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1. Velmurugan B, Singh RP, Kaul N, Agarwal R, Agarwal C: Dietary feeding of grape seed extract prevents intestinal tumorigenesis in APCmin/+ mice. Neoplasia; 2010 Jan;12(1):95-102
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Chemopreventive effects and associated mechanisms of grape seed extract (GSE) against intestinal/colon cancer development are largely unknown.
  • At the end of the experiment, GSE feeding decreased the total number of intestinal polyps by 40%.
  • The decrease in polyp formation in the small intestine was 42%, which was mostly in its middle (51%) and distal (49%) portions compared with the proximal one.
  • GSE also decreased polyp growth where the number of polyps of 1 to 2 mm in size decreased by 42% and greater than 2 mm in size by 71%, without any significant change in polyps less than 1 mm in size.
  • Together, these findings show the chemopreventive potential of GSE against intestinal polyp formation and growth in APC(min/+) mice, which was accompanied with reduced cell proliferation and increased apoptosis together with down-regulation in COX-2, iNOS, beta-catenin, cyclin D1, and c-Myc expression, but increased Cip1/p21.

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  • (PMID = 20072658.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCCIH NIH HHS / AT / AT003623-03; United States / NCCIH NIH HHS / AT / R01 AT003623; United States / NCCIH NIH HHS / AT / R01 AT003623-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Myc protein, mouse; 0 / Plant Extracts; 0 / Proliferating Cell Nuclear Antigen; 0 / Proto-Oncogene Proteins c-myc; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, mouse; EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2
  • [Other-IDs] NLM/ PMC2805888
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2. Dubé C, Rostom A, Lewin G, Tsertsvadze A, Barrowman N, Code C, Sampson M, Moher D, U.S. Preventive Services Task Force: The use of aspirin for primary prevention of colorectal cancer: a systematic review prepared for the U.S. Preventive Services Task Force. Ann Intern Med; 2007 Mar 6;146(5):365-75
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  • DATA SYNTHESIS: Regular use of aspirin reduced the incidence of colonic adenomas in RCTs (relative risk [RR], 0.82 [95% CI, 0.7 to 0.95]), case-control studies (RR, 0.87 [CI, 0.77 to 0.98]), and cohort studies (RR, 0.72 [CI, 0.61 to 0.85]).
  • CONCLUSIONS: Aspirin appears to be effective at reducing the incidence of colonic adenoma and colorectal cancer, especially if used in high doses for more than 10 years.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Colorectal Neoplasms / prevention & control. Primary Prevention
  • [MeSH-minor] Adenoma / prevention & control. Adult. Cardiovascular Diseases / chemically induced. Colonic Polyps / prevention & control. Female. Gastrointestinal Diseases / chemically induced. Humans. Incidence. Male. United States / epidemiology

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  • [CommentIn] ACP J Club. 2007 Jul-Aug;147(1):15-6 [17608380.001]
  • [CommentIn] Gastroenterology. 2007 Aug;133(2):717-8 [17681190.001]
  • [CommentIn] Ann Intern Med. 2007 Nov 6;147(9):674; author reply 674-5 [17975195.001]
  • [SummaryForPatientsIn] Ann Intern Med. 2007 Mar 6;146(5):I35 [17339615.001]
  • (PMID = 17339622.001).
  • [ISSN] 1539-3704
  • [Journal-full-title] Annals of internal medicine
  • [ISO-abbreviation] Ann. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; R16CO5Y76E / Aspirin
  • [Number-of-references] 61
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3. Fujita K, Mondal AM, Horikawa I, Nguyen GH, Kumamoto K, Sohn JJ, Bowman ED, Mathe EA, Schetter AJ, Pine SR, Ji H, Vojtesek B, Bourdon JC, Lane DP, Harris CC: p53 isoforms Delta133p53 and p53beta are endogenous regulators of replicative cellular senescence. Nat Cell Biol; 2009 Sep;11(9):1135-42
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  • The senescence-associated signature of p53 isoform expression (that is, elevated p53beta and reduced Delta133p53) was observed in vivo in colon adenomas with senescent phenotypes.
  • The increased Delta133p53 and decreased p53beta isoform expression found in colon carcinoma may signal an escape from the senescence barrier during the progression from adenoma to carcinoma.

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  • (PMID = 19701195.001).
  • [ISSN] 1476-4679
  • [Journal-full-title] Nature cell biology
  • [ISO-abbreviation] Nat. Cell Biol.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / / Z01 BC005480-22; United States / Intramural NIH HHS / / ZIA BC010878-02; United Kingdom / Cancer Research UK / / ; United States / Intramural NIH HHS / / Z01 BC005795-13; United States / Intramural NIH HHS / / Z01 BC005795-14; United States / Intramural NIH HHS / / ZIA BC005795-15; United States / Intramural NIH HHS / / Z01 BC010878-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MIRN34 microRNA, human; 0 / MicroRNAs; 0 / Protein Isoforms; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ NIHMS161529; NLM/ PMC2802853
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4. Lee SE, Park NH, Park IA, Kang SB, Lee HP: Tubulo-villous adenoma of the vagina. Gynecol Oncol; 2005 Feb;96(2):556-8
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  • [Title] Tubulo-villous adenoma of the vagina.
  • BACKGROUND: Tubulo-villous adenomas are common in the colon and rectum, but extremely rare in the vagina.
  • As far as we know, only two cases of tubulo-villous adenoma have ever been reported.
  • We report the third case of enteric-type tubulo-villous adenoma of the vagina.
  • The tumor was excised and pathologically confirmed as a tubulo-villous adenoma.
  • CONCLUSION: Because some tubulo-villous adenomas in the colon and rectum can progress to the cancer, this case requires long-term follow-up to detect recurrence and malignant transformation.
  • [MeSH-major] Adenoma, Villous / pathology. Vaginal Neoplasms / pathology

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  • (PMID = 15661252.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 17
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5. Valantas MR, Farmer WM, DiPalma JA: Do gastroenterologists notify polyp patients that family members should have screening? South Med J; 2005 Feb;98(2):162-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Do gastroenterologists notify polyp patients that family members should have screening?
  • OBJECTIVE: The objective of this study was to determine whether patients found to have adenomatous polyps or cancer were notified that their relatives should have screening, due to an increased risk of developing colorectal cancer.
  • METHODS: Consecutive (n = 121) colonoscopy patients from December of 1999 to October of 2001 found to have adenomatous colon polyps or colon cancer formed the study group.
  • Adenomatous polyps were seen in 95%, and cancer seen in 5%.
  • Overall, 30% of the patients were notified: 23 of 82 (28%) in the polyp group and 3 of 4 (75%) in the cancer group.
  • Advanced adenomas or multiple adenomas were noted in 28 of the 82 (34%).
  • CONCLUSIONS: Gastroenterologists should be aware of the need for increased attention to family notification, especially in those with advanced adenomas or multiple adenomas.
  • Template notification letters may complement the polyp surveillance programs that many colonoscopists use.
  • [MeSH-major] Colonic Neoplasms / diagnosis. Intestinal Polyps / diagnosis

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  • (PMID = 15759945.001).
  • [ISSN] 0038-4348
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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6. Tan KL, Wilson S, O'Neill C, Gordon D, Napier S: Something not quite right: Gardner syndrome diagnosed by multiple cutaneous lesions and genetic testing. Surgeon; 2005 Dec;3(6):412-5
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  • Gardner syndrome is a variant of familial adenomatous polyposis characterized by intestinal adenomatous polyps, which can progress to adenocarcinoma, and a variety of extraintestinal manifestations, including skin cysts, osteomas, soft tissue fibrous tumours and a characteristic ocular lesion.
  • Gardner syndrome was considered only after excision of subcutaneous fibrous tumours from the mastoid region and paraspinal area and was confirmed by genetic testing in spite of the patient's refusal to undergo colonic endoscopic examination.
  • Subsequent resection revealed approximately 70 adenomatous colonic polyps in the colon and rectum but no invasive tumour, highlighting the benefits of genetic testing in treatment planning.

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  • (PMID = 16353862.001).
  • [ISSN] 1479-666X
  • [Journal-full-title] The surgeon : journal of the Royal Colleges of Surgeons of Edinburgh and Ireland
  • [ISO-abbreviation] Surgeon
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
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7. Zagani R, Hamzaoui N, Cacheux W, de Reyniès A, Terris B, Chaussade S, Romagnolo B, Perret C, Lamarque D: Cyclooxygenase-2 inhibitors down-regulate osteopontin and Nr4A2-new therapeutic targets for colorectal cancers. Gastroenterology; 2009 Oct;137(4):1358-66.e1-3
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  • BACKGROUND & AIMS: Cyclooxygenase-2 inhibitors reduce colon cancer risk by mechanisms that are not fully understood.
  • We performed microarray analysis of adenomas from Apc(Delta14/+) mice to identify genes that respond to these drugs.
  • Findings were further assessed using Apc(lox/lox)vil-CreER(T2) mice, the CT26 cancer cell line, and human colon tumor samples.
  • RESULTS: Microarray analysis revealed that osteopontin, a marker of colon cancer progression, was down-regulated in polyps from Apc(Delta14/+) mice given parecoxib compared with controls.
  • Apc(Delta14/+) mice given parecoxib had longer survival times and reduced polyp burdens.
  • Osteopontin was quickly down-regulated by parecoxib in intestinal polyps from Apc(Delta14/+) mice, and 2 components of the osteopontin regulatory network-the orphan nuclear receptor NR4A2 and Wnt/beta-catenin signaling-were sequentially repressed.
  • NR4A2 levels were reduced in adenomas from patients treated with rofecoxib.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Antineoplastic Agents / pharmacology. Colonic Polyps / drug therapy. Colorectal Neoplasms / drug therapy. Cyclooxygenase 2 / metabolism. Cyclooxygenase Inhibitors / therapeutic use. DNA-Binding Proteins / metabolism. Osteopontin / metabolism. Transcription Factors / metabolism

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  • (PMID = 19549529.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CTNNB1 protein, mouse; 0 / Cyclooxygenase Inhibitors; 0 / DNA-Binding Proteins; 0 / Isoxazoles; 0 / Lactones; 0 / NR4A2 protein, human; 0 / Nr4a2 protein, mouse; 0 / Nuclear Receptor Subfamily 4, Group A, Member 2; 0 / SPP1 protein, human; 0 / Spp1 protein, mouse; 0 / Sulfones; 0 / Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin; 0QTW8Z7MCR / rofecoxib; 106441-73-0 / Osteopontin; 9TUW81Y3CE / parecoxib; EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
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8. Landau D, Garrett C, Chodkiewicz C: A case of primary squamous cell colon cancer. J Oncol Pharm Pract; 2007 Mar;13(1):47-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of primary squamous cell colon cancer.
  • Carcinomas of the colon are a common cancer seen in both inpatient and outpatient settings with approximately 145,000 new cases being diagnosed every year in the USA.
  • Despite the frequency of these cancers being seen, it continues to be a rarity to see a primary squamous cell cancer of the colon.
  • While the exact aetiology of this rare tumour is currently still not completely understood, various aetiologies include chronic irritation leading to squamous differentiation, embryonic migration of ectodermal cells to the colon, or adenomas undergoing squamous transformation.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Colonic Neoplasms / pathology

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  • (PMID = 17621567.001).
  • [ISSN] 1078-1552
  • [Journal-full-title] Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners
  • [ISO-abbreviation] J Oncol Pharm Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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9. Ye C, Shrubsole MJ, Cai Q, Ness R, Grady WM, Smalley W, Cai H, Washington K, Zheng W: Promoter methylation status of the MGMT, hMLH1, and CDKN2A/p16 genes in non-neoplastic mucosa of patients with and without colorectal adenomas. Oncol Rep; 2006 Aug;16(2):429-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter methylation status of the MGMT, hMLH1, and CDKN2A/p16 genes in non-neoplastic mucosa of patients with and without colorectal adenomas.
  • CpG island methylation has been observed in aberrant crypt foci (ACF) and adenomas in the colon, implicating it in the earliest aspects of colon cancer formation.
  • In addition, some investigators have identified an age-related increase in DNA methylation of the ESR1 locus in the colon mucosa, suggesting that DNA methylation may be a pre-neoplastic change that increases the risk of colon adenomas and colon cancer.
  • We investigated the methylation status in the promoter regions of the CDKN2A/p16, hMLH1, and MGMT genes in human non-neoplastic rectal mucosa and evaluated whether these methylation markers may predict the presence of adenomatous polyps in the colon.
  • 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 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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10. García Sánchez Mdel V, González R, Iglesias Flores E, Gómez Camacho F, Casais Juanena L, Cerezo Ruiz A, Montero Pérez-Barquero M, Muntané J, de Dios Vega JF: [Diagnostic value of fecal calprotectin in predicting an abnormal colonoscopy]. Med Clin (Barc); 2006 Jun 10;127(2):41-6
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  • [Transliterated title] Precisión diagnóstica de la calprotectina fecal para predecir una colonoscopia patológica.
  • The colonoscopy is the gold standard method of detecting an organic pathology in the colon.
  • Fecal calprotectin (FCP) is a marker that may detect organic pathologies of the colon.
  • People were divided in: normal colonoscopy: 117 people, and 28 colon adenomas, 20 colorectal cancer (CRC) and 25 IBD.
  • 217 mg/kg was the best cut-off for discriminating patients with organic colon disorders.
  • The measurement of FCP is a non-invasive, inexpensive, reliable and easily measured test.
  • [MeSH-major] Colonic Diseases / diagnosis. Colonic Neoplasms / diagnosis. Colonoscopy. Feces / chemistry. Inflammatory Bowel Diseases / diagnosis. Leukocyte L1 Antigen Complex / analysis

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  • (PMID = 16801001.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] spa
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Leukocyte L1 Antigen Complex
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11. Scott RH, Mansour S, Pritchard-Jones K, Kumar D, MacSweeney F, Rahman N: Medulloblastoma, acute myelocytic leukemia and colonic carcinomas in a child with biallelic MSH6 mutations. Nat Clin Pract Oncol; 2007 Feb;4(2):130-4
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  • [Title] Medulloblastoma, acute myelocytic leukemia and colonic carcinomas in a child with biallelic MSH6 mutations.
  • Background A 13-year-old girl presented with rectal bleeding and was found to have two colonic carcinomas (stage Dukes' C) and multiple colonic polyps.
  • A three-generation family history identified no relatives with colonic carcinomas or polyposis.
  • Investigations Immunohistochemical analysis was performed on a sample of colonic adenoma.
  • [MeSH-major] Cerebellar Neoplasms / genetics. Colonic Neoplasms / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Medulloblastoma / genetics


12. Stănciulea O, Preda C, Herlea V, Popa M, Ulmeanu D, Vasilescu C: [Rare indication of cephalic duodenopancreatectomy with total gastrectomy--periampullary carcinoma in moderate form of familial adenomatous polyposis]. Chirurgia (Bucur); 2007 Mar-Apr;102(2):215-20
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  • [Title] [Rare indication of cephalic duodenopancreatectomy with total gastrectomy--periampullary carcinoma in moderate form of familial adenomatous polyposis].
  • [Transliterated title] Indicaţie rară de duodenopancreatectomie cefalică cu gastrectomie totală-- adenocarcinom periampular cu polipoză adenomatoasă familială forma atenuată.
  • We present the case of a 52 years old man, with significant familial history, diagnosed with familial adenomatous polyposis-attenuated form, with no clinical and endoscopic surveillance until 2001 when he was admitted for an upper gastrointestinal haemorrhage episode.
  • Upper gastrointestinal scopy revealed duodenal adenomatous polyps and gastric hyperplastic polyps.
  • The histopathological exam revealed duodenal G2 adenocarcinoma pT3N0, and gastric hyperplastic polyps with no signs of dysplasia.
  • In 2002 the patient was admitted for rectal bleeding and colonoscopy showed 2 sigmoid polyps, appropriate for endoscopic removal and a poly-lobate polyp in the transverse colon.
  • March 2003--the patient underwent endoscopic removal for a rectal polyp (histopathological exam: moderate dysplasia).
  • The surgical procedure recommended in patients with attenuated form of familial adenomatous polyposis and suspect periampullary lesions is duodenopancreatectomy.
  • The particularity of the case is the association of total gastrectomy for gastric hyperplastic polyps.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Carcinoma / surgery. Duodenal Neoplasms / surgery. Gastrectomy. Neoplasms, Multiple Primary / surgery. Pancreaticoduodenectomy / methods


13. Bretthauer M, Hoff G: [Prevention and early diagnosis of colorectal cancer]. Tidsskr Nor Laegeforen; 2007 Oct 18;127(20):2688-91
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  • CRC develops from benign adenomas in the colon over a long time.
  • RESULTS AND INTERPRETATION: Acetylsalicylic-acid, non-steroidal anti-inflammatory drugs and COX-2 inhibitors are shown to reduce adenoma growth, but it remains uncertain whether these drugs reduce the incidence of CRC.
  • [MeSH-minor] Colon / radiography. Colonoscopy. Early Diagnosis. Evidence-Based Medicine. Humans. Mass Screening. Occult Blood. Prognosis. Randomized Controlled Trials as Topic. Sigmoidoscopy

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  • (PMID = 17952153.001).
  • [ISSN] 0807-7096
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Norway
  • [Number-of-references] 35
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14. Qayyum A, Sawan AS: Profile of colonic biopsies in King Abdul Aziz University Hospital, Jeddah. J Pak Med Assoc; 2009 Sep;59(9):608-11
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  • [Title] Profile of colonic biopsies in King Abdul Aziz University Hospital, Jeddah.
  • OBJECTIVE: To scrutinize all colonic biopsies and document the prevalence and pattern of various colonic diseases amongst the patients presenting at a tertiary care hospital of Western Saudi Arabia.
  • METHODS: We examined the record of all colonic biopsies, processed at Histopathology Department of King Abdul Aziz University Hospital; Jeddah from January 2002 to July 2007.
  • RESULTS: The colonic biopsies received during the study period were 711.
  • Biopsies showing inflammatory, nonspecific/infective and other miscellaneous colonic lesions were 477.
  • Of the 107 benign polyps seen, the most dominant was adenomatous polyp.
  • Tubular adenomas are the most common type of polyps and adenocarcinoma is the most common malignancy of the colon.
  • [MeSH-major] Colonic Diseases / epidemiology
  • [MeSH-minor] Adenocarcinoma / epidemiology. Adolescent. Adult. Aged. Child. Child, Preschool. Colitis, Ulcerative / epidemiology. Colonic Neoplasms / epidemiology. Colonic Polyps / epidemiology. Female. Humans. Male. Middle Aged. Prevalence. Saudi Arabia / epidemiology. Young Adult

