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[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

   

[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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[Cites] Am J Surg. 2001 Jun;181(6):526-8 [11513778.001]

[Cites] Am J Gastroenterol. 2005 Aug;100(8):1813-20 [16086719.001]

[Cites] Am J Epidemiol. 2001 Dec 15;154(12):1089-99 [11744511.001]

[Cites] Br J Cancer. 2003 Jan 13;88(1):79-83 [12556963.001]

[Cites] JAMA. 2003 Dec 10;290(22):2959-67 [14665657.001]

[Cites] Rom J Gastroenterol. 2004 Sep;13(3):187-93 [15470530.001]

[Cites] Gut. 1984 Aug;25(8):863-6 [6745725.001]

[Cites] Am J Epidemiol. 1986 Sep;124(3):453-69 [3740045.001]

[Cites] Gut. 1986 Oct;27(10):1181-5 [3781331.001]

[Cites] Cancer. 1988 Feb 1;61(3):618-21 [3338028.001]

[Cites] Dig Dis Sci. 1988 Sep;33(9):1178-84 [3409804.001]

[Cites] Ann R Coll Surg Engl. 1989 Jan;71(1):37-9 [2923417.001]

[Cites] Epidemiology. 1990 Jan;1(1):58-64 [2081241.001]

[Cites] Cancer. 1991 Oct 1;68(7):1644-7 [1893365.001]

[Cites] Gastroenterology. 1993 Jul;105(1):130-41 [8514030.001]

[Cites] Scand J Gastroenterol. 1996 Feb;31(2):160-9 [8658039.001]

[Cites] Am J Gastroenterol. 1999 Jan;94(1):41-6 [9934729.001]

[Cites] Am J Epidemiol. 1999 Sep 15;150(6):547-51 [10489992.001]

[Cites] Gastroenterology. 2001 Sep;121(3):542-7 [11522737.001]

(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

   

[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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[Cites] Jpn J Cancer Res. 1999 Nov;90(11):1212-7 [10622531.001]

[Cites] Am J Clin Nutr. 2007 Feb;85(2):614S-620S [17284765.001]

[Cites] Nutrition. 2000 Jul-Aug;16(7-8):669-71 [10906592.001]

[Cites] Cancer Res. 2001 May 1;61(9):3599-603 [11325827.001]

[Cites] Oncogene. 2002 Jun 20;21(27):4317-22 [12082619.001]

[Cites] J Nutr. 2003 May;133(5):1291-5 [12730412.001]

[Cites] J Nutr. 2003 May;133(5):1302-7 [12730414.001]

[Cites] Neurosci Biobehav Rev. 2003 Sep;27(4):385-99 [12946691.001]

[Cites] Am J Epidemiol. 2004 Jul 15;160(2):102-9 [15234930.001]

[Cites] Am J Clin Nutr. 2004 Sep;80(3):539-49 [15321791.001]

[Cites] Am J Epidemiol. 1984 May;119(5):837-9 [6720679.001]

[Cites] Am J Epidemiol. 1986 Jul;124(1):17-27 [3521261.001]

[Cites] Carcinogenesis. 1986 Aug;7(8):1309-12 [3731384.001]

[Cites] Carcinogenesis. 1988 Feb;9(2):259-63 [3338109.001]

[Cites] Proc Natl Acad Sci U S A. 1989 Apr;86(8):2703-7 [2649891.001]

[Cites] Biochim Biophys Acta. 1990 May 1;1044(1):1-12 [2187537.001]

[Cites] J Natl Cancer Inst. 1993 Jun 2;85(11):875-84 [8492316.001]

[Cites] Adv Exp Med Biol. 1996;399:143-55 [8937554.001]

[Cites] J Natl Cancer Inst. 1998 Jan 7;90(1):57-62 [9428784.001]

[Cites] J Am Diet Assoc. 1998 Jun;98(6):699-706 [9627630.001]

[Cites] Cancer Res. 1999 Jan 1;59(1):80-4 [9892190.001]

[Cites] Brain Res Dev Brain Res. 1999 Mar 12;113(1-2):13-20 [10064869.001]

[Cites] Am J Clin Nutr. 2005 Feb;81(2):440-4 [15699233.001]

[Cites] Curr Drug Metab. 2005 Feb;6(1):15-22 [15720203.001]

[Cites] Mol Imaging. 2004 Oct;3(4):319-23 [15802048.001]

[Cites] Nat Rev Cancer. 2005 May;5(5):388-96 [15864280.001]

[Cites] Eur J Cancer. 2005 Jul;41(10):1453-9 [15913986.001]

[Cites] Am J Clin Nutr. 2005 Jul;82(1):111-7 [16002808.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):189-93 [16492904.001]

[Cites] Am J Clin Nutr. 2006 Apr;83(4):905-11 [16600945.001]

[Cites] Epidemiology. 2006 May;17(3):285-91 [16570024.001]

[Cites] Annu Rev Nutr. 2006;26:229-50 [16848706.001]

[Cites] Gut. 2006 Oct;55(10):1387-9 [16966698.001]

[Cites] J Pediatr. 2006 Nov;149(5 Suppl):S131-6 [17212955.001]

[CommentIn] J Natl Cancer Inst. 2007 Aug 15;99(16):1214-5 [17686821.001]

(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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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Endoscopic and histopathological features of serrated adenoma of large intestine:an analysis of 71 cases].

