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1. Menigatti M, Cattaneo E, Sabates-Bellver J, Ilinsky VV, Went P, Buffoli F, Marquez VE, Jiricny J, Marra G: The protein tyrosine phosphatase receptor type R gene is an early and frequent target of silencing in human colorectal tumorigenesis. Mol Cancer; 2009 Dec 16;8:124
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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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2. Pufulete M: Intake of dairy products and risk of colorectal neoplasia. Nutr Res Rev; 2008 Jun;21(1):56-67
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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3. Kaindl U, Eyberg I, Rohr-Udilova N, Heinzle C, Marian B: The dietary antioxidants resveratrol and quercetin protect cells from exogenous pro-oxidative damage. Food Chem Toxicol; 2008 Apr;46(4):1320-6
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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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4. Sarebø M, Skjelbred CF, Breistein R, Lothe IM, Hagen PC, Bock G, Hansteen IL, Kure EH: Association between cigarette smoking, APC mutations and the risk of developing sporadic colorectal adenomas and carcinomas. BMC Cancer; 2006 Mar 17;6:71
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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
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  • [Chemical-registry-number] 0 / DNA, Neoplasm
  • [Other-IDs] NLM/ PMC1475604
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5. Skjelbred CF, Saebø M, Hjartåker A, Grotmol T, Hansteen IL, Tveit KM, Hoff G, Kure EH: Meat, vegetables and genetic polymorphisms and the risk of colorectal carcinomas and adenomas. BMC Cancer; 2007 Dec 19;7:228
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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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6. Sharma S, Iwasaki M, Kunieda C, Cao X, Ishihara J, Hamada G, Miyajima NT, Tsugane S, Le Marchand L: 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. Int J Food Sci Nutr; 2009;60 Suppl 7:128-39
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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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7. Zhang W, Bauer M, Croner RS, Pelz JO, Lodygin D, Hermeking H, Stürzl M, Hohenberger W, Matzel KE: DNA stool test for colorectal cancer: hypermethylation of the secreted frizzled-related protein-1 gene. Dis Colon Rectum; 2007 Oct;50(10):1618-26; discussion 1626-7
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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


8. Lobach I, Carroll RJ, Spinka C, Gail MH, Chatterjee N: Haplotype-based regression analysis and inference of case-control studies with unphased genotypes and measurement errors in environmental exposures. Biometrics; 2008 Sep;64(3):673-84
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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]
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  • (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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9. Erdem L, Akbayir N, Yildirim S, Köksal HM, Yenice N, Gültekin OS, Sakiz D, Peker O: Predictive value of morphologic characteristics in rectosigmoid adenomatous polyps for the probability of synchronous polyps or cancer in the proximal colon. Turk J Gastroenterol; 2005 Dec;16(4):207-11
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  • BACKGROUND/AIMS: Sigmoidoscopy is performed more frequently than colonoscopy, especially for screening purposes and searching for colorectal neoplasm.
  • The necessity of colonoscopy in patients with an adenoma of<or=5 mm found on sigmoidoscopy is controversial.
  • The aim of this study was to investigate whether the size of rectosigmoid adenomas is associated with the risk of neoplasm in the proximal colon and to determine whether there is indication for total colonoscopy.
  • These adenomas were grouped as diminutive (<or=5 mm), small (6-10 mm) or large (>or=11 mm) polyps.
  • These groups were compared regarding the presence of proximal adenoma and advanced proximal neoplasia (>10 mm adenoma and/or villous histology and/or high grade dysplasia or cancer).
  • The polyps were diminutive (<or=5 mm) in 105, small (6-10 mm) in 46 and large (>or=11 mm) in 33 patients.
  • Forty-one of the patients (39%) with diminutive polyps, 20 of the patients (43%) with small polyps and 19 of the patients (57%) with large polyps had neoplasm in the proximal bowel.
  • The rate of advanced proximal neoplasm was found to be significantly higher in the group with large polyps in the rectosigmoid area than in the groups with small and diminutive polyps (p<0.05).
  • [MeSH-minor] Colonoscopy. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Male. Middle Aged. Prevalence. Retrospective Studies

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  • (PMID = 16547849.001).
  • [ISSN] 1300-4948
  • [Journal-full-title] The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology
  • [ISO-abbreviation] Turk J Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Turkey
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10. Oh K, Willett WC, Fuchs CS, Giovannucci E: Dietary marine n-3 fatty acids in relation to risk of distal colorectal adenoma in women. Cancer Epidemiol Biomarkers Prev; 2005 Apr;14(4):835-41
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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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11. Fracchia M, Galatola G, Sarotto I, Guraldo V, Perona M, Pera A, Risio M: Serum bile acids, programmed cell death and cell proliferation in the mucosa of patients with colorectal adenomas. Dig Liver Dis; 2005 Jul;37(7):509-14
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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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12. Heijink DM, Kleibeuker JH, Jalving M, Boersma-van Ek W, Koornstra JJ, Wesseling J, de Jong S: Independent induction of caspase-8 and cFLIP expression during colorectal carcinogenesis in sporadic and HNPCC adenomas and carcinomas. Cell Oncol; 2007;29(5):409-19
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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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13. Pufulete M, Al-Ghnaniem R, Khushal A, Appleby P, Harris N, Gout S, Emery PW, Sanders TA: Effect of folic acid supplementation on genomic DNA methylation in patients with colorectal adenoma. Gut; 2005 May;54(5):648-53
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  • [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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  • (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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14. Ding XW, Yan JJ, An P, Lü P, Luo HS: Aberrant expression of ether à go-go potassium channel in colorectal cancer patients and cell lines. World J Gastroenterol; 2007 Feb 28;13(8):1257-61
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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


15. Petrova TV, Nykänen A, Norrmén C, Ivanov KI, Andersson LC, Haglund C, Puolakkainen P, Wempe F, von Melchner H, Gradwohl G, Vanharanta S, Aaltonen LA, Saharinen J, Gentile M, Clarke A, Taipale J, Oliver G, Alitalo K: Transcription factor PROX1 induces colon cancer progression by promoting the transition from benign to highly dysplastic phenotype. Cancer Cell; 2008 May;13(5):407-19
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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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16. Hubner RA, Muir KR, Liu JF, Logan RF, Grainge M, Armitage N, Shepherd V, Popat S, Houlston RS, United Kingdom Colorectal Adenoma Prevention Consortium: Genetic variants of UGT1A6 influence risk of colorectal adenoma recurrence. Clin Cancer Res; 2006 Nov 1;12(21):6585-9
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  • [Title] Genetic variants of UGT1A6 influence risk of colorectal adenoma recurrence.
  • Functional polymorphisms of UGT1A6 (T181A and R184S) and CYP2C9 (R144C and I359L) have been reported to modify the protective effect of aspirin on colorectal adenoma risk.
  • We aimed to further investigate the effect of these genetic variants on the development of colorectal neoplasia.
  • EXPERIMENTAL DESIGN: We examined the relationship between UGT1A6 and CYP2C9 genotype and colorectal adenoma recurrence in 546 patients participating in a randomized placebo-controlled aspirin intervention trial.
  • RESULTS: Although colorectal adenoma recurrence was not significantly influenced by CYP2C9 genotype, carriers of variant UGT1A6 alleles were at significantly reduced risk of colorectal neoplasia recurrence [relative risk (RR), 0.68; 95% confidence interval (95% CI), 0.52-0.89].
  • CONCLUSIONS: These findings confirm that UGT1A6 variants influence colorectal carcinogenesis independent of aspirin intake and suggest that they may have clinical value in secondary prevention programs for patients diagnosed with colorectal adenoma.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Genetic Predisposition to Disease. Glucuronosyltransferase / genetics. Neoplasm Recurrence, Local / genetics

