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1. 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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2. 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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3. Woerner SM, Kloor M, Mueller A, Rueschoff J, Friedrichs N, Buettner R, Buzello M, Kienle P, Knaebel HP, Kunstmann E, Pagenstecher C, Schackert HK, Möslein G, Vogelsang H, von Knebel Doeberitz M, Gebert JF, German HNPCC Consortium: Microsatellite instability of selective target genes in HNPCC-associated colon adenomas. Oncogene; 2005 Apr 7;24(15):2525-35
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  • [Title] Microsatellite instability of selective target genes in HNPCC-associated colon adenomas.
  • Instability at coding microsatellites (cMS) in specific target genes causes frameshift mutations and functional inactivation of affected proteins, thereby providing a selective growth advantage to MMR deficient cells.
  • In this study, we examined 30 HNPCC-associated MSI-H colorectal adenomas of different grades of dysplasia for frameshift mutations in 26 cMS-bearing genes, which, according to our previous model, represent Selective Target genes of MSI.
  • About 30% (8/26) of these genes showed a high mutation frequency (> or =50%) in colorectal adenomas, similar to the frequencies reported for colorectal carcinomas.
  • Mutations in one gene (PTHL3) occurred significantly less frequently in MSI adenomas compared to published mutation rates in MSI carcinomas (36.0 vs 85.7%, P=0.023).
  • [MeSH-major] Adenoma / genetics. Adenoma / physiopathology. Cell Transformation, Neoplastic / genetics. Chromosomal Instability. Colonic Neoplasms / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Microsatellite Repeats

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  • (PMID = 15735733.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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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. 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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6. 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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  • [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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7. Herbst A, Bommer GT, Kriegl L, Jung A, Behrens A, Csanadi E, Gerhard M, Bolz C, Riesenberg R, Zimmermann W, Dietmaier W, Wolf I, Brabletz T, Göke B, Kolligs FT: ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition. Gastroenterology; 2009 Aug;137(2):639-48, 648.e1-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition.
  • RESULTS: ITF-2B is strongly expressed in colon adenomas but frequently down-regulated in carcinomas because of LOH at 18q21.
  • Loss of ITF-2B expression correlates with loss of p21(Cip1) expression in primary colon carcinomas.
  • ITF-2B, which is up-regulated during early colorectal carcinogenesis because of loss of adenomatous polyposis coli, is a target for LOH on chromosome 18q, along with deleted in colorectal carcinoma and Smad4.
  • This finding, along with the fact that ITF-2B is a regulator of the key cell cycle inhibitor p21(Cip1), indicates that ITF-2B is a tumor suppressor that has an important function at the adenoma to carcinoma transition.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyposis Coli / genetics. Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 18 / genetics. Colorectal Neoplasms / genetics. DNA-Binding Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 19394332.001).
  • [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 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / TCF3 protein, human; 0 / TCF4 protein, human; 0 / Transcription Factors
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8. Douma KF, Aaronson NK, Vasen HF, Bleiker EM: Psychosocial issues in genetic testing for familial adenomatous polyposis: a review of the literature. Psychooncology; 2008 Aug;17(8):737-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Psychosocial issues in genetic testing for familial adenomatous polyposis: a review of the literature.
  • OBJECTIVES: Familial adenomatous polyposis (FAP) is characterized by the development of multiple adenomas in the colon that can lead to colorectal cancer.
  • [MeSH-major] Adenomatous Polyps / genetics. Adenomatous Polyps / psychology. Colonic Neoplasms / genetics. Colonic Neoplasms / psychology. Genetic Techniques / instrumentation


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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  • [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. Jones LE Jr, Ying L, Hofseth AB, Jelezcova E, Sobol RW, Ambs S, Harris CC, Espey MG, Hofseth LJ, Wyatt MD: Differential effects of reactive nitrogen species on DNA base excision repair initiated by the alkyladenine DNA glycosylase. Carcinogenesis; 2009 Dec;30(12):2123-9
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  • To understand the effects of RNS on BER in vivo, we examined intestinal adenomas for levels of inducible nitric oxide synthase (iNOS) and AAG.
  • We found AAG to be nitrated in human adenomas, suggesting that this RNS modification is relevant in the human disease.
  • POLbeta protein was increased in nearly all adenomas compared with adjacent non-tumor tissues, whereas APE1 expression was only increased in approximately half of the adenomas and also was relocalized to the cytoplasm in adenomas.
  • Collectively, the results suggest that BER is dysregulated in colon adenomas.

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  • (PMID = 19864471.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR017698; United States / NCRR NIH HHS / RR / P20 RR17698; United States / NCI NIH HHS / CA / R01 CA100450; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Reactive Nitrogen Species; EC 2.7.7.- / DNA Polymerase beta; EC 3.2.2.- / 3-methyladenine-DNA glycosylase; EC 3.2.2.- / DNA Glycosylases; EC 4.2.99.18 / APEX1 protein, human; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase
  • [Other-IDs] NLM/ PMC2792317
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11. 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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12. Yuan B, Jin X, Zhu R, Zhang X, Liu J, Wan H, Lu H, Shen Y, Wang F: Cronkhite-Canada syndrome associated with rib fractures: a case report. BMC Gastroenterol; 2010;10:121
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  • Esophagogastroduodenoscopy, video capsule endoscopy and colonoscopy revealed various sizes of generalized gastrointestinal polyps.
  • Histological examination of the biopsy specimens obtained from the stomach and the colon showed adenomatous polyp and inflammatory polyp respectively.

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  • (PMID = 20955587.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2972238
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13. Micheletto G, Sciannamea I, Zanoni A, Panizzo V, Rubino B, Danelli P: [Intestinal neuroendocrine tumor. Case report and review of the literature]. Ann Ital Chir; 2009 Jul-Aug;80(4):319-24
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  • Symptoms are non specific; the most common are abdominal pain, nausea and vomiting, weight loss and gastrointestinal (GI) blood loss.
  • Here we report a case of a 73-year-old male with an adenomatous colonic polyp, not suitable of endoscopic treatment, and a synchronous carcinoid of small intestine discovered during surgical procedure.
  • [MeSH-major] Adenoma. Carcinoid Tumor. Colonic Polyps. Ileal Neoplasms. Neoplasms, Multiple Primary. Sigmoid Neoplasms


