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[Title] The protein tyrosine phosphatase receptor type R gene is an early and frequent target of silencing in human colorectal tumorigenesis.

RESULTS: A recent high-throughput gene expression analysis conducted by our group identified numerous genes whose transcription was markedly diminished in colorectal tumors.

Here, we show that levels of both major PTPRR transcript variants are markedly decreased (compared with normal mucosal levels) in precancerous and cancerous colorectal tumors, as well in colorectal cancer cell lines.

The expression of the PTPRR-1 isoform was inactivated in colorectal cancer cells as a result of de novo CpG island methylation and enrichment of transcription-repressive histone-tail marks, mainly H3K27me3.

De novo methylation of the PTPRR-1 transcription start site was demonstrated in 29/36 (80%) colorectal adenomas, 42/44 (95%) colorectal adenocarcinomas, and 8/8 (100%) liver metastases associated with the latter tumors.

CONCLUSIONS: Epigenetic downregulation of PTPRR seems to be an early alteration in colorectal cell transformation, which is maintained during the clonal selection associated with tumor progression.

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(PMID = 20015382.001).

[ISSN] 1476-4598

[Journal-full-title] Molecular cancer

[ISO-abbreviation] Mol. Cancer

[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 / RNA, Messenger; EC 3.1.3.48 / PTPRR protein, human; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 7

[Other-IDs] NLM/ PMC2801661

   

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[Title] Intake of dairy products and risk of colorectal neoplasia.

Prospective cohort studies suggest that higher intakes of dairy products, in particular milk, are associated with a decreased risk of colorectal cancer (CRC).

Randomised controlled trials with Ca supplements have been conducted with both colorectal adenoma and CRC as endpoints.

Results suggest that Ca supplementation at a level of 1000-2000 mg/d reduces adenoma recurrence in individuals with a previous adenoma but has no effect on CRC incidence.

[MeSH-major] Anticarcinogenic Agents / administration & dosage. Calcium, Dietary / administration & dosage. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms / prevention & control. Dairy Products

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(PMID = 19079854.001).

[ISSN] 1475-2700

[Journal-full-title] Nutrition research reviews

[ISO-abbreviation] Nutr Res Rev

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Calcium, Dietary; 1406-16-2 / Vitamin D

[Number-of-references] 113

   

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In the colorectal epithelium oxidative stress is observed endogenously in premalignant adenoma cells or induced by nutritional factors like fatty acid hydroperoxides (LOOH).

Our study used colorectal adenoma and carcinoma cell lines to assess antioxidant protective effects of resveratrol and quercetin.

For reduction of endogenous H2O2 levels in colorectal tumor cells higher antioxidant-concentrations are needed in all cell lines.

Quercetin (10 microM) alone even increased H2O2 in LT97 adenoma cells and stimulated VEGF production.

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(PMID = 17936464.001).

[ISSN] 0278-6915

[Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

[ISO-abbreviation] Food Chem. Toxicol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antioxidants; 0 / Oxidants; 0 / Stilbenes; 0 / Vascular Endothelial Growth Factor A; 63231-63-0 / RNA; 9IKM0I5T1E / Quercetin; BBX060AN9V / Hydrogen Peroxide; K7Q1JQR04M / Dinoprostone; Q369O8926L / resveratrol

   

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[Title] Association between cigarette smoking, APC mutations and the risk of developing sporadic colorectal adenomas and carcinomas.

BACKGROUND: The association between colorectal cancer (CRC) and smoking has not been consistent.

METHODS: To evaluate the hypothesis that cigarette smoking is associated with adenoma and carcinoma development and further to investigate whether this association is due to mutations in the APC gene, we used a study population consisting of 133 cases (45 adenomas and 88 carcinomas) and 334 controls.

An overall case-control association was detected for adenomas and "ever smoking" OR = 1.73 (95% CI 0.83-3.58).

When cases were divided based on APC truncation mutation status, an association was detected in adenomas without APC mutation in relation to "ever smoking", with an OR = 3.97 (1.26-12.51).

CONCLUSION: Our data suggest an association between smoking and adenoma and CRC development.

[MeSH-major] Adenoma / genetics. Carcinoma / genetics. Colorectal Neoplasms / genetics. DNA, Neoplasm / genetics. Genes, APC. Smoking / adverse effects

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(PMID = 16545110.001).

[ISSN] 1471-2407

[Journal-full-title] BMC cancer

[ISO-abbreviation] BMC Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / DNA, Neoplasm

[Other-IDs] NLM/ PMC1475604

   

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[Title] Meat, vegetables and genetic polymorphisms and the risk of colorectal carcinomas and adenomas.

BACKGROUND: The risk of sporadic colorectal cancer (CRC) is mainly associated with lifestyle factors, particularly dietary factors.

In this study we aimed to evaluate the role of dietary factors in combination with genetic factors in the different stages of colorectal carcinogenesis in a Norwegian population.

METHODS: We used a case-control study design (234 carcinomas, 229 high-risk adenomas, 762 low-risk adenomas and 400 controls) to test the association between dietary factors (meat versus fruit, berries and vegetables) genetic polymorphisms in biotransformation genes (GSTM1, GSTT1, GSTP1 Ile105Val, EPHX1 Tyr113His and EPHX1 His139Arg), and risk of colorectal carcinomas and adenomas.

RESULTS: A higher ratio of total meat to total fruit, berry and vegetable intake was positively associated with both high and low-risk adenomas, with approximately twice the higher risk in the 2nd quartile compared to the lowest quartile.

For the high-risk adenomas this positive association was more obvious for the common allele (Tyr allele) of the EPHX1 codon 113 polymorphism.

An association was also observed for the EPHX1 codon 113 polymorphism in the low-risk adenomas, although not as obvious.

CONCLUSION: Although, the majority of the comparison groups are not significant, our results suggest an increased risk of colorectal adenomas in individuals for some of the higher ratios of total meat to total fruit, berry and vegetable intake.

In addition the study supports the notion that the biotransformation enzymes GSTM1, GSTP1 and EPHX1 may modify the effect of dietary factors on the risk of developing colorectal carcinoma and adenoma.

[MeSH-major] Adenoma / etiology. Carcinoma / etiology. Colorectal Neoplasms / etiology. Eating / physiology. Meat. Polymorphism, Genetic. Vegetables

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(PMID = 18093316.001).

[ISSN] 1471-2407

[Journal-full-title] BMC cancer

[ISO-abbreviation] BMC Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 3.3.2.- / Epoxide Hydrolases; EC 3.3.2.9 / EPHX1 protein, human

[Other-IDs] NLM/ PMC2228310

   

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[Title] Development of a quantitative food frequency questionnaire for assessing food, nutrient, and heterocyclic aromatic amines intake in Japanese Brazilians for a colorectal adenoma case-control study.

PRIMARY OBJECTIVE: To develop of a quantitative food frequency questionnaire (QFFQ) to assess intake of specific foods, nutrients and heterocyclic aromatic amines (HAAs) in a case-control study of colorectal adenoma.

CONCLUSIONS: We have developed a QFFQ appropriate for Japanese Brazilians that will allow us to estimate HAA intake and will be used to examine our hypotheses related to foods, nutrients and HAAs, and diet-gene interactions in colorectal neoplasia in this population.

[MeSH-major] Adenoma. Amines / administration & dosage. Colorectal Neoplasms. Diet. Diet Surveys. Food Analysis. Polycyclic Hydrocarbons, Aromatic / administration & dosage

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(PMID = 19381993.001).

