-82
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  • [Title] Patients with sporadic duodenal adenoma are a high-risk group for advanced colorectal neoplasia: results of a case-control study.
  • AIM: To evaluate colorectal cancer risk among patients with sporadic duodenal neoplasia using a case-control protocol.
  • METHODS: Cases were 35 patients referred for the management of sporadic duodenal adenoma and who underwent colonoscopy.
  • Colonoscopy findings among cases were compared with those from a control group matched for age and sex (two controls per case) without duodenal adenoma.
  • Colonoscopy findings were categorized as adenoma, advanced adenoma, cancer or advanced neoplasia.
  • RESULTS: Colorectal adenoma was present in 31% of cases vs. 24% of controls, advanced neoplasia in 29% vs. 4%, advanced adenoma in 23% vs. 3% and adenocarcinoma in 6% vs. 1%.
  • The relative risks of advanced colorectal adenoma and advanced colorectal neoplasia in cases were 10.1 (95% CI: 1.8-100.1, P = 0.003) and 8.9 (95% CI: 2.1-53.3, P = 0.001), respectively.
  • CONCLUSIONS: The relative risk of advanced colorectal adenoma and advanced neoplasia in cases was nine- to 10-fold that among controls.
  • Patients with sporadic duodenal adenoma represent a high-risk group for advanced colorectal neoplasia and should therefore undergo complete colonoscopy.
  • [MeSH-major] Adenoma / pathology. Colonoscopy. Colorectal Neoplasms / diagnosis. Duodenal Neoplasms / pathology. Precancerous Conditions / pathology

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  • (PMID = 17593073.001).
  • [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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78. Wagner PL, Chen YT, Yantiss RK: Immunohistochemical and molecular features of sporadic and FAP-associated duodenal adenomas of the ampullary and nonampullary mucosa. Am J Surg Pathol; 2008 Sep;32(9):1388-95
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  • [Title] Immunohistochemical and molecular features of sporadic and FAP-associated duodenal adenomas of the ampullary and nonampullary mucosa.
  • The pathogenesis of duodenal adenomas is not well elucidated.
  • Much of the literature pertains to ampullary adenomas and those associated with familial adenomatous polyposis (FAP).
  • In this study, we evaluated the molecular features of a series of sporadic duodenal adenomas (n=22) that developed distal to the ampulla, and compared them with the features of sporadic ampullary adenomas (n=9) and FAP-related polyps (n=12).
  • Wnt signaling pathway abnormalities occurred in sporadic, nonampullary (82%), and ampullary (77%) adenomas at comparable rates, usually reflecting nuclear beta-catenin immunostaining (64% and 44%, respectively), and APC rather than beta-catenin, mutations.
  • KRAS mutations were infrequent in sporadic, nonampullary adenomas (18%), and FAP-related adenomas (9%); moderately frequent in ampullary adenomas (44%); and none of the cases harbored BRAF mutations.
  • Only 4 (13%) sporadic adenomas showed nuclear p53 staining, but no p53 mutations were detected in exons 5 to 8.
  • Loss of O-methylguanine methyltransferase immunostaining was identified in 1 sporadic, nonampullary adenoma, and none of the polyps in any group showed loss of MLH-1, MSH-2, or MSH-6 staining, or high-frequency microsatellite instability.
  • We conclude that sporadic and FAP-related adenomas show similar molecular features, regardless of their anatomic location.
  • Similar to colorectal adenomas, they harbor APC and KRAS mutations; but BRAF mutations, p53 alterations, and DNA mismatch repair abnormalities are rare.
  • [MeSH-major] Adenoma / genetics. Adenoma / metabolism. Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Duodenal Neoplasms / genetics. Duodenal Neoplasms / metabolism


79. Johnson V, Lipton LR, Cummings C, Eftekhar Sadat AT, Izatt L, Hodgson SV, Talbot IC, Thomas HJ, Silver AJ, Tomlinson IP: Analysis of somatic molecular changes, clinicopathological features, family history, and germline mutations in colorectal cancer families: evidence for efficient diagnosis of HNPCC and for the existence of distinct groups of non-HNPCC families. J Med Genet; 2005 Oct;42(10):756-62
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  • [Title] Analysis of somatic molecular changes, clinicopathological features, family history, and germline mutations in colorectal cancer families: evidence for efficient diagnosis of HNPCC and for the existence of distinct groups of non-HNPCC families.
  • OBJECTIVE: To analyse somatic molecular changes, clinicopathological features, family history, and germline mutations in families with colorectal cancer (CRC).
  • METHODS: Molecular changes (K-ras and beta-catenin mutations, chromosome 18q allele loss (LOH), APC LOH, microsatellite instability (MSI), and expression of beta-catenin and p53) were examined in four series of CRC patients with proven or probable hereditary disease: hereditary non-polyposis colon cancer (HNPCC); MYH associated polyposis (MAP); multiple (>5) colorectal adenomas without familial adenomatous polyposis (FAP); and other families/cases referred to family cancer clinics (FCC series).
  • RESULTS: There was overlap between genetic pathways followed by each type of CRC, but significant differences included: increased frequency of K-ras mutation and reduced frequency of APC LOH in cancers from MAP, but not from multiple adenoma patients; reduced frequency of LOH in HNPCC CRCs; and increased MSI in CRCs from HNPCC, but not from FCC or multiple adenoma patients.
  • Cancers from the FCC, unselected, and multiple adenoma series shared similar molecular characteristics.
  • In the FCC and multiple adenoma series, hierarchical cluster analysis using the molecular features of the cancers consistently identified two distinct groups, distinguished by presence or absence of K-ras mutation.
  • CONCLUSIONS: While K-ras mutation status is known to differentiate hereditary bowel cancer syndromes such as MAP and FAP, it may also distinguish groups of non-HNPCC, FCC patients whose disease has different, as yet unknown, genetic origins.
  • [MeSH-major] Colorectal Neoplasms / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Genetic Predisposition to Disease. Germ-Line Mutation