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  • (PMID = 17085674.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; EC 2.4.1.- / UDP-glucuronosyltransferase, UGT1A6; EC 2.4.1.17 / Glucuronosyltransferase; R16CO5Y76E / Aspirin
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17. Zhu XL, Liang L, Ding YQ: [Galectin-1 expression in human colorectal carcinoma and its clinical significance]. Nan Fang Yi Ke Da Xue Xue Bao; 2007 Sep;27(9):1331-4
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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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18. Dai Q, Shrubsole MJ, Ness RM, Schlundt D, Cai Q, Smalley WE, Li M, Shyr Y, Zheng W: The relation of magnesium and calcium intakes and a genetic polymorphism in the magnesium transporter to colorectal neoplasia risk. Am J Clin Nutr; 2007 Sep;86(3):743-51
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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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19. Borda Martín A, Martínez-Peñuela JM, Muñoz-Navas M, Borda Celaya F, Jiménez Pérez J, Carretero Ribón C: [Do metachronous colorectal adenomas show proximal shift?]. Gastroenterol Hepatol; 2010 Jun-Jul;33(6):419-24
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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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20. Durno CA, Holter S, Sherman PM, Gallinger S: The gastrointestinal phenotype of germline biallelic mismatch repair gene mutations. Am J Gastroenterol; 2010 Nov;105(11):2449-56
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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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21. Holt PR, Kozuch P, Mewar S: Colon cancer and the elderly: from screening to treatment in management of GI disease in the elderly. Best Pract Res Clin Gastroenterol; 2009;23(6):889-907
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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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22. Saito S, Hosoya Y, Togashi K, Kurashina K, Haruta H, Hyodo M, Koinuma K, Horie H, Yasuda Y, Nagai H: Prevalence of synchronous colorectal neoplasms detected by colonoscopy in patients with gastric cancer. Surg Today; 2008;38(1):20-5
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  • [Title] Prevalence of synchronous colorectal neoplasms detected by colonoscopy in patients with gastric cancer.
  • PURPOSE: Our purpose was to study the characteristics of colorectal neoplasms in patients with gastric cancer (GC).
  • We examined the prevalence, site, and histology of colorectal neoplasms, as well as the clinicopathological features and treatment of the patients who had synchronous colorectal cancers (CRC).
  • Synchronous colorectal adenoma and cancer were detected in 182 (39%) and 18 (4%) patients, respectively.
  • CONCLUSIONS: The possibility of synchronous colorectal neoplasms in GC patients cannot be disregarded in clinical practice; however, screening of the large bowel may not be necessary in GC patients younger than 50 years.
  • [MeSH-major] Colonoscopy / methods. Colorectal Neoplasms / epidemiology. Neoplasms, Multiple Primary / epidemiology. Stomach Neoplasms / epidemiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Japan / epidemiology. Male. Middle Aged. Neoplasm Staging / methods. Prevalence. Retrospective Studies. Risk Factors


23. Pinsky PF, Fleshman J, Mutch M, Rall C, Charabaty A, Seligson D, Dry S, Umar A, Schoen RE: One year recurrence of aberrant crypt foci. Cancer Prev Res (Phila); 2010 Jul;3(7):839-43
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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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24. Rubio CA: Serrated neoplasias and de novo carcinomas in ulcerative colitis: a histological study in colectomy specimens. J Gastroenterol Hepatol; 2007 Jul;22(7):1024-31
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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


25. Maaser K, Grabowski P, Oezdem Y, Krahn A, Heine B, Stein H, Buhr H, Zeitz M, Scherübl H: Up-regulation of the peripheral benzodiazepine receptor during human colorectal carcinogenesis and tumor spread. Clin Cancer Res; 2005 Mar 1;11(5):1751-6
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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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26. Günther U, Bojarski C, Buhr HJ, Zeitz M, Heller F: Capsule endoscopy in small-bowel surveillance of patients with hereditary polyposis syndromes. Int J Colorectal Dis; 2010 Nov;25(11):1377-82
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  • [Title] Capsule endoscopy in small-bowel surveillance of patients with hereditary polyposis syndromes.
  • PURPOSE: Familial adenomatous polyposis (FAP) and Peutz-Jeghers syndrome (PJS) are hereditary polyposis syndromes with a high risk for benign small-bowel polyps and cancer.
  • The aim of this study was to assess the prevalence of small-bowel polyps beyond the duodenum in patients with FAP and PJS and to examine the clinical value and the optimal interval of capsule endoscopy (CE) for the surveillance of small-bowel polyps in patients with FAP.
  • RESULTS: In 13 of the 15 (87%) FAP patients, small-bowel polyps were detected by CE ranging from estimated <5 mm to >10 mm in size.
  • Thereof, in four patients, medium-sized (5-10 mm) or large-sized (>10 mm) polyps were seen-all of them located in the proximal jejunum.
  • In three FAP patients with repeated CEs, the latest CE displayed medium- and large-sized polyps in the proximal jejunum, whereas previous CEs had detected only small-sized (<5 mm) polyps.
  • In three of the four PJS patients, large-sized small-bowel polyps were visualized by CE which could then be removed by double-balloon enteroscopy (DBE) or surgical resection.
  • CONCLUSION: CE is an effective and safe method for small-bowel surveillance in FAP and PJS.
  • [MeSH-major] Adenomatous Polyposis Coli / diagnosis. Capsule Endoscopy. Intestine, Small / pathology. Peutz-Jeghers Syndrome / diagnosis
  • [MeSH-minor] Adenoma / classification. Adenoma / diagnosis. Humans. Syndrome

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  • (PMID = 20544205.001).
  • [ISSN] 1432-1262
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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27. Su Y, Shrubsole MJ, Ness RM, Cai Q, Kataoka N, Washington K, Zheng W: 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. Cancer Epidemiol Biomarkers Prev; 2006 Sep;15(9):1719-26
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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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28. Berndt SI, Huang WY, Fallin MD, Helzlsouer KJ, Platz EA, Weissfeld JL, Church TR, Welch R, Chanock SJ, Hayes RB: Genetic variation in base excision repair genes and the prevalence of advanced colorectal adenoma. Cancer Res; 2007 Feb 1;67(3):1395-404
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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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29. Deng ZL, Xie DW, Bostick RM, Miao XJ, Gong YL, Zhang JH, Wargovich MJ: Novel genetic variations of the p53R2 gene in patients with colorectal adenoma and controls. World J Gastroenterol; 2005 Sep 7;11(33):5169-73
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  • [Title] Novel genetic variations of the p53R2 gene in patients with colorectal adenoma and controls.
  • METHODS: We screened the p53R2 gene coding regions and a regulatory region which contains a p53 binding sequence in 100 patients with colorectal adenoma and 100 control subjects using PCR, cold SSCP, and direct DNA sequencing.
  • Additionally, we determined the frequency of these p53R2 variants in a recently concluded case-control study of incident sporadic colorectal adenomas (163 cases and 210 controls).

