BioMedLib Search Engine [ goto HOMEPAGE ]

[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 BRAF gene is mutated in 4% to 12% of unselected colorectal cancers, particularly those with high microsatellite instability and in premalignant lesions, such as serrated adenomas and hyperplastic polyps.

To evaluate the role of oncogenic BRAF mutations in non-hereditary nonpolyposis colorectal cancer/non-familial adenomatous polyposis familial colorectal cancer, we did a mutation screening of the most common BRAF mutation, the V600E mutation, in 194 colorectal tumors from patients with a positive family history of the disease.

Interestingly, families with extracolonic tumors showed a much higher mutation frequency (17.5%) compared with families with colonic cancer only (3.5%; P = 0.009).

Subjects from families where the V600E mutation was identified had less adenomas compared with those from families where no BRAF mutation had been found (odds ratio, 8.5; 95% confidence interval, 1.1-64.6).

These findings indicate that adenomas might be less important in the cancer development in the group of families with BRAF-V600E mutations and indirectly support a previous hypothesis that tumors might develop through the hyperplastic polyp-serrated adenoma pathway.

Genetic Alliance. consumer health - Colorectal Cancer.

Genetic Alliance. consumer health - Familial Colorectal Cancer.

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

(PMID = 17119056.001).

[ISSN] 1055-9965

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

[ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf

   

[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

   

[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] Non-steroidal anti-inflammatory drug use and colorectal polyps in the Prostate, Lung, Colorectal, And Ovarian Cancer Screening Trial.

OBJECTIVES: Non-steroidal anti-inflammatory drugs (NSAIDs) have been documented in animal and human studies to reduce risk for colorectal cancer and adenomatous polyps, but risk modification for subgroups of the population and effects on hyperplastic polyps have been less studied.

Follow-up of detected polyps was accomplished outside the Trial setting and relevant records were sought and abstracted.

Cases (n=4,017) included subjects with a biopsy-proven polyp in the left side of the colon (descending colon, sigmoid, and rectum) detected as a consequence of PLCO screening; controls (n=38,396) were subjects with no left-sided colon polyp.

RESULTS: Regular use of aspirin (≥ 4 times/month) in the past year was inversely associated with hyperplastic polyps (odds ratios (OR)=0.8, 95% confidence interval (CI)=0.7-0.9), adenomatous polyps (OR=0.8, 95% CI=0.8-0.9), and advanced adenomas (OR=0.8, 95% CI=0.7-0.9).

As frequency of aspirin use increased, the prevalence of polyps decreased significantly for each histological classification (P for trend ≤ 0.0004).

Similar patterns were found for adenomas and ibuprofen.

Overall protection was consistent in both the descending colon or sigmoid and the rectum, but more evident in males.

CONCLUSIONS: This study of a large general risk population supports previous work that recent use of aspirin and ibuprofen is associated with a decreased risk of colorectal adenomas and demonstrates that this protective effect may be stronger in certain population subgroups and is also evident for aspirin and hyperplastic polyps.

[MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Colonic Polyps / prevention & control. Ibuprofen / therapeutic use

Genetic Alliance. consumer health - Colorectal Cancer.

Genetic Alliance. consumer health - Lung Cancer.

Genetic Alliance. consumer health - Ovarian cancer.

Genetic Alliance. consumer health - Prostate cancer.

MedlinePlus Health Information. consumer health - Colonic Polyps.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. IBUPROFEN .

Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Cancer Causes Control. 2005 Oct;16(8):965-73 [16132805.001]

[Cites] Curr Ther Res Clin Exp. 2004 Jul;65(4):345-52 [24672089.001]

[Cites] Int J Epidemiol. 2007 Oct;36(5):957-9 [17921194.001]

[Cites] Gastroenterology. 2008 Jan;134(1):341-3 [18166360.001]

[Cites] Ann Intern Med. 2007 Mar 6;146(5):376-89 [17339623.001]

[Cites] N Engl J Med. 2005 Mar 31;352(13):1293-304 [15753114.001]

[Cites] Oncol Rep. 2005 Apr;13(4):559-83 [15756426.001]

[Cites] N Engl J Med. 2003 Mar 6;348(10):891-9 [12621133.001]

[Cites] Annu Rev Med. 2000;51:511-23 [10774479.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2008 Apr;17(4):827-33 [18398023.001]

[Cites] JAMA. 2003 Dec 10;290(22):2959-67 [14665657.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 Jul;14(7):1613-8 [16030091.001]

[Cites] BMJ. 2000 Nov 11;321(7270):1183-7 [11073508.001]

[Cites] Science. 2005 Jun 10;308(5728):1572 [15947169.001]

[Cites] Med Sci Monit. 2001 Jul-Aug;7(4):837-41 [11433218.001]

[Cites] N Engl J Med. 1995 Sep 7;333(10):609-14 [7637720.001]