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  • (PMID = 15788729.001).
  • [ISSN] 1468-6244
  • [Journal-full-title] Journal of medical genetics
  • [ISO-abbreviation] J. Med. Genet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1735937
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80. Flood A, Peters U, Jenkins DJ, Chatterjee N, Subar AF, Church TR, Bresalier R, Weissfeld JL, Hayes RB, Schatzkin A, Prostate, Lung, Colorectal, Ovarian (PLCO) Project Team: Carbohydrate, glycemic index, and glycemic load and colorectal adenomas in the Prostate, Lung, Colorectal, and Ovarian Screening Study. Am J Clin Nutr; 2006 Nov;84(5):1184-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Carbohydrate, glycemic index, and glycemic load and colorectal adenomas in the Prostate, Lung, Colorectal, and Ovarian Screening Study.
  • BACKGROUND: It is possible that high-glycemic-load diets, through their hyperinsulinemic effects, can increase the risk of colorectal cancer.
  • OBJECTIVE: We analyzed data from a cancer screening study to determine whether persons with high-glycemic-load diets would be at an increased risk of distal adenomas.
  • DESIGN: We included subjects with no prior adenoma or cancer from the Prostate, Lung, Colorectal, and Ovarian screening trial and whose results from flexible sigmoidoscopy exams indicated either no lesions (n = 34 817) or >/=1 distal adenoma (n = 3696).
  • Using logistic regression analysis, we calculated, separately for men and women, prevalence odds ratios (ORs) and 95% CIs of sigmoidoscopy-detected, distal adenomas for quintiles of energy-adjusted dietary carbohydrate, glycemic index, and glycemic load.
  • CONCLUSION: Despite expectations that increasing glycemic load and glycemic index would increase the risk of adenoma, we observed no association in women and even an inverse association in men.
  • [MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Dietary Carbohydrates / administration & dosage. Food Habits
  • [MeSH-minor] Adenomatous Polyps / diagnosis. Adenomatous Polyps / epidemiology. Adenomatous Polyps / etiology. Aged. Case-Control Studies. Cohort Studies. Confidence Intervals. Female. Glycemic Index. Humans. Hyperglycemia / complications. Logistic Models. Male. Mass Screening. Middle Aged. Multivariate Analysis. Nutrition Assessment. Odds Ratio. Risk Assessment. Risk Factors. Sigmoidoscopy. Surveys and Questionnaires. United States / epidemiology

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  • (PMID = 17093173.001).
  • [ISSN] 0002-9165
  • [Journal-full-title] The American journal of clinical nutrition
  • [ISO-abbreviation] Am. J. Clin. Nutr.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K07-CA108910-01A1
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Carbohydrates
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81. Risio M, Malacarne D, Giaretti W: KRAS transitions and villous growth in colorectal adenomas. Cell Oncol; 2005;27(5-6):363-6
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  • [Title] KRAS transitions and villous growth in colorectal adenomas.
  • [MeSH-major] Adenoma / genetics. Adenoma, Villous / genetics. Colorectal Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Genes, ras

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  • (PMID = 16373972.001).
  • [ISSN] 1570-5870
  • [Journal-full-title] Cellular oncology : the official journal of the International Society for Cellular Oncology
  • [ISO-abbreviation] Cell. Oncol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC4617505
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82. Dorval E, Jankowski JM, Barbieux JP, Viguier J, Bertrand P, Brondin B, Bougnoux P, Corpet DE, Association Gastro 37: Polyethylene glycol and prevalence of colorectal adenomas. Gastroenterol Clin Biol; 2006 Oct;30(10):1196-9
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  • [Title] Polyethylene glycol and prevalence of colorectal adenomas.
  • This study tests the hypothesis that use of a PEG-based laxative might reduce the prevalence of colorectal tumors.
  • Age, gender, previous polyps, family history of colorectal cancer, constipation, digestive symptoms were also recorded.
  • Among those, 813 had no tumor, 329 had adenomas, and 23 had carcinomas.
  • In a univariate analysis, older age, male gender, lack of digestive symptom, and previous polyps were more common in patients with colorectal tumors.
  • In multivariate analysis, older age and male gender were associated with higher risk, and NSAIDs use with lower risk, of colorectal tumors.
  • CONCLUSION: Forlax users had a halved risk of colorectal tumors in univariate analysis, which suggests that PEG may prevent carcinogenesis.
  • [MeSH-major] Adenoma / epidemiology. Cathartics / therapeutic use. Colorectal Neoplasms / epidemiology. Polyethylene Glycols / therapeutic use