[ISSN] 1465-3478

[Journal-full-title] International journal of food sciences and nutrition

[ISO-abbreviation] Int J Food Sci Nutr

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R03 CA119682

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Amines; 0 / Polycyclic Hydrocarbons, Aromatic

   

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[Title] Interaction between adiponectin and leptin influences the risk of colorectal adenoma.

Obesity has been associated with an increased risk of colorectal neoplasia, but the mechanisms of this potential association have not been elucidated.

We hypothesized that the adipokines adiponectin, leptin, and tumor necrosis factor-alpha (TNF-alpha) may mediate an association between obesity and colorectal cancer.

An inverse association of total and HMW adiponectin was observed with colorectal adenoma (P trend < 0.001 and 0.03, respectively).

Further, total adiponectin interacted with leptin, but not TNF-alpha, in relation to colorectal adenoma (P interaction = 0.007).

An inverse association of total adiponectin with colorectal adenoma was apparent in the highest two tertiles of leptin, particularly the middle (P trend < 0.001), whereas a positive association of leptin was obvious in the lowest tertile of total adiponectin (P trend = 0.01) after adjusting for potential confounders and body mass index, which is a major determinant of insulin resistance.

Adiponectin may exert an anticarcinogenic effect on the large intestine by interfering with leptin, whereas leptin could conversely exert a carcinogenic effect under conditions of a lower abundance of adiponectin.

Our findings provide the first epidemiologic evidence for interactive effects of adiponectin and leptin in the early stage of colorectal tumorigenesis, distinct from their involvement in insulin resistance.

[MeSH-major] Adenoma / blood. Colorectal Neoplasms / blood. Leptin / blood

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[Copyright] Copyright 2010 AACR.

(PMID = 20516125.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / ADIPOQ protein, human; 0 / Adiponectin; 0 / Leptin; 0 / Tumor Necrosis Factor-alpha

   

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[Title] DNA stool test for colorectal cancer: hypermethylation of the secreted frizzled-related protein-1 gene.

PURPOSE: To investigate a potential mode of noninvasive screening for colorectal cancer, we evaluated the hypermethylation of the secreted frizzled-related protein-1 gene promoter in human stool DNA.

METHODS: In stool samples from 36 patients with colorectal neoplasia (7 adenoma, 29 colorectal cancer) and 17 healthy control subjects, isolated DNA was treated with sodium bisulfite and analyzed by methylation-specific polymerase chain reaction with primers specific for methylated or unmethylated promoter sequences of the secreted frizzled-related protein-1 gene.

RESULTS: Hypermethylation of the secreted frizzled-related protein-1 promoter was present in the stool DNA of patients with adenoma and colorectal cancer.

A sensitivity of 89 percent and specificity of 86 percent were achieved in the detection of colorectal neoplasia.

The difference in hypermethylation status of the secreted frizzled-related protein-1 promoter between the patients with colorectal neoplasia and the control group was statistically highly significant (P < 0.001).

Adenoma and early tumor Stage I (International Union Against Cancer) displayed both unmethylated and methylated secreted frizzled-related protein-1 promoter sequences, whereas advanced tumor stages showed only methylated secreted frizzled-related protein-1 (P = 0.05).

It has the potential of a clinically useful test for the early detection of colorectal cancer.

[MeSH-major] Adenoma / metabolism. Carcinoma / metabolism. Colorectal Neoplasms / metabolism. DNA Methylation. Feces. Intercellular Signaling Peptides and Proteins / metabolism. Membrane Proteins / metabolism

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(PMID = 17762966.001).

[ISSN] 0012-3706

[Journal-full-title] Diseases of the colon and rectum

[ISO-abbreviation] Dis. Colon Rectum

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / SFRP1 protein, human

   

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Inferences with measurement error corrections are complicated by the fact that the Wald test often behaves poorly in the presence of large amounts of measurement error.

An application of our method is illustrated using a population-based case-control study of the association between calcium intake and the risk of colorectal adenoma.

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[Cites] Biometrics. 2001 Sep;57(3):795-802 [11550930.001]

[Cites] Cancer Causes Control. 2002 Dec;13(10):937-46 [12588090.001]

[Cites] Am J Epidemiol. 2003 Jul 1;158(1):1-13 [12835280.001]

[Cites] Am J Hum Genet. 2003 Dec;73(6):1316-29 [14631556.001]

[Cites] Genet Epidemiol. 2004 Nov;27(3):192-201 [15372619.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2004 Dec;13(12):2181-6 [15598778.001]

[Cites] Genet Epidemiol. 2005 Sep;29(2):108-27 [16080203.001]

(PMID = 18047538.001).

[ISSN] 1541-0420

[Journal-full-title] Biometrics

[ISO-abbreviation] Biometrics

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / U01 CA057030; United States / NCI NIH HHS / CA / R25 CA090301; United States / NCI NIH HHS / CA / CA57030; United States / NCI NIH HHS / CA / R37 CA057030-20; United States / NCI NIH HHS / CA / R01 CA057030; United States / NCI NIH HHS / CA / CA90301; United States / NCI NIH HHS / CA / CA057030-20; United States / NCI NIH HHS / CA / R37 CA057030; United States / NIEHS NIH HHS / ES / P30 ES009106; United States / NIEHS NIH HHS / ES / P30-ES09106

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Calcium, Dietary

[Other-IDs] NLM/ NIHMS101403; NLM/ PMC2672569

   

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[Title] Dietary marine n-3 fatty acids in relation to risk of distal colorectal adenoma in women.

Epidemiologic studies of dietary marine n-3 fatty acids and risk of colorectal cancer have been inconsistent, and their relation to risk of colorectal adenoma has not been evaluated in detail.

We examined dietary marine n-3 fatty acids and the ratio of marine n-3 to total n-6 fatty acids (n-3/n-6 ratio) in relation to risk of adenoma of the distal colon or rectum among 34,451 U.S. women who were initially free of colorectal cancer or polyps, who completed a semiquantitative food frequency questionnaire in 1980, and who underwent endoscopy from 1980 to 1998.

We documented 1,719 distal colorectal adenoma cases (705 large adenomas, 897 small adenomas, 1,280 distal colon adenomas, and 505 rectal adenomas) during 18 years of follow-up.

Neither dietary marine n-3 fatty acids nor n-3/n-6 ratio were associated with risk of total distal colorectal adenoma after adjustment for age and established risk factors [multivariable relative risk (RR) for extreme quintiles of dietary marine n-3 fatty acids = 1.04; 95% confidence interval (95% CI), 0.84-1.27, P(trend) = 0.66; RR for extreme quintiles of n-3/n-6 ratio = 1.02; 95% CI, 0.83-1.25; P(trend) = 0.86].

Similarly, no significant associations were observed separately for distal colon or rectal adenoma.

However, higher intake of dietary marine n-3 fatty acids was nonsignificantly but suggestively inversely associated with large adenoma (RR, 0.74; 95% CI, 0.54-1.01; P(trend) = 0.16) but directly associated with small adenoma (RR, 1.36; 95% CI, 1.02-1.81; P(trend) = 0.09).

Our findings do not support the hypothesis that a higher intake of marine n-3 fatty acids or a higher n-3/n-6 ratio reduces the risk of distal colorectal adenoma but are suggestive that higher intake may reduce the progression of small adenomas to large adenomas.

[MeSH-major] Adenoma / prevention & control. Colorectal Neoplasms / prevention & control. Diet. Fatty Acids, Omega-3 / therapeutic use

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[CommentIn] Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):406-7 [16492940.001]

(PMID = 15824153.001).