OBJECTIVE: To explore the endoscopic and histopathological morphology of large intestinal serrated adenomas (SA).

RESULTS: Forty-seven of the 71 serrated adenomas were protruded (sessile 23, semipedunculated 5, pedunculated 23) and 24 were superficial (flat 16, laterally spreading 8).

[MeSH-major] Adenoma / pathology. Colonoscopy. Colorectal Neoplasms / pathology

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(PMID = 16721690.001).

[ISSN] 1671-0274

[Journal-full-title] Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery

[ISO-abbreviation] Zhonghua Wei Chang Wai Ke Za Zhi

[Language] chi

[Publication-type] Controlled Clinical Trial; English Abstract; Journal Article

[Publication-country] China

   

[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

   

[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.

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[Cites] J Nutr. 2004 Dec;134(12 Suppl):3421S-3426S [15570048.001]

[Cites] J Natl Cancer Inst. 1999 Jun 2;91(11):916-32 [10359544.001]

[Cites] Carcinogenesis. 2005 Mar;26(3):579-85 [15564289.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):616-9 [15767339.001]

[Cites] Lung Cancer. 2005 Apr;48(1):11-7 [15777967.001]

[Cites] Cancer Lett. 2005 Aug 8;226(1):49-54 [15882925.001]

[Cites] Br J Cancer. 2005 Oct 17;93(8):953-9 [16205694.001]

[Cites] Int J Cancer. 2006 Aug 1;119(3):668-72 [16506214.001]

[Cites] BMC Cancer. 2006;6:70 [16542464.001]

[Cites] Int J Cancer. 2006 Jul 15;119(2):297-303 [16482563.001]

[Cites] Breast Cancer Res. 2006;8(6):R71 [17181859.001]

[Cites] Cancer. 2007 Mar 1;109(5):849-57 [17236225.001]

[Cites] Carcinogenesis. 2007 Jun;28(6):1197-201 [17151091.001]

[Cites] Cancer Sci. 2008 Mar;99(3):576-81 [18167131.001]

[Cites] Oncogene. 1999 Dec 20;18(55):7908-16 [10630643.001]

[Cites] Am J Pathol. 2000 Feb;156(2):545-53 [10666384.001]

[Cites] Biochim Biophys Acta. 2000 Mar 27;1470(2):M69-78 [10722929.001]

[Cites] J Biol Chem. 2000 Apr 21;275(16):11750-7 [10766797.001]

[Cites] Am J Epidemiol. 2001 Feb 15;153(4):394-403 [11207158.001]

[Cites] J Biol Chem. 2001 May 25;276(21):18075-81 [11278548.001]

[Cites] Clin Cancer Res. 2001 Dec;7(12):3971-6 [11751489.001]

[Cites] Arterioscler Thromb Vasc Biol. 2002 Oct 1;22(10):1631-6 [12377741.001]

[Cites] Biomed Pharmacother. 2002 Oct;56(8):380-7 [12442910.001]

[Cites] Clin Pharmacol Ther. 2003 Jan;73(1):122-30 [12545150.001]

[Cites] Carcinogenesis. 2003 May;24(5):985-90 [12771044.001]

[Cites] Mol Cell Biochem. 2003 Nov;253(1-2):141-9 [14619964.001]

[Cites] Prog Lipid Res. 2004 Jan;43(1):3-35 [14636669.001]

[Cites] Curr Pharm Des. 2004;10(6):635-46 [14965326.001]

[Cites] Dis Colon Rectum. 2004 May;47(5):665-73 [15054679.001]

[Cites] Br J Cancer. 2004 May 4;90(9):1760-4 [15150618.001]

[Cites] Br J Cancer. 2004 Jul 19;91(2):339-43 [15173859.001]

[Cites] Am J Epidemiol. 1985 Jul;122(1):51-65 [4014201.001]

[Cites] Gastroenterology. 1990 Feb;98(2):371-9 [2403953.001]

[Cites] Biochem Biophys Res Commun. 1993 Jan 29;190(2):406-11 [8427584.001]

[Cites] Am J Epidemiol. 1993 Jun 1;137(11):1241-50 [8322764.001]

[Cites] Biochem J. 1994 Sep 15;302 ( Pt 3):723-7 [7945196.001]

[Cites] Int J Epidemiol. 1995 Apr;24(2):389-98 [7635601.001]

[Cites] Med Sci Sports Exerc. 1997 Jun;29(6 Suppl):S1-205 [9243481.001]

[Cites] Jpn J Clin Oncol. 1998 Jul;28(7):421-6 [9739782.001]

[Cites] Carcinogenesis. 2005 Feb;26(2):449-57 [15550453.001]

(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 / R01CA-51932; United States / NCRR NIH HHS / RR / P20 RR017698; United States / NCRR NIH HHS / RR / RR017698; United States / NCI NIH HHS / CA / R01 CA134609; United States / NCI NIH HHS / CA / U01 CA114601; United States / NCI NIH HHS / CA / 1 U01 CA114601-01

[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

   

[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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[Cites] Cancer Epidemiol Biomarkers Prev. 2001 May;10(5):559-62 [11352869.001]