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  • (PMID = 17075478.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Cathartics; 30IQX730WE / Polyethylene Glycols
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83. Tao H, Shinmura K, Suzuki M, Kono S, Mibu R, Tanaka M, Kakeji Y, Maehara Y, Okamura T, Ikejiri K, Futami K, Yasunami Y, Maekawa T, Takenaka K, Ichimiya H, Imaizumi N, Sugimura H: Association between genetic polymorphisms of the base excision repair gene MUTYH and increased colorectal cancer risk in a Japanese population. Cancer Sci; 2008 Feb;99(2):355-60
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  • [Title] Association between genetic polymorphisms of the base excision repair gene MUTYH and increased colorectal cancer risk in a Japanese population.
  • Biallelic germline mutations of MUTYH have been shown to predict familial and sporadic multiple colorectal adenomas and carcinomas, however, whether there is an association between single nucleotide polymorphisms (SNPs) of MUTYH and sporadic colorectal cancer (CRC) risk has remained unclear.
  • [MeSH-major] Colorectal Neoplasms / genetics. DNA Glycosylases / genetics. Genetic Predisposition to Disease. Polymorphism, Genetic

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  • (PMID = 18271935.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
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84. Takahashi T, Shigematsu H, Shivapurkar N, Reddy J, Zheng Y, Feng Z, Suzuki M, Nomura M, Augustus M, Yin J, Meltzer SJ, Gazdar AF: Aberrant promoter methylation of multiple genes during multistep pathogenesis of colorectal cancers. Int J Cancer; 2006 Feb 15;118(4):924-31
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  • [Title] Aberrant promoter methylation of multiple genes during multistep pathogenesis of colorectal cancers.
  • The aims of our study were to study the role of methylation of a large panel of genes during multistage pathogenesis and to correlate our findings with patient age and other clinico-pathological features.
  • We investigated the aberrant promoter methylation profile of 19 genes in 92 colorectal cancers (CRCs) and corresponding nonmalignant epithelia (NME) (n = 57), and selected 15 genes for studying 26 colorectal adenomas (CAs).

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  • [CommentIn] NIH Guide Grants Contracts. 2014 Nov 14;:NOT-OD-15-022 [25412515.001]
  • [RetractionIn] Int J Cancer. 2013 Jan 15;132(2):499 [23169200.001]
  • [CommentIn] Fed Regist. 2014 Sep 18;79(181):56075-56076 [27737247.001]
  • (PMID = 16108009.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5U01CA8497102; United States / NCI NIH HHS / CA / CA01808; United States / NCI NIH HHS / CA / CA098450; United States / NCI NIH HHS / CA / CA77057; United States / NCI NIH HHS / CA / CA85069; United States / NCI NIH HHS / CA / CA95323
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Retracted Publication
  • [Publication-country] United States
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85. Paun BC, Kukuruga D, Jin Z, Mori Y, Cheng Y, Duncan M, Stass SA, Montgomery E, Hutcheon D, Meltzer SJ: Relation between normal rectal methylation, smoking status, and the presence or absence of colorectal adenomas. Cancer; 2010 Oct 1;116(19):4495-501
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  • [Title] Relation between normal rectal methylation, smoking status, and the presence or absence of colorectal adenomas.
  • BACKGROUND: Colorectal cancer (CRC) is 1 of the leading causes of death in the Western world.
  • CRC develops from premalignant lesions, chiefly colorectal adenomas.
  • Currently, the most accurate and recommended screening method for finding colorectal adenomas is colonoscopy performed on all individuals aged>50 years.
  • The objectives of the current study were to correlate epigenetic alterations that occur in normal rectal mucosa, smoking status, and age with the presence or absence of concomitant colorectal adenomas and to assess the potential clinical value of methylation in normal rectal biopsies as a screening assay for the presence of polyps and, hence, the need for a full colonoscopy.
  • RESULTS: By using several sets of genes, clinical characteristics, and multivariate analyses, the authors developed a prediction model for the presence of concomitant colorectal adenomas at the time of rectal biopsy.
  • They also observed strong correlations between smoking status and rectal methylation pattern and between smoking status and the presence or risk of concomitant adenomas.
  • CONCLUSIONS: A prediction model was developed for the presence of colorectal adenomas based on gene methylation patterns in the normal rectum.
  • The results indicated that these genes may be involved in early stages of adenoma formation.