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  • (PMID = 16127747.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA066539; United States / NCI NIH HHS / CA / R03 CA092773
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 1.17.4.- / Ribonucleotide Reductases; EC 1.17.4.- / ribonucleotide reductase R2 subunit
  • [Other-IDs] NLM/ PMC4320390
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30. Mitrou PN, Watson MA, Loktionov AS, Cardwell C, Gunter MJ, Atkin WS, Macklin CP, Cecil T, Bishop TD, Primrose J, Bingham SA: MTHFR (C677T and A1298C) polymorphisms and risk of sporadic distal colorectal adenoma in the UK Flexible Sigmoidoscopy Screening Trial (United Kingdom). Cancer Causes Control; 2006 Aug;17(6):793-801
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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31. Miller PE, Lesko SM, Muscat JE, Lazarus P, Hartman TJ: Dietary patterns and colorectal adenoma and cancer risk: a review of the epidemiological evidence. Nutr Cancer; 2010;62(4):413-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dietary patterns and colorectal adenoma and cancer risk: a review of the epidemiological evidence.
  • A number of studies exploring associations between individual dietary components and colorectal adenoma or cancer risk have yielded conflicting results.
  • Results from prospective cohort and population-based case-control studies examining associations between dietary patterns and colorectal cancer or adenoma risk were evaluated and described in this review.
  • Despite notable differences in population characteristics, study design, and methods used for characterizing dietary patterns across the different studies, two general dietary patterns were found to modestly predict colorectal adenoma and cancer risk.
  • A healthier pattern consisting of greater intakes of fruits and vegetables, and lower intakes of red and processed meat, appeared protective against colorectal adenoma and cancer incidence.
  • Continued research efforts are needed to evaluate the cumulative and interactive effects of numerous dietary exposures on colorectal cancer risk.
  • [MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Diet

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  • (PMID = 20432162.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dietary Carbohydrates; 0 / Dietary Fats
  • [Number-of-references] 49
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32. Hall MJ, Liberman E, Dulkart O, Galazan L, Sagiv E, Shmueli E, Kazanov D, Hallak A, Moshkowitz M, Figer A, Kraus S, Inbar M, Neugut AI, Arber N: Risk of colorectal neoplasia associated with the adenomatous polyposis coli E1317Q variant. Ann Oncol; 2009 Sep;20(9):1517-21
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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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33. Ye C, Shrubsole MJ, Cai Q, Ness R, Grady WM, Smalley W, Cai H, Washington K, Zheng W: Promoter methylation status of the MGMT, hMLH1, and CDKN2A/p16 genes in non-neoplastic mucosa of patients with and without colorectal adenomas. Oncol Rep; 2006 Aug;16(2):429-35
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  • [Title] Promoter methylation status of the MGMT, hMLH1, and CDKN2A/p16 genes in non-neoplastic mucosa of patients with and without colorectal adenomas.
  • CpG island methylation has been observed in aberrant crypt foci (ACF) and adenomas in the colon, implicating it in the earliest aspects of colon cancer formation.
  • In addition, some investigators have identified an age-related increase in DNA methylation of the ESR1 locus in the colon mucosa, suggesting that DNA methylation may be a pre-neoplastic change that increases the risk of colon adenomas and colon cancer.
  • 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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34. Jenkins PJ: Cancers associated with acromegaly. Neuroendocrinology; 2006;83(3-4):218-23
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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


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

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  • (PMID = 16981843.001).
  • [ISSN] 1462-2416
  • [Journal-full-title] Pharmacogenomics
  • [ISO-abbreviation] Pharmacogenomics
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-34627; United States / NCI NIH HHS / CA / CA034627-21; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R01 CA034627; United States / NCI NIH HHS / CA / R01 CA034627-21
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Isoenzymes; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / N-acetyltransferase 1; EC 2.3.1.5 / NAT2 protein, human
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36. Zou H, Harrington JJ, Sugumar A, Klatt KK, Smyrk TC, Ahlquist DA: Detection of colorectal disease by stool defensin assay: an exploratory study. Clin Gastroenterol Hepatol; 2007 Jul;5(7):865-8
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  • [Title] Detection of colorectal disease by stool defensin assay: an exploratory study.
  • BACKGROUND & AIMS: Alpha-defensins 1-3 (human neutrophil peptides [HNP]1-3), reported to be elevated in tumor tissue and serum of patients with colorectal cancer (CRC), have not been studied in stool.
  • HNP1-3 proteins in stools were quantified in blinded fashion from 30 normal subjects, 20 patients with CRC, 10 with a large colorectal adenoma, 10 with upper gastrointestinal cancer, and 10 with IBD.
  • Mean stool HPN1-3 levels were 17 ng/mL with normals, 125 ng/mL with CRC, 62 ng/mL with adenoma, 63 ng/mL with upper gastrointestinal cancer, and 231 ng/mL with IBD (P < .01 for each patient group vs normals).
  • At 90% specificity, sensitivity of stool defensins was 35% for CRC, 40% for adenoma, 40% for upper gastrointestinal cancers, and 80% for IBD.
  • CONCLUSIONS: Alpha-defensins 1-3 levels are nonspecifically elevated in stools from patients with colorectal neoplasia and likely originate from white blood cells.
  • Alpha-defensins 1-3 in stool might serve as markers of inflammatory bowel conditions.
  • [MeSH-major] Colonic Diseases / diagnosis. Feces / chemistry. Rectal Diseases / diagnosis. alpha-Defensins / analysis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers / analysis. Cells, Cultured. Diagnosis, Differential. Enzyme-Linked Immunosorbent Assay. Female. Gene Expression. Humans. Male. Middle Aged. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17531545.001).
  • [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
  • [Chemical-registry-number] 0 / Biomarkers; 0 / RNA, Messenger; 0 / alpha-Defensins; 0 / human neutrophil peptide 1; 0 / human neutrophil peptide 2; 0 / human neutrophil peptide 3
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37. Hassan C, Zullo A, Winn S, Eramo A, Tomao S, Rossini FP, Morini S: The colorectal malignant polyp: scoping a dilemma. Dig Liver Dis; 2007 Jan;39(1):92-100
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  • [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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38. Ayanian JZ, Sequist TD, Zaslavsky AM, Johannes RS: Physician reminders to promote surveillance colonoscopy for colorectal adenomas: a randomized controlled trial. J Gen Intern Med; 2008 Jun;23(6):762-7
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  • [Title] Physician reminders to promote surveillance colonoscopy for colorectal adenomas: a randomized controlled trial.
  • BACKGROUND: Most colorectal cancers develop from adenomatous polyps.
  • PATIENTS: Seven hundred seventeen patients who had colorectal adenomas removed during 1995 through 2000 and no follow-up colonoscopy identified via automated review of electronic records through March, 2006.
  • MEASUREMENTS AND MAIN RESULTS: The use of colonoscopy and detection of new adenomas or cancer were assessed at 6 months by a blinded medical record review in all patients.
  • New adenomas or cancer were detected in 14 (3.9%) intervention patients and 6 (1.7%) control patients (P = 0.06), representing 42.4% and 37.5% of patients who underwent colonoscopy in each group, respectively.
  • CONCLUSIONS: Among patients with prior colorectal adenomas, physician reminders increased the use of surveillance colonoscopy, but better systems are needed to identify eligible patients (ClinicalTrials.gov ID number NCT00397969).
  • [MeSH-major] Adenomatous Polyps / diagnosis. Appointments and Schedules. Colonic Polyps / diagnosis. Colonoscopy / utilization. Colorectal Neoplasms / diagnosis. Reminder Systems