[Cites] N Engl J Med. 2005 Mar 31;352(13):1366-8 [15755763.001]

[Cites] Ann Intern Med. 2004 Feb 3;140(3):157-66 [14757613.001]

[Cites] Ann Intern Med. 1994 Aug 15;121(4):241-6 [8037405.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1998 Mar;7(3):227-30 [9521438.001]

[Cites] Gastroenterology. 2008 Jan;134(1):21-8 [18005960.001]

[Cites] Gastroenterology. 2008 Jan;134(1):29-38 [18022173.001]

[Cites] N Engl J Med. 2003 Mar 6;348(10):883-90 [12621132.001]

[Cites] Cancer Res. 2001 May 1;61(9):3566-9 [11325819.001]

[Cites] Br J Cancer. 2006 Nov 6;95(9):1277-9 [17060932.001]

[Cites] N Engl J Med. 2006 Aug 31;355(9):873-84 [16943400.001]

[Cites] Lancet Oncol. 2002 Mar;3(3):166-74 [11902503.001]

[Cites] Am J Med. 2006 Jun;119(6):494-502 [16750963.001]

[Cites] Nat Rev Cancer. 2006 Feb;6(2):130-40 [16491072.001]

[Cites] J Clin Gastroenterol. 2002 Feb;34(2):117-25 [11782603.001]

[Cites] Cancer Causes Control. 2006 Dec;17(10):1299-304 [17111262.001]

[Cites] Ann Intern Med. 2007 Mar 6;146(5):361-4 [17339621.001]

[Cites] N Engl J Med. 2000 Jun 29;342(26):1946-52 [10874062.001]

[Cites] Lancet. 2007 May 12;369(9573):1603-13 [17499602.001]

[Cites] Br J Cancer. 1999 Sep;81(1):62-8 [10487613.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):555-6 [15767326.001]

[Cites] Dis Colon Rectum. 2004 May;47(5):665-73 [15054679.001]

[Cites] Pharmacogenomics J. 2008 Aug;8(4):237-47 [18195728.001]

[Cites] Cancer Causes Control. 2003 Jun;14(5):403-11 [12946034.001]

[Cites] Gastroenterology. 2003 Aug;125(2):328-36 [12891533.001]

[Cites] Gastroenterology. 2008 Apr;134(4):1224-37 [18395100.001]

[Cites] JAMA. 2005 Aug 24;294(8):914-23 [16118381.001]

[Cites] Chest. 2004 Sep;126(3 Suppl):234S-264S [15383474.001]

[Cites] J Natl Cancer Inst. 2002 Feb 20;94(4):252-66 [11854387.001]

[Cites] Eur J Biochem. 1980 Aug;109(1):1-8 [6773769.001]

[Cites] J Natl Cancer Inst. 1998 Oct 21;90(20):1529-36 [9790545.001]

[Cites] Ann Intern Med. 2007 Mar 6;146(5):365-75 [17339622.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2008 Aug;17(8):1858-61 [18708372.001]

[Cites] Br J Cancer. 2005 Mar 28;92 (6):1137-43 [15770215.001]

[Cites] Ann Pharmacother. 2003 Nov;37(11):1664-74 [14565811.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):616-9 [15767339.001]

[Cites] Cochrane Database Syst Rev. 2004;(2):CD004079 [15106236.001]

[Cites] N Engl J Med. 2003 Mar 6;348(10):879-80 [12621130.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2002 Jul;11(7):622-9 [12101109.001]

[Cites] Lancet. 2002 Sep 21;360(9337):942-4 [12354487.001]

[Cites] Epidemiology. 2000 Jul;11(4):376-81 [10874542.001]

[Cites] Postgrad Med J. 2005 Apr;81(954):223-7 [15811884.001]

[Cites] Am J Epidemiol. 2007 Apr 15;165(8):874-81 [17244633.001]

[Cites] J Natl Cancer Inst. 2005 Jul 6;97(13):989-97 [15998952.001]

[Cites] BMJ. 2005 Jun 11;330(7504):1366 [15947398.001]

[Cites] J Natl Cancer Inst. 2005 Mar 16;97(6):457-60 [15770010.001]

[Cites] N Engl J Med. 1991 Dec 5;325(23):1593-6 [1669840.001]

[Cites] Am J Epidemiol. 2005 Sep 15;162(6):548-58 [16093288.001]

[Cites] Drugs Aging. 2006;23(6):513-23 [16872234.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2008 Aug;17(8):1852-7 [18708371.001]

[Cites] Clin Gastroenterol Hepatol. 2004 Jan;2(1):1-8 [15017625.001]

[Cites] JAMA. 2005 Jul 6;294(1):47-55 [15998890.001]

(PMID = 20808298.001).