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  • [Copyright] Copyright © 2010 American Cancer Society.
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  • (PMID = 20572039.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA077057-06; United States / NCI NIH HHS / CA / CA095323-09A2; United States / NIDDK NIH HHS / DK / R01 DK047717; United States / NCI NIH HHS / CA / CA077057-06; United States / NIDDK NIH HHS / DK / DK047717-07; United States / NCI NIH HHS / CA / R01 CA095323-09A2; United States / NCI NIH HHS / CA / R01 CA077057; United States / NCI NIH HHS / CA / R01 CA095323; United States / NIDDK NIH HHS / DK / R01 DK047717-07
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS251065; NLM/ PMC2988654
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86. Zhongyin Z, Hesheng L, Jun L, Jihong C: Association of serum lipids and apolipoprotein E gene polymorphism with the risk of colorectal adenomas. Saudi Med J; 2006 Feb;27(2):161-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of serum lipids and apolipoprotein E gene polymorphism with the risk of colorectal adenomas.
  • OBJECTIVE: To investigate the relationship of serum lipids and apolipoprotein (apoE) gene polymorphism to colorectal adenomas.
  • Ninety-eight patients with colorectal adenomas and 40 healthy subjects were enrolled, and their serum levels of triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), and low density lipoprotein cholesterol (LDL-C) were determined.
  • RESULTS: Serum TC levels of colorectal adenomas group (5.32 +/- 0.85 mmol/L), distal colorectal adenomas group (5.58 +/- 0.63 mmol/L), and villous adenoma group (5.49 +/- 0.69 mmol/L) were higher than the control group (4.28 +/- 0.62 mmol/L, p=0.016), proximal colorectal adenomas group (4.82 +/- 0.58 mmol/L, p=0.038) and non-villous adenoma group (4.76 +/- 0.58 mmol/L, p=0.03).
  • Serum HDL-C levels of colorectal adenomas group (1.39 +/- 0.25 mmol/L) were lower than the control group (1.51 +/- 0.29 mmol/L) (p=0.035).
  • Serum lipids levels of each genotype in colorectal adenomas group were not statistically significant.
  • Apolipoprotein E3/E4 genotypic frequency in colorectal adenomas group (7.1%) was lower than the control group (17.5%) (p=0.012).
  • CONCLUSION: The findings suggest that altered lipid metabolism may be differentially associated with colorectal adenomas and the persons with apoE E3/E4 genotype have lower risk suffering from colorectal adenomas than those with other genotypes.
  • [MeSH-major] Adenoma / blood. Adenoma / genetics. Apolipoproteins E / genetics. Colorectal Neoplasms / blood. Colorectal Neoplasms / genetics. Lipids / blood

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  • (PMID = 16501668.001).
  • [ISSN] 0379-5284
  • [Journal-full-title] Saudi medical journal
  • [ISO-abbreviation] Saudi Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Saudi Arabia
  • [Chemical-registry-number] 0 / Apolipoproteins E; 0 / Cholesterol, HDL; 0 / Cholesterol, LDL; 0 / Lipids; 0 / Triglycerides; 97C5T2UQ7J / Cholesterol
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87. Castellví-Bel S, Balaguer F, Castells A: [MYH and colorectal cancer. A significant advance?]. Gastroenterol Hepatol; 2006 Aug-Sep;29(7):409-13
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  • [Title] [MYH and colorectal cancer. A significant advance?].
  • Colorectal cancer is the second most common neoplasm and the second most frequent cause of cancer-related deaths in Spain.
  • Colorectal polyposis associated with mutations in the MYH gene is an autosomal recessive syndrome characterized by the development of colorectal adenomas and cancer.
  • [MeSH-minor] Base Pair Mismatch / genetics. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms / genetics. Epidemiologic Studies. Genetic Predisposition to Disease. Humans. Myosin Heavy Chains / genetics

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  • (PMID = 16938257.001).
  • [ISSN] 0210-5705
  • [Journal-full-title] Gastroenterología y hepatología
  • [ISO-abbreviation] Gastroenterol Hepatol
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / MYH16 protein, human; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase; EC 3.6.4.1 / Myosin Heavy Chains
  • [Number-of-references] 29
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88. Guilera M, Connelly-Frost A, Keku TO, Martin CF, Galanko J, Sandler RS: Does physical activity modify the association between body mass index and colorectal adenomas? Nutr Cancer; 2005;51(2):140-5
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  • [Title] Does physical activity modify the association between body mass index and colorectal adenomas?
  • Although both physical inactivity and obesity have been associated with an increased risk of colorectal adenomas, it is unclear whether physical activity modifies the relationship between obesity and colorectal adenomas or through what mechanism this might occur.
  • The aim of this study is to evaluate whether physical activity modifies the relationship between body mass index (BMI) and colorectal adenomas and whether apoptosis is a plausible mechanism responsible for this effect modification.
  • Study subjects were part of a large, cross-sectional study, the Diet and Health Study III.
  • There were 226 patients with adenomas and 494 adenoma-free controls.
  • When comparing overweight subjects with the referent group (high physical activity/normal BMI), the relative odds of having an adenoma decreased as physical activity increased: low (odds ratio, OR=1.6; 95% confidence interval, CI=0.7-3.4); moderate (OR=1.1; 95% CI=0.6-2.0); and high (OR=0.8; 95% CI=0.4-1.6).
  • When comparing obese subjects with the referent group, relative odds of having an adenoma were increased regardless of physical activity level.
  • Our results suggest that physical activity may modify the association between obesity and colorectal adenoma until a high level of obesity is achieved.
  • [MeSH-major] Adenoma / epidemiology. Body Mass Index. Colorectal Neoplasms / epidemiology. Motor Activity / physiology. Obesity / epidemiology

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  • (PMID = 15860435.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK34987; United States / NCI NIH HHS / CA / R01 CA44684; United States / NIDDK NIH HHS / DK / T32 DK07634
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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89. Mutch MG, Schoen RE, Fleshman JW, Rall CJ, Dry S, Seligson D, Charabaty A, Chia D, Umar A, Viner J, Hawk E, Pinsky PF: A multicenter study of prevalence and risk factors for aberrant crypt foci. Clin Gastroenterol Hepatol; 2009 May;7(5):568-74
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  • BACKGROUND & AIMS: Aberrant crypt foci (ACF) are the putative precursor of colorectal adenomas.
  • METHODS: Subjects from the Prostate, Lung, Colorectal and Ovarian cancer screening trial were recruited for an ACF study, with subjects with adenoma history being oversampled.
  • RESULTS: A total of 505 (66% male; 55% > or =70 y) subjects from 4 institutions were examined; 42% had no adenoma, 32% had nonadvanced distal adenoma, and 25% had advanced distal adenoma at the baseline Prostate, Lung, Colorectal and Ovarian cancer screening trial examination (8.2 years before ACF examination on average).
  • Baseline adenoma status was not associated with ACF prevalence (range, 66%-69%) or mean number of ACF (range, 3.1-3.5).
  • Age, sex, family history of colorectal cancer, and aspirin/nonsteroidal anti-inflammatory drug use were not associated significantly with ACF prevalence.
  • CONCLUSIONS: ACF prevalence and number were not associated with adenoma history, and only 68.5% of endoscopic ACF were confirmed histologically.
  • These results raise concern about the use of ACF as a surrogate marker of colorectal cancer risk.