14. 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


15. 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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16. 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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17. 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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18. 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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19. 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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20. 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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21. Siddiqui AA, Patel A, Huerta S: Determinants of compliance with colonoscopy in patients with adenomatous colon polyps in a veteran population. Aliment Pharmacol Ther; 2006 Dec;24(11-12):1623-30
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  • [Title] Determinants of compliance with colonoscopy in patients with adenomatous colon polyps in a veteran population.
  • AIM: To determine factors affecting compliance of a follow-up colonoscopy in patients with previously diagnosed adenomatous colon polyps.
  • METHODS: A retrospective review was performed on patients with adenomatous polyps excised between January and December 1998.
  • RESULTS: One hundred and nineteen patients with adenomatous colon polyps were identified.
  • In a univariate analysis, greater number of polyps (P = 0.04), NSAID use (P = 0.02), statin use (P = 0.005), first-degree relatives with colon cancer (P = 0.05) and compliance with out-patient clinic follow-up (P < 0.001) were significantly associated with patient compliance.
  • Multivariate analysis revealed statin use (P = 0.05), first-degree relatives with colon cancer (P = 0.06) and compliance with out-patient clinic follow-up (P < 0.001) were independent predictors of compliance.
  • CONCLUSIONS: History of statin use and family history of colon cancer are good predictors of compliance.
  • Strong efforts should be directed at improving patient education about colon cancer by the physician and facilitating patient compliance.
  • [MeSH-major] Adenomatous Polyps / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Colonoscopy. Patient Compliance

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  • (PMID = 17206950.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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22. 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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23. Knoll N, Weise A, Claussen U, Sendt W, Marian B, Glei M, Pool-Zobel BL: 2-Dodecylcyclobutanone, a radiolytic product of palmitic acid, is genotoxic in primary human colon cells and in cells from preneoplastic lesions. Mutat Res; 2006 Feb 22;594(1-2):10-9
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  • [Title] 2-Dodecylcyclobutanone, a radiolytic product of palmitic acid, is genotoxic in primary human colon cells and in cells from preneoplastic lesions.
  • Results of previous in vitro studies with primary human colon cells and in vivo experiments with rats fed with 2-alkylcyclobutanones indicated that these radiolytic derivatives may be genotoxic and enhance the progression of colon tumors.
  • In particular, we explored the relative sensitivities of human colon cells, representing different stages of tumor development and healthy colon tissues, respectively.
  • HT29clone19A cells, LT97 adenoma cells and primary human epithelial cells were exposed to 2dDCB (150-2097 microM).
  • Genotoxicity, reflected as strand breaks, was assessed using the alkaline version of the comet assay and chromosomal abnormalities were investigated by 24-color fluorescence-in-situ-hybridization.
  • 2dDCB was cytotoxic in a time- and dose-dependent manner in LT97 adenoma cells and in freshly isolated primary cells but not in the human colon tumor cell line.
  • Associated with this was a marked induction of DNA damage by 2dDCB in LT97 adenoma cells and in freshly isolated colonocytes, whereas in the HT29clone19A cells no strand breaks were detectable.
  • A long-term incubation of LT97 adenoma cells with lower concentrations of 2dDCB revealed cytogenetic effects.
  • In summary, 2dDCB was clearly genotoxic in healthy human colon epithelial cells and in cells representing preneoplastic colon adenoma.
  • These findings provide additional evidence that this compound may be regarded as a possible risk factor for processes in colon carcinogenesis related to initiation and progression.
  • [MeSH-major] Colon / drug effects. Cyclobutanes / toxicity. Mutagens / toxicity. Palmitic Acid / metabolism. Precancerous Conditions / genetics

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  • (PMID = 16153665.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cyclobutanes; 0 / Mutagens; 2V16EO95H1 / Palmitic Acid; 35493-46-0 / 2-dodecylcyclobutanone
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24. 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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25. Knöbel Y, Glei M, Weise A, Osswald K, Schäferhenrich A, Richter KK, Claussen U, Pool-Zobel BL: Uranyl nitrilotriacetate, a stabilized salt of uranium, is genotoxic in nontransformed human colon cells and in the human colon adenoma cell line LT97. Toxicol Sci; 2006 Oct;93(2):286-97
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  • [Title] Uranyl nitrilotriacetate, a stabilized salt of uranium, is genotoxic in nontransformed human colon cells and in the human colon adenoma cell line LT97.
  • To assess possible hazards, we investigated the genotoxic effects of uranyl nitrilotriacetate (U-NTA) in human colon tumor cells (HT29 clone 19A), adenoma cells (LT97), and nontransformed primary colon cells.
  • Colon cells were incubated with U-NTA.
  • Cell survival, cytotoxicity, cellular glutathione (GSH) levels, genotoxicity, and DNA repair capacity (comet assay), as well as gene- and chromosome-specific damage combination of comet assay and fluorescence in situ hybridization [FISH], 24-color FISH) were determined.
  • U-NTA was also genotoxic in LT97 cells and primary colon cells, where it additionally increased migration of TP53 into the comet tail.
  • [MeSH-major] Colon / drug effects. Uranium / toxicity
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Cell Line, Tumor. Cell Survival / drug effects. Chromosome Aberrations. Colonic Neoplasms / genetics. Colonic Neoplasms / pathology. DNA Damage. Glutathione / analysis. Humans. In Situ Hybridization, Fluorescence. Reactive Oxygen Species. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 16840563.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 0 / Tumor Suppressor Protein p53; 4OC371KSTK / Uranium; GAN16C9B8O / Glutathione
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26. 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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27. 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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28. 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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29. 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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30. 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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31. 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


32. 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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33. 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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  • [Cites] Eur J Nutr. 2008 Aug;47(5):226-34 [18636219.001]
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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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34. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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35. 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


36. 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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37. 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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38. 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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39. 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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40. 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
  • [Chemical-registry-number] 0 / Interferon Regulatory Factor-1; 0 / PIAS1 protein, human; 0 / Protein Inhibitors of Activated STAT; 0 / Small Ubiquitin-Related Modifier Proteins
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41. 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


42. Galamb O, Gyorffy B, Sipos F, Spisák S, Németh AM, Miheller P, Dinya E, Molnár B, Tulassay Z: [Identification of colorectal cancer, adenoma, and inflammatory bowel disease specific gene expression patterns using whole genomic oligonucleotide microarray system]. Orv Hetil; 2007 Nov 4;148(44):2067-79
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  • [Title] [Identification of colorectal cancer, adenoma, and inflammatory bowel disease specific gene expression patterns using whole genomic oligonucleotide microarray system].
  • [Transliterated title] Vastagbél-adenoma, vastagbélrák és IBD-specifikus génexpressziós mintázatok meghatározása teljes genomszintu oligonukleotid microarray-rendszerrel.
  • BACKGROUND: Discrimination and classification of colorectal diseases (adenoma, colorectal cancer, inflammatory bowel disease) using biopsy samples and expression microarrays, has not been solved yet, nevertheless, it can contribute to the understanding of the colonic diseases.
  • METHODS: Total ribonucleic acid was extracted, amplified and biotinylated from frozen colonic biopsies of 15 patients with colorectal cancer, 15 with adenoma, 14 with inflammatory bowel disease and 8 normal controls.
  • RESULTS: Top validated genes included CD44 antigen, met proto-oncogene, chemokine ligand-12, ADAM-like decysin-1 and ATP-binding casette-A8 genes in adenoma; collagen IValpha1, lipocalin-2, calumenin, aquaporin-8 genes in colorectal cancer; and lipocalin-2, ubiquitin D and interferon induced transmembrane protein 2 genes in inflammatory bowel disease.
  • [MeSH-major] Adenoma / diagnosis. Colorectal Neoplasms / diagnosis. Gene Expression Profiling. Inflammatory Bowel Diseases / diagnosis. Oligonucleotide Array Sequence Analysis