[ISSN] 1572-0241

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

[ISO-abbreviation] Am. J. Gastroenterol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / N01 CN25522; United States / Intramural NIH HHS / /

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

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; R16CO5Y76E / Aspirin; WK2XYI10QM / Ibuprofen

   

Advertisement

[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

   

[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

   

[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] Mucins in the colorectal neoplastic spectrum with reference to conventional and serrated adenomas.

BACKGROUND/AIMS: Alterations in expression of mucins and aberrant expression of various types of mucin genes were observed in colorectal adenomas and carcinomas, though their significance in neoplastic transformation of colorectal epithelium is yet to be determined.

The aim of this study was to determine expression of MUC1, MUC2, MUC5AC, and MUC6 through conventional adenoma-carcinoma sequence and polyps involved in the "serrated" pathway of the colorectum using tissue array technique.

METHODS: In this study, a total of 172 cases including 100 colorectal polyps [8 hyperplastic polyps, 10 sessile serrated adenomas, 19 tubular, 37 tubulovillous, and 26 villous adenomas], 16 adenomas with intramucosal carcinoma, 28 conventional colorectal cancers, and 28 normal mucosae were examined.

Sessile serrated adenomas exhibited the highest MUC5AC expression while adenomatous polyps showed an increase in MUC5AC expression in parallel with neoplastic progression (p<0.001).

Hyperplastic polyps seemed to lie between normal mucosa and sessile serrated adenomas in terms of mucin expression, suggesting that they are morphologically and histogenetically linked.

CONCLUSIONS: Upregulation of MUC1 and MUC6 through the adenoma-carcinoma sequence together with downregulation of MUC2 and MUC5AC at the neoplastic end of the spectrum seem to follow the steps of malignant transformation.

[MeSH-major] Adenoma / metabolism. Colonic Polyps / metabolism. Colorectal Neoplasms / metabolism. Mucins / metabolism

MedlinePlus Health Information. consumer health - Colonic Polyps.

MedlinePlus Health Information. consumer health - Colorectal Cancer.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

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 = 18080919.001).

[ISSN] 2148-5607

[Journal-full-title] The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology

[ISO-abbreviation] Turk J Gastroenterol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Turkey

[Chemical-registry-number] 0 / Mucins

   

[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.

Colo-colic intussusception was diagnosed by means of a colonic contrast X-ray.

Hundreds of polyps were seen throughout the entire colon.

The pathology specimen showed an intramucosal carcinoma and multiple adenomas.

[MeSH-major] Adenomatous Polyposis Coli / diagnosis. Colonic Diseases / diagnosis. DNA Glycosylases / genetics. Intussusception / diagnosis

MedlinePlus Health Information. consumer health - Colonic Diseases.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentIn] Ned Tijdschr Geneeskd. 2008 Jan 5;152(1):56-7; author reply 57 [18240762.001]

(PMID = 17715770.001).

[ISSN] 0028-2162

[Journal-full-title] Nederlands tijdschrift voor geneeskunde

[ISO-abbreviation] Ned Tijdschr Geneeskd

[Language] dut

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Netherlands

[Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase

   

[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

   

[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

   

[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.

Surveillance procedures were classified as: a) Barrett's oesophagus, b) chronic IBD, c) prior adenomatous colorectal polyps and, d) prior surgical resection of colorectal cancer.

Of these, 50 of 133 (37.6%) Barrett's patients, 92 of 213 (43.2%) patients with prior colonic polyps, 36 of 48 (75.0%) patients with prior colonic malignancy and 17 of 47 (36.2%) patients for IBD surveillance were scheduled prematurely.

[MeSH-minor] Adenomatous Polyposis Coli / diagnosis. Barrett Esophagus / diagnosis. Colorectal Neoplasms / diagnosis. Databases as Topic. Great Britain. Humans. Inflammatory Bowel Diseases / diagnosis. Ireland

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18990956.001).

[ISSN] 0332-3102

[Journal-full-title] Irish medical journal

[ISO-abbreviation] Ir Med J

[Language] eng

[Publication-type] Evaluation Studies; Journal Article

[Publication-country] Ireland

   

[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.

Adenomatous polyps are the most common neoplastic findings uncovered in people who undergo colorectal screening or have a diagnostic workup for symptoms.

It was common practice in the 1970s for these patients to have annual follow-up surveillance examinations to detect additional new adenomas as well as missed synchronous adenomas.

As a result of the National Polyp Study report in 1993, which demonstrated clearly in a randomized design that the first postpolypectomy examination could be deferred for 3 years, guidelines published by a gastrointestinal consortium in 1997 recommended that the first follow-up surveillance be 3 years after polypectomy for most patients.

In 2003, these guidelines were updated, colonoscopy was recommended as the only follow-up examination, and stratification at baseline into lower and higher risk for subsequent adenomas was suggested.

In the present paper, a careful analytic approach was designed addressing all evidence available in the literature to delineate predictors of advanced pathology, both cancer and advanced adenomas, so that patients can be more definitely stratified at their baseline colonoscopy into those at lower or increased risk for a subsequent advanced neoplasia.