[ISSN] 1055-9965

[Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

[ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA 87969; United States / NCI NIH HHS / CA / CA55075

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Fatty Acids, Omega-3; 0 / Fatty Acids, Omega-6; 0RBV727H71 / alpha-Linolenic Acid

   

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[Title] Abberant crypt foci -- importance in colorectal carcinogenesis and expression of p53 and mdm2: a changing concept.

BACKGROUND: The presence of aberrant crypt foci (ACF) represents an important preneoplastic condition of the large intestine.

AIMS: To study the significance of ACF in carcinogenesis, the incidence of ACF in colorectal carcinoma (CRC) patients and the expression profiles of the tumor repressor protein p53 and the murine double minute (mdm2) protein in ACF.

RESULT: Aberrant crypt foci were present in a large number of cases (84.4%), of which 65% were hyperplastic.

This results suggests that the conventional adenoma-carcinoma sequence is not completely correct.

[MeSH-major] Adenocarcinoma / chemistry. Cell Transformation, Neoplastic / chemistry. Colorectal Neoplasms / chemistry. Precancerous Conditions / chemistry. Proto-Oncogene Proteins c-mdm2 / analysis. Tumor Suppressor Protein p53 / analysis

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(PMID = 18080767.001).

[ISSN] 0163-2116

[Journal-full-title] Digestive diseases and sciences

[ISO-abbreviation] Dig. Dis. Sci.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.3.2.27 / MDM2 protein, human; EC 2.3.2.27 / Proto-Oncogene Proteins c-mdm2

   

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[Title] Serum bile acids, programmed cell death and cell proliferation in the mucosa of patients with colorectal adenomas.

BACKGROUND: Deoxycholic acid induced programmed cell death and an imbalance with cell proliferation may favour colorectal tumourigenesis according to 'in vitro' studies, but information is lacking on the relationships occurring 'in vivo' in humans.

METHODS: In 10 patients with colorectal adenomas, we measured fasting serum levels of bile acids; and, in normal colonic mucosa, programmed cell death by the TUNEL technique and cell proliferation by immunohistochemical staining with anti-Ki67.

[MeSH-major] Adenoma / blood. Apoptosis / drug effects. Bile Acids and Salts / blood. Cell Proliferation / drug effects. Colorectal Neoplasms / blood. Deoxycholic Acid / blood. Deoxycholic Acid / pharmacology. Intestinal Mucosa / cytology

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(PMID = 15975538.001).

[ISSN] 1590-8658

[Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver

[ISO-abbreviation] Dig Liver Dis

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / Bile Acids and Salts; 0 / Ki-67 Antigen; 0 / MIB-1 antibody; 005990WHZZ / Deoxycholic Acid

   

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[Title] Independent induction of caspase-8 and cFLIP expression during colorectal carcinogenesis in sporadic and HNPCC adenomas and carcinomas.

METHODS: The aim of this study was to investigate basic expression of caspase-8 and cFLIP in normal colorectal epithelium (n=20), colorectal adenomas (n=66) and colorectal carcinomas (n=44) using immunohistochemistry performed on both sporadic and Hereditary Non-Polyposis Colorectal Cancer (HNPCC or Lynch syndrome)-associated adenomas and carcinomas.

Expression of caspase-8 in colorectal adenomas and carcinomas was increased when compared to normal colon tissue (P=0.02).

Immunohistochemistry revealed an upregulation of cFLIP in colorectal carcinomas in comparison to normal epithelium and colorectal adenomas (P<0.001).

A large variation in the caspase-8/cFLIP ratio was observed between the individual adenomas and carcinomas.

CONCLUSION: Caspase-8 and cFLIP are upregulated during colorectal carcinogenesis.

Upregulation of caspase-8 and/or downregulation of cFLIP may be interesting approaches to maximize TRAIL sensitivity in colorectal neoplasms.

[MeSH-major] Adenoma / enzymology. CASP8 and FADD-Like Apoptosis Regulating Protein / metabolism. Caspase 8 / biosynthesis. Colorectal Neoplasms, Hereditary Nonpolyposis / enzymology

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(PMID = 17726263.001).

[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 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; EC 3.4.22.- / Caspase 8

[Other-IDs] NLM/ PMC4617989

   

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[Title] Effect of folic acid supplementation on genomic DNA methylation in patients with colorectal adenoma.

BACKGROUND AND AIMS: A low dietary folate intake can cause genomic DNA hypomethylation and may increase the risk of colorectal neoplasia.

The hypothesis that folic acid supplementation increases DNA methylation in leucocytes and colorectal mucosa was tested in 31 patients with histologically confirmed colorectal adenoma using a randomised, double blind, placebo controlled, parallel design.

[MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. DNA Methylation / drug effects. Dietary Supplements. Folic Acid / pharmacology

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[CommentIn] Gut. 2005 May;54(5):579-81 [15831897.001]

(PMID = 15831910.001).

[ISSN] 0017-5749

[Journal-full-title] Gut

[ISO-abbreviation] Gut

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial

[Publication-country] England

[Chemical-registry-number] 0 / DNA, Neoplasm; 0LVT1QZ0BA / Homocysteine; 935E97BOY8 / Folic Acid

[Other-IDs] NLM/ PMC1774481

   

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[Title] Aberrant expression of ether à go-go potassium channel in colorectal cancer patients and cell lines.

AIM: To study the expression of ether à go-go (Eag1) potassium channel in colorectal cancer and the relation-ship between their expression and clinico-pathological features.

METHODS: The expression levels of Eag1 protein were determined in 76 cancer tissues with paired non-cancerous matched tissues as well as 9 colorectal adenoma tissues by immunohistochemistry.

Eag1 mRNA expression was detected in 13 colorectal cancer tissues with paired non-cancerous matched tissues and 4 colorectal adenoma tissues as well as two colorectal cancer cell lines (LoVo and HT-29) by reverse transcription PCR.

RESULTS: The frequency of positive expression of Eag1 protein was 76.3% (58/76) and Eag1 mRNA was 76.9% (10/13) in colorectal cancer tissue.

Eag1 protein and mRNA were negative in normal colorectal tissue, and absolutely negative in colorectal adenomas except that one case was positively stained for Eag1 protein.

CONCLUSION: Eag1 protein and mRNA are aberrantly expressed in colorectal cancer and occasionally expressed in colorectal adenoma.

[MeSH-major] Adenoma / metabolism. Carcinoma / metabolism. Colorectal Neoplasms / metabolism. Ether-A-Go-Go Potassium Channels / metabolism. Gene Expression Regulation, Neoplastic

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(PMID = 17451210.001).

[ISSN] 1007-9327

[Journal-full-title] World journal of gastroenterology

[ISO-abbreviation] World J. Gastroenterol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Ether-A-Go-Go Potassium Channels; 0 / KCNH1 protein, human

[Other-IDs] NLM/ PMC4147004

   

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However, we show here that PROX1 promotes dysplasia in colonic adenomas and colorectal cancer progression.

PROX1 expression marks the transition from benign colon adenoma to carcinoma in situ, and its loss inhibits growth of human colorectal tumor xenografts and intestinal adenomas in Apc(min/+) mice, while its transgenic overexpression promotes colorectal tumorigenesis.

[MeSH-major] Adenoma / genetics. Colonic Neoplasms / genetics. Homeodomain Proteins / genetics. Tumor Suppressor Proteins / genetics

[MeSH-minor] Carcinoma in Situ / genetics. Cell Line, Tumor. Colorectal Neoplasms / genetics. Disease Progression. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Phenotype. beta Catenin / physiology

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(PMID = 18455124.001).