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  • (PMID = 19418605.001).
  • [ISSN] 1542-7714
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N01 CN25404; United States / NCI NIH HHS / CN / N01-CN2551
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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90. Becker F, Nusko G, Welke J, Hahn EG, Mansmann U: Benefit-risk analysis of different risk-related surveillance schedules following colorectal polypectomy. Hepatogastroenterology; 2007 Dec;54(80):2249-58
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  • [Title] Benefit-risk analysis of different risk-related surveillance schedules following colorectal polypectomy.
  • BACKGROUND/AIMS: For colorectal screening patients a gain of life time was previously calculated to be about 30-50 days.
  • Different recommendations for recognizing at-risk groups and defining surveillance intervals after an initial finding of colorectal adenomas have been published.
  • METHODOLOGY: A Markov model based on time-dependent transition possibilities was developed to compare two surveillance schedules: recommendations based on the Erlangen Registry of Colorectal Polyps (ERCRP) and the National Polyp Study (NPS).
  • The data used in this model were taken from different sources, namely the ERCRP, the German Study Group of Colorectal Cancer, the German Statistical Yearbook, and from meta-analyses of studies reporting data on complications and sensitivity of colonoscopy.
  • Approximately 84% and 79% of deaths from colorectal carcinoma (CRC) could be prevented if patients were followed up according to the recommendations of the ERCRP and the NPS, respectively.
  • CONCLUSIONS: Surveillance using colonoscopy is an effective tool for preventing CRC after colorectal polypectomy and similar to the screening procedure.
  • [MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Colonic Polyps / surgery. Colonoscopy. Continuity of Patient Care / standards. Outcome Assessment (Health Care). Risk Assessment

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  • (PMID = 18265643.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
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91. Daniel P, Wagrowska-Danilewicz M, Danilewicz M, Stasikowska O, Malecka-Panas E: Transforming growth factor beta 1 and metalloproteinase-9 overexpression in colorectal cancer (CC) and adenoma. Int J Colorectal Dis; 2007 Oct;22(10):1165-72
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  • [Title] Transforming growth factor beta 1 and metalloproteinase-9 overexpression in colorectal cancer (CC) and adenoma.
  • BACKGROUND AND AIMS: Although the role of transforming growth factor beta (TGFbeta) 1 and metalloproteinase-9 (MMP-9) is well documented in colorectal cancer (CC), there is a little evidence supporting its role in early carcinogenesis.
  • PATIENT/METHODS: The study group comprised 50 patients with colorectal polyps and 33 patients with CC.
  • RESULTS: Among 62 adenomas, 33 high-grade dysplasia (HGD) and 29 low-grade dysplasia (LGD) had been detected.
  • CONCLUSION: The increased expression of TGFbeta1, MMP-9 observed in colorectal adenomas seems to be related to the grade of dysplasia.
  • We assume that overexpression of TGFbeta1, MMP-9 represent an early event in colorectal carcinogenesis and may possibly have the prognostic value.
  • [MeSH-major] Adenoma / metabolism. Colorectal Neoplasms / metabolism. Matrix Metalloproteinase 9 / metabolism. Transforming Growth Factor beta1 / metabolism

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  • (PMID = 17394006.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Transforming Growth Factor beta1; EC 3.4.24.35 / Matrix Metalloproteinase 9
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92. de Bruin JH, Kievit W, Ligtenberg MJ, Nagengast FM, Adang EM, Ruers TJ, Kleibeuker JH, Sijmons RH, van Krieken JH, Hoogerbrugge N: [More hereditary intestinal cancer can be detected if patients with colorectal carcinoma that are selected by the pathologist are examined for microsatellite instability]. Ned Tijdschr Geneeskd; 2005 Aug 6;149(32):1792-8
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  • [Title] [More hereditary intestinal cancer can be detected if patients with colorectal carcinoma that are selected by the pathologist are examined for microsatellite instability].
  • [Transliterated title] Meer opsporing van erfelijke darmkanker met onderzoek op microsatellietinstabiliteit bij door de patholoog geselecteerde patiënten met een colon-rectumcarcinoom.
  • OBJECTIVE: To determine whether an investigation of microsatellite instability (MSI) in patients with colorectal carcinoma that have been selected by the pathologist could increase the number of detected families with hereditary non-polyposis colorectal carcinoma (HNPCC).
  • METHOD: Pathologists selected patients with a newly diagnosed colorectal carcinoma for MSI analysis of their tumour tissue if they met one of the following four criteria: (a) colorectal carcinoma diagnosed below 50 years of age;.
  • (b) a second colorectal carcinoma;.
  • (c) a combination of colorectal carcinoma and another HNPCC-related cancer;.
  • (d) colorectal adenoma with high-grade dysplasia diagnosed below 40 years of age.
  • [MeSH-major] Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Germ-Line Mutation. Microsatellite Repeats
  • [MeSH-minor] Adult. Colorectal Neoplasms / diagnosis. Diagnosis, Differential. Female. Genetic Testing. Genomic Instability. Humans. Male. Middle Aged. Netherlands. Pedigree. Predictive Value of Tests. Prospective Studies