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  • (PMID = 19750855.001).
  • [ISSN] 0030-9982
  • [Journal-full-title] JPMA. The Journal of the Pakistan Medical Association
  • [ISO-abbreviation] J Pak Med Assoc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
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15. Paskett ED, Reeves KW, Pineau B, Albert PS, Caan B, Hasson M, Iber F, Kikendall JW, Lance P, Shike M, Slattery ML, Weissfeld J, Kahle L, Schatzkin A, Lanza E, Polyp Prevention Trial Study Group: The association between cigarette smoking and colorectal polyp recurrence (United States). Cancer Causes Control; 2005 Nov;16(9):1021-33
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  • [Title] The association between cigarette smoking and colorectal polyp recurrence (United States).
  • OBJECTIVE: Although evidence exists linking smoking to precancerous colorectal adenomatous polyps, few studies have examined the association between cigarette smoking and recurrence of colorectal polyps.
  • This association was investigated prospectively with data from the Polyp Prevention Trial.
  • The study was completed by 1872 men and women with presence of adenomas at baseline colonoscopy.
  • Multiple logistic regression analysis was used to examine the association between cigarette smoking and polyp recurrence (adenomatous and hyperplastic) up to four years from baseline.
  • RESULTS: Adenoma recurrence was not related to cigarette smoking.
  • Current smokers had increased odds of hyperplastic polyps at follow-up compared to never smokers (OR 2.88, 95% CI 2.06-4.01).
  • Current smoking was associated with subsequent distal (OR 3.44, 95% CI 2.38-4.95) and rectal (OR 3.53, 95% CI 2.15-5.78) hyperplastic polyps, but not subsequent proximal hyperplastic polyps.
  • Cigarette smoking was associated with subsequent multiple and small size (4 mm) hyperplastic polyps.
  • Significant linear trends were observed between development of subsequent hyperplastic polyps and all smoking variables.
  • CONCLUSIONS: Although no association with recurrent adenomas was observed, cigarette smoking was significantly associated with hyperplastic polyp development, except for those in the proximal colon.
  • This prospective study confirms that cigarette smoking has a significant effect on the development of hyperplastic colorectal polyps.
  • [MeSH-major] Colonic Polyps / pathology. Precancerous Conditions. Smoking / epidemiology
  • [MeSH-minor] Adenoma / epidemiology. Adenoma / pathology. Aged. Colonoscopy. Epidemiologic Studies. Female. Humans. Hyperplasia / epidemiology. Hyperplasia / pathology. Male. Middle Aged. Recurrence. Risk Assessment. Risk Factors. Surveys and Questionnaires. Time Factors. United States

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  • (PMID = 16184467.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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16. Kim S, Baron JA, Mott LA, Burke CA, Church TR, McKeown-Eyssen GE, Cole BF, Haile RW, Sandler RS: Aspirin may be more effective in preventing colorectal adenomas in patients with higher BMI (United States). Cancer Causes Control; 2006 Dec;17(10):1299-304
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  • [Title] Aspirin may be more effective in preventing colorectal adenomas in patients with higher BMI (United States).
  • Obesity is a risk factor for colon cancer, possibly due to elevated levels of circulating cytokines derived from adipose tissue.
  • Aspirin, which may affect the levels of these cytokines, has been shown in randomized controlled trials to decrease the risk of colorectal adenomas.
  • Data were available from the Aspirin/Folate Polyp Prevention Study, a randomized controlled trial of aspirin and folic acid to prevent recurrent colorectal adenomas.
  • For the analysis of the effect of aspirin on the recurrence of colorectal adenoma by BMI, we computed risk ratios for aspirin versus placebo within the three BMI strata using a modified Poisson model.
  • Overall the risk reduction of adenomas with a daily dose of 325 mg aspirin was greater among subjects with higher BMI.
  • Among obese subjects the risk ratio (RR) for advanced adenomas compared with placebo was 0.44 (95% CI 0.17-1.10), versus RR = 1.23 (95% CI 0.55-2.77) among those with normal weight.
  • However, 81 mg aspirin daily did not interact with BMI to modify the risk of adenomas in such a fashion.
  • [MeSH-major] Adenomatous Polyps / prevention & control. Aspirin / pharmacology. Body Mass Index. Colorectal Neoplasms / prevention & control

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  • (PMID = 17111262.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK34987; United States / NCI NIH HHS / CA / R01 CA59005; United States / NCRR NIH HHS / RR / RR000046
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] R16CO5Y76E / Aspirin
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17. Glei M, Hovhannisyan G, Pool-Zobel BL: Use of Comet-FISH in the study of DNA damage and repair: review. Mutat Res; 2009 Jan-Feb;681(1):33-43
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  • The Comet-FISH technique is a useful tool to detect overall and region-specific DNA damage and repair in individual cells.
  • Whereas the Comet assay allows separating fragmented from non-fragmented DNA, FISH helps to detect specifically labelled DNA sequences of interest, including whole chromosomes.
  • Thus the combination of both techniques has been applied in particular for detection of site-specific breaks in DNA regions which are relevant for development of different diseases.
  • This paper reviews the relevant literature and presents three examples on how Comet-FISH was used for studying the induction of DNA damage by genotoxic compounds related to oxidative stress in colon cancer-relevant genes (TP53, APC, KRAS) of a colon adenoma cell line.
  • A third example relates to measuring repair of specific gene regions using Comet-FISH, a method that can be developed to biomarker application.
  • Taken together, available data suggests that Comet-FISH helps to get further insights into sensitivity of specific DNA regions and consequently in mechanisms of carcinogenesis.
  • Although the nature of the measured Comet-FISH endpoint precludes us from stating basically that damage and repair are occurring within the specific gene, it is at least possible to evaluate whether the damage and repair are occurring within the vicinity of the gene of interest.
  • [MeSH-minor] Cell Line, Tumor. Colonic Neoplasms / genetics. Colonic Neoplasms / metabolism. Genes, APC / drug effects. Genes, p53 / drug effects. Genes, ras / drug effects. Genetic Markers. Humans. Mutagens / toxicity. Oxidative Stress / genetics. Telomere / drug effects. Telomere / genetics

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  • (PMID = 18304859.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Genetic Markers; 0 / Mutagens
  • [Number-of-references] 88
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18. Bartosova Z, Zavodna K, Krivulcik T, Usak J, Mlkva I, Kruzliak T, Hromec J, Usakova V, Kopecka I, Veres P, Bartosova Z, Bujalkova M: STK11/LKB1 germline mutations in the first Peutz-Jeghers syndrome patients identified in Slovakia. Neoplasma; 2007;54(2):101-7
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  • Peutz-Jeghers syndrome (PJS) is characterized by number of hamartomatous polyps in the gastrointestinal tract and by mucocutaneous hypermelanocytic lesions at different sites.
  • Older patients have an increased risk of the cancers of small intestine, stomach, pancreas, colon, esophagus, ovary, testis, uterus, breast and lung.
  • Neither the polyp nor the tumor of the patient displayed the loss of heterozygosity at the site of mutation suggesting different mechanism involved in the formation of polyp and tumor in this case.
  • Interestingly, the patient displayed concomitant occurrence of adenomatous and hamartomatous polyps.
  • [MeSH-minor] Adult. DNA Mutational Analysis. Female. Genotype. Humans. Intestinal Polyps / pathology. Intestine, Small / pathology. Male. Pedigree. Phenotype. Slovakia

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  • (PMID = 17319781.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] EC 2.7.1.- / STK11 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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19. Yoshida I, Suzuki A, Vallée M, Matano Y, Masunaga T, Zenda T, Shinozaki K, Okada T: Serum insulin levels and the prevalence of adenomatous and hyperplastic polyps in the proximal colon. Clin Gastroenterol Hepatol; 2006 Oct;4(10):1225-31
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  • [Title] Serum insulin levels and the prevalence of adenomatous and hyperplastic polyps in the proximal colon.
  • BACKGROUND & AIMS: Obesity and diabetes mellitus are associated with an increased incidence of proximal colon cancer.
  • Colonic adenoma that has been reported to be associated with elevated serum insulin levels and subsets of hyperplastic polyps might serve as a precursor of colon cancer.
  • In this study, we sought to determine segment-specific associations between serum insulin levels and the prevalence of adenoma and hyperplastic polyps in the proximal and distal colon.
  • We performed multinomial logistic regression models by using the outcome categories of none (reference), proximal-only, distal-only, and both-segment lesions for the presence of adenoma/hyperplastic polyp with serum insulin, age, gender, lifestyle characteristics, and the presence of other types of lesions as predictors.
  • RESULTS: Overall, serum insulin levels were significantly associated with adenoma (OR, 1.5; 95% CI, 1.1-2.0; P = .005) and borderline associated with hyperplastic polyps (OR, 1.3; 95% CI, 1.0-1.7; P = .075).
  • In multinomial logistic regression models, elevated serum insulin levels were significantly associated with proximal-only adenoma (OR, 1.8; 95% CI, 1.2-2.5; P = .002), both-side hyperplastic polyp (OR, 1.7; 95% CI, 1.1-2.5; P = .015), and proximal-only hyperplastic polyp (OR, 1.5; 95% CI, 1.0-2.1; P = .048) and borderline associated with distal-only adenoma (OR, 1.5; 95% CI, 1.0-2.1; P =.059) but not with distal-only hyperplastic polyp.
  • CONCLUSIONS: Serum insulin levels directly correlate with the presence of adenoma and hyperplastic polyps in the proximal colon and might also less strongly correlate with the presence of distal adenoma.
  • [MeSH-major] Adenomatous Polyposis Coli / blood. Biomarkers, Tumor / blood. Colonic Polyps / blood. Colonic Polyps / epidemiology. Insulin / blood

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  • [ErratumIn] Clin Gastroenterol Hepatol. 2007 Jan;5(1):137
  • (PMID = 16979948.001).
  • [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
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Insulin
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20. Ashktorab H, Belgrave K, Hosseinkhah F, Brim H, Nouraie M, Takkikto M, Hewitt S, Lee EL, Dashwood RH, Smoot D: Global histone H4 acetylation and HDAC2 expression in colon adenoma and carcinoma. Dig Dis Sci; 2009 Oct;54(10):2109-17
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  • [Title] Global histone H4 acetylation and HDAC2 expression in colon adenoma and carcinoma.
  • Chromatin remodeling and activation of transcription are important aspects of gene regulation, but these often go awry in disease progression, including during colon cancer development.
  • We investigated the status of global histone acetylation (by measuring H3, H4 acetylation of lysine residues, which also occur over large regions of chromatin including coding regions and non-promoter sequences) and expression of histone deacetylase 2 (HDAC2) in colorectal cancer (CRC) tissue microarrays using immunohistochemical staining.
  • Specifically, HDAC2 and the acetylation of histones H4K12 and H3K18 were evaluated in 134 colonic adenomas, 55 moderate to well differentiated carcinomas, and 4 poorly differentiated carcinomas compared to matched normal tissue.
  • HDAC2 nuclear expression was detected at high levels in 81.9%, 62.1%, and 53.1% of CRC, adenomas, and normal tissue, respectively (P = 0.002).
  • HDAC2 expression was correlated significantly with progression of adenoma to carcinoma (P = 0.002), with a discriminative power of 0.74, when comparing cancer and non-cancer cases.

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  • (PMID = 19057998.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA122959; United States / NCI NIH HHS / CA / CA122959-02; United States / NCI NIH HHS / CA / R01 CA122959-02; United States / PHS HHS / / A102681; United States / NCI NIH HHS / CA / R01 CA122959
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Histones; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ NIHMS118762; NLM/ PMC2737733
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21. Suzuki R, Kohno H, Sugie S, Tanaka T: Dose-dependent promoting effect of dextran sodium sulfate on mouse colon carcinogenesis initiated with azoxymethane. Histol Histopathol; 2005 04;20(2):483-92
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  • [Title] Dose-dependent promoting effect of dextran sodium sulfate on mouse colon carcinogenesis initiated with azoxymethane.
  • We previously reported a powerful tumor-promoting ability of dextran sodium sulfate (DSS) in a novel mouse model for colitis-related colon carcinogenesis initiated with azoxymethane (AOM).
  • All animals were sacrificed at week 14 and histological alterations in their colon and nitrotyrosine immunohistochemistry were examined to evaluate the nitrosative stress.
  • In the mice which received AOM and 2% DSS, the incidences (multiplicity) of colonic tubular adenoma and adenocarcinoma were 75% (1.25+/-1.26/mouse) and 100% (2.75+/-2.22/mouse), respectively.
  • Mice given AOM and 1% DSS had 80% incidence of adenoma (1.00+/-0.71/mouse) and 60% incidence of adenocarcinoma (1.40+/-2.07/mouse) in the colon.
  • In a mouse treated with AOM and 0.5% DSS, only one colonic adenoma (20% incidence with 0.20+/-0.45 multiplicity) developed.
  • Higher frequency of high-grade colonic dysplasia was noted in mice given AOM and 2% or 1% DSS when compared with mice treated with AOM and lower doses of DSS.
  • Also, scoring of inflammation and nitrotyrosine immunoreactivity suggested that severe inflammation and nitrosation stress caused by high-doses (2% and 1%) of DSS contribute its tumor-promoting effects in mouse colon carcinogenesis initiated with a low dose of AOM.
  • [MeSH-major] Carcinogens / toxicity. Colonic Neoplasms / chemically induced. Dextran Sulfate / toxicity. Tyrosine / analogs & derivatives
  • [MeSH-minor] Animals. Azoxymethane / administration & dosage. Azoxymethane / toxicity. Cocarcinogenesis. Colitis / chemically induced. Colitis / pathology. Colonic Diseases / chemically induced. Colonic Diseases / pathology. Dose-Response Relationship, Drug. Intestinal Mucosa / drug effects. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Male. Mice. Mice, Inbred ICR. Ulcer / chemically induced. Ulcer / pathology

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  • (PMID = 15736053.001).
  • [ISSN] 0213-3911
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Carcinogens; 3604-79-3 / 3-nitrotyrosine; 42HK56048U / Tyrosine; 9042-14-2 / Dextran Sulfate; MO0N1J0SEN / Azoxymethane
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22. Jurek D, Fleckl E, Marian B: Bile acid induced gene expression in LT97 colonic adenoma cells. Food Chem Toxicol; 2005 Jan;43(1):87-93
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  • [Title] Bile acid induced gene expression in LT97 colonic adenoma cells.
  • LT97 human colonic adenoma cells reflecting early premalignant genotype and growth characteristics have been posed to tumor promoting bile acids in order to identify marker genes that permit identification of tumor promoters in vitro.
  • Transient induction of c-fos was seen with the non-promoting taurodesoxycholate (TDOC) as well as DOC, however extended induction at 3 h was only achieved by DOC and CDC reaching 3-6-fold as compared to the control.
  • Stimulation of COX-2 expression was completely specific for the tumor promoting analogs DOC and CDC.
  • Expression of VEGF was stimulated 4-5-fold in the tumor promoter (DOC and CDC) groups and about 2-fold in the non-promoting controls TDOC and GCDC.
  • At later times the tumor promoter specific difference was lost.
  • Our results show that all three genes are modulated in a tumor promoter dependent way and that their upregulation in LT97 adenoma cells can be used for in vitro testing of colon tumor promoters and chemopreventive compounds.
  • [MeSH-major] Adenoma / metabolism. Bile Acids and Salts / pharmacology. Biomarkers, Tumor / metabolism. Colonic Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / drug effects

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  • (PMID = 15582199.001).
  • [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 / Bile Acids and Salts; 0 / Biomarkers, Tumor; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins c-fos; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 005990WHZZ / Deoxycholic Acid; 0GEI24LG0J / Chenodeoxycholic Acid; 516-50-7 / Taurodeoxycholic Acid; 63231-63-0 / RNA; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases
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23. van Kouwen MC, Laverman P, van Krieken JH, Oyen WJ, Nagengast FM, Drenth JP: Noninvasive monitoring of colonic carcinogenesis: feasibility of [(18)F]FDG-PET in the azoxymethane model. Nucl Med Biol; 2006 Feb;33(2):245-8
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  • [Title] Noninvasive monitoring of colonic carcinogenesis: feasibility of [(18)F]FDG-PET in the azoxymethane model.
  • BACKGROUND: Azoxymethane (AOM) is a potent carcinogen that induces colorectal cancer and adenomas in rats.
  • At present, it is unknown at which stage FDG accumulation occurs during the adenoma carcinoma sequence.
  • RESULTS: Macroscopic examination revealed 21 tumors (7 located in the small bowel and 14 in the colon) in 19 rats.
  • On histological examination, we found 10 colonic adenocarcinomas (the first being observed at Week 22) and 7 adenocarcinoma in the small bowel.
  • In total, seven colon adenomas were found in five rats, six of which expressed high-grade dysplasia.
  • [(18)F]FDG uptake was lower in adenomas than in carcinomas.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / radionuclide imaging. Colonic Neoplasms / metabolism. Colonic Neoplasms / radionuclide imaging. Disease Models, Animal. Fluorodeoxyglucose F18 / pharmacokinetics

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  • (PMID = 16546679.001).
  • [ISSN] 0969-8051
  • [Journal-full-title] Nuclear medicine and biology
  • [ISO-abbreviation] Nucl. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; MO0N1J0SEN / Azoxymethane
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24. Kurland JE, Beck SE, Solomon CJ, Brann OS, Carethers JM, Huang SC: Cyclooxygenase-2 expression in polyps from a patient with juvenile polyposis syndrome with mutant BMPR1A. J Pediatr Gastroenterol Nutr; 2007 Mar;44(3):318-25
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  • [Title] Cyclooxygenase-2 expression in polyps from a patient with juvenile polyposis syndrome with mutant BMPR1A.
  • OBJECTIVES: Cyclooxygenase-2 (COX-2) expression is increased in colorectal cancers and has been reported to be upregulated in Peutz-Jeghers polyps.
  • To determine whether germline and somatic loss of BMPR1A in polyps from a patient with juvenile polyposis syndrome have altered COX-2 expression, we characterized a patient with juvenile polyposis syndrome for BMPR1A germline mutations and examined the polyps for BMPR1A expression and COX-2 expression.
  • Multiple polypectomies were performed, and several polyps showed adenomatous change.
  • Genomic DNA was extracted from polyp material for loss of heterozygosity (LOH) analyses with microsatellite markers.
  • In polyp domains containing cystic and adenomatous epithelium, no LOH was observed using markers near the BMPR1A locus.
  • Immunostaining indicated decreased expression of phospho-SMAD1 (pSMAD1), functionally downstream of the mutant BMPR1A receptor in the cystic epithelium, with further reduction in adenomatous portions within the polyp.
  • COX-2 protein, normally not expressed in the colon, was present and increased in polyp epithelium.
  • CONCLUSIONS: Decreased expression of pSMAD1 in the cystic epithelium with further reduction in the adenomatous area, and increase in COX-2 expression within polyps from the BMPR1A heterozygote, suggest a potential mechanism for adenomatous pathogenesis in these hamartomatous polyps.