[Cites] Carcinogenesis. 2007 Sep;28(9):2019-27 [17690112.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2000 Jun;9(6):625-30 [10868699.001]

[Cites] Eur J Cancer Prev. 2000 Jun;9(3):151-64 [10954254.001]

[Cites] Carcinogenesis. 2000 Oct;21(10):1909-15 [11023550.001]

[Cites] Carcinogenesis. 2001 Jan;22(1):199-202 [11159760.001]

[Cites] Nutr Rev. 2001 May;59(5):140-8 [11396694.001]

[Cites] Am J Epidemiol. 2001 Dec 15;154(12):1089-99 [11744511.001]

[Cites] Jpn J Cancer Res. 2002 May;93(5):478-83 [12036442.001]

[Cites] Mutat Res. 2002 Aug 26;519(1-2):151-61 [12160900.001]

[Cites] J Natl Cancer Inst. 2002 Aug 7;94(15):1126-33 [12165637.001]

[Cites] Cancer Res. 2003 May 15;63(10):2358-60 [12750250.001]

[Cites] J Natl Cancer Inst. 2004 Mar 3;96(5):403-7 [14996862.001]

[Cites] Environ Mol Mutagen. 2004;44(1):44-55 [15199546.001]

[Cites] J Nutr. 2004 Oct;134(10):2711-6 [15465771.001]

[Cites] Int J Cancer. 1981;27(4):471-4 [7275353.001]

[Cites] J Am Diet Assoc. 1982 Apr;80(4):307-11 [7061776.001]

[Cites] J Nutr. 1986 Sep;116(9):1720-5 [3761027.001]

[Cites] Gastroenterology. 1987 Nov;93(5):1009-13 [3653628.001]

[Cites] Stat Med. 1989 May;8(5):551-61 [2657958.001]

[Cites] Mutat Res. 1991 Mar-Apr;259(3-4):399-410 [2017219.001]

[Cites] Carcinogenesis. 1991 Aug;12(8):1503-6 [1860171.001]

[Cites] J Natl Cancer Inst. 1993 Jun 2;85(11):884-91 [8388061.001]

[Cites] N Engl J Med. 1993 Dec 30;329(27):1977-81 [8247072.001]

[Cites] Int J Cancer. 1994 Feb 1;56(3):379-82 [8314326.001]

[Cites] Cancer Res. 1995 Oct 15;55(20):4516-9 [7553619.001]

[Cites] Am J Epidemiol. 1995 Oct 1;142(7):692-8 [7572938.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1996 Jul;5(7):503-7 [8827353.001]

[Cites] Am J Epidemiol. 1996 Dec 1;144(11):1005-14 [8942430.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1997 Dec;6(12):1029-32 [9419398.001]

[Cites] Food Chem Toxicol. 1998 Apr;36(4):279-87 [9651044.001]

[Cites] Food Chem Toxicol. 1998 Apr;36(4):289-97 [9651045.001]

[Cites] Int J Cancer. 1999 Mar 15;80(6):852-6 [10074917.001]

[Cites] Cancer Res. 1999 Sep 1;59(17):4320-4 [10485479.001]

[Cites] J Natl Cancer Inst. 2005 Feb 2;97(3):232-3; author reply 233-4 [15687367.001]

[Cites] Carcinogenesis. 2005 Mar;26(3):637-42 [15579480.001]

[Cites] N Engl J Med. 2005 May 19;352(20):2061-8 [15901859.001]

[Cites] J Natl Cancer Inst. 2005 Jun 15;97(12):917-26 [15956653.001]

[Cites] Mol Nutr Food Res. 2005 Jul;49(7):648-55 [15986387.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 Aug;14(8):2030-4 [16103456.001]

[Cites] Cancer Res. 2005 Sep 1;65(17):8034-41 [16140978.001]

[Cites] Int J Cancer. 2006 Jun 15;118(12):3147-52 [16425287.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2006 Apr;15(4):717-25 [16614114.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2006 Jun;15(6):1120-5 [16775169.001]

[Cites] Med Hypotheses. 2007;68(3):562-4 [17045417.001]

[Cites] J Nutr. 2007 Apr;137(4):999-1004 [17374667.001]

[Cites] Int J Cancer. 2007 Jul 1;121(1):136-42 [17354224.001]

[Cites] Carcinogenesis. 2007 Jun;28(6):1210-6 [17277235.001]

[Cites] Br J Cancer. 2007 Jul 2;97(1):118-22 [17551493.001]

[Cites] Cancer Res. 1999 Nov 15;59(22):5704-9 [10582688.001]

(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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[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

   

[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

   

[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^INK4a, MGMT, p14^ARF 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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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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[Cites] Gastrointest Endosc. 2000 Apr;51(4 Pt 1):433-7 [10744815.001]

[Cites] Gastroenterology. 2006 May;130(6):1872-85 [16697750.001]

[Cites] Gastroenterology. 2001 Apr;120(5):1077-83 [11266371.001]

[Cites] Gut. 2001 Jun;48(6):812-5 [11358901.001]

[Cites] Am J Gastroenterol. 2002 Jun;97(6):1524-9 [12094877.001]

[Cites] Dis Colon Rectum. 2004 Mar;47(3):323-33 [14991494.001]