93. Chan AT, Tranah GJ, Giovannucci EL, Hunter DJ, Fuchs CS: Genetic variants in the UGT1A6 enzyme, aspirin use, and the risk of colorectal adenoma. J Natl Cancer Inst; 2005 Mar 16;97(6):457-60
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  • [Title] Genetic variants in the UGT1A6 enzyme, aspirin use, and the risk of colorectal adenoma.
  • To determine whether polymorphisms in the UGT1A6 enzyme modulate the protective benefit of regular aspirin use on colorectal adenoma, we conducted a prospective, nested case-control study of 1062 women who provided blood specimens and detailed data on aspirin use before undergoing lower endoscopy.
  • Although UGT1A6 genotype was not associated with overall adenoma risk (multivariable odds ratio [OR] = 1.10, 95% confidence interval [CI] = 0.85 to 1.41), functional variant genotypes statistically significantly modified the effect of aspirin on adenoma (P(interaction) = .02).
  • Among the 616 women with variant genotypes, regular use of aspirin (two or more standard tablets per week) was associated with a decreased risk of adenoma (multivariable OR for adenoma = 0.66 [95% CI = 0.45 to 0.95], OR = 0.63 [95% CI = 0.43 to 0.91] for 0.5-7 standard tablets per week and OR = 0.41 [95% CI = 0.24 to 0.71] for more than 7 tablets per week; P(trend) = .001).
  • These results were consistent among women with advanced adenomas (P(interaction) = .003).
  • Thus, functional polymorphisms in the UGT1A6 enzyme statistically significantly modify the effect of aspirin on colorectal neoplasia, and certain subsets of the population, defined by genotype, may obtain differential benefit from aspirin chemoprevention.
  • [MeSH-major] Adenoma / genetics. Adenoma / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Aspirin / administration & dosage. Colorectal Neoplasms / genetics. Colorectal Neoplasms / prevention & control. Glucuronosyltransferase / genetics

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  • [ErratumIn] J Natl Cancer Inst. 2005 Aug 17;97(16):1227
  • (PMID = 15770010.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 09001-27; United States / NCI NIH HHS / CA / CA 55075; United States / NCI NIH HHS / CA / CA 87969; United States / NHLBI NIH HHS / HL / HL 34594
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; EC 2.4.1.- / UDP-glucuronosyltransferase, UGT1A6; EC 2.4.1.17 / Glucuronosyltransferase; R16CO5Y76E / Aspirin
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94. Fedirko V, Bostick RM, Flanders WD, Long Q, Shaukat A, Rutherford RE, Daniel CR, Cohen V, Dash C: Effects of vitamin D and calcium supplementation on markers of apoptosis in normal colon mucosa: a randomized, double-blind, placebo-controlled clinical trial. Cancer Prev Res (Phila); 2009 Mar;2(3):213-23
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  • To further clarify and/or develop calcium and vitamin D as chemopreventive agents against colorectal cancer in humans, understand the mechanisms by which these agents reduce risk for the disease, and develop "treatable" biomarkers of risk for colorectal cancer, we conducted a pilot, randomized, double-blind, placebo-controlled, 2 x 2 factorial clinical trial to test the effects of calcium and vitamin D3, alone and in combination on markers of apoptosis, in the normal colorectal mucosa.
  • Ninety-two men and women with at least one pathology-confirmed colorectal adenoma were treated with 2.0 g/d calcium or 800 IU/d vitamin D3, alone or in combination, versus placebo over 6 months.
  • Overall expression and colorectal crypt distributions of Bcl-2 (an apoptosis inhibitor) and Bax (an apoptosis promoter) in biopsies of normal-appearing rectal mucosa were detected by automated immunohistochemistry and quantified by image analysis.
  • Overall, these preliminary results suggest that calcium and vitamin D, individually or together, may enhance apoptosis in the normal human colorectal epithelium, and the strongest treatment effects may be vitamin D related and in the upper sections of the colorectal crypts.