People at increased risk have either three or more adenomas, or high-grade dysplasia, or villous features, or an adenoma > or =1 cm in size.

People at lower risk who have one or two small (< 1 cm) tubular adenomas with no high-grade dysplasia can have a follow-up in 5 to 10 years, whereas people with hyperplastic polyps only should have a 10-year follow-up as average-risk people.

It has been shown that the first screening colonoscopy and polypectomy produces the greatest effects on reducing the incidence of colorectal cancer in patients with adenomatous polyps.

[MeSH-minor] Adenomatous Polyps / epidemiology. Adenomatous Polyps / prevention & control. Adenomatous Polyps / surgery. American Cancer Society. Colonic Polyps / epidemiology. Colonic Polyps / prevention & control. Colonic Polyps / surgery. Humans. Societies, Medical. United States / epidemiology

Genetic Alliance. consumer health - Colorectal Cancer.

MedlinePlus Health Information. consumer health - Colonoscopy.

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 = 16737947.001).

[ISSN] 0007-9235

[Journal-full-title] CA: a cancer journal for clinicians

[ISO-abbreviation] CA Cancer J Clin

[Language] eng

[Publication-type] Journal Article; Practice Guideline

[Publication-country] United States

   

[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

   

[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.

Data on its prevalence are lacking in Iran, as well as for adenomatous polyps.

This study was conducted to estimate prevalence of CRC in patients with long lasting colonic symptoms (except for known risk factors for cancer and those with rectal bleeding) who underwent total colonoscopy.

RESULTS: Thirty four subjects (14.9%) were found to have colorectal neoplasia and 112 (49.1%) had a completely normal colon.

Adenomatous polyps were detected in 27 patients, which included 15.6% of men and 7.0% of women.

Mean age of patients with a polyp (51.1+/-12.5 years) was not significantly different compared to others (p=0.381) nor mean duration of symptoms (21.1 months, p=0.435).

None of the symptoms were predictors of cancer or polyps.

CONCLUSION: The low prevalence of colorectal neoplasms as well as the less advanced pattern of adenomas in Iran are compatible with other data from Asia and the Middle East, contrasting with western countries.

[MeSH-major] Adenoma / diagnosis. Colonic Polyps / diagnosis. Colorectal Neoplasms / diagnosis

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 = 18260716.001).

[ISSN] 2476-762X

[Journal-full-title] Asian Pacific journal of cancer prevention : APJCP

[ISO-abbreviation] Asian Pac. J. Cancer Prev.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Thailand

   

[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] CYP27A1 and CYP24 expression as a function of malignant transformation in the colon.

However, vitamin D precursors do not present toxicity concerns and may be sufficient for CRC chemoprevention or chemotherapy, providing the appropriate enzymes are present in colonic epithelia.

We previously showed that CYP27B1 is present at equally high levels in the colon and CRC irrespective of differentiation but was not present in metastases.

In this study we used quantitative immunohistochemistry to show that CYP27A1, converting D3 to 25-hydroxycholecalciferol, is present in increasing concentrations in the nuclei of normal colonic epithelia, aberrant crypt foci (ACF), and adenomatous polyps.

Similarly, increasing amounts of the deactivating enzyme CYP24 are present in the nuclei of normal colonic epithelia, ACFs, and adenomatous polyps.

These data indicate that non-toxic vitamin D precursors should be sufficient for CRC chemoprevention, but that neither vitamin D nor its precursors may be sufficient for CRC chemotherapy.

[MeSH-minor] Adenomatous Polyps / enzymology. Adenomatous Polyps / ultrastructure. Colon / enzymology. Colon / pathology. Colon / ultrastructure. Humans. Immunohistochemistry. Intestinal Mucosa / enzymology. Intestinal Mucosa / ultrastructure. Lymphatic Metastasis. Vitamin D3 24-Hydroxylase

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 = 17875655.001).

[ISSN] 0022-1554

[Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society

[ISO-abbreviation] J. Histochem. Cytochem.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA-094346

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

[Publication-country] United States

[Chemical-registry-number] EC 1.14.- / Steroid Hydroxylases; EC 1.14.13.126 / Vitamin D3 24-Hydroxylase; EC 1.14.13.15 / CYP27A1 protein, human; EC 1.14.13.15 / Cholestanetriol 26-Monooxygenase

   

[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.

Herein, we describe the clinical, pathologic, immunohistochemical, and molecular features of 3 unique patients with long standing inflammatory bowel disease, all of whom developed numerous discrete hyperplastic/serrated colonic polyps similar to those described in the hyperplastic/serrated polyposis syndrome.

The 3 patients (2 with ulcerative colitis and 1 with Crohn ileo-colitis) were evaluated for a variety of clinical, histologic (including the type, location and number of polyps in the colon), and immunohistochemical features [MLH-1, MSH-2, MGMT (O(6)-methylguanine-DNA methyltransferase), beta-catenin, and p53].