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  • (PMID = 17325551.001).
  • [ISSN] 1536-4801
  • [Journal-full-title] Journal of pediatric gastroenterology and nutrition
  • [ISO-abbreviation] J. Pediatr. Gastroenterol. Nutr.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA090231-05; United States / NIDDK NIH HHS / DK / T32 DK007202-32; United States / NCI NIH HHS / CA / R01 CA090231-05; United States / NCI NIH HHS / CA / R01 CA090231; United States / NCI NIH HHS / CA / R01-CA90231; United States / NIDDK NIH HHS / DK / K08-DK64560A; United States / NIDDK NIH HHS / DK / T32 DK007202; United States / NIDDK NIH HHS / DK / DK007202-32
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Smad1 Protein; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.30 / BMPR1A protein, human; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type I
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25. Beggs AD, Hodgson SV: The genomics of colorectal cancer: state of the art. Curr Genomics; 2008 Mar;9(1):1-10
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  • The concept of the adenoma-carcinoma sequence, as first espoused by Morson et al. whereby the development of colorectal cancer is dependent on a stepwise progression from adenomatous polyp to carcinoma is well documented.
  • Initial studies of the genetics of inherited colorectal cancer susceptibility concentrated on the inherited colorectal cancer syndromes, such as Familial Adenomatous Polyposis (FAP) and Lynch Syndrome (also known as HNPCC).
  • Recent research has concentrated on the pathways by which colorectal adenomatous polyps not due to one of these known inherited susceptibilities undergo malignant transformation, and determination of the types of polyps most likely to do so.
  • We will also discuss in detail the genetic changes in polyps that undergo malignant transformation as well as current knowledge with regards to the epigenomic changes found in colorectal polyps.

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  • (PMID = 19424478.001).
  • [ISSN] 1389-2029
  • [Journal-full-title] Current genomics
  • [ISO-abbreviation] Curr. Genomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC2674304
  • [Keywords] NOTNLM ; Colorectal / cancer / epigenomics. / genomics
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26. Lee HL, Son BK, Lee OY, Jeon YC, Han DS, Sohn JH, Yoon BC, Choi HS, Hahm JS, Lee MH, Lee DH, Kee CS: [Abdominal obesity, insulin resistance, and the risk of colonic adenoma]. Korean J Gastroenterol; 2007 Mar;49(3):147-51
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  • [Title] [Abdominal obesity, insulin resistance, and the risk of colonic adenoma].
  • BACKGROUND/AIMS: Abdominal obesity and hyperinsulinemia or insulin resistance are of interest in connection with colon carcinogenesis.
  • We conducted a prospective case controlled study for the evaluation of relationship between abdominal obesity, insulin resistance, and colorectal adenoma.
  • METHODS: Fifty patients with colorectal adenoma and fifty healthy subjects were included in this study.
  • RESULTS: There were no differences in sex, serum insulin, FBS, HOMA-IR, TG, CROL between adenoma and control group.
  • Subjects with high BMI, WHR, percent body fat, and obesity were more likely to have colonic adenoma.
  • Multiple logistic regression analysis after adjusting confounding factors, had revealed that WHR was the most important independent risk factor for colon adenoma.
  • CONCLUSIONS: Abdominal obesity was most closely related to colonic adenoma.
  • However, insulin resistance was not related to colonic adenoma.
  • [MeSH-major] Abdominal Fat. Adenoma / etiology. Colonic Neoplasms / etiology. Insulin Resistance. Obesity / complications

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  • [CommentIn] Korean J Gastroenterol. 2007 Mar;49(3):192-5 [18172350.001]
  • (PMID = 18172342.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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27. Poshkus T, Samalavichus NE, Dracutene G: [Flat adenomas of the colon]. Ter Arkh; 2007;79(2):77-81
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  • [Title] [Flat adenomas of the colon].
  • [MeSH-major] Adenoma / pathology. Adenomatous Polyps / pathology. Colonic Neoplasms / pathology

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  • (PMID = 17460974.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Number-of-references] 79
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28. Varey AH, Rennel ES, Qiu Y, Bevan HS, Perrin RM, Raffy S, Dixon AR, Paraskeva C, Zaccheo O, Hassan AB, Harper SJ, Bates DO: VEGF 165 b, an antiangiogenic VEGF-A isoform, binds and inhibits bevacizumab treatment in experimental colorectal carcinoma: balance of pro- and antiangiogenic VEGF-A isoforms has implications for therapy. Br J Cancer; 2008 Apr 22;98(8):1366-79
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  • Using isoform-specific enzyme-linked immunosorbent assay and quantitative polymerase chain reaction, we found that over 90% of the VEGF in normal colonic tissue was VEGF(xxx)b, but there was a variable upregulation of VEGF(xxx) and downregulation of VEGF(xxx)b in paired human CRC samples.
  • Furthermore, cultured colonic adenoma cells expressed predominantly VEGF(xxx)b, whereas colonic carcinoma cells expressed predominantly VEGF(xxx).
  • However, adenoma cells exposed to hypoxia switched their expression from predominantly VEGF(xxx)b to predominantly VEGF(xxx).
  • VEGF(165)b overexpression in LS174t colon cancer cells inhibited colon carcinoma growth in mouse xenograft models.
  • However, although bevacizumab effectively inhibited the rapid growth of colon carcinomas expressing VEGF(165), it did not affect the slower growth of tumours from colonic carcinoma cells expressing VEGF(165)b.
  • Both bevacizumab and anti-VEGF(165)b-specific antibodies were cytotoxic to colonic epithelial cells, but less so to colonic carcinoma cells.
  • Together with the identification of an autocrine cytoprotective role for VEGF(165)b in colonic epithelial cells, these results indicate that bevacizumab treatment of human CRC may depend upon this balance of VEGF isoforms.
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Bevacizumab. Cell Line, Tumor. Cell Proliferation. Colon / metabolism. Humans. Mice. Protein Isoforms. RNA Splicing. RNA, Messenger / analysis

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  • (PMID = 18349829.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / British Heart Foundation / / FS/06/038; United Kingdom / British Heart Foundation / / BS/06/005/20340; United Kingdom / British Heart Foundation / / FS/04/22; United Kingdom / Cancer Research UK / / A8451; United Kingdom / Cancer Research UK / / ; United Kingdom / British Heart Foundation / / BS/2001003/12790; United Kingdom / British Heart Foundation / / BB2000003
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 2S9ZZM9Q9V / Bevacizumab
  • [Other-IDs] NLM/ PMC2361696; NLM/ UKMS2582
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29. Knöbel Y, Weise A, Glei M, Sendt W, Claussen U, Pool-Zobel BL: Ferric iron is genotoxic in non-transformed and preneoplastic human colon cells. Food Chem Toxicol; 2007 May;45(5):804-11
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  • [Title] Ferric iron is genotoxic in non-transformed and preneoplastic human colon cells.
  • We previously demonstrated genotoxic effects by ferric iron using the human colon cancer cell line HT29.
  • Here we investigated ferric iron in primary non-transformed colon cells and in a preneoplastic colon adenoma cell line (LT97), which both are suitable models to study effects of carcinogens during early stages of cell transformation.
  • Comet FISH (fluorescence in situ hybridization) was used to assess specific effects on TP53.
  • Fe-NTA (0-1000 microM, 30 min, 37 degrees C) significantly induced single strand breaks in primary colon cells (500 microM Fe-NTA: Tail intensity [TI] 22.6%+/-5.0% versus RPMI control: TI 10.6%+/-3.9%, p<0.01) and in LT97 cells (1000 microM Fe-NTA: TI 26.8%+/-7.3% versus RPMI control: TI 11.1%+/-3.7%, p<0.01).
  • With the Comet FISH protocol lower concentrations of Fe-NTA significantly increased DNA damage already at 100 and 250 microM Fe-NTA in primary colon and LT97 adenoma cells, respectively.
  • In conclusion, Fe-NTA acts genotoxic in non-transformed and in preneoplastic human colon cells, in which it also enhances migration of TP53 at relatively low concentrations.
  • Translated to the in vivo situation these results suggest that iron overload putatively contributes to a genotoxic risk during early stages of colorectal carcinogenesis on account of its genotoxic potential in non-tumorigenic human colon cells.
  • [MeSH-major] Colon / drug effects. DNA Damage / drug effects. Ferric Compounds / toxicity. Nitrates / toxicity
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Cell Line, Tumor. Chromosome Aberrations. Colonic Neoplasms / genetics. Colonic Neoplasms / pathology. Comet Assay. Dose-Response Relationship, Drug. Humans. In Situ Hybridization, Fluorescence. Reactive Oxygen Species / metabolism. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 17157427.001).
  • [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 / Ferric Compounds; 0 / Nitrates; 0 / Reactive Oxygen Species; 0 / Tumor Suppressor Protein p53; N8H8402XOB / ferric nitrate
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30. Roberts ML, Drosopoulos KG, Vasileiou I, Stricker M, Taoufik E, Maercker C, Guialis A, Alexis MN, Pintzas A: Microarray analysis of the differential transformation mediated by Kirsten and Harvey Ras oncogenes in a human colorectal adenocarcinoma cell line. Int J Cancer; 2006 Feb 1;118(3):616-27
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  • Colorectal cancer arises after a series of mutational events in the colon epithelia and is often used as a model of the multistep progression of tumorigenesis.
  • In order to examine the distinctive function that Ki-Ras plays in cancer development in the colon, we introduced constitutively active mutant Ki- and Ha-Ras genes into an intermediate-stage colon adenoma cell line (Caco-2).
  • We found that mutant active Ha-RasV12 was more efficient at transforming these colon epithelial cells as assessed by anchorage-independent growth, tumor formation in SCID mice and the development of mesenchymal morphology compared to transformation by Ki-RasV12.
  • Specifically, we found that Ki-RasV12 regulated genes involved in cytokine signaling, cell adhesion and colon development, whereas Ha-RasV12 mainly regulated genes involved in controlling cell morphology, correlating to an epithelial-mesenchymal transition only observed in these cells.
  • Our results demonstrate how 2 Ras isoforms regulate disparate biologic processes, revealing a number of genes whose deregulated expression may influence colon carcinogenesis (supplementary material for this article can be found on the International Journal of Cancer website at http://www.interscience.wiley.com/jpages/0020-7136/suppmat/index.html).

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16152623.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Protein Isoforms
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31. Colao A, Pivonello R, Auriemma RS, Galdiero M, Ferone D, Minuto F, Marzullo P, Lombardi G: The association of fasting insulin concentrations and colonic neoplasms in acromegaly: a colonoscopy-based study in 210 patients. J Clin Endocrinol Metab; 2007 Oct;92(10):3854-60
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  • [Title] The association of fasting insulin concentrations and colonic neoplasms in acromegaly: a colonoscopy-based study in 210 patients.
  • CONTEXT: Hyperinsulinemia is associated with colon carcinoma in the general population.
  • PATIENTS with acromegaly are considered to be at risk for developing colonic lesions and typically have hyperinsulinemia.
  • OBJECTIVE: Our objective was to evaluate the role of fasting insulin levels on the prevalence of colonic adenomatous polyps or adenocarcinoma in acromegaly.
  • RESULTS: Colonic lesions were found in 81 patients (38.6%), and consisted of hyperplastic polyps in 33 (15.7%), adenomatous polyps in 42 (20.0%), and adenocarcinoma in six patients (2.8%).
  • Polyps were single in 22 cases (27.1%).
  • Fasting insulin levels were significantly lower in patients without lesions (16.0 +/- 7.5 mU/liter) than in patients with hyperplastic polyps (22.4 +/- 8.8 mU/liter; P < 0.01), adenomatous polyps (38.0 +/- 15.9 mU/liter; P < 0.0001), and adenocarcinoma (59.0 +/- 30.6 mU/liter; P < 0.0001).
  • Fasting insulin levels were also lower in patients with hyperplastic polyps than in those with adenomatous polyps (P < 0.01).
  • The odds ratio for harboring colonic adenomas was 14.8 (95% confidence interval 4.4-51.2; P < 0.0001) and 8.6 times higher (95% confidence interval 2.8-29.0; P < 0.0001) in patients with fasting insulin levels in the upper tertile [>/=27.1 mIU/liter (n = 28)] compared with the lower [</=12.1 mIU/liter (n = 40)] and middle tertiles [>12.1 to <27.1 mIU/liter (n = 74)], respectively.
  • CONCLUSION: An increase in fasting insulin levels is associated with an 8.6- to 14.8-fold increased risk of presenting with colonic adenomas in acromegaly.
  • [MeSH-major] Acromegaly / epidemiology. Adenocarcinoma / epidemiology. Adenomatous Polyps / epidemiology. Colonic Neoplasms / epidemiology. Insulin / blood

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  • (PMID = 17652220.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
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32. Shin JE, Jung SA, Kim SE, Joo YH, Shim KN, Kim TH, Yoo K, Moon IH: [Expression of MMP-2, HIF-1alpha and VEGF in colon adenoma and colon cancer]. Korean J Gastroenterol; 2007 Jul;50(1):9-18
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  • [Title] [Expression of MMP-2, HIF-1alpha and VEGF in colon adenoma and colon cancer].
  • BACKGROUND/AIMS: This study was aimed to investigate the expression of matrix metalloproteinase-2 (MMP-2), hypoxia-inducible factor (HIF)-1alpha, and vascular endothelial growth factor (VEGF) in colonic adenoma-carcinoma sequence.
  • METHODS: Thirty-two tissue samples of colon adenoma, 11 of early colon cancer and 36 of advanced colon cancer were collected by colonoscopic biopsy.
  • Normal colonic tissues were also collected from the same subjects.
  • RESULTS: The expression level of MMP-2 mRNA showed a progressive increase in the advance of the colorectal adenoma-carcinoma sequence (p<0.05).
  • In colon cancer tissues, the expression level of MMP-2 mRNA showed an increasing trend according to differentiation, lymphatic invasion and Dukes' stage (p<0.05).
  • The mRNA expression levels of HIF-1alpha and VEGF were greater in tissues of early and advanced colon cancer compared with colon adenoma (p<0.05; p<0.001).
  • CONCLUSIONS: MMP-2, HIF-1alpha, and VEGF may be useful in detecting early carcinogenesis and progression of colon cancer.
  • [MeSH-major] Adenoma / metabolism. Colonic Neoplasms / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Matrix Metalloproteinase 2 / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 18172354.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; EC 3.4.24.24 / Matrix Metalloproteinase 2
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33. Li SR, Wang HH, Hu JC, Li N, Liu YL, Wu ZT, Zheng Y, Wang HH, Wu K, Ye H: [Comparison of three FOBT protocols for colorectal cancer screening in Chinese--a multicenter study]. Zhonghua Yi Xue Za Zhi; 2005 Mar 16;85(10):697-700
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  • RESULTS: 323 eligible patients including 49 colorectal cancers, 60 colon adenomas, 60 chronic colitis, 15 hemorrhoids and 139 normal colon were observed.
  • 41.6% approximately 48.3% of adenomas was found by the 3 protocols, and 87.5% of adenomas over 2 cm in diameter were detected by any one of FOBT.
  • The majority of adenomas in that advanced lesion existed might be detected by FOBT.
  • [MeSH-minor] Adenoma / prevention & control. Colonoscopy. Cost-Benefit Analysis. Female. Humans. Male


34. Alferez DG, Ryan AJ, Goodlad RA, Wright NA, Wilkinson RW: Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model. Int J Oncol; 2010 Oct;37(4):767-72
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  • [Title] Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model.
  • The Apc(MIN/+) mouse is a well-characterised model of intestinal tumourigenesis in which animals develop macroscopically detectable adenomas.
  • However, most of the adenomas are formed in the small intestine and resolution of events in the colon, the most relevant site for human disease, is limited.
  • Inducing colitis with dextran sodium sulphate (DSS) can selectively enhance the development of lesions in the colon.
  • We demonstrated that a DSS pre-treatment is well tolerated and effective at inducing colon adenomas in an Apc(MIN/+) mouse model.
  • We then investigated the effect of inhibiting vascular endothelial growth factor (VEGFR)- and epidermal growth factor receptor (EGFR)-dependent signalling pathways on the development of adenomas induced in DSS-pretreated (DSS/Apc(MIN/+)) or non-DSS-pretreated (Apc(MIN/+)) mice using vandetanib (ZD6474), a potent and selective inhibitor of VEGFR and EGFR tyrosine kinase activity.
  • Eight-week old Apc(MIN/+) mice were given either drinking water or 1.8% DSS and then vandetanib (ZD6474) (50 mg/kg/day) or vehicle by oral gavage for 28 days and sacrificed 24 h after the last dose and assessed for adenoma formation in the intestines.
  • DSS pre-treatment was well tolerated and significantly enhanced formation of adenomas in the colon of control Apc(MIN/+) mice.
  • Vandetanib treatment significantly reduced adenoma formation in the small intestine by 68% (P=0.001) and the colon by 77% (from 13.8 to 3.1, P=0.01) of DSS-pretreated Apc(MIN/+) mice.
  • In the Apc(MIN/+) group, vandetanib also reduced the mean number of adenomas in the small intestine by 76% (P<0.001) and in the colon by 60% (from 3.9 to 1.5, P=0.1).
  • DSS-pre-treatment increased the resolution of the model, allowing us to confirm statistically significant effects of vandetanib on the development and growth of colon adenomas in the Apc(MIN/+) mouse.
  • [MeSH-major] Adenoma / prevention & control. Antineoplastic Agents / pharmacology. Colitis / chemically induced. Colonic Neoplasms / prevention & control. Dextran Sulfate. Genes, APC. Piperidines / pharmacology. Protein Kinase Inhibitors / pharmacology. Quinazolines / pharmacology

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  • (PMID = 20811697.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CTNNB1 protein, mouse; 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Piperidines; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / beta Catenin; 9042-14-2 / Dextran Sulfate; EC 2.7.10.1 / EGFR protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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35. Habermann N, Lund EK, Pool-Zobel BL, Glei M: Modulation of gene expression in eicosapentaenoic acid and docosahexaenoic acid treated human colon adenoma cells. Genes Nutr; 2009 Mar;4(1):73-6
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  • [Title] Modulation of gene expression in eicosapentaenoic acid and docosahexaenoic acid treated human colon adenoma cells.
  • The aim of the study was to compare the modulation of gene expression in LT97 colon adenoma cells in response to EPA and DHA treatment.
  • In our approach, we used preneoplastic adenoma cells which are a relevant model for target cells of chemoprevention.
  • If verified with real time PCR, these results identify genes and targets for chemoprevention of colon cancer.