43. 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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44. 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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45. 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


46. 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


47. 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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48. 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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  • [Other-IDs] NLM/ PMC4124439
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49. 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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50. 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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51. 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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52. 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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53. 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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54. 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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55. 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


56. 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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57. 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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58. 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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59. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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60. 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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61. 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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62. 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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63. 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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64. 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


65. Kekilli M, Dagli U, Kalkan IH, Tunc B, Disibeyaz S, Ulker A, Sahin B: Low incidence of colorectal dysplasia and cancer among patients with ulcerative colitis: a Turkish referral centre study. Scand J Gastroenterol; 2010 Apr;45(4):434-9
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  • OBJECTIVES: To determine the incidences of dysplasia, adenomatous polyp and colon cancer in patients with ulcerative colitis (UC) and to evaluate the risk factors.
  • Adenomatous polyp was found in six patients (2.2%).
  • Five cases (83.3% of the polyps) were in the diseased segment and one case (16.7%) was in the non-diseased segment.
  • Adenomatous polyp was not found in cases with colon cancer.
  • The difference in rates may be explained by racial factors, specific environmental factors, intensive control of disease activity through medical therapy and effective colonoscopic surveillance programmes.
  • [MeSH-major] Colitis, Ulcerative / epidemiology. Colonic Polyps / epidemiology. Colorectal Neoplasms / epidemiology. Precancerous Conditions / epidemiology


66. 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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67. 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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68. 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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  • [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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69. 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


70. 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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71. 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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  • [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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72. 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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73. 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


74. Cavalcanti JL, Núñez RF, Yeung HW, Mehran RJ, Macapinlac HA: Incidental finding of prostate cancer and adenomatous colon polyp in a patient with lung cancer. Clin Nucl Med; 2007 Nov;32(11):871-3
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  • [Title] Incidental finding of prostate cancer and adenomatous colon polyp in a patient with lung cancer.
  • [MeSH-major] Adenomatous Polyps / complications. Adenomatous Polyps / diagnosis. Colonic Polyps / diagnosis. Incidental Findings. Lung Neoplasms / complications. Prostatic Neoplasms / complications. Prostatic Neoplasms / diagnosis


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

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  • (PMID = 17379616.001).
  • [ISSN] 0002-9262
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK040561; None / None / / P30 DK040561-12; United States / NCI NIH HHS / CA / CA 87969; United States / NIDDK NIH HHS / DK / P30 DK040561-12; United States / NCI NIH HHS / CA / CA 55075
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium, Dietary; 11103-57-4 / Vitamin A; 1406-16-2 / Vitamin D
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77. Emmons KM, McBride CM, Puleo E, Pollak KI, Clipp E, Kuntz K, Marcus BH, Napolitano M, Onken J, Farraye F, Fletcher R: Project PREVENT: a randomized trial to reduce multiple behavioral risk factors for colon cancer. Cancer Epidemiol Biomarkers Prev; 2005 Jun;14(6):1453-9
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  • [Title] Project PREVENT: a randomized trial to reduce multiple behavioral risk factors for colon cancer.
  • BACKGROUND: This report examines the outcome data for Project PREVENT, a two-site randomized control trial designed to reduce behavioral risk factors for colorectal cancer among individuals who have been diagnosed with adenomatous colon polyps.
  • METHODS: The study sample included 1,247 patients with recent diagnosis of adenomatous colorectal polyps.
  • [MeSH-major] Colonic Neoplasms / prevention & control. Diet. Health Behavior
  • [MeSH-minor] Adenomatous Polyposis Coli / complications. Adult. Aged. Alcohol Drinking. Exercise. Female. Humans. Male. Middle Aged. Risk Factors. Smoking. Telephone

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  • (PMID = 15941955.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 R01 CA74000-04
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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78. O'Sullivan J, Risques RA, Mandelson MT, Chen L, Brentnall TA, Bronner MP, Macmillan MP, Feng Z, Siebert JR, Potter JD, Rabinovitch PS: Telomere length in the colon declines with age: a relation to colorectal cancer? Cancer Epidemiol Biomarkers Prev; 2006 Mar;15(3):573-7
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  • [Title] Telomere length in the colon declines with age: a relation to colorectal cancer?
  • Using Q-FISH, we also examined the histologically normal epithelium adjacent to, or distant from, colon adenomas and cancers, in addition to the neoplasms.
  • Telomere length in larger adenoma lesions (>2 cm) was significantly shorter than in normal adjacent (P = 0.004) or normal distant (P = 0.05) tissue from the same individuals.
  • However, telomere length in histologically normal epithelium adjacent to cancers or in adenomas <2 cm was not statistically different from that of the normal distant mucosa or from normal controls, evidence that a telomere-shortening field effect was not present.
  • [MeSH-major] Cell Aging / genetics. Colonic Neoplasms / genetics. Colonic Neoplasms / pathology. Telomere / ultrastructure
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Aging / genetics. Biomarkers, Tumor / analysis. Child. Child, Preschool. Colon / pathology. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Intestinal Mucosa / pathology. Intestinal Mucosa / physiology. Male. Middle Aged. Predictive Value of Tests. Reference Values. Reverse Transcriptase Polymerase Chain Reaction. Risk Assessment. Sampling Studies. Sensitivity and Specificity. Tissue Culture Techniques