[ISSN] 1878-3686

[Journal-full-title] Cancer cell

[ISO-abbreviation] Cancer Cell

[Language] eng

[Grant] United Kingdom / Worldwide Cancer Research / / 09-0791; United Kingdom / Medical Research Council / / G0301154

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Tumor Suppressor Proteins; 0 / beta Catenin; 0 / prospero-related homeobox 1 protein

   

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[Title] Genetic variants of UGT1A6 influence risk of colorectal adenoma recurrence.

Functional polymorphisms of UGT1A6 (T181A and R184S) and CYP2C9 (R144C and I359L) have been reported to modify the protective effect of aspirin on colorectal adenoma risk.

We aimed to further investigate the effect of these genetic variants on the development of colorectal neoplasia.

EXPERIMENTAL DESIGN: We examined the relationship between UGT1A6 and CYP2C9 genotype and colorectal adenoma recurrence in 546 patients participating in a randomized placebo-controlled aspirin intervention trial.

RESULTS: Although colorectal adenoma recurrence was not significantly influenced by CYP2C9 genotype, carriers of variant UGT1A6 alleles were at significantly reduced risk of colorectal neoplasia recurrence [relative risk (RR), 0.68; 95% confidence interval (95% CI), 0.52-0.89].

CONCLUSIONS: These findings confirm that UGT1A6 variants influence colorectal carcinogenesis independent of aspirin intake and suggest that they may have clinical value in secondary prevention programs for patients diagnosed with colorectal adenoma.

[MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Genetic Predisposition to Disease. Glucuronosyltransferase / genetics. Neoplasm Recurrence, Local / genetics

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(PMID = 17085674.001).

[ISSN] 1078-0432

[Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research

[ISO-abbreviation] Clin. Cancer Res.

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; EC 2.4.1.- / UDP-glucuronosyltransferase, UGT1A6; EC 2.4.1.17 / Glucuronosyltransferase; R16CO5Y76E / Aspirin

   

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[Title] [Galectin-1 expression in human colorectal carcinoma and its clinical significance].

OBJECTIVE: To investigate the correlation between galectin-1 expression and the biological behaviors of human colorectal carcinoma.

METHODS: SP immunohistochemistry was used to detect the expression of galectin-1 in 158 paraffin-embedded specimens including 30 normal mucosa, 25 adenoma, 65 colorectal carcinoma and 38 metastatic tumor specimens.

Real-time RT-PCR was used to detect galectin-1 mRNA expression in 32 fresh specimens of colorectal carcinoma and normal mucosa.

RESULTS: The positive expression level of galectin-1 was significantly different between normal mucosa, adenoma, colorectal carcinomas and metastatic tumors, with positivity rate of 0, 8%, 66% and 86%, respectively (P<0.05).

Galectin-1 expression in moderately or well differentiated colorectal carcinomas was significantly lower than that in poorly differentiated ones (P=0.031), and its expression in invasive carcinomas was significantly higher than that in non-invasive carcinomas (P=0.000).

Galectin-1 expression in colorectal carcinomas was significantly related with lymph node metastasis (P=0.004).

In poorly differentiated colorectal carcinomas, the expression of galectin-1 mRNA was about 2.27 times that in moderately or well differentiated colorectal carcinomas (P=0.00); galectin-1 mRNA expression in invasive carcinoma was 1.98 times that in non-invasive carcinoma (P=0.002).

CONCLUSION: Galectin-1 can be involved in the development and progression of colorectal carcinoma, and may relate to the infiltration, differentiation and lymph node metastasis of colorectal carcinoma.

[MeSH-major] Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Galectin 1 / genetics. Galectin 1 / metabolism. Gene Expression Regulation, Neoplastic

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(PMID = 17884770.001).

[ISSN] 1673-4254

[Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University

[ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Galectin 1; 0 / RNA, Messenger

   

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[Title] The relation of magnesium and calcium intakes and a genetic polymorphism in the magnesium transporter to colorectal neoplasia risk.

BACKGROUND: Mean magnesium intake in the US population does not differ from that in East Asian populations with traditionally low risks of colorectal cancer and other chronic diseases, but the ratio of calcium to magnesium (Ca:Mg) intake is much higher in the US population.

OBJECTIVE: We aimed to test whether the association of colorectal polyps with intake of calcium, magnesium, or both and Thr1482Ile polymorphism in the TRPM7 gene is modified by the Ca:Mg intake.

DESIGN: Included in the study were a total of 688 adenoma cases, 210 hyperplastic polyp cases, and 1306 polyp-free controls from the Tennessee Colorectal Polyp Study.

RESULTS: We found that total magnesium consumption was linked to a significantly lower risk of colorectal adenoma, particularly in those subjects with a low Ca:Mg intake.

The subjects who carried >or=1 1482Ile allele and who consumed diets with a high Ca:Mg intake were at a higher risk of adenoma (odds ratio: 1.60; 95% CI: 1.12, 2.29) and hyperplastic polyps (odds ratio: 1.85; 95% CI: 1.09, 3.14) than were the subjects who did not carry the polymorphism.

CONCLUSION: These findings, if confirmed, may provide a new avenue for the personalized prevention of magnesium deficiency and, thus, colorectal cancer.

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(PMID = 17823441.001).

[ISSN] 0002-9165

[Journal-full-title] The American journal of clinical nutrition

[ISO-abbreviation] Am. J. Clin. Nutr.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / P50 CA 95103; United States / NCI NIH HHS / CA / R01 CA072784; United States / NCI NIH HHS / CA / R01 CA072784-05; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / R01 CA97386; United States / NCI NIH HHS / CA / CA072784-05

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Calcium, Dietary; 0 / TRPM Cation Channels; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / TRPM7 protein, human; I38ZP9992A / Magnesium

[Other-IDs] NLM/ NIHMS33891; NLM/ PMC2082111

   

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[Title] [Do metachronous colorectal adenomas show proximal shift?].

[Transliterated title] ¿Presentan un desplazamiento hacia segmentos más proximales los adenomas metacrónicos en el cáncer colorrectal?

OBJECTIVE: To study the possibility of shift toward more proximal sites in colorectal cancer (CRC) after resection of tumors and synchronous lesions.

The localization of metachronous adenomas was compared with that of synchronous lesions overall and by sex, tumoral size and the number of synchronous lesions.

The frequency of exclusively proximal localization in first-, second- and third-generation metachronous adenomas was compared with that of synchronous adenomas.

RESULTS: A total of 54.5% of patients with CRC had synchronous adenomas.

After a median follow-up of 48 months, with 2.74+/-1.47 colonoscopies/case, 42.4% developed metachronous adenomas, 16.8% second-generation adenomas and 7.3% third-generation lesions.

Proximal shift was found in metachronous adenomas in both sexes, independently of tumoral size and the number of initial lesions.

The frequency of exclusively proximal localization in adenomas was 21.2% in synchronous lesions, 39.5% in first-generation metachronous adenomas (p=0.0001; OR=2.46 [1.50-3.95]), 42.6% in second-generation metachronous adenomas (p=0.0008; OR=2.77 [1.44-5.31]) and 39.3% in third-generation metachronous lesions (p=0.0003; OR=2.41 [0.97-5.93]).

CONCLUSIONS: We found a high incidence of synchronous and metachronous adenomas.

Metachronous adenomas showed a proximal shift, independently of sex, tumoral size and the number of synchronous lesions.