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  • (PMID = 19234733.001).
  • [ISSN] 1555-8932
  • [Journal-full-title] Genes & nutrition
  • [ISO-abbreviation] Genes Nutr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2654050
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36. Phelps RA, Broadbent TJ, Stafforini DM, Jones DA: New perspectives on APC control of cell fate and proliferation in colorectal cancer. Cell Cycle; 2009 Aug 15;8(16):2549-56
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  • Aberrant Wnt/beta-catenin signaling following loss of the tumor suppressor adenomatous polyposis coli (APC) is thought to initiate colon adenoma formation.
  • However, examination of tumors from familial adenomatous polyposis coli (FAP) patients has failed to confirm the presence of nuclear beta-catenin in early lesions following APC loss despite robust staining in later lesions.
  • This observation presents the possibility that colon adenomas arise through a beta-catenin-independent function of APC.
  • Though there are currently contrasting models to explain colon tumorigenesis, our goal is to begin to reconcile data from multiple different model systems and provide a functional view into the initiation and progression of colon cancer.
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Cell Differentiation / physiology. Colorectal Neoplasms / pathology

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  • (PMID = 19597346.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 94
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37. Boissan M, De Wever O, Lizarraga F, Wendum D, Poincloux R, Chignard N, Desbois-Mouthon C, Dufour S, Nawrocki-Raby B, Birembaut P, Bracke M, Chavrier P, Gespach C, Lacombe ML: Implication of metastasis suppressor NM23-H1 in maintaining adherens junctions and limiting the invasive potential of human cancer cells. Cancer Res; 2010 Oct 1;70(19):7710-22
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  • We silenced NM23-H1 expression in human hepatoma and colon carcinoma cells and methodologically investigated effects on cell-cell adhesion, migration, invasion, and signaling linked to cancer progression.
  • Analysis of NM23-H1 expression in clinical specimens revealed high expression in premalignant lesions (liver cirrhosis and colon adenoma) and the central body of primary liver or colon tumors, but downregulation at the invasive front of tumors.
  • [MeSH-minor] Actins / metabolism. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cell Line, Tumor. Cell Movement / genetics. Colonic Neoplasms / genetics. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Cytoskeleton / metabolism. Cytoskeleton / pathology. Gene Silencing. Humans. Liver Neoplasms / genetics. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Matrix Metalloproteinase 14 / metabolism. Neoplasm Invasiveness. Wnt Proteins / metabolism


38. Militsa NN, Postolenko ND, Kotelevets VV, Lazareva NV: [Successful operative treatment of multiple intestinal invagination, caused by adenomatous polyp of colon transversum]. Klin Khir; 2008 Jun;(6):57-8
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  • [Title] [Successful operative treatment of multiple intestinal invagination, caused by adenomatous polyp of colon transversum].

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  • (PMID = 18982730.001).
  • [ISSN] 0023-2130
  • [Journal-full-title] Klinichna khirurhiia
  • [ISO-abbreviation] Klin Khir
  • [Language] RUS
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ukraine
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39. 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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  • [Title] Predictive value of morphologic characteristics in rectosigmoid adenomatous polyps for the probability of synchronous polyps or cancer in the proximal colon.
  • 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.
  • METHODS: Patients found to have rectosigmoid adenomatous polyps on colonoscopy were included in the study.
  • 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).
  • Polyps found in the rectum and sigmoid colon were considered as distal polyps and polyps other than these were considered as proximal polyps.
  • RESULTS: In this study, of 1124 consecutive patients who underwent colonoscopy between April 1997 and January 2002, 184 (16%) had 258 adenomatous polyps in the rectosigmoid area.
  • 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.
  • There was no difference regarding the presence of neoplasm in the proximal colon between these groups.
  • 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).
  • In 104 patients (57%) with polyp(s) in rectum and sigmoid colon, no associated polyp or cancer was encountered in the proximal colon.
  • CONCLUSION: Colonoscopy is indicated when adenomatous polyp, regardless of size, is found on rectosigmoidoscopy performed because of symptoms.
  • [MeSH-major] Adenomatous Polyps / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Neoplasms, Multiple Primary. Rectal Neoplasms / pathology. Sigmoid Neoplasms / pathology

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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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40. Loffeld SM, Loffeld RJ: Colorectal cancer and adenomas are rare in individuals of Turkish descent living in the Zaanstreek region in the Netherlands. J Cancer Res Clin Oncol; 2010 Sep;136(9):1439-43
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  • [Title] Colorectal cancer and adenomas are rare in individuals of Turkish descent living in the Zaanstreek region in the Netherlands.
  • Screening and detection of its precursor lesion, the adenoma could prevent development of colorectal cancer.
  • AIM: To evaluate the prevalence of colorectal cancer and adenoma in patients living in the Zaanstreek region, the Netherlands, and correlate these findings with ethnicity.
  • MATERIALS AND METHODS: All patients undergoing endoscopy of the colon and rectum during a period of 16 consecutive years in whom colorectal cancer and/or a polyp were diagnosed, were included in this study.
  • A total of 2,744 patients had one or more polyp(s) during endoscopy.
  • CONCLUSION: Colorectal cancer and colonic adenoma are rare in patients of Turkish descent living in the Zaanstreek region, the Netherlands.
  • [MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology

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  • (PMID = 20140623.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2908754
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41. Lee GE, Park HS, Yun KE, Jun SH, Kim HK, Cho SI, Kim JH: Association between BMI and metabolic syndrome and adenomatous colonic polyps in Korean men. Obesity (Silver Spring); 2008 Jun;16(6):1434-9
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  • [Title] Association between BMI and metabolic syndrome and adenomatous colonic polyps in Korean men.
  • Obesity and insulin resistance are associated with the risk of colon cancer.
  • Adenomatous colonic polyps are precancerous lesions of colon cancer.
  • We investigated whether BMI and the metabolic syndrome are associated with the presence of adenomatous colonic polyps in Korean men.
  • Multiple logistic regression analysis was used to evaluate the association between BMI and the metabolic syndrome and adenomatous polyps.
  • Compared with men in the 1st quintile of the BMI, the adjusted odds ratio (OR) and 95% confidence interval (CI) for adenomatous polyps in men in the 2nd, 3rd, 4th, and 5th quintiles of the BMI were 1.55 (1.10-2.19), 1.57 (1.10-2.24), 1.94 (1.34-2.81), and 1.99 (1.31-3.01), respectively (P for trend <0.0001).
  • Men with triglycerides (TGs) > or = 150 mg/dl were significantly more likely to have adenomatous polyps than were men with TG <150 mg/dl (OR 1.29; 95% CI 1.03-1.62).
  • As a function of the number of metabolic risk factors, the ORs for adenomatous polyps were 1.41 (1.03-1.93), 1.52 (1.08-2.12), 1.46 (1.01-2.12), and 1.77 (1.08-2.90) for 1, 2, 3, and > or = 4 risk factors, respectively (P for trend <0.05).
  • Adenomatous colonic polyps were significantly associated with increased BMI levels.
  • Subjects with even one component of the metabolic syndrome had a significantly higher risk for developing adenomatous polyps compared to those subjects without any component in Korean men.
  • [MeSH-major] Adenomatous Polyps / epidemiology. Body Mass Index. Colonic Polyps / epidemiology. Metabolic Syndrome X / physiopathology

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  • (PMID = 18388894.001).
  • [ISSN] 1930-7381
  • [Journal-full-title] Obesity (Silver Spring, Md.)
  • [ISO-abbreviation] Obesity (Silver Spring)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Triglycerides
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42. Cirocchi R, Coccetta M, De Sol A, Morelli U, Spizzirri A, Cattorini L, Farinella E, Giustozzi G, Sciannameo F: [Minimally invasive treatment of synchronous colorectal tumours]. Chir Ital; 2008 Mar-Apr;60(2):237-41
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  • [Transliterated title] Trattamento mini-invasivo delle neoplasie sincrone del colon-retto.
  • In patients with colorectal cancers synchronous neoplastic lesions are an increasingly frequent finding at preoperative staging; 3% of the cases are other cancers while 33-35% of the synchronous lesions are villous adenomas.
  • The treatment of most colorectal adenomas can be performed by endoscopic poplypectomy.
  • Surgical timing involved performing a sequential exeresis characterised by a cancer resection, followed by resection of the voluminous adenoma: TEM for rectal cancer followed by a laparoscopic right hemicolectomy with an extracorporeal anastomosis for a voluminous villous adenoma (1 patient) and laparoscopic right hemicolectomy with an extracorporeal anastomosis for cancer followed by TEM for a voluminous villous adenoma (2 patients).
  • One patient with left colon cancer associated with a voluminous villous rectal adenoma first underwent TEM for the rectal adenoma and then a left laparoscopic hemicolectomy with an extracorporeal anastomosis in order to ease the transit of the circular mechanical stapler.
  • Another patient with rectal and right colon adenomas first underwent TEM for a voluminous rectal sessile adenoma and later a right hemicolectomy.
  • [MeSH-major] Adenoma / surgery. Colectomy / methods. Colorectal Neoplasms / surgery. Laparoscopy. Microsurgery

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  • (PMID = 18689172.001).
  • [ISSN] 0009-4773
  • [Journal-full-title] Chirurgia italiana
  • [ISO-abbreviation] Chir Ital
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
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43. Coppola D, Parikh V, Boulware D, Blanck G: Substantially reduced expression of PIAS1 is associated with colon cancer development. J Cancer Res Clin Oncol; 2009 Sep;135(9):1287-91
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  • [Title] Substantially reduced expression of PIAS1 is associated with colon cancer development.
  • This project was designed to assess PIAS1 expression in colon cancer.
  • METHODS: To determine whether PIAS1, one of the PIAS family members, or IFN-gamma signaling pathway components could be used to stratify colon tumors, we stained tissue microarrays for PIAS1, interferon regulatory factor-1 (IRF-1) and STAT1alpha.
  • RESULTS: PIAS1 staining of the colon cancer tissue microarrays indicated a strong correlation of normal colon cells, and adenomas, with high expression of both PIAS1 and IRF-1.
  • CONCLUSION: The PIAS1 results in particular may represent a basis for new approaches for efficiently distinguishing adenomas from colon cancer.
  • [MeSH-major] Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Disease Progression. Down-Regulation. Protein Inhibitors of Activated STAT / biosynthesis. Protein Inhibitors of Activated STAT / deficiency. Small Ubiquitin-Related Modifier Proteins / biosynthesis. Small Ubiquitin-Related Modifier Proteins / deficiency

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  • (PMID = 19288270.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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44. Durno CA: Colonic polyps in children and adolescents. Can J Gastroenterol; 2007 Apr;21(4):233-9
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  • [Title] Colonic polyps in children and adolescents.
  • Colonic polyps most commonly present with rectal bleeding in children.
  • The isolated juvenile polyp is the most frequent kind of polyp identified in children.
  • 'Juvenile' refers to the histological type of polyp and not the age of onset of the polyp.
  • Adolescents and adults with multiple juvenile polyps are at a significant risk of intestinal cancer.
  • Attenuated familial adenamatous polyposis (AFAP) can occur either by a mutation at the extreme ends of the adenomatous polyposis coli gene or by biallelic mutations in the mutY homologue (MYH) gene.
  • Colonic polyps, including isolated juvenile polyps, juvenile polyposis syndrome, FAP, AFAP and MYH-associated polyposis, are discussed in the present review.
  • [MeSH-major] Colonic Polyps
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / pathology. Adolescent. Child. DNA Glycosylases / genetics. Genes, APC. Genetic Counseling. Genetic Predisposition to Disease. Genetic Testing. Humans. Mutation

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  • (PMID = 17431512.001).
  • [ISSN] 0835-7900
  • [Journal-full-title] Canadian journal of gastroenterology = Journal canadien de gastroenterologie
  • [ISO-abbreviation] Can. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Canada
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
  • [Number-of-references] 47
  • [Other-IDs] NLM/ PMC2657698
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45. Fernández-Suárez A, Cordero Fernández C, García Lozano R, Pizarro A, Garzón M, Núñez Roldán A: Clinical and ethical implications of genetic counselling in familial adenomatous polyposis. Rev Esp Enferm Dig; 2005 Sep;97(9):654-65
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  • [Title] Clinical and ethical implications of genetic counselling in familial adenomatous polyposis.
  • The association of specific genetic disturbances with the development of hereditary cancer helps us to understand the risk of suffering from it, the possibility of an earlier diagnosis, and the treatment and prevention of this disease.
  • Familial adenomatous polyposis (FAP) is a pre-neoplastic syndrome characterized by the presence of hundreds of adenomatous polyps in the colon, which develop into a carcinoma.
  • FAP can be diagnosed using sequencing techniques to detect mutations in the germinal line of the APC (adenomatous polyposis coli) gene.
  • [MeSH-major] Adenomatous Polyposis Coli / prevention & control. Genetic Counseling


46. Pickhardt PJ, Schumacher C, Kim DH: Polyp detection at 3-dimensional endoluminal computed tomography colonography: sensitivity of one-way fly-through at 120 degrees field-of-view angle. J Comput Assist Tomogr; 2009 Jul-Aug;33(4):631-5
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  • [Title] Polyp detection at 3-dimensional endoluminal computed tomography colonography: sensitivity of one-way fly-through at 120 degrees field-of-view angle.
  • PURPOSE: To investigate whether increasing the visual field-of-view (FOV) angle at 3-dimensional (3D) endoluminal computed tomography colonography (CTC) from 90 degrees to 120 degrees allows for single pass fly-through examination of the supine and prone views without sacrificing polyp detection.
  • METHODS: Primary 3D endoluminal CTC evaluation using a 120 degree FOV was performed by 2 experienced radiologists on 73 patients harboring 104 colonoscopy-proven polyps measuring 6 mm or larger.
  • RESULTS: All 104 (100%) polyps were detectable with the single-pass 3D evaluation on either the retrograde supine or antegrade prone fly-through, with 86 (82.7%) of 104 polyps seen on both fly-through views.
  • Of the 18 polyps detected on only one of the two 3D endoluminal passes (10 prone, 8 supine), 13 were either submerged under fluid (n = 12) or within a collapsed segment (n = 1); therefore, these were also undetectable on the corresponding 90 degrees bidirectional fly-through.
  • The remaining 5 (4.8%) polyps were located behind a fold, but these polyps were all detectable on the other fly-through in the reverse direction.
  • CONCLUSIONS: Increasing the visual FOV angle to 120 degrees allows for a decrease in the total number of supine and prone 3D endoluminal fly-through passes from 4 to 2 without negatively impacting overall polyp detection.
  • [MeSH-major] Adenocarcinoma / radiography. Adenomatous Polyps / radiography. Colonic Neoplasms / radiography. Colonic Polyps / radiography. Colonography, Computed Tomographic / methods. Imaging, Three-Dimensional / methods. Radiographic Image Enhancement / methods
  • [MeSH-minor] Cohort Studies. Colon / radiography. Contrast Media. Female. Humans. Male. Middle Aged. Observer Variation. Posture. Retrospective Studies. Sensitivity and Specificity

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  • (PMID = 19638863.001).
  • [ISSN] 1532-3145
  • [Journal-full-title] Journal of computer assisted tomography
  • [ISO-abbreviation] J Comput Assist Tomogr
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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47. Siddiqui AA, Nazario H, Mahgoub A, Pandove S, Cipher D, Spechler SJ: The long-term use of statins is associated with a decreased incidence of adenomatous colon polyps. Digestion; 2009;79(1):17-22
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  • [Title] The long-term use of statins is associated with a decreased incidence of adenomatous colon polyps.
  • BACKGROUND/AIMS: Studies have suggested that statins may protect against colorectal cancer (CRC), but it is not clear whether that protection results from effects on established adenomatous polyps (APs) or from preventing the development of new APs.
  • Statin use was associated with a smaller mean number of polyps (2.6 vs. 3.1; p = 0.002), a smaller mean polyp size (7.1 vs. 7.9 mm; p = 0.03) and a significant reduction in the incidence of advanced APs (OR 0.74, 95% CI 0.52-0.96; p = 0.03).
  • [MeSH-major] Adenomatous Polyps / epidemiology. Colonic Polyps / epidemiology. Colorectal Neoplasms / epidemiology. Hydroxymethylglutaryl-CoA Reductase Inhibitors / administration & dosage

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  • (PMID = 19246916.001).
  • [ISSN] 1421-9867
  • [Journal-full-title] Digestion
  • [ISO-abbreviation] Digestion
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors
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48. Fujiya M, Moriichi K, Saitoh Y, Watari J, Kohgo Y: Endoscopic piecemeal resection is a practical option to cure colorectal tumors. Dig Endosc; 2009 Jul;21 Suppl 1:S28-30
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  • Endoscopic mucosal resection (EMR) and endoscopic piecemeal resection (EPMR) are therapeutic options widely accepted for the treatment of colon adenoma, intramucosal cancer and minimally invasive submucosal cancer.
  • [MeSH-major] Adenoma / surgery. Colonoscopy / methods. Colorectal Neoplasms / surgery. Intestinal Mucosa / surgery

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  • (PMID = 19691729.001).
  • [ISSN] 1443-1661
  • [Journal-full-title] Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society
  • [ISO-abbreviation] Dig Endosc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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49. Ye YN, Wu WK, Shin VY, Bruce IC, Wong BC, Cho CH: Dual inhibition of 5-LOX and COX-2 suppresses colon cancer formation promoted by cigarette smoke. Carcinogenesis; 2005 Apr;26(4):827-34
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  • [Title] Dual inhibition of 5-LOX and COX-2 suppresses colon cancer formation promoted by cigarette smoke.
  • Previous studies indicate that the arachidonic acid-metabolizing enzymes COX-2 and 5-LOX are overexpressed during the process of colonic adenoma formation promoted by cigarette smoke.
  • The aims of the present study were to investigate whether there exists a relationship between COX-2 and 5-LOX, and whether dual inhibition of COX-2 and 5-LOX has an anticarcinogenic effect in the colonic tumorigenesis promoted by cigarette smoke.
  • Results showed that pretreating colon cancer cells with cigarette smoke extract (CSE) promoted colon cancer growth in the nude mouse xenograft model.
  • In an in vitro study, we found that the action of CSE on colon cancer cells was mediated by 5-LOX DNA demethylation.
  • In summary, these results indicate that inhibition of COX-2 may lead to a shunt of arachidonic acid metabolism towards the leukotriene pathway during colonic tumorigenesis promoted by CSE.
  • [MeSH-major] Adenocarcinoma / prevention & control. Colonic Neoplasms / prevention & control. Cyclooxygenase Inhibitors / therapeutic use. Lipoxygenase Inhibitors / therapeutic use. Prostaglandin-Endoperoxide Synthases / drug effects

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  • (PMID = 15637091.001).
  • [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 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Lipoxygenase Inhibitors; 0 / RNA, Messenger; 0 / Smoke; 1HGW4DR56D / Leukotriene B4; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; K7Q1JQR04M / Dinoprostone
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50. Qasim A, Muldoon C, McKiernan S: Colonic adenoma patients have higher incidence of hyperplastic polyps on surveillance colonoscopy. Eur J Gastroenterol Hepatol; 2009 Aug;21(8):877-81
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  • [Title] Colonic adenoma patients have higher incidence of hyperplastic polyps on surveillance colonoscopy.
  • OBJECTIVES: To determine the incidence of hyperplastic polyps in patients undergoing surveillance colonoscopy and to compare with the prevalence in individuals undergoing index colonoscopy.
  • PATIENTS AND METHODS: This prospective observational study included patients with index colonoscopy findings of adenomas, adenoma with concomitant hyperplastic polyps and advanced neoplasia who subsequently underwent surveillance colonoscopy.
  • On index colonoscopy, adenomas, adenoma with concomitant hyperplastic polyps and advanced neoplasia were present in 61, 35 and 12 patients, respectively.
  • Findings on surveillance examination included hyperplastic polyps in 35 and 57% of patients with past adenomas and adenoma with concomitant hyperplastic polyps, respectively.
  • Hyperplastic polyps, adenomas and advanced neoplasia were found in 155 (4%), 388 (10%) and 60 (1.5%) of patients, respectively.
  • Hyperplastic polyps and adenoma were significantly higher in study group as compared with control group (P >0.5).
  • CONCLUSION: Incidence of hyperplastic polyps is significantly higher on surveillance colonoscopy as compared with the prevalence on index colonoscopy.
  • This may signify a continuous spectrum of biological evolution between hyperplastic polyps and adenomas.
  • [MeSH-major] Adenoma / pathology. Colonic Polyps / pathology. Colonoscopy / methods. Colorectal Neoplasms / pathology


