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1. Sinha R, Kulldorff M, Gunter MJ, Strickland P, Rothman N: Dietary benzo[a]pyrene intake and risk of colorectal adenoma. Cancer Epidemiol Biomarkers Prev; 2005 Aug;14(8):2030-4
Hazardous Substances Data Bank. Benzo(a)pyrene .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dietary benzo[a]pyrene intake and risk of colorectal adenoma.
  • We carried out a clinic-based case-control study specifically designed to address the hypothesis that dietary intake of polycyclic aromatic hydrocarbons (PAH) is associated with colorectal adenoma risk.
  • We estimated BaP intake derived from meat and from all foods to test its relationship with risk of colorectal adenomas.
  • Increased risk of colorectal adenomas was more strongly associated with BaP intake estimated from all foods: 2.61 (1.08-6.29) for the second quintile, 4.21 (1.79-9.91) for the third quintile, 2.45 (0.98-6.12) for the fourth quintile, and 5.60 (2.20-14.20) for the fifth quintile (Ptrend=0.002).
  • This study provides evidence that dietary BaP plays a role in colorectal adenoma etiology.
  • [MeSH-major] Adenoma / chemically induced. Benzo(a)pyrene / adverse effects. Colorectal Neoplasms / chemically induced. Diet. Meat

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  • (PMID = 16103456.001).
  • [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 / PHS HHS / / P01-E506052
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 3417WMA06D / Benzo(a)pyrene
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2. Vinikoor LC, Galanko JA, Sandler RS: Cholecystectomy and the risk of colorectal adenomas. Dig Dis Sci; 2008 Mar;53(3):730-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cholecystectomy and the risk of colorectal adenomas.
  • Cholecystectomy has been identified as a risk factor for colorectal cancer, yet little attention has been given to the relationship between cholecystectomy and colorectal adenomas.
  • Utilizing data collected in two large cross-sectional studies of colorectal adenoma risk factors, we examined the association between cholecystectomy and colorectal adenomas.
  • In the adjusted logistic regression model, both men and women showed no effect of cholecystectomy on risk of colorectal adenomas (men: OR 0.67 [95% CI 0.30-1.47]; women: OR 1.46 [95% CI 0.92-2.29]).
  • Thus, we conclude that, although cholecystectomy is a risk factor for colorectal cancer, cholecystectomy is not a risk factor for colorectal adenomas.

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  • (PMID = 17710546.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA044684; United States / NCI NIH HHS / CA / R01 CA044684-17; United States / NIDDK NIH HHS / DK / P30 DK034987-24; United States / NIDDK NIH HHS / DK / P30 DK034987; United States / NIDDK NIH HHS / DK / T32 DK07634; United States / NCI NIH HHS / CA / CA044684-17; United States / NIDDK NIH HHS / DK / DK034987-24; United States / NIDDK NIH HHS / DK / T32 DK007634-19; United States / NIDDK NIH HHS / DK / T32 DK007634; United States / NIDDK NIH HHS / DK / R01 DK 44684; United States / NIDDK NIH HHS / DK / P30 DK34987
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS92903; NLM/ PMC2647516
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3. Cho E, Willett WC, Colditz GA, Fuchs CS, Wu K, Chan AT, Zeisel SH, Giovannucci EL: Dietary choline and betaine and the risk of distal colorectal adenoma in women. J Natl Cancer Inst; 2007 Aug 15;99(16):1224-31
Hazardous Substances Data Bank. CHOLINE CHLORIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dietary choline and betaine and the risk of distal colorectal adenoma in women.
  • BACKGROUND: Choline and betaine are involved in methyl-group metabolism as methyl-group donors; thus, like folate, another methyl-group donor, they may be associated with a reduced risk of colorectal adenomas.
  • No epidemiologic study has examined the association of intake of these nutrients and colorectal adenoma risk.
  • METHODS: We investigated the relationship between intakes of choline and betaine and risk of colorectal adenoma in US women enrolled in the Nurses' Health Study.
  • Logistic regression models were used to calculate adjusted odds ratios (as approximations for relative risks) and 95% confidence intervals (CIs) of colorectal adenoma.
  • RESULTS: Among 39246 women who were initially free of cancer or polyps and who had at least one endoscopy from 1984 through 2002, 2408 adenoma cases were documented.
  • Increasing choline intake was associated with an elevated risk of colorectal adenoma; the multivariable relative risks (95% CIs) for increasing quintiles of intake, relative to the lowest quintile, were 1.03 (0.90 to 1.18), 1.01 (0.88 to 1.16), 1.23 (1.07 to 1.41), and 1.45 (1.27 to 1.67; P(trend)<.001).
  • Betaine intake had a nonlinear inverse association with colorectal adenoma; the multivariable relative risks (95% CIs) for increasing quintiles of intake were 0.94 (0.83 to 1.07), 0.85 (0.75 to 0.97), 0.86 (0.75 to 0.98), and 0.90 (95% CI = 0.78 to 1.04; P(trend) = .09).
  • Among individual sources of choline, choline from phosphatidylcholine and from sphingomyelin were each positively related to adenoma risk.
  • CONCLUSIONS: Our findings do not support an inverse association between choline intake and risk of colorectal adenoma.
  • The positive association between choline intake and colorectal adenoma that we observed could represent effects of other components in the foods from which choline was derived and should be investigated further.

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  • (PMID = 17686825.001).
  • [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 / CA108341; United States / NIDDK NIH HHS / DK / P30 DK040561; United States / NIDDK NIH HHS / DK / P30 DK056350-08; United States / NIDDK NIH HHS / DK / DK55865; United States / NCI NIH HHS / CA / P01 CA087969; United States / NIDDK NIH HHS / DK / R01 DK055865; None / None / / P30 DK040561-12; United States / NCI NIH HHS / CA / CA87969; United States / NIDDK NIH HHS / DK / P30 DK040561-12; United States / NCI NIH HHS / CA / R03 CA108341; United States / NIDDK NIH HHS / DK / DK56350; United States / NIDDK NIH HHS / DK / DK055865-07; United States / NIDDK NIH HHS / DK / R01 DK055865-07; United States / NIDDK NIH HHS / DK / P30 DK056350
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 3SCV180C9W / Betaine; N91BDP6H0X / Choline
  • [Other-IDs] NLM/ NIHMS50988; NLM/ PMC2441932
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4. Ferrucci LM, Sinha R, Graubard BI, Mayne ST, Ma X, Schatzkin A, Schoenfeld PS, Cash BD, Flood A, Cross AJ: Dietary meat intake in relation to colorectal adenoma in asymptomatic women. Am J Gastroenterol; 2009 May;104(5):1231-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dietary meat intake in relation to colorectal adenoma in asymptomatic women.
  • OBJECTIVES: No previous study has concurrently assessed the associations between meat intake, meat-cooking methods and doneness levels, meat mutagens (heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons), heme iron, and nitrite from meat and colorectal adenoma in asymptomatic women undergoing colonoscopy.
  • METHODS: Of the 807 eligible women in a cross-sectional multicenter colonoscopy screening study, 158 prevalent colorectal adenoma cases and 649 controls satisfactorily completed the validated food frequency and meat questionnaires.
  • RESULTS: Red meat was associated positively with colorectal adenoma (OR fourth vs. first quartile = 2.02; 95% CI = 1.06-3.83; P trend = 0.38).
  • Intake of pan-fried meat (OR = 1.72; 95% CI = 0.96-3.07; P trend = 0.01) and the HCA: 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) (OR = 1.90; 95% CI = 1.05-3.42; P trend = 0.07) were also associated with an increased risk of colorectal adenoma.
  • Although not statistically significant, there were positive associations between iron and heme iron from meat and colorectal adenoma.
  • CONCLUSIONS: In asymptomatic women undergoing colonoscopy, colorectal adenomas were associated with high intake of red meat, pan-fried meat, and the HCA MeIQx.

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  • (PMID = 19367270.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA105666-01; United States / NCI NIH HHS / CA / TU2 CA105666; United States / Intramural NIH HHS / / Z01 CP010127-12; United States / NCI NIH HHS / CA / TU2 CA105666-01
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Heterocyclic Compounds
  • [Other-IDs] NLM/ NIHMS114849; NLM/ PMC2891034
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5. Connelly-Frost A, Poole C, Satia JA, Kupper LL, Millikan RC, Sandler RS: Selenium, apoptosis, and colorectal adenomas. Cancer Epidemiol Biomarkers Prev; 2006 Mar;15(3):486-93
Hazardous Substances Data Bank. SELENIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selenium, apoptosis, and colorectal adenomas.
  • OBJECTIVES: The relation between selenium and colorectal adenomas was evaluated because the colorectal adenoma is the established precursor lesion of most colorectal cancers.
  • Apoptosis was a pathway of interest because decreased apoptosis has been associated with an increased prevalence of adenomas.
  • Our objectives were as follows: to investigate the association between (a) selenium and colorectal adenomas and (b) selenium and apoptosis.
  • There were 451 participants in the analysis of selenium and adenoma prevalence and 351 participants in the analysis of selenium and apoptosis.
  • RESULTS: Participants in the highest fifth of serum selenium were less likely to have adenomas in comparison with those in the lowest fifth (prevalence ratio, 0.6; 95% confidence interval, 0.4-1.1).
  • CONCLUSIONS: High selenium was associated with a reduced prevalence of colorectal adenomas.
  • Apoptosis, however, did not seem to be the mechanism by which selenium was related to adenoma prevalence in our data.
  • [MeSH-major] Adenoma / blood. Adenoma / pathology. Biomarkers, Tumor / blood. Colorectal Neoplasms / blood. Colorectal Neoplasms / epidemiology. Selenium / blood

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  • (PMID = 16537706.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK34987; United States / NIEHS NIH HHS / ES / P30 ES10126; United States / NCI NIH HHS / CA / R01 CA44684; United States / NCI NIH HHS / CA / R03 CA101132
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; H6241UJ22B / Selenium
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6. Gong Z, Bostick RM, Xie D, Hurley TG, Deng Z, Dixon DA, Zhang J, Hebert JR: Genetic polymorphisms in the cyclooxygenase-1 and cyclooxygenase-2 genes and risk of colorectal adenoma. Int J Colorectal Dis; 2009 Jun;24(6):647-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphisms in the cyclooxygenase-1 and cyclooxygenase-2 genes and risk of colorectal adenoma.
  • PURPOSE: Cyclooxygenase (COX) enzymes, COX1 and COX2, are key in converting arachidonic acid (AA) into prostaglandins that have been associated with colorectal carcinogenesis.
  • The aim of our study was to investigate associations of polymorphisms in COX genes, alone and in interaction with exposures known to be related to inflammation and AA metabolism, with risk of colorectal adenomas.
  • MATERIALS AND METHODS: In a community-, colonoscopy-based case-control study with 162 incident, sporadic colorectal adenoma cases and 211 controls, we investigated associations of two promoter polymorphisms (-842 A > G in COX1 and -765 G > C in COX2) and two polymorphisms in the 3'-UTR of COX2 (8473 T > C and 9850 A > G) with risk of adenomas.
  • Multiple logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (CI) of colorectal adenoma after adjusting for potential confounders.
  • RESULTS: Overall, there was no evidence for an association between any of the four polymorphisms and colorectal adenomas.
  • CONCLUSION: These results suggest that the C allele of COX2 8473 T > C polymorphism may interact with NSAIDs to reduce risk for colorectal adenoma.
  • [MeSH-major] Adenoma / enzymology. Colorectal Neoplasms / enzymology. Colorectal Neoplasms / genetics. Cyclooxygenase 1 / genetics. Cyclooxygenase 2 / genetics. Genetic Predisposition to Disease. Polymorphism, Single Nucleotide / genetics

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  • (PMID = 19205707.001).
  • [ISSN] 1432-1262
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA134609; United States / NCRR NIH HHS / RR / RR017698; United States / NCI NIH HHS / CA / 1 U01 CA114601-01; United States / NCI NIH HHS / CA / R01CA-51932
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS1 protein, human; EC 1.14.99.1 / PTGS2 protein, human
  • [Other-IDs] NLM/ NIHMS377403; NLM/ PMC3461962
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7. Fentz AK, Spörl M, Spangenberg J, List HJ, Zornig C, Dörner A, Layer P, Juhl H, David KA: Detection of colorectal adenoma and cancer based on transthyretin and C3a-desArg serum levels. Proteomics Clin Appl; 2007 Jun;1(6):536-44
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of colorectal adenoma and cancer based on transthyretin and C3a-desArg serum levels.
  • Colorectal cancer is the second leading cause of cancer death, and it develops from benign colorectal adenomas in over 95% of patients.
  • Early detection of these cancer precursors by screening tests and their removal can potentially eradicate more than 95% of colorectal cancers before they develop.
  • To discover sensitive and specific biomarkers for improvement of pre-clinical diagnosis of colorectal adenoma and cancer, we analysed in two independent studies (n = 87 and n = 83 patients) serum samples from colorectal cancer (stage III), colorectal adenoma and control patients using SELDI-TOF-MS.
  • Two biomarkers that were each able to distinguish control patients from either colorectal adenoma or colorectal cancer patients (p<0.001) were identified as transthyretin (pre-albumin) and C3a-desArg by MS/MS and were further validated by antibody-based assays (radial immunodiffusion, ELISA).
  • A combination of both proteins clearly indicated the presence of colorectal adenoma or carcinoma.
  • Using a cut-off of <0.225 g/L for transthyretin and >1974 ng/mL for C3a-desArg, we found a sensitivity and specificity for colorectal adenoma of 96% and 70%, respectively.

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  • [Copyright] Copyright © 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
  • (PMID = 21136704.001).
  • [ISSN] 1862-8346
  • [Journal-full-title] Proteomics. Clinical applications
  • [ISO-abbreviation] Proteomics Clin Appl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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8. Yang MH, Son HJ, Lee JH, Kim MH, Kim JY, Kim YH, Chang DK, Rhee PL, Kim JJ, Rhee JC: Do we need colonoscopy in patients with gastric adenomas? The risk of colorectal adenoma in patients with gastric adenomas. Gastrointest Endosc; 2010 Apr;71(4):774-81
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  • [Title] Do we need colonoscopy in patients with gastric adenomas? The risk of colorectal adenoma in patients with gastric adenomas.
  • Genetic alterations of several genes occur in gastric adenomas and colorectal adenomas.
  • However, it is unknown whether patients with gastric adenomas are at higher risk for colorectal adenomas.
  • OBJECTIVE: To investigate the prevalence rate of colorectal adenoma in patients with gastric adenomas and to determine the association between the presence of gastric adenomas and synchronous colorectal adenomas.
  • PATIENTS: This study involved 87 patients with gastric adenomas and 174 sex-matched and age-matched controls among 19,019 participants who underwent EGD and colonoscopy simultaneously or within 6 months of each other from January 2001 to December 2008 at the Center for Health Promotion of Samsung Medical Center.
  • MAIN OUTCOME MEASUREMENTS: The prevalence rate of colorectal adenoma in patients with gastric adenomas.
  • RESULTS: The 87 gastric adenoma patients included 72 men and 15 women.
  • Colorectal adenomas were identified in 42 (48.3%) of 87 cases and in 58 (33.3%) of 174 controls (P = .022).
  • The prevalence of colorectal adenoma was significantly higher in the gastric adenoma group than in the control group.
  • The mean size and number of colorectal adenomas were not significantly different between the two groups.
  • The majority of colorectal adenomas were located in distal colonic segments in the gastric adenoma group in contrast with proximal colonic segments in the control group.
  • Multivariate logistic regression analysis revealed that independent risk factors for colorectal adenoma were the presence of gastric adenomas (odds ratio [OR], .915; 95% confidence interval [CI], 1.044-3.513) and increasing age over 55 years (OR, 2.943; 95% CI, 1.558-5.560).
  • LIMITATIONS: Lack of data on previous colorectal adenomas and possible confounding factors such as hyperlipidemia or diabetes mellitus.
  • CONCLUSION: The risk of colorectal adenoma increases significantly in patients with gastric adenomas and in patients over age 55.
  • A screening colonoscopy may be necessary for patients with gastric adenomas to detect colorectal adenomas.
  • [MeSH-major] Adenoma / diagnosis. Colonoscopy. Colorectal Neoplasms / diagnosis. Gastroscopy. Neoplasms, Multiple Primary / diagnosis. Stomach Neoplasms / diagnosis

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  • [Copyright] Copyright 2010 American Society for Gastrointestinal Endoscopy. Published by Mosby, Inc. All rights reserved.
  • (PMID = 20363417.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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9. Gunter MJ, Divi RL, Kulldorff M, Vermeulen R, Haverkos KJ, Kuo MM, Strickland P, Poirier MC, Rothman N, Sinha R: Leukocyte polycyclic aromatic hydrocarbon-DNA adduct formation and colorectal adenoma. Carcinogenesis; 2007 Jul;28(7):1426-9
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  • [Title] Leukocyte polycyclic aromatic hydrocarbon-DNA adduct formation and colorectal adenoma.
  • Consumption of charbroiled red meat and meat-derived polycyclic aromatic hydrocarbons (PAHs) has been associated with risk of colorectal adenoma, a precursor of colorectal cancer.
  • Furthermore, leukocyte PAH-DNA adduct levels have been demonstrated to increase in response to charbroiled red meat intake but to date there have been no studies that have investigated the relationship between leukocyte PAH-DNA adduct levels and risk of colorectal adenoma.
  • We investigated the relation of leukocyte PAH-DNA adduct formation and colorectal adenoma in a clinic-based case-control study of colorectal adenomas.
  • The study comprised 82 cases of colorectal adenoma and 111 polyp-free controls, none of whom were current smokers.
  • Leukocyte PAH-DNA adduct levels were higher among colorectal adenoma cases (median, 1.4 adducts per 10(8) nucleotides) than polyp-free controls (median, 1.2 adducts per 10(8) nucleotides) (P = 0.02).
  • There was a positive association between PAH-DNA adduct level and adenoma prevalence: each unit increase in PAH-DNA adduct level (per 10(8) nucleotides) was associated with an odds ratio (OR) of 1.5 [95% confidence interval (CI), 1.1-2.2].
  • In addition, a comparison of the lowest quartile for PAH-DNA adduct level with the highest quartile yielded an OR of 2.8 (95% CI, 1.2-6.5; P(trend) = 0.048) for risk of colorectal adenoma.
  • These data support a link between PAH exposure and colorectal adenoma.
  • [MeSH-major] Adenoma / metabolism. Carcinogens / metabolism. Colorectal Neoplasms / metabolism. DNA Adducts / blood. Leukocytes / metabolism. Polycyclic Hydrocarbons, Aromatic / metabolism

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  • (PMID = 17277232.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / DNA Adducts; 0 / Polycyclic Hydrocarbons, Aromatic; 55097-80-8 / 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide
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10. Yamaji Y, Okamoto M, Yoshida H, Kawabe T, Wada R, Mitsushima T, Omata M: Cholelithiasis is a risk factor for colorectal adenoma. Am J Gastroenterol; 2008 Nov;103(11):2847-52
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  • [Title] Cholelithiasis is a risk factor for colorectal adenoma.
  • OBJECTIVES: Postcholecystectomy patients show moderate risk of colorectal cancer.
  • However, few studies have investigated the relationship between cholelithiasis and colorectal adenoma.
  • We investigated whether subjects with cholelithiasis or a previous cholecystectomy showed an increased risk of colorectal adenoma, as compared with subjects with normal gallbladders.
  • The prevalence of colorectal adenoma was 29.6% (61/206) in subjects with cholelithiasis, which was significantly higher when compared with normal subjects, with a prevalence of 17.7% (741/4,189, P < 0.001).
  • In cholecystectomy patients, only 15.9% (10/63) developed colorectal adenomas, which was not significantly different from the control group.
  • In a multivariate analysis controlling for sex, age, family history of colorectal cancer, alcohol, smoking, and body mass index, cholelithiasis was shown to be an independent risk factor for colorectal adenoma (adjusted OR 1.57, 95% CI 1.14-2.18).
  • Cholelithiasis was strongly associated with multiple (> or = 3 lesions, adjusted OR 2.39, 95% CI 1.21-4.72) and left-sided colorectal adenomas (adjusted OR 1.82, 95% CI 1.28-2.59).
  • CONCLUSIONS: Cholelithiasis is a risk factor for colorectal adenoma.
  • [MeSH-major] Adenoma / etiology. Cholelithiasis / complications. Colorectal Neoplasms / etiology

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  • (PMID = 18684172.001).
  • [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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11. Lai R Sr, Feng L, Liu L, Xie L, Wu X, Zhang S, Tang X, Geng J, Chen T: The clinical pathogensis significance associated with mutation of APC MCR in colorectal neoplasms. J Clin Oncol; 2009 May 20;27(15_suppl):e15119

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinical pathogensis significance associated with mutation of APC MCR in colorectal neoplasms.
  • : e15119 Background: To explore the clinical pathogensis evalution of codon 1493,1367 and 1328 mutations in MCR (mutation cluster region) of exon 15 of APC (Adenomatous polyposis coli) gene in cases of colorectal neoplasm and the family history.
  • METHODS: The specimens from 21 colorectal adenoma specimens groups,16 colorectal carcinoma groups, 20 healthy germline groups with positive familial history and 8 healthy germline groups without familial history.
  • The allele mutations were checked out four genotypes such as 4478(G→A), 41/69(59.4%); 4478(G/A), 22/69(31.9%); 4096(C/T), 1/69 (1.4%) and 3979(C/T), 5/69(7.2%); but the significant groups status (P<0.05) were shown between the adenoma and nonfamily history group on the analysis of 4478(G→A) and (G/A), also the significant differences were tested between the with and without family history on the analysis of 4478(G→A).
  • CONCLUSIONS: In our data, the highest mutant frequency 4478(G→A) of 1493(ACG>ACA) presented to the significant phenotype of positive history and adenoma, but 4478 (G/A) were associated with colorectal adenocancer, which was discovered in the different effect to candidators despite the same synonymous mutation.
  • In researches, APC MCR codon 1367 and 1328 genotyping were significantly presented in the colorectal cancergenetic phenotypes in somatic cells only.