This tendency was maintained in successive generations of metachronous adenomas, thus demonstrating the need to perform complete colonoscopies throughout the postoperative follow-up period.

[MeSH-major] Adenoma / pathology. Colon / pathology. Colorectal Neoplasms / pathology. Neoplasms, Second Primary / pathology

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[Copyright] Copyright 2009 Elsevier España, S.L. All rights reserved.

(PMID = 20374971.001).

[ISSN] 0210-5705

[Journal-full-title] Gastroenterología y hepatología

[ISO-abbreviation] Gastroenterol Hepatol

[Language] spa

[Publication-type] English Abstract; Journal Article; Multicenter Study

[Publication-country] Spain

   

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The aim of this study was to characterize patients with GI small bowel and/or colorectal cancers (CRCs) who have germline biallelic MMR mutations.

Among the 29 patients with CRCs, the mean age of first cancer diagnosis was 16.4 years (range: 5-28).

More than one-third of patients had multiple colorectal adenomas (>10 polyps).

Six individuals with biallelic MMR gene mutations have been reported with small bowel adenocarcinoma (mean age 20 years (range: 11-41)).

CONCLUSIONS: Biallelic MMR mutations are an underrecognized cause of small bowel and colonic cancers in children and young adults.

[MeSH-major] Alleles. Colorectal Neoplasms / genetics. DNA Mismatch Repair. Genetic Predisposition to Disease. Germ-Line Mutation. Intestinal Neoplasms / genetics

[MeSH-minor] Adolescent. Adult. Child. Child, Preschool. DNA Mutational Analysis. Databases, Factual. Humans. Intestine, Small. Microsatellite Instability. Phenotype. Registries

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(PMID = 20531397.001).

[ISSN] 1572-0241

[Journal-full-title] The American journal of gastroenterology

[ISO-abbreviation] Am. J. Gastroenterol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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Colorectal cancer is one of the commonest tumours in the Westernized world affecting mainly the elderly.

Effective screening permits discovery of colorectal cancer at an early highly treatable stage and allows for detection and removal of premalignant colorectal adenomas.

Screening methods that focus on cancer detection use fecal assays for the presence of blood or altered DNA, those for detection of adenomas (and early cancer) use endoscopic or computerised radiologic techniques.

Broad use of screening methods has lowered colorectal cancer development by about 50%.

Since 1996 the chemotherapeutic armamentarium for metastatic colorectal cancer has grown beyond 5-fluorouracil to include an oral 5-fluorouracil prodrug, capecitabine as well as irinotecan and oxaliplatin.

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(PMID = 19942166.001).

[ISSN] 1532-1916

[Journal-full-title] Best practice & research. Clinical gastroenterology

[ISO-abbreviation] Best Pract Res Clin Gastroenterol

[Language] ENG

[Grant] United States / NCATS NIH HHS / TR / UL1 TR000043; United States / NCRR NIH HHS / RR / UL1RR024143; United States / NCRR NIH HHS / RR / UL1 RR024143; United States / NCI NIH HHS / CA / U54CA100926; United States / NCI NIH HHS / CA / U54 CA100926

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review

[Publication-country] Netherlands

[Number-of-references] 163

[Other-IDs] NLM/ NIHMS160270; NLM/ PMC3742312

   

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Aberrant crypt foci (ACF) are putative precursors of colorectal adenomas and have been postulated as a potential biomarker for colorectal cancer.

Subjects enrolled in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial were recruited for a study of ACF.

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[Copyright] 2010 AACR.

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(PMID = 20570885.001).

[ISSN] 1940-6215

[Journal-full-title] Cancer prevention research (Philadelphia, Pa.)

[ISO-abbreviation] Cancer Prev Res (Phila)

[Language] eng

[Grant] United States / Intramural NIH HHS / / Z99 CA999999

[Publication-type] Journal Article

[Publication-country] United States

[Other-IDs] NLM/ NIHMS195702; NLM/ PMC2900400

   

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[Title] Serrated neoplasias and de novo carcinomas in ulcerative colitis: a histological study in colectomy specimens.

BACKGROUND AND AIM: Cancer in ulcerative colitis (UC) originates in dysplastic crypts, adenomatous growths (UCAG), and UC-associated adenomas (UCAD).

The aim of the present study was to compare the histological phenotypes between UCAG, UCAD, and sporadic colorectal adenomas in non-colitics (non-UCAD), as well as between UC-associated carcinomas (UCC) and carcinomas in non-colitic patients (non-UCC).

Six UCC (5.6%) were de novo carcinomas.

This is the first study reporting the occurrence of serrated and microtubular UCAG and of de novo carcinomas in UC.

[MeSH-major] Adenoma / pathology. Adenoma / surgery. Colectomy. Colitis, Ulcerative / pathology. Colitis, Ulcerative / surgery. Colonic Neoplasms / pathology. Colonic Neoplasms / surgery. Colorectal Neoplasms / pathology. Colorectal Neoplasms / surgery

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(PMID = 17559365.001).

[ISSN] 0815-9319

[Journal-full-title] Journal of gastroenterology and hepatology

[ISO-abbreviation] J. Gastroenterol. Hepatol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Australia

   

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[Title] Up-regulation of the peripheral benzodiazepine receptor during human colorectal carcinogenesis and tumor spread.

In Unio Internationale Contra Cancrum (UICC) III colorectal cancers, a high level of PBR overexpression correlates with poor prognosis.

However, little is known about the role of PBR in the development and progression of colorectal cancer.

This study addresses the up-regulation of PBR during colorectal carcinogenesis and tumor spread.

One hundred sixteen consecutive patients undergoing surgery for colorectal cancer with either regional (59 patients) or distant metastases (57 patients) were followed-up for 5 years or until death.

UICC stage III patients with colorectal primaries highly overexpressing PBR developed metastases significantly more often than patients with low PBR overexpression in their primary carcinoma.

In 54 of the 116 patients adenomas and/or metastases and/or recurrences were available to be studied for PBR up-regulation during colorectal carcinogenesis and tumor spread.

PBR was found to be overexpressed in 86% of early and late adenomas.

The extent of PBR protein overexpression was equivalent in colorectal adenomas and carcinomas but slightly increased in metastases.

These data suggest a functional role of PBR during colorectal carcinogenesis and tumor spread.

[MeSH-major] Adenoma / genetics. Adenoma / pathology. Carcinoma / genetics. Carcinoma / pathology. Cell Transformation, Neoplastic / genetics. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Neoplasm Metastasis. Receptors, GABA / biosynthesis

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[ErratumIn] Clin Cancer Res. 2005 Sep 1;11(17):6408

(PMID = 15755996.001).

[ISSN] 1078-0432

[Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research

[ISO-abbreviation] Clin. Cancer Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Receptors, GABA; 0 / TSPO protein, human

   

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[Title] Immunohistochemical expressions of Ki-67, cyclin D1, beta-catenin, cyclooxygenase-2, and epidermal growth factor receptor in human colorectal adenoma: a validation study of tissue microarrays.

OBJECTIVES: In this study, we evaluated the validity and reliability of using TMA to assess biomarkers in colorectal adenomas.

METHODS: Sixty-three consecutive patients with colorectal adenomas were recruited in this study.

Two TMA blocks were constructed using four punches from each adenoma (one periphery, one deep, and two middle zones).

RESULTS: Colorectal adenoma exhibited zonal, heterogeneous expression patterns for all five markers.

CONCLUSION: Our study indicates that TMA can be used to reliably assess the expression levels of Ki-67, cyclin D1, beta-catenin, cyclooxygenase-2, and epidermal growth factor receptor in colorectal adenoma tissues.