51. du Toit J, Hamilton W, Barraclough K: Risk in primary care of colorectal cancer from new onset rectal bleeding: 10 year prospective study. BMJ; 2006 Jul 8;333(7558):69-70
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  • OBJECTIVE: To measure the risk of colorectal cancer and adenoma with new onset rectal bleeding reported to primary care.
  • MAIN OUTCOME MEASURES: Percentage of participants in whom colorectal cancer or colonic adenoma was identified after investigation of the bowel.
  • Of these, 15 (5.7%, 95% confidence interval 3.2% to 9.2%) had colorectal cancer, and 13 (4.9%, 2.6% to 8.4%) had colonic adenoma.
  • CONCLUSIONS: One in 10 patients aged 45 or more with new onset rectal bleeding had colonic neoplasia, so investigation of the bowel should be offered to all such patients, whether or not they have other symptoms.
  • [MeSH-major] Adenoma / etiology. Colorectal Neoplasms / etiology. Gastrointestinal Hemorrhage / etiology. Rectal Diseases / etiology


52. Gurudu SR, Heigh RI, De Petris G, Heigh EG, Leighton JA, Pasha SF, Malagon IB, Das A: Sessile serrated adenomas: demographic, endoscopic and pathological characteristics. World J Gastroenterol; 2010 Jul 21;16(27):3402-5
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  • [Title] Sessile serrated adenomas: demographic, endoscopic and pathological characteristics.
  • AIM: To study the demographic and endoscopic characteristics of patients with sessile serrated adenoma (SSA) in a single center.
  • A retrospective chart review was performed to extract data on demographics, polyp characteristics, presence of synchronous adenomatous polyps or cancer, polypectomy methods, and related complications.
  • Fifty-one per cent of SSAs were located in the cecum or ascending colon.
  • Approximately half of the patients had synchronous polyps of other histological types, including hyperplastic and adenomatous polyps.
  • Ninety-seven percent of polyps were removed by colonoscopy.
  • CONCLUSION: Among patients with colon polyps, 2.9% were found to have SSAs.
  • [MeSH-major] Adenoma / pathology. Colorectal Neoplasms / pathology. Polyps / pathology

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  • (PMID = 20632442.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
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53. García-Faroldi G, Sánchez-Jiménez F, Fajardo I: The polyamine and histamine metabolic interplay in cancer and chronic inflammation. Curr Opin Clin Nutr Metab Care; 2009 Jan;12(1):59-65
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  • RECENT FINDINGS: The most recent and relevant findings that might reflect a link between the polyamines/histamine metabolic interplay and the development of cancer and chronic inflammation-related diseases include: the observation that histamine catabolism is downregulated in the colonic mucosa of patients with colonic adenoma; the finding that some polyamine and histamine-related metabolites are different between a breast cancer cell line and a reference mammary epithelial cell line; and the demonstration of the critical role that mast cells (a cell type in which the polyamine/histamine metabolic interplay has been confirmed) play in the development of pancreatic tumors.
  • There is still, however, a lack of specific studies elucidating the exact contribution of the polyamine/histamine metabolic interplay in these clinical settings.

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  • (PMID = 19057189.001).
  • [ISSN] 1473-6519
  • [Journal-full-title] Current opinion in clinical nutrition and metabolic care
  • [ISO-abbreviation] Curr Opin Clin Nutr Metab Care
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Polyamines; 7LP2MPO46S / S-Adenosylmethionine; 820484N8I3 / Histamine
  • [Number-of-references] 64
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54. Tabuchi M, Kitayama J, Nagawa H: Hypertriglyceridemia is positively correlated with the development of colorectal tubular adenoma in Japanese men. World J Gastroenterol; 2006 Feb 28;12(8):1261-4
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  • [Title] Hypertriglyceridemia is positively correlated with the development of colorectal tubular adenoma in Japanese men.
  • AIM: To determine the real association between serum lipid levels and colonic polyp formation.
  • METHODS: We performed a large scale retrospective study to analyze the correlation between the incidence of colorectal adenoma or carcinoma and the fasting serum levels of total cholesterol (TC) and triglycerides (TG) in patients who underwent total colonoscopy for screening for colon cancer.
  • RESULTS: Both levels were significantly elevated in patients with adenomas as compared with patients without any neoplastic lesion (TC 207.6+/-29.5 vs 199.5+/-34.3, n=4883, P<0.001; TG 135.0+/-82.2 vs 108.7+/-71.5, n=4874, P<0.001).
  • The difference was significant in patients with tubular adenoma but not in those with villous or serrated adenoma.
  • The level of TG in patients with invasive carcinoma did not show a significant elevation from that in patients with adenoma.
  • These findings suggest that hypertriglyceridemia is an independent risk factor for colonic adenoma in men.
  • [MeSH-major] Adenoma / blood. Adenoma / etiology. Colorectal Neoplasms / blood. Colorectal Neoplasms / etiology. Hypertriglyceridemia / complications

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  • [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
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55. Phelps RA, Chidester S, Dehghanizadeh S, Phelps J, Sandoval IT, Rai K, Broadbent T, Sarkar S, Burt RW, Jones DA: A two-step model for colon adenoma initiation and progression caused by APC loss. Cell; 2009 May 15;137(4):623-34
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  • [Title] A two-step model for colon adenoma initiation and progression caused by APC loss.
  • Aberrant Wnt/beta-catenin signaling following loss of the tumor suppressor adenomatous polyposis coli (APC) is thought to initiate colon adenoma formation.
  • These findings suggest that, following APC loss, CtBP1 contributes to adenoma initiation as a first step, whereas KRAS activation and beta-catenin nuclear localization promote adenoma progression to carcinomas as a second step.
  • Consistent with this model, human FAP adenomas showed robust upregulation of CtBP1 in the absence of detectable nuclear beta-catenin, whereas nuclear beta-catenin was detected in carcinomas.

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  • (PMID = 19450512.001).
  • [ISSN] 1097-4172
  • [Journal-full-title] Cell
  • [ISO-abbreviation] Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA073992; United States / NCI NIH HHS / CA / CA116468-03; United States / NCI NIH HHS / CA / CA073992-06A10003; United States / NCI NIH HHS / CA / R01 CA116468-03; United States / NCI NIH HHS / CA / CA96934; United States / NCI NIH HHS / CA / P01 CA073992-06A10003; United States / NCI NIH HHS / CA / R01 CA116468; United States / NCI NIH HHS / CA / P01 CA073992; United States / NCI NIH HHS / CA / CA116468-04; United States / NCI NIH HHS / CA / CA042014; United States / NCI NIH HHS / CA / P30 CA042014; United States / NCI NIH HHS / CA / R01 CA116468-04
  • [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 / Adenomatous Polyposis Coli Protein; 0 / DNA-Binding Proteins; 0 / Peptide Fragments; 0 / Rac1 GTP-binding protein (17-32); 0 / beta Catenin; EC 1.1.- / Alcohol Oxidoreductases; EC 1.1.1.- / C-terminal binding protein; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf; EC 3.6.5.2 / rac1 GTP-Binding Protein; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS102940; NLM/ PMC2706149
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56. Wei HJ, Guo ZY, Xie SS, He BH, Li LB, Chen XM, Wu GY, Lu JJ: [Colon adenoma detection using Kubelka-Munk spectral function of DNA and protein bands]. Guang Pu Xue Yu Guang Pu Fen Xi; 2009 Jun;29(6):1473-7
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  • [Title] [Colon adenoma detection using Kubelka-Munk spectral function of DNA and protein bands].
  • Differential diagnosis of human colon adenoma was studied using the Kubelka-Munk spectral function of the DNA and protein absorption bands at 260 and 280 nm in vitro.
  • The results of measurement showed that for the spectral range from 590 to 1 064 nm pathological changes of colon epithelial tissues were induced so that there were significant differences in the averaged values of the Kubelka-Munk function f(r infinity) and logarithmic Kubelka-Munk function log [f(r infinity)] of the DNA absorption bands at 260 nm between normal and adenomatous colon epithelial tissues, and the differences were 218% (p < 0.05) and 68.5% (p < 0.05) respectively.
  • Pathological changes of colon epithelial tissues were induced so that there were significant differences in the averaged values of the Kubelka-Munk function f(r infinity) and logarithmic Kubelka-Munk function log [f(r infinity)] of the protein absorption bands at 280 nm between normal and adenomatous colon epithelial tissues, and the differences were 208% (p < 0.05) and 59.0% (p < 0.05) respectively.
  • Pathological changes of colon epithelial tissues were induced so that there were significant differences in the averaged values of the Kubelka-Munk function f(r infinity) and logarithmic Kubelka-Munk function log [f(r infinity)] of the beta-carotene absorption bands at 480 nm between normal and adenomatous colon epithelial tissues, and the differences were 41.7% (p < 0.05) and 32.9% (p < 0.05) respectively.
  • Obviously, pathological changes of colon epithelial tissues were induced so that there were significant changes in the contents of the DNA, protein and beta-carotene of colon epithelial tissues.
  • The conclusion can be applied to rapid, low-cost and noninvasive optical biopsy of colon adenoma, and provides a useful reference.
  • [MeSH-major] Adenoma / diagnosis. Colonic Neoplasms / diagnosis. DNA / chemistry. Proteins / chemistry. Spectrum Analysis

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  • (PMID = 19810511.001).
  • [ISSN] 1000-0593
  • [Journal-full-title] Guang pu xue yu guang pu fen xi = Guang pu
  • [ISO-abbreviation] Guang Pu Xue Yu Guang Pu Fen Xi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Proteins; 9007-49-2 / DNA
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57. Oh SJ, Lee SJ, Lee HY, Paik YH, Lee DK, Lee KS, Chung JB, Yu JS, Yoon DS: [Extrapancreatic tumors in intraductal papillary mucinous neoplasm of the pancreas]. Korean J Gastroenterol; 2009 Sep;54(3):162-6
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  • As benign tumor, there were two gallbladder adenoma, one gastric adenoma, one colonic adenoma and one benign ovarian cystic neoplasm, respectively.

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  • [CommentIn] Korean J Gastroenterol. 2009 Sep;54(3):196-8 [19844158.001]
  • (PMID = 19844152.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
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58. Burke CA: Colonic complications of obesity. Gastroenterol Clin North Am; 2010 Mar;39(1):47-55
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  • [Title] Colonic complications of obesity.
  • Obesity is a risk factor for colorectal cancer and adenomatous polyps.
  • The increased prevalence of neoplasia coupled with the observation that obesity may be associated with a suboptimal bowel preparation may diminish the adequate detection of adenomas for obese who undergo colonoscopy.
  • The colonic complications of obesity are reviewed in this article.
  • [MeSH-major] Colonic Diseases / etiology. Obesity / complications
  • [MeSH-minor] Adenoma / epidemiology. Animals. Body Mass Index. Colonoscopy. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms / physiopathology. Comorbidity. Diverticulitis, Colonic / epidemiology. Humans. Insulin Resistance / physiology. Intra-Abdominal Fat / physiopathology. Leptin / physiology. Metabolic Syndrome X / epidemiology. Metabolic Syndrome X / physiopathology

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20202578.001).
  • [ISSN] 1558-1942
  • [Journal-full-title] Gastroenterology clinics of North America
  • [ISO-abbreviation] Gastroenterol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Leptin
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59. Khatibzadeh N, Ziaee SA, Rahbar N, Molanie S, Arefian L, Fanaie SA: The indirect role of site distribution in high-grade dysplasia in adenomatous colorectal polyps. J Cancer Res Ther; 2005 Oct-Dec;1(4):204-7
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  • [Title] The indirect role of site distribution in high-grade dysplasia in adenomatous colorectal polyps.
  • BACKGROUND: The appropriate application of Endoscopic modalities for polypectomy depends on the likelihood that the adenoma in question harbors invasive cancer.
  • While prior studies have evaluated polyp size and morphology in assessing the risk of malignancy, in recent decay some authorities have paid more attention to dysplasia.
  • All in all, the relative risk of cancer based on polyp distribution in correlation with dysplasia has not been statistically studied which is done in our study.
  • METHODS AND MATERIALS: Between June 2001 and March 2004, the distribution of 130 adenomatous polyps was compared with synchronous invasive or in situ cancer.
  • Factors such as Patient age, Patients gender, location of lesion, size of polyp, histological subtype of adenoma on biopsy, degree of dysplasia, synchronous cancer, color of polyp, and number of polyps were included in the data collection.
  • CONCLUSION: Lesions greater than 1 cm in diameter with high-grade dysplasia after splenic flexure should be managed as presumptive malignancies with segmental colon resection.
  • [MeSH-major] Adenomatous Polyps / pathology. Colorectal Neoplasms / pathology

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  • (PMID = 17998654.001).
  • [ISSN] 1998-4138
  • [Journal-full-title] Journal of cancer research and therapeutics
  • [ISO-abbreviation] J Cancer Res Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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60. Kita H, Hikichi Y, Hikami K, Tsuneyama K, Cui ZG, Osawa H, Ohnishi H, Mutoh H, Hoshino H, Bowlus CL, Yamamoto H, Sugano K: Differential gene expression between flat adenoma and normal mucosa in the colon in a microarray analysis. J Gastroenterol; 2006 Nov;41(11):1053-63
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  • [Title] Differential gene expression between flat adenoma and normal mucosa in the colon in a microarray analysis.
  • BACKGROUND: Flat adenomas in the colon are associated with a relatively higher potential for malignancy.
  • Distinct genes may be involved in the development of flat adenoma.
  • The aim of this study was to profile gene expression changes in flat adenomas in the colon.
  • METHODS: A genomewide expression analysis was carried out by using flat adenoma and adjacent normal mucosa in the colon to detect differences in gene expression.
  • Because the right and left colon have different embryonic origins, each sample was classified according to its location, and the gene expression levels between flat adenoma and adjacent normal mucosa were also compared among samples derived from the right or left colon.
  • RESULTS: A total of 180 genes were differentially expressed between flat adenoma and normal mucosa in the colon, including matrix metalloproteinase 7 (MMP7), cadherin 3 (CDH3), S100P, and dual oxidase 2 (DUOX2).
  • In addition, a total of 89 and 49 genes were differentially expressed between flat adenoma and normal mucosa among the samples from the right and left colon, respectively.
  • CONCLUSIONS: This is the first report characterizing the genes differentially expressed in flat adenomas using a microarray analysis.
  • Considerable differences in the gene expression profiles of flat adenomas also exist between the right and left colon.
  • These data should lead to new insights into the pathogenesis of flat adenomas in the colon as well as to new therapeutic strategies.
  • [MeSH-major] Adenoma / genetics. Biomarkers, Tumor / genetics. Colonic Neoplasms / genetics. DNA, Neoplasm / genetics. Gene Expression Regulation, Neoplastic. Intestinal Mucosa / metabolism. Oligonucleotide Array Sequence Analysis / methods

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  • (PMID = 17160516.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Calcium-Binding Proteins; 0 / DNA, Neoplasm; 0 / Flavoproteins; 0 / Neoplasm Proteins; 0 / S100P protein, human; EC 1.6.3.1 / DUOX2 protein, human; EC 1.6.3.1 / NADPH Oxidase; EC 3.4.24.23 / Matrix Metalloproteinase 7
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61. Watanabe M, Tsunoda A, Narita K, Kusano M, Miwa M: Colonic tattooing using fluorescence imaging with light-emitting diode-activated indocyanine green: a feasibility study. Surg Today; 2009;39(3):214-8
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  • [Title] Colonic tattooing using fluorescence imaging with light-emitting diode-activated indocyanine green: a feasibility study.
  • METHODS: Indocyanine green injections were given to patients undergoing preoperative colonoscopy for early colon cancer or colon adenoma.
  • During subsequent laparotomy, the colon was first observed with the naked eye, and then using a prototype machine with a charge-coupled device (CCD) video camera equipped with a cutoff filter and a LED at a wavelength of 760 nm as the light source.
  • CONCLUSIONS: Colonic tattooing using this fluorescence imaging technique of LED-activated ICG fluorescence is a new concept of colonic marking based on the characteristics that ICG is a near infrared fluorescent dye, and is useful, without any adverse effects, to identify perioperatively the tumor localization.
  • [MeSH-major] Colonic Neoplasms / diagnosis. Fluorescent Dyes. Indocyanine Green. Tattooing / methods

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  • (PMID = 19280280.001).
  • [ISSN] 1436-2813
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Fluorescent Dyes; IX6J1063HV / Indocyanine Green
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62. Ivanov D, Toyonaga T: The first case of endoscopic submucosal dissection of cecal adenoma in Serbia. Med Pregl; 2009 Jan-Feb;62(1-2):27-30
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  • [Title] The first case of endoscopic submucosal dissection of cecal adenoma in Serbia.
  • In 2006, we performed a colonic ESD in Serbia.
  • The adenoma was removed en bloc and prepared for further histopathological examination.
  • Histopathological examination showed that the tumor was a "flat adenoma" of the colon mucosa with a low grade dysplasia.
  • [MeSH-major] Adenoma / surgery. Cecal Neoplasms / surgery. Colonoscopy

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  • (PMID = 19514597.001).
  • [ISSN] 0025-8105
  • [Journal-full-title] Medicinski pregled
  • [ISO-abbreviation] Med. Pregl.
  • [Language] eng; srp
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Serbia
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63. Cholongitas E, Pipili C, Dasenaki M, Plexousakis E, Delibaltadakis G: Is diabetes mellitus or obesity a more important risk factor for colonic adenoma? Am J Gastroenterol; 2007 Mar;102(3):692
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is diabetes mellitus or obesity a more important risk factor for colonic adenoma?
  • [MeSH-major] Adenoma / etiology. Colonic Neoplasms / etiology. Diabetes Complications / complications. Obesity / complications