[Cites] Ann Surg. 1975 Oct;182(4):511-5 [1180587.001]

[Cites] Cancer. 1978 Dec;42(6):2839-48 [728878.001]

[Cites] Cancer. 1979 May;43(5):1847-57 [445371.001]

[Cites] Cancer. 1982 Feb 15;49(4):819-25 [7055790.001]

[Cites] Endoscopy. 1985 Sep;17(5):175-81 [4054062.001]

[Cites] Scand J Gastroenterol. 1987 Sep;22(7):833-41 [3672041.001]

[Cites] J Natl Cancer Inst. 1990 Nov 21;82(22):1769-72 [2231773.001]

[Cites] Gastroenterology. 1991 Jan;100(1):64-7 [1796931.001]

[Cites] World J Surg. 1991 Jan-Feb;15(1):3-6 [1994603.001]

[Cites] Am J Gastroenterol. 1991 Aug;86(8):941-5 [1858757.001]

[Cites] N Engl J Med. 1993 Apr 1;328(13):901-6 [8446136.001]

[Cites] Scand J Gastroenterol. 1993 Oct;28(10):869-74 [8266015.001]

[Cites] Gastroenterology. 1995 Feb;108(2):402-8 [7835580.001]

[Cites] Gastroenterology. 1997 Jan;112(1):24-8 [8978338.001]

[Cites] Gastroenterology. 1997 Feb;112(2):594-642 [9024315.001]

[Cites] Gastroenterology. 1998 Jul;115(1):13-8 [9649453.001]

[Cites] J Natl Cancer Inst. 1998 Nov 4;90(21):1661-5 [9811316.001]

[Cites] Hepatogastroenterology. 1998 Sep-Oct;45(23):1565-72 [9840106.001]

[Cites] Am J Gastroenterol. 2006 Feb;101(2):343-50 [16454841.001]

[Cites] Am J Gastroenterol. 2000 Nov;95(11):3053-63 [11095318.001]

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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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[Cites] Br J Cancer. 2001 Aug 3;85(3):357-61 [11487265.001]

[Cites] Am J Pathol. 2006 Nov;169(5):1505-22 [17071576.001]

[Cites] J Nutr. 2001 Nov;131(11 Suppl):3109S-20S [11694656.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2002 Apr;11(4):385-91 [11927499.001]

[Cites] J Womens Health (Larchmt). 2003 Mar;12(2):173-82 [12737716.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):412-8 [12750235.001]

[Cites] Int J Cancer. 2003 Oct 20;107(1):89-93 [12925961.001]

[Cites] J Natl Cancer Inst. 2004 Apr 7;96(7):546-53 [15069117.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2004 Jun;13(6):915-9 [15184246.001]

[Cites] Ann Clin Lab Sci. 1980 Mar-Apr;10(2):111-5 [6770740.001]

[Cites] Arteriosclerosis. 1987 May-Jun;7(3):211-25 [3593067.001]

[Cites] J Biol Chem. 1991 Oct 5;266(28):18868-76 [1717456.001]

[Cites] J Natl Cancer Inst. 1991 Oct 2;83(19):1403-7 [1920483.001]

[Cites] Cancer Causes Control. 1993 Mar;4(2):117-21 [8481490.001]

[Cites] Ann Intern Med. 1995 Mar 1;122(5):327-34 [7847643.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1994 Dec;3(8):687-95 [7881343.001]

[Cites] Cancer Causes Control. 1995 Mar;6(2):164-79 [7749056.001]

[Cites] Cancer Causes Control. 1996 Mar;7(2):253-63 [8740738.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1996 Aug;5(8):607-12 [8824362.001]

[Cites] Scand J Gastroenterol. 1997 Feb;32(2):162-8 [9051877.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1997 Sep;6(9):661-70 [9298572.001]

[Cites] Cancer Causes Control. 1999 Oct;10(5):379-86 [10530607.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 Apr;14(4):850-5 [15824155.001]

[Cites] Nutr Metab Cardiovasc Dis. 2004 Dec;14(6):334-43 [15853117.001]

[Cites] J Gastroenterol Hepatol. 2005 Sep;20(9):1410-5 [16105129.001]

[Cites] Lancet. 2005 Sep 24-30;366(9491):1059-62 [16182882.001]

[Cites] J Natl Cancer Inst. 2005 Nov 16;97(22):1679-87 [16288121.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 Dec;14(12):3010-2 [16365028.001]

[Cites] Asian Pac J Cancer Prev. 2005 Oct-Dec;6(4):485-9 [16435997.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2006 Apr;15(4):750-5 [16614119.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2391-7 [17164361.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2007 Jan;16(1):161-4 [17220346.001]

[Cites] Int J Cancer. 2007 May 1;120(9):2007-12 [17266031.001]

[Cites] Int J Cancer. 2007 Jul 15;121(2):368-76 [17372899.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2007 Aug;16(8):1543-6 [17684126.001]

[Cites] Int J Obes (Lond). 2008 Feb;32(2):304-14 [17878894.001]

[Cites] Cancer Causes Control. 2008 Aug;19(6):559-67 [18214695.001]

[Cites] J Natl Cancer Inst. 2000 Oct 4;92(19):1592-600 [11018095.001]

[Cites] Clin Chem. 2001 Mar;47(3):444-50 [11238295.001]