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(PMID = 16985035.001).

[ISSN] 1055-9965

[Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

[ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / P50 CA95103; United States / NCI NIH HHS / CA / R01 CA97386

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Validation Studies

[Publication-country] United States

[Chemical-registry-number] 0 / Ki-67 Antigen; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Receptor, Epidermal Growth Factor

   

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[Title] Genetic variation in base excision repair genes and the prevalence of advanced colorectal adenoma.

Base excision repair (BER) corrects DNA damage caused by oxidative stress and low folate intake, which are putative risk factors for colorectal neoplasia.

To examine the relationship between genetic variation in BER genes and colorectal adenoma risk, we conducted a case-control study of 767 cases of advanced colorectal adenoma and 773 controls from the baseline screening exam of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial.

Cases included participants diagnosed with advanced left-sided adenoma, and controls were subjects without evidence of a left-sided polyp by sigmoidoscopy, frequency-matched to cases on race and gender.

Twenty single nucleotide polymorphisms were genotyped in four BER genes (APEX1, PARP1, POLB, and XRCC1), and conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI) for the association with colorectal adenoma.

The APEX1 51H variant was associated with a borderline significant decreased risk of colorectal adenoma (OR, 0.66; 95% CI, 0.44-1.00), and the XRCC1 399Q variant was inversely associated with risk among Caucasians (OR, 0.80; 95% CI, 0.64-0.99).

Homozygotes at two PARP1 loci (A284A and IVS13+118G>A) were also associated with a decreased risk of colorectal adenoma compared with wild-type carriers (OR, 0.70; 95% CI, 0.49-0.98 for both), which was restricted to advanced adenomas displaying histologically aggressive characteristics (OR, 0.51; 95% CI, 0.33-0.78, P = 0.002 for PARP1 A284A).

This study suggests that polymorphisms in APEX1, XRCC1, and PARP1 may be associated with advanced colorectal adenoma.

[MeSH-major] Adenomyoma / epidemiology. Adenomyoma / genetics. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms / genetics. DNA Repair / genetics

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(PMID = 17283177.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Grant] United States / Intramural NIH HHS / /

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Intramural

[Publication-country] United States

   

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[Title] Serrated polyps of the large intestine: a morphologic and molecular review of an evolving concept.

Serrated polyps of the large intestine, including traditional hyperplastic polyps, traditional serrated adenomas, and more recently described sessile serrated adenomas, have gained increased recognition in recent years because of growing evidence that one of these lesions, the sessile serrated adenoma, might be the precursor lesion for some cases of microsatellite unstable colorectal carcinoma.

Nevertheless, there has been some reluctance to embrace the concept of sessile serrated adenoma, and numerous diagnostic challenges exist.

Haggitt Gastrointestinal Pathology Society Forum presented in Vancouver, Canada, March 6, 2004 as part of the annual meeting of the United States-Canadian Academy of Pathology, reviews the morphologic and molecular evidence for the concept of various polyps in the general category of serrated polyps of the large intestine, in particular the lesion known as the sessile serrated adenoma, and provides a conceptual framework for diagnosis of these lesions.

[MeSH-major] Colonic Polyps / pathology. Colorectal Neoplasms / pathology. Intestinal Polyps / pathology

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[CommentIn] Am J Clin Pathol. 2006 Jun;125(6):951; author reply 952-3 [16761354.001]

(PMID = 16191506.001).

[ISSN] 0002-9173

[Journal-full-title] American journal of clinical pathology

[ISO-abbreviation] Am. J. Clin. Pathol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 36

   

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[Title] Novel genetic variations of the p53R2 gene in patients with colorectal adenoma and controls.

METHODS: We screened the p53R2 gene coding regions and a regulatory region which contains a p53 binding sequence in 100 patients with colorectal adenoma and 100 control subjects using PCR, cold SSCP, and direct DNA sequencing.

Additionally, we determined the frequency of these p53R2 variants in a recently concluded case-control study of incident sporadic colorectal adenomas (163 cases and 210 controls).

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(PMID = 16127747.001).

[ISSN] 1007-9327

[Journal-full-title] World journal of gastroenterology

[ISO-abbreviation] World J. Gastroenterol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA066539; United States / NCI NIH HHS / CA / R03 CA092773

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 1.17.4.- / Ribonucleotide Reductases; EC 1.17.4.- / ribonucleotide reductase R2 subunit

[Other-IDs] NLM/ PMC4320390

   

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[Title] Comparative evaluation of immunochemical fecal occult blood tests for colorectal adenoma detection.

BACKGROUND: Different immunochemical fecal occult blood tests (FOBTs) have been proposed for noninvasive colorectal cancer screening.

Large-scale, colonoscopy-based screening studies that allow evaluation of these tests for the detection of precursor lesions are scarce.

OBJECTIVE: To determine and compare performance characteristics of 6 qualitative immunochemical FOBTs for identifying colorectal adenomas among adults who attended screening colonoscopy examinations.

PATIENTS: 1319 participants at average risk for colorectal neoplasia who were undergoing screening colonoscopy (mean age, 63 years; 50% men).

MEASUREMENTS: 6 different qualitative immunochemical FOBTs were done with stool samples collected before bowel preparation for colonoscopy.

RESULTS: Overall, 405 participants (31%) had an adenoma and 130 participants (10%) had an advanced adenoma.

For the 2 best-performing tests (immoCARE-C [CAREdiagnostica, Voerde, Germany] and FOB advanced [ulti med, Ahrensburg, Germany]), the sensitivity for detection of advanced adenomas was 25% (95% CI, 18% to 34%) and 27% (CI, 20% to 35%), respectively; specificity was 97% (CI, 95% to 98%) and 93% (CI, 91% to 95%); and the positive likelihood ratio was 3.5 (CI, 2.2 to 5.4) and 2.5 (CI, 1.9 to 3.5).

CONCLUSION: Qualitative immunochemical FOBTs could be an option for future colorectal cancer screening because they showed better performance characteristics for precursor lesions than guaiac-based FOBTs and are practical for mass screening.

However, given the large differences in diagnostic performance among tests, careful evaluation of the different test variants is important.

[MeSH-major] Adenoma / diagnosis. Colorectal Neoplasms / diagnosis. Immunohistochemistry / methods. Occult Blood

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[SummaryForPatientsIn] Ann Intern Med. 2009 Feb 3;150(3):I34 [19189901.001]

(PMID = 19189905.001).

[ISSN] 1539-3704

[Journal-full-title] Annals of internal medicine

[ISO-abbreviation] Ann. Intern. Med.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Indicators and Reagents; 9000-29-7 / Guaiac

   

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[Title] MTHFR (C677T and A1298C) polymorphisms and risk of sporadic distal colorectal adenoma in the UK Flexible Sigmoidoscopy Screening Trial (United Kingdom).

OBJECTIVE: The purpose of this study was to further evaluate the role of low activity MTHFR variants as well as to explore interactive effects between alcoholic drink consumption and MTHFR variants and risk of distal colorectal adenomatous polyps.

METHODS: We examined the relationship between MTHFR C677T and A1298C gene polymorphisms and risk of distal adenomas in one of the largest case control studies of 946 polyp-free controls and 894 cases, all participants of the UK Flexible Sigmoidoscopy Screening Trial (UKFSS).

RESULTS: Investigation of the effect of the MTHFR C677T polymorphism in this large UKFSS study revealed no overall association on adenoma risk (P>0.05).