KRAS and BRAF mutation analysis was also performed on a subset of polyps from 2 patients.

All patients had moderate-severe pancolitis of more than 10 years duration and had >20 colonic polyps.

None had polyps in the upper gastrointestinal tract.

Pathologically, a combination of conventional hyperplastic polyps and sessile serrated polyps (adenomas) were present in the 3 cases.

In addition, serrated adenomas were present in 2 and conventional adenomas in 1.

However, 2 cases showed loss of MGMT in several serrated polyps, and one also in adjacent colitic mucosa.

KRAS mutations were detected in 5/11 serrated polyps.

However, BRAF mutations were not present in any of the polyps tested.

[MeSH-major] Adenomatous Polyps / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Inflammatory Bowel Diseases / pathology. Precancerous Conditions / pathology

MedlinePlus Health Information. consumer health - Colonic Polyps.

COS Scholar Universe. author profiles.

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 = 18223333.001).

[ISSN] 0147-5185

[Journal-full-title] The American journal of surgical pathology

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

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Biomarkers, Tumor; 0 / MLH1 protein, human; 0 / MLH2 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf

   

[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] Noninvasive detection of candidate molecular biomarkers in subjects with a history of insulin resistance and colorectal adenomas.

We have developed novel molecular methods using a stool sample, which contains intact sloughed colon cells, to quantify colonic gene expression profiles.

For this purpose, the effects of a legume-enriched, low glycemic index, high fermentable fiber diet was evaluated in subjects with four possible combinations of risk factors, including insulin resistance and a history of adenomatous polyps.

Linear discriminant analysis was successfully used to identify the best single genes and two- to three-gene combinations for distinguishing subjects with insulin resistance, a history of polyps, or exposure to a chemoprotective legume-rich diet.

These results support our premise that gene products (RNA) isolated from stool have diagnostic value in terms of assessing colon cancer risk.

MedlinePlus Health Information. consumer health - Bowel Movement.

MedlinePlus Health Information. consumer health - Colonic Polyps.

MedlinePlus Health Information. consumer health - Colorectal Cancer.

MedlinePlus Health Information. consumer health - Dietary Fiber.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Cell Death Differ. 2009 Jan;16(1):87-93 [18806760.001]

[Cites] Cell Cycle. 2008 May 1;7(9):1178-83 [18418037.001]

[Cites] Gastroenterology. 2009 Feb;136(2):459-70 [19026650.001]

[Cites] Gastroenterology. 2000 Nov;119(5):1219-27 [11054379.001]

[Cites] Eur J Cancer. 2001 Jan;37(2):224-33 [11166150.001]

[Cites] Mol Cancer Ther. 2002 Nov;1(13):1229-36 [12479704.001]

[Cites] Cancer Res. 2003 Jan 1;63(1):60-6 [12517778.001]

[Cites] Biomarkers. 2003 Jan-Feb;8(1):51-61 [12519636.001]

[Cites] J Virol. 2003 Feb;77(3):2233-42 [12525658.001]

[Cites] Trends Genet. 2003 Jul;19(7):362-5 [12850439.001]

[Cites] Int J Oncol. 2003 Sep;23(3):617-25 [12888896.001]

[Cites] Gastroenterology. 2008 Sep;135(3):907-16, 916.e1-2 [18655788.001]

[Cites] Ann Intern Med. 2008 Oct 7;149(7):441-50, W81 [18838724.001]

[Cites] Cancer Res. 2003 Nov 15;63(22):7708-16 [14633695.001]

[Cites] Gastroenterology. 2004 Aug;127(2):422-7 [15300574.001]

[Cites] Cancer Res. 2004 Sep 15;64(18):6797-804 [15374999.001]

[Cites] Biochim Biophys Acta. 1979 Aug 10;560(2):281-99 [380653.001]

[Cites] Diabetes Care. 1988 Feb;11(2):149-59 [3383733.001]

[Cites] Int J Cancer. 1992 Sep 30;52(3):347-50 [1383164.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1995 Sep;4(6):643-7 [8547831.001]

[Cites] Carcinogenesis. 1997 Feb;18(2):351-7 [9054628.001]

[Cites] Carcinogenesis. 1998 Feb;19(2):253-7 [9498273.001]

[Cites] Am J Physiol. 1999 May;276(5 Pt 1):G1087-93 [10329998.001]

[Cites] N Engl J Med. 2004 Dec 23;351(26):2704-14 [15616205.001]

[Cites] Nat Rev Cancer. 2005 Mar;5(3):199-209 [15738983.001]

[Cites] Cancer Causes Control. 2005 Apr;16(3):225-33 [15947874.001]

[Cites] J Natl Cancer Inst. 2005 Aug 3;97(15):1124-32 [16077070.001]