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  • (PMID = 27960846.001).
  • [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
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Azuara D, Rodriguez-Moranta F, Soriano-Izquierdo A, Guardiola J, de Oca J, Biondo S, Blanco I, Esteller M, Capella G: Evaluation of stool melting curve analysis of methylated CpG island promoters as an alternative for early noninvasive diagnosis of colorectal tumors. J Clin Oncol; 2009 May 20;27(15_suppl):e15036

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of stool melting curve analysis of methylated CpG island promoters as an alternative for early noninvasive diagnosis of colorectal tumors.
  • : e15036 Background: Previous studies have shown that assessment of promoter hypermethylation of a limited number of genes in tumor biopsies may identify all colorectal tumors analyzed.
  • The aim of the present study was to assess the clinical usefulness of a panel of methylation biomarkers in stool DNA in the diagnosis of colorectal tumors using Methylation Curve (MC) analyses, a technique that simultaneously analyze all CpG residues within a promoter.
  • METHODS: Promoter methylation status of 5 tumor-related genes (RARB2, p16<sup>INK4a</sup>, MGMT, p14<sup>ARF</sup> and APC) was analyzed in DNA stool samples and corresponding tissues in an initial set of 12 newly diagnosed patients with primary colorectal carcinomas and 20 with colorectal adenomas using Methylation-specific PCR (MSP).
  • Results were validated in a set of 88 patients (20 healthy subjects, 17 inflammatory bowel disease, 23 adenomas, 28 carcinomas) using MC analyses.
  • RESULTS: In the initial set, the majority [10 of 12 (83%) carcinomas and 18 of 20 (90%) adenomas] of biopsies were positive for at least one marker.
  • In stool DNA prevalence was 75% for carcinomas (9 of 12) and 60% for adenomas (12 of 20) with no false positive in stools.
  • In the validation set MC analyses of biopsies showed that at least one marker was positive in 22 of 28 (79%) carcinomas and 16 of 23 (70%) adenomas.
  • In stool DNA, these percentages were 64% (18 of 28) for carcinomas and 42% (9 of 23) for adenomas.
  • CONCLUSIONS: Melting Curve analysis of a panel of methylation markers in stool DNA is a good alternative for the early non-invasive diagnosis of colorectal tumors.

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  • (PMID = 27964470.001).
  • [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
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Capella G, Castellsague E, Rennert G, Gruber S: APC allele-specific expression in carriers of Ashkenazi Jewish mutation I1307K. J Clin Oncol; 2009 May 20;27(15_suppl):e22181

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e22181 Background: I1307K is a missense APC variant with incomplete penetrance that has been found in 6% of Jewish Ashkenazi population and confers a two-fold increased risk to develop multiple adenomas and colorectal tumours.

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  • (PMID = 27963596.001).
  • [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
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Sinha R, Peters U, Cross AJ, Kulldorff M, Weissfeld JL, Pinsky PF, Rothman N, Hayes RB: Meat, meat cooking methods and preservation, and risk for colorectal adenoma. Cancer Res; 2005 Sep 1;65(17):8034-41
Hazardous Substances Data Bank. 2-Amino-3,8-dimethylimidazo[4,5-f]quinoxaline .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Meat, meat cooking methods and preservation, and risk for colorectal adenoma.
  • We investigated meat, processed meat, HCAs, and the PAH benzo(a)pyrene and the risk of colorectal adenoma in 3,696 left-sided (descending and sigmoid colon and rectum) adenoma cases and 34,817 endoscopy-negative controls.
  • Intake of red meat, with known doneness/cooking methods, was associated with an increased risk of adenoma in the descending and sigmoid colon [odds ratio (OR), 1.26; 95% confidence interval (95% CI), 1.05-1.50 comparing extreme quintiles of intake] but not rectal adenoma.
  • Well-done red meat was associated with increased risk of colorectal adenoma (OR, 1.21; 95% CI, 1.06-1.37).
  • Increased risks for adenoma of the descending colon and sigmoid colon were observed for the two HCAs: 2-amino-3,8-dimethylimidazo[4,5]quinoxaline and 2-amino-1-methyl-6-phenylimidazo[4,5]pyridine (OR, 1.18; 95% CI, 1.01-1.38 and OR, 1.17, 95% CI, 1.01-1.35, respectively) as well as benzo(a)pyrene (OR, 1.18; 95% CI, 1.02-1.35).
  • Greater intake of bacon and sausage was associated with increased colorectal adenoma risk (OR, 1.14; 95% CI, 1.00-1.30); however, total intake of processed meat was not (OR, 1.04; 95% CI, 0.90-1.19).
  • Our study of screening-detected colorectal adenomas shows that red meat and meat cooked at high temperatures are associated with an increased risk of colorectal adenoma.
  • [MeSH-major] Adenoma / etiology. Colorectal Neoplasms / etiology. Cooking. Food Preservation. Meat

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  • (PMID = 16140978.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Imidazoles; 0 / Mutagens; 0 / Quinoxalines; 3417WMA06D / Benzo(a)pyrene; 77500-04-0 / 2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline; 909C6UN66T / 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine
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15. 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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16. Tsilidis KK, Brancati FL, Pollak MN, Rifai N, Clipp SL, Hoffman-Bolton J, Helzlsouer KJ, Platz EA: Metabolic syndrome components and colorectal adenoma in the CLUE II cohort. Cancer Causes Control; 2010 Jan;21(1):1-10
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  • [Title] Metabolic syndrome components and colorectal adenoma in the CLUE II cohort.
  • BACKGROUND: Metabolic syndrome components have been associated with colorectal cancer in several studies; however, evidence for colorectal adenomas is limited.
  • Thus, we evaluated the association between markers of the metabolic syndrome with colorectal adenoma development in a nested case-control study.
  • METHODS: Colorectal adenoma cases (n = 132) and matched controls, who had a negative sigmoidoscopy or a colonoscopy (n = 260), were identified between baseline in 1989 and 2000 among participants in the CLUE II cohort of Washington County, Maryland.
  • RESULTS: No statistically significant associations with adenomas were observed for the markers of the metabolic syndrome, with the exception of a strong positive association for use of diabetes medications (OR, 8.00; 95% CI, 1.70-37.67), albeit based on small numbers.
  • CONCLUSION: Our findings do not support that components of the metabolic syndrome influence risk of colorectal adenomas, except possibly for severe diabetes mellitus warranting medical treatment.

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  • (PMID = 19774471.001).
  • [ISSN] 1573-7225
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA086308-05; United States / NIA NIH HHS / AG / AG18033; United States / NCI NIH HHS / CA / U01 CA086308; United States / NIA NIH HHS / AG / U01 AG018033-05; United States / NCI NIH HHS / CA / CA086308-05; United States / NCI NIH HHS / CA / CA86308; United States / NIA NIH HHS / AG / AG018033-05; United States / NIA NIH HHS / AG / U01 AG018033
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers
  • [Other-IDs] NLM/ NIHMS257633; NLM/ PMC3010872
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17. Hubner RA, Muir KR, Liu JF, Sellick GS, Logan RF, Grainge M, Armitage N, Chau I, Houlston RS: Folate metabolism polymorphisms influence risk of colorectal adenoma recurrence. Cancer Epidemiol Biomarkers Prev; 2006 Sep;15(9):1607-13
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  • [Title] Folate metabolism polymorphisms influence risk of colorectal adenoma recurrence.
  • Folate intake is inversely related to risk of developing colorectal neoplasia.
  • Associations between risk of colorectal neoplasia and polymorphisms in genes coding for enzymes involved in folate metabolism have also been reported, suggesting a relationship between genotype and development of colorectal neoplasia.
  • To further investigate the effects of folate metabolism genotypes on colorectal neoplasia, we genotyped 546 patients participating in a randomized controlled trial of folate supplementation for the prevention of colorectal adenoma recurrence.
  • These findings provide additional support for the hypothesis that germ line variants in folate metabolism genes influence the development of colorectal adenomas.
  • [MeSH-major] Adenoma / etiology. Colorectal Neoplasms / etiology. Folic Acid / metabolism. Neoplasm Recurrence, Local / etiology. Polymorphism, Genetic

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  • (PMID = 16985020.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 935E97BOY8 / Folic Acid; EC 1.18.1.- / methionine synthase reductase; EC 1.18.1.2 / Ferredoxin-NADP Reductase; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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18. Kang WY, Chen WT, Wu MT, Chai CY: The expression of CD66a and possible roles in colorectal adenoma and adenocarcinoma. Int J Colorectal Dis; 2007 Aug;22(8):869-74
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  • [Title] The expression of CD66a and possible roles in colorectal adenoma and adenocarcinoma.
  • BACKGROUND: The aim of our study was to analyze the expression and possible role of CD66a in colorectal adenoma and adenocarcinoma and the relationship between its expression and pre-operation serum carcinoembryonic antigen (CEA) level and tumor stage in patients with colorectal adenocarcinomas.
  • METHODS: Paraffin-embedded sections from 184 patients including 42 colorectal adenomas with low-grade dysplasia, 43 adenomas with high-grade dysplasia, and 99 adenocarcinomas were collected for this study.
  • RESULTS: The expression of CD66a was found not only in the apical membrane of neoplastic glands but also in secretion within the lumen of the neoplastic glands including adenomas and adenocarcinomas.
  • Expressions of secreted CD66a were of higher level in adenocarcinoma than in adenoma with high-grade dysplasia and adenoma with low-grade dysplasia (p < 0.0001).
  • High expression of secreted CD66a was also associated with tumor stage, invasion, and pre-operation serum CEA level of patients with colorectal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / immunology. Adenoma / immunology. Antigens, CD / analysis. Cell Adhesion Molecules / analysis. Colorectal Neoplasms / immunology

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  • (PMID = 17143599.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD66 antigens; 0 / CTNNB1 protein, human; 0 / Carcinoembryonic Antigen; 0 / Cell Adhesion Molecules; 0 / beta Catenin
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19. Park SY, Kim HS, Yoon KW, Cho SB, Lee WS, Park CH, Joo YE, Choi SK, Rew JS: [Prevalence of colorectal adenoma is increased in patients with gastric adenoma]. Korean J Gastroenterol; 2009 Oct;54(4):220-6
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  • [Title] [Prevalence of colorectal adenoma is increased in patients with gastric adenoma].
  • BACKGROUND/AIMS: It has been reported that patients with gastric cancer may be at increased risk of synchronous or metachronous colorectal cancer.
  • However, the incidence of colorectal adenoma in patients with gastric adenoma has not been discussed earlier.
  • The aims of this study were to investigate the incidence of colorectal adenoma and to evaluate the necessity of colonoscopic surveillance in patients with gastric adenoma.
  • METHODS: We performed colonoscopy in 221 patients with gastric adenoma between January 2002 and June 2008.
  • As a control group, 387 consecutive patients without gastric adenoma on gastroscopy who underwent colonoscopy were included.
  • RESULTS: Colorectal adenoma were diagnosed in 57.5% (127/221) of the gastric adenoma group and 38.0% (147/387) of the control group (p<0.001).
  • Univariate analysis demonstrated that gender, age, past history of diabetes, and past history of gastric adenoma were associated with the risk of colorectal adenoma.
  • Multivariate analysis demonstrated that gender (male, aOR 2.31, 95% CI 1.61-3.31), age (> or =50 years, aOR 2.47, 95% CI 1.53-4.01), past history of diabetes (aOR 2.35, 95% CI 1.32-4.20), and presence of gastric adenoma (aOR 1.63, 95% CI 1.13-2.36) appeared to be independent risk factors for colorectal adenoma.
  • CONCLUSIONS: The risk of colorectal adenoma increases significantly in patients with gastric adenoma.
  • We suggest that colonoscopic surveillance may be necessary in patients with gastric adenoma.
  • [MeSH-major] Adenoma / diagnosis. Colorectal Neoplasms / diagnosis. Stomach Neoplasms / diagnosis
  • [MeSH-minor] Age Factors. Aged. Colonoscopy. Diabetes Mellitus / diagnosis. Female. Humans. Male. Middle Aged. Prevalence. Retrospective Studies. Risk Factors. Sex Factors

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  • (PMID = 19844141.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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20. Chia VM, Newcomb PA, Lampe JW, White E, Mandelson MT, McTiernan A, Potter JD: Leptin concentrations, leptin receptor polymorphisms, and colorectal adenoma risk. Cancer Epidemiol Biomarkers Prev; 2007 Dec;16(12):2697-703
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  • [Title] Leptin concentrations, leptin receptor polymorphisms, and colorectal adenoma risk.
  • Obesity has been shown to be associated with an increased risk of both colorectal cancer and adenomatous polyps.
  • We conducted a gastroenterology clinic-based, case-control study to evaluate the relationship between circulating leptin concentrations and colorectal adenoma risk; in addition, we evaluated the relationship between leptin receptor polymorphisms and adenoma risk.
  • Individuals with adenomas (n = 157) and colonoscopy-negative controls (n = 191), who had a clinically indicated colonoscopy, were recruited from a large health maintenance organization in the Seattle metropolitan area from 1999 to 2003.
  • Odds ratios and 95% confidence intervals were obtained using logistic regression, adjusting for age at diagnosis, body mass index, family history of colorectal cancer, smoking history, nonsteroidal anti-inflammatory drug use, physical activity, and, among women, menopausal status and postmenopausal hormone use.
  • Among men, those in the highest tertile of leptin concentrations had a 3.3-fold (95% confidence interval, 1.2-8.7) increased adenoma risk compared with those in the lowest tertile (P trend = 0.01).
  • There were no associations between leptin concentrations and adenoma risk in women.
  • There were no associations of leptin receptor genotypes or haplotypes and adenoma risk.
  • The results of this study suggest that, in men, leptin may be associated with risk of colorectal adenomas.

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  • (PMID = 18086776.001).
  • [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 / P01CA74184; United States / NCI NIH HHS / CA / R03 CA110852; United States / NCI NIH HHS / CA / R25 CA094880; United States / NCI NIH HHS / CA / U01 CA074794; United States / NCI NIH HHS / CA / P01 CA074184; United States / NCI NIH HHS / CA / R25CA094880; United States / NCI NIH HHS / CA / R03CA11085
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Leptin; 0 / Receptors, Leptin
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21. Kim KS, Moon HJ, Choi CH, Baek EK, Lee SY, Cha BK, Lee HW, Kim HJ, Do JH, Chang SK: The Frequency and Risk Factors of Colorectal Adenoma in Health-Check-up Subjects in South Korea: Relationship to Abdominal Obesity and Age. Gut Liver; 2010 Mar;4(1):36-42
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  • [Title] The Frequency and Risk Factors of Colorectal Adenoma in Health-Check-up Subjects in South Korea: Relationship to Abdominal Obesity and Age.
  • BACKGROUND/AIMS: Obesity is associated with the risk of colorectal cancer.
  • However, there is a lack of information about the relationship between obesity and colorectal adenoma.
  • We investigated whether general and abdominal obesity are risk factors for colorectal adenoma.
  • The frequency and characteristics of colorectal adenomas were analyzed according to demographic features, past history, blood tests, body mass index, and components of metabolic syndrome.
  • In univariate analysis, abdominal obesity was significantly associated with the frequency of colorectal adenoma (26.5% "yes" vs 16.9% "no"; p<0.001).
  • The frequency of colorectal adenoma was significantly higher among males, older patients, current smokers, and subjects with fasting hyperglycemia (>/=100 mg/dL) or fatty liver (p<0.05).
  • Multivariate analysis identified that male sex (odds ratio [OR], 1.5; 95% confidence interval [CI], 1.0-2.2), old age (age >/=60 years; OR, 6.7; 95% CI, 3.5-12.5), and abdominal obesity (OR, 1.5; 95% CI, 1.0-2.2) were independent risk factors for colorectal adenoma (p<0.05).
  • The frequency of multiple adenomas (more than two sites) was also significantly higher in subjects with abdominal obesity.
  • However, the effect of abdominal obesity on the development of colorectal adenoma decreased in elderly people.
  • CONCLUSIONS: Abdominal obesity is an independent risk factor for colorectal adenoma and its multiplicity, especially in younger people in South Korea.

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  • (PMID = 20479911.001).
  • [ISSN] 2005-1212
  • [Journal-full-title] Gut and liver
  • [ISO-abbreviation] Gut Liver
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2871608
  • [Keywords] NOTNLM ; Abdominal obesity / Colorectal adenoma
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22. Lin YL, Chiang JK, Lin SM, Tseng CE: Helicobacter pylori infection concomitant with metabolic syndrome further increase risk of colorectal adenomas. World J Gastroenterol; 2010 Aug 14;16(30):3841-6
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  • [Title] Helicobacter pylori infection concomitant with metabolic syndrome further increase risk of colorectal adenomas.
  • AIM: To investigate the association of colorectal adenomas with both Helicobacter pylori (H. pylori) infection and metabolic syndrome.
  • Examined data included gender, age, life style, anthropometric measurements, blood pressure, biochemical and hematological studies, H. pylori infection detected by esophagogastroduodenoscopy and biopsy urease tests, and colorectal adenomas detected with a complete total colonoscopy.
  • RESULTS: The prevalence values for H. pylori infection, metabolic syndrome, and colorectal adenoma were 39.2%, 18.7%, and 20.7%, respectively.
  • Colorectal adenoma risk factors included male gender [odd ratio (OR): 2.005, 95% confidence interval (CI): 1.740-2.310, P < 0.001], advanced age (OR: 1.046, 95% CI: 1.040-1.052, P < 0.001), smoking (OR: 1.377, 95% CI: 1.146-1.654, P = 0.001), increased body fat (OR: 1.016, 95% CI: 1.007-1.026, P = 0.001), higher white blood cell count (OR: 1.038, 95% CI: 1.005-1.073, P = 0.025), H. pylori infection (OR: 1.366, 95% CI: 1.230-1.517, P < 0.001), and metabolic syndrome (OR: 1.408, 95% CI: 1.231-1.610, P < 0.001).
  • In addition, concomitant H. pylori infection with metabolic syndrome further increased the probability of colorectal adenomas.
  • CONCLUSION: Our study revealed H. pylori infection with concomitant metabolic syndrome might further increase the risk of colorectal adenomas.
  • [MeSH-major] Adenoma / etiology. Colorectal Neoplasms / etiology. Helicobacter Infections / complications. Helicobacter pylori / pathogenicity. Metabolic Syndrome X / complications

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  • (PMID = 20698048.001).
  • [ISSN] 2219-2840
  • [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
  • [Other-IDs] NLM/ PMC2921097
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23. Lim YJ, Kwack WG, Lee YS, Hahm KB, Kim YK: Increased pulse wave velocity reflecting arterial stiffness in patients with colorectal adenomas. J Clin Biochem Nutr; 2010 Nov;47(3):261-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased pulse wave velocity reflecting arterial stiffness in patients with colorectal adenomas.
  • The obese patients with diabetes or cardiovascular risk factors are associated with increased risk of colorectal cancer as well as adenomas under the shared pathogenesis related to atherosclerosis.
  • Here we determined the association between increased arterial stiffness and colorectal adenomas incorporating parameters including age, gender, waist circumference, body mass index, lipid profiles, fasting glucose, and blood pressure.
  • Subjects who simultaneously underwent colonoscopies and pulse wave velocity (PWV) determinations between July 2005 and September 2006 were analyzed, based on which the subjects were classified into two groups as patients group with colorectal adenomas (n = 49) and control group (n = 200) with normal, non-polypoid benign lesions or hyperplastic polyps.
  • Uni- and multi-variate analyses were performed to calculate the odd ratio for colon adenomas.
  • Based on uni-variate analysis, age, waist circumference, body mass index, heart-femoral PWV (hfPWV), and brachial-ankle PWV were significantly associated with adenomas (p<0.05) and multiple logistic regression analysis showed that the heart-femoral PWV, waist circumference, and the levels of LDL-C were significant risk factor for colorectal adenoma.
  • However, arterial stiffness did not affect the progression of colon adenoma.
  • The finding that hfPWV, reflecting aortic stiffness, was increased in patients with colorectal adenomas lead to conclusion that patients who have prominently increased arterial stiffness can be recommended to undergo colonoscopic examinations and at the same time we also recommend counseling about the risk for atherosclerosis in those who have colorectal adenomas.