However the MTHFR 1298C allele was linked, for the first time, to high risk adenomas, although in males only (odds ratio (OR) for A/C+C/C compared with A/A 1.55; 95% confidence interval (CI), 1.08-2.22; P=0.018).

CONCLUSIONS: In this, the largest study of these polymorphisms in relation to colorectal adenoma, there was no evidence for an interaction with alcohol in combination with the variant forms of MTHFR (P>0.05).

[MeSH-major] 5,10-Methylenetetrahydrofolate Reductase (FADH2) / genetics. Adenoma / genetics. Adenomatous Polyps / genetics. Colorectal Neoplasms / genetics. Polymorphism, Single Nucleotide / genetics

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(PMID = 16783607.001).

[ISSN] 0957-5243

[Journal-full-title] Cancer causes & control : CCC

[ISO-abbreviation] Cancer Causes Control

[Language] eng

[Grant] United Kingdom / Cancer Research UK / / A4994; United Kingdom / Medical Research Council / / G9615910

[Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] Netherlands

[Chemical-registry-number] EC 1.5.1.20 / 5,10-Methylenetetrahydrofolate Reductase (FADH2)

   

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[Title] Dietary patterns and colorectal adenoma and cancer risk: a review of the epidemiological evidence.

A number of studies exploring associations between individual dietary components and colorectal adenoma or cancer risk have yielded conflicting results.

Results from prospective cohort and population-based case-control studies examining associations between dietary patterns and colorectal cancer or adenoma risk were evaluated and described in this review.

Despite notable differences in population characteristics, study design, and methods used for characterizing dietary patterns across the different studies, two general dietary patterns were found to modestly predict colorectal adenoma and cancer risk.

A healthier pattern consisting of greater intakes of fruits and vegetables, and lower intakes of red and processed meat, appeared protective against colorectal adenoma and cancer incidence.

Continued research efforts are needed to evaluate the cumulative and interactive effects of numerous dietary exposures on colorectal cancer risk.

[MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Diet

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(PMID = 20432162.001).

[ISSN] 1532-7914

[Journal-full-title] Nutrition and cancer

[ISO-abbreviation] Nutr Cancer

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / Dietary Carbohydrates; 0 / Dietary Fats

[Number-of-references] 49

   

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[Title] Risk of colorectal neoplasia associated with the adenomatous polyposis coli E1317Q variant.

BACKGROUND: Reports of the risk of colorectal neoplasia associated with a variant of the adenomatous polyposis coli (APC E1317Q) gene are conflicting.

Subjects underwent colonoscopic evaluation (+/-biopsy and/or polypectomy) and had cancer history and colorectal neoplasia risk factors assessed.

When stratified by neoplasia type, adenoma risk was significantly elevated in carriers (OR 4.1, 95% CI 1.8-9.4) but colorectal cancer risk was not (OR 2.1, 95% CI 0.8-5.3).

After adjustment, the E1317Q variant remained a significant predictor of colorectal adenoma (OR 4.6, 95% CI 2.0-10.8).

CONCLUSIONS: The APC E1317Q variant is associated with colorectal neoplasia, particularly colorectal adenomas, but further studies are still needed.

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(PMID = 19474113.001).

[ISSN] 1569-8041

[Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology

[ISO-abbreviation] Ann. Oncol.

[Language] ENG

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein

   

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[Title] Promoter methylation status of the MGMT, hMLH1, and CDKN2A/p16 genes in non-neoplastic mucosa of patients with and without colorectal adenomas.

CpG island methylation has been observed in aberrant crypt foci (ACF) and adenomas in the colon, implicating it in the earliest aspects of colon cancer formation.

In addition, some investigators have identified an age-related increase in DNA methylation of the ESR1 locus in the colon mucosa, suggesting that DNA methylation may be a pre-neoplastic change that increases the risk of colon adenomas and colon cancer.

The promoter methylation patterns of these genes were examined in rectal biopsies (mucosa samples) of 97 colorectal adenoma cases and 94 healthy controls using methylation-specific PCR (MSP) assays.

The frequency of CDKN2A/p16 promoter methylation was very rare in normal colorectal tissue with a frequency of approximately 2%.

The methylation status of these genes in rectal mucosa biopsies detected by MSP assays may not distinguish between patients with and without adenomas in the colon.

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(PMID = 16820927.001).

[ISSN] 1021-335X

[Journal-full-title] Oncology reports

[ISO-abbreviation] Oncol. Rep.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / P50 CA95103; United States / NCI NIH HHS / CA / R01CA97386

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural

[Publication-country] Greece

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / MLH1 protein, human; 0 / Nuclear Proteins; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase

   

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More recently, it has become apparent that patients with acromegaly may also have an increased prevalence of colorectal adenomas and cancer.

This may be due to elevated IGF-I, which is implicated in the development of sporadic colorectal cancer, and environmental factors, such as the bile acid deoxycholic acid, the levels of which are also increased in acromegaly.

Large-scale epidemiological studies are required to clarify this issue.

[MeSH-major] Acromegaly / complications. Breast Neoplasms / etiology. Colorectal Neoplasms / etiology. Prostatic Neoplasms / etiology

[MeSH-minor] Adenoma / blood. Adenoma / epidemiology. Adenoma / etiology. Carcinoma / blood. Carcinoma / epidemiology. Carcinoma / etiology. Female. Human Growth Hormone / blood. Humans. Male

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(PMID = 17047386.001).

[ISSN] 0028-3835

[Journal-full-title] Neuroendocrinology

[ISO-abbreviation] Neuroendocrinology

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Switzerland

[Chemical-registry-number] 12629-01-5 / Human Growth Hormone

[Number-of-references] 56

   

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[Title] Cigarette smoking, N-acetyltransferase genes and the risk of advanced colorectal adenoma.

BACKGROUND: Cigarette use is associated with greater risk for colorectal adenoma, a colorectal cancer precursor.

Our interest is in the polymorphisms within the NAT1 and NAT2 genes that influence the tobacco-colorectal tumor relationship by impacting on the metabolic activation and detoxification of tobacco smoke-derived carcinogens.

METHODS: In the Prostate, Lung, Colorectal and Ovarian (PLCO) cancer screening trial, we compared NAT1 and NAT2 gene variant distributions for 772 cases with left-sided advanced adenoma and 777 gender and age-matched controls.

RESULTS: Risks for advanced colorectal adenoma were significantly increased among recent smokers (current smokers or those who quit less than 10 years ago) (odds ratio [OR] = 2.3, 95% confidence interval [CI]: 1.7-3.1) and among those who smoked more than 20 cigarettes per day (OR = 1.7, 95% CI: 1.3-2.2), compared with nonsmokers.

CONCLUSIONS: Our study indicated that NAT2 gene variants associated with a slow acetylator phenotype were more susceptible to the effects of tobacco smoking with respect to adenoma risk, providing leads for disease prevention.

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(PMID = 16981843.001).

[ISSN] 1462-2416

[Journal-full-title] Pharmacogenomics

[ISO-abbreviation] Pharmacogenomics

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA-34627; United States / NCI NIH HHS / CA / CA034627-21; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R01 CA034627; United States / NCI NIH HHS / CA / R01 CA034627-21

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural

[Publication-country] England

[Chemical-registry-number] 0 / Isoenzymes; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / N-acetyltransferase 1; EC 2.3.1.5 / NAT2 protein, human

   

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[Title] The colorectal malignant polyp: scoping a dilemma.

Colorectal adenomas containing invasive carcinoma represent the majority of early colorectal cancers.