[Cites] Mol Cell Biol. 2005 Dec;25(23):10454-64 [16287858.001]

[Cites] Cancer Res. 2006 Apr 1;66(7):3942-53 [16585224.001]

[Cites] Gastroenterology. 2006 Apr;130(4):1030-8 [16618396.001]

[Cites] Ann Surg. 2006 May;243(5):619-25; discussion 625-7 [16632996.001]

[Cites] J Nutr. 2006 Jul;136(7):1896-903 [16772456.001]

[Cites] Bioinformatics. 2006 Oct 1;22(19):2430-6 [16870934.001]

[Cites] Nat Med. 2006 Nov;12(11):1294-300 [17057710.001]

[Cites] Clin Gastroenterol Hepatol. 2007 Jan;5(1):111-7 [17161655.001]

[Cites] Nutr Rev. 2007 Feb;65(2):51-62 [17345958.001]

[Cites] Nat Cell Biol. 2007 Apr;9(4):445-52 [17351641.001]

[Cites] Clin Chem. 2007 Sep;53(9):1646-51 [17712002.001]

[Cites] J Cell Biochem. 2007 Dec 15;102(6):1420-31 [17471513.001]

[Cites] Biochimie. 2008 Feb;90(2):313-23 [17928127.001]

[Cites] Oncogene. 2008 Feb 21;27(9):1315-9 [17704798.001]

[Cites] N Engl J Med. 2008 Mar 13;358(11):1148-59 [18337604.001]

[Cites] Cancer Res. 2008 Apr 15;68(8):2813-9 [18413749.001]

[Cites] Nutr Cancer. 2008;60(3):373-81 [18444172.001]

[Cites] Cancer Prev Res (Phila). 2009 Jan;2(1):60-9 [19139019.001]

(PMID = 19470793.001).

[ISSN] 1940-6215

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

[ISO-abbreviation] Cancer Prev Res (Phila)

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / R01 DK071707-02; United States / NCI NIH HHS / CA / R01 CA129444-01; United States / NIDDK NIH HHS / DK / R01 DK071707-01A2; United States / NIDDK NIH HHS / DK / R01 DK071707-01A2S1; United States / NCI NIH HHS / CA / R01 CA059034-05; United States / NCI NIH HHS / CA / CA059034-12; United States / NCI NIH HHS / CA / CA059034-08; United States / NIEHS NIH HHS / ES / P30ES09106; United States / NCI NIH HHS / CA / R01 CA059034-07; United States / NCI NIH HHS / CA / CA059034-13; United States / NCI NIH HHS / CA / R01 CA059034; United States / NIDDK NIH HHS / DK / DK071707; United States / NCI NIH HHS / CA / R01 CA059034-15; United States / NCI NIH HHS / CA / R01 CA059034-11; United States / NCI NIH HHS / CA / CA059034-06; United States / NCI NIH HHS / CA / R01 CA059034-09; United States / NIDDK NIH HHS / DK / R01 DK071707-03; United States / NCI NIH HHS / CA / CA059034-09; United States / NIDDK NIH HHS / DK / DK071707-03; United States / NCI NIH HHS / CA / R01 CA129444-02; United States / NCI NIH HHS / CA / R01 CA059034-08; United States / NCI NIH HHS / CA / CA59034; United States / NCI NIH HHS / CA / CA059034-05; United States / NCI NIH HHS / CA / R01 CA059034-10; United States / NCI NIH HHS / CA / CA129444-01; United States / NCI NIH HHS / CA / CA059034-10; United States / NCI NIH HHS / CA / R01 CA059034-14; United States / NCI NIH HHS / CA / R01 CA059034-12; United States / NIDDK NIH HHS / DK / DK071707-01A2S1; United States / NIDDK NIH HHS / DK / DK071707-01A2; United States / NCI NIH HHS / CA / CA129444-02; United States / NCI NIH HHS / CA / CA059034-15; United States / NIDDK NIH HHS / DK / DK071707-02; United States / NCI NIH HHS / CA / CA059034-11; United States / NCI NIH HHS / CA / CA129444; United States / NCI NIH HHS / CA / CA059034-14; United States / NIDDK NIH HHS / DK / R01 DK071707; United States / NIEHS NIH HHS / ES / P30 ES009106; United States / NCI NIH HHS / CA / CA059034-07; United States / NCI NIH HHS / CA / R01 CA059034-06; United States / NCI NIH HHS / CA / R01 CA059034-13; United States / NCI NIH HHS / CA / R01 CA129444

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

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger

[Other-IDs] NLM/ NIHMS120536; NLM/ PMC2745241

   

[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

   

[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

   

[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] Pigmented mesenteric lymphadenopathy in familial adenomatous polyposis - an unusual cause of intraoperative abandonment of ileo-anal pouch.

