[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 466
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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .
  • PubMed Health. DARE review .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2008 Mar 6;27(11):1562-71 [17873905.001]
  • [Cites] Cell. 2008 Feb 8;132(3):363-74 [18267069.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3193-203 [18451145.001]
  • [Cites] Cell. 2008 Jun 13;133(6):1006-18 [18555777.001]
  • [Cites] Cell. 2008 Jun 13;133(6):1019-31 [18555778.001]
  • [Cites] Oncogene. 2008 Sep 4;27(39):5204-13 [18504438.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Sep 9;105(36):13421-6 [18755897.001]
  • [Cites] Genes Dev. 2009 Feb 1;23(3):278-90 [19204115.001]
  • [Cites] Mol Cell Biol. 2000 Apr;20(8):2803-8 [10733583.001]
  • [Cites] Gastroenterology. 2000 Oct;119(4):929-42 [11040180.001]
  • [Cites] EMBO J. 2003 Mar 3;22(5):1210-22 [12606585.001]
  • [Cites] Mol Cell. 2004 May 21;14(4):501-13 [15149599.001]
  • [Cites] Carcinogenesis. 1980 May;1(5):375-80 [7273277.001]
  • [Cites] Nature. 1990 Aug 30;346(6287):866-8 [2392154.001]
  • [Cites] Cell. 1992 Sep 18;70(6):937-48 [1525830.001]
  • [Cites] Exp Gerontol. 1992 Jul-Aug;27(4):375-82 [1459213.001]
  • [Cites] Hum Mol Genet. 1995 Feb;4(2):313-4 [7757087.001]
  • [Cites] Cell. 1997 Mar 7;88(5):593-602 [9054499.001]
  • [Cites] Science. 1997 Aug 8;277(5327):831-4 [9242615.001]
  • [Cites] Cell. 1998 Feb 6;92(3):401-13 [9476899.001]
  • [Cites] J Biol Chem. 1998 May 15;273(20):11995-8 [9575138.001]
  • [Cites] J Clin Invest. 2004 Nov;114(9):1299-307 [15520862.001]
  • [Cites] J Cell Sci. 2005 Feb 1;118(Pt 3):485-96 [15657080.001]
  • [Cites] Nature. 2005 Aug 4;436(7051):642 [16079833.001]
  • [Cites] Genes Dev. 2005 Sep 15;19(18):2122-37 [16131611.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Mar;15(3):573-7 [16537718.001]
  • [Cites] Nat Cell Biol. 2006 Aug;8(8):877-84 [16862142.001]
  • [Cites] Nature. 2006 Nov 30;444(7119):633-7 [17136093.001]
  • [Cites] Cell Death Differ. 2007 Jan;14(1):3-9 [17068503.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 15;104(20):8334-9 [17488820.001]
  • [Cites] Mol Cell. 2007 Jun 8;26(5):731-43 [17540598.001]
  • [Cites] Mol Cell. 2007 Jun 8;26(5):745-52 [17540599.001]
  • [Cites] Nature. 2007 Jun 28;447(7148):1130-4 [17554337.001]
  • [Cites] Cell. 2007 Jul 27;130(2):223-33 [17662938.001]
  • [Cites] Curr Biol. 2007 Aug 7;17(15):1298-307 [17656095.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Sep 25;104(39):15472-7 [17875987.001]
  • [Cites] Oncogene. 2007 Nov 15;26(52):7302-12 [17533371.001]
  • [Cites] Cancer Res. 2007 Dec 15;67(24):11677-86 [18089797.001]
  • [Cites] JAMA. 2008 Jan 30;299(4):425-36 [18230780.001]
  • [Cites] Science. 2008 Mar 7;319(5868):1352-5 [18323444.001]
  • (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
  •  go-up   go-down


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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


Advertisement
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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Vaginal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Gardner Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


6. Beggs AD, Hodgson SV: The genomics of colorectal cancer: state of the art. Curr Genomics; 2008 Mar;9(1):1-10
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The concept of the adenoma-carcinoma sequence, as first espoused by Morson et al. whereby the development of colorectal cancer is dependent on a stepwise progression from adenomatous polyp to carcinoma is well documented.
  • Initial studies of the genetics of inherited colorectal cancer susceptibility concentrated on the inherited colorectal cancer syndromes, such as Familial Adenomatous Polyposis (FAP) and Lynch Syndrome (also known as HNPCC).
  • Recent research has concentrated on the pathways by which colorectal adenomatous polyps not due to one of these known inherited susceptibilities undergo malignant transformation, and determination of the types of polyps most likely to do so.
  • We will also discuss in detail the genetic changes in polyps that undergo malignant transformation as well as current knowledge with regards to the epigenomic changes found in colorectal polyps.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Lancet. 1978 Feb 4;1(8058):245-7 [74668.001]
  • [Cites] Gastroenterology. 1978 Jun;74(6):1325-30 [348556.001]
  • [Cites] Hum Mutat. 2004 Oct;24(4):353-4 [15366000.001]
  • [Cites] Nature. 2004 Sep 2;431(7004):80-4 [15343335.001]
  • [Cites] Nutrition. 2004 Jan;20(1):63-8 [14698016.001]
  • [Cites] Oncogene. 2004 Aug 23;23(38):6445-70 [15322516.001]
  • [Cites] Nat Genet. 2004 Aug;36(8):790-2 [15284845.001]
  • [Cites] J Med Genet. 2004 Jul;41(7):484-91 [15235019.001]
  • [Cites] Genes Dev. 2004 Jul 1;18(13):1533-8 [15231735.001]
  • [Cites] Gastroenterology. 2004 Jun;126(7):1681-5 [15188161.001]
  • [Cites] Trends Genet. 2004 Apr;20(4):177-81 [15041171.001]
  • [Cites] Nat Genet. 2008 Jan;40(1):26-8 [18084292.001]
  • [Cites] Gut. 2007 Nov;56(11):1498-500 [17938428.001]
  • [Cites] Gut. 2007 Nov;56(11):1564-71 [17339237.001]
  • [Cites] World J Gastroenterol. 2007 Jul 28;13(28):3792-8 [17657832.001]
  • [Cites] J Pathol. 2007 Aug;212(4):378-85 [17503413.001]
  • [Cites] Gut. 2007 Mar;56(3):417-25 [16840506.001]
  • [Cites] Nat Rev Cancer. 2007 Jan;7(1):35-45 [17167516.001]
  • [Cites] Cancer Res. 2006 Oct 15;66(20):9837-44 [17047044.001]
  • [Cites] Cell Mol Life Sci. 2006 Sep;63(18):2135-44 [16952058.001]
  • [Cites] Cancer Lett. 2006 Sep 28;241(2):184-96 [16412571.001]
  • [Cites] Cell. 2006 Jul 28;126(2):297-308 [16873062.001]
  • [Cites] Nat Genet. 2006 Jul;38(7):787-93 [16804544.001]
  • [Cites] Annu Rev Biochem. 2006;75:137-63 [16756488.001]
  • [Cites] Cell. 2006 May 5;125(3):509-22 [16678095.001]
  • [Cites] J Med Genet. 2006 May;43(5):e18 [16648371.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):2-5 [16397205.001]
  • [Cites] JAMA. 2005 Nov 16;294(19):2465-73 [16287957.001]
  • [Cites] Biochem Soc Trans. 2005 Aug;33(Pt 4):679-83 [16042573.001]
  • [Cites] Cancer Causes Control. 2005 Apr;16(3):201-13 [15947872.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):2078-93 [15774796.001]
  • [Cites] Am J Dig Dis. 1960 Jun;5:576-7 [14412980.001]
  • [Cites] EMBO J. 1997 Jul 1;16(13):3797-804 [9233789.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8681-6 [10411935.001]
  • [Cites] Am J Pathol. 1999 Jun;154(6):1637-41 [10362787.001]
  • [Cites] Gut. 1999 Jun;44(6):826-33 [10323885.001]
  • [Cites] Oncogene. 1999 Jan 28;18(4):855-67 [10023661.001]
  • [Cites] Br J Cancer. 1998 Dec;78(12):1615-9 [9862572.001]
  • [Cites] Cancer Res. 1998 Nov 15;58(22):5023-6 [9823302.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10596-601 [9724749.001]
  • [Cites] Oncogene. 1998 Aug 13;17(6):719-25 [9715273.001]
  • [Cites] Cancer Res. 1998 Jul 15;58(14):3101-4 [9679977.001]
  • [Cites] Cancer Res. 1998 Apr 15;58(8):1713-8 [9563488.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2412-6 [9482899.001]
  • [Cites] Cell. 1998 Mar 6;92(5):645-56 [9506519.001]
  • [Cites] Genes Dev. 1997 Dec 15;11(24):3286-305 [9407023.001]
  • [Cites] Adv Cancer Res. 1998;72:141-96 [9338076.001]
  • [Cites] Cancer Res. 1997 Aug 15;57(16):3370-4 [9269998.001]
  • [Cites] Oncogene. 1997 Sep 4;15(10):1179-89 [9294611.001]
  • [Cites] Cancer Res. 1997 Jun 15;57(12):2485-92 [9192830.001]
  • [Cites] Cell. 1996 Oct 18;87(2):175-85 [8861902.001]
  • [Cites] Cell. 1996 Oct 18;87(2):159-70 [8861899.001]
  • [Cites] Int J Colorectal Dis. 1996;11(2):88-91 [8739833.001]
  • [Cites] Cell. 1996 Aug 23;86(4):543-52 [8752209.001]
  • [Cites] Genes Chromosomes Cancer. 1996 Apr;15(4):234-45 [8703849.001]
  • [Cites] Nat Genet. 1996 Jul;13(3):347-9 [8673135.001]
  • [Cites] Nat Genet. 1996 Jul;13(3):343-6 [8673134.001]
  • [Cites] Science. 1996 May 17;272(5264):1023-6 [8638126.001]
  • [Cites] Science. 1996 Jan 19;271(5247):350-3 [8553070.001]
  • [Cites] Science. 1987 Oct 9;238(4824):193-7 [2889267.001]
  • [Cites] Dis Colon Rectum. 1988 Jun;31(6):439-44 [3378468.001]
  • [Cites] Am J Surg Pathol. 1987 Apr;11(4):323-7 [3565675.001]
  • [Cites] Clin Genet. 1986 Mar;29(3):222-33 [3698331.001]
  • [Cites] Ann Surg Oncol. 1995 Sep;2(5):386-91 [7496832.001]
  • [Cites] Cancer Res. 1995 Dec 1;55(23):5548-50 [7585632.001]
  • [Cites] Cancer Res. 1994 Jun 1;54(11):3011-20 [8187091.001]
  • [Cites] Genomics. 1994 Feb;19(3):525-31 [8188295.001]
  • [Cites] Cancer Res. 1995 Jul 15;55(14):2972-7 [7606712.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 May 9;92(10):4482-6 [7753829.001]
  • [Cites] Neth J Med. 1995 Apr;46(4):185-8 [7760968.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Mar 28;92(7):3046-50 [7708772.001]
  • [Cites] Cancer. 1995 Mar 15;75(6 Suppl):1520-6 [7889485.001]
  • [Cites] Science. 1994 Mar 18;263(5153):1625-9 [8128251.001]
  • [Cites] Nat Genet. 1994 Aug;7(4):536-40 [7951326.001]
  • [Cites] Cancer Res. 1994 Nov 1;54(21):5523-6 [7923189.001]
  • [Cites] Gastroenterology. 1994 Oct;107(4):1183-8 [7926468.001]
  • [Cites] Cancer Detect Prev. 1994;18(3):187-95 [8076381.001]
  • [Cites] Cancer Res. 1994 Sep 1;54(17):4798-804 [8062281.001]
  • [Cites] Cancer Res. 1994 Jul 15;54(14):3676-81 [8033083.001]
  • [Cites] Nature. 1994 Mar 17;368(6468):258-61 [8145827.001]
  • [Cites] Am J Pathol. 1993 Jan;142(1):87-93 [7678722.001]
  • [Cites] Cell. 1993 Dec 17;75(6):1215-25 [8261515.001]
  • [Cites] Cell. 1993 Dec 17;75(6):1227-36 [8261516.001]
  • [Cites] Cell. 1993 Dec 3;75(5):1027-38 [8252616.001]
  • [Cites] Gut. 1993 May;34(5):621-4 [8504962.001]
  • [Cites] Nature. 1990 Nov 8;348(6297):125-32 [2122258.001]
  • [Cites] Lancet. 1992 Sep 12;340(8820):626-30 [1355210.001]
  • [Cites] EMBO J. 1992 Dec;11(13):5013-20 [1464323.001]
  • [Cites] Cell. 1992 Jun 26;69(7):1237-45 [1535557.001]
  • [Cites] Nature. 1992 Sep 17;359(6392):235-7 [1528264.001]
  • [Cites] Nature. 1992 Jul 2;358(6381):15-6 [1614522.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7555-9 [1699228.001]
  • [Cites] Arch Dis Child. 1991 Aug;66(8):971-5 [1656892.001]
  • [Cites] Am J Gastroenterol. 1991 Aug;86(8):946-51 [1858758.001]
  • [Cites] Am J Gastroenterol. 1991 Aug;86(8):941-5 [1858757.001]
  • [Cites] Cancer Res. 1991 Jun 15;51(12):3075-9 [2039987.001]
  • [Cites] Histopathology. 1988 Dec;13(6):619-30 [2853131.001]
  • [Cites] Nature. 1987 Aug 13-19;328(6131):614-6 [3039373.001]
  • [Cites] Cancer Res. 1989 Sep 1;49(17):4682-9 [2547513.001]
  • [Cites] Cancer Res. 2003 Aug 15;63(16):4878-81 [12941809.001]
  • [Cites] Lancet. 2003 Jul 5;362(9377):39-41 [12853198.001]
  • [Cites] Am J Clin Pathol. 2003 Jun;119(6):773-5 [12817423.001]
  • [Cites] N Engl J Med. 2003 Feb 27;348(9):791-9 [12606733.001]
  • [Cites] Carcinogenesis. 2003 Feb;24(2):283-90 [12584179.001]
  • [Cites] Hum Mol Genet. 2002 Nov 1;11(23):2961-7 [12393807.001]
  • [Cites] Scand J Gastroenterol. 2002 Sep;37(9):1048-53 [12374230.001]
  • [Cites] Nature. 2002 Jun 27;417(6892):949-54 [12068308.001]
  • [Cites] Br J Surg. 2002 Jul;89(7):845-60 [12081733.001]
  • [Cites] Am J Hum Genet. 2002 Apr;70(4):829-44 [11875759.001]
  • [Cites] Nat Genet. 2002 Feb;30(2):227-32 [11818965.001]
  • [Cites] Biol Cell. 2001 Sep;93(1-2):53-62 [11730323.001]
  • [Cites] Gastroenterology. 2001 Oct;121(4):830-8 [11606497.001]
  • [Cites] Nat Cell Biol. 2001 Apr;3(4):433-8 [11283620.001]
  • [Cites] Nat Cell Biol. 2001 Apr;3(4):429-32 [11283619.001]
  • [Cites] Cell. 2000 Oct 13;103(2):295-309 [11057902.001]
  • [Cites] Biochem J. 2000 Oct 15;351 Pt 2:289-305 [11023813.001]
  • [Cites] J Pathol. 2000 Dec;192(4):440-5 [11113860.001]
  • [Cites] Gastroenterology. 2000 Dec;119(6):1447-53 [11113065.001]
  • [Cites] Gastroenterology. 2000 Aug;119(2):323-32 [10930367.001]
  • [Cites] Gut. 2000 Jul;47(1):148-53 [10861278.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4820-5 [10781087.001]
  • [Cites] J Pathol. 2000 Mar;190(4):450-6 [10699994.001]
  • [Cites] Science. 1989 Apr 14;244(4901):217-21 [2649981.001]
  • [Cites] Cell. 1990 Jun 1;61(5):759-67 [2188735.001]
  • [Cites] Science. 1990 Jan 5;247(4938):49-56 [2294591.001]
  • [Cites] Cancer Res. 1990 Jan 15;50(2):261-5 [2295065.001]
  • [Cites] Endoscopy. 1982 Jan;14(1):28-30 [7056242.001]
  • (PMID = 19424478.001).
  • [ISSN] 1389-2029
  • [Journal-full-title] Current genomics
  • [ISO-abbreviation] Curr. Genomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC2674304
  • [Keywords] NOTNLM ; Colorectal / cancer / epigenomics. / genomics
  •  go-up   go-down