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  • (PMID = 16537718.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA74184; United States / NCI NIH HHS / CA / P20 CA103728; United States / NIA NIH HHS / AG / P30 AG13280; United States / NCI NIH HHS / CA / R01 CA68124-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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79. Kim SE, Shim KN, Jung SA, Yoo K, Moon IH: An association between obesity and the prevalence of colonic adenoma according to age and gender. J Gastroenterol; 2007 Aug;42(8):616-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An association between obesity and the prevalence of colonic adenoma according to age and gender.
  • BACKGROUND: Epidemiologic data on obesity as a risk factor for colonic adenoma with respect to gender have not yet been confirmed.
  • Here, we aimed to compare the prevalence of colonic adenoma and of advanced polyps in age-stratified men and women at baseline, to examine the role of body mass index (BMI) on colonic adenoma risk according to age and gender, and to examine the influence of menopausal status.
  • BMI was assessed, and histology, size, and location of the adenoma were examined for each patient.
  • RESULTS: A significant increase in the prevalence of colonic adenoma and of advanced polyps was found to occur with age (P for trend < 0.01).
  • The prevalences of adenoma and advanced polyps were higher in men in most age groups (P < 0.01), but no significant difference in prevalences was observed between genderes in patients 70 years of age or older.
  • Moreover, a positive association between BMI and the prevalence of colonic adenoma and advanced polyps was shown in relatively young individuals of both gender (men in their thirties, P < 0.05; women in their forties, P < 0.05), and premenopausal women according to hormonal status (P = 0.01).
  • CONCLUSIONS: Our data suggest that obesity increases the risk of colonic adenoma in relatively young people and in premenopausal women subject to estrogen effects.
  • [MeSH-major] Adenoma / epidemiology. Colonic Neoplasms / epidemiology. Obesity / complications
  • [MeSH-minor] Adult. Age Factors. Aged. Biopsy. Body Mass Index. Colonic Polyps / epidemiology. Colonic Polyps / etiology. Colonic Polyps / pathology. Colonoscopy. Female. Humans. Korea / epidemiology. Male. Menopause. Middle Aged. Prevalence. Retrospective Studies. Risk Factors. Sex Factors

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  • (PMID = 17701124.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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80. Lim YJ, Kwack WG, Lee YS, Hahm KB, Kim YK: Increased pulse wave velocity reflecting arterial stiffness in patients with colorectal adenomas. J Clin Biochem Nutr; 2010 Nov;47(3):261-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased pulse wave velocity reflecting arterial stiffness in patients with colorectal adenomas.
  • The obese patients with diabetes or cardiovascular risk factors are associated with increased risk of colorectal cancer as well as adenomas under the shared pathogenesis related to atherosclerosis.
  • Here we determined the association between increased arterial stiffness and colorectal adenomas incorporating parameters including age, gender, waist circumference, body mass index, lipid profiles, fasting glucose, and blood pressure.
  • Subjects who simultaneously underwent colonoscopies and pulse wave velocity (PWV) determinations between July 2005 and September 2006 were analyzed, based on which the subjects were classified into two groups as patients group with colorectal adenomas (n = 49) and control group (n = 200) with normal, non-polypoid benign lesions or hyperplastic polyps.
  • Uni- and multi-variate analyses were performed to calculate the odd ratio for colon adenomas.
  • Based on uni-variate analysis, age, waist circumference, body mass index, heart-femoral PWV (hfPWV), and brachial-ankle PWV were significantly associated with adenomas (p<0.05) and multiple logistic regression analysis showed that the heart-femoral PWV, waist circumference, and the levels of LDL-C were significant risk factor for colorectal adenoma.
  • However, arterial stiffness did not affect the progression of colon adenoma.
  • The finding that hfPWV, reflecting aortic stiffness, was increased in patients with colorectal adenomas lead to conclusion that patients who have prominently increased arterial stiffness can be recommended to undergo colonoscopic examinations and at the same time we also recommend counseling about the risk for atherosclerosis in those who have colorectal adenomas.

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  • (PMID = 21103036.001).
  • [ISSN] 1880-5086
  • [Journal-full-title] Journal of clinical biochemistry and nutrition
  • [ISO-abbreviation] J Clin Biochem Nutr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Other-IDs] NLM/ PMC2966937
  • [Keywords] NOTNLM ; atherosclerosis / colon adenoma / pulse wave velocity / risk factors
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81. Al-Thihli K, Palma L, Marcus V, Cesari M, Kushner YB, Barkun A, Foulkes WD: A case of Cowden's syndrome presenting with gastric carcinomas and gastrointestinal polyposis. Nat Clin Pract Gastroenterol Hepatol; 2009 Mar;6(3):184-9
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  • BACKGROUND: A 73-year-old white man was referred to a cancer genetics clinic for evaluation of a approximately 20-year history of mixed upper and lower gastrointestinal polyposis, including hyperplastic, inflammatory and adenomatous polyps, colonic ganglioneuromas, and associated diffuse, esophageal glycogenic acanthosis.
  • Multiple hyperplastic polyps and small, sessile polyps were also observed in the gastrectomy specimen.
  • [MeSH-major] Carcinoma / etiology. Gastrointestinal Diseases / etiology. Hamartoma Syndrome, Multiple / complications. Polyps / etiology. Stomach Neoplasms / etiology

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  • (PMID = 19190598.001).
  • [ISSN] 1743-4386
  • [Journal-full-title] Nature clinical practice. Gastroenterology & hepatology
  • [ISO-abbreviation] Nat Clin Pract Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] P6YC3EG204 / Vitamin B 12
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82. Hurlstone DP, George R, Brown S: Novel clinical in vivo roles for indigo carmine: high-magnification chromoscopic colonoscopy. Biotech Histochem; 2007 Apr;82(2):57-71
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  • Since the adenoma-carcinoma sequence was first proposed by Morson in the 1970s, it has become widely accepted that detection and subsequent removal of polypoid adenomas from the colon reduces the incidence of colorectal cancer.
  • These adenomas are relatively easy to detect by conventional colonoscopy; however, large population studies have shown that despite resection of polypoid adenomas, interval colorectal cancers still occurred.
  • Current data suggest that such morphologically distinct lesions may account for up to 30% of all colorectal adenomas.
  • Furthermore, flat and depressed lesions of the large bowel may confer greater malignant potential compared to polypoid adenomas.
  • [MeSH-major] Adenoma / diagnosis. Carcinoma / diagnosis. Colonoscopy / methods. Colorectal Neoplasms / diagnosis. Coloring Agents / chemistry. Indigo Carmine / chemistry
  • [MeSH-minor] Adenomatous Polyposis Coli / diagnosis. Adenomatous Polyposis Coli / pathology. Adult. Female. Humans. Male. Middle Aged