[Cites] Cancer. 2006 Jul 1;107(1):28-36 [16721800.001]

[Cites] Am J Epidemiol. 2006 Oct 1;164(7):652-64 [16877536.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2001 Sep;10(9):937-41 [11535544.001]

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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)

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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)

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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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[Cites] Gastroenterology. 2005 Aug;129(2):464-75 [16083703.001]

[Cites] Lancet. 2005 Apr 16-22;365(9468):1415-28 [15836891.001]

[Cites] Gut. 2006 Feb;55(2):285-91 [16239255.001]

[Cites] Asian Pac J Cancer Prev. 2005 Oct-Dec;6(4):485-9 [16435997.001]

[Cites] Clin Gastroenterol Hepatol. 2006 Oct;4(10):1225-31 [16979948.001]

[Cites] Genet Med. 2006 Sep;8(9):571-5 [16980813.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2007 Aug;16(8):1543-6 [17684126.001]

[Cites] Cancer Res. 2008 Jan 1;68(1):329-37 [18172327.001]

[Cites] JAMA. 2008 Dec 17;300(23):2765-78 [19088354.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):275-81 [19124509.001]

[Cites] Hepatogastroenterology. 2009 May-Jun;56(91-92):677-81 [19621679.001]

[Cites] Lancet. 1978 Feb 4;1(8058):245-7 [74668.001]

[Cites] Int J Cancer. 1990 Feb 15;45(2):372-5 [2406206.001]

[Cites] Jpn J Cancer Res. 1989 Jan;80(1):51-8 [2540132.001]

[Cites] Am J Gastroenterol. 1986 Feb;81(2):101-3 [3946362.001]

[Cites] Ann Intern Med. 1995 Mar 1;122(5):327-34 [7847643.001]

[Cites] Ann Epidemiol. 1995 Nov;5(6):478-83 [8680611.001]

[Cites] Int J Epidemiol. 1998 Oct;27(5):794-8 [9839735.001]

[Cites] J Natl Cancer Inst. 1999 Mar 17;91(6):542-7 [10088625.001]

[Cites] Am J Med. 1999 Jan 25;106(1A):24S-27S [10089111.001]

[Cites] Jpn J Cancer Res. 1999 Aug;90(8):805-11 [10543250.001]

[Cites] J Natl Cancer Inst. 2000 Oct 4;92(19):1592-600 [11018095.001]

[Cites] Br J Cancer. 2001 Feb 2;84(3):417-22 [11161410.001]

[Cites] Jpn J Cancer Res. 2001 Aug;92(8):836-40 [11509114.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2002 Oct;11(10 Pt 1):1012-8 [12376501.001]

[Cites] Cancer Causes Control. 2002 Dec;13(10):917-21 [12588087.001]

[Cites] Am J Med. 1954 Apr;16(4):555-64 [13148199.001]

[Cites] Surg Gynecol Obstet. 1951 Sep;93(3):327-30 [14866716.001]

[Cites] Ann Intern Med. 2004 Apr 20;140(8):603-13 [15096331.001]

[Cites] Cancer Causes Control. 2004 Aug;15(6):581-9 [15280637.001]

[Cites] Lancet. 2005 Sep 24-30;366(9491):1059-62 [16182882.001]

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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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[Cites] JAMA. 1999 Dec 15;282(23):2240-5 [10605976.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2007 Aug;16(8):1543-6 [17684126.001]

[Cites] J Natl Cancer Inst. 2000 Sep 20;92(18):1472-89 [10995803.001]

[Cites] Am J Gastroenterol. 2001 Jan;96(1):84-8 [11197293.001]

[Cites] Am J Physiol Endocrinol Metab. 2001 May;280(5):E745-51 [11287357.001]

[Cites] Am J Gastroenterol. 2001 Dec;96(12):3406-10 [11774957.001]

[Cites] JAMA. 2002 May 15;287(19):2559-62 [12020337.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2002 Oct;11(10 Pt 1):1095-9 [12376513.001]

[Cites] Gastroenterol Clin North Am. 2002 Dec;31(4):925-43 [12489270.001]

[Cites] Microbes Infect. 2003 Jul;5(8):693-703 [12814770.001]

[Cites] Cancer Sci. 2004 Jan;95(1):72-6 [14720330.001]

[Cites] JAMA. 2004 Feb 4;291(5):585-90 [14762037.001]

[Cites] Diabetes Care. 2004 May;27(5):1182-6 [15111542.001]

[Cites] Mutat Res. 1990 May;238(3):313-20 [2188127.001]

[Cites] Cell. 1990 Jun 1;61(5):759-67 [2188735.001]

[Cites] Science. 1990 Aug 31;249(4972):970-1 [2136249.001]

[Cites] N Engl J Med. 1991 Sep 26;325(13):938-48 [1881419.001]

[Cites] Lancet. 1992 May 9;339(8802):1128-30 [1349365.001]

[Cites] Lancet. 1992 Nov 14;340(8829):1194-5 [1359263.001]

[Cites] Environ Health Perspect. 1995 Nov;103 Suppl 8:263-8 [8741796.001]

[Cites] J Natl Cancer Inst. 1996 Dec 4;88(23):1717-30 [8944002.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1996 Dec;5(12):1013-5 [8959325.001]