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  • (PMID = 21103036.001).
  • [ISSN] 1880-5086
  • [Journal-full-title] Journal of clinical biochemistry and nutrition
  • [ISO-abbreviation] J Clin Biochem Nutr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Other-IDs] NLM/ PMC2966937
  • [Keywords] NOTNLM ; atherosclerosis / colon adenoma / pulse wave velocity / risk factors
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24. Nam SY, Kim BC, Han KS, Ryu KH, Park BJ, Kim HB, Nam BH: Abdominal visceral adipose tissue predicts risk of colorectal adenoma in both sexes. Clin Gastroenterol Hepatol; 2010 May;8(5):443-50.e1-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Abdominal visceral adipose tissue predicts risk of colorectal adenoma in both sexes.
  • BACKGROUND & AIMS: Small studies have shown inconsistent results regarding the association between abdominal visceral adipose tissue and colorectal adenomas.
  • We evaluated the effects of visceral adipose tissue volume on the development and growth of colorectal adenomas.
  • The associations between waist circumference, visceral adipose tissue volume, and colorectal adenomas were estimated with adjusted odds ratios and 95% confidence intervals (CIs).
  • In addition, the association between characteristics of colorectal adenomas and visceral adipose tissue volume was evaluated.
  • RESULTS: Compared with participants who had visceral adipose tissue volume of less than 500 cm(3), the odds ratio for colorectal adenoma was 1.09 (95% CI, 0.87-1.36) for a volume of 500 to 999 cm(3), 1.33 (95% CI, 1.04-1.69) for a volume of 1000 to 1499 cm(3), and 1.43 (95% CI, 1.06-1.94) for a volume of 1500 cm(3) or greater.
  • The risk of colorectal adenomas increased with increasing visceral adipose tissue volume in both sexes (P trend = .004 in men and .009 in women).
  • Waist circumference was associated with colorectal adenomas in men (P trend = .02), but not in women.
  • High volume of visceral adipose tissue (>or=1000 cm(3)) had a positive association with larger adenomas (>or=10 mm) and multiple adenomas.
  • CONCLUSIONS: Abdominal visceral adipose tissue volume can contribute to the development and growth of colorectal adenomas, and it was a better predictor for risk of colorectal adenomas than body mass index or waist circumference in both sexes.
  • [MeSH-major] Adenoma / epidemiology. Intra-Abdominal Fat / pathology. Obesity / complications

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  • [Copyright] Copyright (c) 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20144736.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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25. Jacobs ET, Martínez ME, Alberts DS, Jiang R, Lance P, Lowe KA, Thompson PA: Association between body size and colorectal adenoma recurrence. Clin Gastroenterol Hepatol; 2007 Aug;5(8):982-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association between body size and colorectal adenoma recurrence.
  • BACKGROUND & AIMS: Obesity has been associated with increased risk for colorectal adenoma, although its role as a risk factor after polypectomy for recurrence is unclear.
  • Therefore, we sought to evaluate the effect of anthropometric measures of obesity on adenoma after polypectomy.
  • METHODS: Subjects with baseline adenomas (n = 2465) and follow-up colonoscopy data were drawn from 2 randomized trials designed to prevent adenoma recurrence.
  • RESULTS: Over a mean follow-up period of 3.1 years presence of a body mass index (BMI) > or = 30 kg/m2 was associated with a nonsignificant 17% increase in the odds for any adenoma recurrence among all subjects (odds ratio [OR], 1.17; 95% confidence interval [CI], 0.92-1.48).
  • Analyses of the effects of obesity on more clinically significant lesions demonstrated that high BMI was a slightly stronger risk factor for advanced adenoma recurrences in men (OR, 1.62; 95% CI, 1.04-2.53) when compared with non-advanced lesions (OR, 1.26; 95% CI, 0.91-1.75).
  • In addition, we observed an association for obesity and odds of adenoma recurrence among participants reporting a family history of colorectal cancer (OR, 2.25; 95% CI, 1.32-3.84) but not for those without (OR, 1.00; 95% CI, 0.77 to 1.31; P(int) = P = .008).
  • CONCLUSIONS: Our results support obesity as a risk factor for subsequent short-interval (mean follow-up time 3.1 years) development of colorectal adenomas, particularly among men and persons with a family history of colorectal cancer.

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  • (PMID = 17553754.001).
  • [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 / K07 CA106269; United States / NCI NIH HHS / CA / P30 CA023074; United States / NCI NIH HHS / CA / 1K07CA10629-01A1; United States / NCI NIH HHS / CA / CA95060; United States / NCI NIH HHS / CA / CA-41108; United States / NCI NIH HHS / CA / P01 CA041108; United States / NCI NIH HHS / CA / P50 CA095060; United States / NCI NIH HHS / CA / CA-23074; United States / NCI NIH HHS / CA / K07 CA106269-01A1; United States / NCI NIH HHS / CA / CA106269-01A1; United States / NCI NIH HHS / CA / CA-77145
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS29366; NLM/ PMC2729188
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26. Keku TO, Lund PK, Galanko J, Simmons JG, Woosley JT, Sandler RS: Insulin resistance, apoptosis, and colorectal adenoma risk. Cancer Epidemiol Biomarkers Prev; 2005 Sep;14(9):2076-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Insulin resistance, apoptosis, and colorectal adenoma risk.
  • Compelling evidence from epidemiologic studies indicates that elevated circulating insulin-like growth factor (IGF)-I, insulin resistance, and associated complications, such as elevated fasting plasma insulin, glucose and free fatty acids, glucose intolerance, increased body mass index, and visceral adiposity, are linked with increased risk of colorectal cancer.
  • However, the role of insulin and markers of glucose control in the development of adenomas, precursors to colorectal cancer, has not been fully explored.
  • We evaluated the relationship between plasma insulin, glucose, IGF-I, IGF-II, IGF-binding protein-3 (IGFBP-3), apoptosis, and colorectal adenomas in a case-control study.
  • Participants were classified as cases or controls based on whether they had one or more colorectal adenomatous polyps.
  • Logistic regression was used to examine the association between adenoma status and insulin-IGF markers.
  • Adenoma cases (n = 239) and adenoma-free controls (n = 517) provided rectal biopsies and/or blood samples and interview data.
  • Those in the highest quartile of insulin (adjusted odds ratio, 2.2; 95% confidence interval, 1.1-4.2) and glucose (adjusted odds ratio, 1.8; 95% confidence interval, 0.9-3.6) were more likely to have an adenoma compared with the lowest quartile.
  • The results provide novel evidence that elevated insulin and glucose are associated with increased adenoma risk and decreased apoptosis in normal rectal mucosa.
  • These findings suggest that insulin may act early in the adenoma-carcinoma sequence to promote the development of colorectal adenoma by decreasing apoptosis in the normal mucosa.
  • [MeSH-major] Apoptosis. Colorectal Neoplasms / physiopathology. Insulin / physiology. Insulin Resistance
  • [MeSH-minor] Adenoma / epidemiology. Adenoma / etiology. Adenoma / physiopathology. Blood Glucose / analysis. Case-Control Studies. Cell Transformation, Neoplastic. Diet. Female. Humans. Life Style. Male. Middle Aged. Risk Assessment. Somatomedins / analysis

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  • (PMID = 16172212.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK34987; United States / NCI NIH HHS / CA / R01 CA 44684; United States / NCI NIH HHS / CA / R01 CA93654-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 0 / Somatomedins
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27. Sedjo RL, Byers T, Levin TR, Haffner SM, Saad MF, Tooze JA, D'Agostino RB Jr: Change in body size and the risk of colorectal adenomas. Cancer Epidemiol Biomarkers Prev; 2007 Mar;16(3):526-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Change in body size and the risk of colorectal adenomas.
  • Adiposity has been recognized as a risk factor for colorectal adenoma, but the influence of weight gain, adipose tissue distribution, and possible differences between ethnic/racial and gender groups remains unanswered.
  • The aim of this prospective study was to examine the association between adiposity and weight change and colorectal adenoma risk.
  • Multivariate logistic regression analyses were used to assess the association between colorectal adenomas and measures of adiposity and weight change over the approximately 10-year period before colonoscopy.
  • Obesity was positively associated with risk of colorectal adenomas at the time of colonoscopy [adjusted odds ratio (OR(adj)), 2.16; 95% confidence interval (95% CI), 1.13-4.14] and was stronger in women (OR(adj), 4.42; 95% CI, 1.53-12.78) than in men (OR(adj), 1.26; 95% CI, 0.52-3.07).
  • The risk of adenomas increased among participants who gained weight compared with those who maintained weight over the approximately 5 years (OR(adj), 2.30; 95% CI, 1.25-4.22) and approximately 10 years (OR(adj), 2.12; 95% CI, 1.25-3.62).
  • These associations were similar for both advanced and nonadvanced adenomas.
  • These results suggest a positive association between obesity, weight gain, and colorectal adenoma risk.
  • Stronger associations were observed when obesity was measured at the time of colonoscopy, suggesting that obesity may be a promoting factor in the growth of colorectal adenomas.
  • [MeSH-major] Adenomatous Polyps / epidemiology. Body Size. Colorectal Neoplasms / epidemiology

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  • (PMID = 17372248.001).
  • [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 / 1R01CA88007; United States / NIDDK NIH HHS / DK / DK07658; United States / NCI NIH HHS / CA / R01 CA88008
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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28. Gunter MJ, Canzian F, Landi S, Chanock SJ, Sinha R, Rothman N: Inflammation-related gene polymorphisms and colorectal adenoma. Cancer Epidemiol Biomarkers Prev; 2006 Jun;15(6):1126-31
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inflammation-related gene polymorphisms and colorectal adenoma.
  • Chronic inflammation has been reported to be a risk factor for colorectal neoplasia.
  • We hypothesized that a proinflammatory genotype would be positively associated with colorectal adenoma, a precursor of colorectal cancer.
  • We investigated the association of colorectal adenoma with 19 single nucleotide polymorphisms in a range of important proinflammatory (IL1B, IL6, IL8, TNF, and LTA) and anti-inflammatory (IL4, IL10, and IL13) cytokines and other inflammation-related genes (PTGS2 and PPARG) in a case-control study of risk factors for colorectal polyps in which all participants (ages 18-74 years) had undergone colonoscopy or sigmoidoscopy.
  • The study sample comprised 244 cases of colorectal adenoma and 231 polyp-free controls.
  • Compared with being homozygous for the common allele, heterozygosity at the IL1B -31 (C>T) locus was associated with an odds ratio (OR) for colorectal adenoma of 1.8 [95% confidence interval (95% CI), 1.2-2.9].
  • Homozygous carriers of the IL8 -251-A allele were at 2.7-fold increased risk of adenoma (95% CI, 1.5-4.9) compared with homozygosity for the common T allele, whereas carriage of at least one IL8 -251-A allele conferred a 1.5 increased odds of disease (95% CI, 1.0-2.4).
  • Among non-nonsteroidal anti-inflammatory drug users, there was a statistically significant association between the IL10 -819-T/T genotype and adenoma compared with the common IL10 -819-C/C genotype (OR, 3.9; 95% CI, 1.1-13.6), which was not evident among nonsteroidal anti-inflammatory drug users (OR, 0.7; 95% CI, 0.3-1.5; P(interaction) = 0.01).
  • These exploratory data provide evidence that polymorphic variation in genes that regulate inflammation could alter risk for colorectal adenoma.
  • [MeSH-major] Adenomatous Polyps / genetics. Biomarkers, Tumor / genetics. Colorectal Neoplasms / genetics. Cytokines / genetics. Cytokines / metabolism. Inflammation / genetics. Polymorphism, Single Nucleotide / genetics

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  • (PMID = 16775170.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Biomarkers, Tumor; 0 / Cytokines
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29. Legras A, Lièvre A, Bonaiti-Pellié C, Cottet V, Pariente A, Nalet B, Lafon J, Faivre J, Bonithon-Kopp C, Goasguen N, Penna C, Olschwang S, Laurent-Puig P, ANGH group: Mitochondrial D310 mutations in colorectal adenomas: an early but not causative genetic event during colorectal carcinogenesis. Int J Cancer; 2008 May 15;122(10):2242-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mitochondrial D310 mutations in colorectal adenomas: an early but not causative genetic event during colorectal carcinogenesis.
  • Somatic mutations of the D310 sequence of the mitochondrial DNA are reported in human cancers, including colorectal cancers (CRC).
  • The presence of these mutations at early or late steps of colorectal carcinogenesis is unknown.
  • The aim of this study was (i) to investigate the prevalence of D310 mutations in 64 colorectal adenomas and 36 liver metastases from 15 CRC patients, (ii) to assess the relation between D310 polymorphism and the risk of colorectal adenoma in a case-control study including 613 cases with colorectal adenoma and 572 polyp-free (PF) controls.
  • D310 mutations were found in colorectal adenomas and liver metastases from CRC patients in 27 and 33%, respectively and so are an early genetic event in colorectal carcinogenesis.
  • The frequency of the mutations increased significantly with the number of cytosines in the matched normal tissue D310 sequence (p < 0.001) but the distribution of D310 polymorphisms was not significantly different between adenoma cases (large (>9 mm) and small (<5 mm) adenomas) and PF controls (C(4)-C(7)TC(6): 47, 52 and 49%; C(8)TC(6): 44, 39 and 41%; C(9)-C(10)TC(6): 9, 9 and 10%, respectively; p > 0.05), suggesting that germline D310 polymorphism is not a risk factor for colorectal adenomas.
  • Considering their high frequency in colorectal adenomas, mitochondrial D310 mutations could represent a biomarker for early detection of CRC although their causative role in colorectal carcinogenesis remains uncertain.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. DNA, Mitochondrial / genetics. Germ-Line Mutation / genetics

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18224678.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Mitochondrial
  • [Investigator] Berthelémy P; Cassan P; Glikmanas M; Gatineau-Sailliant G; Courrier A; Pillon D; Michalet JP; Latrive JP; Guillan J; Blanchi A; Bour B; Morin T; Druart F; Legoux JL; Labarrière D; Naudy B; Goldfain D; Rotenberg A; Bories C; Andrieu A; Doll J; Staub JL
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30. Pendergrass CJ, Edelstein DL, Hylind LM, Phillips BT, Iacobuzio-Donahue C, Romans K, Griffin CA, Cruz-Correa M, Tersmette AC, Offerhaus GJ, Giardiello FM: Occurrence of colorectal adenomas in younger adults: an epidemiologic necropsy study. Clin Gastroenterol Hepatol; 2008 Sep;6(9):1011-5
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  • [Title] Occurrence of colorectal adenomas in younger adults: an epidemiologic necropsy study.
  • BACKGROUND & AIMS: The colorectal adenoma is the precursor lesion in virtually all colorectal cancers.
  • Occurrence of colorectal adenomas has been studied in older adults but analysis in younger adults is lacking.
  • METHODS: The prevalence by age, sex, race, and location, and the number of colorectal adenomas detected was investigated using epidemiologic necropsy in 3558 persons ages 20 to 89 autopsied from 1985 to 2004 at the Johns Hopkins Hospital.
  • RESULTS: The prevalence of colorectal adenomas in younger adults increased from 1.72% to 3.59% from the third to the fifth decade of life and then sharply increased after age 50.
  • In younger adults, adenomas were more prevalent in men than in women (risk ratio, 1.09; 95% confidence interval, 1.07-1.11) and in whites than in blacks (risk ratio, 1.28; 95% confidence interval, 1.26-1.31).
  • Overall, both younger and older adults had predominately left-sided adenomas, but blacks in both age groups had more right-sided adenomas.
  • Occurrence of 2 or more adenomas in younger adults and 5 or more in older adults was greater than 2 SDs from the mean.
  • CONCLUSIONS: Colorectal adenomas infrequently occur in younger adults and are more prevalent in the left colon.
  • Irrespective of age, blacks have more right-sided adenomas, suggesting the need for screening the entire colorectum.
  • Two or more adenomas in younger adults and 5 or more in older adults represents polyp burden outside the normal expectation.

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  • (PMID = 18558514.001).
  • [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 / K07 CA092445; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / P50 CA062924-06; United States / NCI NIH HHS / CA / P50 CA 62924-10
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS85837; NLM/ PMC2629450
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31. Ok KS, Kim YS, Kim HH, Ryu SH, Lee JH, Moon JS, Kang YK: [The difference of clinicopathologic features according to leptin expression in colorectal adenoma]. Korean J Gastroenterol; 2010 Jul;56(1):20-6
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  • [Title] [The difference of clinicopathologic features according to leptin expression in colorectal adenoma].
  • BACKGROUND/AIMS: Colorectal adenoma and cancer are known to be associated with obesity.
  • However, the association between adenoma and leptin remains controversial.
  • We evaluated the leptin expression in human colorectal adenoma and its correlation to clinicopathologic factors.
  • METHODS: Leptin expression was assessed by immunohistochemistry in 91 samples of colorectal adenoma larger than 5 mm, which were removed by endoscopic polypectomy.
  • In leptin positive group, the correlation of leptin expression with adenoma size and histological showed positive tendency without statistical significance.
  • CONCLUSIONS: Leptin expression of colorectal adenoma was associated with BMI.
  • The question of whether leptin contributes to colorectal adenoma development is unresolved and will require additional studies.
  • [MeSH-major] Adenoma / pathology. Colorectal Neoplasms / pathology. Leptin / metabolism

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  • (PMID = 20664314.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Leptin
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32. Ueda N, Maehara Y, Tajima O, Tabata S, Wakabayashi K, Kono S: Genetic polymorphisms of cyclooxygenase-2 and colorectal adenoma risk: the Self Defense Forces Health Study. Cancer Sci; 2008 Mar;99(3):576-81
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  • [Title] Genetic polymorphisms of cyclooxygenase-2 and colorectal adenoma risk: the Self Defense Forces Health Study.
  • Cyclooxygenase (COX) is a key enzyme in the formation of prostaglandins, and an inducible isoform of COX, COX-2, has been implicated in colorectal carcinogenesis.
  • This study investigated the relation of COX-2 polymorphisms (-1195G>A, -765G>C and 8160A>G) to colorectal adenomas in a case-control study of male officials in the Self Defense Forces (SDF).
  • The study subjects were 455 cases of colorectal adenoma and 1052 controls with no polyps who underwent total colonoscopy.
  • A statistically non-significant decrease in the risk of colorectal adenomas was observed for the AA versus GG genotype of -1195G>A polymorphism and for the GC versus GG genotype of -765G>C polymorphism.
  • A haplotype of -1195G, -765G and 8160A alleles was associated with a modest increase in the risk (adjusted odds ratio [OR] 1.38, 95% confidence interval [CI] 0.99-1.91), and the increase was more evident for distal adenomas (adjusted OR 1.57, 95% CI 1.04-2.38).
  • These findings add to evidence for the role of COX-2 in colorectal carcinogenesis and warrant further studies focusing on haplotypes.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Cyclooxygenase 2 / genetics. Polymorphism, Single Nucleotide

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  • (PMID = 18167131.001).
  • [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 1.14.99.1 / Cyclooxygenase 2
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33. Soreide K, Buter TC, Janssen EA, Gudlaugsson E, Skaland I, Körner H, Baak JP: Cell-cycle and apoptosis regulators (p16INK4A, p21CIP1, beta-catenin, survivin, and hTERT) and morphometry-defined MPECs predict metachronous cancer development in colorectal adenoma patients. Cell Oncol; 2007;29(4):301-13
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  • [Title] Cell-cycle and apoptosis regulators (p16INK4A, p21CIP1, beta-catenin, survivin, and hTERT) and morphometry-defined MPECs predict metachronous cancer development in colorectal adenoma patients.
  • BACKGROUND AND AIMS: Although adenomas may be precursors to colorectal cancers (CRC), knowledge concerning the development of metachronous CRC is scarce.
  • We assessed whether differential expression of cell-cycle and apoptosis-regulating proteins and a monotonous population of elongated cells (MPECs) in colorectal adenomas could predict metachronous CRC.
  • METHODS: Application of immunohistochemistry on tissue microarrays in consecutive, population-based colorectal adenomas.
  • RESULTS: Of 171 patients with colorectal adenoma 86% (n=147) were eligible for study; 10 (7%) developed metachronous CRC.
  • Within adenomas containing MPECs, several molecular markers further defined high-risk patients.
  • CONCLUSIONS: Among several markers predictive for metachronous CRC development in colorectal adenomas, MPECs, survivin and hTERT may, when validated, provide information superior to conventional histology, with relevance for the clinical management of patients with colorectal adenoma.
  • [MeSH-major] Adenoma / pathology. Apoptosis Regulatory Proteins / metabolism. Cell Cycle Proteins / metabolism. Colorectal Neoplasms / pathology. Neoplasms, Second Primary / pathology

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  • (PMID = 17641414.001).
  • [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] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / beta Catenin; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC4617994
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34. 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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35. Lièvre A, Milet J, Carayol J, Le Corre D, Milan C, Pariente A, Nalet B, Lafon J, Faivre J, Bonithon-Kopp C, Olschwang S, Bonaiti-Pellié C, Laurent-Puig P, members of the ANGH group: Genetic polymorphisms of MMP1, MMP3 and MMP7 gene promoter and risk of colorectal adenoma. BMC Cancer; 2006;6:270
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  • [Title] Genetic polymorphisms of MMP1, MMP3 and MMP7 gene promoter and risk of colorectal adenoma.
  • BACKGROUND: Matrix metalloproteinases (MMP) have been shown to play a role in colorectal cancer (CRC).
  • To document the role of MMP polymorphisms in the early step of colorectal carcinogenesis, we investigated their association with colorectal adenoma risk in a case-control study comprising 295 patients with large adenomas (LA), 302 patients with small adenomas (SA) and 568 polyp-free (PF) controls.
  • Association between MMP genotypes and colorectal adenomas was first tested for each polymorphism separately and then for combined genotypes using the combination test.
  • CONCLUSION: These data show a relation between MMP1 -1607 ins/del G and MMP3 -1612 ins/delA combined polymorphisms and risk of SA, suggesting their potential role in the early steps of colorectal carcinogenesis.
  • [MeSH-major] Adenomatous Polyps / genetics. Colorectal Neoplasms / genetics. Matrix Metalloproteinase 1 / genetics. Matrix Metalloproteinase 3 / genetics. Matrix Metalloproteinase 7 / genetics. Polymorphism, Genetic / genetics

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  • (PMID = 17125518.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.24.17 / Matrix Metalloproteinase 3; EC 3.4.24.23 / Matrix Metalloproteinase 7; EC 3.4.24.7 / Matrix Metalloproteinase 1
  • [Other-IDs] NLM/ PMC1687194
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36. Elwing JE, Gao F, Davidson NO, Early DS: Type 2 diabetes mellitus: the impact on colorectal adenoma risk in women. Am J Gastroenterol; 2006 Aug;101(8):1866-71
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  • [Title] Type 2 diabetes mellitus: the impact on colorectal adenoma risk in women.
  • OBJECTIVES: Increased risk for colorectal cancer (CRC) has been associated with type 2 diabetes.
  • Despite several studies linking insulin resistance to increased CRC risk, there are limited data on colorectal adenoma risk in diabetic women.
  • We hypothesized that diabetic women would have increased rates of colorectal adenomas relative to a group of nondiabetic women.
  • METHODS: Colorectal adenoma rates were determined in 100 estrogen-negative women with type 2 diabetes mellitus and compared with 500 nondiabetic, estrogen-negative controls.
  • Adenomas were defined as any adenoma or advanced adenoma (villous or tubulovillous features, size >1 cm or high-grade dysplasia).
  • A multivariate model including age, race, diabetes, hypertension, hypercholesterolemia, body mass index, and nonsteroidal anti-inflammatory drug status was used to determine the independent effects of diabetes on colorectal adenoma incidence.
  • RESULTS: Diabetics as compared with nondiabetics had greater rates of any adenoma (37%vs 24%, p= 0.009) and advanced adenomas (14%vs 6%, p= 0.009).
  • Two hundred forty-five obese subjects compared with 355 nonobese subjects had a higher rate of any adenoma (32%vs 22%, p= 0.001).
  • Obese diabetics compared with nonobese, nondiabetics had greater rates of any adenoma (42%vs 23%, p< or = 0.001) and advanced adenomas (19%vs 7%, p< or = 0.001).
  • Multivariate analysis showed that adenomas and advanced adenomas were independently predicted by diabetes (p < 0.05) and adenomas by age.
  • DISCUSSION: Women with type 2 diabetes mellitus had higher rates of colorectal adenomas as compared with lean and nondiabetic women.
  • This finding adds to the evidence that type 2 diabetes is an important factor in the progression of the adenoma-carcinoma sequence.