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  • (PMID = 17577700.001).
  • [ISSN] 1052-0295
  • [Journal-full-title] Biotechnic & histochemistry : official publication of the Biological Stain Commission
  • [ISO-abbreviation] Biotech Histochem
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Coloring Agents; D3741U8K7L / Indigo Carmine
  • [Number-of-references] 96
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83. Pap Z, Pávai Z, Dénes L, Kovalszky I, Jung J: An immunohistochemical study of colon adenomas and carcinomas: E-cadherin, Syndecan-1, Ets-1. Pathol Oncol Res; 2009 Dec;15(4):579-87
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  • [Title] An immunohistochemical study of colon adenomas and carcinomas: E-cadherin, Syndecan-1, Ets-1.
  • Our goal was to study the changes in the expression of these molecules during colon carcinoma development and progression.
  • We tested 117 colon adenomas and 149 de novo and ex adenoma carcinomas of the colon, using the Ultravision Polymer system.
  • The positive reaction rate was 100% for E-cadherin, 98.3% for syndecan-1 and 22.4% for Ets-1 in adenomas, while in carcinomas it was 88.5%, 62.4% and 56.3% respectively.
  • We found decreasing expression of E-cadherin and syndecan-1 throughout colon carcinoma progression and an opposite regulation for the Ets-1 protein.
  • De novo carcinomas have lower E-cadherin and syndecan-1 expression, and higher Ets-1 expression compared to ex adenoma carcinomas.
  • [MeSH-major] Adenoma / metabolism. Cadherins / metabolism. Carcinoma / metabolism. Colonic Neoplasms / metabolism. Proto-Oncogene Protein c-ets-1 / metabolism. Syndecan-1 / metabolism

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  • (PMID = 19253033.001).
  • [ISSN] 1532-2807
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Proto-Oncogene Protein c-ets-1; 0 / Syndecan-1
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84. Galitskiĭ MV, Khomeriki SG, Nikiforov PA: [Expression of proliferation and apoptosis markers in neoplasms of colon mucosa after cholecystectomy]. Eksp Klin Gastroenterol; 2009;(5):28-32
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  • [Title] [Expression of proliferation and apoptosis markers in neoplasms of colon mucosa after cholecystectomy].
  • The goal of the study was to investigate immunohistochemical markers of proliferation and apoptosis in colorectal adenomas and adenocarcinomas at the patients with cholecystectomy.
  • Fifty patients (40 with retained function of gallbladder and 10 patients with cholecystectomy) histologically diagnosed as proximal colon adenoma or adenocarcinoma were included into the study.
  • Colonoscopic biopsies have been taken from the lesion in cancer patients, and colonoscopic polypectomy has been performed for adenomas.
  • In addition, biopsies have been taken from the adjacent healthy colon mucosa at least 5 cm from the lesion in each patient.
  • The index of Ki-67 expression in healthy colon mucosa at the patients with cholecystectomy was 37,5 +/- 1,8% (p < 0,05) as compared to 31,36 +/- 1,9 at the patients without cholecystectomy.
  • No significant difference was detected in the comparison of Ki-67 expression levels between the healthy mucosa and adenomas at the patients with cholecystectomy 43,4 +/- 3,45 (p > 0,05), but more prominent increase was revealed in adenocarcinomas 64,33 +/- 7,67% (p < 0,01).
  • At the patients without cholecystectomy the frequency of revealing p53 in adenomas does not vary, compared with healthy mucosa, however in adenocarcinomas p53 was not revealed at none case.
  • As a contrast, in group of the patients with cholecystectomy the frequency of revealing p53 in adenomas is considerably increased (up to 80%), and even in adenocarcinomas, p53 was revealed in 30,8% of cases.
  • At the patients with a cholecystectomy, the increase of proliferative activity is accompanied by increased apoptosis in adenomas and maintained apoptosis in adenocarcinomas.
  • [MeSH-major] Apoptosis. Biomarkers, Tumor / biosynthesis. Cell Proliferation. Cholecystectomy. Colon / metabolism. Colonic Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Intestinal Mucosa / metabolism. Ki-67 Antigen / biosynthesis. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 20205327.001).
  • [ISSN] 1682-8658
  • [Journal-full-title] Ėksperimental'nai︠a︡ i klinicheskai︠a︡ gastroėnterologii︠a︡ = Experimental & clinical gastroenterology
  • [ISO-abbreviation] Eksp Klin Gastroenterol
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
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85. Moore LE, Huang WY, Chatterjee N, Gunter M, Chanock S, Yeager M, Welch B, Pinsky P, Weissfeld J, Hayes RB: GSTM1, GSTT1, and GSTP1 polymorphisms and risk of advanced colorectal adenoma. Cancer Epidemiol Biomarkers Prev; 2005 Jul;14(7):1823-7
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  • [Title] GSTM1, GSTT1, and GSTP1 polymorphisms and risk of advanced colorectal adenoma.
  • Cigarette smoking is a risk factor for colon adenoma.
  • We examined the prevalence of GSTM1 and GSTT1 gene deletions, and two GSTP1 polymorphisms in 772 cases with advanced colorectal adenomas (>1 cm, villous elements or high-grade dysplasia) of the distal colon (descending or sigmoid colon or rectum) and 777 sigmoidoscopy negative controls enrolled in the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial.
  • Advanced adenoma risk was increased in current/former smokers (OR, 1.4; 95% CI, 1.2-1.8).
  • In summary, this is the first study to report associations between colorectal adenomas and GSTM1 wild-type and GSTT1 null allele among smokers.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Glutathione Transferase / genetics. Isoenzymes / genetics. Polymorphism, Genetic

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  • (PMID = 16030123.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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86. M Bustamante-Balén, Bernet L, Cano R, Morell L, López A: Assessing the reproducibility of the microscopic diagnosis of sessile serrated adenoma of the colon. Rev Esp Enferm Dig; 2009 Apr;101(4):258-64
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  • [Title] Assessing the reproducibility of the microscopic diagnosis of sessile serrated adenoma of the colon.
  • INTRODUCTION: sessile serrated adenoma (SSA) is a recently described lesion that may be related to the development of up to 15% of colorectal cancers (CRCs).
  • MATERIAL AND METHODS: concordance between two pathologists in the diagnosis of serrated lesions of the colon was studied for 195 lesions (187 hyperplastic polyps and 7 serrated adenomas).
  • Possible diagnoses were: SSA, traditional serrated adenoma (TSA), hyperplastic polyp (HP), serrated polyp, tubular adenoma, or mixed lesions.
  • [MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology


87. Siddiqui AA, Maddur H, Naik S, Cryer B: The association of elevated HbA1c on the behavior of adenomatous polyps in patients with type-II diabetes mellitus. Dig Dis Sci; 2008 Apr;53(4):1042-7
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  • [Title] The association of elevated HbA1c on the behavior of adenomatous polyps in patients with type-II diabetes mellitus.
  • The aim of our study was to determine whether poor control of diabetes mellitus (DM) is associated with increased prevalence of colonic adenomatous polyps (APs), especially those that are advanced .
  • Significant variables by UA were included in a stepwise logistic regression analysis to determine independent predictors of aggressive clinical behavior by the polyps.
  • Logistic regression, as measured by HbA1c, demonstrated that poorly controlled DM-2 independently predicted a greater prevalence of right-sided AP, a more advanced lesion at the time of presentation, a greater number of polyps, and greater use of exogenous insulin.
  • [MeSH-major] Adenomatous Polyps / blood. Adenomatous Polyps / pathology. Colonic Neoplasms / blood. Colonic Neoplasms / pathology. Diabetes Mellitus, Type 2 / blood. Hemoglobin A, Glycosylated / metabolism