[Cites] Nutr Cancer. 1997;27(3):316-20 [9101563.001]

[Cites] J Clin Gastroenterol. 1997 Dec;25(4):605-7 [9451672.001]

[Cites] J Clin Endocrinol Metab. 1998 Mar;83(3):859-62 [9506740.001]

[Cites] Diabetes Care. 1998 Sep;21(9):1414-31 [9727886.001]

[Cites] Digestion. 1999;60(3):210-5 [10343134.001]

[Cites] Lancet. 2005 Apr 16-22;365(9468):1415-28 [15836891.001]

[Cites] J Gastroenterol Hepatol. 2005 Sep;20(9):1410-5 [16105129.001]

[Cites] J Med Microbiol. 2005 Nov;54(Pt 11):1031-5 [16192433.001]

[Cites] Lancet. 2005 Oct 1;366(9492):1197-209 [16198769.001]

[Cites] J Gastroenterol. 2005 Sep;40(9):887-93 [16211345.001]

[Cites] J Gastroenterol. 2005 Sep;40(9):919-20 [16211355.001]

[Cites] Int J Cancer. 2005 Dec 20;117(6):1058-9 [15986436.001]

[Cites] Asian Pac J Cancer Prev. 2005 Oct-Dec;6(4):485-9 [16435997.001]

[Cites] Helicobacter. 2006 Apr;11(2):75-80 [16579836.001]

[Cites] World J Surg Oncol. 2007;5:51 [17498313.001]

[Cites] Cytokine. 2000 Jan;12(1):78-85 [10623446.001]

(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

   

[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

   

[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

   

[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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[Cites] N Engl J Med. 2000 Apr 20;342(16):1149-55 [10770979.001]

[Cites] N Engl J Med. 1992 Nov 5;327(19):1350-5 [1406836.001]

[Cites] Am J Physiol Endocrinol Metab. 2000 May;278(5):E941-8 [10780952.001]

[Cites] Horm Res. 2005;64 Suppl 2:37-40 [16286769.001]

[Cites] Gut. 2006 Jan;55(1):62-7 [15972299.001]

[Cites] Int J Cancer. 2006 Mar 15;118(6):1496-500 [16187280.001]

[Cites] Am J Gastroenterol. 2006 Feb;101(2):343-50 [16454841.001]

[Cites] BMC Gastroenterol. 2006;6:5 [16412216.001]

[Cites] Int J Obes (Lond). 2006 Mar;30(3):475-83 [16261188.001]

[Cites] CA Cancer J Clin. 2006 May-Jun;56(3):143-59; quiz 184-5 [16737947.001]

[Cites] J Natl Cancer Inst. 2006 Jul 5;98(13):920-31 [16818856.001]

[Cites] Br J Cancer. 1993 Jan;67(1):177-84 [8381298.001]

[Cites] Cancer Causes Control. 1994 Jan;5(1):38-52 [8123778.001]

[Cites] Gynecol Endocrinol. 1993 Dec;7(4):251-8 [8147234.001]

[Cites] Eur J Cancer. 1994;30A(3):344-50 [8204357.001]

[Cites] Ann Intern Med. 1995 Mar 1;122(5):327-34 [7847643.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1996 Apr;5(4):313-5 [8722224.001]

[Cites] Cancer Causes Control. 1996 Mar;7(2):253-63 [8740738.001]

[Cites] J Natl Cancer Inst. 1997 Jul 2;89(13):948-55 [9214674.001]

[Cites] Am J Epidemiol. 1998 Apr 1;147(7):670-80 [9554606.001]

[Cites] Int J Cancer. 1998 Oct 5;78(2):161-5 [9754646.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1999 Jan;8(1):45-51 [9950239.001]

[Cites] Annu Rev Med. 2005;56:45-62 [15660501.001]

[Cites] J Natl Cancer Inst. 2005 Jun 1;97(11):846-53 [15928305.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 Sep;14(9):2082-6 [16172213.001]

[Cites] Gastroenterology. 1993 Jan;104(1):137-44 [8419236.001]

[Cites] Jpn J Cancer Res. 1999 Aug;90(8):805-11 [10543250.001]

[Cites] Am J Epidemiol. 2000 Nov 1;152(9):847-54 [11085396.001]

[Cites] Gastroenterology. 2001 Apr;120(5):1077-83 [11266371.001]

[Cites] Am J Gastroenterol. 2001 Jul;96(7):2238-46 [11467659.001]

[Cites] Nutr Cancer. 2001;39(1):50-7 [11588902.001]

[Cites] Eur J Nutr. 2002 Feb;41(1):35-43 [11990006.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2002 Jul;11(7):622-9 [12101109.001]

[Cites] Gut. 2002 Aug;51(2):147 [12117867.001]

[Cites] Gut. 2002 Aug;51(2):191-4 [12117878.001]

[Cites] Cancer Causes Control. 2003 Feb;14(1):75-84 [12708728.001]

[Cites] Diabetologia. 2003 Apr;46(4):459-69 [12687327.001]

[Cites] Trends Pharmacol Sci. 2003 Sep;24(9):479-85 [12967773.001]

[Cites] Cancer Causes Control. 2003 Nov;14(9):879-87 [14682445.001]