64. 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.
  • Future studies in a larger number of patients are needed to evaluate the relationship of histopathological features of colonic polyps and detectability of these lesions by FDG-PET.
  • [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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65. Kahveci A, Ari E, Arikan H, Koc M, Tuglular S, Ozener C: Streptococcus bovis bacteremia related to colon adenoma in a chronic hemodialysis patient. Hemodial Int; 2010 Jan;14(1):91-3
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  • [Title] Streptococcus bovis bacteremia related to colon adenoma in a chronic hemodialysis patient.
  • Abstract We report the case of a 54-year-old hemodialysis patient who presented with recurrent fever due to Streptococcus bovis bacteremia related to colonic tubulovillous adenoma.
  • In this paper, we discussed the relation between S. bovis bacteremia, colonic adenomas, and hemodialysis.
  • [MeSH-major] Adenoma / microbiology. Bacteremia / etiology. Colonic Neoplasms / microbiology. Kidney Failure, Chronic / therapy. Renal Dialysis / adverse effects. Streptococcal Infections / pathology. Streptococcus bovis / isolation & purification

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  • (PMID = 19758303.001).
  • [ISSN] 1542-4758
  • [Journal-full-title] Hemodialysis international. International Symposium on Home Hemodialysis
  • [ISO-abbreviation] Hemodial Int
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Canada
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66. Nikpour S, Ali Asgari A: Colonoscopic evaluation of minimal rectal bleeding in average-risk patients for colorectal cancer. World J Gastroenterol; 2008 Nov 14;14(42):6536-40
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  • Neoplastic polyps, colorectal carcinoma, and IBD were defined as significant lesions.
  • Significant lesions were found in 121 (30.1%) patients, including 26 patients (6.5%) with adenocarcinoma and 30 (7.5%) with adenomatous polyps.
  • Almost all patients with significant lesions had at least one lesion in the distal colon; an adenocarcinoma and an adenomatous polyp in the proximal colon were found in 2 patients with hemorrhoids.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenomatous Polyps / diagnosis. Colonic Polyps / diagnosis. Colonoscopy. Colorectal Neoplasms / diagnosis. Hemorrhage / etiology


67. Johnson CC, Hayes RB, Schoen RE, Gunter MJ, Huang WY, PLCO Trial Team: Non-steroidal anti-inflammatory drug use and colorectal polyps in the Prostate, Lung, Colorectal, And Ovarian Cancer Screening Trial. Am J Gastroenterol; 2010 Dec;105(12):2646-55
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  • [Title] Non-steroidal anti-inflammatory drug use and colorectal polyps in the Prostate, Lung, Colorectal, And Ovarian Cancer Screening Trial.
  • OBJECTIVES: Non-steroidal anti-inflammatory drugs (NSAIDs) have been documented in animal and human studies to reduce risk for colorectal cancer and adenomatous polyps, but risk modification for subgroups of the population and effects on hyperplastic polyps have been less studied.
  • Follow-up of detected polyps was accomplished outside the Trial setting and relevant records were sought and abstracted.
  • Cases (n=4,017) included subjects with a biopsy-proven polyp in the left side of the colon (descending colon, sigmoid, and rectum) detected as a consequence of PLCO screening; controls (n=38,396) were subjects with no left-sided colon polyp.
  • RESULTS: Regular use of aspirin (≥ 4 times/month) in the past year was inversely associated with hyperplastic polyps (odds ratios (OR)=0.8, 95% confidence interval (CI)=0.7-0.9), adenomatous polyps (OR=0.8, 95% CI=0.8-0.9), and advanced adenomas (OR=0.8, 95% CI=0.7-0.9).
  • As frequency of aspirin use increased, the prevalence of polyps decreased significantly for each histological classification (P for trend ≤ 0.0004).
  • Similar patterns were found for adenomas and ibuprofen.
  • Overall protection was consistent in both the descending colon or sigmoid and the rectum, but more evident in males.
  • CONCLUSIONS: This study of a large general risk population supports previous work that recent use of aspirin and ibuprofen is associated with a decreased risk of colorectal adenomas and demonstrates that this protective effect may be stronger in certain population subgroups and is also evident for aspirin and hyperplastic polyps.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Colonic Polyps / prevention & control. Ibuprofen / therapeutic use

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  • (PMID = 20808298.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / N01 CN25522; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; R16CO5Y76E / Aspirin; WK2XYI10QM / Ibuprofen
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68. Hao CY, Moore DH, Wong P, Bennington JL, Lee NM, Chen LC: Alteration of gene expression in macroscopically normal colonic mucosa from individuals with a family history of sporadic colon cancer. Clin Cancer Res; 2005 Feb 15;11(4):1400-7
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  • [Title] Alteration of gene expression in macroscopically normal colonic mucosa from individuals with a family history of sporadic colon cancer.
  • PURPOSE: We have shown that the expression of several genes associated with human colon cancer is altered in the morphologically normal colonic mucosa (MNCM) of APC(min) mice and humans with colon cancers.
  • To determine whether these alterations also occur in the MNCM of individuals who have not developed colon cancer but are at high risk of doing so, we measured gene expression in the MNCM of individuals with a family history of colon cancer.
  • METHODS: Expression of 16 genes in the MNCM of 12 individuals with a first-degree relative with sporadic colon cancer and 16 normal controls were measured by quantitative reverse transcription-PCR.
  • Biopsy samples of MNCM were obtained from the ascending, transverse, descending, and rectosigmoid regions of the colon (2-8 biopsy samples were obtained from each region).
  • RESULTS: Relative to normal controls, the expression of several genes, including PPAR-gamma, SAA1, and IL-8 were significantly altered in the macroscopically normal rectosigmoid mucosa from individuals with a family history of colon cancer.
  • CONCLUSIONS: Molecular abnormalities that precede the appearance of adenomatous polyp are present in the MNCM of individuals who have a family history of colon cancer.
  • This observation raises the possibility of screening for individuals who are at an increased risk of developing colon cancer by analysis of gene expression in rectosigmoid biopsy samples.
  • To assess this possibility, prospective studies will be needed to determine whether or not altered gene expression is associated with the subsequent development of adenomatous polyps and/ or colonic carcinomas.
  • [MeSH-major] Colon / metabolism. Colonic Neoplasms / genetics. Gene Expression / genetics. Intestinal Mucosa / metabolism

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  • (PMID = 15746039.001).
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-8; 0 / Membrane Proteins; 0 / PPAR delta; 0 / PPAR gamma; 0 / Serum Amyloid A Protein; 63231-63-0 / RNA; 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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69. Pulitzer M, Xu R, Suriawinata AA, Waye JD, Harpaz N: Microcarcinoids in large intestinal adenomas. Am J Surg Pathol; 2006 Dec;30(12):1531-6
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  • [Title] Microcarcinoids in large intestinal adenomas.
  • Composite adenoma-carcinoid tumors are rare colorectal lesions consisting of intermingled adenomatous and carcinoid components.
  • We present 4 cases of colonic adenomas containing microcarcinoids, a hitherto undescribed lesion that is either a precursor of composite adenoma-carcinoids or a related but independent entity.
  • The cases, identified among our surgical and consultation files, were endoscopically routine sessile polyps removed from 4 otherwise normal individuals, 3 from the cecum and 1 from the distal colon.
  • The microcarcinoids were 0.5 to 1.5 mm in size and situated within the basal lamina propria, where they interposed between the crypts and muscularis mucosae without disturbing the overall polyp architecture.
  • Endocrine differentiation of the microcarcinoids was confirmed by the expression of 3 or more of the following: Grimelius argyrophil, chromogranin, synaptophysin, neuron-specific enolase and somatostatin.
  • The glandular component of the polyps was unremarkable in 3 cases, but 1 polyp, in addition to a microcarcinoid, showed a diffuse pattern of mixed adenomatous-endocrine differentiation.
  • Awareness of microcarcinoids in colonic adenomas should help avert potential diagnostic pitfalls posed by their pleomorphism, basal location, and infiltrative patterns, and may help clarify their natural history and possible relationship to composite glandular-carcinoid tumors.
  • [MeSH-major] Adenoma / pathology. Carcinoid Tumor / pathology. Intestinal Neoplasms / pathology. Intestine, Large / pathology. Neoplasms, Multiple Primary / pathology

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  • (PMID = 17122508.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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70. Benes Z, Antos Z: Optical biopsy system distinguishing between hyperplastic and adenomatous polyps in the colon during colonoscopy. Anticancer Res; 2009 Nov;29(11):4737-9
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  • [Title] Optical biopsy system distinguishing between hyperplastic and adenomatous polyps in the colon during colonoscopy.
  • BACKGROUND: It has been established that the removal of adenomatous colon polyps drastically reduces the incidence of colorectal cancer (CRC), but polypectomy is not without risk.
  • The aim was to determine the correlation between the results of an optical biopsy system and the histopathology report of the physical biopsy specimens of the same polyps removed at colonoscopy.
  • PATIENTS AND METHODS: Paired optical and physical biopsies were performed on 55 polyps with complete polypectomy of the same tissue.
  • RESULTS: Fifty-three adenomatous polyps and two hyperplastic polyps were identified by the hospital pathologist.
  • The optical biopsy system identified 52 polyps as suspect (adenomatous) and 2 as non-suspect (hyperplastic).
  • One villous adenoma could not be optically analyzed due to friability.
  • CONCLUSION: The WavSTAT Optical Biopsy System provides accurate information to the gastroenterologist to assist in distinguishing between hyperplastic and adenomatous polyps.
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Colon / pathology
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / pathology. Adult. Aged. Aged, 80 and over. Biopsy / methods. Colonic Neoplasms / diagnosis. Colonic Neoplasms / pathology. Colonoscopy / methods. Diagnosis, Differential. Humans. Hyperplasia / diagnosis. Middle Aged. Optics and Photonics / methods. Prospective Studies

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  • (PMID = 20032428.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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71. Patel VG, Darko ND, Martin DM, Lyons R, Marantz D: Serrated adenoma of the colon: an under-recognized premalignant variant of adenomatous polyp. Am Surg; 2010 Sep;76(9):E190-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serrated adenoma of the colon: an under-recognized premalignant variant of adenomatous polyp.
  • [MeSH-major] Adenoma / pathology. Adenomatous Polyps / pathology. Colorectal Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Age Distribution. Aged. Aged, 80 and over. Biopsy, Needle. Cohort Studies. Colectomy / methods. Colonic Polyps / epidemiology. Colonic Polyps / pathology. Colonic Polyps / surgery. Female. Humans. Immunohistochemistry. Incidence. Male. Middle Aged. Prognosis. Retrospective Studies. Risk Assessment. Sex Distribution. Survival Analysis. Treatment Outcome

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  • (PMID = 21396285.001).
  • [ISSN] 0003-1348
  • [Journal-full-title] The American surgeon
  • [ISO-abbreviation] Am Surg
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] United States
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72. Jannasch O, Dombrowski F, Lippert H, Meyer F: Rare coincidence of familial adenomatous polyposis and a retroperitoneal fibromyxoid sarcoma: report of a case. Dis Colon Rectum; 2008 Apr;51(4):477-81
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  • [Title] Rare coincidence of familial adenomatous polyposis and a retroperitoneal fibromyxoid sarcoma: report of a case.
  • PURPOSE: Familial adenomatous polyposis is an autosomal-dominant inherited disease with development of as many as thousands of adenomas within colon and rectum.
  • An association of familial adenomatous polyposis and sarcomas was reported in a few cases only.
  • METHODS: We present the exceptional case of a 24-year-old male with genetically verified familial adenomatous polyposis (deletion of 10 base pairs at position 228-237 of exon 15A).
  • CONCLUSIONS: To our knowledge, this is the first reported case of familial adenomatous polyposis with metachronous retroperitoneal fibromyxoid sarcoma.
  • In addition to more common semimalignant retroperitoneal desmoid tumors in familial adenomatous polyposis patients, a malignant soft-tissue tumor also has to be considered for differential diagnosis.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Fibrosarcoma / complications. Retroperitoneal Neoplasms / complications
  • [MeSH-minor] Adult. Anastomosis, Surgical / methods. Colonic Pouches. Colonoscopy. Diagnosis, Differential. Follow-Up Studies. Humans. Laparotomy. Male. Proctocolectomy, Restorative / methods. Rectum / surgery. Time Factors. Tomography, X-Ray Computed

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  • (PMID = 18180996.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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73. Cappell MS: From colonic polyps to colon cancer: pathophysiology, clinical presentation, screening and colonoscopic therapy. Minerva Gastroenterol Dietol; 2007 Dec;53(4):351-73
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  • [Title] From colonic polyps to colon cancer: pathophysiology, clinical presentation, screening and colonoscopic therapy.
  • Colon cancer is the most common nondermatologic cancer in Italy and throughout Europe, with about 250,000 cases annually in Europe, about half of whom die.
  • Yet, colon cancer is largely preventable through intensive, mass screening programs to remove premalignant colonic polyps.
  • Colon cancer mostly arises from adenomas, recognized as colonic polyps, but may occasionally arise from the sessile serrated adenoma.
  • Adenomatous polyposis coli (APC) gene mutation is the key molecular step in adenoma formation.
  • Progression from adenomas to colon cancer is a multistep process, involving mutations of the DCC, k-ras, and p53 genes; loss of heterozygosity in which cells loose one allele of some genes from chromosomal loss; and DNA methylation which can silence DNA expression.
  • Numerous environmental factors can increase the risk of colon cancer, presumably by modulating these molecular pathways.
  • While colon cancer in an advanced and incurable stage often produces clinical findings, premalignant adenomatous polyps and early, highly curable, colon cancer are often asymptomatic.
  • This phenomenon renders adenomas or early cancers difficult to detect by clinical presentation and provides the rationale for mass screening of asymptomatic adults over 50 years old for early detection and prevention of colon cancer.
  • All polyps identified at colonoscopy are removed by colonoscopic polypectomy.
  • Endoscopic mucosal resection is required for deeply penetrating noncancerous polyps.
  • Colonoscopy is repeated every ten years if the index colonoscopy revealed no lesions, but is repeated more frequently if adenomatous polyps were identified at this colonoscopy due to an increased risk of subsequent polyps or colon cancer.
  • Virtual colonoscopy is controversial as a screening test due to widely variable reported RESULTS: Computerized tomography is standardly used to preoperatively detect distant colon cancer metastases, while endosonography is being increasingly used for locoregional staging of rectal cancer.
  • [MeSH-major] Adenoma. Colonic Neoplasms. Colonic Polyps / complications. Colonoscopy
  • [MeSH-minor] Aged. Colon / pathology. Endosonography. Humans. Mass Screening. Middle Aged. Mutation. Neoplasm Staging. Risk Factors. Tomography, X-Ray Computed

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  • (PMID = 18043553.001).
  • [ISSN] 1121-421X
  • [Journal-full-title] Minerva gastroenterologica e dietologica
  • [ISO-abbreviation] Minerva Gastroenterol Dietol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 113
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74. Sztarkier I, Levy I, Walfisch S, Delgado J, Benharroch D: Mantle cell lymphoma in a tubular adenoma: unusual presentation with synchronous colonic carcinoma. Ann Diagn Pathol; 2009 Feb;13(1):47-9
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  • [Title] Mantle cell lymphoma in a tubular adenoma: unusual presentation with synchronous colonic carcinoma.
  • Colonoscopy at this time revealed 3 colonic tubular adenomas.
  • Reassessment of the histology of the colonic polyps and appropriate immunohistochemical stains showed that the lamina propria of one of the tubular adenomas was infiltrated by MCL.
  • Reexamination of the sections taken at the time of the original sigmoidectomy showed MCL in 2 of the regional lymph nodes removed at that time, but no evidence of lymphoma in the colon was found.
  • To our knowledge, this is the fifth reported case of synchronous occurrence of intestinal MCL and colonic carcinoma and the first report of MCL presenting in a tubular adenoma of the colon.
  • [MeSH-minor] Aged, 80 and over. Bone Marrow / pathology. Colonic Polyps / pathology. Humans. Lymph Nodes / pathology. Male

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  • (PMID = 19118782.001).
  • [ISSN] 1532-8198
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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75. Schreibman IR, Baker M, Amos C, McGarrity TJ: The hamartomatous polyposis syndromes: a clinical and molecular review. Am J Gastroenterol; 2005 Feb;100(2):476-90
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  • Familial adenomatous polyposis and hereditary nonpolyposis colon cancer are the two most common heritable colon cancer syndromes.
  • Inherited polyposis syndromes are characterized by the dominant type of polyp (whether adenomatous or hamartomatous) present and by the polyp's location within the gastrointestinal tract.
  • They represent a small but appreciable number of the gastrointestinal inherited cancer predisposition syndromes; it is now known that many of these syndromes carry a substantial risk for developing colon cancer as well as other gastrointestinal and pancreatic cancers.
  • Hereditary mixed polyposis syndrome is a variant of juvenile polyposis characterized by both hamartomatous and adenomatous polyps.
  • The hamartomatous syndromes occur at approximately 1/10th the frequency of the adenomatous syndromes and account for <1% of colorectal cancer in Northern America.
  • [MeSH-major] Intestinal Polyps / genetics. Neoplastic Syndromes, Hereditary
  • [MeSH-minor] Abnormalities, Multiple. Adenomatous Polyposis Coli / diagnosis. Adenomatous Polyposis Coli / genetics. Hamartoma Syndrome, Multiple / diagnosis. Hamartoma Syndrome, Multiple / genetics. Humans. Neurofibromatosis 1 / diagnosis. Neurofibromatosis 1 / genetics. Peutz-Jeghers Syndrome / diagnosis. Peutz-Jeghers Syndrome / genetics. Syndrome

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  • (PMID = 15667510.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 113
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76. Mochizuka A, Uehara T, Nakamura T, Kobayashi Y, Ota H: Hyperplastic polyps and sessile serrated 'adenomas' of the colon and rectum display gastric pyloric differentiation. Histochem Cell Biol; 2007 Nov;128(5):445-55
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  • [Title] Hyperplastic polyps and sessile serrated 'adenomas' of the colon and rectum display gastric pyloric differentiation.
  • The serrated polyp-neoplasia pathway is a novel concept that has been demonstrated to differ from the conventional adenoma-carcinoma pathway.
  • To characterize the phenotypic patterns of differentiation in colorectal serrated polyps, we examined the immunohistochemical expression profile of gastric (MUC5AC, TFF1, MUC6, GlcNAcalpha1 --> 4Gal --> R, and PDX1) and intestinal (MUC2, TFF3, and CDX2) epithelial markers in 15 hyperplastic polyps (HPs), 29 sessile serrated adenomas (SSAs),12 traditional serrated adenomas (TSAs), and 16 conventional adenomas (CAs).
  • The colorectal serrated polyps showed higher expression of gastric makers than CAs.
  • PDX1 up-regulation and CDX2 down-regulation could be important for the induction of a gastric pyloric pattern of cell differentiation in colorectal serrated polyps.
  • [MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Intestinal Polyps / pathology. Pylorus / cytology. Rectal Neoplasms / pathology

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  • (PMID = 17851679.001).
  • [ISSN] 0948-6143
  • [Journal-full-title] Histochemistry and cell biology
  • [ISO-abbreviation] Histochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mucins
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77. Cleary SP, Kim H, Croitoru ME, Redston M, Knight JA, Gallinger S, Gryfe R: Missense polymorphisms in the adenomatous polyposis coli gene and colorectal cancer risk. Dis Colon Rectum; 2008 Oct;51(10):1467-73; discussion 1473-4
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  • [Title] Missense polymorphisms in the adenomatous polyposis coli gene and colorectal cancer risk.
  • PURPOSE: Whereas truncating germline mutations of the adenomatous polyposis coli (APC) gene give rise to familial adenomatous polyposis, missense polymorphisms of APC may confer a weaker risk for colorectal cancer.
  • METHODS: We sequenced the entire open reading frame of the APC gene and tested for two common MYH mutations in a population-based series of patients with colorectal cancer and 5 to 99 adenomas.
  • Missense adenomatous polyposis coli alterations identified in this colorectal cancer multiple-polyp population were analyzed in a population-based series of patients with colorectal cancer and healthy control subjects.
  • RESULTS: Germline APC or mutY human homologue (MYH) alterations were identified in 16 of 39 colorectal cancer-multiple polyp patients.