[MeSH-major] Adenomatous Polyps / pathology. Colonic Polyps / pathology. Colorectal Neoplasms / pathology

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(PMID = 17113842.001).

[ISSN] 1590-8658

[Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver

[ISO-abbreviation] Dig Liver Dis

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Netherlands

[Number-of-references] 80

   

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[Title] Physician reminders to promote surveillance colonoscopy for colorectal adenomas: a randomized controlled trial.

BACKGROUND: Most colorectal cancers develop from adenomatous polyps.

PATIENTS: Seven hundred seventeen patients who had colorectal adenomas removed during 1995 through 2000 and no follow-up colonoscopy identified via automated review of electronic records through March, 2006.

MEASUREMENTS AND MAIN RESULTS: The use of colonoscopy and detection of new adenomas or cancer were assessed at 6 months by a blinded medical record review in all patients.

New adenomas or cancer were detected in 14 (3.9%) intervention patients and 6 (1.7%) control patients (P = 0.06), representing 42.4% and 37.5% of patients who underwent colonoscopy in each group, respectively.

CONCLUSIONS: Among patients with prior colorectal adenomas, physician reminders increased the use of surveillance colonoscopy, but better systems are needed to identify eligible patients (ClinicalTrials.gov ID number NCT00397969).

[MeSH-major] Adenomatous Polyps / diagnosis. Appointments and Schedules. Colonic Polyps / diagnosis. Colonoscopy / utilization. Colorectal Neoplasms / diagnosis. Reminder Systems

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

[Cites] Arch Intern Med. 2007 Mar 12;167(5):507-12 [17353500.001]

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(PMID = 18386103.001).

[ISSN] 1525-1497

[Journal-full-title] Journal of general internal medicine

[ISO-abbreviation] J Gen Intern Med

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00397969

[Grant] United States / NCI NIH HHS / CA / R21 CA112365; United States / NCI NIH HHS / CA / R21-CA112365

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural

[Publication-country] United States

[Other-IDs] NLM/ PMC2517870

   

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BACKGROUND AND OBJECTIVES: The diagnostic feasibility of optical coherence tomography (OCT) and laser-induced fluorescence (LIF) have been evaluated for human colorectal cancer.

This study applies these technologies to a murine model of colorectal adenoma.

One adenoma was histologically identified; OCT visualized mucosal thickening/abnormal mass development over the imaging timepoints.

CONCLUSIONS: These preliminary data indicate endoscopic OCT-LIF has the potential to identify colorectal adenomas in murine models.

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[Copyright] Copyright 2006 Wiley-Liss, Inc.

(PMID = 16596657.001).

[ISSN] 0196-8092

[Journal-full-title] Lasers in surgery and medicine

[ISO-abbreviation] Lasers Surg Med

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA109385; United States / NCI NIH HHS / CA / CA083148; United States / NCI NIH HHS / CA / CA095060; United States / NCI NIH HHS / CA / CA109385

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

   

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[Title] Serrated adenoma: a distinct form of non-polypoid colorectal neoplasia?

Until recently, 2 major forms of colorectal polyp were recognized: the adenoma and the hyperplastic polyp.

Adenomas were known to represent a precursor to colorectal cancer, whereas hyperplastic polyps were viewed as nonneoplastic, having no potential for progression to malignancy.

We now recognize, however, that the lesions diagnosed as hyperplastic polyps in the past represent a heterogeneous group of polyps, some of which truly are hyperplastic, and others that truly have a significant risk for transformation to colorectal cancer.

These polyps have a characteristic serrated architecture, and include not only hyperplastic polyps but also the recently recognized serrated adenomas.

Serrated adenomas occur in 2 forms: the traditional serrated adenoma, which is usually a polypoid lesion endoscopically, and the sessile serrated adenoma, a flat or slightly raised, usually right-sided lesion.

Serrated adenomas of both types show characteristic molecular alterations not commonly seen in traditional colorectal adenomas, and probably progress to colorectal cancer by means of a different pathway, the so-called serrated neoplasia pathway.

The morphologic features of serrated colorectal lesions, the molecular alterations that characterize them, and their role in colorectal cancer development are discussed.

[MeSH-major] Adenoma / diagnosis. Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis

[MeSH-minor] Apoptosis. Colonic Polyps / diagnosis. Colonic Polyps / genetics. Colonic Polyps / pathology. CpG Islands / genetics. DNA Methylation. Disease Progression. Humans. Microsatellite Instability. Mutation. Phenotype. Polymorphism, Genetic. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics. Receptor, EphB2 / genetics. Risk Assessment. ras Proteins / genetics

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[Copyright] Copyright 2010 Elsevier Inc. All rights reserved.

(PMID = 20656251.001).

[ISSN] 1558-1950

[Journal-full-title] Gastrointestinal endoscopy clinics of North America

[ISO-abbreviation] Gastrointest. Endosc. Clin. N. Am.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Receptor, EphB2; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / ras Proteins

   

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[Title] The effect of body weight reduction on the incidence of colorectal adenoma.

OBJECTIVES: Obesity is thought to be associated with colorectal cancer and adenoma.

We aimed to investigate the effect of body weight on the risk of colorectal adenoma both in cross-sectional and longitudinal analyses.

METHODS: This is a retrospective cohort study in a large-scale health appraisal institution in Japan.

The association with the prevalence of colorectal adenoma was evaluated according to the body mass index (BMI) at the initial examination.

The incidence of colorectal adenoma at the second colonoscopy was investigated according to the initial BMI and body weight changes during the year.

RESULTS: The prevalence of colorectal adenoma increased in relation to increases in the BMI: 15.4%, 20.6%, 22.7%, and 24.2%, respectively, in the first (BMI < 21.350), second (21.350 < or = BMI < 23.199), third (23.199 < or = BMI < 25.156), and fourth (25.156 < or = BMI) quartiles.

The incidence rates of colorectal adenoma after 1 yr also increased proportionally according to the initial BMI: Group Q1 (12.9%), Group Q2 (15.7%), Group Q3 (18.3%), and Group Q4 (19.0%).

CONCLUSIONS: Obesity was associated with the risk for colorectal adenoma, and body weight reduction was suggested to decrease this risk.

[MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Obesity / complications. Weight Loss

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(PMID = 18796100.001).

[ISSN] 1572-0241

[Journal-full-title] The American journal of gastroenterology

[ISO-abbreviation] Am. J. Gastroenterol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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They affect the management of inflammatory bowel disease, colorectal cancer and the chemoprevention of colorectal adenoma by influencing the metabolism of their respective substrates, azathioprine/6-mercaptopurine, 5-fluorouracil and sulindac.

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(PMID = 17133087.001).

[ISSN] 0267-1379

[Journal-full-title] Current opinion in gastroenterology

[ISO-abbreviation] Curr. Opin. Gastroenterol.

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / R01 DK052230; United States / NIDDK NIH HHS / DK / DK064399-05; United States / NCI NIH HHS / CA / R01 CA084197-09; United States / NIDDK NIH HHS / DK / R24 DK064399-05; United States / NCI NIH HHS / CA / CA084197-09; United States / NIDDK NIH HHS / DK / R01 DK052230-11; United States / NCI NIH HHS / CA / R01 CA084197; United States / NIDDK NIH HHS / DK / R24 DK064399; United States / NIDDK NIH HHS / DK / DK52230; United States / NIDDK NIH HHS / DK / DK052230-11; United States / NCI NIH HHS / CA / CA84197

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Number-of-references] 57

[Other-IDs] NLM/ NIHMS37179; NLM/ PMC2213557