[Cites] Horm Metab Res. 2003 Nov-Dec;35(11-12):694-704 [14710348.001]

[Cites] Dis Colon Rectum. 2004 Mar;47(3):323-33 [14991494.001]

[Cites] Int J Obes Relat Metab Disord. 2004 Apr;28(4):559-67 [14770200.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2004 Apr;13(4):553-9 [15066919.001]

[Cites] Am J Gastroenterol. 2004 Apr;99(4):687-93 [15089903.001]

[Cites] Am J Epidemiol. 2004 May 15;159(10):983-92 [15128611.001]

[Cites] J Natl Cancer Inst. 2004 Jun 16;96(12):921-5 [15199111.001]

[Cites] JAMA. 2004 Jun 16;291(23):2847-50 [15199035.001]

[Cites] Cancer Causes Control. 2004 Aug;15(6):581-9 [15280637.001]

[Cites] J Chronic Dis. 1979;32(8):563-76 [468958.001]

[Cites] J Natl Cancer Inst. 1985 Feb;74(2):307-17 [3856044.001]

[Cites] Am J Clin Nutr. 1988 Feb;47(2):312-7 [3341261.001]

[Cites] Am J Epidemiol. 1988 Sep;128(3):490-503 [2843038.001]

[Cites] Am J Epidemiol. 1989 Jan;129(1):125-37 [2910056.001]

[Cites] J Natl Cancer Inst. 1991 Mar 6;83(5):359-61 [1995919.001]

[Cites] Cancer Causes Control. 1992 Jul;3(4):349-54 [1617122.001]

[Cites] J Natl Cancer Inst. 1992 Sep 2;84(17):1326-31 [1495102.001]

[Cites] N Engl J Med. 2000 Apr 20;342(16):1156-62 [10770980.001]

(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

   

[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

   

[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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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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[Cites] Cancer. 1982 Feb 15;49(4):819-25 [7055790.001]

[Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]

[Cites] Gastroenterology. 2001 Jul;121(1):198-213 [11438509.001]

[Cites] Int J Colorectal Dis. 2001 Aug;16(4):257-61 [11515686.001]

[Cites] CA Cancer J Clin. 2001 Jan-Feb;51(1):38-75; quiz 77-80 [11577479.001]

[Cites] Cancer. 1977 Jan;39(1):274-8 [832242.001]

[Cites] Cancer. 1978 Dec;42(6):2839-48 [728878.001]

[Cites] Cancer. 1979 May;43(5):1847-57 [445371.001]

[Cites] Dis Colon Rectum. 1981 Jan-Feb;24(1):29-36 [7472099.001]

[Cites] Gut. 1982 Oct;23(10):835-42 [7117903.001]

[Cites] Int J Cancer. 1985 Aug 15;36(2):179-86 [4018911.001]

[Cites] JAMA. 1987 Jul 17;258(3):331-8 [3599325.001]

[Cites] Virchows Arch A Pathol Anat Histopathol. 1987;411(6):591-8 [3118568.001]

[Cites] Cancer. 1988 Apr 1;61(7):1472-6 [3345499.001]

[Cites] Scand J Gastroenterol. 1989 Sep;24(7):799-806 [2799283.001]

[Cites] Gut. 1992 Nov;33(11):1508-14 [1452076.001]

[Cites] Gastroenterology. 1997 Feb;112(2):594-642 [9024315.001]

[Cites] Natl Vital Stat Rep. 2006 Jun 28;54(19):1-49 [16850709.001]

[Cites] Cancer. 2006 Sep 1;107(5 Suppl):1153-61 [16862554.001]

[Cites] N Engl J Med. 2006 Nov 2;355(18):1863-72 [17079760.001]

[Cites] N Engl J Med. 2002 Jun 6;346(23):1781-5 [12050337.001]

(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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[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.

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[CommentIn] JAMA. 2007 Jun 6;297(21):2408-9 [17551134.001]

[CommentIn] JAMA. 2007 Sep 26;298(12):1397; author reply 1397 [17895454.001]

(PMID = 17551129.001).

[ISSN] 1538-3598

[Journal-full-title] JAMA

[ISO-abbreviation] JAMA

[Language] ENG

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00272324

[Grant] United States / NCI NIH HHS / CA / R01 CA059005; United States / NCI NIH HHS / CA / R01 CA059005; United States / NCI NIH HHS / CA / U54 CA100971; United States / NCI NIH HHS / CA / U54 CA100971

[Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 935E97BOY8 / Folic Acid; R16CO5Y76E / Aspirin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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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[Cites] Can J Physiol Pharmacol. 1999 Jul;77(7):465-80 [10535707.001]

[Cites] Cell. 1990 Jun 1;61(5):759-67 [2188735.001]

[Cites] J Clin Oncol. 2000 Mar;18(5):1135-49 [10694567.001]

[Cites] Arterioscler Thromb Vasc Biol. 2000 Jun;20(6):1600-5 [10845878.001]

[Cites] Br J Surg. 2000 Sep;87(9):1215-21 [10971431.001]

[Cites] Mod Pathol. 2000 Sep;13(9):925-33 [11007031.001]

[Cites] Matrix Biol. 2000 Dec;19(7):623-9 [11102751.001]

[Cites] J Biol Chem. 2001 Jun 8;276(23):20108-15 [11274170.001]