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  • (PMID = 19258546.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA104637-01; United States / NCI NIH HHS / CA / R01 CA104637; United States / NCI NIH HHS / CA / R01 CA104637-01
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Placebos; 1406-16-2 / Vitamin D; 1C6V77QF41 / Cholecalciferol; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ NIHMS120314; NLM/ PMC2712935
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95. Wolpin BM, Wei EK, Ng K, Meyerhardt JA, Chan JA, Selhub J, Giovannucci EL, Fuchs CS: Prediagnostic plasma folate and the risk of death in patients with colorectal cancer. J Clin Oncol; 2008 Jul 1;26(19):3222-8
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  • [Title] Prediagnostic plasma folate and the risk of death in patients with colorectal cancer.
  • PURPOSE: Although previous studies have demonstrated an inverse relationship between folate intake and colorectal cancer risk, a recent trial suggests that supplemental folic acid may accelerate tumorigenesis among patients with a history of colorectal adenoma.
  • Therefore, high priority has been given to research investigating the influence of folate on cancer progression in patients with colorectal cancer.
  • PATIENTS AND METHODS: To investigate whether prediagnostic levels of plasma folate are associated with colorectal cancer-specific and overall mortality, we performed a prospective, nested observational study within two large US cohorts: the Nurses' Health Study and Health Professionals Follow-Up Study.
  • We measured folate levels among 301 participants who developed colorectal cancer 2 or more years after their plasma was collected and compared participants using Cox proportional hazards models by quintile of plasma folate.
  • RESULTS: Higher levels of plasma folate were not associated with an increased risk of colorectal cancer-specific or overall mortality.
  • Compared with participants in the lowest quintile of plasma folate, those in the highest quintile experienced a multivariable-adjusted hazard ratio for colorectal cancer-specific mortality of 0.42 (95% CI, 0.20 0.88) and overall mortality of 0.46 (95% CI, 0.24 0.88).
  • When the analysis was limited to participants whose plasma was collected within 5 years of cancer diagnosis, no detrimental effect of high plasma folate was noted.
  • CONCLUSION: In two large prospective cohorts, higher prediagnostic levels of plasma folate were not associated with an increased risk of colorectal cancer-specific or overall mortality.

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  • (PMID = 18591557.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA108341; United States / NCI NIH HHS / CA / R01 CA118553; United States / NCI NIH HHS / CA / P01 CA087969; United States / NCI NIH HHS / CA / CA87969; United States / NCI NIH HHS / CA / T32 CA009172; United States / NCI NIH HHS / CA / R03 CA108341; United States / NCI NIH HHS / CA / CA118553; United States / NCI NIH HHS / CA / CA09001; United States / NCI NIH HHS / CA / T32 CA009001
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 935E97BOY8 / Folic Acid
  • [Other-IDs] NLM/ NIHMS557427; NLM/ PMC3962289
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96. Kim S, Baron JA, Mott LA, Burke CA, Church TR, McKeown-Eyssen GE, Cole BF, Haile RW, Sandler RS: Aspirin may be more effective in preventing colorectal adenomas in patients with higher BMI (United States). Cancer Causes Control; 2006 Dec;17(10):1299-304
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  • [Title] Aspirin may be more effective in preventing colorectal adenomas in patients with higher BMI (United States).
  • Aspirin, which may affect the levels of these cytokines, has been shown in randomized controlled trials to decrease the risk of colorectal adenomas.
  • Data were available from the Aspirin/Folate Polyp Prevention Study, a randomized controlled trial of aspirin and folic acid to prevent recurrent colorectal adenomas.
  • For the analysis of the effect of aspirin on the recurrence of colorectal adenoma by BMI, we computed risk ratios for aspirin versus placebo within the three BMI strata using a modified Poisson model.
  • Overall the risk reduction of adenomas with a daily dose of 325 mg aspirin was greater among subjects with higher BMI.
  • Among obese subjects the risk ratio (RR) for advanced adenomas compared with placebo was 0.44 (95% CI 0.17-1.10), versus RR = 1.23 (95% CI 0.55-2.77) among those with normal weight.
  • However, 81 mg aspirin daily did not interact with BMI to modify the risk of adenomas in such a fashion.
  • [MeSH-major] Adenomatous Polyps / prevention & control. Aspirin / pharmacology. Body Mass Index. Colorectal Neoplasms / prevention & control

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  • (PMID = 17111262.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK34987; United States / NCI NIH HHS / CA / R01 CA59005; United States / NCRR NIH HHS / RR / RR000046
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] R16CO5Y76E / Aspirin
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97. Ji JS, Choi KY, Lee WC, Lee BI, Park SH, Choi H, Kim BW, Chae HS, Park YM, Park YJ: Endoscopic and histopathologic predictors of recurrence of colorectal adenoma on lowering the miss rate. Korean J Intern Med; 2009 Sep;24(3):196-202
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  • [Title] Endoscopic and histopathologic predictors of recurrence of colorectal adenoma on lowering the miss rate.
  • BACKGROUND/AIMS: Although colorectal adenoma is reported to recur frequently, this may result from missing it at baseline.
  • This study evaluated the recurrence rate prospectively and clinical predictors of recurrence in colorectal adenoma after lowering the miss rate.
  • METHODS: The study population comprised 128 patients who underwent baseline colonoscopy with resection of colorectal adenomas.
  • Thirty patients had a recurrent adenoma, for a recurrence rate of 23.4%.
  • Patients with three or four adenomas at baseline colonoscopy had a two-fold greater risk than those with one adenoma (hazard ratio, 2.44; 95% CI, 1.11-5.35).
  • Patients with advanced adenoma had a two-fold greater risk than those with no advanced adenoma (hazard ratio, 2.88; 95% CI, 1.40-5.95).
  • In multivariate analysis, only the presence of three or four adenomas independently predicted the recurrence of adenoma (hazard ratio, 3.19; 95% CI, 1.04-9.79).
  • CONCLUSIONS: The recurrence rate of colorectal adenoma corrected by lowering the miss rate was lower than reported rates.
  • The presence of multiple adenomas on initial colonoscopy was an important predictor of recurrence.
  • [MeSH-major] Adenoma / diagnosis. Colonoscopy. Colorectal Neoplasms / diagnosis. Neoplasm Recurrence, Local / diagnosis
  • [MeSH-minor] Adult. Aged. Colonic Polyps / diagnosis. Colonic Polyps / pathology. Female. Follow-Up Studies. Humans. Male. Middle Aged