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  • [CommentIn] Am J Gastroenterol. 2007 Feb;102(2):466-7 [17311671.001]
  • [CommentIn] Am J Gastroenterol. 2007 Mar;102(3):692 [17335459.001]
  • (PMID = 16790036.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK056341-05S2; United States / NIDDK NIH HHS / DK / P30 DK056341; United States / NHLBI NIH HHS / HL / HL38180; None / None / / P30 DK056341-06; United States / NIDDK NIH HHS / DK / P30 DK056341-06; United States / NIDDK NIH HHS / DK / DK52574; None / None / / P30 DK056341-05S2; United States / NIDDK NIH HHS / DK / DK56260
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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37. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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38. Hubner RA, Muir KR, Liu JF, Logan RF, Grainge M, Armitage N, Shepherd V, Popat S, Houlston RS, United Kingdom Colorectal Adenoma Prevention Consortium: Genetic variants of UGT1A6 influence risk of colorectal adenoma recurrence. Clin Cancer Res; 2006 Nov 1;12(21):6585-9
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  • [Title] Genetic variants of UGT1A6 influence risk of colorectal adenoma recurrence.
  • Functional polymorphisms of UGT1A6 (T181A and R184S) and CYP2C9 (R144C and I359L) have been reported to modify the protective effect of aspirin on colorectal adenoma risk.
  • We aimed to further investigate the effect of these genetic variants on the development of colorectal neoplasia.
  • EXPERIMENTAL DESIGN: We examined the relationship between UGT1A6 and CYP2C9 genotype and colorectal adenoma recurrence in 546 patients participating in a randomized placebo-controlled aspirin intervention trial.
  • RESULTS: Although colorectal adenoma recurrence was not significantly influenced by CYP2C9 genotype, carriers of variant UGT1A6 alleles were at significantly reduced risk of colorectal neoplasia recurrence [relative risk (RR), 0.68; 95% confidence interval (95% CI), 0.52-0.89].
  • CONCLUSIONS: These findings confirm that UGT1A6 variants influence colorectal carcinogenesis independent of aspirin intake and suggest that they may have clinical value in secondary prevention programs for patients diagnosed with colorectal adenoma.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Genetic Predisposition to Disease. Glucuronosyltransferase / genetics. Neoplasm Recurrence, Local / genetics

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  • (PMID = 17085674.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; EC 2.4.1.- / UDP-glucuronosyltransferase, UGT1A6; EC 2.4.1.17 / Glucuronosyltransferase; R16CO5Y76E / Aspirin
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39. Yamaji T, Iwasaki M, Sasazuki S, Kurahashi N, Mutoh M, Yamamoto S, Suzuki M, Moriyama N, Wakabayashi K, Tsugane S: Visceral fat volume and the prevalence of colorectal adenoma. Am J Epidemiol; 2009 Dec 15;170(12):1502-11
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  • [Title] Visceral fat volume and the prevalence of colorectal adenoma.
  • Few epidemiologic investigations of visceral adiposity and colorectal neoplasms have attempted the direct quantification of visceral fat.
  • The authors measured visceral fat volume among middle-aged and elderly Japanese men and women who underwent colonoscopy and positron emission tomography/computed tomography for cancer screening in Tokyo, Japan, between February 2004 and February 2005, and examined the association between visceral adiposity and colorectal adenoma in 1,205 eligible subjects.
  • Odds ratios and 95% confidence intervals for colorectal adenoma were estimated by using an unconditional logistic regression model after adjustment for potential confounders.
  • Despite its high correlation with body mass index, visceral fat volume was associated with the prevalence of colorectal adenoma independently of body mass index in both sexes.
  • After further adjustment for body mass index, the odds ratio of colorectal adenoma for the highest compared with the lowest quartile of visceral fat volume was 1.58 (95% confidence interval: 1.11, 2.24) for men and women combined.
  • Conversely, body mass index was unlikely to modify the association between visceral fat volume and colorectal adenoma (P(interaction) = 0.39).
  • These findings add to accumulating evidence that visceral adiposity exerts an important influence on the pathogenesis of colorectal neoplasms.
  • The mechanisms of this potential association between visceral adiposity and colorectal carcinogenesis warrant further investigation.
  • [MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Intra-Abdominal Fat / pathology

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  • (PMID = 19923108.001).
  • [ISSN] 1476-6256
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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40. Hamilton KE, Lund PK, Galanko JA, Sandler RS, Keku TO: Suppressor of cytokine signaling 3 (SOCS3) is not an independent biomarker of colorectal adenoma risk. BMC Res Notes; 2010;3:144
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  • [Title] Suppressor of cytokine signaling 3 (SOCS3) is not an independent biomarker of colorectal adenoma risk.
  • BACKGROUND: Inflammation and its associated pathologies are increasingly suggested as risk factors for colorectal cancer (CRC) development.
  • Previous research from our group has shown that increased levels of circulating, pro-inflammatory cytokines IL-6 and TNFalpha promote colorectal adenoma risk.
  • Emerging data in mice and humans suggest that Suppressor of Cytokine Signaling 3 (SOCS3) may act as a tumor suppressor in the intestine, and decreased SOCS3 expression may promote CRC.
  • As SOCS3 has been shown to inhibit the actions of IL-6 and TNFalpha in the intestine, we hypothesized that decreased SOCS3 expression in normal mucosa may predispose to adenomas and thus increase risk for CRC.
  • FINDINGS: We examined SOCS3 mRNA levels in normal mucosa biopsies of 322 screening colonoscopy patients (93 with adenoma and 229 without adenoma) using real-time qRT-PCR.
  • Logistic regression analysis was used to generate odds ratios (OR) and 95% confidence intervals to determine if low SOCS3 expression was associated with adenoma status.
  • Median SOCS3 values did not differ between patients with or without adenoma.
  • Logistic regression analysis showed no association (unadjusted or adjusted for age and sex) between SOCS3 and colorectal adenomas.
  • CONCLUSIONS: Low SOCS3 mRNA expression is not an independent biomarker of colorectal adenoma risk in the normal mucosa.

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  • [Cites] J Exp Med. 2001 Feb 19;193(4):471-81 [11181699.001]
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  • (PMID = 20500855.001).
  • [ISSN] 1756-0500
  • [Journal-full-title] BMC research notes
  • [ISO-abbreviation] BMC Res Notes
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES010126; United States / NIDDK NIH HHS / DK / R01 DK047769
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2883989
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41. Martínez ME, Giovannucci E, Jiang R, Henning SM, Jacobs ET, Thompson P, Smith-Warner SA, Alberts DS: Folate fortification, plasma folate, homocysteine and colorectal adenoma recurrence. Int J Cancer; 2006 Sep 15;119(6):1440-6
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  • [Title] Folate fortification, plasma folate, homocysteine and colorectal adenoma recurrence.
  • In 1996, the US Food and Drug Administration mandated the fortification of grain products with folic acid, a nutrient that has been associated with lower risk of colorectal neoplasia.
  • We assessed the relation of plasma folate and homocysteine and colorectal adenoma recurrence separately in 2 studies: the first involved an intervention of a cereal supplement that contained folic acid, wheat bran fiber (WBF), and the second was conducted primarily during postfortification of the food supply using ursodeoxycholic acid (UDCA).
  • Results show that plasma folate and homocysteine concentrations were associated with adenoma recurrence among nonusers of multivitamins only.
  • Among nonmultivitamin users, the odds ratio [OR] (95% confidence interval [CI]) for those in the highest versus the lowest folate quartile was 0.65 (0.40-1.06) for the WBF study and 0.56 (0.31-1.02) for the UDCA; likewise, individuals in the highest versus the lowest quartile of homocysteine had higher odds of adenoma recurrence, in both the WBF (OR = 2.25; 95% CI = 1.38-3.66) and UDCA (OR = 1.93; 95% CI = 1.07-3.49) populations.
  • [MeSH-major] Adenoma / blood. Colorectal Neoplasms / blood. Folic Acid / blood. Food, Fortified. Homocysteine / blood. Neoplasm Recurrence, Local / blood

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  • (PMID = 16615116.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA23074; United States / NCI NIH HHS / CA / CA41108; United States / NCI NIH HHS / CA / CA42710; United States / NCI NIH HHS / CA / CA95060
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0LVT1QZ0BA / Homocysteine; 12001-76-2 / Vitamin B Complex; 724L30Y2QR / Ursodeoxycholic Acid; 935E97BOY8 / Folic Acid
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42. Hou L, Chatterjee N, Huang WY, Baccarelli A, Yadavalli S, Yeager M, Bresalier RS, Chanock SJ, Caporaso NE, Ji BT, Weissfeld JL, Hayes RB: CYP1A1 Val462 and NQO1 Ser187 polymorphisms, cigarette use, and risk for colorectal adenoma. Carcinogenesis; 2005 Jun;26(6):1122-8
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  • [Title] CYP1A1 Val462 and NQO1 Ser187 polymorphisms, cigarette use, and risk for colorectal adenoma.
  • Cigarette use is a risk factor for colorectal adenoma, a known precursor of colorectal cancer.
  • Polymorphic variants in NQO1 and CYP1A1 influence the activation of carcinogenic substances in tobacco smoke, possibly impacting on tobacco-associated risks for colorectal tumors.
  • We investigated the association of cigarette smoking with risk for advanced colorectal adenoma in relation to the CYP1A1 Val(462) and NQO1 Ser(187) polymorphic variants.
  • Subjects were 725 non-Hispanic Caucasian cases with advanced colorectal adenoma of the distal colon (descending colon, sigmoid and rectum) and 729 gender- and ethnicity-matched controls, randomly selected from participants in the prostate, lung, colorectal and ovarian cancer screening trial.
  • Subjects carrying either CYP1A1 Val(462) or NQO1 Ser(187) alleles were weakly associated with risk of colorectal adenoma; however, subjects carrying both CYP1A1 Val(462) and NQO1 Ser(187) alleles showed increased risks (OR = 2.2, 95% CI = 1.1-4.5), particularly among recent (including current) (OR = 17.4, 95% CI = 3.8-79.8, P for interaction = 0.02) and heavy cigarette smokers (>20 cigarettes/day) (OR = 21.1, 95% CI = 3.9-114.4, P for interaction = 0.03) compared with non-smokers who did not carry either of these variants.
  • In analysis of adenoma subtypes, the combined gene variants were most strongly associated with the presence of multiple adenoma (P = 0.002).
  • In summary, joint carriage of CYP1A1 Val(462) and NQO1 Ser(187) alleles, particularly in smokers, was related to colorectal adenoma risk, with a propensity for formation of multiple lesions.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Cytochrome P-450 CYP1A1 / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Polymorphism, Genetic. Smoking / adverse effects

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  • (PMID = 15731166.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
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43. Perfumo C, Bonelli L, Menichini P, Inga A, Gismondi V, Ciferri E, Percivale P, Bianchi Scarrà G, Nasti S, Fronza G, Varesco L: Increased risk of colorectal adenomas in Italian subjects carrying the p53 PIN3 A2-Pro72 haplotype. Digestion; 2006;74(3-4):228-35
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  • [Title] Increased risk of colorectal adenomas in Italian subjects carrying the p53 PIN3 A2-Pro72 haplotype.
  • BACKGROUND: Few reports have investigated the association of two p53 polymorphisms (Arg72Pro and PIN3-A2) with colorectal cancer (CRC) risk, and no previous study has analyzed their role as susceptibility alleles for colorectal adenoma.
  • AIM: To explore the impact of the p53 PIN3-Arg72Pro haplotype on colorectal adenoma formation and progression to cancer.
  • METHODS: One hundred and eighty-four colorectal tumor patients (124 with adenomas and 60 with adenocarcinoma) and 188 controls (42 subjects with a clean colon, 54 hospital controls and 92 blood donors) from the Italian population were tested for PIN3-Arg72Pro haplotype status.
  • RESULTS: A significantly increased risk of colorectal adenomas was observed in patients carrying the PIN3 A2-Pro72 haplotype (OR = 2.02, 95% CI: 1.17-3.48; p = 0.01), while those carrying the PIN3 A1-Pro72 haplotype had a significantly increased risk of developing CRC (OR = 3.33; 95% CI: 1.40-7.89; p = 0.006).
  • No association was observed between the pathologic features of adenomas, the Arg72Pro and PIN3 polymorphisms, and the PIN3-Arg72Pro haplotype.
  • CONCLUSIONS: Our finding that two different p53 haplotypes are associated with colorectal adenoma and cancer, respectively, suggests that each of these haplotypes may independently impact on p53 function(s) within different genetic pathways of colorectal carcinogenesis.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Genes, p53 / genetics. Genetic Predisposition to Disease / epidemiology. Heterozygote. Polymorphism, Genetic

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  • [Copyright] 2006 S. Karger AG, Basel
  • (PMID = 17374954.001).
  • [ISSN] 1421-9867
  • [Journal-full-title] Digestion
  • [ISO-abbreviation] Digestion
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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44. Hermann S, Rohrmann S, Linseisen J: Lifestyle factors, obesity and the risk of colorectal adenomas in EPIC-Heidelberg. Cancer Causes Control; 2009 Oct;20(8):1397-408
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  • [Title] Lifestyle factors, obesity and the risk of colorectal adenomas in EPIC-Heidelberg.
  • OBJECTIVE: We investigated the association of lifestyle and obesity with colorectal adenoma risk in a prospective setting.
  • Until June 2007, 536 verified incident colorectal adenomas were identified.
  • RESULTS: In multivariate logistic regression analyses, participants with highest alcohol intake had an increased adenoma risk (odds ratio [OR] = 1.63; 95% CI 1.21-2.22) compared with lowest intake group.
  • Current smokers had a significantly increased adenoma risk compared with never smokers (OR = 1.40; 95% CI 1.16-1.84).
  • Physical activity, body mass index, and waist-to-hip ratio were not consistently associated with adenoma risk.
  • CONCLUSIONS: The results of this prospective cohort study showed that alcohol intake and smoking are important risk factors for colorectal adenoma, and regular NSAID use decreases the risk.
  • The relationship between alcohol consumption and adenoma risk was modified by folate intake.
  • However, we could not confirm an effect of obesity or physical activity on adenoma risk.
  • [MeSH-major] Adenoma / etiology. Colorectal Neoplasms / etiology. Life Style. Obesity / complications

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  • (PMID = 19466571.001).
  • [ISSN] 1573-7225
  • [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 / Anti-Inflammatory Agents, Non-Steroidal
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45. 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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46. Pot GK, Geelen A, van Heijningen EM, Siezen CL, van Kranen HJ, Kampman E: Opposing associations of serum n-3 and n-6 polyunsaturated fatty acids with colorectal adenoma risk: an endoscopy-based case-control study. Int J Cancer; 2008 Oct 15;123(8):1974-7
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  • [Title] Opposing associations of serum n-3 and n-6 polyunsaturated fatty acids with colorectal adenoma risk: an endoscopy-based case-control study.
  • Several human and animal studies have shown that n-3 polyunsaturated fatty acids (PUFA) might be associated with a decreased risk, whereas other studies showed that n-6 PUFA may be associated with an increased risk of colorectal cancer.
  • We evaluated the associations between serum n-3 and n-6 PUFA levels and colorectal adenoma risk in an endoscopy-based case-control study, conducted in The Netherlands between 1997 and 2002.
  • We included 363 cases of colorectal adenomas and 498 adenoma-free controls.
  • Total serum n-3 PUFA levels were inversely associated with colorectal adenoma risk, the OR comparing the third tertile with the first tertile was 0.67 [95% confidence interval (CI) 0.46-0.96, p for trend = 0.03].
  • Serum eicosapentaenoic acid (EPA; C20:5n-3) and docosahexaenoic acid (DHA; C22:6n-3) and the n-3/n-6 ratio were inversely associated with colorectal adenoma risk, but these were not statistically significant.
  • In contrast, the risk of colorectal adenomas was increased by total n-6 PUFA with an OR of 1.68 (95% CI, 1.17-2.42, p for trend = 0.006) and by linoleic acid (LA; C18:2n-6) with an OR of 1.65 (95% CI, 1.15-2.38, p for trend = 0.007).
  • This is the first observational study that simultaneously finds an inverse association of serum n-3 PUFA and a positive association of n-6 PUFA with colorectal adenoma risk.
  • [MeSH-major] Adenoma / blood. Colorectal Neoplasms / blood. Fatty Acids, Omega-3 / blood. Fatty Acids, Omega-6 / blood

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  • (PMID = 18661525.001).
  • [ISSN] 1097-0215
  • [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 / Fatty Acids, Omega-3; 0 / Fatty Acids, Omega-6
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47. Deng ZL, Xie DW, Bostick RM, Miao XJ, Gong YL, Zhang JH, Wargovich MJ: Novel genetic variations of the p53R2 gene in patients with colorectal adenoma and controls. World J Gastroenterol; 2005 Sep 7;11(33):5169-73
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  • [Title] Novel genetic variations of the p53R2 gene in patients with colorectal adenoma and controls.
  • METHODS: We screened the p53R2 gene coding regions and a regulatory region which contains a p53 binding sequence in 100 patients with colorectal adenoma and 100 control subjects using PCR, cold SSCP, and direct DNA sequencing.
  • Additionally, we determined the frequency of these p53R2 variants in a recently concluded case-control study of incident sporadic colorectal adenomas (163 cases and 210 controls).