Familial adenomatous polyposis (FAP) is an autosomal dominant condition with near complete penetrance, characterised by the presence of numerous adenomatous polyps of the colon and rectum.

Melanosis coli describes the brownish-black discolouration of the colon resulting from the accumulation of a granular pigment in the phagosomes of macrophages in the colonic lamina propria.

The presence of melanosis pigment in pericolonic lymph nodes has been reported in patients with coincidental melanosis coli, following segmental colonic resection.

[MeSH-major] Adenomatous Polyposis Coli / surgery. Lymphatic Diseases / complications. Melanosis / complications. Mesentery. Peritoneal Diseases / complications

[MeSH-minor] Adolescent. Colonic Pouches. Female. Humans. Intraoperative Complications / etiology. Proctocolectomy, Restorative. Reoperation

Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).

Genetic Alliance. consumer health - Familial Polyposis.

MedlinePlus Health Information. consumer health - Lymphatic Diseases.

MedlinePlus Health Information. consumer health - Peritoneal Disorders.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16884599.001).

[ISSN] 0035-8843

[Journal-full-title] Annals of the Royal College of Surgeons of England

[ISO-abbreviation] Ann R Coll Surg Engl

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC1963935

   

[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 (FAP) and results in the manifestation of numerous external and internal symptoms including gastrointestinal polyps, osteomas, tumors, and epidermoid cysts.

Stemming from a mutation in the adenomatous polyposis coli (APC) gene, Gardner syndrome shares genetic correlations with the FAP phenotype; as a result, it becomes all the more crucial for physicians to be able to discern Gardner syndrome from other differential diagnoses such as Turcot syndrome, FAP, and other attenuated forms of familial polyposis.

Fortunately, Gardner syndrome has characteristic polyps in the colon, osteomas, and also exhibits abnormalities in the retinal epithelium that discern it from others.

Surgery is the most effective method of management for Gardner syndrome; restorative proctocolectomy with ileal pouch anal anastomosis with mucosectomy is the top choice for colonic malignancies, and skin manifestations can be treated through a variety of excisions and therapy depending on location, size, and number of malignancies.

Currently, there are no specific screening recommendations for Gardner syndrome, but testing following general screening recommendations for extra-colonic malignancies, genetic counseling, and endoscopy are encouraged.

[MeSH-minor] Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis. Colorectal Neoplasms, Hereditary Nonpolyposis / pathology. Colorectal Neoplasms, Hereditary Nonpolyposis / therapy. Diagnosis, Differential. Genetic Counseling / methods. Humans. Mutation

Genetic Alliance. consumer health - Gardner Syndrome.

The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for gardner syndrome .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20141232.001).

[ISSN] 1175-0561

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

[ISO-abbreviation] Am J Clin Dermatol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] New Zealand

[Number-of-references] 29

   

[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

   

[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

   

[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 is a risk factor for subsequent adenomatous polyps.

BACKGROUND: Serrated adenomas (SA) are histologically defined by the presence of both hyperplastic and adenomatous features.

These uncommon polyps are thought to play an important role in the development of sporadic colorectal cancers (CRC) with microsatellite instability (MSI).

This study was undertaken to define the relationship between SA and the future development of adenomatous polyps.

These were matched to controls by age, sex, indication for colonoscopy, polyp type and number and duration of follow-up.

Of these, 80 patients (0.5%) with SA were found, and of these SA, 80% were found in the left colon.

On follow-up examination four patients (24%) and no controls had adenomatous polyps (P = 0.01).

Serrated adenomas appear to be found more commonly in the left colon and in older patients.

This study found a significant association between SA and the subsequent development of adenomatous polyps.

[MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Precancerous Conditions / pathology

MedlinePlus Health Information. consumer health - Colonic Polyps.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Surg Pathol. 1990 Jun;14(6):524-37 [2186644.001]

[Cites] Am J Surg Pathol. 1984 Jul;8(7):551-6 [6742315.001]

[Cites] Am J Clin Pathol. 2005 Mar;123(3):349-59 [15716230.001]

[Cites] Clin Cancer Res. 2004 May 1;10 (9):3082-90 [15131047.001]

[Cites] Am J Gastroenterol. 2004 Nov;99(11):2242-55 [15555008.001]

[Cites] Gastroenterology. 2001 Dec;121(6):1300-9 [11729109.001]

[Cites] J Pathol. 2001 Mar;193(3):286-94 [11241406.001]

[Cites] Am J Clin Pathol. 2005 Sep;124(3):380-91 [16191506.001]

[Cites] Gut. 2004 Aug;53(8):1137-44 [15247181.001]

[Cites] J Natl Cancer Inst. 2001 Sep 5;93(17 ):1307-13 [11535705.001]

[Cites] N Engl J Med. 1988 Sep 1;319(9):525-32 [2841597.001]

[Cites] Am J Pathol. 2003 Mar;162(3):815-22 [12598316.001]

[Cites] Science. 1989 Apr 14;244(4901):207-11 [2565047.001]

[Cites] Anticancer Res. 2000 Mar-Apr;20(2B):1141-7 [10810411.001]

[Cites] J Clin Pathol. 1999 Jan;52(1):5-9 [10343605.001]

[Cites] Gastrointest Endosc. 1995 Aug;42(2):114-22 [7590045.001]

(PMID = 18320324.001).