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  • (PMID = 19721855.001).
  • [ISSN] 1226-3303
  • [Journal-full-title] The Korean journal of internal medicine
  • [ISO-abbreviation] Korean J. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2732778
  • [Keywords] NOTNLM ; Colorectal adenoma / Miss rate / Recurrence rate
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98. Schroy PC 3rd, Lal SK, Wilson S, Heeren T, Farraye FA: Deficiencies in knowledge and familial risk communication among colorectal adenoma patients. J Clin Gastroenterol; 2005 Apr;39(4):298-302
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  • [Title] Deficiencies in knowledge and familial risk communication among colorectal adenoma patients.
  • GOALS: Our primary objectives were to assess knowledge about familial risk and risk communication among colorectal adenoma patients.
  • BACKGROUND: The first-degree relatives (FDRs) of colorectal adenoma patients diagnosed before the age of 60 years may be at increased risk of colorectal cancer and should begin screening by the age of 40 years.
  • STUDY: We conducted a telephone survey of 129 consecutive English-speaking adenoma patients younger than 60 years treated by 11 endoscopists at two medical centers.
  • Few responders (n = 25, 33%) were aware that their FDRs were at increased risk of colorectal cancer, and only 56% of knowledgeable patients identified a physician as the source of information.
  • Most knowledgeable patients (n = 20, 80%) reported that they had informed > or = 1 FDRs about their diagnosis, and most (68%) felt that it was the patient's responsibility to notify at-risk relatives.
  • CONCLUSIONS: Most colorectal adenoma patients younger than 60 years are unaware of the familial implications of their diagnosis and therefore unlikely to notify at-risk FDRs.
  • [MeSH-major] Adenoma / psychology. Colorectal Neoplasms / psychology. Communication. Family Health. Patient Education as Topic

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  • (PMID = 15758623.001).
  • [ISSN] 0192-0790
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / KO7-CA68058
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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99. van den Donk M, Pellis L, Crott JW, van Engeland M, Friederich P, Nagengast FM, van Bergeijk JD, de Boer SY, Mason JB, Kok FJ, Keijer J, Kampman E: Folic acid and vitamin B-12 supplementation does not favorably influence uracil incorporation and promoter methylation in rectal mucosa DNA of subjects with previous colorectal adenomas. J Nutr; 2007 Sep;137(9):2114-20
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  • [Title] Folic acid and vitamin B-12 supplementation does not favorably influence uracil incorporation and promoter methylation in rectal mucosa DNA of subjects with previous colorectal adenomas.
  • Subjects (n = 86) with a history of colorectal adenoma and MTHFR CC or TT genotype were randomly assigned to receive folic acid plus vitamin B-12 or placebo for 6 mo.
  • This study suggests that supplementation with high doses of folic acid and vitamin B-12 may not favorably influence uracil incorporation and promoter methylation in subjects with previous colorectal adenomas.
  • [MeSH-major] Colorectal Neoplasms / genetics. Colorectal Neoplasms / metabolism. Intestinal Mucosa / metabolism. Promoter Regions, Genetic / genetics. Uracil / metabolism

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  • (PMID = 17709451.001).
  • [ISSN] 0022-3166
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K05 CA100048; United States / NCI NIH HHS / CA / U54 CA100971
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0LVT1QZ0BA / Homocysteine; 56HH86ZVCT / Uracil; 935E97BOY8 / Folic Acid; EC 1.5.- / Oxidoreductases Acting on CH-NH Group Donors; P6YC3EG204 / Vitamin B 12
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100. Zhang CH, He YL, Zhan WH, Cai SR, Huang MJ, Wang JP, Peng JJ: [Clinical analysis of multiple primary carcinomas in colorectal cancer patients]. Zhonghua Wei Chang Wai Ke Za Zhi; 2005 Jan;8(1):38-40
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  • [Title] [Clinical analysis of multiple primary carcinomas in colorectal cancer patients].
  • OBJECTIVE: To explore the prevalence, clinical features and prognosis of multiple primary neoplasms in patients with colorectal carcinoma (CRC).
  • METHODS: Data of colorectal cancer patients admitted to our hospital from June 1994 to June 2002 were analyzed retrospectively.
  • Forty- seven patients had multiple colorectal cancers metachronous CRC(S) in 12 and synchronous CRC(S) in 35.
  • Thirty- six patients 5 patients with synchronous cancers had malignant tumors outside colorectal tract,12 of whom were gastric carcinomas.
  • Cancer family history (P=0.002) and colorectal adenoma (P=0.036) were significantly more common in MCG than those in SCG.
  • The secondary tumors were mainly adenoma cancerization in MCG.
  • CONCLUSION: Cancer family history and colorectal adenoma seems to be at high risk for developing multiple cancers in CRC patients.
  • Gastric cancer and colorectal adenoma cancerization were common secondary tumors of multiple primary neoplasms in patients with colorectal carcinoma.
  • [MeSH-major] Colorectal Neoplasms / epidemiology. Neoplasms, Multiple Primary / epidemiology

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  • (PMID = 16148997.001).
  • [ISSN] 1671-0274
  • [Journal-full-title] Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery
  • [ISO-abbreviation] Zhonghua Wei Chang Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] Controlled Clinical Trial; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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