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  • (PMID = 18386103.001).
  • [ISSN] 1525-1497
  • [Journal-full-title] Journal of general internal medicine
  • [ISO-abbreviation] J Gen Intern Med
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00397969
  • [Grant] United States / NCI NIH HHS / CA / R21 CA112365; United States / NCI NIH HHS / CA / R21-CA112365
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2517870
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39. Hariri LP, Tumlinson AR, Besselsen DG, Utzinger U, Gerner EW, Barton JK: Endoscopic optical coherence tomography and laser-induced fluorescence spectroscopy in a murine colon cancer model. Lasers Surg Med; 2006 Apr;38(4):305-13
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  • 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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40. Noffsinger AE, Hart J: Serrated adenoma: a distinct form of non-polypoid colorectal neoplasia? Gastrointest Endosc Clin N Am; 2010 Jul;20(3):543-63
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  • [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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41. Yamaji Y, Okamoto M, Yoshida H, Kawabe T, Wada R, Mitsushima T, Omata M: The effect of body weight reduction on the incidence of colorectal adenoma. Am J Gastroenterol; 2008 Aug;103(8):2061-7
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  • [Title] The effect of body weight reduction on the incidence of colorectal adenoma.
  • OBJECTIVES: Obesity is thought to be associated with colorectal cancer and adenoma.
  • We aimed to investigate the effect of body weight on the risk of colorectal adenoma both in cross-sectional and longitudinal analyses.
  • METHODS: This is a retrospective cohort study in a large-scale health appraisal institution in Japan.
  • The association with the prevalence of colorectal adenoma was evaluated according to the body mass index (BMI) at the initial examination.
  • The incidence of colorectal adenoma at the second colonoscopy was investigated according to the initial BMI and body weight changes during the year.
  • RESULTS: The prevalence of colorectal adenoma increased in relation to increases in the BMI: 15.4%, 20.6%, 22.7%, and 24.2%, respectively, in the first (BMI < 21.350), second (21.350 < or = BMI < 23.199), third (23.199 < or = BMI < 25.156), and fourth (25.156 < or = BMI) quartiles.
  • The incidence rates of colorectal adenoma after 1 yr also increased proportionally according to the initial BMI: Group Q1 (12.9%), Group Q2 (15.7%), Group Q3 (18.3%), and Group Q4 (19.0%).
  • CONCLUSIONS: Obesity was associated with the risk for colorectal adenoma, and body weight reduction was suggested to decrease this risk.
  • [MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Obesity / complications. Weight Loss

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

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

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  • (PMID = 17295810.001).
  • [ISSN] 1445-1433
  • [Journal-full-title] ANZ journal of surgery
  • [ISO-abbreviation] ANZ J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Number-of-references] 72
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44. Chlumská A, Boudová L, Zámecník M: Sessile serrated adenomas of the large bowel. Clinicopathologic and immunohistochemical study including comparison with common hyperplastic polyps and adenomas. Cesk Patol; 2006 Jul;42(3):133-8
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  • [Title] Sessile serrated adenomas of the large bowel. Clinicopathologic and immunohistochemical study including comparison with common hyperplastic polyps and adenomas.
  • Sessile serrated adenoma (SSA) is a newly characterized type of the large bowel adenoma.
  • It arises in hyperplastic polyp (HP) and represents a precursor lesion of colorectal carcinoma with microsatellite instability.
  • For comparison, we examined 10 conventional tubular adenomas and 10 common HPs with vesicular cells.
  • However, our study found positivity of MUC2 and MUC5A also in conventional adenomas.
  • SSAs have malignant potential comparable with conventional adenomas and for this reason they must be distinguished from HPs.
  • [MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology. Intestinal Polyps / pathology. Rectal Neoplasms / pathology

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  • (PMID = 16955561.001).
  • [ISSN] 1210-7875
  • [Journal-full-title] Československá patologie
  • [ISO-abbreviation] Cesk Patol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / Mucin 5AC; 0 / Mucin-2; 0 / Mucins
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45. Alberts DS, Martínez ME, Hess LM, Einspahr JG, Green SB, Bhattacharyya AK, Guillen J, Krutzsch M, Batta AK, Salen G, Fales L, Koonce K, Parish D, Clouser M, Roe D, Lance P, Phoenix and Tucson Gastroenterologist Networks: Phase III trial of ursodeoxycholic acid to prevent colorectal adenoma recurrence. J Natl Cancer Inst; 2005 Jun 1;97(11):846-53
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  • [Title] Phase III trial of ursodeoxycholic acid to prevent colorectal adenoma recurrence.
  • We conducted a phase III, double-blind placebo-controlled trial of UDCA to evaluate its ability to prevent colorectal adenoma recurrence.
  • METHODS: We randomly assigned 1285 individuals who had undergone removal of a colorectal adenoma within the past 6 months to daily treatment with UDCA (8-10 mg/kg of body weight; 661 participants) or with placebo (624 participants) for 3 years or until follow-up colonoscopy.
  • Recurrence rates (number of recurrent adenomas per unit time) were compared by use of a Huber-White variance estimator.
  • Proportions of participants with one or more recurrent adenomas were compared with a Pearson chi-square statistic; adjusted odds ratios (ORs) were obtained by logistic regression.
  • RESULTS: We observed a non-statistically significant 12% reduction in the adenoma recurrence rate associated with UDCA treatment, compared with placebo treatment.
  • However, UDCA treatment was associated with a statistically significant reduction (P = .03) in the recurrence of adenomas with high-grade dysplasia (adjusted OR = 0.61, 95% confidence interval = 0.39 to 0.96).
  • We observed no statistically significant differences between UDCA and placebo groups in recurrence with regard to adenoma size, villous histology, or location.
  • CONCLUSIONS: UDCA treatment was associated with a non-statistically significant reduction in total colorectal adenoma recurrence but with a statistically significant 39% reduction in recurrence of adenomas with high-grade dysplasia.
  • Because severely dysplastic lesions have a high risk of progression to invasive colorectal carcinoma, this finding indicates that future chemoprevention trials of UDCA in individuals with such lesions should be considered.
  • [MeSH-major] Adenoma / prevention & control. Antineoplastic Agents / therapeutic use. Colorectal Neoplasms / prevention & control. Neoplasm Recurrence, Local / prevention & control. Ursodeoxycholic Acid / therapeutic use