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  • (PMID = 16127747.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA066539; United States / NCI NIH HHS / CA / R03 CA092773
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 1.17.4.- / Ribonucleotide Reductases; EC 1.17.4.- / ribonucleotide reductase R2 subunit
  • [Other-IDs] NLM/ PMC4320390
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48. Morita T, Tabata S, Mineshita M, Mizoue T, Moore MA, Kono S: The metabolic syndrome is associated with increased risk of colorectal adenoma development: the Self-Defense Forces health study. Asian Pac J Cancer Prev; 2005 Oct-Dec;6(4):485-9
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  • [Title] The metabolic syndrome is associated with increased risk of colorectal adenoma development: the Self-Defense Forces health study.
  • Hyperinsulinemia is also a postulated biological risk factor for colorectal carcinogenesis.
  • We therefore here examined the relation between the metabolic syndrome and colorectal adenoma development.
  • The study subjects were 756 cases of colorectal adenoma and 1751 controls with no polyps who underwent total colonoscopy during the period January 1995 to March 2002 at two Self Defense Forces (SDF) hospitals in Japan.
  • The metabolic syndrome was found to be associated with a moderately increased risk of colorectal adenomas whether either of the Japanese and Asian criteria was used; adjusted odds ratios with the Japanese and Asian criteria were 1.38 (95% confidence interval [CI] 1.13-1.69) and 1.48 (95% CI 1.13-1.93), respectively.
  • Increased risk was more evident for proximal than distal colon or rectal adenomas, and was almost exclusively observed for large lesions (5 mm in diameter).
  • Thus the metabolic syndrome appears to be an important entity with regard to the prevention of colorectal cancer, as well as cardiovascular disease and type 2 diabetes.
  • [MeSH-major] Adenoma / etiology. Asian Continental Ancestry Group. Colonic Neoplasms / etiology. Metabolic Syndrome X / complications. Military Personnel. Rectal Neoplasms / etiology

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  • (PMID = 16435997.001).
  • [ISSN] 1513-7368
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Thailand
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49. 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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50. Wei MY, Garland CF, Gorham ED, Mohr SB, Giovannucci E: Vitamin D and prevention of colorectal adenoma: a meta-analysis. Cancer Epidemiol Biomarkers Prev; 2008 Nov;17(11):2958-69
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  • [Title] Vitamin D and prevention of colorectal adenoma: a meta-analysis.
  • BACKGROUND: Vitamin D status is associated inversely with risk of colorectal cancer, but the association with adenoma risk is less clear.
  • This meta-analysis examined the overall relationship between circulating (plasma or serum) 25-hydroxyvitamin D [25(OH)D], vitamin D intake (dietary, supplemental, or total), and colorectal adenoma incidence in published studies.
  • METHODS: A meta-analysis composed of 17 epidemiologic studies [1 cross-sectional, 9 case-control, and 7 cohort or nested case-control studies; 7 on 25(OH)D and 12 on vitamin D intake] published before December 2007 was done to examine the association between circulating 25(OH)D, vitamin D intake, and colorectal adenomas.
  • RESULTS: Circulating 25(OH)D was inversely associated with risk of colorectal adenomas: the OR was 0.70 [95% confidence interval (95% CI), 0.56-0.87] for high versus low circulating 25(OH)D.
  • The highest quintile of vitamin D intake was associated with an 11% marginally decreased risk of colorectal adenomas compared with low vitamin D intake (OR, 0.89; 95% CI, 0.78-1.02).
  • For recurrent adenomas, there was a decreased risk of 12% (95% CI, 0.72-1.07) among individuals with high versus low vitamin D intake.
  • The inverse associations appeared stronger for advanced adenoma [OR, 0.64; 95% CI, 0.45-0.90 for serum 25(OH)D and OR, 0.77; 95% CI, 0.63-0.95 for vitamin D intake], but the number of studies was small.
  • CONCLUSIONS: Both circulating 25(OH)D and vitamin D intake were inversely associated with colorectal adenoma incidence and recurrent adenomas.
  • These results further support a role of vitamin D in prevention of colorectal adenoma incidence and recurrence.
  • [MeSH-major] Adenoma / prevention & control. Colorectal Neoplasms / prevention & control. Vitamin D / analogs & derivatives

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  • (PMID = 18990737.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 1406-16-2 / Vitamin D; 64719-49-9 / 25-hydroxyvitamin D
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51. Kim JH, Lim YJ, Kim YH, Sung IK, Shim SG, Oh SO, Park SS, Yang S, Son HJ, Rhee PL, Kim JJ, Rhee JC, Choi YH: Is metabolic syndrome a risk factor for colorectal adenoma? Cancer Epidemiol Biomarkers Prev; 2007 Aug;16(8):1543-6
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  • [Title] Is metabolic syndrome a risk factor for colorectal adenoma?
  • BACKGROUND AND AIMS: Epidemiologic studies provide evidence for a link between obesity or diabetes and the risk for colorectal cancer.
  • However, there is a lack of information about the relationship between metabolic syndrome and colorectal adenoma.
  • Therefore, we investigated whether metabolic syndrome is a risk factor for colorectal adenoma.
  • We classified a total of 2,531 subjects into the adenoma group (n = 731) and the control group (n = 1,800), including normal colonoscopic finding, nonpolyp benign lesions, or histologically confirmed hyperplastic polyp.
  • RESULTS: The prevalence for metabolic syndrome was 17% in the adenoma group and 11% in the control group.
  • On the multiple logistic regression analyses, metabolic syndrome was found to be associated with an increased risk of colorectal adenoma (odds ratio, 1.51; 95% confidence interval, 1.18-1.93).
  • Also, waist circumference among the individual components of metabolic syndrome was an independent risk factor for colorectal adenoma.
  • An increased risk for metabolic syndrome was more evident for proximal than distal colon, for multiple (>/=3), and for advanced adenoma in the adenoma group.
  • CONCLUSION: Metabolic syndrome was associated with colorectal adenoma.
  • Abdominal obesity of the individual components of metabolic syndrome was an important risk factor for colorectal adenoma.
  • [MeSH-major] Adenoma / epidemiology. Colonic Neoplasms / epidemiology. Metabolic Syndrome X / epidemiology. Rectal Neoplasms / epidemiology
  • [MeSH-minor] Adenoma, Villous / epidemiology. Age Factors. Alcohol Drinking / epidemiology. Body Weights and Measures. Colonic Polyps / epidemiology. Colonoscopy. Diabetes Mellitus / epidemiology. Female. Humans. Hyperlipidemias / epidemiology. Hyperplasia. Hypertension / epidemiology. Korea / epidemiology. Male. Mass Screening. Middle Aged. Obesity / epidemiology. Precancerous Conditions / epidemiology. Risk Factors. Sex Factors. Smoking / epidemiology

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  • (PMID = 17684126.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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52. Cottet V, Bonithon-Kopp C, Kronborg O, Santos L, Andreatta R, Boutron-Ruault MC, Faivre J, European Cancer Prevention Organisation Study Group: Dietary patterns and the risk of colorectal adenoma recurrence in a European intervention trial. Eur J Cancer Prev; 2005 Feb;14(1):21-9
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  • [Title] Dietary patterns and the risk of colorectal adenoma recurrence in a European intervention trial.
  • The relations between individual foods and nutrients to colorectal tumours are conflicting.
  • The aim of the study was to examine the associations between dietary patterns and the risk of colorectal adenoma recurrence in the European fibre-calcium intervention trial.
  • Among the 640 patients with confirmed adenomas at the index colonoscopy, 592 had an initial dietary assessment using a diet history questionnaire.
  • The present analysis was restricted to 277 men and 165 women without history of adenoma prior to the index colonoscopy and who completed the study.
  • The main end point was the 3-year recurrence of adenomas.
  • Ninety-two patients presented new colorectal adenomas at the 3-year colonoscopy (65 men and 27 women).
  • None of them were significantly related to the overall recurrence of colorectal adenomas either in univariate or multivariate analyses.
  • The 'Mediterranean' pattern characterized by a high consumption of olive oil, vegetables, fruit, fish and lean meat significantly reduced adenoma recurrence [second tertile: adjusted odds ratio (OR)=0.50, 95% confidence interval (CI)=0.18-1.42; third tertile: adjusted OR=0.30, 95% CI=0.09-0.98; P for linear trend=0.04].
  • In conclusion, this study suggests that the Mediterranean dietary pattern may reduce the recurrence of colorectal adenomas, at least in women.
  • [MeSH-major] Adenoma / etiology. Adenoma / pathology. Calcium, Dietary. Colorectal Neoplasms / etiology. Colorectal Neoplasms / pathology. Dietary Fiber. Neoplasm Recurrence, Local

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  • (PMID = 15677892.001).
  • [ISSN] 0959-8278
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Calcium, Dietary
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53. Bjelakovic G, Nagorni A, Nikolova D, Simonetti RG, Bjelakovic M, Gluud C: Meta-analysis: antioxidant supplements for primary and secondary prevention of colorectal adenoma. Aliment Pharmacol Ther; 2006 Jul 15;24(2):281-91
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  • [Title] Meta-analysis: antioxidant supplements for primary and secondary prevention of colorectal adenoma.
  • BACKGROUND: Colorectal cancer may be prevented by reducing the development of adenomatous polyps.
  • AIM: To assess the benefits and harms of antioxidant supplements in preventing colorectal adenoma.
  • Outcome measures were development of colorectal adenoma adverse events.
  • Antioxidant supplements seemed to increase the development of colorectal adenoma in three low-bias risk trials (1.2, 0.99-1.4) and significantly decrease its development in five high-bias risk trials (0.59, 0.47-0.74).
  • CONCLUSION: We found no convincing evidence that antioxidant supplements have significant beneficial effect on primary or secondary prevention of colorectal adenoma.
  • [MeSH-major] Antioxidants / therapeutic use. Colorectal Neoplasms / prevention & control

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  • (PMID = 16842454.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants
  • [Number-of-references] 68
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54. Carvalho B, Postma C, Mongera S, Hopmans E, Diskin S, van de Wiel MA, van Criekinge W, Thas O, Matthäi A, Cuesta MA, Terhaar Sive Droste JS, Craanen M, Schröck E, Ylstra B, Meijer GA: Multiple putative oncogenes at the chromosome 20q amplicon contribute to colorectal adenoma to carcinoma progression. Gut; 2009 Jan;58(1):79-89
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  • [Title] Multiple putative oncogenes at the chromosome 20q amplicon contribute to colorectal adenoma to carcinoma progression.
  • OBJECTIVE: This study aimed to identify the oncogenes at 20q involved in colorectal adenoma to carcinoma progression by measuring the effect of 20q gain on mRNA expression of genes in this amplicon.
  • METHODS: Segmentation of DNA copy number changes on 20q was performed by array CGH (comparative genomic hybridisation) in 34 non-progressed colorectal adenomas, 41 progressed adenomas (ie, adenomas that present a focus of cancer) and 33 adenocarcinomas.
  • Moreover, a robust analysis of altered expression of genes in these segments was performed by microarray analysis in 37 adenomas and 31 adenocarcinomas.
  • RESULTS: The genes C20orf24, AURKA, RNPC1, TH1L, ADRM1, C20orf20 and TCFL5, mapping at 20q, were significantly overexpressed in carcinomas compared with adenomas as a consequence of copy number gain of 20q.
  • CONCLUSION: This approach revealed C20orf24, AURKA, RNPC1, TH1L, ADRM1, C20orf20 and TCFL5 genes to be important in chromosomal instability-related adenoma to carcinoma progression.
  • These genes therefore may serve as highly specific biomarkers for colorectal cancer with potential clinical applications.
  • [MeSH-major] Adenoma / genetics. Chromosome Aberrations. Chromosomes, Human, Pair 20 / genetics. Colorectal Neoplasms / genetics. Oncogenes

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  • (PMID = 18829976.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins
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55. Wu XL, Li DQ, Liu ZS, Wan XY, Wu YH, Jiang CQ, Zhang ZL, Qin QB, Qian Q: [Association of vascular endothelial growth factor 936C/T polymorphism and the susceptibility to colorectal adenoma]. Zhonghua Wei Chang Wai Ke Za Zhi; 2010 Apr;13(4):286-8
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  • [Title] [Association of vascular endothelial growth factor 936C/T polymorphism and the susceptibility to colorectal adenoma].
  • OBJECTIVE: To examine the association between polymorphism of vascular endothelial growth factor(VEGF)1498 C/T,936 C/T and colorectal adenoma genetic susceptibility.
  • METHODS: A case-control study of 224 colorectal adenomas and 200 controls was conducted and VEGF genotypes were determined based on TaqMan-probe assay.
  • RESULTS: The carriage of 936 CT and CT+TT genotypes had significantly higher risk of colorectal adenoma (CT vs. CC, OR=2.00, 95% CI: 1.23-3.25, P=0.006; CT+TT vs. CC, OR=2.04, 95% CI:1.28-3.26, P=0.003).
  • 936-T allele carriage had increased risk of colorectal adenoma (OR=1.91, 95% CI:1.25-2.91, P=0.003).
  • In patients with 936 CT+TT and 936-T allele implied a tendency of villous adenoma category (CT+TT vs. CC, OR=2.54, 95% CI:1.12-5.75, P=0.040; T allele vs. C allele, OR=3.08, 95% CI, 1.64-5.80, P=0.001).
  • CONCLUSION: VEGF 936 C/T polymorphism can influence susceptibility to colorectal adenoma.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Polymorphism, Single Nucleotide. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 20422487.001).
  • [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] 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
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56. Guan J, Chen J, Luo YF, Cao JL, Zhao H, Hao J: [Expression of survivin in colorectal adenoma and adenocarcinoma]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao; 2007 Jun;29(3):398-401
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  • [Title] [Expression of survivin in colorectal adenoma and adenocarcinoma].
  • OBJECTIVE: To explore the expression of Survivin (SVV) protein in colorectal carcinogenesis and its clinical significance.
  • METHODS Immunohistochemistry staining was performed by two-step EnVision technique for the paraffin sections, which included 90 adenomas, 25 ademomas with high-grade glandular intraepithelial neoplasia, and 108 colorectal adenocarcinomas.
  • The positive rate of SVV in tubular adenomas, villous adenomas, and tubulovillous adenomas were 30% (12/40), 40.9% (9/22), and 35.8% (10/28), respectively.
  • The positive rate of SVV in tubulovillous adenomas with high-grade glandular intraepithelial neoplasia were 68% (17/25).
  • SVV expressions among the three types of adenomas without neoplasia were not significantly different (P > 0.05).
  • SVV expression between each type of the above-mentioned ademoma and tubulovillous adenoma with high-grade glandular intraepithelial neoplasia or different Dukes stages of colorectal carcinoma was significantly different (P < 0.05).
  • SVV expressions in adenocarcinomas and adenomas with high grade glandular intraepithelial neoplasia were significantly higher than those in adenomas (P < 0.01).
  • CONCLUSIONS: SVV is abnormally expressed in the early stage of colorectal carcinogenesis, which may be correlated with the carcinogenesis of colorectal ademoma.
  • SVV expression may be useful to distinguish adenocarcinoma from adenoma in colorectal carcinogenesis.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenoma / metabolism. Colorectal Neoplasms / metabolism. Microtubule-Associated Proteins / biosynthesis

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  • (PMID = 17633470.001).
  • [ISSN] 1000-503X
  • [Journal-full-title] Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae
  • [ISO-abbreviation] Zhongguo Yi Xue Ke Xue Yuan Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins
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57. van den Donk M, Buijsse B, van den Berg SW, Ocké MC, Harryvan JL, Nagengast FM, Kok FJ, Kampman E: Dietary intake of folate and riboflavin, MTHFR C677T genotype, and colorectal adenoma risk: a Dutch case-control study. Cancer Epidemiol Biomarkers Prev; 2005 Jun;14(6):1562-6
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  • [Title] Dietary intake of folate and riboflavin, MTHFR C677T genotype, and colorectal adenoma risk: a Dutch case-control study.
  • We investigated the associations between dietary intake of folate and vitamin B2, MTHFR C677T genotype, and colorectal adenomas in a Dutch case-control study.
  • Data of cases with at least one histologically confirmed colorectal adenoma (n = 768) and controls with no history of any type of colorectal polyp (n = 709) were included.
  • Folate seemed to be a risk factor, especially when vitamin B2 intake was low; vitamin B2 was inversely associated with adenomas, especially with relatively high folate intake.
  • No association was observed between MTHFR C677T genotype and colorectal adenomas.
  • The inverse association between vitamin B2 intake and colorectal adenoma risk seemed to be more pronounced among those with the MTHFR TT genotype.
  • We conclude that this study does not provide evidence for a decreased colorectal adenoma risk for subjects with high dietary intake of folate.
  • It suggests, however, an inverse association between vitamin B2 and colorectal adenomas, which may be more relevant for those with the MTHFR TT genotype.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Folic Acid. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Riboflavin

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  • (PMID = 15941973.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 935E97BOY8 / Folic Acid; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2); TLM2976OFR / Riboflavin
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58. Yamaji T, Iwasaki M, Sasazuki S, Tsugane S: Interaction between adiponectin and leptin influences the risk of colorectal adenoma. Cancer Res; 2010 Jul 1;70(13):5430-7
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  • [Title] Interaction between adiponectin and leptin influences the risk of colorectal adenoma.
  • Obesity has been associated with an increased risk of colorectal neoplasia, but the mechanisms of this potential association have not been elucidated.
  • We hypothesized that the adipokines adiponectin, leptin, and tumor necrosis factor-alpha (TNF-alpha) may mediate an association between obesity and colorectal cancer.
  • An inverse association of total and HMW adiponectin was observed with colorectal adenoma (P trend < 0.001 and 0.03, respectively).
  • Further, total adiponectin interacted with leptin, but not TNF-alpha, in relation to colorectal adenoma (P interaction = 0.007).
  • An inverse association of total adiponectin with colorectal adenoma was apparent in the highest two tertiles of leptin, particularly the middle (P trend < 0.001), whereas a positive association of leptin was obvious in the lowest tertile of total adiponectin (P trend = 0.01) after adjusting for potential confounders and body mass index, which is a major determinant of insulin resistance.
  • Adiponectin may exert an anticarcinogenic effect on the large intestine by interfering with leptin, whereas leptin could conversely exert a carcinogenic effect under conditions of a lower abundance of adiponectin.
  • Our findings provide the first epidemiologic evidence for interactive effects of adiponectin and leptin in the early stage of colorectal tumorigenesis, distinct from their involvement in insulin resistance.
  • [MeSH-major] Adenoma / blood. Colorectal Neoplasms / blood. Leptin / blood

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  • [Copyright] Copyright 2010 AACR.
  • (PMID = 20516125.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ADIPOQ protein, human; 0 / Adiponectin; 0 / Leptin; 0 / Tumor Necrosis Factor-alpha
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59. Thompson PA, Wertheim BC, Roe DJ, Ashbeck EL, Jacobs ET, Lance P, Martínez ME, Alberts DS: Gender modifies the effect of ursodeoxycholic acid in a randomized controlled trial in colorectal adenoma patients. Cancer Prev Res (Phila); 2009 Dec;2(12):1023-30
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  • [Title] Gender modifies the effect of ursodeoxycholic acid in a randomized controlled trial in colorectal adenoma patients.
  • PURPOSE: Ursodeoxycholic acid (UDCA) was one of the earliest agents investigated as a drug for colorectal cancer prevention.
  • However, UDCA failed to show efficacy to prevent the development of colorectal adenomas in a large, phase III, randomized, placebo-controlled trial.
  • We re-evaluated the effect of UDCA in men and women separately, based on sex-specific differences in bile acid metabolism and suspected variation in etiologic factors contributing to colorectal cancer risk.
  • EXPERIMENTAL DESIGN: We conducted a secondary analysis of the efficacy of UDCA to prevent colorectal adenoma in men (n = 804) and women (n = 388).
  • RESULTS: We found no reduction in risk of any metachronous adenoma with UDCA treatment in men or women.
  • CONCLUSION: Our findings support the use of UDCA for preventing advanced colorectal adenomas in men.
  • The increased odds of adenoma among women with high fat intake suggest a previously unrecognized harm that warrants further study, especially given the chronic exposure to UDCA in patients with primary biliary cirrhosis and the increasing investigational use of UDCA for several other conditions.
  • [MeSH-major] Adenoma / prevention & control. Cholagogues and Choleretics / therapeutic use. Colorectal Neoplasms / prevention & control. Ursodeoxycholic Acid / therapeutic use

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  • (PMID = 19952360.001).
  • [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 / P01 CA041108; United States / NCI NIH HHS / CA / 1K07CA10629-01A1; United States / NCI NIH HHS / CA / P01 CA4108; United States / NCI NIH HHS / CA / P01-CA-41108
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cholagogues and Choleretics; 0 / Placebos; 724L30Y2QR / Ursodeoxycholic Acid
  • [Other-IDs] NLM/ NIHMS157373; NLM/ PMC4120755
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60. Methy N, Binquet C, Boutron-Ruault MC, Paillot B, Faivre J, Bonithon-Kopp C: Dietary fatty acids and recurrence of colorectal adenomas in a European intervention trial. Nutr Cancer; 2008;60(5):560-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dietary fatty acids and recurrence of colorectal adenomas in a European intervention trial.
  • Epidemiological studies have provided inconsistent data about the role of dietary fatty acids in colorectal cancer, and few studies have addressed their role in colorectal adenoma.
  • The aim of the study was to assess the risk of overall adenoma recurrence associated with dietary consumption of total fat, subtypes of fat, and specific fatty acids (oleic acid, linoleic acid, alpha-linolenic acid).
  • The study sample was composed of 523 patients with confirmed adenomas at the index colonoscopy, 35 to 75 yr old, who completed the European fiber-calcium intervention trial and had an initial dietary assessment using a qualitative and quantitative food questionnaire.
  • There were no significant associations between overall adenoma recurrence and either total fat, subtypes of fat, or specific fatty acids.
  • No significant associations were observed with recurrence of proximal or advanced adenomas.
  • Our findings do not support the hypothesis of strong associations between dietary fatty acids and recurrence of colorectal adenomas.
  • The hypothesis of a differential role of specific fatty acids according to colorectal subsites deserves further investigation.
  • [MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Dietary Fats / administration & dosage. Fatty Acids / administration & dosage. Neoplasm Recurrence, Local / epidemiology

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  • (PMID = 18791918.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Fats; 0 / Fatty Acids; 0 / Fatty Acids, Unsaturated; 9KJL21T0QJ / Linoleic Acid
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61. Barry EL, Sansbury LB, Grau MV, Ali IU, Tsang S, Munroe DJ, Ahnen DJ, Sandler RS, Saibil F, Gui J, Bresalier RS, McKeown-Eyssen GE, Burke C, Baron JA: Cyclooxygenase-2 polymorphisms, aspirin treatment, and risk for colorectal adenoma recurrence--data from a randomized clinical trial. Cancer Epidemiol Biomarkers Prev; 2009 Oct;18(10):2726-33
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  • [Title] Cyclooxygenase-2 polymorphisms, aspirin treatment, and risk for colorectal adenoma recurrence--data from a randomized clinical trial.
  • Chronic inflammation plays an important role in the development and progression of colorectal cancer.
  • Aspirin inhibits COX-2 activity and lowers the risk for colorectal adenomas and cancer.
  • We investigated whether common genetic variation in COX-2 influenced risk for colorectal adenoma recurrence among 979 participants in the Aspirin/Folate Polyp Prevention Study who were randomly assigned to placebo or aspirin and followed for 3 years for the occurrence of new adenomas.
  • Of these participants, 44.2% developed at least one new adenoma during follow-up.
  • Adjusted relative risks and 95% confidence intervals (95% CI) were calculated to test the association between genetic variation at six COX-2 single-nucleotide polymorphisms and adenoma occurrence and interaction with aspirin treatment.
  • Two single-nucleotide polymorphisms were significantly associated with increased adenoma recurrence: for rs5277, homozygous carriers of the minor C allele had a 51% increased risk compared with GG homozygotes (relative risk, 1.51; 95% CI, 1.01-2.25), and for rs4648310, heterozygous carriers of the minor G allele had a 37% increased risk compared with AA homozygotes (relative risk, 1.37; 95% CI, 1.05-1.79). (There were no minor allele homozygotes.
  • These results support the hypothesis that COX-2 plays a role in the etiology of colon cancer and may be a target for aspirin chemoprevention and warrant further investigation in other colorectal adenoma and cancer populations.