7. Voloyiannis T, Snyder MJ, Bailey RR, Pidala M: Management of the difficult colon polyp referred for resection: resect or rescope? Dis Colon Rectum; 2008 Mar;51(3):292-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of the difficult colon polyp referred for resection: resect or rescope?
  • PURPOSE: Patients are frequently referred for resection of difficult colon polyps.
  • Before colectomy the experienced surgeon has the option of repeating the colonoscopy to assess the polyp, tattoo the site, and potentially remove the polyp.
  • METHODS: All new patients referred during a five-year period to an 11-physician colon and rectal surgical group with the diagnosis of colon polyp (CPT 211.3) that was not previously removed were retrospectively reviewed.
  • Patients with rectal polyps, inflammatory bowel disease, previous cancer, or familial adenomatous polyposis were excluded.
  • Patient demographics, details of the polyps, success of polypectomy, reasons for surgical resection, pathology, and complications were analyzed.
  • The remaining 71 patients had a subsequent colon resection after at least one repeat colonoscopy.
  • In 26 cases the polyp site was tattooed for later localization.
  • Patients with large difficult polyps referred for resection should be considered for repeat colonoscopy before surgery.
  • [MeSH-major] Colonic Polyps / surgery. Colonoscopy / utilization

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • MedlinePlus Health Information. consumer health - Colonoscopy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Dis Colon Rectum. 2008 Aug;51(8):1300
  • (PMID = 18202891.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


8. Velmurugan B, Singh RP, Kaul N, Agarwal R, Agarwal C: Dietary feeding of grape seed extract prevents intestinal tumorigenesis in APCmin/+ mice. Neoplasia; 2010 Jan;12(1):95-102
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Immunol. 2000 Apr 15;164(8):4032-6 [10754295.001]
  • [Cites] Br J Nutr. 2008 Jul;100(1):36-43 [18298868.001]
  • [Cites] Carcinogenesis. 2000 Oct;21(10):1909-15 [11023550.001]
  • [Cites] Biofactors. 2000;12(1-4):129-33 [11216473.001]
  • [Cites] Anticancer Res. 2001 Mar-Apr;21(2A):911-5 [11396184.001]
  • [Cites] J Agric Food Chem. 2001 Nov;49(11):5348-55 [11714327.001]
  • [Cites] Nutr Cancer. 2001;39(2):252-8 [11759289.001]
  • [Cites] Ann N Y Acad Sci. 2002 May;957:260-70 [12074978.001]
  • [Cites] Cell. 2002 Oct 18;111(2):241-50 [12408868.001]
  • [Cites] Rapid Commun Mass Spectrom. 2003;17(1):9-16 [12478550.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):391-400 [12750232.001]
  • [Cites] Cancer Res. 2003 Jul 15;63(14):4037-43 [12874003.001]
  • [Cites] Curr Pharm Des. 2003;9(27):2229-51 [14529404.001]
  • [Cites] Cancer Res. 2003 Dec 1;63(23):8516-22 [14679019.001]
  • [Cites] Int J Cancer. 2004 Feb 20;108(5):733-40 [14696100.001]
  • [Cites] Breast Cancer Res Treat. 2004 May;85(1):1-12 [15039593.001]
  • [Cites] Oncogene. 2004 Oct 21;23(49):8128-34 [15377995.001]
  • [Cites] Science. 1992 May 1;256(5057):668-70 [1350108.001]
  • [Cites] Nature. 1992 Sep 17;359(6392):235-7 [1528264.001]
  • [Cites] Mol Biol Cell. 1993 Sep;4(9):897-906 [7903056.001]
  • [Cites] Nature. 1994 Jun 16;369(6481):574-8 [7911228.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1994;59:517-21 [7587107.001]
  • [Cites] Science. 1996 May 17;272(5264):1023-6 [8638126.001]
  • [Cites] Cell. 1996 Oct 18;87(2):159-70 [8861899.001]
  • [Cites] Science. 1997 Mar 21;275(5307):1787-90 [9065402.001]
  • [Cites] Biochim Biophys Acta. 1997 Jun 7;1332(3):F127-47 [9196022.001]
  • [Cites] Horm Res. 1997;48 Suppl 3:2-4 [9267809.001]
  • [Cites] Cancer Res. 1998 Mar 15;58(6):1130-4 [9515795.001]
  • [Cites] Mol Cell Biochem. 1999 Jun;196(1-2):99-108 [10448908.001]
  • [Cites] Carcinogenesis. 1999 Sep;20(9):1737-45 [10469619.001]
  • [Cites] J Nutr. 2004 Dec;134(12 Suppl):3445S-3452S [15570052.001]
  • [Cites] Recent Results Cancer Res. 2005;166:177-211 [15648191.001]
  • [Cites] Antioxid Redox Signal. 2005 Jan-Feb;7(1-2):108-18 [15650400.001]
  • [Cites] Life Sci. 2005 May 6;76(25):2995-3000 [15820509.001]
  • [Cites] Carcinogenesis. 2005 May;26(5):892-9 [15695237.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Jul;14(7):1608-12 [16030090.001]
  • [Cites] Am J Surg. 2006 Apr;191(4):517-26 [16531147.001]
  • [Cites] J Agric Food Chem. 2006 Mar 22;54(6):2392-7 [16536624.001]
  • [Cites] Mol Carcinog. 2006 Jun;45(6):447-54 [16688727.001]
  • [Cites] Clin Cancer Res. 2006 Oct 15;12(20 Pt 1):6194-202 [17062697.001]
  • [Cites] Int J Cancer. 2006 Dec 1;119(11):2657-64 [16991129.001]
  • [Cites] J Agric Food Chem. 2006 Dec 13;54(25):9322-8 [17147414.001]
  • [Cites] Methods Mol Biol. 2007;361:63-91 [17172707.001]
  • [Cites] Cancer Biol Ther. 2006 Dec;5(12):1658-64 [17106247.001]
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5976-82 [17575168.001]
  • [Cites] Cancer Res. 2007 Oct 15;67(20):9937-44 [17942926.001]
  • [Cites] Neoplasma. 2008;55(3):165-76 [18348648.001]
  • [Cites] Carcinogenesis. 2000 Jul;21(7):1319-27 [10874009.001]
  • (PMID = 20072658.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCCIH NIH HHS / AT / AT003623-03; United States / NCCIH NIH HHS / AT / R01 AT003623; United States / NCCIH NIH HHS / AT / R01 AT003623-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Myc protein, mouse; 0 / Plant Extracts; 0 / Proliferating Cell Nuclear Antigen; 0 / Proto-Oncogene Proteins c-myc; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, mouse; EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2
  • [Other-IDs] NLM/ PMC2805888
  •  go-up   go-down


9. Landau D, Garrett C, Chodkiewicz C: A case of primary squamous cell colon cancer. J Oncol Pharm Pract; 2007 Mar;13(1):47-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of primary squamous cell colon cancer.
  • Carcinomas of the colon are a common cancer seen in both inpatient and outpatient settings with approximately 145,000 new cases being diagnosed every year in the USA.
  • Despite the frequency of these cancers being seen, it continues to be a rarity to see a primary squamous cell cancer of the colon.
  • While the exact aetiology of this rare tumour is currently still not completely understood, various aetiologies include chronic irritation leading to squamous differentiation, embryonic migration of ectodermal cells to the colon, or adenomas undergoing squamous transformation.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Colonic Neoplasms / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


10. Valantas MR, Farmer WM, DiPalma JA: Do gastroenterologists notify polyp patients that family members should have screening? South Med J; 2005 Feb;98(2):162-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Do gastroenterologists notify polyp patients that family members should have screening?
  • OBJECTIVE: The objective of this study was to determine whether patients found to have adenomatous polyps or cancer were notified that their relatives should have screening, due to an increased risk of developing colorectal cancer.
  • METHODS: Consecutive (n = 121) colonoscopy patients from December of 1999 to October of 2001 found to have adenomatous colon polyps or colon cancer formed the study group.
  • Adenomatous polyps were seen in 95%, and cancer seen in 5%.
  • Overall, 30% of the patients were notified: 23 of 82 (28%) in the polyp group and 3 of 4 (75%) in the cancer group.
  • Advanced adenomas or multiple adenomas were noted in 28 of the 82 (34%).
  • CONCLUSIONS: Gastroenterologists should be aware of the need for increased attention to family notification, especially in those with advanced adenomas or multiple adenomas.
  • Template notification letters may complement the polyp surveillance programs that many colonoscopists use.
  • [MeSH-major] Colonic Neoplasms / diagnosis. Intestinal Polyps / diagnosis

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15759945.001).
  • [ISSN] 0038-4348
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


11. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


12. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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


13. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter methylation status of the MGMT, hMLH1, and CDKN2A/p16 genes in non-neoplastic mucosa of patients with and without colorectal adenomas.
  • CpG island methylation has been observed in aberrant crypt foci (ACF) and adenomas in the colon, implicating it in the earliest aspects of colon cancer formation.
  • In addition, some investigators have identified an age-related increase in DNA methylation of the ESR1 locus in the colon mucosa, suggesting that DNA methylation may be a pre-neoplastic change that increases the risk of colon adenomas and colon cancer.
  • We investigated the methylation status in the promoter regions of the CDKN2A/p16, hMLH1, and MGMT genes in human non-neoplastic rectal mucosa and evaluated whether these methylation markers may predict the presence of adenomatous polyps in the colon.
  • The promoter methylation patterns of these genes were examined in rectal biopsies (mucosa samples) of 97 colorectal adenoma cases and 94 healthy controls using methylation-specific PCR (MSP) assays.
  • The methylation status of these genes in rectal mucosa biopsies detected by MSP assays may not distinguish between patients with and without adenomas in the colon.

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


14. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Cancer. 2000 Jul 1;87(1):1-4 [10861445.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Nov 25;94(24):13087-92 [9371804.001]
  • [Cites] Free Radic Biol Med. 2000 May 15;28(10):1478-86 [10927172.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 5;97(25):13573-8 [11106395.001]
  • [Cites] J Biol Chem. 2001 Aug 10;276(32):30085-91 [11404354.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6388-93 [11522631.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3481-6 [11904413.001]
  • [Cites] Carcinogenesis. 2002 Jun;23(6):993-1001 [12082021.001]
  • [Cites] J Biol Chem. 2002 Jul 26;277(30):26987-93 [12016206.001]
  • [Cites] J Biol Chem. 2002 Aug 30;277(35):31673-8 [12077143.001]
  • [Cites] Chem Biol. 2002 Sep;9(9):1033-41 [12323378.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):12691-6 [12226478.001]
  • [Cites] Biochemistry. 2003 Apr 1;42(12):3608-16 [12653565.001]
  • [Cites] Arch Biochem Biophys. 2003 Sep 1;417(1):3-11 [12921773.001]
  • [Cites] Trends Biochem Sci. 2003 Dec;28(12):646-54 [14659696.001]
  • [Cites] J Clin Invest. 2003 Dec;112(12):1887-94 [14679184.001]
  • [Cites] Arch Biochem Biophys. 2004 Mar 1;423(1):12-22 [14989259.001]
  • [Cites] J Biol Chem. 2004 Mar 12;279(11):9750-7 [14688248.001]
  • [Cites] J Comput Chem. 2004 Oct;25(13):1605-12 [15264254.001]
  • [Cites] J Biol Chem. 2004 Sep 10;279(37):38177-83 [15247209.001]
  • [Cites] J Med Chem. 1991 Nov;34(11):3242-7 [1956043.001]
  • [Cites] Cancer Res. 1994 Nov 15;54(22):5947-52 [7954427.001]
  • [Cites] J Biol Chem. 1996 Sep 27;271(39):23690-7 [8798591.001]
  • [Cites] EMBO J. 1998 Jan 15;17(2):363-7 [9430628.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):9997-10002 [9707589.001]
  • [Cites] Cell. 1998 Oct 16;95(2):249-58 [9790531.001]
  • [Cites] J Natl Cancer Inst. 1999 Jan 6;91(1):86-8 [9890175.001]
  • [Cites] Mutat Res. 1999 Mar 8;424(1-2):37-49 [10064848.001]
  • [Cites] J Surg Oncol. 1999 Apr;70(4):222-9 [10219017.001]
  • [Cites] Chem Res Toxicol. 2005 Jan;18(1):87-94 [15651853.001]
  • [Cites] Antioxid Redox Signal. 2005 Mar-Apr;7(3-4):367-84 [15706084.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9132-6 [16230367.001]
  • [Cites] Mutat Res. 2005 Dec 11;591(1-2):34-44 [16099477.001]
  • [Cites] J Biol Chem. 2005 Dec 9;280(49):40684-98 [16176930.001]
  • [Cites] Chem Res Toxicol. 2006 Jan;19(1):50-7 [16411656.001]
  • [Cites] Mol Carcinog. 2006 Feb;45(2):93-105 [16329147.001]
  • [Cites] Mol Cancer Res. 2006 Apr;4(4):221-33 [16603636.001]
  • [Cites] Chem Res Toxicol. 2006 Dec;19(12):1580-94 [17173371.001]
  • [Cites] DNA Repair (Amst). 2007 Jun 1;6(6):695-711 [17337257.001]
  • [Cites] Nucleic Acids Res. 2007;35(8):2522-32 [17403694.001]
  • [Cites] Nat Rev Drug Discov. 2007 Aug;6(8):662-80 [17667957.001]
  • [Cites] Carcinogenesis. 2007 Aug;28(8):1807-13 [17347141.001]
  • [Cites] J Biol Chem. 2007 Oct 12;282(41):30078-84 [17716976.001]
  • [Cites] Science. 2008 May 23;320(5879):1050-4 [18497292.001]
  • [Cites] Cancer Res. 2008 Jun 1;68(11):4142-9 [18519673.001]
  • [Cites] Free Radic Biol Med. 2008 Jul 1;45(1):18-31 [18439435.001]
  • [Cites] J Clin Invest. 2008 Jul;118(7):2516-25 [18521188.001]
  • [Cites] Nitric Oxide. 2008 Sep;19(2):146-51 [18474261.001]
  • [Cites] Mol Pharmacol. 2008 Aug;74(2):505-16 [18477668.001]
  • [Cites] Carcinogenesis. 2008 Sep;29(9):1799-806 [18567620.001]
  • [Cites] DNA Repair (Amst). 2008 Oct 1;7(10):1731-45 [18706524.001]
  • [Cites] Arch Biochem Biophys. 2009 Apr 15;484(2):134-45 [19056332.001]
  • [Cites] Cancer Res. 1997 May 1;57(9):1794-7 [9135024.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Nov 25;94(24):12869-74 [9371767.001]
  • [Cites] Ann N Y Acad Sci. 2000;899:209-21 [10863541.001]
  • (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
  •  go-up   go-down


15. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Bowel Movement.
  • MedlinePlus Health Information. consumer health - Colonic Diseases.
  • MedlinePlus Health Information. consumer health - Colonoscopy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


16. Tony J, Harish K, Ramachandran TM, Sunilkumar K, Thomas V: Profile of colonic polyps in a southern Indian population. Indian J Gastroenterol; 2007 May-Jun;26(3):127-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17704579.001).
  • [ISSN] 0254-8860
  • [Journal-full-title] Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology
  • [ISO-abbreviation] Indian J Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  •  go-up   go-down


17. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


18. Zagani R, Hamzaoui N, Cacheux W, de Reyniès A, Terris B, Chaussade S, Romagnolo B, Perret C, Lamarque D: Cyclooxygenase-2 inhibitors down-regulate osteopontin and Nr4A2-new therapeutic targets for colorectal cancers. Gastroenterology; 2009 Oct;137(4):1358-66.e1-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND & AIMS: Cyclooxygenase-2 inhibitors reduce colon cancer risk by mechanisms that are not fully understood.
  • We performed microarray analysis of adenomas from Apc(Delta14/+) mice to identify genes that respond to these drugs.
  • Findings were further assessed using Apc(lox/lox)vil-CreER(T2) mice, the CT26 cancer cell line, and human colon tumor samples.
  • RESULTS: Microarray analysis revealed that osteopontin, a marker of colon cancer progression, was down-regulated in polyps from Apc(Delta14/+) mice given parecoxib compared with controls.
  • Apc(Delta14/+) mice given parecoxib had longer survival times and reduced polyp burdens.
  • Osteopontin was quickly down-regulated by parecoxib in intestinal polyps from Apc(Delta14/+) mice, and 2 components of the osteopontin regulatory network-the orphan nuclear receptor NR4A2 and Wnt/beta-catenin signaling-were sequentially repressed.
  • NR4A2 levels were reduced in adenomas from patients treated with rofecoxib.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Antineoplastic Agents / pharmacology. Colonic Polyps / drug therapy. Colorectal Neoplasms / drug therapy. Cyclooxygenase 2 / metabolism. Cyclooxygenase Inhibitors / therapeutic use. DNA-Binding Proteins / metabolism. Osteopontin / metabolism. Transcription Factors / metabolism

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19549529.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CTNNB1 protein, mouse; 0 / Cyclooxygenase Inhibitors; 0 / DNA-Binding Proteins; 0 / Isoxazoles; 0 / Lactones; 0 / NR4A2 protein, human; 0 / Nr4a2 protein, mouse; 0 / Nuclear Receptor Subfamily 4, Group A, Member 2; 0 / SPP1 protein, human; 0 / Spp1 protein, mouse; 0 / Sulfones; 0 / Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin; 0QTW8Z7MCR / rofecoxib; 106441-73-0 / Osteopontin; 9TUW81Y3CE / parecoxib; EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
  •  go-up   go-down


19. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


20. Bretthauer M, Hoff G: [Prevention and early diagnosis of colorectal cancer]. Tidsskr Nor Laegeforen; 2007 Oct 18;127(20):2688-91
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


21. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


22. Ji JH, Park BJ, Park YS, Hwang JH, Chung SH, Kim N, Lee DH, Jung HC, Song IS: [Clinicopathologic study of colorectal polyps and obesity in Korean adult]. Korean J Gastroenterol; 2007 Jan;49(1):10-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinicopathologic study of colorectal polyps and obesity in Korean adult].
  • Numerous epidemiologic studies have shown a positive association between obesity and colorectal polyps.
  • There are few studies investigating the association between colorectal adenomatous polyps and body fat composition in Korea.
  • We tried to examine the relationship between body fatness and colorectal adenomatous polyps in health check-up subjects in Korea.
  • METHODS: Six thousand seven hundred and six routine health check-up subjects, who visited our hospital between March 2002 and April 2005 and underwent distal colon examimation with sigmoidoscopy, were enrolled in this study.
  • Among them, colonoscopy was done in 860 patients to evaluate the entire colon.
  • We tried to reveal the relationship between body mass index (BMI) and size, location, number and histopathological type of polyps.
  • RESULTS: The mean value of BMI in total polyp-free group (23.8+/-2.9) was not different from that of the polyp group (24.5+/-2.8, p=0.09).
  • The frequency of rectosigmoid polyps in obese patients (20.4%) was higher than that in non-obese patients (16.0%, p<0.05).
  • The frequency of adenomatous polyp was not different between obese and non-obese group.
  • Number of polyps (> or=4) correlated well with obesity.
  • Moreover, age and triglyceride level in patients with colonic adenoma were significantly higher than in patients without colonic adenom.
  • CONCLUSIONS: This study shows that obesity is not associated with colonic adenomatous polyp in Korean population.
  • However, we observed that obesity may be associated with rectosigmoid colon polyps.
  • Furthermore, age and triglyceride level might be the risk factors of colonic adenomatous polyps in Korean population.
  • [MeSH-major] Adenomatous Polyps / complications. Colonic Neoplasms / complications. Obesity / complications
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Body Mass Index. Colonic Polyps / complications. Colonic Polyps / epidemiology. Colonic Polyps / pathology. Comorbidity. Female. Humans. Korea. Male. Middle Aged. Retrospective Studies. Sigmoidoscopy

  • Genetic Alliance. consumer health - Obesity.
  • MedlinePlus Health Information. consumer health - Obesity.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18167428.001).
  • [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)
  •  go-up   go-down


23. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Biol. 2000 Aug;20(15):5540-53 [10891493.001]
  • [Cites] Lung Cancer. 2008 Jan;59(1):24-31 [17854949.001]
  • [Cites] J Natl Cancer Inst. 2001 Jun 6;93(11):824-42 [11390532.001]
  • [Cites] Science. 2001 Aug 10;293(5532):1074-80 [11498575.001]
  • [Cites] Curr Opin Oncol. 2001 Nov;13(6):477-83 [11673688.001]
  • [Cites] J Cell Sci. 2002 Feb 15;115(Pt 4):689-98 [11865025.001]
  • [Cites] Nature. 2002 May 23;417(6887):455-8 [12024216.001]
  • [Cites] Br J Cancer. 2002 Jun 5;86(11):1817-23 [12087472.001]
  • [Cites] Oncogene. 2002 Aug 12;21(35):5427-40 [12154405.001]
  • [Cites] J Exp Clin Cancer Res. 2002 Sep;21(3):377-82 [12385581.001]
  • [Cites] Chem Biol. 2002 Nov;9(11):1167-73 [12445767.001]
  • [Cites] Cancer Res. 2002 Dec 15;62(24):7213-8 [12499261.001]
  • [Cites] Biochem J. 2003 Mar 15;370(Pt 3):737-49 [12429021.001]
  • [Cites] Clin Cancer Res. 2003 Mar;9(3):1112-7 [12631615.001]
  • [Cites] Ann N Y Acad Sci. 2003 Mar;983:220-31 [12724227.001]
  • [Cites] J Biol Chem. 2003 Sep 12;278(37):35775-80 [12837748.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 11;101(19):7398-403 [15123805.001]
  • [Cites] Mol Cell Biol. 2004 Jun;24(12):5106-18 [15169878.001]
  • [Cites] J Cell Physiol. 2000 Jul;184(1):1-16 [10825229.001]
  • [Cites] J Assoc Acad Minor Phys. 1999;10(3):59-67 [10826011.001]
  • [Cites] Cancer. 1980 Mar 15;45(5 Suppl):1185-92 [7357511.001]
  • [Cites] Cell. 1997 Aug 22;90(4):595-606 [9288740.001]
  • [Cites] Cancer. 1997 Nov 1;80(9):1803-4 [9351551.001]
  • [Cites] Cancer. 1999 Apr 15;85(8):1670-6 [10223559.001]
  • [Cites] J Pathol. 2005 Jan;205(1):65-73 [15586362.001]
  • [Cites] Nat Genet. 2005 Apr;37(4):391-400 [15765097.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2684-9 [15805266.001]
  • [Cites] Nature. 2005 Jun 30;435(7046):1262-6 [15988529.001]
  • [Cites] Int J Cancer. 2005 Oct 10;116(6):914-9 [15856472.001]
  • [Cites] Ann Thorac Surg. 2006 Aug;82(2):396-401; discussion 401 [16863736.001]
  • [Cites] Methods Enzymol. 2006;410:400-15 [16938563.001]
  • [Cites] Science. 2006 Oct 13;314(5797):268-74 [16959974.001]
  • [Cites] Histopathology. 2007 Jan;50(1):113-30 [17204026.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] Cell. 2007 Feb 23;128(4):669-81 [17320505.001]
  • [Cites] Cancer Res. 2007 Mar 15;67(6):2685-92 [17363589.001]
  • [Cites] Semin Cancer Biol. 2007 Oct;17(5):363-9 [17555985.001]
  • [Cites] Virchows Arch. 2007 Oct;451(4):763-9 [17674041.001]
  • [Cites] J Clin Oncol. 2007 Oct 1;25(28):4358-64 [17906200.001]
  • [Cites] Science. 2007 Nov 16;318(5853):1108-13 [17932254.001]
  • [Cites] Hum Mol Genet. 2001 Apr;10(7):687-92 [11257100.001]
  • (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
  •  go-up   go-down


24. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Hazardous Substances Data Bank. L-TYROSINE .
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


25. Bazan HA, Legmann MD, Dardik H: A replaced right hepatic artery and a large duodenal polyp in attenuated familial polyposis. Dig Dis Sci; 2005 Aug;50(8):1523-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A replaced right hepatic artery and a large duodenal polyp in attenuated familial polyposis.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Duodenal Obstruction / etiology. Hepatic Artery / abnormalities. Intestinal Polyps / etiology

  • Genetic Alliance. consumer health - Familial Polyposis.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Dis Colon Rectum. 2002 Jan;45(1):127-34; discussion 134-6 [11786778.001]
  • [Cites] Am Surg. 1998 Aug;64(8):758-61 [9697907.001]
  • (PMID = 16110846.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


26. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Hazardous Substances Data Bank. DEOXYCHOLIC ACID .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


27. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


28. Gonzalez AB, Stafford I, Mancuso P, Carney S: Delivery of a polyp. Obstet Gynecol; 2008 Aug;112(2 Pt 2):488-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Delivery of a polyp.
  • Although there is overlap between symptoms of colon cancer and normal pregnancy, clinicians should be vigilant identifying those at risk and offer colorectal cancer screening when appropriate.
  • CASES: Three women in their 30s passed or prolapsed adenomatous tissue per rectum during the second stage of labor.
  • [MeSH-major] Colonic Polyps / diagnosis. Delivery, Obstetric. Incidental Findings
  • [MeSH-minor] Adenoma / pathology. Adult. Colon / pathology. Colonic Neoplasms / pathology. Female. Humans. Pregnancy. Pregnancy Complications, Neoplastic / diagnosis

  • MedlinePlus Health Information. consumer health - Childbirth.
  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18669775.001).
  • [ISSN] 0029-7844
  • [Journal-full-title] Obstetrics and gynecology
  • [ISO-abbreviation] Obstet Gynecol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


29. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • MedlinePlus Health Information. consumer health - Colonoscopy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


30. Ramirez M, Schierling S, Papaconstantinou HT, Thomas JS: Management of the malignant polyp. Clin Colon Rectal Surg; 2008 Nov;21(4):286-90
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of the malignant polyp.
  • In the United States, the prevalence of adenomatous polyps found during colonoscopic evaluation ranges from 25 to 41%, and of these, 2 to 5% contain invasive malignancy.
  • The management of the malignant polyp continues to be challenging.
  • Endoscopic resection by polypectomy has been shown to be sufficient for management of certain polyps containing cancer; however, it is important to keep in mind that polypectomy does not remove the lymph node drainage basin and may be an inadequate resection for some adenocarcinoma containing polyps that have specific histologic features.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Surg Endosc. 1999 Mar;13(3):231-2 [10064752.001]
  • [Cites] Gastroenterology. 1990 Feb;98(2):371-9 [2403953.001]
  • [Cites] Dis Colon Rectum. 2000 Sep;43(9):1246-9 [11005491.001]
  • [Cites] World J Surg. 2000 Sep;24(9):1047-51 [11036280.001]
  • [Cites] Dis Colon Rectum. 2001 May;44(5):746-8 [11357040.001]
  • [Cites] Ann Surg. 1975 Oct;182(4):516-25 [1180588.001]
  • [Cites] Dis Colon Rectum. 2002 Feb;45(2):200-6 [11852333.001]
  • [Cites] Cancer. 1975 Dec;36(6):2251-70 [1203876.001]
  • [Cites] Surg Clin North Am. 2002 Oct;82(5):959-66 [12507202.001]
  • [Cites] J Am Coll Surg. 2003 Aug;197(2):177-81 [12892794.001]
  • [Cites] Dis Colon Rectum. 2005 Aug;48(8):1588-96 [15937622.001]
  • [Cites] Gastroenterology. 1991 Jan;100(1):64-7 [1796931.001]
  • [Cites] Am J Gastroenterol. 1991 Aug;86(8):941-5 [1858757.001]
  • [Cites] Am J Gastroenterol. 1991 Aug;86(8):946-51 [1858758.001]
  • [Cites] World J Surg. 1991 Jan-Feb;15(1):35-40 [1994604.001]
  • [Cites] Cancer. 1989 Nov 1;64(9):1937-47 [2477139.001]
  • [Cites] Gastroenterology. 1986 Aug;91(2):419-27 [3721127.001]
  • [Cites] Gastroenterology. 1995 Jun;108(6):1657-65 [7768369.001]
  • [Cites] Am J Gastroenterol. 1994 Oct;89(10):1775-80 [7942665.001]
  • [Cites] Endoscopy. 1993 Sep;25(7):455-61 [8261988.001]
  • [Cites] Surg Endosc. 1997 Jun;11(6):643-4 [9171124.001]
  • [Cites] Gastroenterology. 1985 Aug;89(2):328-36 [4007423.001]
  • [Cites] Ann Surg. 2003 Jul;238(1):67-72 [12832967.001]
  • [Cites] Arch Surg. 2004 Jan;139(1):39-42 [14718273.001]
  • [Cites] Zentralbl Chir. 2004 Aug;129(4):291-5 [15354251.001]
  • [Cites] Dis Colon Rectum. 2004 Nov;47(11):1789-96; discussion 1796-7 [15622570.001]
  • [Cites] Surg Endosc. 2005 Sep;19(9):1252-5 [16132333.001]
  • [Cites] Curr Opin Gastroenterol. 2006 Jan;22(1):54-9 [16319677.001]
  • [Cites] CA Cancer J Clin. 1997 Mar-Apr;47(2):93-112 [9074488.001]
  • [Cites] Cancer. 1992 Sep 1;70(5 Suppl):1236-45 [1511370.001]
  • [Cites] Gastrointest Endosc. 1999 Jun;49(6):731-5 [10343218.001]
  • (PMID = 20011440.001).
  • [ISSN] 1530-9681
  • [Journal-full-title] Clinics in colon and rectal surgery
  • [ISO-abbreviation] Clin Colon Rectal Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2780260
  • [Keywords] NOTNLM ; Haggitt level / Malignant polyp / adenocarcinoma / adenomatous polyp / endoscopic polypectomy / segmental colectomy
  •  go-up   go-down