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  • (PMID = 18612690.001).
  • [ISSN] 1530-0358
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA074783-06; United States / NCI NIH HHS / CA / CA074783-06; United States / NCI NIH HHS / CA / CA074783-07; United States / NCI NIH HHS / CA / U01 CA074783; United States / NCI NIH HHS / CA / U01 CA074783-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS139709; NLM/ PMC2768068
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78. Rock CL: Primary dietary prevention: is the fiber story over? Recent Results Cancer Res; 2007;174:171-7
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  • Among the various dietary factors that have been proposed to affect the risk and progression of colon cancer, dietary fiber has been of greatest interest, due to the effects of fiber on the function of the large bowel.
  • To date, intervention studies testing the relationship between dietary fiber and colon cancer have focused on whether fiber supplementation or diet modification can affect the risk for adenoma recurrence and growth in individuals with a history of adenomatous polyps.
  • In four of these intervention studies, subjects in the intervention arm were prescribed dietary fiber supplements, and beneficial effects on adenoma recurrence were not observed over 3-5 years of follow-up.
  • In a large randomized U.S. study, the Polyp Prevention Trial, the effect of prescribing diet modification (increased fiber and reduced fat intakes) was tested, and no effects on adenoma recurrence were observed, although dietary biomarker data suggest that the change in dietary intakes in the intervention arm was not substantial.

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  • (PMID = 17302194.001).
  • [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
  • [Number-of-references] 32
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79. Xin B, Platzer P, Fink SP, Reese L, Nosrati A, Willson JK, Wilson K, Markowitz S: Colon cancer secreted protein-2 (CCSP-2), a novel candidate serological marker of colon neoplasia. Oncogene; 2005 Jan 20;24(4):724-31
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  • [Title] Colon cancer secreted protein-2 (CCSP-2), a novel candidate serological marker of colon neoplasia.
  • Cancers of the colon and rectum are the second leading cause of cancer death among adult Americans.
  • When detected at early stages, colon cancer is highly curable.
  • The goal of this study was to identify novel serum markers of colon cancers and precancerous colon adenomas as potential candidates for noninvasive detection of early colon neoplasms.
  • Employing expression microarrays, we identified colon cancer secreted protein-2 (CCSP-2) as a novel transcript whose expression is generally absent in normal colon and other normal body tissues, but that is induced an average of 78-fold in Stage II, III, and IV colon cancers, as well as in colon adenomas and colon cancer cell lines.
  • These findings were validated by real-time PCR analysis in an independent panel of colon cancer cases.
  • As a novel secreted protein that is markedly induced in colon adenomas and cancers, CCSP-2 is a novel candidate for development as a diagnostic serum marker of early stage colon cancer.
  • [MeSH-major] Biomarkers, Tumor / blood. Colonic Neoplasms / blood. Colonic Neoplasms / pathology. Transcription Factors / blood

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  • (PMID = 15580307.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30CA43703; United States / NCI NIH HHS / CA / U01CA88130
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / VWA2 protein, human
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80. Cohen M, Thomson M, Taylor C, Donatone J, Quijano G, Drut R: Colonic and duodenal flat adenomas in children with classical familial adenomatous polyposis. Int J Surg Pathol; 2006 Apr;14(2):133-40
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  • [Title] Colonic and duodenal flat adenomas in children with classical familial adenomatous polyposis.
  • Flat adenomas of the colon and duodenum have been described as associating with familial adenomatous polyposis (FAP), its attenuated variant, and the so-called hereditary nonpolyposis colorectal cancer.
  • There seem to be no report on the occurrence of flat adenomas in pediatric patients with family history of FAP.
  • We are reporting 4 children from 2 cancer-prone families in whom colonic and duodenal moderately dysplastic flat adenomas were found.
  • The colonic videoendoscopy showed in 2/3 siblings hundreds of flat or slightly raised plaques less than 1 cm in diameter as well as some classic polyps throughout the colon.
  • The colonic videoendoscopy performed on the 9-year-old boy revealed multiple small sessile polyps.
  • Microscopic study demonstrated tubular adenomas with a few neoplastic crypts, slight disarray of the overall architecture, and moderate (low-grade) dysplasia of the epithelium.
  • These features were more obvious at the center and superficial areas of the adenomas.
  • The 4 children had multiple flat adenomas of the colon and duodenum (2/4) matching with those described in adult patients.
  • Flat adenomas in the context of FAP probably represent early stages of the adenoma development.
  • [MeSH-major] Adenoma / etiology. Adenomatous Polyposis Coli / complications. Colorectal Neoplasms / etiology. Duodenal Neoplasms / etiology. Precancerous Conditions / etiology


81. Tony J, Harish K, Ramachandran TM, Sunilkumar K, Thomas V: Profile of colonic polyps in a southern Indian population. Indian J Gastroenterol; 2007 May-Jun;26(3):127-9
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  • [Title] Profile of colonic polyps in a southern Indian population.
  • BACKGROUND: In Western countries, colonic polyps are usually adenomatous in nature, are evenly distributed along the entire colon in asymptomatic per-sons and show a left-sided predominance in symptomatic patients.
  • Clinical features, colonoscopic description and histologic findings of all patients with polyps were noted.
  • Association of the degree of dysplasia with the size, site and type of polyps and the person's age was assessed.
  • RESULTS: Polyps were seen in 124 (5.1%) of 2412 complete colonoscopies.
  • Mean age of patients with polyps was 58.1 (SD 19.9) years; ninety were men.
  • A majority of polyps (92%) were located in the left colon.
  • They were adenomatous in 99 (79.8%), juvenile in 12 (9.8%), hyperplastic in 11 (8.8 %), inflammatory in 1 (0.8%) and Peutz-Jegher's polyp in 1 (0.8%).
  • Dysplasia was severe in large (>2 cm) polyps compared to small (< 1 cm) ones (p< 0.001).
  • Age of patient and location of polyp had no association with degree of dysplasia.
  • CONCLUSIONS: In southern Indian adults, most colonic polyps are adenomatous and are in the left colon.
  • Large polyps are associated with severe dysplasia.
  • [MeSH-major] Colonic Polyps / epidemiology

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  • (PMID = 17704579.001).
  • [ISSN] 0254-8860
  • [Journal-full-title] Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology
  • [ISO-abbreviation] Indian J Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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82. Tobi M, Kam M, Ullah N, Qureshi K, Yordanova V, Hatfield J, Fligiel SE, Sochacki P, McGarrity T, Cole C, Lawson M, Jacoby R: An anti-adenoma antibody, Adnab-9, may reflect the risk for neoplastic progression in familial hamartomatous polyposis syndromes. Dig Dis Sci; 2008 Mar;53(3):723-9
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  • [Title] An anti-adenoma antibody, Adnab-9, may reflect the risk for neoplastic progression in familial hamartomatous polyposis syndromes.
  • Patients with the hamartomatous polyposis Peutz-Jeghers and familial juvenile polyposis syndromes are predisposed to colorectal cancer but lack early genetic alterations found in adenomatous premalignant lesions.
  • We studied hamartomatous polyps for the expression of an early preneoplastic colorectal neoplasia risk marker also found in familial adenomatous polyposis patients.
  • Retrospective, genetic, and hospital archival tissue immunohistochemistry using Adnab-9, a premalignant marker often found in Paneth-like cells (PCs), was performed on sections of polyps from eight patients with Peutz-Jeghers syndrome, eight patients with familial juvenile polyposis, and 36 hyperplastic polyp control sections.
  • Hamartomatous polyposis patients also underwent specific genetic analysis.
  • Eighty-nine percent of Peutz-Jeghers syndrome polyps labeled with Adnab-9 compared with 63% for AD5; 88% of familial juvenile polyposis sections also labeled with Adnab-9.
  • Of the 36 hyperplastic polyp sections, only four (11%) labeled with Adnab-9 and one (3%) with AD5.
  • Adnab-9 labeling of PCs in the epithelial elements of hamartomatous colonic lesions of hereditary hamartomatous syndrome patients reflects the predisposition to colorectal cancer, further justifying early intervention strategies.
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Antibodies, Monoclonal. Biomarkers, Tumor. Colon / pathology. Colonic Polyps / pathology. Peutz-Jeghers Syndrome / pathology

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  • (PMID = 17934846.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adnab-9; 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / alpha-Defensins; 0 / alpha-defensin 5, human; EC 2.7.1.- / STK11 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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83. Yantiss RK, Oh KY, Chen YT, Redston M, Odze RD: Filiform serrated adenomas: a clinicopathologic and immunophenotypic study of 18 cases. Am J Surg Pathol; 2007 Aug;31(8):1238-45
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  • [Title] Filiform serrated adenomas: a clinicopathologic and immunophenotypic study of 18 cases.
  • In this study, we describe a previously uncharacterized type of adenomatous polyp of the colorectum that shows prominent, thin, elongated projections of neoplastic epithelium with a serrated contour, which we have termed "filiform serrated adenoma" (SA).
  • Five cases contained sufficient non-neoplastic tissue for dissection and DNA extraction, allowing analysis of loss of heterozygosity.
  • All 18 filiform SAs were located in the left colon, including 15 (83%) that occurred in the rectum, compared with 43% of the control group (P=0.03).
  • Four (22%) filiform SAs also contained nonserrated adenomatous elements with a villous (3 cases) or tubular (1 case) growth pattern.
  • None of the polyps in the control group showed stromal edema, high-grade dysplasia, or mixed elements.
  • Polyps in both groups demonstrated comparable staining patterns for O-methylguanine methyltransferase, MLH-1, MSH-2, CDX2, beta-catenin, and Ki-67, and none showed increased nuclear p53 expression.
  • Four cases showed silent p53 mutations upon direct sequencing and 4 revealed loss of heterozygosity at the loci evaluated, including 1 at D5S346 [adenomatous polyposis coli (APC) gene], 1 at D17S250 (p53 gene), and 2 at MYCL (chromosome 1p34).
  • We conclude that filiform SA potentially represents an unusual variant of SA with a predilection for the left colon, particularly the rectum.
  • [MeSH-major] Adenomatous Polyps / pathology. Colorectal Neoplasms / pathology

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  • (PMID = 17667549.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Genetic Markers; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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84. Oh K, Redston M, Odze RD: Support for hMLH1 and MGMT silencing as a mechanism of tumorigenesis in the hyperplastic-adenoma-carcinoma (serrated) carcinogenic pathway in the colon. Hum Pathol; 2005 Jan;36(1):101-11
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  • [Title] Support for hMLH1 and MGMT silencing as a mechanism of tumorigenesis in the hyperplastic-adenoma-carcinoma (serrated) carcinogenic pathway in the colon.
  • BACKGROUND: Down-regulation of DNA repair genes has been proposed as an important mechanism of tumorigenesis in some colon cancers.
  • This mechanism has also recently been implicated in the newly postulated hyperplastic polyp-serrated adenoma-carcinoma ("serrated") pathway of carcinogenesis, although this has never been investigated thoroughly.
  • The aim of this study was to evaluate hMLH1, hMSH2, MGMT, as well as MIB-1, p53, and beta-catenin immunoexpression in an uncommon cohort of mixed colonic polyps that contain a combination of hyperplastic and adenomatous features (n = 21), and in some (n = 7), carcinoma as well.
  • DESIGN: The clinical, pathological, and immunophenotypic (hMLH1, hMSH2, MGMT, MIB-1, p53, and beta-catenin) properties of 28 mixed hyperplastic and adenomatous polyps of the colon (7 of which also contained carcinoma within the same lesion) were evaluated for the above immunopeptides in each of the different morphologic areas of the polyps, and the results were compared to traditional hyperplastic polyps, serrated adenomas, and conventional (nonserrated) adenomas.
  • RESULTS: Clinically, most mixed polyps with carcinoma occurred in the ascending colon (86%), and pathologically, the adenomatous component of most mixed polyps was serrated (96%).
  • Mixed polyps, particularly those with carcinoma, showed loss of hMLH1 (33%), MGMT (37%), and even hMSH2 (11%) with significantly higher frequency compared to hyperplastic polyps, conventional adenomas, and serrated adenomas.
  • More specifically, loss of hMLH1 and MGMT were more frequent in epithelium of higher neoplastic grade in mixed polyps.
  • However, hMSH2 loss was only present in the adenoma component and never in the hyperplastic or carcinomatous areas of these polyps.
  • Defects in MIB-1 proliferation indices and p53 were not significantly different among the same epithelial components in each of the polyp groups.
  • However, conventional adenomas showed significantly higher rates of nuclear beta -catenin staining (100%) in comparison to the adenomatous component of mixed polyps (60%).
  • CONCLUSIONS: Loss of hMLH1 and MGMT play a prominent role in the serrated pathway of carcinogenesis in the colon.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Colonic Neoplasms / genetics. Colonic Polyps / genetics. Gene Silencing. Neoplasm Proteins / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adult. Aged. Aged, 80 and over. Carcinoma / genetics. Carcinoma / metabolism. Carcinoma / pathology. Carrier Proteins. Cytoskeletal Proteins / metabolism. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Female. Humans. Hyperplasia / genetics. Hyperplasia / metabolism. Hyperplasia / pathology. Immunohistochemistry. Ki-67 Antigen / metabolism. Male. Middle Aged. MutS Homolog 2 Protein. Nuclear Proteins. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Trans-Activators / metabolism. Tumor Suppressor Protein p53 / metabolism. beta Catenin

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  • (PMID = 15712188.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / CTNNB1 protein, human; 0 / Carrier Proteins; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / MLH1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / Tumor Suppressor Protein p53; 0 / beta Catenin; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein
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85. Half E, Arber N: Colon cancer: preventive agents and the present status of chemoprevention. Expert Opin Pharmacother; 2009 Feb;10(2):211-9
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  • [Title] Colon cancer: preventive agents and the present status of chemoprevention.
  • CRC has a natural history of transition from a precursor lesion, ie adenomatous polyp to cancer, that spans over 10 to 15 years providing an extended opportunity for intervention and cancer prevention.
  • All articles and other referenced materials were retrieved using the keywords "colon cancer", "adenoma", "chemoprevention", "non steroidal anti-inflammatory drugs", "aspirin", "HMG-CoA reductase inhibitors", "bile acids", "Difluoromethylornithine", "hormone replacement therapy", "mesalamine", "curcumin", and "calcium".
  • Currently, only celecoxib is FDA approved for chemoprevention of CRC and only for high-risk patients with Familial Adenomatous Polyposis (FAP).
  • This is mainly due to cardiovascular toxicity reported in individuals with a personal history of sporadic adenomas.
  • [MeSH-major] Adenomatous Polyps / prevention & control. Anticarcinogenic Agents. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Animals. Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Bile Acids and Salts / therapeutic use. Cyclooxygenase 2 Inhibitors / adverse effects. Cyclooxygenase 2 Inhibitors / therapeutic use. Drug Therapy, Combination. Hormone Replacement Therapy. Humans. Hydroxymethylglutaryl-CoA Reductase Inhibitors / adverse effects. Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use

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  • (PMID = 19236194.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents; 0 / Bile Acids and Salts; 0 / Cyclooxygenase 2 Inhibitors; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • [Number-of-references] 87
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86. Jonsson C, Stål P, Sjöqvist U, Akerlund JE, Löfberg R, Möller L: DNA adducts in normal colonic mucosa from healthy controls and patients with colon polyps and colorectal carcinomas. Mutagenesis; 2010 Sep;25(5):499-504
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  • [Title] DNA adducts in normal colonic mucosa from healthy controls and patients with colon polyps and colorectal carcinomas.
  • Colon cancer is a multistage process where adenomatous polyps developing in a normal mucosa may further progress to neoplasia.
  • Such DNA adducts have been detected in the mucosa of colon cancer patients.
  • The aim of this study was to investigate whether there are differences in DNA adduct levels and patterns in mucosa from patients with colon cancer, polyps and non-cancerous controls and whether some DNA adducts could be markers for colon cancer development.
  • Human colonic biopsies were collected from healthy controls (n = 10), polyp patients (n = 22) (from both normal and polyp tissue) and colon cancer patients (n = 32) (from both tumour tissue and adjacent normal mucosa).
  • One DNA adduct was found only in tumour tissue and adjacent mucosa from the colon cancer patients.
  • A food derived, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-related DNA adduct was detected in 106 of the 150 tissues analysed, but in similar levels in tissues from controls, polyp patients or cancer patients.
  • Furthermore, a food-derived PhIP-related adduct contributes to the general DNA adduct pattern in most individuals, indicating a minor role of this adduct in human colon carcinogenesis.
  • [MeSH-major] Colonic Polyps / metabolism. Colorectal Neoplasms / metabolism. DNA Adducts / metabolism. Health. Intestinal Mucosa / metabolism

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  • (PMID = 20551081.001).
  • [ISSN] 1464-3804
  • [Journal-full-title] Mutagenesis
  • [ISO-abbreviation] Mutagenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-amino-1-methyl-6-phenolimidazo(4,5-b)pyridine-DNA adduct; 0 / DNA Adducts; 0 / Imidazoles
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87. Kline CL, Jackson R, Engelman R, Pledger WJ, Yeatman TJ, Irby RB: Src kinase induces tumor formation in the c-SRC C57BL/6 mouse. Int J Cancer; 2008 Jun 15;122(12):2665-73
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  • Src kinase has been linked as a causative agent in the progression of a number of cancers including colon, breast, lung and melanoma.
  • Src protein and activity levels are increased in colorectal cancer and liver metastases arising secondary to colon cancer.
  • However, although Src protein is increased in colon cancer as early as the adenomatous polyp stage, a role for Src in carcinogenesis has not been established.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18351644.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 9038-94-2 / Metallothionein; EC 2.7.10.2 / src-Family Kinases
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88. Leng Q, Wu KL, Jin HY, Liu P, Lin HP, Zhang JH, Ye H, Zhu Y, Zhang JC: [Distribution characteristics of colorectal neoplasm in 4450 patients and implication for colorectal cancer screening]. Zhonghua Wei Chang Wai Ke Za Zhi; 2010 Nov;13(11):822-4
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  • RESULTS: Colorectal neoplasm was found in 24.8% (4450/17,939) of the patients during colonoscopy, including adenomatous polyp (n=3410, 19.0%) and adenocarcinoma (n=1040, 5.8%).
  • 63.3% of the lesions located at the distal colon (sigmoid colon and rectum) and 36.7% at the proximal colon (36.7%).
  • In patients with adenomatous polyp, 52.8% (1802/3410) of the lesions were at the distal colon, 30.8% (1049/3410) at the proximal colon, and 16.4% (559/3410) at both distal and proximal colon.
  • In patients with carcinoma (n=1040), 921 (88.6%) lesions located at the distal colon, 118 (11.3%) at the proximal colon, and 1 (0.1%) at both segments.