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  • (PMID = 15928305.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-23074; United States / NCI NIH HHS / CA / P01-CA-41108
  • [Publication-type] Clinical Trial; Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 724L30Y2QR / Ursodeoxycholic Acid
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46. Wang JY, Wang YH, Jao SW, Lu CY, Kuo CH, Hu HM, Hsieh JS, Chong IW, Cheng TL, Lin SR: Molecular mechanisms underlying the tumorigenesis of colorectal adenomas: correlation to activated K-ras oncogene. Oncol Rep; 2006 Dec;16(6):1245-52
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  • [Title] Molecular mechanisms underlying the tumorigenesis of colorectal adenomas: correlation to activated K-ras oncogene.
  • Mutations of K-ras gene have been demonstrated in 40-50% of colorectal cancer and large adenoma (>1 cm).
  • This study was intended to clarify the correlation between the existence of K-ras oncogene and the pathological features of colorectal adenomas using our recently developed membrane arrays.
  • Moreover, the downstream genes regulated by K-ras oncogene were explored to serve as potential biomarkers in the early diagnosis and risk assessment of patients with colorectal adenoma.
  • Specimens were collected from 70 patients with colorectal adenoma.
  • Furthermore, activated K-ras oncogene was identified in 18 of 70 (25.7%) adenoma by membrane arrays.
  • The analysis of the correlation between the experimental data and pathological characteristics of adenoma showed that activated K-ras oncogenes were significantly associated with the size, number and histology of adenomas (all P<0.001).
  • Finally, we found the downstream genes activated by K-ras oncogene, including B-cell CLL/lymphoma 2 (BCL2), Homo sapiens H2A histone family, member Z (H2AFZ), Homo sapiens RAP1B, member of RAS oncogene family (RAP1B), Homo sapiens T-box 19 (TBX19), Homo sapiens E2F transcription factor 4, p107/p130-binding (E2F4) and matrix metallopeptidase 1 (MMP1), of which were overexpressed in most of all examined adenomas.
  • Therefore, we propose that activated K-ras oncogene in colorectal adenomas may play an important role in the subsequent colorectal carcinogenesis through a group of K-ras-related molecular targets.
  • [MeSH-major] Adenoma / genetics. Adenoma / pathology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Genes, ras

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

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

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  • (PMID = 17111255.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Triglycerides
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49. Goodlad RA, Ryan AJ, Wedge SR, Pyrah IT, Alferez D, Poulsom R, Smith NR, Mandir N, Watkins AJ, Wilkinson RW: Inhibiting vascular endothelial growth factor receptor-2 signaling reduces tumor burden in the ApcMin/+ mouse model of early intestinal cancer. Carcinogenesis; 2006 Oct;27(10):2133-9
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  • We used AZD2171, an oral, highly potent and selective vascular endothelial growth factor (VEGF) signaling inhibitor, to investigate the role of VEGF receptor-2 (VEGFR-2) signaling in adenoma development and growth in Apc(Min/+) mice.
  • In the early-intervention study, AZD2171 reduced the number of macroscopic polyps in the small bowel and colon.
  • Macropolyp diameter was lower in the small bowel, but remained unchanged in the colon.
  • In animals receiving AZD2171, microscopic evaluation of the small intestine showed a significant reduction in the number of larger lesions.
  • In the late-intervention study, AZD2171 treatment reduced macropolyp diameter (but not number) in the small intestine.
  • Microscopic analysis revealed that AZD2171 significantly reduced the number of larger micropolyps in the small bowel, with no large micropolyps present in the colon.
  • AZD2171 treatment had no effect on microvessel density or localization of beta-catenin staining in adenomas or non-tumor intestinal tissue, but significantly reduced the number of cells expressing VEGFR-2 mRNA.
  • In conclusion, the effects of AZD2171 in the small intestine of Apc(Min/+) mice are consistent with an antiangiogenic mechanism of action, limiting growth of adenomas to < or =1 mm.
  • These data also suggest that an early step in adenoma development may depend on VEGFR-2 signaling.
  • Together, these results indicate that VEGFR-2 signaling may play key roles in the development and progression of intestinal adenomas.
  • [MeSH-major] Adenoma / prevention & control. Genes, APC / physiology. Intestinal Neoplasms / prevention & control. Intestinal Polyps / drug therapy. Quinazolines / therapeutic use. Signal Transduction / drug effects. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors

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  • (PMID = 16782971.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Quinazolines; 0 / RNA, Messenger; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; NQU9IPY4K9 / cediranib
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50. Caswell S, Anderson AS, Steele RJ: Diet and physical activity in patients with colorectal adenomas: directions for intervention programmes. J Hum Nutr Diet; 2008 Oct;21(5):494-501
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  • [Title] Diet and physical activity in patients with colorectal adenomas: directions for intervention programmes.
  • The aim of the current exploratory research was to identify diet and activity habits in adults diagnosed with colorectal adenomas on screening colonoscopy in order to inform the development of an intervention study in this patient group.
  • [MeSH-major] Adenoma / prevention & control. Colorectal Neoplasms / prevention & control. Diet. Exercise

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

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

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  • (PMID = 20348947.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A5301; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BAD protein, human; 0 / BCL2L11 protein, human; 0 / Bcl-2-Like Protein 11; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / bcl-Associated Death Protein; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.25.1 / Proteasome Endopeptidase Complex; K7Q1JQR04M / Dinoprostone
  • [Other-IDs] NLM/ PMC2883743; NLM/ UKMS28872
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53. Neri E, Faggioni L, Cini L, Bartolozzi C: Colonic polyps: inheritance, susceptibility, risk evaluation, and diagnostic management. Cancer Manag Res; 2010;3:17-24
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  • Colorectal cancer (CRC) is the third-ranked neoplasm in order of incidence and mortality, worldwide, and the second cause of cancer death in industrialized countries.
  • Up to 25% of patients with CRC have a family history for CRC, and a fraction of these patients are affected by hereditary syndromes, such as familial adenomatous polyposis, Gardner or Turcot syndromes, or hereditary nonpolyposis colorectal cancer.
  • The onset of CRC is triggered by a well-defined combination of genetic alterations, which form the bases of the adenoma-carcinoma sequence hypothesis and justify the set-up of CRC screening techniques.
  • Moreover, especially with the advent and widespread availability of modern multidetector CT scanners, excellent quality 2D and 3D reconstructions of the large bowel can be obtained routinely with a relatively low radiation dose.