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  • (PMID = 19755647.001).
  • [ISSN] 1538-7755
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-059005; United States / NCI NIH HHS / CA / R01 CA059005-06A1; United States / NCI NIH HHS / CA / R01 CA059005-13; United States / NCI NIH HHS / CA / R01 CA059005-14; United States / NCI NIH HHS / CA / CA059005-13; United States / NCI NIH HHS / CA / P30 CA023108; United States / NCI NIH HHS / CA / R01 CA059005-11A2; United States / PHS HHS / / HHSN261200800001E; United States / NCI NIH HHS / CA / CA059005-12; United States / NCI NIH HHS / CA / CA059005-14; United States / NCI NIH HHS / CA / CA059005-11A2; United States / CCR NIH HHS / RC / HHSN261200800001C; United States / NCI NIH HHS / CA / R01 CA059005-12; United States / NCI NIH HHS / CA / R01 CA059005; United States / NCI NIH HHS / CA / HHSN261200800001E
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 935E97BOY8 / Folic Acid; EC 1.14.99.1 / Cyclooxygenase 2; R16CO5Y76E / Aspirin
  • [Other-IDs] NLM/ NIHMS140209; NLM/ PMC2769932
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62. F Lam F, Jankova L, Dent OF, Molloy MP, Kwun SY, Clarke C, Chapuis P, Robertson G, Beale P, Clarke S, Bokey EL, Chan C: Identification of distinctive protein expression patterns in colorectal adenoma. Proteomics Clin Appl; 2010 Jan;4(1):60-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of distinctive protein expression patterns in colorectal adenoma.
  • PURPOSE: As a pre-malignant precursor, adenoma provides an ideal tissue for proteome profiling to investigate early colorectal cancer development and provide possible targets for preventive interventions.
  • The aim of this study was to identify patterns of differential protein expression that distinguish colorectal adenoma from normal tissue.
  • EXPERIMENTAL DESIGN: Twenty paired samples of adenoma and normal mucosa were analysed by 2-DE and MALDI-TOF/TOF MS to detect proteins with ≥2-fold differential expression.
  • RESULTS: Four proteins were up-regulated in adenoma (Annexin A3, S100A11, S100P and eIF5A-1) and three were down-regulated (Galectin-1, S100A9 and FABPL).
  • CONCLUSIONS AND CLINICAL RELEVANCE: Distinctive patterns of in vivo protein expression in colorectal adenoma were identified for the first time.
  • These proteins have important functions in cell differentiation, proliferation and metabolism, and may play a crucial role in early colorectal carcinogenesis.
  • [MeSH-major] Adenoma / genetics. Adenoma / metabolism. Colorectal Neoplasms / genetics. Colorectal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Proteome / metabolism. Proteomics / methods

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  • [Copyright] Copyright © 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
  • (PMID = 21137016.001).
  • [ISSN] 1862-8354
  • [Journal-full-title] Proteomics. Clinical applications
  • [ISO-abbreviation] Proteomics Clin Appl
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Proteome
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63. Bertagnolli MM, Hsu M, Hawk ET, Eagle CJ, Zauber AG, Adenoma Prevention with Celecoxib (APC) Study Investigators: Statin use and colorectal adenoma risk: results from the adenoma prevention with celecoxib trial. Cancer Prev Res (Phila); 2010 May;3(5):588-96
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  • [Title] Statin use and colorectal adenoma risk: results from the adenoma prevention with celecoxib trial.
  • Statins are widely prescribed for cardiovascular disease prevention and also commonly used in patients at high risk for colorectal cancer.
  • We report the results of a planned secondary analysis of the relationship between statin use and colorectal adenoma risk in a large chemoprevention trial.
  • The Adenoma Prevention with Celecoxib (APC) trial randomized 2,035 adenoma patients to receive placebo (679 patients), 200 mg celecoxib twice daily (bid; 685 patients), or 400 mg celecoxib bid (671 patients).
  • The effects of statin use on newly detected adenomas and cardiovascular adverse events were analyzed as time-dependent variables by multivariable Cox regression.
  • Statin use for >3 years increased adenoma risk over 5 years (risk ratio, 1.39; 95% confidence interval, 1.04-1.86; P = 0.024).
  • For all comparisons of patients treated with celecoxib, adenoma detection rates for statin users and nonusers were equivalent.
  • For patients at high risk of colorectal cancer, statins do not protect against colorectal neoplasms and may even increase the risk of developing colorectal adenomas.

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  • (PMID = 20403998.001).
  • [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 / K05 CA131504; United States / NCI NIH HHS / CA / K05 CA131504-04; United States / NCI NIH HHS / CA / P30 CA008748; United States / NCI NIH HHS / CA / CA-N01-95015
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; JCX84Q7J1L / Celecoxib
  • [Other-IDs] NLM/ NIHMS236429; NLM/ PMC2990920
  • [Investigator] Bertagnolli MM; Hawk ET; Eagle CJ; Zauber AG; Kim KM; Corle D; Rosenstein R; Tang J; Hess T; Wilton A; Hsu M; Anderson W; Doody L; Redston M; Geisinger KR; Woloj GM; Bagheri D; Crawford A; Schietrum M; Ladouceur V; Rosen S; Friedman L; Makuch R; Phillips R; Taylor P; Auerbach S; Barish CF; Barringer T; Bennetts RW; Blitstein M; Bruggen J; Carricaburu P; Chung D; Colizzo F; Curtis R; Dewar T; DuBois R; Feinstat T; Foley TR; Gabbaizadeh D; Geenen J; Giardiello F; Goetsch A; Goldberg M; Goldstein JL; Harlan W 3rd; Hogan R; Kamionkowski M; Kelfer M; Kerzner B; Kim K; Klimberg I; Koval G; Krone C; Krumholz S; Layton MW; Lightdale C; Limburg PJ; Lind C; Lipkis D; Lloyd M; Maccini D; MacMillan F Sr; Madoff R; Malik A; Markowitz A; Marks R; McDougall CJ; Miner P; Murphy M; Namais A; Nickl N; Pochapin M; Pruitt RE; Puolos J; Riff DS; Roman R; Rubin L; Safdi M; Saltzman J; Salzberg B; Sattler JA; Schleinitz P; Schwartz J; Schwartz M; Silpa M; Silvers D; Smoot D; Sontag S; Sorrell RJ; Stanton D; Sturgeon J; Tracey JP; Werth T; Wilcox CM; Wohlman R; Woods S; Burn J; Ee H; Korman M; Lee A; Leggett B; Macrae F; Mollison L; Yeomans N; Young G; Aumais G; Bailey R; Bernstein C; Cohen L; Dallaire C; Morgan D; Sylwestrowicz T; Van Rosendaal G; Van Zantan SJ
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64. 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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  • [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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65. Tabata S, Yin G, Ogawa S, Yamaguchi K, Mineshita M, Kono S: Genetic polymorphism of cholesterol 7alpha-hydroxylase (CYP7A1) and colorectal adenomas: Self Defense Forces Health Study. Cancer Sci; 2006 May;97(5):406-10
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  • [Title] Genetic polymorphism of cholesterol 7alpha-hydroxylase (CYP7A1) and colorectal adenomas: Self Defense Forces Health Study.
  • Bile acids have long been implicated in colorectal carcinogenesis, but epidemiological evidence is limited.
  • The present study examined the relationship between the CYP7A1 A-203C polymorphism and colorectal adenoma, which is a well-established precursor lesion of colorectal cancer.
  • The study subjects comprised 446 cases of colorectal adenomas and 914 controls of normal total colonoscopy among men receiving a preretirement health examination at two hospitals of the Self Defense Forces (SDF).
  • Statistical adjustment was made for age, hospital, rank in the SDF, smoking, alcohol use, body mass index, physical activity and parental history of colorectal cancer.
  • The CYP7A1 polymorphism was not measurably related to the overall risk of colorectal adenomas.
  • However, the CC genotype was associated with a decreased risk of proximal colon adenomas, but not of distal colon and rectal adenomas.
  • Adjusted odds ratios of proximal colon adenomas (95% confidence intervals) for the AC and CC genotype versus AA genotype were 0.82 (0.54-1.24) and 0.56 (0.34-0.95), respectively.
  • The findings add to evidence for the role of bile acids in colorectal carcinogenesis.
  • [MeSH-major] Adenoma / genetics. Cholesterol 7-alpha-Hydroxylase / genetics. Colorectal Neoplasms / genetics. Polymorphism, Genetic

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  • (PMID = 16630139.001).
  • [ISSN] 1347-9032
  • [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] 0 / Bile Acids and Salts; EC 1.14.13.17 / Cholesterol 7-alpha-Hydroxylase
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66. Diosdado B, van de Wiel MA, Terhaar Sive Droste JS, Mongera S, Postma C, Meijerink WJ, Carvalho B, Meijer GA: MiR-17-92 cluster is associated with 13q gain and c-myc expression during colorectal adenoma to adenocarcinoma progression. Br J Cancer; 2009 Aug 18;101(4):707-14
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  • [Title] MiR-17-92 cluster is associated with 13q gain and c-myc expression during colorectal adenoma to adenocarcinoma progression.
  • In colorectal tumours, the combination of gain of 8q and 13q is one of the major factors associated with colorectal adenoma to adenocarcinoma progression.
  • We investigated the contribution of the miR-17-92 cluster during colorectal adenoma to adenocarcinoma progression.
  • METHODS: Expression levels of the miR-17-92 cluster were determined in 55 colorectal tumours and in 10 controls by real-time RT-PCR.
  • RESULTS: From the six members of the miR-17-92 cluster, all except miR-18a, showed significant increased expression in colorectal tumours with miR-17-92 locus gain compared with tumours without miR-17-92 locus gain.
  • CONCLUSION: Increased expression of miR-17-92 cluster during colorectal adenoma to adenocarcinoma progression is associated to DNA copy number gain of miR17-92 locus on 13q31 and c-myc expression.
  • [MeSH-major] Adenocarcinoma / genetics. Adenoma / genetics. Chromosomes, Human, Pair 13 / genetics. Colorectal Neoplasms / genetics. MicroRNAs / genetics. Proto-Oncogene Proteins c-myc / biosynthesis

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  • (PMID = 19672269.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MIRN17 microRNA, human; 0 / MYC protein, human; 0 / MicroRNAs; 0 / Proto-Oncogene Proteins c-myc
  • [Other-IDs] NLM/ PMC2736819
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67. Hazra A, Wu K, Kraft P, Fuchs CS, Giovannucci EL, Hunter DJ: Twenty-four non-synonymous polymorphisms in the one-carbon metabolic pathway and risk of colorectal adenoma in the Nurses' Health Study. Carcinogenesis; 2007 Jul;28(7):1510-9
Hazardous Substances Data Bank. CYANOCOBALAMIN .

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  • [Title] Twenty-four non-synonymous polymorphisms in the one-carbon metabolic pathway and risk of colorectal adenoma in the Nurses' Health Study.
  • Dietary folate and alcohol consumption as well as polymorphic variants in one-carbon metabolism genes may modulate risk of colorectal adenoma through aberrant DNA methylation and altered nucleotide synthesis and repair.
  • We assessed the association of 24 non-synonymous single nucleotide polymorphisms (nsSNPs) in 13 genes in the one-carbon metabolism pathway and risk of colorectal adenoma in 556 incident cases and 557 controls nested in the Nurses' Health Study.
  • Most of the SNPs were not associated with risk of colorectal adenoma.
  • We did, however, observe a modest increased risk among carriers of the transcobalamin (TCN) II 259 Pro/Arg + Arg/Arg variant (odds ratio 1.48, 95% confidence interval 1.09-2.02) for colorectal adenoma.
  • In addition, the methionine synthase reductase (MTRR) Arg415Cys and MTRR Ser284Thr variant carriers, also in the vitamin B(12) pathway, have suggestive associations with advanced colorectal adenoma (defined as being larger than 1 cm, villous, tubular-villous or carcinoma in situ histology).
  • We observed significant evidence for departure from multiplicative interaction for the betaine-homocysteine methyltransferase (BHMT) Arg239Gln with dietary methyl status (based on intake of dietary folate, methionine and alcohol intake) in relation to colorectal adenoma; no such interaction was observed for the other 23 SNPs.
  • Further investigation is required to validate the association of the polymorphisms in the one-carbon metabolic genes and risk of colorectal adenoma.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Genetics, Population. One-Carbon Group Transferases / genetics. Polymorphism, Single Nucleotide

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  • (PMID = 17389618.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA87969; United States / NCI NIH HHS / CA / P01-CA087969; United States / NCI NIH HHS / CA / T-32 CA 09001-30; United States / NCI NIH HHS / CA / U54 CA100971
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Transcobalamins; 935E97BOY8 / Folic Acid; AE28F7PNPL / Methionine; EC 1.18.1.- / methionine synthase reductase; EC 1.18.1.2 / Ferredoxin-NADP Reductase; EC 2.1.- / One-Carbon Group Transferases; EC 2.1.1.5 / BHMT protein, human; EC 2.1.1.5 / Betaine-Homocysteine S-Methyltransferase; P6YC3EG204 / Vitamin B 12
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68. Raimondi S, Botteri E, Iodice S, Lowenfels AB, Maisonneuve P: Gene-smoking interaction on colorectal adenoma and cancer risk: review and meta-analysis. Mutat Res; 2009 Nov 2;670(1-2):6-14
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  • [Title] Gene-smoking interaction on colorectal adenoma and cancer risk: review and meta-analysis.
  • The etiology of colorectal cancer is complex and multifactorial.
  • Tobacco smoke has been found to be associated both with colorectal adenoma and cancer development.
  • We found a weak suggestion of an antagonistic effect of mEH3 low or medium metabolizer with smoking on colorectal adenoma risk (pooled P-value for the interaction: 0.02): smokers carriers of mEH3 low or medium metabolizer had slightly lower risk (Odds Ratio; 95% Confidence Interval: 1.6; 1.2-2.1) than smokers with mEH3 high metabolizer (1.8; 1.4-2.4).
  • A non-significant positive interaction between GSTT1 null genotype and smoking was suggested for colorectal adenoma risk.
  • None of the other common genetic polymorphisms involved in tobacco carcinogens metabolism seemed to modify the smoking-related risk of colorectal adenoma or cancer.
  • [MeSH-major] Colorectal Neoplasms / etiology. Colorectal Neoplasms / genetics. Polymorphism, Genetic. Smoking / adverse effects. Smoking / genetics
  • [MeSH-minor] Adenoma / etiology. Adenoma / genetics. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Humans. Risk

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  • (PMID = 19589345.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 2.5.1.18 / Glutathione Transferase
  • [Number-of-references] 64
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69. Botma A, Nagengast FM, Braem MG, Hendriks JC, Kleibeuker JH, Vasen HF, Kampman E: Body mass index increases risk of colorectal adenomas in men with Lynch syndrome: the GEOLynch cohort study. J Clin Oncol; 2010 Oct 1;28(28):4346-53
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  • [Title] Body mass index increases risk of colorectal adenomas in men with Lynch syndrome: the GEOLynch cohort study.
  • PURPOSE: High body mass index (BMI) is an established risk factor for sporadic colorectal cancer.
  • Still, the influence of BMI on hereditary colorectal cancer (eg, Lynch syndrome [LS]), is unknown.
  • The objective of this study was to assess whether BMI is associated with colorectal adenoma occurrence in persons with LS.
  • Cox regression models with robust sandwich estimates controlling for age, sex, extent of colon surgery, smoking, and alcohol intake were used to evaluate associations between BMI, height, weight, weight change, and risk of colorectal adenomas.
  • Analyses were performed separately for those without (incident cohort; n = 243) and those with (prevalent cohort; n = 243) a history of colorectal cancer neoplasms at baseline.
  • RESULTS: A statistically significant association between current overweight (≥ 25 kg/m(2)) and developing colorectal adenomas was seen among men in the incident cohort (overweight v normal weight hazard ratio [HR], 8.72; 95% CI, 2.06 to 36.96).
  • CONCLUSION: Excess body weight increased the risk of incident colorectal adenomas in people with LS.
  • [MeSH-major] Adenoma / epidemiology. Body Mass Index. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms, Hereditary Nonpolyposis / epidemiology

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  • (PMID = 20733131.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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70. 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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71. 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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72. Bobe G, Murphy G, Albert PS, Sansbury LB, Lanza E, Schatzkin A, Colburn NH, Cross AJ: Serum cytokine concentrations, flavonol intake and colorectal adenoma recurrence in the Polyp Prevention Trial. Br J Cancer; 2010 Oct 26;103(9):1453-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum cytokine concentrations, flavonol intake and colorectal adenoma recurrence in the Polyp Prevention Trial.
  • BACKGROUND: Serum cytokine concentrations may reflect inflammatory processes occurring during the development of colorectal neoplasms.
  • Flavonols, bioactive compounds found in plant-based foods and beverages, may inhibit colorectal neoplasms partly by attenuating inflammation.
  • METHODS: Using logistic regression, we estimated odds ratios (ORs) and 95% confidence intervals (CIs) to investigate the association between serum concentrations of interleukin (IL) β, 2, 8, 10, 12p70, granulocyte macrophage colony stimulating factor, interferon-γ, and tumour necrosis factor-α, measured over time, flavonol intake, estimated from a flavonol database used in conjunction with a food frequency questionnaire, and adenoma recurrence in 872 participants from the intervention arm of the Polyp Prevention Trial.
  • RESULTS: Decreased IL-2 concentration during the trial increased the risk of any adenoma recurrence (4th vs 1st quartile, OR=1.68, 95% CI=1.13-2.49), whereas decreased IL-1β or IL-10 reduced the risk of advanced adenoma recurrence (OR=0.37, 95% CI=0.15-0.94; OR=0.39, 95% CI=0.15-0.98, respectively).
  • Individuals with flavonol intake above the median (29.7 mg per day) and decreased cytokine concentrations had the lowest risk of advanced adenoma recurrence.
  • CONCLUSION: Overall, no consistent associations were observed between serum cytokine profile and colorectal adenoma recurrence; however, decreased cytokine concentrations during high flavonol consumption may indicate prevention of colorectal neoplasms.

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  • (PMID = 20924374.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Flavonols; 0 / Interleukins
  • [Other-IDs] NLM/ PMC2990604
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73. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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74. Koushik A, Tranah GJ, Ma J, Stampfer MJ, Sesso HD, Fuchs CS, Giovannucci EL, Hunter DJ: p53 Arg72Pro polymorphism and risk of colorectal adenoma and cancer. Int J Cancer; 2006 Oct 15;119(8):1863-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] p53 Arg72Pro polymorphism and risk of colorectal adenoma and cancer.
  • We investigated this SNP in relation to colorectal adenoma and cancer among men and women from case-control studies nested within the Nurses' Health Study, the Health Professionals Follow-up Study and the Physicians' Health Study.
  • Among 856 colorectal adenoma cases and 1,184 controls, we observed a modest association with p53 Arg72Pro genotype (multivariate odds ratio (OR) = 1.25, 95% confidence interval (CI) = 1.04-1.50 for Arg/Pro and Pro/Pro vs. Arg/Arg).
  • This association did not vary by colorectal site or by sex.
  • Among 442 colorectal cancer cases and 904 controls, we observed no significant overall association between p53 Arg72Pro genotype and colorectal cancer (multivariate OR = 1.14, 95% CI = 0.90-1.45).
  • However, when colorectal site and sex was accounted for, the Pro carrier genotypes compared to Arg/Arg were associated with an increased risk of proximal colon cancers in women (multivariate OR = 2.59, 95% CI = 1.49-4.52) though not with distal colon or rectal cancers, while among men the same genotypes were associated with an increased risk of distal colon cancers (multivariate OR = 2.09, 95% CI = 1.28-3.40) but not proximal colon or rectal cancers.
  • Our results suggest that Arg72Pro may play a role in the early stages of colorectal neoplasia and possibly in progression to invasive disease, depending on site and sex.
  • [MeSH-major] Adenoma / genetics. Adenoma / pathology. Arginine / genetics. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Polymorphism, Genetic / genetics. Tumor Suppressor Protein p53 / genetics

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16721787.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA42182; United States / NCI NIH HHS / CA / CA55075; United States / NCI NIH HHS / CA / CA70817; United States / NCI NIH HHS / CA / CA87969
  • [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 / Tumor Suppressor Protein p53; 94ZLA3W45F / Arginine; 9DLQ4CIU6V / Proline
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75. Ashktorab H, Tsang S, Luke B, Sun Z, Adam-Campbell L, Kwagyan J, Poirier R, Akter S, Akhgar A, Smoot D, Munroe DJ, Ali IU: Protective effect of Cox-2 allelic variants on risk of colorectal adenoma development in African Americans. Anticancer Res; 2008 Sep-Oct;28(5B):3119-23
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  • [Title] Protective effect of Cox-2 allelic variants on risk of colorectal adenoma development in African Americans.
  • BACKGROUND: Recent evidence indicates that single nucleotide polymorphisms (SNPs) in the Cox-2 gene may modulate the risk of colorectal adenoma development.
  • PATIENTS AND METHODS: We explored possible associations between Cox-2 polymorphisms and risk of adenoma development in an African American case-control study comprising 72 cases of advanced adenomas and 146 polyp-free controls.
  • RESULTS: Statistically significant inverse associations were observed between the heterozygous genotypes at the 5229 G>T polymorphism in intron 5 [odds ratio (OR)=0.42; confidence interval (CI)=0.19-0.92; p=0.03] and at the 10935 A>G polymorphism in the 3' flanking region downstream from the poly A signals (OR=0.39; CI=0.18-0.83;p=0.01) and the risk for colorectal adenoma development.
  • CONCLUSION: The data from our pilot study suggest that allelic variants of the COX-2 gene significantly influence the risk of adenoma development in the African American population.
  • [MeSH-major] Adenoma / genetics. African Americans / genetics. Colorectal Neoplasms / genetics. Cyclooxygenase 2 / genetics