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  • (PMID = 21108058.001).
  • [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
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89. Singh M, Dhindsa G, Friedland S, Triadafilopoulos G: Long-term use of proton pump inhibitors does not affect the frequency, growth, or histologic characteristics of colon adenomas. Aliment Pharmacol Ther; 2007 Oct 1;26(7):1051-61
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  • [Title] Long-term use of proton pump inhibitors does not affect the frequency, growth, or histologic characteristics of colon adenomas.
  • BACKGROUND: The clinical significance of the trophic effects of long-term proton pump inhibitors (PPI)-related hypergastrinemia on colon polyps remains unknown.
  • AIM: To study the frequency, growth, and histology of colon polyps in patients on chronic PPI therapy (cases), compared to those not receiving acid suppression (controls).
  • RESULTS: Demographics and risk factors for colon cancer were comparable between the two groups.
  • At baseline the mean frequency and size of adenomatous polyps were similar in cases and controls (P > 0.05) and at follow-up, these were 0.89 and 1.18 (P > 0.05; 95% CI of -0.08 to 0.66) and 4.09 mm and 4.00 mm (P > 0.05; 95% CI -2.29 to 2.11), respectively with no significant change.
  • However, control group had a higher mean frequency and size of hyperplastic polyps at baseline as well as at follow-up colonoscopy (P < 0.05).
  • CONCLUSIONS: The long-term use of PPI does not influence the frequency, growth, or histology of adenomatous polyps, but is associated with a reduction in both baseline and interval development of hyperplastic polyps.
  • [MeSH-major] Adenomatous Polyps / drug therapy. Colonic Polyps / drug therapy. Proton Pump Inhibitors / therapeutic use

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  • (PMID = 17877512.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK063624
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proton Pump Inhibitors
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90. Farah-Klibi F, Kourda-Boujemaa J, Bouaskar I, Dziri C, Rachida Z, Jilani-Baltagi SB: Cystadenocarcinoma of the appendix: an incidental perioperatory finding in a patient with adenocarcinoma of the ascending and sigmoid colon: case report and review of literature. Pathologica; 2009 Dec;101(6):255-60
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  • [Title] Cystadenocarcinoma of the appendix: an incidental perioperatory finding in a patient with adenocarcinoma of the ascending and sigmoid colon: case report and review of literature.
  • We present a unique case of primary cystadenocarcinoma of the appendix occurring concurrently with adenocarcinoma of the colon, and overview the clinical and therapeutic difficulties posed by this rare entity.
  • Degenerated adenomatous polyp of the ascending colon and mucinous adenocarcinoma of the sigmoid colon invading the parietal peritoneum of the uterine and vagina was diagnosed.
  • Synchronous colon cancer may occur in patients with appendiceal mucoceles.
  • In such patients, the colon should be investigated.
  • [MeSH-major] Adenocarcinoma / pathology. Appendiceal Neoplasms / pathology. Colonic Neoplasms / pathology. Cystadenocarcinoma / pathology. Neoplasms, Multiple Primary / pathology

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  • (PMID = 20387715.001).
  • [ISSN] 0031-2983
  • [Journal-full-title] Pathologica
  • [ISO-abbreviation] Pathologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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91. Giardiello FM, Hylind LM, Trimbath JD, Hamilton SR, Romans KE, Cruz-Correa M, Corretti MC, Offerhaus GJ, Yang VW: Oral contraceptives and polyp regression in familial adenomatous polyposis. Gastroenterology; 2005 Apr;128(4):1077-80
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  • [Title] Oral contraceptives and polyp regression in familial adenomatous polyposis.
  • We describe a patient in the placebo arm of a 4-year primary chemoprevention trial who developed adenomatous polyps and then had eradication of polyps after the administration of oral contraceptives.
  • No change in the prostaglandin levels in the colonic mucosa was noted after polyp elimination, making nonsteroidal anti-inflammatory drug ingestion unlikely as a cause.
  • This report represents the regression of colorectal adenomas with the use of estrogen/progesterone compounds.
  • [MeSH-major] Adenomatous Polyposis Coli / physiopathology. Contraceptives, Oral / therapeutic use
  • [MeSH-minor] Child. Colon / metabolism. Female. Humans. Intestinal Mucosa / metabolism. Menstruation Disturbances / drug therapy. Prostaglandins / metabolism. Remission Induction

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  • (PMID = 15825088.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 51085; United States / NCI NIH HHS / CA / CA 53801; United States / NCI NIH HHS / CA / CA 63721; United States / NCI NIH HHS / CA / P50 CA 9316
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contraceptives, Oral; 0 / Prostaglandins
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92. Poole EM, Bigler J, Whitton J, Sibert JG, Potter JD, Ulrich CM: C-reactive protein genotypes and haplotypes, polymorphisms in NSAID-metabolizing enzymes, and risk of colorectal polyps. Pharmacogenet Genomics; 2009 Feb;19(2):113-20
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  • [Title] C-reactive protein genotypes and haplotypes, polymorphisms in NSAID-metabolizing enzymes, and risk of colorectal polyps.
  • INTRODUCTION: C-reactive protein (CRP) is a nonspecific marker of inflammation linked to cardiovascular disease and possibly colon cancer.
  • In a case-control study of adenomatous (n=491) or hyperplastic (n=184) polyps versus polyp-free controls (n=583) we investigated these SNPs in relation to colorectal polyp risk.
  • RESULTS: Individuals with 838 GC or CC genotypes had a modestly, although not statistically significantly, increased risk of adenomas (odds ratio: 1.4 95% confidence interval: 0.9-2.1) and a nearly 2-fold increased risk of concurrent adenomas and hyperplastic polyps (odds ratio: 2.0 95% confidence interval: 1.1-3.6).
  • Increased risk for concurrent adenomas and hyperplastic polyps was also observed for haplotype ACACAC.
  • Risk of adenomas associated with 2043G>A differed with nonsteroidal anti-inflammatory drug (NSAID) use.
  • Among NSAID nonusers, there was a suggestion that the GA or AA genotypes were associated with decreased risk of adenomas; this was not seen among NSAID users (P interaction=0.03).
  • We also observed interactions between UGT1A1 [TA](7) promoter repeat polymorphism and CRP tagSNPs -390C>T/A and 90A>T, in which only the homozygous variant CRP genotype was associated with increased risk of adenoma among those with the UGT1A1 6rpt/6rpt genotype (P interaction=0.02 and 0.04 for -390C>T/A and 90A>T, respectively).
  • CONCLUSION: These results provide limited support for associations between genetic variation in CRP and colorectal polyp risk.

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  • (PMID = 19077918.001).
  • [ISSN] 1744-6872
  • [Journal-full-title] Pharmacogenetics and genomics
  • [ISO-abbreviation] Pharmacogenet. Genomics
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA89445; United States / NCI NIH HHS / CA / R01 CA59045; United States / NCI NIH HHS / CA / R25 CA094880; United States / NCI NIH HHS / CA / R01 CA089445; United States / NCI NIH HHS / CA / R01 CA114467; United States / NCI NIH HHS / CA / T32 CA009661
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 9007-41-4 / C-Reactive Protein; EC 1.14.13.- / CYP2C9 protein, human; EC 1.14.13.- / Cytochrome P-450 CYP2C9; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 2.4.1.- / UGT1A1 enzyme; EC 2.4.1.17 / Glucuronosyltransferase
  • [Other-IDs] NLM/ NIHMS133466; NLM/ PMC3690930
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93. Schmitz KJ, Hey S, Schinwald A, Wohlschlaeger J, Baba HA, Worm K, Schmid KW: Differential expression of microRNA 181b and microRNA 21 in hyperplastic polyps and sessile serrated adenomas of the colon. Virchows Arch; 2009 Jul;455(1):49-54
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  • [Title] Differential expression of microRNA 181b and microRNA 21 in hyperplastic polyps and sessile serrated adenomas of the colon.
  • This study was designed to analyse the potential diagnostic value of miR-181b and miR-21 for discriminating hyperplastic polyps (HP) from sessile serrated adenomas (SSA) without cytologic dysplasia.
  • Using real-time polymerase chain reaction expression levels of miR-181b and miR-21 in 18 HPs, 19 SSAs without cytologic dysplasia and 20 normal colonic mucosal specimens were examined.
  • A differential expression of miR-181b and miR-21 was found in HPs, SSAs, and normal colonic mucosa with highest expression levels in SSAs.
  • [MeSH-major] Adenoma / genetics. Colonic Neoplasms / genetics. Colonic Polyps / genetics. MicroRNAs / analysis


94. Leuhuber K, Klepal W, Hausott B, Marian B: Apoptosis in a tissue-like culture model of human colorectal adenoma cells. Tissue Cell; 2006 Jun;38(3):203-8
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  • [Title] Apoptosis in a tissue-like culture model of human colorectal adenoma cells.
  • Tissue-like cultures of LT97 human colonic adenoma cells were produced by plating on reconstructed connective tissue supports (CTR) containing colon-associated fibroblasts to form mucosal monolayers and polyp-like structures closely resembling the in vivo situation.
  • While LT97 cultures on plastic shed apoptotic bodies into the medium, they collected at the basal pole of the cell layer in the CTR cultures as is also observed in adenoma tissue.
  • Only a small proportion was released into the medium as shown by the detection of apoptosis specific keratin fragments, which could be increased by 100microM of quercetin and resveratrol.
  • [MeSH-major] Adenoma / metabolism. Apoptosis. Colorectal Neoplasms / metabolism. Models, Biological

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  • (PMID = 16730771.001).
  • [ISSN] 0040-8166
  • [Journal-full-title] Tissue & cell
  • [ISO-abbreviation] Tissue Cell
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Stilbenes; 9007-34-5 / Collagen; 9IKM0I5T1E / Quercetin; Q369O8926L / resveratrol
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95. Laos S, Baeckström D, Hansson GC: Inhibition of NF-kappaB activation and chemokine expression by the leukocyte glycoprotein, CD43, in colon cancer cells. Int J Oncol; 2006 Mar;28(3):695-704
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of NF-kappaB activation and chemokine expression by the leukocyte glycoprotein, CD43, in colon cancer cells.
  • It is frequently overexpressed in early colon adenomas, but not in normal colon epithelial cells.
  • To identify CD43 target genes, gene array analysis was performed using a tetracycline-inducible CD43 expression system in human colon adenocarcinoma SW480 cells.
  • [MeSH-minor] Active Transport, Cell Nucleus / drug effects. Blotting, Western. Cell Line, Tumor. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Chemokine CCL2 / genetics. Chemokine CCL2 / metabolism. Chemokine CXCL1. Chemokines, CXC / genetics. Chemokines, CXC / metabolism. Colonic Neoplasms / genetics. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Gene Expression Regulation, Neoplastic / genetics. Humans. I-kappa B Proteins / metabolism. Intercellular Signaling Peptides and Proteins / genetics. Intercellular Signaling Peptides and Proteins / metabolism. Interleukin-8 / genetics. Interleukin-8 / metabolism. PPAR gamma / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Time Factors. Transcription Factor RelA / genetics. Transcription Factor RelA / metabolism. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16465375.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD43; 0 / CCL2 protein, human; 0 / CXCL1 protein, human; 0 / Chemokine CCL2; 0 / Chemokine CXCL1; 0 / Chemokines; 0 / Chemokines, CXC; 0 / I-kappa B Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Interleukin-8; 0 / NF-kappa B; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha; 139874-52-5 / NF-kappaB inhibitor alpha
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96. Fan XS, Wu HY, Yu HP, Zhou Q, Zhang YF, Huang Q: Expression of Lgr5 in human colorectal carcinogenesis and its potential correlation with beta-catenin. Int J Colorectal Dis; 2010 May;25(5):583-90
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  • METHODS: The study was carried out on a tissue microarray that consisted of 102 colorectal carcinomas (CRC; M:F = 55:47), 18 colon adenoma, and 12 colon normal mucosa cases.
  • RESULTS: Lgr5 immunoreactivity was observed only in single cells in the base of normal colon mucosal crypts but high in 28% (five out of 18) adenomas, and significantly higher in 54% (55/102, p = 0.016) CRC cases.
  • In normal mucosa, adenoma, and CRC, beta-catenin expression was seen in 25% (three out of 12), 27% (five out of 18), and 81% (83/102) cases, respectively, in contrast to 0, 0, and 40% (41/102) for p53 expression, respectively.
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Male. Middle Aged. Neoplasm Invasiveness. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 20195621.001).
  • [ISSN] 1432-1262
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / LGR5 protein, human; 0 / Receptors, G-Protein-Coupled; 0 / Tumor Suppressor Protein p53; 0 / beta Catenin
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97. Kodach LL, Bleuming SA, Musler AR, Peppelenbosch MP, Hommes DW, van den Brink GR, van Noesel CJ, Offerhaus GJ, Hardwick JC: The bone morphogenetic protein pathway is active in human colon adenomas and inactivated in colorectal cancer. Cancer; 2008 Jan 15;112(2):300-6
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  • [Title] The bone morphogenetic protein pathway is active in human colon adenomas and inactivated in colorectal cancer.
  • METHODS: The authors used a tissue microarray and immunohistochemistry of BMP receptors and signal transduction elements in adenomas and CRC specimens to elucidate the role of BMP signaling in CRC carcinogenesis.
  • RESULTS: The adenoma specimens expressed all 3 BMP receptors (BMPRs) (BMPR type 1a [BMPR1a], BMPR1b, and BMPR2) and expressed SMAD family member 4 (SMAD4); and 20 of 22 adenomas (90.9%) exhibited active BMP signaling, as determined by nuclear phosphorylated SMAD1,5,8 (pSMAD1,5,8) expression.
  • In contrast, pSMAD1,5,8 nuclear staining was present in 5 CRC specimens (22.7%) but was lost in 17 CRC specimens (77.3%; cancer vs adenoma; P< .0001).
  • The earliest loss of pSMAD1,5,8 nuclear staining was detected in regions of high-grade dysplasia/carcinoma in situ within adenomas.
  • CRCs showed frequent loss of BMPR2 (P< .0001) and SMAD4 (P< .01) compared with adenomas.
  • CONCLUSIONS: Taken together, the current results indicated that loss of BMP signaling correlates tightly with progression of adenomas to cancer and occurs relatively early during cancer progression.
  • [MeSH-major] Adenoma / etiology. Bone Morphogenetic Proteins / physiology. Colonic Neoplasms / etiology. Colorectal Neoplasms / etiology. Signal Transduction / physiology


98. Wassenaar MJ, Biermasz NR, Pereira AM, van der Klaauw AA, Smit JW, Roelfsema F, van der Straaten T, Cazemier M, Hommes DW, Kroon HM, Kloppenburg M, Guchelaar HJ, Romijn JA: The exon-3 deleted growth hormone receptor polymorphism predisposes to long-term complications of acromegaly. J Clin Endocrinol Metab; 2009 Dec;94(12):4671-8
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  • METHODS: The presence of the d3GHR polymorphism was assessed in 86 acromegalic patients with long-term disease control and related to anthropometric parameters, cardiovascular risk factors, osteoarthritis, bone mineral density, colonic polyps and diverticulae, and dolichocolon.
  • Carriers of the d3GHR isoform showed increased prevalence of osteoarthritis, especially of the hip [adjusted odds ratio (OR), 5.2; 95% confidence interval (CI), 3.2-7.1], of adenomatous polyps (adjusted OR, 4.1; 95% CI, 2.4-5.6), and dolichocolon (adjusted OR, 3.2; 95% CI, 1.8-4.6).
  • Anthropometric parameters, cardiovascular risk factors, bone mineral density, and (non)vertebral fractures were not significantly different between patients with and without the d3GHR allele.
  • CONCLUSION: In patients with long-term cured acromegaly, the d3GHR polymorphism is associated with an increased prevalence of irreversible comorbidities such as osteoarthritis, dolichocolon, and adenomatous colonic polyps, but not with other comorbidities such as cardiovascular risk factors.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Anthropometry. Bone Density / genetics. Bone Density / physiology. Cardiovascular Diseases / epidemiology. Cardiovascular Diseases / genetics. Cohort Studies. Colonic Diseases / epidemiology. Colonic Diseases / genetics. DNA / genetics. DNA / isolation & purification. Female. Gene Deletion. Genetic Predisposition to Disease. Human Growth Hormone / metabolism. Human Growth Hormone / physiology. Humans. Insulin-Like Growth Factor I / metabolism. Male. Middle Aged. Osteoarthritis / epidemiology. Osteoarthritis / genetics. Osteoarthritis / radiography. Osteoporosis / epidemiology. Osteoporosis / genetics. Risk Factors. Spinal Fractures / epidemiology. Spinal Fractures / genetics. Treatment Outcome

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  • (PMID = 19864451.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Somatotropin; 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9007-49-2 / DNA
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99. Oh K, Willett WC, Wu K, Fuchs CS, Giovannucci EL: Calcium and vitamin D intakes in relation to risk of distal colorectal adenoma in women. Am J Epidemiol; 2007 May 15;165(10):1178-86
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  • [Title] Calcium and vitamin D intakes in relation to risk of distal colorectal adenoma in women.
  • The authors examined intakes of calcium and vitamin D, and interaction with retinol, in relation to risk of adenoma of the distal colon or rectum among 48,115 US women who were free of colorectal cancer or polyps, completed a food frequency questionnaire in 1980, and underwent endoscopy by 2002.
  • They documented 2,747 cases of adenoma (1,064 large, 1,531 small, 2,085 distal colon, and 779 rectal).
  • Total calcium intake was weakly associated with distal colorectal adenoma risk (multivariable relative risk (RR) for extreme quintiles = 0.88, 95% confidence interval (CI): 0.74, 1.04; p(trend) = 0.06), particularly for large adenoma (RR = 0.73, 95% CI: 0.56, 0.96; p(trend) = 0.02).
  • Total vitamin D intake was weakly associated with reduced risk of distal colorectal adenoma (RR = 0.79, 95% CI: 0.63, 0.99; p(trend) = 0.07), but more strongly with distal colon adenoma risk (RR = 0.67, 95% CI: 0.52, 0.87; p(trend) = 0.004).
  • The combinations of high vitamin D and low retinol intake (RR = 0.55, 95% CI: 0.28, 1.10) further decreased risk of distal colorectal adenoma when compared with the opposite extreme.