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  • (PMID = 21407996.001).
  • [ISSN] 1179-1322
  • [Journal-full-title] Cancer management and research
  • [ISO-abbreviation] Cancer Manag Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3048090
  • [Keywords] NOTNLM ; colonic polyps / colonoscopy / colorectal cancer / computed tomography colonography / double contrast barium enema
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54. Trecca A, Gaj F, Di Lorenzo GP, Ricciardi MR, Silano M, Bella A, Sperone M: Improved detection of colorectal neoplasms with selective use of chromoendoscopy in 2005 consecutive patients. Tech Coloproctol; 2006 Dec;10(4):339-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improved detection of colorectal neoplasms with selective use of chromoendoscopy in 2005 consecutive patients.
  • BACKGROUND: Colorectal cancer mortality is decreased by endoscopic polypectomy, but conventional colonoscopy may be inadequate for detecting subtle colonic lesions.
  • Patients with a history of colorectal polyps, inflammatory bowel disease, colorectal surgery or coagulopathy and those with poor bowel preparation were excluded from this analysis.
  • Overall, 56 large, ulcerated, advanced cancers and 696 non-advanced neoplasms were found.
  • [MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology. Colonoscopy / methods. Coloring Agents. Indigo Carmine

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  • [ErratumIn] Tech Coloproctol. 2009 Mar;13(1):103
  • (PMID = 17115312.001).
  • [ISSN] 1123-6337
  • [Journal-full-title] Techniques in coloproctology
  • [ISO-abbreviation] Tech Coloproctol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Coloring Agents; D3741U8K7L / Indigo Carmine
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55. Hsu CH, Taylor JM, Long Q, Alberts DS: Analysis of colorectal adenoma recurrence data subject to informative censoring. Cancer Epidemiol Biomarkers Prev; 2009 Mar;18(3):712-7
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  • [Title] Analysis of colorectal adenoma recurrence data subject to informative censoring.
  • The treatment effect of a colorectal polyp prevention trial is often evaluated from the colorectal adenoma recurrence status at the end of the trial.

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  • [Cites] Br J Surg. 2002 Jul;89(7):845-60 [12081733.001]
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  • (PMID = 19240239.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA023074; United States / NCI NIH HHS / CA / P30 CA023074-30; United States / NCI NIH HHS / CA / CA041108-22; United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / CA041108-21; United States / NCI NIH HHS / CA / P30 CA023074-28; None / None / / P30 CA023074-30; United States / NCI NIH HHS / CA / P01 CA041108; United States / NCI NIH HHS / CA / CA23074; United States / NCI NIH HHS / CA / P01 CA041108-21; United States / NCI NIH HHS / CA / P01 CA041108-22; United States / NCI NIH HHS / CA / CA41108
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cholagogues and Choleretics; 724L30Y2QR / Ursodeoxycholic Acid
  • [Other-IDs] NLM/ NIHMS104698; NLM/ PMC2668929
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56. Iarŭmov N, Toshev S, Petrova D, Angelov K, Gribnev P, Sokolov M: [Genetic counseling, surgical prophylaxis and treatment for familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer]. Khirurgiia (Sofiia); 2007;(3):46-53
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  • [Title] [Genetic counseling, surgical prophylaxis and treatment for familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer].
  • FAP is an autosomal dominant disorder characterized by the appearance of thousands of adenomatous polyps.
  • Surgical prophylaxis in FAP consists of resection of the entire large bowel, to prevent malignant transformation.
  • Hereditary Nonpolyposis Colorectal Cancer(HNPCC), like FAP, is an autosomal dominant disorder.
  • In contrast to FAP, HNPCC is associated with an unusually high frequency of cancers in the proximal large bowel.
  • If an adenoma or adenocarcinoma of the colon is identified, total abdominal colectomy with an ileorectal anastomosis is recommended.
  • [MeSH-major] Adenomatous Polyposis Coli. Colorectal Neoplasms, Hereditary Nonpolyposis. Genetic Counseling. Intestine, Large / surgery


57. Bertagnolli MM: Cox-2 and cancer chemoprevention: picking up the pieces. Recent Results Cancer Res; 2007;174:73-8
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  • The recent reports of cardiovascular adverse events in patients treated with selective Cox-2 inhibitors for colorectal adenoma prevention remind us that all therapies carry risks as well as benefits.
  • This article will discuss the biologic rationale for using selective Cox-2 inhibitors in cancer chemoprevention, and outline new avenues of research necessary to allow their successful use in patients at risk for colorectal cancer.

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

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  • [CommentIn] Am J Gastroenterol. 2010 Jul;105(7):1677 [20606672.001]
  • (PMID = 19755965.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipids
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59. Bresalier RS: Chemoprevention of colorectal cancer: why all the confusion? Curr Opin Gastroenterol; 2008 Jan;24(1):48-50
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  • [Title] Chemoprevention of colorectal cancer: why all the confusion?
  • PURPOSE OF REVIEW: Chemoprevention provides an opportunity to complement screening for the prevention of colorectal neoplasia.
  • RECENT FINDINGS: A recent prospective randomized trial demonstrates that folic acid supplementation in patients with a previous history of colorectal adenomas does not reduce future colorectal adenoma risk, and may possibly increase the risk of colorectal neoplasia.
  • [MeSH-major] Colorectal Neoplasms / prevention & control. Diet. Folic Acid / pharmacology