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  • (PMID = 19031967.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA102681
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] EC 1.14.99.1 / Cyclooxygenase 2
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76. Hubner RA, Muir KR, Liu JF, Logan RF, Grainge MJ, Houlston RS, Members of the UKCAP Consortium: Ornithine decarboxylase G316A genotype is prognostic for colorectal adenoma recurrence and predicts efficacy of aspirin chemoprevention. Clin Cancer Res; 2008 Apr 15;14(8):2303-9
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  • [Title] Ornithine decarboxylase G316A genotype is prognostic for colorectal adenoma recurrence and predicts efficacy of aspirin chemoprevention.
  • PURPOSE: The chemopreventive activity of aspirin in colorectal neoplasia may be explained in part by its effect on polyamine metabolism.
  • We investigated the influence of ODC G316A on the chemopreventive activity of aspirin in colorectal adenoma (CRA) recurrence.
  • EXPERIMENTAL DESIGN: We genotyped ODC G316A in 546 individuals in the United Kingdom Colorectal Adenoma Prevention trial of aspirin for CRA recurrence prevention and pooled our findings with data from two other randomized intervention trials.
  • RESULTS: The United Kingdom Colorectal Adenoma Prevention participants with homozygous ODC 316AA genotype were at reduced CRA recurrence risk [relative risk (RR), 0.43; 95% confidence interval (95% CI), 0.16-1.15], particularly if also exposed to aspirin (RR, 0.24; 95% CI, 0.03-1.71).
  • [MeSH-major] Adenoma / genetics. Anticarcinogenic Agents / therapeutic use. Aspirin / therapeutic use. Colorectal Neoplasms / genetics. Neoplasm Recurrence, Local / genetics. Ornithine Decarboxylase / genetics

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  • (PMID = 18413818.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; EC 4.1.1.17 / Ornithine Decarboxylase; R16CO5Y76E / Aspirin
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77. Wang Y, Ma Y, Lü B, Xu E, Huang Q, Lai M: Differential expression of mimecan and thioredoxin domain-containing protein 5 in colorectal adenoma and cancer: a proteomic study. Exp Biol Med (Maywood); 2007 Oct;232(9):1152-9
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  • [Title] Differential expression of mimecan and thioredoxin domain-containing protein 5 in colorectal adenoma and cancer: a proteomic study.
  • Adenoma is the major precursor lesion of colorectal cancer, one of the most common cancers worldwide.
  • The elucidation of the molecular mechanism underlying adenoma is essential for early detection, prevention, and intervention of colorectal cancer.
  • Using a combination of two-dimensional gel electrophoresis and mass spectrometry, we identified 27 differentially expressed proteins in adenoma, compared with matched normal mucosa and cancer tissue.
  • Seventeen proteins were upregulated and six downregulated in adenoma when compared with the same proteins in individual-matched normal mucosa.
  • Four were downregulated, but none upregulated in adenoma when compared with the same proteins in matched cancer tissue.
  • Two novel proteins, mimecan and thioredoxin domain-containing protein 5 (TXNDC5), were further validated by Western blot in 8 colorectal adenomas and 19 cancers that were matched with normal mucosa.
  • All adenoma and cancer tissues did not express mimecan, but all normal mucosa did (P < 0.01).
  • In contrast, TXNDC5 was significantly upregulated in colorectal adenoma and cancer tissues as compared with that in normal mucosa (P < 0.05).
  • This study clearly demonstrated that absence of mimecan and upregulation of TXNDC5 are involved in the early development of colorectal cancer.
  • Thus, the differentially expressed proteins might serve as potential biomarkers for colorectal cancer detection and intervention.
  • [MeSH-major] Adenoma / metabolism. Colorectal Neoplasms / metabolism. Intercellular Signaling Peptides and Proteins / metabolism. Protein Disulfide-Isomerases / metabolism. Thioredoxins / metabolism

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  • (PMID = 17895523.001).
  • [ISSN] 1535-3702
  • [Journal-full-title] Experimental biology and medicine (Maywood, N.J.)
  • [ISO-abbreviation] Exp. Biol. Med. (Maywood)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / OGN protein, human; 52500-60-4 / Thioredoxins; EC 5.3.4.1 / Protein Disulfide-Isomerases; EC 5.3.4.1 / TXNDC5 protein, human
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78. Park SK, Park DI, Park JH, Kim HJ, Cho YK, Sohn CI, Jeon WK, Kim BI, Kim JE, Son HJ: [C-reactive protein level and colorectal adenoma]. Korean J Gastroenterol; 2008 Apr;51(4):225-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [C-reactive protein level and colorectal adenoma].
  • BACKGROUND/AIMS: Recent studies implicated inflammation playing an important role in the occurrence and advancement of colorectal cancer.
  • Colorectal adenoma as the representative precursor lesion of colorectal cancer has meaningful association with inflammation.
  • Accordingly, the purpose of this study was to evaluate the association between serum C-reactive protein (CRP) levels and the risk of colorectal adenoma.
  • The subjects were allocated into 3,505 normal control subjects and 1,982 patients with colorectal adenoma.
  • Also, the risk of colorectal adenoma according to CRP level and difference of CRP level according to the characteristics of adenomas were analyzed.
  • RESULTS: There was no significant difference in serum CRP level between normal and colorectal adenoma group.
  • After adjusting for the clinically significant variables of colorectal adenoma, multiple logistic regression analysis of the risk of colorectal adenoma according to the CRP level (<1, 1-3, >3) and the CRP level according to characteristics of adenomas showed no significant difference.
  • CONCLUSIONS: An inflammatory marker, CRP is not a risk factor for colorectal adenoma development.
  • [MeSH-major] Adenoma / etiology. C-Reactive Protein / analysis. Colorectal Neoplasms / etiology

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  • [CommentIn] Korean J Gastroenterol. 2008 Apr;51(4):265-8 [18516007.001]
  • (PMID = 18516001.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 9007-41-4 / C-Reactive Protein
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79. Otake T, Uezono K, Takahashi R, Fukumoto J, Tabata S, Abe H, Tajima O, Mizoue T, Ohnaka K, Kono S: C-reactive protein and colorectal adenomas: Self Defense Forces Health Study. Cancer Sci; 2009 Apr;100(4):709-14
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  • [Title] C-reactive protein and colorectal adenomas: Self Defense Forces Health Study.
  • Chronic inflammation has been implicated in colorectal carcinogenesis.
  • Several studies have investigated the relationship between C-reactive protein (CRP), a biomarker of inflammation, and colorectal cancer and adenomas, resulting in inconsistent findings.
  • The present study examined the relationship between circulating levels of high-sensitivity CRP and colorectal adenomas.
  • The study subjects comprised 646 cases of colorectal adenoma and 635 controls of normal total colonoscopy among men receiving a preretirement health examination at two hospitals of the Self Defense Forces.
  • The multivariate-adjusted geometric means showed no measurable differences between adenoma cases and controls, but were higher among cases with larger adenomas (trend P = 0.03).
  • Likewise, although the prevalence odds of colorectal adenomas did not differ according to CRP levels as categorized at the 30th, 60th, and 90th percentiles in the controls, higher levels of CRP were associated with a statistically significant increase in the prevalence odds of large adenomas (> or = 5 mm), but not of small adenomas (<5 mm).
  • The multivariate-adjusted odds ratios of large adenomas for the lowest to highest categories of CRP were 1.00 (referent), 1.81 (95% confidence interval 1.17-2.80), 1.61 (95% confidence interval 1.03-2.52), and 2.21 (95% confidence interval 1.28-3.84), respectively (trend P = 0.01).
  • A positive association between CRP and prevalence odds of large adenomas was not modified by either smoking or overweight.
  • These findings suggest that inflammation is linked to the growth of colorectal adenomas.
  • [MeSH-major] Adenoma / genetics. C-Reactive Protein / genetics. Colorectal Neoplasms / genetics. Health Surveys. Military Personnel / statistics & numerical data

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  • (PMID = 19469014.001).
  • [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] 9007-41-4 / C-Reactive Protein
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80. Gao F, Liao C, Liu L, Tan A, Cao Y, Mo Z: The effect of aspirin in the recurrence of colorectal adenomas: a meta-analysis of randomized controlled trials. Colorectal Dis; 2009 Nov;11(9):893-901
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  • [Title] The effect of aspirin in the recurrence of colorectal adenomas: a meta-analysis of randomized controlled trials.
  • PURPOSE: Colorectal adenomas are precursors of most colorectal cancers and are important targets for chemoprevention.
  • However, the role of aspirin in preventing recurrence of adenomas is controversial.
  • We performed a systematic review and meta-analysis to evaluate the effect of aspirin in preventing the recurrence of colorectal adenoma.
  • Main outcome measures were the recurrence of any new adenoma and advanced adenoma.
  • We found that the relative risks of any adenoma (when compared with the placebo group) were 0.859 in the high dose of aspirin groups (95% confidence interval (CI), 0.756-0.976, P = 0.019), 0.826 in the low dose of aspirin groups (95% CI 0.706-0.965, P = 0.016) and 0.836 in the both aspirin combined groups (95% CI 0.746-0.937, P = 0.002).
  • For the recurrence of advanced adenoma, the relative risk (when compared with the placebo group) was 0.655 (95% CI 0.513-0.837, P = 0.001) in the aspirin groups without considering the dose.
  • CONCLUSION: This meta-analysis suggests that aspirin prevents recurrent colorectal adenomas among patients with a history of colorectal adenomas.
  • [MeSH-major] Adenoma / drug therapy. Aspirin / therapeutic use. Colorectal Neoplasms / drug therapy. Cyclooxygenase Inhibitors / therapeutic use. Neoplasm Recurrence, Local / prevention & control

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  • (PMID = 19055515.001).
  • [ISSN] 1463-1318
  • [Journal-full-title] Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland
  • [ISO-abbreviation] Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; R16CO5Y76E / Aspirin
  • [Number-of-references] 53
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81. Hirose M, Kono S, Tabata S, Ogawa S, Yamaguchi K, Mineshita M, Hagiwara T, Yin G, Lee KY, Tsuji A, Ikeda N: Genetic polymorphisms of methylenetetrahydrofolate reductase and aldehyde dehydrogenase 2, alcohol use and risk of colorectal adenomas: Self-Defense Forces Health Study. Cancer Sci; 2005 Aug;96(8):513-8
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  • [Title] Genetic polymorphisms of methylenetetrahydrofolate reductase and aldehyde dehydrogenase 2, alcohol use and risk of colorectal adenomas: Self-Defense Forces Health Study.
  • Methylenetetrahydrofolate reductase is a key enzyme in folate metabolism, which affects DNA synthesis and methylation and is possibly linked to colorectal carcinogenesis.
  • This study investigated the relationship of functional MTHFR C677T and ALDH2 polymorphisms to colorectal adenomas with reference to alcohol consumption in a case-control study of male officials in the Self-Defense Forces (SDF) who received a preretirement health examination at two SDF hospitals.
  • The study subjects were 452 cases of colorectal adenoma and 1050 controls with no polyp who underwent total colonoscopy.
  • Neither MTHFR C677T nor ALDH2 showed a measurable association with colorectal adenoma.
  • While high alcohol consumption was associated with a moderately increased risk of colorectal adenoma, neither of the two polymorphisms showed a significant effect on the association between alcohol and colorectal adenoma.
  • Individuals with the variant alleles ALDH2*2 and MTHFR 677T had a decreased risk of colorectal adenomas, showing adjusted odds ratios of 0.70 (95% confidence interval 0.49-1.00) for all adenomas and 0.57 (0.34-0.95) for large adenomas (> or = 5 mm), as compared to individuals with ALDH2*1/1 and MTHFR 677CC genotypes combined.
  • The findings may be interpreted as suggesting that folate inhibits the growth of colorectal adenomas, but further confirmation is needed.
  • [MeSH-major] Adenoma / genetics. Alcohol Drinking. Aldehyde Dehydrogenase / genetics. Colorectal Neoplasms / genetics. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Single Nucleotide

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  • (PMID = 16108833.001).
  • [ISSN] 1347-9032
  • [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 1.2.1.3 / ALDH2 protein, human; EC 1.2.1.3 / Aldehyde Dehydrogenase; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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82. Morita M, Tabata S, Tajima O, Yin G, Abe H, Kono S: Genetic polymorphisms of CYP2E1 and risk of colorectal adenomas in the Self Defense Forces Health Study. Cancer Epidemiol Biomarkers Prev; 2008 Jul;17(7):1800-7
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  • [Title] Genetic polymorphisms of CYP2E1 and risk of colorectal adenomas in the Self Defense Forces Health Study.
  • Functional RsaI and 96-bp insertion polymorphisms in 5'-flanking region have drawn interest in relation to the risk of colorectal cancer.
  • We investigated the relation of these genetic polymorphisms and colorectal adenoma, a well-established precursor lesion of colorectal cancer.
  • Subjects were 455 cases of colorectal adenomas and 1,052 controls of normal colonoscopy among men receiving a preretirement health examination in the Self Defense Forces.
  • Individuals with RsaI c2 allele showed a decreased risk of proximal colon adenomas; adjusted odds ratios (95% confidence interval) of proximal and distal adenomas for the c1/c2 or c2/c2 genotype versus c1/c1 was 0.61 (0.41-0.88) and 0.95 (0.71-1.27), respectively.
  • CYP2E1 96-bp insertion allele was associated with an increased risk of large (> or = 5 mm) adenomas; adjusted odds ratios (95% confidence interval) of large and small adenomas for having at least one insertion allele were 1.41 (1.03-1.94) and 0.94 (0.71-1.25), respectively.
  • A suggestive effect modification was noted for alcohol consumption on the association between RsaI polymorphism and proximal adenomas (P(interaction) = 0.09) as well as on the association between 96-bp insertion and large adenomas (P(interaction) = 0.05).
  • These findings indicate that variation in activity and inducibility of CYP2E1 contribute to the development of colorectal carcinogenesis.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Cytochrome P-450 CYP2E1 / genetics. DNA, Neoplasm / genetics. Health Surveys. Military Personnel / statistics & numerical data. Polymorphism, Genetic

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  • (PMID = 18628434.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 1.14.13.- / Cytochrome P-450 CYP2E1
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83. Lim U, Flood A, Choi SW, Albanes D, Cross AJ, Schatzkin A, Sinha R, Katki HA, Cash B, Schoenfeld P, Stolzenberg-Solomon R: Genomic methylation of leukocyte DNA in relation to colorectal adenoma among asymptomatic women. Gastroenterology; 2008 Jan;134(1):47-55
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  • [Title] Genomic methylation of leukocyte DNA in relation to colorectal adenoma among asymptomatic women.
  • We examined genomic methylation of leukocyte DNA in relation to colorectal adenoma (CRA) among asymptomatic women (40-79 years of age) participating in a multicenter colonoscopy screening study (CONCeRN Study, 2000-2002).
  • The inverse relationship was stronger for nonadvanced than for advanced adenoma and, less notably, for proximal than for distal adenoma.
  • The association was also moderately more protective with low rather than high total folate intake but did not differ by other nutrients involved in 1-carbon metabolism or colorectal cancer risk factors.

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  • (PMID = 18166347.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K07 CA108910-01A1; United States / NCI NIH HHS / CA / K07-CA108910-01A1; United States / Intramural NIH HHS / / NIH0011451923; United States / PHS HHS / / NIH0011451923; None / None / / K07 CA108910-01A1; United States / NCI NIH HHS / CA / K07 CA108910
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS36885; NLM/ PMC2211566
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84. Bai Y, Gao J, Zou DW, Li ZS: Distribution trends of colorectal adenoma and cancer: a colonoscopy database analysis of 11,025 Chinese patients. J Gastroenterol Hepatol; 2010 Oct;25(10):1668-73
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  • [Title] Distribution trends of colorectal adenoma and cancer: a colonoscopy database analysis of 11,025 Chinese patients.
  • BACKGROUND AND AIM: A left-to-right shift of colorectal cancer (CRC) has been reported in Western studies.
  • However, few Asian studies have investigated the anatomic distribution of colorectal adenoma and CRC.
  • We aimed to describe the time trends in the distribution of colorectal adenoma and CRC in a Chinese population.
  • Data, including patients' sex, age, symptoms, and the number and anatomic locations of colorectal adenoma and CRC, were documented.
  • RESULTS: A total of 11,025 patients were included in the final analysis; 1012 and 363 patients were diagnosed with colorectal adenoma and CRC, respectively.
  • Overall, there were more distal than proximal adenomas (54.4% vs 37.9%), and the proportion of proximal adenomas remained stable from 1998-2006 to 2007-2009 (38.2% vs 37.6%).
  • Colorectal adenoma and CRC were equally distributed among both sexes.
  • For elderly patients (> 50 years), there was a non-significant trend towards more proximal adenoma and CRC.
  • CONCLUSIONS: The present study suggests no distal-to-proximal shift of colorectal adenoma and CRC among the Chinese population in Shanghai over the past 12 years.
  • The distribution pattern of colorectal adenoma and CRC of Chinese patients is different from that of Western patients, who had more colorectal lesions located in the distal part.
  • [MeSH-major] Adenoma / diagnosis. Colonoscopy / statistics & numerical data. Colorectal Neoplasms / diagnosis

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  • [Copyright] © 2010 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd.
  • (PMID = 20880177.001).
  • [ISSN] 1440-1746
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
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85. Ward MH, Cross AJ, Divan H, Kulldorff M, Nowell-Kadlubar S, Kadlubar FF, Sinha R: Processed meat intake, CYP2A6 activity and risk of colorectal adenoma. Carcinogenesis; 2007 Jun;28(6):1210-6
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  • [Title] Processed meat intake, CYP2A6 activity and risk of colorectal adenoma.
  • Red and processed meat intake is associated with increased risks of both colorectal adenoma and cancer.
  • We conducted a case-control study of 146 cases of colorectal adenoma, diagnosed at sigmoidoscopy or colonoscopy, and 228 polyp-free controls.
  • Our results suggest that nitrite and nitrate intake from processed meat intake increases the risk of colorectal adenoma after accounting for HCA and PAH.
  • [MeSH-major] Adenoma / enzymology. Aryl Hydrocarbon Hydroxylases / physiology. Colorectal Neoplasms / enzymology. Diet. Meat Products. Mixed Function Oxygenases / physiology

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  • (PMID = 17277235.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CYP2A6 protein, human; EC 1.- / Mixed Function Oxygenases; EC 1.14.13.- / Cytochrome P-450 CYP2A6; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases
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86. Yamaji T, Iwasaki M, Sasazuki S, Sakamoto H, Yoshida T, Tsugane S: Methionine synthase A2756G polymorphism interacts with alcohol and folate intake to influence the risk of colorectal adenoma. Cancer Epidemiol Biomarkers Prev; 2009 Jan;18(1):267-74
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  • [Title] Methionine synthase A2756G polymorphism interacts with alcohol and folate intake to influence the risk of colorectal adenoma.
  • Genomic DNA hypomethylation has been associated with colorectal carcinogenesis.
  • We therefore hypothesized that minor allele carriers possess a decreased risk of colorectal adenoma, and examined this hypothesis in a case-control study of colorectal adenoma in Japan involving 723 cases and 670 controls.
  • An unconditional logistic regression model was used to estimate odds ratios (OR) and their 95% confidence intervals (95% CI) for colorectal adenoma after adjustment for potential confounders.
  • The G allele may confer protection against colorectal adenoma in the presence of a considerably good folate status.
  • Our findings add to increasing evidence that DNA methylation plays an important role even at an early stage of colorectal carcinogenesis.
  • [MeSH-major] 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase / genetics. Adenoma / genetics. Alcohol Drinking / adverse effects. Colorectal Neoplasms / genetics. Folic Acid / blood. Polymorphism, Genetic

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  • (PMID = 19124508.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 935E97BOY8 / Folic Acid; EC 2.1.1.13 / 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase
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87. Bobe G, Murphy G, Rogers CJ, Hance KW, Albert PS, Laiyemo AO, Sansbury LB, Lanza E, Schatzkin A, Cross AJ: Serum adiponectin, leptin, C-peptide, homocysteine, and colorectal adenoma recurrence in the Polyp Prevention Trial. Cancer Epidemiol Biomarkers Prev; 2010 Jun;19(6):1441-52
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  • [Title] Serum adiponectin, leptin, C-peptide, homocysteine, and colorectal adenoma recurrence in the Polyp Prevention Trial.
  • BACKGROUND: Serum adiponectin, leptin, C-peptide, and homocysteine are indicators for obesity, hyperinsulinemia, and chronic inflammation, which have all been associated with colorectal cancer.
  • AIMS: To determine whether serum adiponectin, leptin, C-peptide, and homocysteine are associated with fat, fiber, fruit and vegetable, flavonol, or dry bean intake and colorectal adenoma recurrence.
  • METHODS: Using logistic regression, we estimated odds ratios (OR) and 95% confidence intervals (95% CI) for adenoma recurrence in 627 participants from the control arm of the Polyp Prevention Trial, a 4-year trial that examined the effectiveness of a low-fat, high-fiber, high-fruit and vegetable diet on adenoma recurrence.
  • High homocysteine concentrations were associated with any (4th versus 1st quartile: OR, 2.26; 95% CI, 1.30-3.94) and more than one adenoma recurrence (OR, 2.11; 95% CI, 1.01-4.40).
  • Individuals in the highest, versus lowest, tertile of serum leptin concentration had a decreased risk of advanced adenoma recurrence (OR, 0.22; 95% CI, 0.06-0.79).
  • CONCLUSION: Our results suggest that serum homocysteine may serve as an indicator of dietary exposure, including a low-fat and high-fiber, high-fruit and vegetable, and high-flavonol diet, as well as colorectal adenoma recurrence.
  • We identified serum homocysteine as a novel indicator that is modified by diet and predicts risk of adenoma recurrence.
  • [MeSH-major] Adenoma / blood. Colorectal Neoplasms / blood. Neoplasm Recurrence, Local / blood