[Cites] Clin Cancer Res. 2001 Aug;7(8):2344-6 [11489811.001]

[Cites] Arterioscler Thromb Vasc Biol. 2001 Nov;21(11):1834-9 [11701474.001]

[Cites] Nat Rev Cancer. 2002 Mar;2(3):161-74 [11990853.001]

[Cites] Cancer Res. 2002 Jul 1;62(13):3855-60 [12097300.001]

[Cites] Int J Cancer. 2002 Dec 10;102(5):526-9 [12432557.001]

[Cites] Circ Res. 2003 May 2;92(8):827-39 [12730128.001]

[Cites] J Am Coll Cardiol. 2003 Jun 18;41(12):2130-7 [12821236.001]

[Cites] J Pathol. 2003 Aug;200(5):568-76 [12898592.001]

[Cites] Genet Epidemiol. 2003 Sep;25(2):158-67 [12916024.001]

[Cites] Clin Chem. 2003 Nov;49(11):1940-2 [14578330.001]

[Cites] Int J Cancer. 1991 Nov 11;49(5):666-72 [1657796.001]

[Cites] N Engl J Med. 1993 Dec 30;329(27):1977-81 [8247072.001]

[Cites] Biochem Biophys Res Commun. 1994 Jun 15;201(2):657-64 [8002999.001]

[Cites] Mol Carcinog. 1994 Aug;10(4):199-206 [8068180.001]

[Cites] Cancer. 1995 Mar 15;75(6 Suppl):1516-9 [7889484.001]

[Cites] Int J Cancer. 1995 Apr 10;61(2):218-22 [7705951.001]

[Cites] Br Heart J. 1995 Mar;73(3):209-15 [7727178.001]

[Cites] Transplantation. 1995 Aug 27;60(4):375-83 [7652768.001]

[Cites] Nat Med. 1996 Apr;2(4):461-2 [8597958.001]

[Cites] J Biol Chem. 1996 May 31;271(22):13055-60 [8662692.001]

[Cites] Dis Colon Rectum. 1996 Nov;39(11):1255-64 [8918435.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Feb 18;94(4):1402-7 [9037065.001]

[Cites] Mol Carcinog. 1997 Aug;19(4):225-9 [9290698.001]

[Cites] Atherosclerosis. 1998 Jul;139(1):49-56 [9699891.001]

[Cites] Cancer Res. 1998 Dec 1;58(23):5321-5 [9850057.001]

[Cites] Cancer Res. 1999 Sep 1;59(17):4225-7 [10485461.001]

[Cites] Clin Cancer Res. 2005 Jan 15;11(2 Pt 1):594-9 [15701845.001]

[Cites] Carcinogenesis. 2005 May;26(5):892-9 [15695237.001]

[Cites] Aliment Pharmacol Ther. 2006 Jul 1;24(1):101-9 [16803608.001]

[Cites] J Pathol. 2003 Dec;201(4):528-34 [14648655.001]

[Cites] Cancer Metastasis Rev. 2004 Jan-Jun;23(1-2):101-17 [15000152.001]

[Cites] Clin Cancer Res. 2004 Apr 15;10(8):2594-9 [15102660.001]

[Cites] Am J Hum Genet. 2004 Oct;75(4):561-70 [15290652.001]

[Cites] Cancer. 1974 Sep;34(3):suppl:936-9 [4853883.001]

[Cites] J Chronic Dis. 1982;35(5):313-20 [7068807.001]

[Cites] Int J Cancer. 1986 Dec 15;38(6):789-94 [3793259.001]

[Cites] Oncogene. 1999 Dec 20;18(55):7908-16 [10630643.001]

(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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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]

[Cites] Gut. 2010 Feb;59(2):227-35 [19926618.001]

[Cites] Gastroenterology. 2002 Dec;123(6):1770-7 [12454832.001]

[Cites] Nat Immunol. 2003 Jun;4(6):540-5 [12754505.001]

[Cites] J Biol Chem. 2003 Aug 22;278(34):31972-9 [12783885.001]

[Cites] J Immunol. 2003 Sep 15;171(6):3194-201 [12960348.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14133-8 [14617776.001]

[Cites] Oncogene. 2005 Oct 6;24(44):6699-708 [16007169.001]

[Cites] Oncogene. 2005 Sep 22;24(42):6406-17 [16007195.001]

[Cites] Am J Pathol. 2005 Oct;167(4):969-80 [16192633.001]

[Cites] Oncogene. 2007 Jul 19;26(33):4833-41 [17297444.001]

[Cites] Cancer Res. 2008 Jan 1;68(1):323-8 [18172326.001]

[Cites] BMC Cancer. 2008;8:143 [18498652.001]

[Cites] World J Gastroenterol. 2009 Jan 7;15(1):61-6 [19115469.001]

[Cites] Am J Physiol Gastrointest Liver Physiol. 2009 Apr;296(4):G850-9 [19179628.001]

[Cites] Cancer Cell. 2009 Feb 3;15(2):91-102 [19185844.001]

[Cites] Clin Cancer Res. 2009 Apr 1;15(7):2248-58 [19276252.001]

[Cites] Scand J Gastroenterol. 2002 Aug;37(8):944-8 [12229970.001]

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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