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

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

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  • (PMID = 19064714.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ PMC2664982
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62. Arslan N, Dehdashti F, Siegel BA: FDG uptake in colonic villous adenomas. Ann Nucl Med; 2005 Jun;19(4):331-4
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  • [Title] FDG uptake in colonic villous adenomas.
  • Colonic adenomas constitute 70-80% of all colorectal polyps, and their clinical significance relates primarily to their relationship with colorectal cancer.
  • The malignant potential of the polyps detected by FDG-PET is unknown, as not all the colonic lesions identified by FDG-PET represent colorectal malignancies.
  • The purpose of this study was to investigate the rate of FDG-PET positivity within colonic villous adenomas.
  • A pathology database search was performed to identify all patients diagnosed with colonic villous adenoma between June 1, 1996 and December 1, 2000.
  • Patients with a pathologic diagnosis of colonic villous adenoma and who also had a FDG-PET study up to 1 month before colonoscopy were included in this study.
  • Of more than 4,000 patients, six patients were diagnosed with colonic adenoma on subsequent colonoscopy following FDG-PET study.
  • Based on the pathological findings, these 6 patients had a total of 2 villous and 9 tubulovillous adenomas.
  • Five of the 6 patients showed foci of increased FDG uptake in the region of the colon that corresponded to the villous adenoma(s) detected on colonoscopy, which accounted for a true-positive rate of 83.3% (5/6 subjects).
  • Focal lesions in the colon seen on FDG-PET examinations need to be investigated further, even though some of these will prove to be villous adenomas rather than colorectal carcinomas.
  • [MeSH-major] Adenoma, Villous / radionuclide imaging. Colorectal Neoplasms / radionuclide imaging. Fluorodeoxyglucose F18 / pharmacokinetics. Positron-Emission Tomography / methods

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

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

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

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

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  • [CommentOn] Cancer Prev Res (Phila). 2010 May;3(5):588-96 [20403998.001]
  • [CommentOn] Cancer Prev Res (Phila). 2010 May;3(5):597-603 [20403997.001]
  • (PMID = 20403999.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] eng
  • [Publication-type] Comment; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticholesteremic Agents; 0 / Antineoplastic Agents; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • [Number-of-references] 27
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67. Nuzzo V, Tauchmanová L, Falchetti A, Faggiano A, Marini F, Piantadosi S, Brandi ML, Leopaldi L, Colao A: MEN1 family with a novel frameshift mutation. J Endocrinol Invest; 2006 May;29(5):450-6
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  • He reported a previous intestinal resection for bowel occlusion with a histological diagnosis of unspecified mesenchymal neoplasia.
  • He had also undergone a left adrenalectomy for a large nonfunctioning adrenal adenoma.

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  • [Cites] Surg Oncol. 2002 Nov;11(3):143-50 [12356510.001]
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  • (PMID = 16794369.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
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68. Kloor M, Michel S, Buckowitz B, Rüschoff J, Büttner R, Holinski-Feder E, Dippold W, Wagner R, Tariverdian M, Benner A, Schwitalle Y, Kuchenbuch B, von Knebel Doeberitz M: Beta2-microglobulin mutations in microsatellite unstable colorectal tumors. Int J Cancer; 2007 Jul 15;121(2):454-8
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  • [Title] Beta2-microglobulin mutations in microsatellite unstable colorectal tumors.
  • MSI-H cancers may develop either sporadically or in the context of the hereditary nonpolyposis colorectal cancer (HNPCC) syndrome that is caused by germline mutations of MMR genes.
  • In colorectal cancer (CRC), MSI-H is characterized by a dense lymphocytic infiltration, reflecting a high immunogenicity of these cancers.
  • To examine the implications of beta2m mutations during MSI-H colorectal tumor development, we analyzed the prevalence of beta2m mutations in MSI-H colorectal adenomas (n=38) and carcinomas (n=104) of different stages.
  • Mutations were observed in 6/38 (15.8%) MSI-H adenomas and 29/104 (27.9%) MSI-H CRCs.
  • The high frequency of beta2m mutations in HNPCC-associated MSI-H CRCs is in line with the hypothesis that immunoselection may be particularly pronounced in HNPCC patients with inherited predisposition to develop MSI-H cancers. beta2m mutations were positively related to stage in tumors without distant metastases (UICC I-III), suggesting that loss of beta2m expression may promote local progression of colorectal MSI-H tumors.
  • [MeSH-major] Colorectal Neoplasms / pathology. Microsatellite Repeats / genetics. Mutation. beta 2-Microglobulin / genetics

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

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

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

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

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

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

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  • (PMID = 17373735.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; 0 / fragile histidine triad protein; EC 3.6.- / Acid Anhydride Hydrolases
  • [Other-IDs] NLM/ PMC4146863
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75. Sun Y, Tian H, Xiao FM, Xie XY, Song YG: [PI3K p85alpha expression and its role in the progression of colorectal cancer]. Nan Fang Yi Ke Da Xue Xue Bao; 2009 Mar;29(3):416-8
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  • [Title] [PI3K p85alpha expression and its role in the progression of colorectal cancer].
  • OBJECTIVE: To investigate the expression of PI3K p85alpha in normal colorectal tissue, colorectal adenoma and primary colorectal carcinoma and explore its significance in the progression of colorectal cancer.
  • METHODS: The expression of PI3K p85alpha was detected in 116 normal colorectal tissue, colorectal adenoma and primary colorectal carcinoma specimens using immunohistochemical staining, and the relationship between the expression of PI3K p85alpha protein and the clinicopathological factors was analyzed.
  • RESULTS: The positivity rates of the expression of PI3K p85alpha protein increased gradually in the progression of colorectal cancer and showed significant differences between the tissues (P<0.05).
  • A significant difference was also noted in the positivity rates of the PI3K p85alpha expression in colorectal carcinoma tissues at different Dukes' stages (P<0.05).
  • CONCLUSIONS: Abnormal PI3K p85alpha expression occurs in the progression of colorectal cancer in close relation to the clinical stage, and the PI3K/AKT pathway plays an important role in the progression of colorectal cancer.
  • [MeSH-major] Carcinoma / enzymology. Colorectal Neoplasms / enzymology. Disease Progression. Phosphatidylinositol 3-Kinases / metabolism
  • [MeSH-minor] Adenoma / enzymology. Adenoma / pathology. Adult. Aged. Humans. Immunohistochemistry. Middle Aged. Signal Transduction. Young Adult

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

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

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  • (PMID = 18559549.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 BC010025-12
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Flavonoids
  • [Other-IDs] NLM/ NIHMS56510; NLM/ PMC2517243
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78. Wu H, Dai Q, Shrubsole MJ, Ness RM, Schlundt D, Smalley WE, Chen H, Li M, Shyr Y, Zheng W: Fruit and vegetable intakes are associated with lower risk of colorectal adenomas. J Nutr; 2009 Feb;139(2):340-4
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  • [Title] Fruit and vegetable intakes are associated with lower risk of colorectal adenomas.
  • Participants were part of the Tennessee Colorectal Polyp Study.
  • Cases had at least one adenoma and controls were polyp free.
  • Associations between dietary intakes and adenoma risk were evaluated using unconditional logistic regression with restricted cubic function spline.
  • In multivariate analyses of 764 cases and 1517 controls, increased intakes of total fruits, berries, fruit juice, and green leafy vegetables were associated with reduced adenoma risk.
  • This study provides additional evidence that high total fruit intake and certain fruit and vegetable intakes may be associated with a reduced risk of colorectal adenomas.