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  • (PMID = 17939046.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Hemoglobin A, Glycosylated; 0 / hemoglobin A1c protein, human
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88. Ichihara T, Yoshino H, Doi Y, Nabae K, Imai N, Hagiwara A, Tamano S, Morita O, Tamaki Y, Suzuki H: No enhancing effects of diacylglycerol oil on tumor development in a medium-term multi-organ carcinogenesis bioassay using male F344 rats. Food Chem Toxicol; 2008 Jan;46(1):157-67
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  • Controls received standard diet without any supplementation as non-treated control.
  • The incidence of colon adenomas was significantly increased in rats given 1.375% DAG oil, but not 2.75% and 5.5% DAG oil, when compared to the control (5.5% TG group) value.
  • Furthermore, incidences and multiplicity of hyperplasias and adenomas and/or adenocarcinomas were comparable across all DAG oil-treated groups.
  • In contrast, incidences of colon adenomas and/or adenocarcinomas were significantly increased in rats given 5.5% HOTG, and adenomas with MCTG, but not 5.5% HLTG, as compared to the 5.5% TG value.
  • Thus, the current results indicate that DAG oil may not exert modifying potential on tumor development, even in the colon because of the lack of dose-dependence.
  • DAG oil was equivalent to HOTG (standard cocking oil composed of naturally occurring fatty acids), with regard to colon tumor development.
  • [MeSH-minor] Animals. Body Weight / drug effects. Colonic Neoplasms / chemically induced. Colonic Neoplasms / pathology. Diet. Drinking / drug effects. Drug Interactions. Eating / drug effects. Glutathione Transferase / metabolism. Male. Organ Size / drug effects. Rats. Rats, Inbred F344. Survival Analysis. Triglycerides / analysis

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  • (PMID = 17728035.001).
  • [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
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Diglycerides; 0 / Triglycerides; EC 2.5.1.18 / Glutathione Transferase
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89. Zhou JN, Chen SQ, Zhang XM, Zhou X, Zhu M, Feng B, Li JT, Ma GJ, Zhang YY: [A novel APC gene germline mutation in a familial adenomatous polyposis pedigree]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2006 Aug;23(4):388-91
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  • [Title] [A novel APC gene germline mutation in a familial adenomatous polyposis pedigree].
  • OBJECTIVE: To detect the adenomatous polyposis coli (APC) gene germline mutation in the proband and her family members with familial adenomatous polyposis (FAP).
  • This mutation manifested an aggressive form of FAP with early onset of colorectal adenocarcinoma and colonic adenoma.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli Protein / genetics. Germ-Line Mutation

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  • (PMID = 16883523.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein
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90. Hensley HH, Merkel CE, Chang WC, Devarajan K, Cooper HS, Clapper ML: Endoscopic imaging and size estimation of colorectal adenomas in the multiple intestinal neoplasia mouse. Gastrointest Endosc; 2009 Mar;69(3 Pt 2):742-9
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  • [Title] Endoscopic imaging and size estimation of colorectal adenomas in the multiple intestinal neoplasia mouse.
  • OBJECTIVE: To develop an endoscopy-based protocol for the accurate estimation of adenoma size in vivo from images obtained during colonoscopy.
  • SUBJECTS: Adenomatous polyposis coli multiple intestinal metaplasia Fox Chase Cancer Center mice that develop multiple colorectal adenomas.
  • METHODS: The mice received colonoscopic examination by using a rigid endoscope, and high-resolution images of colon adenomas were captured by using a charge-coupled-device camera.
  • Lesion size was estimated by comparing the dimensions of the adenoma relative to a reference rod by using a novel geometric construction.
  • MAIN OUTCOME MEASUREMENTS: Cross-sectional area of colon adenomas.
  • RESULTS: The cross-sectional area of 20 adenomas was measured in vivo during colonoscopy and compared with the size as measured at necropsy, which yielded a Pearson correlation coefficient of 0.94 (P = 6.52 x 10(-9)).
  • Assessment of interoperator variability, when using measurements from 11 adenomas, yielded a Pearson correlation coefficient of 0.85 (P = 4.35 x 10(-3)) and demonstrated excellent reproducibility.
  • LIMITATIONS: Only the distal colon could be viewed, and endoscopic measurements were 2-dimensional.
  • CONCLUSIONS: An endoscopic method for the reliable measurement of colorectal adenomas in vivo was established.
  • The application of this technique to mouse models of colon carcinogenesis will provide unique insight into the dynamics of adenoma growth.

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  • (PMID = 19251020.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA105008-010003; United States / NCI NIH HHS / CA / CA006927-47S5; United States / NCI NIH HHS / CA / P30 CA006927-47S5; United States / NCI NIH HHS / CA / U54 CA-105008; United States / NCI NIH HHS / CA / U54 CA105008-010003; United States / NCI NIH HHS / CA / U54 CA105008; United States / NCI NIH HHS / CA / P30 CA006927; United States / NCI NIH HHS / CA / CA-06927
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS100772; NLM/ PMC2821747
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91. Klenow S, Glei M, Haber B, Owen R, Pool-Zobel BL: Carob fibre compounds modulate parameters of cell growth differently in human HT29 colon adenocarcinoma cells than in LT97 colon adenoma cells. Food Chem Toxicol; 2008 Apr;46(4):1389-97
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  • [Title] Carob fibre compounds modulate parameters of cell growth differently in human HT29 colon adenocarcinoma cells than in LT97 colon adenoma cells.
  • An extract of the Mediterranean carob (Ceratonia siliqua L.) pod (carob fibre extract), products formed after its fermentation by the gut flora and the major phenolic ingredient gallic acid (GA), were comparatively investigated for their influence on survival and growth parameters of colon adenocarcinoma HT29 cells and adenoma LT97 cells.
  • The differently modulated growth of human colon cell lines was more related to proliferation rates and impairment of DNA-synthesis than to H2O2 formation.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Antineoplastic Agents, Phytogenic. Cell Division / drug effects. Colonic Neoplasms / pathology. Dietary Fiber / pharmacology. Fabaceae / chemistry