31. Cappell MS: Reducing the incidence and mortality of colon cancer: mass screening and colonoscopic polypectomy. Gastroenterol Clin North Am; 2008 Mar;37(1):129-60, vii-viii
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reducing the incidence and mortality of colon cancer: mass screening and colonoscopic polypectomy.
  • Most colon cancers arise from conventional adenomatous polyps (conventional adenoma-to-carcinoma sequence), while some colon cancers appear to arise from the recently recognized serrated adenomatous polyp (serrated adenoma-to-carcinoma theory).
  • Because conventional adenomas and serrated adenomas are usually asymptomatic, mass screening of asymptomatic patients has become the cornerstone for detecting and eliminating these precursor lesions to reduce the risk of colon cancer.
  • A minimal colonoscopic withdrawal time of 6 minutes is important to maximize polyp detection at colonoscopy.
  • Chromoendoscopy is an experimental technique used to highlight abnormal colonic areas to identify neoplastic tissue and to potentially determine the histology of colonic polyps at colonoscopy based on superficial pit anatomy.
  • [MeSH-major] Colonic Neoplasms. Colonoscopy / methods. Mass Screening / methods


32. Stănciulea O, Preda C, Herlea V, Popa M, Ulmeanu D, Vasilescu C: [Rare indication of cephalic duodenopancreatectomy with total gastrectomy--periampullary carcinoma in moderate form of familial adenomatous polyposis]. Chirurgia (Bucur); 2007 Mar-Apr;102(2):215-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Rare indication of cephalic duodenopancreatectomy with total gastrectomy--periampullary carcinoma in moderate form of familial adenomatous polyposis].
  • [Transliterated title] Indicaţie rară de duodenopancreatectomie cefalică cu gastrectomie totală-- adenocarcinom periampular cu polipoză adenomatoasă familială forma atenuată.
  • We present the case of a 52 years old man, with significant familial history, diagnosed with familial adenomatous polyposis-attenuated form, with no clinical and endoscopic surveillance until 2001 when he was admitted for an upper gastrointestinal haemorrhage episode.
  • Upper gastrointestinal scopy revealed duodenal adenomatous polyps and gastric hyperplastic polyps.
  • The histopathological exam revealed duodenal G2 adenocarcinoma pT3N0, and gastric hyperplastic polyps with no signs of dysplasia.
  • In 2002 the patient was admitted for rectal bleeding and colonoscopy showed 2 sigmoid polyps, appropriate for endoscopic removal and a poly-lobate polyp in the transverse colon.
  • March 2003--the patient underwent endoscopic removal for a rectal polyp (histopathological exam: moderate dysplasia).
  • The surgical procedure recommended in patients with attenuated form of familial adenomatous polyposis and suspect periampullary lesions is duodenopancreatectomy.
  • The particularity of the case is the association of total gastrectomy for gastric hyperplastic polyps.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Carcinoma / surgery. Duodenal Neoplasms / surgery. Gastrectomy. Neoplasms, Multiple Primary / surgery. Pancreaticoduodenectomy / methods


33. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • Genetic Alliance. consumer health - Obesity.
  • MedlinePlus Health Information. consumer health - Obesity.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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)
  •  go-up   go-down


34. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Hazardous Substances Data Bank. PALMITIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


35. Barreda B F, Combe G J, Valdez P LA, Sánchez L J: [Clinical aspects in polyps of the colon]. Rev Gastroenterol Peru; 2007 Apr-Jun;27(2):131-47
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical aspects in polyps of the colon].
  • [Transliterated title] Aspectos clínicos de los pólipos colónicos.
  • INTRODUCTION: The colonics polyps according to their number, size, location, age of presentation and mainly, according to their histology, have the potentiality of malignant degeneration, which makes of a continuous study and pursuit susceptible.
  • OBJECTIVES: To evaluate the relation between the histologic type of the colon polyps, its location, the degree of dysplasia, the size, its possible commitment by carcinoma, the age, sex and the handling that has occurred them, in a series of 684 patients of the National Institute of Enfermedades Neoplásicas (INEN) between the 1 of January from 1974 to the 31 of March of the 2004.
  • MATERIAL AND METHODS: The revision of clinical histories of 840 patients with the diagnosis of colon polyp was made who attended the service of Gastroenterology of the INEN between the 1 of January from 1974 to the 31 of March of 2004 and a card predesigned for each clinical history filled.
  • 1162 resecteds polyps evaluated themselves in this period.
  • The final sample was of 684 patients, in whom it was 1057 polyps.
  • Other endoscopic findings were: internal hemorrhoids (172), colonic diverticulosis (50), anal fissure (4), and nonspecific ulcerative colitis (2).
  • RESULTS: 1057 polyps extirpated, by means of the endoscopy polipectomy were 1016, with colectomy were 32 and with transanal resection without colectomy they 9.
  • Within the histology of the 1057 polyps, 331 was briefed (31.3%) that were hyperplasic, 448 (42.4%) adenomas, 278 (26.3%) others and 35 (8.2%) adenocarcinomas on adenomas.
  • The location but frequence of the adenomas was in the left colon (76.6%).
  • Adenocarcinoma (carcinomas on adenomas), was present mainly in polyps villous type, with dysplasia severe and greater to 10 mm.
  • Nevertheless, in smaller polyps of 5mm with dysplasia severe, was a polyp invaded by cancer, that represents the 0,8% of millimetric polyps.
  • The made handling was mainly endoscopic, with 96% of the resected polyps this way, also slogan transanal resection and segmental colonic resection.
  • The colectomy was necessary in 3% of all the made interventions, dysplasia severe or carcinoma was made in adenomatous polyps with, and in greater percentage in greater polyps of 20 mm (53%).
  • On the other hand, in polyps with level of invasion Haggitt 3 and 4, the colectomy was the election treatment.
  • CONCLUSIONS: The Evaluation of colonic polyps in INEN is predominantly by endoscopy.
  • The polyps are more frequent over the 50 years and have preferred location in the left colon.
  • The carcinoma is more probable with severe dysplasia and greater size of the adenoma.
  • All polyps, from the millimetric ones, including the hyperplasic, must be considered marks of neoplasia and extirpated in its totality.
  • [MeSH-major] Colonic Polyps / pathology. Colonic Polyps / surgery

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17712391.001).
  • [ISSN] 1022-5129
  • [Journal-full-title] Revista de gastroenterología del Perú : órgano oficial de la Sociedad de Gastroenterología del Perú
  • [ISO-abbreviation] Rev Gastroenterol Peru
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Peru
  •  go-up   go-down


36. Kim S, Baron JA, Mott LA, Burke CA, Church TR, McKeown-Eyssen GE, Cole BF, Haile RW, Sandler RS: Aspirin may be more effective in preventing colorectal adenomas in patients with higher BMI (United States). Cancer Causes Control; 2006 Dec;17(10):1299-304
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aspirin may be more effective in preventing colorectal adenomas in patients with higher BMI (United States).
  • Obesity is a risk factor for colon cancer, possibly due to elevated levels of circulating cytokines derived from adipose tissue.
  • Aspirin, which may affect the levels of these cytokines, has been shown in randomized controlled trials to decrease the risk of colorectal adenomas.
  • Data were available from the Aspirin/Folate Polyp Prevention Study, a randomized controlled trial of aspirin and folic acid to prevent recurrent colorectal adenomas.
  • For the analysis of the effect of aspirin on the recurrence of colorectal adenoma by BMI, we computed risk ratios for aspirin versus placebo within the three BMI strata using a modified Poisson model.
  • Overall the risk reduction of adenomas with a daily dose of 325 mg aspirin was greater among subjects with higher BMI.
  • Among obese subjects the risk ratio (RR) for advanced adenomas compared with placebo was 0.44 (95% CI 0.17-1.10), versus RR = 1.23 (95% CI 0.55-2.77) among those with normal weight.
  • However, 81 mg aspirin daily did not interact with BMI to modify the risk of adenomas in such a fashion.
  • [MeSH-major] Adenomatous Polyps / prevention & control. Aspirin / pharmacology. Body Mass Index. Colorectal Neoplasms / prevention & control

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17111262.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK34987; United States / NCI NIH HHS / CA / R01 CA59005; United States / NCRR NIH HHS / RR / RR000046
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] R16CO5Y76E / Aspirin
  •  go-up   go-down


37. Poshkus T, Samalavichus NE, Dracutene G: [Flat adenomas of the colon]. Ter Arkh; 2007;79(2):77-81
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Flat adenomas of the colon].
  • [MeSH-major] Adenoma / pathology. Adenomatous Polyps / pathology. Colonic Neoplasms / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


38. Govindarajan R, Ratnasinghe L, Simmons DL, Siegel ER, Midathada MV, Kim L, Kim PJ, Owens RJ, Lang NP: Thiazolidinediones and the risk of lung, prostate, and colon cancer in patients with diabetes. J Clin Oncol; 2007 Apr 20;25(12):1476-81
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thiazolidinediones and the risk of lung, prostate, and colon cancer in patients with diabetes.
  • PURPOSE: Peroxisome proliferator-activated receptor gamma (PPARgamma) mediates cell cycle arrest and adipocyte differentiation; has tumor suppressor activity in liposarcoma, lung, and prostate cancers; and suppresses colonic polyp formation in adenomatous polyposis coli (APC)min/+ mice.
  • [MeSH-major] Colonic Neoplasms / epidemiology. Diabetes Mellitus, Type 2 / drug therapy. Diabetes Mellitus, Type 2 / epidemiology. Lung Neoplasms / epidemiology. Prostatic Neoplasms / epidemiology. Thiazolidinediones / therapeutic use


39. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Hazardous Substances Data Bank. URANIUM, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


40. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncologist. 2000;5 Suppl 1:11-5 [10804085.001]
  • [Cites] Biomed Pharmacother. 2008 Mar;62(3):158-63 [17851027.001]
  • [Cites] Hepatogastroenterology. 2002 Jan-Feb;49(43):116-23 [11941933.001]
  • [Cites] Cancer Res. 2002 Jul 15;62(14):4123-31 [12124351.001]
  • [Cites] Microsc Res Tech. 2003 Feb 1;60(2):199-207 [12539174.001]
  • [Cites] J Clin Invest. 2003 Mar;111(5):649-58 [12618519.001]
  • [Cites] Br J Cancer. 2003 Jun 16;88(12):1979-86 [12799646.001]
  • [Cites] N Engl J Med. 2003 Jul 31;349(5):427-34 [12890841.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2004 Apr;16(4):397-402 [15028972.001]
  • [Cites] N Engl J Med. 2004 Jun 3;350(23):2335-42 [15175435.001]
  • [Cites] Adv Cancer Res. 1985;43:175-203 [2581424.001]
  • [Cites] Anal Biochem. 1987 Apr;162(1):156-9 [2440339.001]
  • [Cites] Int J Cancer. 1988 Jun 15;41(6):908-12 [3372063.001]
  • [Cites] Cancer Res. 1990 Aug 1;50(15):4724-30 [2369746.001]
  • [Cites] Growth Factors. 1992;7(1):53-64 [1380254.001]
  • [Cites] Nature. 1993 Apr 29;362(6423):841-4 [7683111.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Nov 15;90(22):10705-9 [8248162.001]
  • [Cites] Nat Med. 1995 Jan;1(1):27-31 [7584949.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14765-70 [8962129.001]
  • [Cites] Cancer Res. 1997 Oct 15;57(20):4593-9 [9377574.001]
  • [Cites] Structure. 1997 Oct 15;5(10):1325-38 [9351807.001]
  • [Cites] Nature. 1997 Nov 27;390(6658):404-7 [9389480.001]
  • [Cites] Eur Surg Res. 1998;30(4):273-8 [9704754.001]
  • [Cites] Int J Cancer. 1998 Sep 11;77(6):933-6 [9714067.001]
  • [Cites] Hepatogastroenterology. 1999 Mar-Apr;46(26):920-3 [10370639.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):7822-35 [15520188.001]
  • [Cites] World J Gastroenterol. 2005 Mar 14;11(10):1535-9 [15770733.001]
  • [Cites] J Natl Cancer Inst. 2005 Jul 6;97(13):981-9 [15998951.001]
  • [Cites] Diabetologia. 2005 Nov;48(11):2422-7 [16193288.001]
  • [Cites] J Clin Oncol. 2006 Jan 10;24(2):217-27 [16365183.001]
  • [Cites] J Physiol. 2006 Apr 1;572(Pt 1):243-57 [16423853.001]
  • [Cites] Arch Surg. 2006 Apr;141(4):367-74; discussion 374 [16618894.001]
  • [Cites] Clin Cancer Res. 2006 May 15;12(10):3124-9 [16707611.001]
  • [Cites] Mol Vis. 2006;12:626-32 [16735996.001]
  • [Cites] Cell Mol Life Sci. 2006 Sep;63(17):2067-77 [16909199.001]
  • [Cites] Br J Cancer. 2007 Jul 16;97(2):223-30 [17595666.001]
  • [Cites] Cancer Res. 2000 Oct 1;60(19):5565-70 [11034104.001]
  • (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
  •  go-up   go-down


41. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Hazardous Substances Data Bank. FERRIC NITRATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


42. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


43. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Acromegaly.
  • MedlinePlus Health Information. consumer health - Diabetes Medicines.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


44. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


45. Park KJ, Choi HJ, Kim SH, Han SY, Hong SH, Cho JH, Kim HH: Sigmoidorectal intussusception of adenoma of sigmoid colon treated by laparoscopic anterior resection after sponge-on-the-stick-assisted manual reduction. World J Gastroenterol; 2006 Jan 7;12(1):146-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sigmoidorectal intussusception of adenoma of sigmoid colon treated by laparoscopic anterior resection after sponge-on-the-stick-assisted manual reduction.
  • We present herein a case report of sigmoidorectal intussusception as an unusual case of sigmoid adenomatous polyp.
  • An emergency colonoscopy revealed that the invaginated colon with polypoid mass was protruded to the lower rectum.
  • The permanent pathologic finding showed villotubular adenoma of the sigmoid colon.
  • [MeSH-major] Adenoma / complications. Intussusception / surgery. Laparoscopy / methods. Rectal Diseases / surgery. Sigmoid Neoplasms / complications

  • MedlinePlus Health Information. consumer health - Rectal Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Surg Today. 2000;30(2):188-90 [10664347.001]
  • [Cites] J Am Coll Surg. 1999 Apr;188(4):390-5 [10195723.001]
  • [Cites] J Clin Gastroenterol. 2003 Jan;36(1):18-21 [12488701.001]
  • [Cites] Surg Today. 2003;33(10):768-71 [14513327.001]
  • [Cites] Radiol Clin North Am. 2003 Nov;41(6):1137-51 [14661662.001]
  • [Cites] N Engl J Med. 2004 May 13;350(20):2050-9 [15141043.001]
  • [Cites] Am J Surg. 1971 May;121(5):531-5 [5557762.001]
  • [Cites] Ann Surg. 1981 Feb;193(2):230-6 [7469558.001]
  • [Cites] Acta Chir Scand. 1989 Mar;155(3):201-4 [2741629.001]
  • [Cites] Br J Surg. 1989 Jul;76(7):727 [2765810.001]
  • [Cites] Am Surg. 1995 Apr;61(4):320-1 [7893095.001]
  • [Cites] Am J Surg. 1997 Feb;173(2):88-94 [9074370.001]
  • [Cites] Ann Surg. 1997 Aug;226(2):134-8 [9296505.001]
  • [Cites] Clin Radiol. 1998 Jan;53(1):53-7 [9464437.001]
  • [Cites] Aust N Z J Surg. 1998 Sep;68(9):683-5 [9737271.001]
  • [Cites] Anticancer Res. 2000 Nov-Dec;20(6C):4697-700 [11205203.001]
  • (PMID = 16440436.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC4077479
  •  go-up   go-down


46. Kurland JE, Beck SE, Solomon CJ, Brann OS, Carethers JM, Huang SC: Cyclooxygenase-2 expression in polyps from a patient with juvenile polyposis syndrome with mutant BMPR1A. J Pediatr Gastroenterol Nutr; 2007 Mar;44(3):318-25
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclooxygenase-2 expression in polyps from a patient with juvenile polyposis syndrome with mutant BMPR1A.
  • OBJECTIVES: Cyclooxygenase-2 (COX-2) expression is increased in colorectal cancers and has been reported to be upregulated in Peutz-Jeghers polyps.
  • To determine whether germline and somatic loss of BMPR1A in polyps from a patient with juvenile polyposis syndrome have altered COX-2 expression, we characterized a patient with juvenile polyposis syndrome for BMPR1A germline mutations and examined the polyps for BMPR1A expression and COX-2 expression.
  • Multiple polypectomies were performed, and several polyps showed adenomatous change.
  • Genomic DNA was extracted from polyp material for loss of heterozygosity (LOH) analyses with microsatellite markers.
  • In polyp domains containing cystic and adenomatous epithelium, no LOH was observed using markers near the BMPR1A locus.
  • Immunostaining indicated decreased expression of phospho-SMAD1 (pSMAD1), functionally downstream of the mutant BMPR1A receptor in the cystic epithelium, with further reduction in adenomatous portions within the polyp.
  • COX-2 protein, normally not expressed in the colon, was present and increased in polyp epithelium.
  • CONCLUSIONS: Decreased expression of pSMAD1 in the cystic epithelium with further reduction in the adenomatous area, and increase in COX-2 expression within polyps from the BMPR1A heterozygote, suggest a potential mechanism for adenomatous pathogenesis in these hamartomatous polyps.

  • Genetic Alliance. consumer health - Juvenile polyposis syndrome.
  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17325551.001).
  • [ISSN] 1536-4801
  • [Journal-full-title] Journal of pediatric gastroenterology and nutrition
  • [ISO-abbreviation] J. Pediatr. Gastroenterol. Nutr.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA090231-05; United States / NIDDK NIH HHS / DK / T32 DK007202-32; United States / NCI NIH HHS / CA / R01 CA090231-05; United States / NCI NIH HHS / CA / R01 CA090231; United States / NCI NIH HHS / CA / R01-CA90231; United States / NIDDK NIH HHS / DK / K08-DK64560A; United States / NIDDK NIH HHS / DK / T32 DK007202; United States / NIDDK NIH HHS / DK / DK007202-32
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Smad1 Protein; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.30 / BMPR1A protein, human; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type I
  •  go-up   go-down


47. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


48. Voutsadakis IA: Pathogenesis of colorectal carcinoma and therapeutic implications: the roles of the ubiquitin-proteasome system and Cox-2. J Cell Mol Med; 2007 Mar-Apr;11(2):252-85
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • High up in the list of colorectal cancer lesions are APC (adenomatous polyposis coli), K-ras, Smad4 (or DPC4-deleted in pancreatic cancer 4) and p53 genes.
  • Inhibition of Cox-2 by aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) has been found to inhibit proliferation of colorectal cancer cells and in epidemiologic studies has been shown to reduce colon polyp formation in genetically predisposed populations and in the general population.

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17488476.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Ubiquitin; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Number-of-references] 298
  • [Other-IDs] NLM/ PMC3822826
  •  go-up   go-down


49. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


50. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Eur J Nutr. 2008 Aug;47(5):226-34 [18636219.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 May;17(5):1136-43 [18483335.001]
  • [Cites] Int J Cancer. 2008 Jun 15;122(12):2647-55 [18351577.001]
  • [Cites] J Nutr. 2008 Feb;138(2):250-6 [18203887.001]
  • [Cites] Am J Epidemiol. 2007 Nov 15;166(10):1116-25 [17823383.001]
  • [Cites] Int J Oncol. 2001 Dec;19(6):1255-62 [11713597.001]
  • [Cites] J Natl Cancer Inst. 2005 Jun 15;97(12):906-16 [15956652.001]
  • [Cites] Carcinogenesis. 1999 Apr;20(4):645-50 [10223194.001]
  • [Cites] Cancer. 2003 Sep 15;98(6):1262-72 [12973851.001]
  • [Cites] Eur J Cancer. 2002 Sep;38(14):1937-45 [12204677.001]
  • [Cites] Mutat Res. 2006 Feb 22;594(1-2):10-9 [16153665.001]
  • (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
  •  go-up   go-down


51. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


52. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


53. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer. 2000 May 15;88(10):2398-424 [10820364.001]
  • [Cites] Cancer. 2009 May 1;115(9):1967-76 [19235249.001]
  • [Cites] J Natl Cancer Inst. 2003 Sep 3;95(17):1276-99 [12953083.001]
  • [Cites] Int J Cancer. 2004 Jan 10;108(2):287-92 [14639617.001]
  • [Cites] Dis Esophagus. 2004;17(1):87-90 [15209748.001]
  • [Cites] Eur J Epidemiol. 1992 Nov;8(6):845-50 [1294390.001]
  • [Cites] Arch Fam Med. 1995 Oct;4(10):849-56 [7551132.001]
  • [Cites] Colorectal Dis. 2005 Nov;7(6):559-62 [16232235.001]
  • [Cites] Int J Cancer. 2006 Dec 1;119(11):2665-72 [16929492.001]
  • [Cites] Am J Clin Nutr. 2007 Dec;86(6):1754-64 [18065596.001]
  • [Cites] Int J Cancer. 2008 May 1;122(9):2106-14 [18183593.001]
  • [Cites] Turk J Gastroenterol. 2008 Mar;19(1):22-7 [18386236.001]
  • [Cites] J Natl Med Assoc. 2008 Dec;100(12):1441-4 [19110912.001]
  • [Cites] Cancer. 2009 Jan 15;115(2):259-70 [19109815.001]
  • [Cites] Cancer. 2009 Jan 15;115(2):419-27 [19109819.001]
  • [Cites] J Nutr. 2009 Feb;139(2):340-4 [19091801.001]
  • [Cites] Genet Mol Res. 2009;8(1):64-75 [19283674.001]
  • [Cites] Am J Epidemiol. 2002 Jun 15;155(12):1104-13 [12048224.001]
  • (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
  •  go-up   go-down


54. Levy BT, Daly JM, Luxon B, Merchant ML, Xu Y, Levitz CE, Wilbur JK: The "Iowa get screened" colon cancer screening program. J Prim Care Community Health; 2010 Apr 1;1(1):43-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The "Iowa get screened" colon cancer screening program.
  • OBJECTIVE: To implement a colon cancer screening program for uninsured or underinsured Iowans.
  • Individuals with colonic symptoms or who were up to date with screening were ineligible.
  • Thirty of the 49 (61%) individuals had a colonoscopy, and 20 individuals had at least 1 polyp biopsied.
  • Thirteen individuals had at least 1 tubular adenoma; 2 had adenomas more than 1 cm in diameter, with no colon cancers identified.
  • CONCLUSION: There was high interest in and compliance with colon cancer screening using a FIT among underinsured individuals.
  • Population-based strategies for offering FIT could significantly increase colon cancer screening among disadvantaged individuals, but programs will have to develop sustainable mechanisms to include the necessary organization and address substantial costs of providing mass screening, as well as facilitating and providing colonoscopies for those who test positive.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 23804068.001).
  • [ISSN] 2150-1319
  • [Journal-full-title] Journal of primary care & community health
  • [ISO-abbreviation] J Prim Care Community Health
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; adenomatous polyp / colorectal cancer screening / fecal immunochemical testing / prevention / recruitment strategies / screening program / tubular adenoma / underinsured / uninsured
  •  go-up   go-down


55. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • MedlinePlus Health Information. consumer health - Metabolic Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


56. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


57. Paskett ED, Reeves KW, Pineau B, Albert PS, Caan B, Hasson M, Iber F, Kikendall JW, Lance P, Shike M, Slattery ML, Weissfeld J, Kahle L, Schatzkin A, Lanza E, Polyp Prevention Trial Study Group: The association between cigarette smoking and colorectal polyp recurrence (United States). Cancer Causes Control; 2005 Nov;16(9):1021-33
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The association between cigarette smoking and colorectal polyp recurrence (United States).
  • OBJECTIVE: Although evidence exists linking smoking to precancerous colorectal adenomatous polyps, few studies have examined the association between cigarette smoking and recurrence of colorectal polyps.
  • This association was investigated prospectively with data from the Polyp Prevention Trial.
  • The study was completed by 1872 men and women with presence of adenomas at baseline colonoscopy.
  • Multiple logistic regression analysis was used to examine the association between cigarette smoking and polyp recurrence (adenomatous and hyperplastic) up to four years from baseline.
  • RESULTS: Adenoma recurrence was not related to cigarette smoking.
  • Current smokers had increased odds of hyperplastic polyps at follow-up compared to never smokers (OR 2.88, 95% CI 2.06-4.01).
  • Current smoking was associated with subsequent distal (OR 3.44, 95% CI 2.38-4.95) and rectal (OR 3.53, 95% CI 2.15-5.78) hyperplastic polyps, but not subsequent proximal hyperplastic polyps.
  • Cigarette smoking was associated with subsequent multiple and small size (4 mm) hyperplastic polyps.
  • Significant linear trends were observed between development of subsequent hyperplastic polyps and all smoking variables.
  • CONCLUSIONS: Although no association with recurrent adenomas was observed, cigarette smoking was significantly associated with hyperplastic polyp development, except for those in the proximal colon.
  • This prospective study confirms that cigarette smoking has a significant effect on the development of hyperplastic colorectal polyps.
  • [MeSH-major] Colonic Polyps / pathology. Precancerous Conditions. Smoking / epidemiology
  • [MeSH-minor] Adenoma / epidemiology. Adenoma / pathology. Aged. Colonoscopy. Epidemiologic Studies. Female. Humans. Hyperplasia / epidemiology. Hyperplasia / pathology. Male. Middle Aged. Recurrence. Risk Assessment. Risk Factors. Surveys and Questionnaires. Time Factors. United States

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • MedlinePlus Health Information. consumer health - Smoking.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16184467.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  •  go-up   go-down


58. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochem Soc Trans. 2007 Dec;35(Pt 6):1405-8 [18031232.001]
  • [Cites] J Biol Chem. 2005 Oct 28;280(43):36228-36 [16085646.001]
  • [Cites] Carcinogenesis. 2005 Sep;26(9):1527-35 [15878912.001]
  • [Cites] Biochem Biophys Res Commun. 1996 Dec 4;229(1):21-6 [8954078.001]
  • [Cites] Oncogene. 1999 Oct 21;18(43):5889-903 [10557076.001]
  • [Cites] Stat Appl Genet Mol Biol. 2007;6:Article3 [17402918.001]
  • [Cites] J Biol Chem. 2004 Jul 16;279(29):30358-68 [15123634.001]
  • [Cites] J Immunol. 2001 Jan 15;166(2):1041-8 [11145683.001]
  • [Cites] Lupus. 2001;10 (10 ):691-9 [11721695.001]
  • [Cites] Ann Surg Oncol. 1999 Sep;6(6):604-8 [10493631.001]
  • [Cites] J Biol Chem. 2004 May 7;279(19):19712-20 [14993214.001]
  • [Cites] Gut. 2001 Aug;49(2):251-62 [11454803.001]
  • [Cites] J Biol Chem. 2007 Mar 30;282(13):9797-804 [17251186.001]
  • [Cites] J Biol Chem. 2007 Jul 13;282(28):20059-63 [17502367.001]
  • (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
  •  go-up   go-down


59. Rocha Ramírez JL, Villanueva Sáenz E, Hernández-Magro PM, Sierra Montenegro E, Soto Quirino R, Pérez Aguirre J, Blanco Lemus E: [Hereditary mixed polyposis syndrome. First report in Mexico]. Rev Gastroenterol Mex; 2005 Oct-Dec;70(4):430-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Síndrome de poliposis mixta hereditaria. Primer reporte en México.
  • BACKGROUND: The hereditary mixed polyposis syndrome (HMPS) is an uncommon condition, distinguished by presence of a different histological pattern of polyps in digestive tract, clinically manifested by diarrhea, anemia and weight loss.
  • CASE REPORT: Male patient, 38 years old, with familiar antecedent (dead sister) with polyps and gastric cancer.
  • At blood test with hemoglobin of 9.7 g/dL, and colonoscopy with multiple polyps within colon and rectum, upper endoscopy with a big esophageal polyp and multiple polyps in gastric and duodenal lining smaller than 1 cm.
  • Histopathologic study of the polyps report mixed pattern of polyps: (hyperplasic-adenomatous, juvenile-adenomatous, adenoma-inflammatory-hyperplasic, hyperplasic-adenomatous with a high degree dysplasia); juvenile in esophagus, and hyperplasic in stomach and duodenum.
  • [MeSH-major] Adenomatous Polyposis Coli / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17058983.001).
  • [ISSN] 0375-0906
  • [Journal-full-title] Revista de gastroenterología de México
  • [ISO-abbreviation] Rev Gastroenterol Mex
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Mexico
  •  go-up   go-down


60. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


61. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


62. Khatibzadeh N, Ziaee SA, Rahbar N, Molanie S, Arefian L, Fanaie SA: The indirect role of site distribution in high-grade dysplasia in adenomatous colorectal polyps. J Cancer Res Ther; 2005 Oct-Dec;1(4):204-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The indirect role of site distribution in high-grade dysplasia in adenomatous colorectal polyps.
  • BACKGROUND: The appropriate application of Endoscopic modalities for polypectomy depends on the likelihood that the adenoma in question harbors invasive cancer.
  • While prior studies have evaluated polyp size and morphology in assessing the risk of malignancy, in recent decay some authorities have paid more attention to dysplasia.
  • All in all, the relative risk of cancer based on polyp distribution in correlation with dysplasia has not been statistically studied which is done in our study.
  • METHODS AND MATERIALS: Between June 2001 and March 2004, the distribution of 130 adenomatous polyps was compared with synchronous invasive or in situ cancer.
  • Factors such as Patient age, Patients gender, location of lesion, size of polyp, histological subtype of adenoma on biopsy, degree of dysplasia, synchronous cancer, color of polyp, and number of polyps were included in the data collection.
  • CONCLUSION: Lesions greater than 1 cm in diameter with high-grade dysplasia after splenic flexure should be managed as presumptive malignancies with segmental colon resection.
  • [MeSH-major] Adenomatous Polyps / pathology. Colorectal Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17998654.001).
  • [ISSN] 1998-4138
  • [Journal-full-title] Journal of cancer research and therapeutics
  • [ISO-abbreviation] J Cancer Res Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  •  go-up   go-down


63. Yoshida I, Suzuki A, Vallée M, Matano Y, Masunaga T, Zenda T, Shinozaki K, Okada T: Serum insulin levels and the prevalence of adenomatous and hyperplastic polyps in the proximal colon. Clin Gastroenterol Hepatol; 2006 Oct;4(10):1225-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum insulin levels and the prevalence of adenomatous and hyperplastic polyps in the proximal colon.
  • BACKGROUND & AIMS: Obesity and diabetes mellitus are associated with an increased incidence of proximal colon cancer.
  • Colonic adenoma that has been reported to be associated with elevated serum insulin levels and subsets of hyperplastic polyps might serve as a precursor of colon cancer.
  • In this study, we sought to determine segment-specific associations between serum insulin levels and the prevalence of adenoma and hyperplastic polyps in the proximal and distal colon.
  • We performed multinomial logistic regression models by using the outcome categories of none (reference), proximal-only, distal-only, and both-segment lesions for the presence of adenoma/hyperplastic polyp with serum insulin, age, gender, lifestyle characteristics, and the presence of other types of lesions as predictors.
  • RESULTS: Overall, serum insulin levels were significantly associated with adenoma (OR, 1.5; 95% CI, 1.1-2.0; P = .005) and borderline associated with hyperplastic polyps (OR, 1.3; 95% CI, 1.0-1.7; P = .075).
  • In multinomial logistic regression models, elevated serum insulin levels were significantly associated with proximal-only adenoma (OR, 1.8; 95% CI, 1.2-2.5; P = .002), both-side hyperplastic polyp (OR, 1.7; 95% CI, 1.1-2.5; P = .015), and proximal-only hyperplastic polyp (OR, 1.5; 95% CI, 1.0-2.1; P = .048) and borderline associated with distal-only adenoma (OR, 1.5; 95% CI, 1.0-2.1; P =.059) but not with distal-only hyperplastic polyp.
  • CONCLUSIONS: Serum insulin levels directly correlate with the presence of adenoma and hyperplastic polyps in the proximal colon and might also less strongly correlate with the presence of distal adenoma.
  • [MeSH-major] Adenomatous Polyposis Coli / blood. Biomarkers, Tumor / blood. Colonic Polyps / blood. Colonic Polyps / epidemiology. Insulin / blood

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • MedlinePlus Health Information. consumer health - Diabetes Medicines.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Clin Gastroenterol Hepatol. 2007 Jan;5(1):137
  • (PMID = 16979948.001).
  • [ISSN] 1542-3565
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Insulin
  •  go-up   go-down


64. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colonoscopy.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


65. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


66. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


67. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


68. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Hazardous Substances Data Bank. HISTAMINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


69. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Triglycerides.
  • Hazardous Substances Data Bank. CHOLESTEROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nutr Cancer. 2000;37(1):19-26 [10965515.001]
  • [Cites] Int J Epidemiol. 1998 Oct;27(5):794-8 [9839735.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):412-8 [12750235.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):6090-5 [14522940.001]
  • [Cites] Cancer Sci. 2003 Nov;94(11):960-4 [14611672.001]
  • [Cites] Cancer. 1977 Jun;39(6):2533-9 [872053.001]
  • [Cites] Cancer Res. 1981 Sep;41(9 Pt 2):3700-5 [6266660.001]
  • [Cites] J Chronic Dis. 1982;35(5):313-20 [7068807.001]
  • [Cites] JAMA. 1986 Jan 17;255(3):365-7 [3941515.001]
  • [Cites] N Engl J Med. 1986 Dec 25;315(26):1634-8 [3785334.001]
  • [Cites] Br J Cancer. 1987 Oct;56(4):451-4 [3689662.001]
  • [Cites] Am J Clin Nutr. 1988 Feb;47(2):312-7 [3341261.001]
  • [Cites] Hematol Oncol Clin North Am. 1989 Mar;3(1):35-63 [2537285.001]
  • [Cites] Cancer. 1992 Feb 15;69(4):883-8 [1735079.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1994 Dec;3(8):687-95 [7881343.001]
  • [Cites] Cancer Causes Control. 1995 Mar;6(2):164-79 [7749056.001]
  • [Cites] Eur J Cancer. 1995 Jul-Aug;31A(7-8):1033-8 [7576987.001]
  • [Cites] Scand J Gastroenterol. 1997 Feb;32(2):162-8 [9051877.001]
  • [Cites] Carcinogenesis. 1998 Sep;19(9):1679-84 [9771941.001]
  • [Cites] Climacteric. 2002 Mar;5(1):3-14 [11974557.001]
  • (PMID = 16534881.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Triglycerides; 97C5T2UQ7J / Cholesterol
  • [Other-IDs] NLM/ PMC4124439
  •  go-up   go-down


70. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • ZFIN. ZFIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Bioessays. 1999 Dec;21(12):1021-30 [10580987.001]
  • [Cites] J Clin Oncol. 2004 Nov 15;22(22):4456-62 [15483017.001]
  • [Cites] EMBO J. 2000 May 15;19(10):2270-9 [10811618.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):51581-9 [15358764.001]
  • [Cites] Oncogene. 2004 Dec 16;23(58):9369-80 [15516977.001]
  • [Cites] J Biol Chem. 2005 Jul 15;280(28):26565-72 [15899904.001]
  • [Cites] J Biol Chem. 2005 Aug 26;280(34):30490-5 [15967793.001]
  • [Cites] Gene. 2005 Nov 21;361:1-12 [16185824.001]
  • [Cites] Science. 2005 Dec 2;310(5753):1504-10 [16293724.001]
  • [Cites] Genes Dev. 2006 Mar 1;20(5):586-600 [16510874.001]
  • [Cites] EMBO Rep. 2006 Apr;7(4):444-9 [16439994.001]
  • [Cites] J Biol Chem. 2006 Apr 14;281(15):9971-6 [16476742.001]
  • [Cites] EMBO J. 2006 Jun 21;25(12):2735-45 [16710294.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Sep 5;103(36):13409-14 [16938888.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Sep 19;103(38):14122-7 [16959882.001]
  • [Cites] Cell. 2006 Nov 3;127(3):469-80 [17081971.001]
  • [Cites] J Biol Chem. 2006 Dec 8;281(49):37828-35 [17028196.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4036-41 [17360473.001]
  • [Cites] Cancer Res. 2007 Mar 15;67(6):2469-79 [17363564.001]
  • [Cites] Am J Med Genet A. 2007 Jul 1;143A(13):1472-80 [17551924.001]
  • [Cites] J Biol Chem. 2007 Oct 5;282(40):29394-400 [17673467.001]
  • [Cites] Cancer Res. 2007 Oct 15;67(20):9721-30 [17942902.001]
  • [Cites] Science. 2008 Jan 18;319(5861):333-6 [18202290.001]
  • [Cites] Cell. 2008 Apr 18;133(2):340-53 [18423204.001]
  • [Cites] Nat Genet. 2008 May;40(5):600-8 [18372904.001]
  • [Cites] Gastroenterology. 2006 Oct;131(4):1096-109 [17030180.001]
  • [Cites] Cell. 2000 Oct 13;103(2):311-20 [11057903.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Feb 5;99(3):1521-6 [11818567.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 25;99(13):8683-8 [12072559.001]
  • [Cites] Curr Biol. 2002 Jul 23;12(14):R499-R501 [12176352.001]
  • [Cites] Am J Clin Pathol. 2003 Sep;120(3):418-23 [14502807.001]
  • [Cites] Nature. 2003 Oct 9;425(6958):633-7 [14534590.001]
  • [Cites] Genes Dev. 2004 Jun 15;18(12):1385-90 [15198980.001]
  • [Cites] Curr Opin Cell Biol. 2004 Oct;16(5):528-35 [15363803.001]
  • [Cites] J Biol Chem. 2004 Oct 8;279(41):43261-72 [15294912.001]
  • [Cites] Nature. 1987 May 28-Jun 3;327(6120):293-7 [3587348.001]
  • [Cites] Nature. 1987 May 28-Jun 3;327(6120):298-303 [2438556.001]
  • [Cites] Cell. 1990 Jun 1;61(5):759-67 [2188735.001]
  • [Cites] Cell. 1996 Oct 18;87(2):159-70 [8861899.001]
  • [Cites] Science. 1997 Mar 21;275(5307):1787-90 [9065402.001]
  • [Cites] Cancer Res. 1997 Oct 15;57(20):4624-30 [9377578.001]
  • [Cites] Cancer Res. 1998 Mar 1;58(5):1021-6 [9500465.001]
  • [Cites] Cancer Res. 1998 Mar 15;58(6):1130-4 [9515795.001]
  • [Cites] Science. 1998 Sep 4;281(5382):1509-12 [9727977.001]
  • [Cites] Curr Opin Genet Dev. 1999 Feb;9(1):15-21 [10072352.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7):1442-4 [10197610.001]
  • [Cites] Nature. 1999 Apr 1;398(6726):422-6 [10201372.001]
  • [Cites] Cancer Res. 1999 Aug 15;59(16):3875-9 [10463573.001]
  • [Cites] Dev Cell. 2004 Nov;7(5):677-85 [15525529.001]
  • [Cites] Oncogene. 1999 Dec 2;18(51):7219-25 [10602475.001]
  • (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
  •  go-up   go-down


71. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


72. Nam JH, Yang CH: [Clinical characteristics and risk factors of colon polyps in gyeongju and pohang area]. Korean J Gastroenterol; 2008 Sep;52(3):142-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical characteristics and risk factors of colon polyps in gyeongju and pohang area].
  • BACKGROUND/AIMS: The purposes of this study were to investigate various environmental factors for colon polyps and to analyze locoregional clinical characteristics of colon polyps in Gyeongju and Pohang area.
  • METHODS: From October 2005 to September 2006, patients who underwent colonoscopy were analyzed based on their ages, genders, body mass indices (BMI), dietary habits, smoking behaviors, accompaying diseases, and medications as risk factors for the occurrence of colon polyps.
  • Then clinical manifestations, gross appearances and pathologic findings of polyps were investigated.
  • RESULTS: Among 253 patients enrolled, a total of 296 colon polyps were found in 108 patients.
  • The incidence of colon polyps in more than 50-year old patients was 3.2-fold greater compared to less than 50-year old patients.
  • Smoking habits were also significantly associated with the occurence of colon polyps.
  • Among adenomatous polyps, tubulovillous type and moderate to severe dysplasia were frequently observed as the size increased, yet the location of polyps was not significantly associated.
  • CONCLUSIONS: Older age and smoking habit increase the risk of colon polyps.
  • Rectal polyps have less chance to be adenomatous type.
  • The larger the polyp grows, the more likely it to be tubulovillous and dysplastic.
  • [MeSH-major] Colonic Polyps / diagnosis. Colorectal Neoplasms / diagnosis
  • [MeSH-minor] Adenomatous Polyps / pathology. Adult. Aged. Aged, 80 and over. Female. Humans. Korea. Male. Middle Aged. Multivariate Analysis. Odds Ratio. Risk Factors. Rural Population. Surveys and Questionnaires

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19077510.001).
  • [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)
  •  go-up   go-down


73. Traboulsi EI: Ocular manifestations of familial adenomatous polyposis (Gardner syndrome). Ophthalmol Clin North Am; 2005 Mar;18(1):163-6, x
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ocular manifestations of familial adenomatous polyposis (Gardner syndrome).
  • Familial adenomatous polyposis (FAP) is a colon cancer predisposition syndrome in which hundreds to thousands of precancerous colonic polyp become evident at a mean age of 16 years (range, 7-36 years).
  • By age 35 years, 95% of patients have polyps.


74. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • As benign tumor, there were two gallbladder adenoma, one gastric adenoma, one colonic adenoma and one benign ovarian cystic neoplasm, respectively.

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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)
  •  go-up   go-down


75. Fidder HH, Figer A, Geva R, Flex D, Schayek H, Avidan B, Meir SB, Friedman E: Genetic analyses in consecutive israeli jewish colorectal cancer patients. Am J Gastroenterol; 2005 Jun;100(6):1376-80
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In addition, the rate of the I1307K APC missense mutation and the two predominant Jewish mutations in hMSH2, A636P, and 324delCA, associated with hereditary nonpolyposis colon cancer (HNPCC), were determined.
  • Carriers and noncarrier CRC patients did not differ in age of onset or associated colonic adenomatous polyps.
  • The carrier rate among controls was 5% among Ashkenazim and 1.6% among non-Ashkenazi individuals.
  • The I1307K mutation is associated with a moderate excess risk for CRC, but age of onset seems not to be earlier and this variant is not associated with a multiple colonic polyp phenotype.