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  • [Copyright] Copyright 2010 AACR.
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  • (PMID = 20501764.001).
  • [ISSN] 1538-7755
  • [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 CN000151-19
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / C-Peptide; 0 / Leptin; 0LVT1QZ0BA / Homocysteine
  • [Other-IDs] NLM/ NIHMS192819; NLM/ PMC2882997
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88. Akhter M, Iwasaki M, Yamaji T, Sasazuki S, Tsugane S: Dietary isoflavone and the risk of colorectal adenoma: a case-control study in Japan. Br J Cancer; 2009 Jun 2;100(11):1812-6
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  • [Title] Dietary isoflavone and the risk of colorectal adenoma: a case-control study in Japan.
  • We conducted a case-control study in a Japanese population to investigate the association between dietary isoflavone intake and the risk of colorectal adenoma.
  • We found a significant inverse association between dietary isoflavone intake and the risk of colorectal adenoma in men and women combined.
  • The observed ceiling effect associated with higher isoflavone intake suggests that a lower intake of dietary isoflavone might be associated with an increased risk of colorectal adenoma in Japanese populations.
  • [MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Diet. Isoflavones / pharmacology

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  • (PMID = 19417743.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Isoflavones
  • [Other-IDs] NLM/ PMC2695684
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89. Grau MV, Baron JA, Sandler RS, Wallace K, Haile RW, Church TR, Beck GJ, Summers RW, Barry EL, Cole BF, Snover DC, Rothstein R, Mandel JS: Prolonged effect of calcium supplementation on risk of colorectal adenomas in a randomized trial. J Natl Cancer Inst; 2007 Jan 17;99(2):129-36
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  • [Title] Prolonged effect of calcium supplementation on risk of colorectal adenomas in a randomized trial.
  • BACKGROUND: Calcium supplementation has been shown to decrease the risk of recurrence of colorectal adenomas in randomized trials.
  • METHODS: In the Calcium Polyp Prevention Study, 930 subjects with a previous colorectal adenoma were randomly assigned from November 1988 through April 1992 to receive placebo or 1200 mg of elemental calcium daily for 4 years.
  • The Calcium Follow-up Study was an observational phase of the trial that tracked adenoma occurrence for an average of 7 years after the end of randomized treatment and gathered information regarding the use of medications, vitamins, and supplements during that time.
  • Generalized linear models were used to compute relative risks (RRs) and 95% confidence intervals (CIs) for the effect of randomized calcium treatment on risk of adenoma recurrence during the first 5 years after study treatment ended and during the subsequent 5 years.
  • RESULTS: During the first 5 years after randomized treatment ended, subjects in the calcium group still had a substantially and statistically significantly lower risk of any adenoma than those in the placebo group (31.5% versus 43.2%; adjusted RR = 0.63, 95% CI = 0.46 to 0.87, P = .005) and a smaller and not statistically significant reduction in risk of advanced adenomas (adjusted RR = 0.85, 95% CI = 0.43 to 1.69, P = .65).
  • CONCLUSION: The protective effect of calcium supplementation on risk of colorectal adenoma recurrence extends up to 5 years after cessation of active treatment, even in the absence of continued supplementation.

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  • [CommentIn] J Natl Cancer Inst. 2007 Jan 17;99(2):99-100 [17227988.001]
  • (PMID = 17227996.001).
  • [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 / R01 CA098286; United States / NCI NIH HHS / CA / U01 CA046927; United States / NCI NIH HHS / CA / 5 U01 CA46927; United States / NCI NIH HHS / CA / R01 CA98286
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Calcium, Dietary
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90. Hiripi E, Bermejo JL, Sundquist J, Hemminki K: Association of colorectal adenoma with other malignancies in Swedish families. Br J Cancer; 2008 Mar 11;98(5):997-1000
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  • [Title] Association of colorectal adenoma with other malignancies in Swedish families.
  • Using the Swedish Family-Cancer Database covering over 11.5 million individuals, estimated relative risks (RRs) for colorectal adenoma were using Poisson's regression.
  • The RR of colorectal adenoma was found to be increased among first-degree relatives of patients with colorectal cancer (2.72; 95% confidence interval=2.46-3.00) and among the offspring and siblings of patients with endometrial and prostate cancers.
  • We also found an increased risk of colorectal adenoma for the offspring of individuals with stomach cancer and leukaemia, and for siblings of those with pancreatic cancer and multiple myeloma.
  • Our results suggest that colorectal adenoma may share a genetic aetiology with cancer even at extracolorectal sites.
  • Increases of colorectal adenoma in families affected by prostate cancer and acute leukaemia cannot be attributed to known cancer syndromes, although the play of chance cannot be excluded.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics

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  • (PMID = 18283306.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2266856
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91. Miller PE, Lesko SM, Muscat JE, Lazarus P, Hartman TJ: Dietary patterns and colorectal adenoma and cancer risk: a review of the epidemiological evidence. Nutr Cancer; 2010;62(4):413-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dietary patterns and colorectal adenoma and cancer risk: a review of the epidemiological evidence.
  • A number of studies exploring associations between individual dietary components and colorectal adenoma or cancer risk have yielded conflicting results.
  • Results from prospective cohort and population-based case-control studies examining associations between dietary patterns and colorectal cancer or adenoma risk were evaluated and described in this review.
  • Despite notable differences in population characteristics, study design, and methods used for characterizing dietary patterns across the different studies, two general dietary patterns were found to modestly predict colorectal adenoma and cancer risk.
  • A healthier pattern consisting of greater intakes of fruits and vegetables, and lower intakes of red and processed meat, appeared protective against colorectal adenoma and cancer incidence.
  • Continued research efforts are needed to evaluate the cumulative and interactive effects of numerous dietary exposures on colorectal cancer risk.
  • [MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Diet

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  • (PMID = 20432162.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dietary Carbohydrates; 0 / Dietary Fats
  • [Number-of-references] 49
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92. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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93. Otake S, Takeda H, Suzuki Y, Fukui T, Watanabe S, Ishihama K, Saito T, Togashi H, Nakamura T, Matsuzawa Y, Kawata S: Association of visceral fat accumulation and plasma adiponectin with colorectal adenoma: evidence for participation of insulin resistance. Clin Cancer Res; 2005 May 15;11(10):3642-6
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  • [Title] Association of visceral fat accumulation and plasma adiponectin with colorectal adenoma: evidence for participation of insulin resistance.
  • PURPOSE: Colorectal carcinogenesis is thought to be related to abdominal obesity and insulin resistance.
  • To investigate whether visceral fat accumulation contributes to colorectal carcinogenesis, we examined its accumulation and the levels of the adipose tissue-derived hormone adiponectin in Japanese patients with colorectal adenoma.
  • EXPERIMENTAL DESIGN: Fifty-one consecutive Japanese patients ages >/=40 years and with colorectal adenoma were subjected to measurement of visceral fat area by computed tomography scanning and plasma adiponectin concentration.
  • The controls were 52 Japanese subjects ages >/=40 years and without colorectal polyp.
  • RESULTS: The patients with colorectal adenoma showed significantly more visceral fat area and significantly less plasma adiponectin concentration in comparison with the controls [odds ratio (OR), 2.19; 95% confidence interval (95% CI), 1.47-3.28; P < 0.001 and OR, 0.24; 95% CI, 0.14-0.41; P < 0.001, respectively] by logistic regression analysis.
  • HOMA-IR index was also associated with colorectal adenoma (OR 2.60; 95% CI, 1.20-5.64; P = 0.040).
  • Visceral fat area and adiponectin were associated with adenoma number (1, 2, >/= 3), the size of the largest adenoma (<10 and >/=10 mm), and adenoma histology (tubular and tubulovillous/villous).
  • CONCLUSIONS: These results suggest an association of visceral fat accumulation and decreased plasma adiponectin concentration with colorectal adenoma in Japanese patients.
  • This study may offer a new insight to understanding the relationship of colorectal carcinogenesis with abdominal obesity and insulin resistance.
  • [MeSH-major] Adenoma / physiopathology. Adipose Tissue. Body Composition. Colorectal Neoplasms / physiopathology. Insulin Resistance. Intercellular Signaling Peptides and Proteins / blood

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  • (PMID = 15897559.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Intercellular Signaling Peptides and Proteins
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94. Le Marchand L, Wang H, Rinaldi S, Kaaks R, Vogt TM, Yokochi L, Decker R: Associations of plasma C-peptide and IGFBP-1 levels with risk of colorectal adenoma in a multiethnic population. Cancer Epidemiol Biomarkers Prev; 2010 Jun;19(6):1471-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Associations of plasma C-peptide and IGFBP-1 levels with risk of colorectal adenoma in a multiethnic population.
  • BACKGROUND: Circulating levels of insulin and insulin-like growth factor (IGF) hormones have been associated with colorectal cancer risk, but few studies have examined their associations with colorectal adenoma.
  • METHODS: We measured plasma C-peptide, a marker of insulin secretion, and IGF hormones in a case-control study of 554 pathologically confirmed, first-time adenoma cases and 786 controls with normal endoscopy among Caucasians, Japanese, and Native Hawaiians in Hawaii.
  • RESULTS: High plasma levels of C-peptide were statistically significantly associated with risk of colorectal adenoma [multivariate odds ratio (95% confidence interval) for increasing quartiles: 1.0, 0.91 (0.65-1.27), 1.21 (0.86-1.71), and 1.79 (1.23-2.60); P(trend) = 0.0002].
  • We also observed a statistically significant inverse association between levels of plasma IGF binding protein-1 (IGFBP-1) and adenoma risk [1.0, 0.97 (0.70-1.34), 0.82 (0.58-1.15), and 0.47 (0.32-0.70); P(trend) <0.0001].
  • IGF-I, IGFBP-3, body mass index, and waist or hip circumference were not independently associated with adenoma risk.
  • CONCLUSION: These results provide evidence for an association of insulin and IGFBP-1 levels with colorectal adenoma.
  • IMPACT: This study suggests that hyperinsulinemia and IGF hormones may act as etiologic factors in colorectal carcinogenesis, as early as during adenoma formation.

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  • [Copyright] Copyright 2010 AACR.
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  • (PMID = 20501760.001).
  • [ISSN] 1538-7755
  • [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 / CA072520-09; United States / NCI NIH HHS / CA / R01 CA072520; United States / NCI NIH HHS / CA / R01 CA072520-09; United States / NCI NIH HHS / CA / R01 CA72520
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / C-Peptide; 0 / Insulin-Like Growth Factor Binding Protein 1
  • [Other-IDs] NLM/ NIHMS192089; NLM/ PMC2882992
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95. Liu CS, Hsu HS, Li CI, Jan CI, Li TC, Lin WY, Lin T, Chen YC, Lee CC, Lin CC: Central obesity and atherogenic dyslipidemia in metabolic syndrome are associated with increased risk for colorectal adenoma in a Chinese population. BMC Gastroenterol; 2010;10:51
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  • [Title] Central obesity and atherogenic dyslipidemia in metabolic syndrome are associated with increased risk for colorectal adenoma in a Chinese population.
  • The purpose of this study was to evaluate the relationship between individual components of MetS and colorectal adenoma.
  • Among the patients with MetS, 34.6% had adenoma, 31.7% had hyperplastic polyps and 23.3% were polyp-free (p < 0.0001, Chi-square test).
  • The adjusted OR for colorectal adenoma was significantly higher in the subjects with MetS (OR, 1.31, CI: 1.09-1.57).
  • A stronger association between MetS and colorectal adenoma was found in men (OR:1.44, CI:1.16-1.80) than in women (OR:1.04, CI:0.74-1.46).
  • The adjusted OR for adenoma increased as the number of MetS components increased (p for trend = 0.0001 ).
  • When the individual components of MetS were analyzed separately, only central obesity (OR:1.36, CI:1.14-1.63), low HDL cholesterol levels (OR:1.30, CI:1.10-1.54) and high triglyceride levels (OR:1.26, CI:1.04-1.53) were independently associated with colorectal adenoma.
  • CONCLUSIONS: Of the components of MetS analyzed in this study, central obesity and dyslipidemia are independent risk factors for colorectal adenoma.
  • With regard to the prevention of colorectal neoplasm, life-style modification such as weight reduction is worthwhile.
  • [MeSH-major] Adenoma / epidemiology. Adenoma / ethnology. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms / ethnology. Dyslipidemias / complications. Metabolic Syndrome X / complications. Obesity, Abdominal / complications

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  • (PMID = 20507579.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2894746
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96. Pufulete M, Al-Ghnaniem R, Khushal A, Appleby P, Harris N, Gout S, Emery PW, Sanders TA: Effect of folic acid supplementation on genomic DNA methylation in patients with colorectal adenoma. Gut; 2005 May;54(5):648-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of folic acid supplementation on genomic DNA methylation in patients with colorectal adenoma.
  • BACKGROUND AND AIMS: A low dietary folate intake can cause genomic DNA hypomethylation and may increase the risk of colorectal neoplasia.
  • The hypothesis that folic acid supplementation increases DNA methylation in leucocytes and colorectal mucosa was tested in 31 patients with histologically confirmed colorectal adenoma using a randomised, double blind, placebo controlled, parallel design.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. DNA Methylation / drug effects. Dietary Supplements. Folic Acid / pharmacology

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  • [CommentIn] Gut. 2005 May;54(5):579-81 [15831897.001]
  • (PMID = 15831910.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0LVT1QZ0BA / Homocysteine; 935E97BOY8 / Folic Acid
  • [Other-IDs] NLM/ PMC1774481
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97. Tsilidis KK, Erlinger TP, Rifai N, Hoffman S, Hoffman-Bolton J, Helzlsouer KJ, Platz EA: C-reactive protein and colorectal adenoma in the CLUE II cohort. Cancer Causes Control; 2008 Aug;19(6):559-67
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] C-reactive protein and colorectal adenoma in the CLUE II cohort.
  • OBJECTIVE: Circulating C-reactive protein concentration has been associated with colorectal cancer in some studies.
  • Thus, we evaluated the association between plasma C-reactive protein concentration and development of colorectal adenoma in a nested case-control study.
  • METHODS: Colorectal adenoma cases (n = 135) and matched controls (n = 269) who had a negative sigmoidoscopy or colonoscopy were identified between baseline in 1989 and 2000 from among participants in the CLUE II cohort of Washington County, Maryland.
  • The odds ratio (OR) of adenoma was estimated from conditional logistic regression models.
  • RESULTS: C-reactive protein concentrations were similar between colorectal adenoma cases and controls (median C-reactive protein, 1.31 vs. 1.38 mg/l; p = 0.13).
  • The OR of colorectal adenoma among those in the highest fourth (>2.95 mg/l) of C-reactive protein concentration compared with the lowest fourth (<0.65 mg/l) was 0.61 (95% confidence interval, 0.29-1.25; p for trend = 0.25).
  • CONCLUSIONS: Pre-diagnostic plasma C-reactive protein concentration was not associated with an increased risk of colorectal adenoma.
  • More work is needed to determine whether C-reactive protein is a valid marker of intra-colonic inflammation, and whether such inflammation contributes to the etiology of colorectal neoplasia.
  • [MeSH-major] Adenoma / blood. Biomarkers, Tumor / blood. C-Reactive Protein / analysis. Colorectal Neoplasms / blood

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  • (PMID = 18214695.001).
  • [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 / Biomarkers, Tumor; 9007-41-4 / C-Reactive Protein
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98. Cole BF, Baron JA, Sandler RS, Haile RW, Ahnen DJ, Bresalier RS, McKeown-Eyssen G, Summers RW, Rothstein RI, Burke CA, Snover DC, Church TR, Allen JI, Robertson DJ, Beck GJ, Bond JH, Byers T, Mandel JS, Mott LA, Pearson LH, Barry EL, Rees JR, Marcon N, Saibil F, Ueland PM, Greenberg ER, Polyp Prevention Study Group: Folic acid for the prevention of colorectal adenomas: a randomized clinical trial. JAMA; 2007 Jun 6;297(21):2351-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Folic acid for the prevention of colorectal adenomas: a randomized clinical trial.
  • CONTEXT: Laboratory and epidemiological data suggest that folic acid may have an antineoplastic effect in the large intestine.
  • OBJECTIVE: To assess the safety and efficacy of folic acid supplementation for preventing colorectal adenomas.
  • Participants included 1021 men and women with a recent history of colorectal adenomas and no previous invasive large intestine carcinoma.
  • MAIN OUTCOME MEASURES: The primary outcome measure was occurrence of at least 1 colorectal adenoma.
  • Secondary outcomes were the occurrence of advanced lesions (> or =25% villous features, high-grade dysplasia, size > or =1 cm, or invasive cancer) and adenoma multiplicity (0, 1-2, or > or =3 adenomas).
  • RESULTS: During the first 3 years, 987 participants (96.7%) underwent colonoscopic follow-up, and the incidence of at least 1 colorectal adenoma was 44.1% for folic acid (n = 221) and 42.4% for placebo (n = 206) (unadjusted risk ratio [RR], 1.04; 95% confidence interval [CI], 0.90-1.20; P = .58).
  • A total of 607 participants (59.5%) underwent a second follow-up, and the incidence of at least 1 colorectal adenoma was 41.9% for folic acid (n = 127) and 37.2% for placebo (n = 113) (unadjusted RR, 1.13; 95% CI, 0.93-1.37; P = .23); and incidence of at least 1 advanced lesion was 11.6% for folic acid (n = 35) and 6.9% for placebo (n = 21) (unadjusted RR, 1.67; 95% CI, 1.00-2.80; P = .05).
  • Folic acid was associated with higher risks of having 3 or more adenomas and of noncolorectal cancers.
  • CONCLUSIONS: Folic acid at 1 mg/d does not reduce colorectal adenoma risk.
  • Further research is needed to investigate the possibility that folic acid supplementation might increase the risk of colorectal neoplasia.


99. Goodman M, Bostick RM, Gross M, Thyagarajan B, Dash C, Flanders WD: Combined measure of pro- and anti-oxidant exposures in relation to prostate cancer and colorectal adenoma risk: an update. Ann Epidemiol; 2010 Dec;20(12):955-7
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  • [Title] Combined measure of pro- and anti-oxidant exposures in relation to prostate cancer and colorectal adenoma risk: an update.
  • PURPOSE: We previously proposed an oxidative balance score (OBS) and illustrated its practical application by using data from previously completed case-control studies of two neoplasms - sporadic colorectal adenoma and prostate cancer.
  • When the OBS was divided into three approximately equal intervals, a comparison of the lowest to highest category showed similar adjusted ORs (95% CIs) of 0.34 (0.13-0.88) and 0.34 (0.14-0.86) for colorectal adenoma and prostate cancer, respectively.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 21074110.001).
  • [ISSN] 1873-2585
  • [Journal-full-title] Annals of epidemiology
  • [ISO-abbreviation] Ann Epidemiol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA116795-03; United States / NCI NIH HHS / CA / R01 CA116795; United States / NCI NIH HHS / CA / R01 CA116795-01; United States / NCI NIH HHS / CA / R01 CA116795-03
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Biomarkers
  • [Other-IDs] NLM/ NIHMS242540; NLM/ PMC3008422
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100. Chung SJ, Kim YS, Yang SY, Song JH, Park MJ, Kim JS, Jung HC, Song IS: Prevalence and risk of colorectal adenoma in asymptomatic Koreans aged 40-49 years undergoing screening colonoscopy. J Gastroenterol Hepatol; 2010 Mar;25(3):519-25
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  • [Title] Prevalence and risk of colorectal adenoma in asymptomatic Koreans aged 40-49 years undergoing screening colonoscopy.
  • BACKGROUND AND AIM: Colorectal cancer screening is recommended for average-risk persons beginning at age 50.
  • However, information about the incidence and risk factors of precursor adenoma in preceding decades is limited.
  • The aim of this study was to determine the prevalence and risk factors of colorectal adenoma in persons aged 40-49 years and to compare the data with those aged 30-39 years and 50-59 years.
  • RESULTS: Prevalence of overall adenomas was 10.4% in the 30-39 years age group, 22.2% in the 40-49 years age group, and 32.8% in the 50-59 years age group.
  • Advanced adenoma was found in 0.7% of the 30-39 years age group, 2.7% of the 40-49 years age group, and 4.1% of the 50-59 years age group.
  • In the 40-49 years age group, male sex and current smoking habits showed associations with low-risk adenoma after multiple adjustments.
  • Moreover, male sex (odds ratio [OR] = 1.55, 95% confidence interval [CI]: 1.02-3.23), current smoking (OR = 1.58, 95%CI: 1.06-3.50), and family history of colorectal cancer (OR = 2.54, 95%CI: 1.16-5.56) were independent predictors of advanced adenoma in this age group.
  • CONCLUSIONS: Prevalence of adenoma in subjects aged 40-49 years was higher than in previous studies.
  • Male sex and current smoking habits along with a family history of colorectal cancer were associated with advanced adenoma in this age group.
  • [MeSH-major] Adenoma / diagnosis. Adenoma / epidemiology. Asian Continental Ancestry Group / statistics & numerical data. Colonoscopy. Colorectal Neoplasms / diagnosis. Colorectal Neoplasms / epidemiology. Mass Screening

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  • (PMID = 20370730.001).
  • [ISSN] 1440-1746
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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