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  • (PMID = 17950517.001).
  • [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 / Antineoplastic Agents, Phytogenic; 0 / Culture Media; 0 / DNA, Neoplasm; 0 / Phenols; 0 / Sulfoxides; 0 / Xylenes; BBX060AN9V / Hydrogen Peroxide; S2VDY878QD / xylenol orange
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92. Kaz A, Kim YH, Dzieciatkowski S, Lynch H, Watson P, Kay Washington M, Lin L, Grady WM: Evidence for the role of aberrant DNA methylation in the pathogenesis of Lynch syndrome adenomas. Int J Cancer; 2007 May 1;120(9):1922-9
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  • [Title] Evidence for the role of aberrant DNA methylation in the pathogenesis of Lynch syndrome adenomas.
  • Colorectal cancer (CRC) forms through a series of histologic steps that are accompanied by mutations and epigenetic alterations, which is called the polyp-cancer sequence.
  • The role of epigenetic alterations, such as aberrant DNA methylation, in the polyp-cancer sequence in sporadic CRC and particularly in hereditary colon cancer is not well understood.
  • Consequently, we assessed the methylation status of CDKN2A/p16, MGMT, MLH1 and p14(ARF) in adenomas arising in the Lynch syndrome, a familial colon cancer syndrome caused by MLH1 and MSH2 mutations, to determine if DNA methylation is a "second hit" mechanism in CRC and to characterize the role of DNA methylation in the polyp phase of the Lynch syndrome.
  • We found MLH1 and p14(ARF) are methylated in 53 and 60% of the Lynch syndrome adenomas and in 4 and 20% of sporadic adenomas, whereas CDKN2A/p16 and MGMT are methylated in 6 and 14% of the Lynch syndrome adenomas versus 50 and 64% of sporadic adenomas.
  • Therefore, the frequency and pattern of gene methylation varies between the Lynch syndrome and sporadic colon adenomas, implying differences in the molecular pathogenesis of the tumors.
  • MLH1 methylation in the Lynch syndrome adenomas suggests gene methylation might have a role in the initiation of these neoplasms.
  • [MeSH-major] Adenoma / genetics. Colonic Neoplasms / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. DNA Methylation

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17278092.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / MLH1 protein, human; 0 / Nuclear Proteins; 0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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93. Luo F, Ye H, Hamoudi R, Dong G, Zhang W, Patek CE, Poulogiannis G, Arends MJ: K-ras exon 4A has a tumour suppressor effect on carcinogen-induced murine colonic adenoma formation. J Pathol; 2010 Apr;220(5):542-50
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  • [Title] K-ras exon 4A has a tumour suppressor effect on carcinogen-induced murine colonic adenoma formation.
  • The present study evaluated whether K-ras 4A expression can suppress colonic adenoma development in the absence of its oncogenic allele.
  • Mice with homozygous targeted deletions of K-ras exon 4A (K-ras(tmDelta4A/tmDelta4A)) that can express the K-ras 4B isoform only, along with heterozygous K-ras(tmDelta4A/+) and wild-type mice, were given ten weekly 1,2-dimethylhydrazine (DMH) treatments to induce colonic adenomas.
  • There was a significant increase in both the number and the size of colonic adenomas in DMH-treated K-ras(tmDelta4A/tmDelta4A) mice, with reduced survival, compared with heterozygous and wild-type mice.
  • Lack of expression of K-ras 4A transcripts was confirmed, whereas the relative expression levels of K-ras 4B transcripts were significantly increased in the adenomas of K-ras(tmDelta4A/tmDelta4A) mice compared with K-ras(tmDelta4A/+) and wild-type mice.
  • Immunohistochemical studies showed that adenomas of K-ras(tmDelta4A/tmDelta4A) mice had significantly increased cell proliferation and significantly decreased apoptosis with evidence of activation of MapKinase and Akt pathways, with increased phospho-Erk1/2 and both phospho-Akt-Thr308 and phospho-Akt-Ser473 immunostaining, compared with adenomas from K-ras(tmDelta4A/+) and wild-type mice.
  • In conclusion, following DMH treatment, K-ras exon 4A deletion promoted increased number and size of colonic adenomas showing increased K-ras 4B expression, increased proliferation, decreased apoptosis, and activation of MapKinase and Akt pathways, in the absence of K-ras mutations.
  • Therefore, K-ras 4A expression had a tumour suppressor effect on carcinogen-induced murine colonic adenoma formation, explaining the selective advantage of the altered K-ras 4A : 4B isoform ratio found in human colorectal cancer.
  • [MeSH-major] Adenoma / genetics. Colonic Neoplasms / genetics. Genes, Tumor Suppressor. Genes, ras. Proto-Oncogene Proteins p21(ras) / genetics

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  • (PMID = 20087880.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras); IX068S9745 / 1,2-Dimethylhydrazine
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94. Park YS: [COX-2 inhibitors in inflammatory bowel disease: friends or foes?]. Korean J Gastroenterol; 2007 Dec;50(6):350-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • COX-2 is frequently overexpressed in colonic adenoma and carcinoma.
  • Specific inhibitors of COX-2 have been shown to induce apoptosis in tumor cells and to inhibit tumor growth in animal models and in humans.
  • In a recent study, powerful chemopreventive ability of selective COX-2 inhibitor was observed in colitis-related colon carcinogenesis in mouse model.
  • But it was reported that even selective COX inhibitors aggravated the DSS-induced colonic inflammation.
  • It is assumed that endogenous PGs are involved in the mucosal defense against DSS-induced colonic ulcerations which are produced by COX-1 at early phase and by COX-2 at late phase.
  • Long-term use of COX-2 inhibitors for the chemoprevention of colitic cancer is needed to define their mechanism of action, that reduce side effects and have specific tumor target.
  • [MeSH-minor] Animals. Colonic Neoplasms / diagnosis. Cyclooxygenase 1 / metabolism. Cyclooxygenase 2 / metabolism. Humans. Mice. Models, Animal

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  • (PMID = 18159171.001).
  • [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; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2
  • [Number-of-references] 59
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95. Ispas C, Yu J, Tarantino DR, Lara JF: Pathologic quiz case: a 44-year-old woman with a tubulovillous adenoma of the colon and liver and bone lesions. Small cell (neuroendocrine) carcinoma of the colon with metastasis and an associated, overlying villous adenoma. Arch Pathol Lab Med; 2005 Mar;129(3):412-4
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  • [Title] Pathologic quiz case: a 44-year-old woman with a tubulovillous adenoma of the colon and liver and bone lesions. Small cell (neuroendocrine) carcinoma of the colon with metastasis and an associated, overlying villous adenoma.
  • [MeSH-major] Adenoma, Villous / diagnosis. Bone Neoplasms / secondary. Carcinoma, Small Cell / diagnosis. Carcinoma, Small Cell / secondary. Colonic Neoplasms / diagnosis. Liver Neoplasms / secondary. Neoplasms, Multiple Primary / diagnosis