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  • (PMID = 19091801.001).
  • [ISSN] 1541-6100
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / CA095103-010005; United States / NCI NIH HHS / CA / R01 CA097386-01; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / R01CA97386; United States / NCI NIH HHS / CA / P50CA95103; United States / NCI NIH HHS / CA / CA097386-01; United States / NCI NIH HHS / CA / P50 CA095103-010005
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS92794; NLM/ PMC2646202
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79. Hata K, Tanaka T, Kohno H, Suzuki R, Qiang SH, Yamada Y, Oyama T, Kuno T, Hirose Y, Hara A, Mori H: beta-Catenin-accumulated crypts in the colonic mucosa of juvenile ApcMin/+ mice. Cancer Lett; 2006 Jul 28;239(1):123-8
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  • Although Apc(Min/+) mice are widely used for an animal model of human familial adenomatous polyposis (FAP), a majority of intestinal polyps locate in the small intestine.
  • We recently reported that numerous beta-catenin-accumulated crypts (BCAC), which are reliable precursor lesions for colonic adenocarcinoma, develop in the large bowel of aged Apc(Min/+) mice.
  • In this study, we determined the presence and location of BCAC in the large intestine of juvenile Apc(Min/+) mice (3 and 5 weeks of age).
  • Our results may indicate need of further investigation of the colorectal mucosa of Apc(Min/+) mice for examining colorectal carcinogenesis using Apc(Min/+) mice.
  • [MeSH-major] Adenoma / metabolism. Adenomatous Polyposis Coli / metabolism. Colon / metabolism. Colonic Neoplasms / metabolism. Intestinal Mucosa / metabolism. beta Catenin / metabolism

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  • (PMID = 16168560.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / beta Catenin
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80. Skjelbred CF, Saebø M, Wallin H, Nexø BA, Hagen PC, Lothe IM, Aase S, Johnson E, Hansteen IL, Vogel U, Kure EH: Polymorphisms of the XRCC1, XRCC3 and XPD genes and risk of colorectal adenoma and carcinoma, in a Norwegian cohort: a case control study. BMC Cancer; 2006 Mar 16;6:67
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  • [Title] Polymorphisms of the XRCC1, XRCC3 and XPD genes and risk of colorectal adenoma and carcinoma, in a Norwegian cohort: a case control study.
  • For colorectal cancer the importance of mutations in mismatch repair genes has been extensively documented.
  • Less is known about other DNA repair pathways in colorectal carcinogenesis.
  • METHODS: We used a case-control study design (157 carcinomas, 983 adenomas and 399 controls) to test the association between five polymorphisms in these DNA repair genes (XRCC1 Arg194Trp, Arg280His, Arg399Gln, XRCC3 Thr241Met and XPD Lys751Gln), and risk of colorectal adenomas and carcinomas in a Norwegian cohort.
  • RESULTS: The XRCC1 280His allele was associated with an increased risk of adenomas (OR 2.30, 95% CI 1.19-4.46).
  • The XRCC1 399Gln allele was associated with a reduction of risk of high-risk adenomas (OR 0.62, 95% CI 0.41-0.96).
  • Carriers of the variant XPD 751Gln allele had an increased risk of low-risk adenomas (OR 1.40, 95% CI 1.03-1.89), while no association was found with risk of carcinomas.
  • CONCLUSION: Our results suggest an increased risk for advanced colorectal neoplasia in individuals with the XRCC1 Arg280His polymorphism and a reduced risk associated with the XRCC1 Arg399Gln polymorphism.
  • Interestingly, individuals with the XPD Lys751Gln polymorphism had an increased risk of low-risk adenomas.
  • This may suggest a role in regression of adenomas.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. DNA-Binding Proteins / genetics. Polymorphism, Genetic. Xeroderma Pigmentosum Group D Protein / genetics

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  • (PMID = 16542436.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1; 0 / X-ray repair cross complementing protein 3; EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human
  • [Other-IDs] NLM/ PMC1458350
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81. Mathers JC: Folate intake and bowel cancer risk. Genes Nutr; 2009 Sep;4(3):173-8
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  • [Title] Folate intake and bowel cancer risk.
  • However, human intervention studies using relatively large doses (500-5,000 mug/day) of folic acid (a synthetic form of folate) have provided no evidence of benefit in terms of adenoma recurrence.
  • Possible reasons for the apparent divergence in findings from the observational and intervention studies include the use of (unphysiologically) large doses of folic acid in the intervention studies whereas smaller intakes of food folates appeared to offer "protection" against CRC in case-control and prospective cohort studies.
  • Until the benefit-risk relationship associated with mandatory fortification with folic acid has been clarified (and, in particular, the possible risk of inducing extra cases of bowel or other cancer), it would seem wise to delay further mandatory folic acid fortification.

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  • (PMID = 19499262.001).
  • [ISSN] 1555-8932
  • [Journal-full-title] Genes & nutrition
  • [ISO-abbreviation] Genes Nutr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2745742
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82. Pokala N, Delaney CP, Kiran RP, Brady K, Senagore AJ: Outcome of laparoscopic colectomy for polyps not suitable for endoscopic resection. Surg Endosc; 2007 Mar;21(3):400-3
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  • BACKGROUND: Large colonic polyps or polyps that lie in anatomical locations that are difficult to access at endoscopy may not be suitable for endoscopic resection and therefore may require partial colectomy.
  • METHODS: Patients referred for laparoscopic colectomy for colonic polyps were identified from the prospective colorectal laparoscopic surgery database.
  • There were six complications (17.7%), including anastomotic leak (n = 1), small bowel obstruction (n = 2), abscess (n = 1), and exacerbation of preexisting medical conditions (n = 2).
  • Mean polyp size was 3.1 cm, and pathology revealed tubular (n = 14), tubulovillous (n = 33) and villous adenoma (n = 2), pseudopolyp (n = 1), and prolapse of the appendix into the cecum mimicking an adenoma (n = 1).
  • High-grade dysplasia was seen in four tubular (33%) and five tubulovillous adenomas (15.5%).
  • Adenocarcinoma not identified at colonoscopy was found in 11 polyps (20%), 9 tubulovillous (27.8%) and both villous adenomas (100%).
  • CONCLUSIONS: Large colonic polyps unresectable at colonoscopy are associated with a high rate of unsuspected cancer.

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  • (PMID = 17180271.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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83. Rubie C, Frick VO, Wagner M, Schuld J, Gräber S, Brittner B, Bohle RM, Schilling MK: ELR+ CXC chemokine expression in benign and malignant colorectal conditions. BMC Cancer; 2008;8:178
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  • [Title] ELR+ CXC chemokine expression in benign and malignant colorectal conditions.
  • Here, we comparatively analyzed their expression profile in resection specimens from patients with colorectal adenoma (CRA) (n = 30) as well as colorectal carcinoma (CRC) (n = 48) and corresponding colorectal liver metastases (CRLM) (n = 16).
  • [MeSH-major] Adenoma / metabolism. Carcinoma / metabolism. Chemokines, CXC / biosynthesis. Colorectal Neoplasms / metabolism

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


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

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