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15929773.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [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
  •  go-up   go-down


76. Pickhardt PJ, Schumacher C, Kim DH: Polyp detection at 3-dimensional endoluminal computed tomography colonography: sensitivity of one-way fly-through at 120 degrees field-of-view angle. J Comput Assist Tomogr; 2009 Jul-Aug;33(4):631-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19638863.001).
  • [ISSN] 1532-3145
  • [Journal-full-title] Journal of computer assisted tomography
  • [ISO-abbreviation] J Comput Assist Tomogr
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
  •  go-up   go-down


77. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Cancer. 2002 Oct 10;101(5):403-8 [12216066.001]
  • [Cites] Dis Colon Rectum. 2005 Jan;48(1):101-7 [15690665.001]
  • [Cites] Am J Pathol. 1999 Oct;155(4):1033-8 [10514384.001]
  • [Cites] Mod Pathol. 2004 Sep;17(9):1141-9 [15167936.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3544-9 [11325815.001]
  • [Cites] Gut. 2002 Oct;51(4):550-5 [12235079.001]
  • [Cites] Trends Endocrinol Metab. 2000 Sep;11(7):281-5 [10920385.001]
  • [Cites] Gut. 1998 Aug;43(2):229-31 [10189849.001]
  • [Cites] Clin Gastroenterol Hepatol. 2005 Jul;3(7 Suppl 1):S33-6 [16012993.001]
  • [Cites] Hum Pathol. 1991 Jan;22(1):70-4 [1985081.001]
  • [Cites] Lab Invest. 1998 Sep;78(9):1155-67 [9759659.001]
  • [Cites] Aliment Pharmacol Ther. 2005 Nov 1;22(9):859-64 [16225496.001]
  • [Cites] Cancer Res. 2001 Mar 15;61(6):2676-83 [11289147.001]
  • [Cites] Cancer Res. 1994 Jun 1;54(11):2841-4 [8187064.001]
  • [Cites] Eur J Cancer Prev. 2000 Aug;9(4):265-8 [10958329.001]
  • [Cites] Am J Pathol. 2003 Jul;163(1):287-94 [12819033.001]
  • [Cites] Dis Colon Rectum. 1995 Oct;38(10):1075-9 [7555422.001]
  • [Cites] Oncogene. 2003 Nov 27;22(54):8662-70 [14647460.001]
  • [Cites] Nature. 2004 Dec 23;432(7020):1027-32 [15616563.001]
  • [Cites] Lancet. 2000 Apr 8;355(9211):1211-4 [10770302.001]
  • [Cites] Gut. 1999 Aug;45(2):252-8 [10403738.001]
  • [Cites] Gut. 2005 Mar;54(3):374-84 [15710986.001]
  • [Cites] Oncogene. 1995 Apr 6;10(7):1413-6 [7731692.001]
  • [Cites] Int J Cancer. 1998 Jul 29;77(3):366-9 [9663597.001]
  • [Cites] Int J Cancer. 1994 Apr 1;57(1):51-5 [8150541.001]
  • [Cites] Cell. 1990 Jun 1;61(5):759-67 [2188735.001]
  • [Cites] Am J Gastroenterol. 2003 Nov;98 (11):2543-9 [14638361.001]
  • [Cites] Dig Dis. 1997 Jul-Oct;15(4-5):302-11 [9359018.001]
  • [Cites] Gut. 2002 Apr;50(4):513-9 [11889072.001]
  • [Cites] Pathol Int. 1994 Jul;44(7):520-7 [7921196.001]
  • [Cites] Dis Colon Rectum. 1985 Nov;28(11):847-51 [4053897.001]
  • [Cites] Gastroenterology. 2001 Jun;120(7):1657-65 [11375947.001]
  • [Cites] Cancer. 1995 Feb 15;75(4):953-7 [7842415.001]
  • [Cites] Clin Cancer Res. 2005 Aug 1;11(15):5356-64 [16061848.001]
  • [Cites] Cancer Res. 2001 Nov 1;61(21):7792-7 [11691794.001]
  • [Cites] J Pathol. 2001 Sep;195(2):171-8 [11592095.001]
  • [Cites] World J Surg. 2000 Sep;24(9):1081-90 [11036286.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):3124-30 [11306497.001]
  • [Cites] Gut. 1994 Sep;35(9):1258-61 [7959233.001]
  • [Cites] Virchows Arch. 2000 Jul;437(1):17-24 [10963375.001]
  • (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
  •  go-up   go-down


78. Fireman Z, Zachlka R, Abu Mouch S, Kopelman Y: The role of endoscopy in the evaluation of iron deficiency anemia in premenopausal women. Isr Med Assoc J; 2006 Feb;8(2):88-90
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Twenty-eight upper gastrointestinal lesions were demonstrated in 24 of the 43 patients (55.8%): erosive gastritis in 12 (27.9%), erosive duodenitis in 4 (9.3%), erosive esophagitis in 3 (7.0%), hiatus hernia (with Cameron lesions) in 3 (7.0%), active duodenal ulcer in 1 (2.3%) and hyperplastic polyp (10 mm) in 1 (2.3%).
  • Five lower gastrointestinal lesions were detected in 5 patients (16.3%): 2 (4.6%) had adenocarcinoma of the right colon, 2 (4.6%) had pedunculate adenomatous polyp > 10 mm, and 1 (2.3%) had segmental colitis (Crohn's disease).


79. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serrated adenoma of the colon: an under-recognized premalignant variant of adenomatous polyp.
  • [MeSH-major] Adenoma / pathology. Adenomatous Polyps / pathology. Colorectal Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Age Distribution. Aged. Aged, 80 and over. Biopsy, Needle. Cohort Studies. Colectomy / methods. Colonic Polyps / epidemiology. Colonic Polyps / pathology. Colonic Polyps / surgery. Female. Humans. Immunohistochemistry. Incidence. Male. Middle Aged. Prognosis. Retrospective Studies. Risk Assessment. Sex Distribution. Survival Analysis. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


80. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Hazardous Substances Data Bank. INDOCYANINE GREEN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Gastroenterol. 2000 Oct;31(3):233-6 [11034004.001]
  • [Cites] Am J Surg Pathol. 1996 Oct;20(10):1266-70 [8827034.001]
  • [Cites] Breast Cancer. 2005;12(3):211-5 [16110291.001]
  • [Cites] Gastrointest Endosc. 1975 Aug;22(1):42-3 [1205106.001]
  • [Cites] Ann Thorac Surg. 2003 Mar;75(3):870-3 [12645709.001]
  • [Cites] Gastrointest Endosc. 2005 Jan;61(1):186-7 [15672088.001]
  • [Cites] Swiss Surg. 2003;9(6):307-10 [14725100.001]
  • [Cites] Cancer Control. 2003 May-Jun;10(3):219-23 [12794620.001]
  • [Cites] Dis Colon Rectum. 1994 Aug;37(8):775-6 [7519975.001]
  • [Cites] Gastrointest Endosc. 1991 Jan-Feb;37(1):65-8 [1706285.001]
  • [Cites] Am J Surg. 2003 Jan;185(1):88-9 [12531454.001]
  • [Cites] Gastrointest Endosc. 2000 Apr;51(4 Pt 1):438-42 [10744816.001]
  • [Cites] Dig Surg. 2008;25(2):103-8 [18379188.001]
  • [Cites] Am Surg. 1989 Jul;55(7):457-61 [2472762.001]
  • [Cites] Surg Today. 2007;37(2):127-32 [17243031.001]
  • [Cites] Dis Colon Rectum. 2003 Jul;46(7):987 [12847379.001]
  • (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
  •  go-up   go-down


81. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colonoscopy.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


82. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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


83. Gurudu SR, Heigh RI, De Petris G, Heigh EG, Leighton JA, Pasha SF, Malagon IB, Das A: Sessile serrated adenomas: demographic, endoscopic and pathological characteristics. World J Gastroenterol; 2010 Jul 21;16(27):3402-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sessile serrated adenomas: demographic, endoscopic and pathological characteristics.
  • AIM: To study the demographic and endoscopic characteristics of patients with sessile serrated adenoma (SSA) in a single center.
  • A retrospective chart review was performed to extract data on demographics, polyp characteristics, presence of synchronous adenomatous polyps or cancer, polypectomy methods, and related complications.
  • Fifty-one per cent of SSAs were located in the cecum or ascending colon.
  • Approximately half of the patients had synchronous polyps of other histological types, including hyperplastic and adenomatous polyps.
  • Ninety-seven percent of polyps were removed by colonoscopy.
  • CONCLUSION: Among patients with colon polyps, 2.9% were found to have SSAs.
  • [MeSH-major] Adenoma / pathology. Colorectal Neoplasms / pathology. Polyps / pathology

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Pathol. 2001 Mar;193(3):286-94 [11241406.001]
  • [Cites] Gastrointest Endosc. 2009 Dec;70(6):1182-99 [19879563.001]
  • [Cites] Am J Clin Pathol. 2003 Jun;119(6):773-5 [12817423.001]
  • [Cites] Am J Clin Pathol. 2003 Jun;119(6):778-96 [12817424.001]
  • [Cites] J Clin Pathol. 2004 Jul;57(7):682-6 [15220357.001]
  • [Cites] N Engl J Med. 1988 Sep 1;319(9):525-32 [2841597.001]
  • [Cites] Am J Surg Pathol. 1990 Jun;14(6):524-37 [2186644.001]
  • [Cites] Cancer Res. 1997 Mar 1;57(5):808-11 [9041175.001]
  • [Cites] J Clin Pathol. 1999 Jan;52(1):5-9 [10343605.001]
  • [Cites] Gastroenterology. 2006 May;130(6):1872-85 [16697750.001]
  • [Cites] World J Gastroenterol. 2006 May 7;12(17):2770-2 [16718767.001]
  • [Cites] Gastroenterology. 2006 Nov;131(5):1400-7 [17101316.001]
  • [Cites] Histopathology. 2007 Jan;50(1):131-50 [17204027.001]
  • [Cites] World J Gastroenterol. 2007 Jul 28;13(28):3792-8 [17657832.001]
  • [Cites] Gastroenterol Clin North Am. 2007 Dec;36(4):947-68, viii [17996799.001]
  • [Cites] Am J Surg Pathol. 2008 Jan;32(1):21-9 [18162766.001]
  • [Cites] Am J Surg Pathol. 2008 Jan;32(1):30-5 [18162767.001]
  • [Cites] Digestion. 2008;77(3-4):178-83 [18617741.001]
  • [Cites] Curr Gastroenterol Rep. 2008 Oct;10(5):490-8 [18799125.001]
  • [Cites] Gastroenterology. 2008 Oct;135(4):1100-5 [18691580.001]
  • [Cites] Dig Dis Sci. 2009 Apr;54(4):906-9 [18688718.001]
  • [Cites] J Clin Oncol. 2002 Feb 15;20(4):1043-8 [11844828.001]
  • (PMID = 20632442.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2904886
  •  go-up   go-down


84. Arslan N, Dehdashti F, Siegel BA: FDG uptake in colonic villous adenomas. Ann Nucl Med; 2005 Jun;19(4):331-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


85. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Dialysis.
  • MedlinePlus Health Information. consumer health - Kidney Failure.
  • MedlinePlus Health Information. consumer health - Streptococcal Infections.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


86. Burke CA: Colonic complications of obesity. Gastroenterol Clin North Am; 2010 Mar;39(1):47-55
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Colonic complications of obesity.
  • Obesity is a risk factor for colorectal cancer and adenomatous polyps.
  • The increased prevalence of neoplasia coupled with the observation that obesity may be associated with a suboptimal bowel preparation may diminish the adequate detection of adenomas for obese who undergo colonoscopy.
  • The colonic complications of obesity are reviewed in this article.
  • [MeSH-major] Colonic Diseases / etiology. Obesity / complications
  • [MeSH-minor] Adenoma / epidemiology. Animals. Body Mass Index. Colonoscopy. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms / physiopathology. Comorbidity. Diverticulitis, Colonic / epidemiology. Humans. Insulin Resistance / physiology. Intra-Abdominal Fat / physiopathology. Leptin / physiology. Metabolic Syndrome X / epidemiology. Metabolic Syndrome X / physiopathology

  • Genetic Alliance. consumer health - Obesity.
  • MedlinePlus Health Information. consumer health - Colonic Diseases.
  • MedlinePlus Health Information. consumer health - Obesity.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20202578.001).
  • [ISSN] 1558-1942
  • [Journal-full-title] Gastroenterology clinics of North America
  • [ISO-abbreviation] Gastroenterol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Leptin
  •  go-up   go-down


87. Fenoglio L, Castagna E, Comino A, Luchino C, Senore C, Migliore E, Capucci F, Panzone S, Silvestri A, Ghezzo L, Ferrigno D: A shift from distal to proximal neoplasia in the colon: a decade of polyps and CRC in Italy. BMC Gastroenterol; 2010;10:139
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A shift from distal to proximal neoplasia in the colon: a decade of polyps and CRC in Italy.
  • This study aims to evaluate the distribution of CRC and adenomatous polyps (ADP) to establish the presence of proximalization and to assess the potential predictors.
  • METHODS: We retrieved histology reports of colonic specimens excised during colonoscopy, considering the exams performed between 1997 and 2006 at Cuneo Hospital, Italy.
  • Adjusting for gender, age, diagnostic period, symptoms and number of polyps the prevalence of proximal advanced ADP was increased among people ≥ 70 years compared to those aged 55-69 years (OR 1.49; 95% CI: 1.032.16).
  • The main predictor of proximal advanced neoplasia was the number of polyps detected per exam (> 1 polyp versus 1 polyp: considering all ADP: OR 2.16; 95% CI: 1.59-2.93; considering advanced ADP OR 1.63; 95% CI: 1.08-2.46).
  • CONCLUSIONS: CRC do not proximalize while a trend towards a proximal shift in adenomas was observed among people ≥ 70 years.
  • [MeSH-major] Adenomatous Polyps / pathology. Colon / pathology. Colonic Neoplasms / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 2000 Jan 13;342(2):69-77 [10631274.001]
  • [Cites] Annu Rev Pathol. 2009;4:343-64 [19400693.001]
  • [Cites] N Engl J Med. 2000 Jul 20;343(3):169-74 [10900275.001]
  • [Cites] N Engl J Med. 2000 Jul 20;343(3):207-8 [10900282.001]
  • [Cites] Br J Surg. 2000 Sep;87(9):1197-202 [10971428.001]
  • [Cites] Ann Oncol. 2001 Jan;12(1):13-22 [11249040.001]
  • [Cites] Gut. 2001 Apr;48(4):449-50 [11288733.001]
  • [Cites] Br J Cancer. 2001 Sep 28;85(7):972-6 [11592768.001]
  • [Cites] Eur J Cancer. 2001 Oct;37 Suppl 8:S4-66 [11602373.001]
  • [Cites] Gastrointest Endosc. 2002 Apr;55(4):548-51 [11923770.001]
  • [Cites] Oncologist. 2003;8(6):541-52 [14657533.001]
  • [Cites] Gastroenterology. 2004 Feb;126(2):394-401 [14762775.001]
  • [Cites] Cancer Metastasis Rev. 2004 Jan-Jun;23(1-2):11-27 [15000146.001]
  • [Cites] Ann Oncol. 2004 Jun;15(6):940-6 [15151952.001]
  • [Cites] J Natl Cancer Inst. 2004 Oct 6;96(19):1420-5 [15467030.001]
  • [Cites] Cancer. 1974 Sep;34(3):suppl:845-9 [4851945.001]
  • [Cites] Radiology. 1985 Apr;155(1):35-8 [3975415.001]
  • [Cites] Arch Surg. 1993 May;128(5):505-9 [8489383.001]
  • [Cites] Cancer Genet Cytogenet. 1997 Jan;93(1):84-99 [9062584.001]
  • [Cites] Ann Surg. 1998 Jan;227(1):51-6 [9445110.001]
  • [Cites] Br J Surg. 1998 Feb;85(2):246-8 [9501827.001]
  • [Cites] Am J Med. 1999 Jan 25;106(1A):3S-6S; discussion 50S-51S [10089106.001]
  • [Cites] J Natl Cancer Inst. 1999 Jun 2;91(11):916-32 [10359544.001]
  • [Cites] Dis Colon Rectum. 1999 Jun;42(6):741-52 [10378598.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8681-6 [10411935.001]
  • [Cites] Ann Surg. 1954 Jun;139(6):846-52 [13159135.001]
  • [Cites] Scand J Gastroenterol. 2004 Aug;39(8):783-6 [15513366.001]
  • [Cites] Postgrad Med J. 2004 Nov;80(949):667-9 [15537853.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2005 May;17(5):567-72 [15827448.001]
  • [Cites] Clin Cancer Res. 2005 Dec 1;11(23):8332-40 [16322293.001]
  • [Cites] Gastrointest Endosc. 2006 Mar;63(3):453-8; quiz 464 [16500395.001]
  • [Cites] Ann Oncol. 2007 Mar;18(3):581-92 [17287242.001]
  • [Cites] J Chemother. 2007 Apr;19(2):115-22 [17434818.001]
  • [Cites] Dig Dis Sci. 2008 Mar;53(3):736-40 [17717749.001]
  • [Cites] CA Cancer J Clin. 2008 May-Jun;58(3):130-60 [18322143.001]
  • [Cites] Surg Oncol. 1998 Nov-Dec;7(3-4):115-23 [10677163.001]
  • (PMID = 21108823.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3001711
  •  go-up   go-down


88. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20032428.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  •  go-up   go-down


89. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).
  • Genetic Alliance. consumer health - Familial Polyposis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


90. Cappell MS: From colonic polyps to colon cancer: pathophysiology, clinical presentation, screening and colonoscopic therapy. Minerva Gastroenterol Dietol; 2007 Dec;53(4):351-73
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • MedlinePlus Health Information. consumer health - Colonoscopy.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


91. Chen AL, Soman KV, Rychahou PG, Luxon BA, Evers BM: Proteomic analysis of colonic myofibroblasts and effect on colon cancer cell proliferation. Surgery; 2005 Aug;138(2):382-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proteomic analysis of colonic myofibroblasts and effect on colon cancer cell proliferation.
  • The phosphatidylinositol 3-kinase (PI3K)/Akt pathway transduces signals initiated by growth factors and is involved in colonic epithelial proliferation.
  • The purpose of this study was to determine (1) the influence of myofibroblasts on colon cancer cell proliferation and PI3K activity, and (2) the protein alterations associated with myofibroblasts derived from polyp versus normal margins.
  • METHODS: Myofibroblasts were derived from polyps and corresponding normal mucosa.
  • Myofibroblasts were cocultured with colon cancer cells HT29 stably transfected with green fluorescent protein and KM20 cells.
  • However, polyp myofibroblasts enhanced proliferation of the cancer cells to a greater extent than normal myofibroblasts.
  • One protein was differentially expressed in polyps versus normal cells.
  • CONCLUSIONS: Utilizing a novel proteomic approach, we identify distinct protein profiles in myofibroblasts of polyps compared with stromal cells of normal mucosa.
  • Moreover, myofibroblasts can stimulate indirectly PI3K activity and enhance colon cancer cell proliferation.
  • [MeSH-major] Adenomatous Polyps / pathology. Cell Communication / physiology. Colon / cytology. Colonic Neoplasms / pathology. Fibroblasts / cytology. Proteomics

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16153451.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / 1U01 AI-054827; United States / NIA NIH HHS / AG / 2R37 AG10885; United States / NHLBI NIH HHS / HV / N01 HV-28184; United States / NIDDK NIH HHS / DK / P01 DK35608; United States / NCI NIH HHS / CA / R01 CA104748; United States / NIDDK NIH HHS / DK / R01 DK48489
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  •  go-up   go-down


92. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


93. Nikpour S, Ali Asgari A: Colonoscopic evaluation of minimal rectal bleeding in average-risk patients for colorectal cancer. World J Gastroenterol; 2008 Nov 14;14(42):6536-40
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Neoplastic polyps, colorectal carcinoma, and IBD were defined as significant lesions.
  • Significant lesions were found in 121 (30.1%) patients, including 26 patients (6.5%) with adenocarcinoma and 30 (7.5%) with adenomatous polyps.
  • Almost all patients with significant lesions had at least one lesion in the distal colon; an adenocarcinoma and an adenomatous polyp in the proximal colon were found in 2 patients with hemorrhoids.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenomatous Polyps / diagnosis. Colonic Polyps / diagnosis. Colonoscopy. Colorectal Neoplasms / diagnosis. Hemorrhage / etiology


94. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pathol Int. 1997 Dec;47(12):831-41 [9503464.001]
  • [Cites] Am J Surg Pathol. 1990 Jun;14(6):524-37 [2186644.001]
  • [Cites] Acta Pathol Jpn. 1992 Feb;42(2):104-10 [1373263.001]
  • [Cites] J Histochem Cytochem. 1999 Aug;47(8):1039-48 [10424888.001]
  • [Cites] Hum Pathol. 1995 Jul;26(7):725-34 [7628843.001]
  • [Cites] Cell Mol Life Sci. 2004 Aug;61(15):1946-54 [15289936.001]
  • [Cites] Am J Surg Pathol. 2003 Jan;27(1):65-81 [12502929.001]
  • [Cites] Gastroenterology. 2002 Sep;123(3):862-76 [12198712.001]
  • [Cites] J Gastroenterol. 2002;37(2):94-100 [11871772.001]
  • [Cites] Biochem J. 1996 Sep 1;318 ( Pt 2):409-16 [8809027.001]
  • [Cites] Cancer Lett. 2002 Feb 8;176(1):47-55 [11790453.001]
  • [Cites] Hum Pathol. 1992 Aug;23(8):925-33 [1379573.001]
  • [Cites] Front Biosci. 2001 Oct 01;6:D1192-206 [11578969.001]
  • [Cites] Histopathology. 2005 Jul;47(1):32-40 [15982321.001]
  • [Cites] Am J Clin Pathol. 1998 Apr;109 (4):423-30 [9535396.001]
  • [Cites] J Histochem Cytochem. 2003 Dec;51(12):1689-98 [14623937.001]
  • [Cites] J Histochem Cytochem. 2000 Dec;48(12):1667-76 [11101635.001]
  • [Cites] Pathol Int. 1997 Jun;47(6):416-9 [9211531.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7318-23 [10377412.001]
  • [Cites] Am J Clin Pathol. 2005 Sep;124(3):380-91 [16191506.001]
  • [Cites] Am J Clin Pathol. 2007 Jun;127(6):938-45 [17509991.001]
  • [Cites] J Histochem Cytochem. 1978 Apr;26(4):233-50 [351046.001]
  • [Cites] Gastroenterology. 1993 Oct;105(4):1110-6 [8405856.001]
  • [Cites] Gut. 2004 Aug;53(8):1137-44 [15247181.001]
  • [Cites] Gut. 2004 Mar;53(3):323-30 [14960508.001]
  • [Cites] Peptides. 2004 May;25(5):727-30 [15177865.001]
  • [Cites] Gastroenterology. 2005 May;128(5):1292-305 [15887112.001]
  • [Cites] Hum Pathol. 2007 May;38(5):710-7 [17391730.001]
  • [Cites] J Pathol. 2002 Aug;197(5):632-7 [12210083.001]
  • [Cites] J Clin Pathol. 1968 Nov;21(6):735-43 [5717544.001]
  • [Cites] Histopathology. 2003 Apr;42(4):357-64 [12653947.001]
  • [Cites] J Biol Chem. 1993 Mar 25;268(9):6694-702 [8454642.001]
  • [Cites] Cancer Sci. 2003 Feb;94(2):135-41 [12708487.001]
  • [Cites] J Pathol. 1999 Apr;187(5):511-7 [10398114.001]
  • [Cites] Endocrinology. 1999 Nov;140(11):5374-81 [10537169.001]
  • [Cites] J Histochem Cytochem. 2000 Dec;48(12):1657-66 [11101634.001]
  • [Cites] Am J Clin Pathol. 2001 Jan;115(1):69-79 [11190809.001]
  • [Cites] Am J Clin Pathol. 2003 Jun;119(6):778-96 [12817424.001]
  • [Cites] J Natl Cancer Inst. 2001 Sep 5;93(17 ):1307-13 [11535705.001]
  • [Cites] Histochem J. 2001 Mar;33(3):183-91 [11508342.001]
  • [Cites] J Pathol. 2004 Aug;203(4):904-8 [15258992.001]
  • [Cites] Am J Surg Pathol. 2006 Dec;30(12 ):1491-501 [17122504.001]
  • [Cites] Clin Cancer Res. 2000 May;6(5):1909-16 [10815915.001]
  • [Cites] Pathol Int. 2004 Jun;54(6):401-7 [15144398.001]
  • [Cites] Virchows Arch. 1998 Apr;432(4):315-22 [9565340.001]
  • [Cites] Dev Biol. 2001 Oct 1;238(1):185-201 [11784003.001]
  • [Cites] J Clin Pathol. 1999 Jan;52(1):5-9 [10343605.001]
  • (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
  •  go-up   go-down


95. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • SciCrunch. HGNC: Data: Gene Annotation .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


96. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


97. Byun TJ, Han DS, Ahn SB, Cho HS, Eun CS, Jeon YC, Sohn JH, Oh YH: Pseudoinvasion in an adenomatous polyp of the colon mimicking invasive colon cancer. Gut Liver; 2009 Jun;3(2):130-3
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pseudoinvasion in an adenomatous polyp of the colon mimicking invasive colon cancer.
  • Pseudoinvasion or pseudocarcinomatous invasion in an adenomatous polyp of the colon can be unfamiliar to an endoscopist.
  • Pseudoinvasion in an adenomatous polyp represents prolapse of the adenomatous epithelium into its stalk.
  • In most cases its morphology does not differ from of general adenomatous polyps, but in some cases it can morphologically mimic a malignant polyp with submucosal invasion due to mass-like lesioning of its stalk.
  • This makes it difficult for endoscopists to differentiate pseudoinvasion in an adenoma from an invasive carcinoma by conventional endoscopy; instead, endoscopic ultrasonography can provide useful information for differentiating these conditions.
  • We report on an 82-year-old man who presented with a large pedunculated polyp with a thick stalk in the sigmoid colon, which mimicked a submucosal invasive carcinoma.
  • The patient was diagnosed with pseudoinvasion in an adenomatous polyp after segmental resection of the sigmoid colon.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Pathol. 1973 Jan;26(1):25-31 [4540378.001]
  • [Cites] Cancer. 1974 Jan;33(1):206-17 [4810096.001]
  • [Cites] Dis Colon Rectum. 1980 Nov-Dec;23(8):529-35 [7460689.001]
  • [Cites] Endoscopy. 2001 Aug;33(8):709-18 [11490390.001]
  • [Cites] Adv Anat Pathol. 2008 Jan;15(1):1-17 [18156808.001]
  • [Cites] Gastrointest Endosc. 2003 May;57(6):722 [12709708.001]
  • [Cites] Pathol Int. 2003 Sep;53(9):584-90 [14507314.001]
  • [Cites] Gastrointest Endosc. 2005 Jan;61(1):1-7 [15672048.001]
  • [Cites] Am J Surg Pathol. 2002 Feb;26(2):206-15 [11812942.001]
  • (PMID = 20431736.001).
  • [ISSN] 2005-1212
  • [Journal-full-title] Gut and liver
  • [ISO-abbreviation] Gut Liver
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2852693
  • [Keywords] NOTNLM ; Adenomatous polyps / EUS / Malignant polyp / Pseudoinvasion
  •  go-up   go-down


98. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


99. Kline CL, Jackson R, Engelman R, Pledger WJ, Yeatman TJ, Irby RB: Src kinase induces tumor formation in the c-SRC C57BL/6 mouse. Int J Cancer; 2008 Jun 15;122(12):2665-73
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Src kinase induces tumor formation in the c-SRC C57BL/6 mouse.
  • Src kinase has been linked as a causative agent in the progression of a number of cancers including colon, breast, lung and melanoma.
  • Src protein and activity levels are increased in colorectal cancer and liver metastases arising secondary to colon cancer.
  • However, although Src protein is increased in colon cancer as early as the adenomatous polyp stage, a role for Src in carcinogenesis has not been established.
  • We developed the c-SRC transgenic mouse in the C57BL/6 strain to address the issue of carcinogenesis in cells with high levels of Src expression.
  • Addition of the c-SRC transgene to the p21-/- background increased tumor formation almost 3-fold, while it increased metastasis 6-fold.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18351644.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 9038-94-2 / Metallothionein; EC 2.7.10.2 / src-Family Kinases
  •  go-up   go-down


100. Jo WS, Bandipalliam P, Shannon KM, Niendorf KB, Chan-Smutko G, Hur C, Syngal S, Chung DC: Correlation of polyp number and family history of colon cancer with germline MYH mutations. Clin Gastroenterol Hepatol; 2005 Oct;3(10):1022-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correlation of polyp number and family history of colon cancer with germline MYH mutations.
  • BACKGROUND & AIMS: Affected individuals with biallelic MYH mutations are believed to display multiple adenomatous polyps without evidence of vertical transmission.
  • Our goal was to determine the detection rate of germline MYH mutations in a high-risk gastrointestinal cancer clinic population by using polyp number as a selection criterion.
  • RESULTS: Among 45 patients with more than 15 adenomatous polyps not diagnosed with familial adenomatous polyposis, 7 (15.6%) had biallelic MYH mutations.
  • Both had young-onset colorectal cancer (age, <50 y) with fewer than 15 polyps.
  • CONCLUSIONS: Most individuals with MYH mutations exhibit multiple adenomatous polyps.
  • [MeSH-major] Colonic Neoplasms / genetics. Colonic Neoplasms / pathology. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / pathology. DNA Glycosylases / genetics. Mutation

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16234049.001).
  • [ISSN] 1542-3565
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
  •  go-up   go-down






Advertisement