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  • (PMID = 15737043.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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96. Pranesh N, Haboubi NY, O'Dwyer ST: Pigmented mesenteric lymphadenopathy in familial adenomatous polyposis - an unusual cause of intraoperative abandonment of ileo-anal pouch. Ann R Coll Surg Engl; 2005 Jul;87(4):W1-4
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  • [Title] Pigmented mesenteric lymphadenopathy in familial adenomatous polyposis - an unusual cause of intraoperative abandonment of ileo-anal pouch.
  • Familial adenomatous polyposis (FAP) is an autosomal dominant condition with near complete penetrance, characterised by the presence of numerous adenomatous polyps of the colon and rectum.
  • Melanosis coli describes the brownish-black discolouration of the colon resulting from the accumulation of a granular pigment in the phagosomes of macrophages in the colonic lamina propria.
  • The presence of melanosis pigment in pericolonic lymph nodes has been reported in patients with coincidental melanosis coli, following segmental colonic resection.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Lymphatic Diseases / complications. Melanosis / complications. Mesentery. Peritoneal Diseases / complications
  • [MeSH-minor] Adolescent. Colonic Pouches. Female. Humans. Intraoperative Complications / etiology. Proctocolectomy, Restorative. Reoperation


97. Lardinois D, Weder W, Roudas M, von Schulthess GK, Tutic M, Moch H, Stahel RA, Steinert HC: Etiology of solitary extrapulmonary positron emission tomography and computed tomography findings in patients with lung cancer. J Clin Oncol; 2005 Oct 1;23(28):6846-53
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  • PURPOSE: The aim of this prospective study was to assess the incidence and the nature of solitary extrapulmonary [18F] fluorodeoxyglucose (FDG) accumulations in patients with non-small-cell lung cancer (NSCLC) staged with integrated positron emission tomography and computed tomography (PET/CT) and to evaluate the impact on management.
  • The six malignancies consisted of carcinoma of the breast in two patients, and carcinoma of the orbit, esophagus, prostate, and non-Hodgkin's lymphoma in one patient each.
  • Benign tumors and inflammatory lesions included eight colon adenomas, four Warthin's tumors, one granuloma of the lower jaw, one adenoma of the thyroid gland, one compensatory muscle activity due to vocal chord palsy, two occurrences of arthritis, three occurrences of reflux esophagitis, two occurrences of pancreatitis, two occurrences of diverticulitis, one hemorrhoidal inflammation, and one rib fracture.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / radionuclide imaging. Lung Neoplasms / radionuclide imaging. Neoplasm Metastasis / radionuclide imaging. Positron-Emission Tomography

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  • (PMID = 16192576.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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98. Deutscher N, Bataille F, Hausmann M, Kiessling S, Muller-Newen G, Leeb SN, Herfarth H, Heinrich PC, Schölmerich J, Rogler G: Functional expression of the interleukin-11 receptor alpha-chain in normal colonic epithelium and colon cancer. Int J Colorectal Dis; 2006 Sep;21(6):573-81
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  • [Title] Functional expression of the interleukin-11 receptor alpha-chain in normal colonic epithelium and colon cancer.
  • The aim of this study was to investigate the expression profiling of IL-11Ralpha and its downstream signaling cascade in colonic adenoma and carcinoma.
  • MATERIALS AND METHODS: The expression of IL-11Ralpha in normal colonic mucosa, 11 colonic adenomas, and 10 carcinomas was analyzed by immunohistochemistry.
  • RESULTS: Immunohistochemistry revealed significant IL-11-Ralpha expression in epithelial cells of normal colonic mucosa.
  • In contrast, the expression of IL-11-Ralpha in colon adenomas and carcinomas was either absent or only detectable in very few scattered epithelial cells.
  • Densitometric analysis of Western blots confirmed these results, showing a decrease of IL-11Ralpha-protein in cells isolated from adenomas or carcinomas.
  • CONCLUSION: This study demonstrates a decrease of IL-11-Ralpha-protein expression in epithelial cells isolated from colon carcinomas and adenomas compared to normal colonic mucosa and a reduced STAT3 signaling.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Colonic Neoplasms / metabolism. Interleukin-11 Receptor alpha Subunit / biosynthesis. Intestinal Mucosa / metabolism

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  • (PMID = 16292518.001).
  • [ISSN] 0179-1958
  • [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 / Biomarkers, Tumor; 0 / Interleukin-11 Receptor alpha Subunit
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99. Habermann N, Schön A, Lund EK, Glei M: Fish fatty acids alter markers of apoptosis in colorectal adenoma and adenocarcinoma cell lines but fish consumption has no impact on apoptosis-induction ex vivo. Apoptosis; 2010 May;15(5):621-30
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  • [Title] Fish fatty acids alter markers of apoptosis in colorectal adenoma and adenocarcinoma cell lines but fish consumption has no impact on apoptosis-induction ex vivo.
  • Previous studies suggest that the n-3 polyunsaturated fatty acids (PUFAs) eicosapenteinoic acid (EPA) and docosahexaenoic acid (DHA), constituents of fish oil, exert chemopreventive activity in colon cancer.
  • LT97 human colon adenoma and HT29 human colon adenocarcinoma cells were used to investigate modulation of apoptosis by EPA, DHA or linoleic acid (LA) using a set of endpoints, namely phosphatidylserine staining with Annexin-V (flow cytometry), Bcl-2 expression (Real-time RT-PCR), and Bid, caspase 3, 8 and 9 expression as well as PARP cleavage (Western Blot).
  • Taken together, our results show that adenoma cells are highly susceptible to n-3 PUFA-induced apoptosis.

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  • (PMID = 20107900.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BH3 Interacting Domain Death Agonist Protein; 0 / Biomarkers; 0 / Caspase Inhibitors; 0 / Dietary Fats; 0 / Fatty Acids, Omega-3; 0 / Fish Oils; 0 / Proto-Oncogene Proteins c-bcl-2; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspases
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100. Agostini M, Tibiletti MG, Lucci-Cordisco E, Chiaravalli A, Morreau H, Furlan D, Boccuto L, Pucciarelli S, Capella C, Boiocchi M, Viel A: Two PMS2 mutations in a Turcot syndrome family with small bowel cancers. Am J Gastroenterol; 2005 Aug;100(8):1886-91
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  • The tumor family history of a patient with cafè-au-lait spots (CALS) and early onset adenomas, duodenal cancer, and glioblastoma was positive for colonic adenoma (mother), jejunal (maternal grandfather), lung (father), and colorectal (paternal uncle) cancers.
  • Our findings point out the association between PMS2 and TS, and support the hypothesis that patients with a few polyps, small bowel tumors with a very early onset, glioblastoma, and CALS should be considered as a variant of hereditary nonpolyposis colorectal cancer.

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  • (PMID = 16144131.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / PMS2 protein, human; EC 6.5.1.- / DNA Repair Enzymes
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