[ISSN] 0163-2116

[Journal-full-title] Digestive diseases and sciences

[ISO-abbreviation] Dig. Dis. Sci.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[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

   

[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

   

[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.

Esophagogastroduodenoscopy, video capsule endoscopy and colonoscopy revealed various sizes of generalized gastrointestinal polyps.

Histological examination of the biopsy specimens obtained from the stomach and the colon showed adenomatous polyp and inflammatory polyp respectively.

MedlinePlus Health Information. consumer health - Chest Injuries and Disorders.

MedlinePlus Health Information. consumer health - Osteoporosis.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Gastrointest Endosc. 2001 Sep;54(3):388-91 [11522989.001]

[Cites] Aliment Pharmacol Ther. 2002 Mar;16(3):333-42 [11876685.001]

[Cites] Expert Opin Pharmacother. 2003 Mar;4(3):385-9 [12614190.001]

[Cites] Am J Gastroenterol. 2003 Jun;98(6):1444-6 [12818298.001]

[Cites] Gastrointest Endosc. 2008 Mar;67(3):570-2 [18294523.001]

[Cites] Medicine (Baltimore). 1982 Sep;61(5):293-309 [7109958.001]

[Cites] Gastrointest Endosc. 1997 Dec;46(6):537-41 [9434222.001]

[Cites] N Engl J Med. 1955 Jun 16;252(24):1011-5 [14383952.001]

[Cites] Digestion. 2007;75(2-3):96-7 [17510553.001]

[Cites] Digestion. 2004;69(1):57-62 [14755154.001]

(PMID = 20955587.001).

[ISSN] 1471-230X

[Journal-full-title] BMC gastroenterology

[ISO-abbreviation] BMC Gastroenterol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2972238

   

[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] Sporadic adenomatous polyp regression with exisulind is effective but toxic: a randomised, double blind, placebo controlled, dose-response study.

The aim of our study was to investigate if exisulind induces regression of sporadic colonic adenomas.

At baseline colonoscopy, left sided polyps (3-10 mm) were tattooed, measured, and left in place.

Follow up sigmoidoscopy was performed after six months, and removal of any remaining polyps at the 12 month colonoscopy.

The primary efficacy variable was change in polyp size from baseline.

The decrease in median polyp size was significantly greater (p=0.03) in patients who received exisulind 400 mg (-10 mm2) compared with those who received placebo (-4 mm2).

CONCLUSION: Exisulind caused significant regression of sporadic adenomatous polyps but was associated with more toxicity.

This model of polyp regression, short in its term and involving a comparatively small patient sample size, may be the best available tool to assess a therapeutic regimen before launching into large preventive clinical studies.

[MeSH-major] Adenomatous Polyposis Coli / drug therapy. Antineoplastic Agents / therapeutic use. Sulindac / analogs & derivatives

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] N Engl J Med. 1993 Dec 30;329(27):1977-81 [8247072.001]

[Cites] Am J Gastroenterol. 1993 Oct;88(10):1652-6 [8213705.001]

[Cites] Gastroenterology. 1995 Apr;108(4):1083-7 [7698575.001]

[Cites] Gastroenterology. 1996 Feb;110(2):654-5 [8566622.001]

[Cites] Cancer Res. 1997 Jun 15;57(12):2452-9 [9192825.001]

[Cites] Am J Gastroenterol. 1997 Jul;92(7):1117-20 [9219781.001]

[Cites] Cancer Res. 1997 Jul 15;57(14):2909-15 [9230200.001]

[Cites] J Clin Invest. 1997 Sep 15;100(6):1325-9 [9294096.001]

[Cites] Eur J Surg Suppl. 1998;(582):111-4 [10029375.001]

[Cites] Scand J Gastroenterol. 1999 Jan;34(1):4-11 [10048725.001]

[Cites] N Engl J Med. 1999 Jun 17;340(24):1888-99 [10369853.001]

[Cites] Gut. 1997 Mar;40(3):344-9 [9135523.001]

[Cites] Clin Cancer Res. 2000 Jan;6(1):78-89 [10656435.001]

[Cites] Can J Gastroenterol. 2000 Apr;14(4):299-307 [10799083.001]

[Cites] Cancer Res. 2000 Jul 1;60(13):3338-42 [10910034.001]

[Cites] Gastroenterology. 2000 Sep;119(3):837-53 [10982778.001]

[Cites] Gastroenterology. 2000 Sep;119(3):854-65 [10982779.001]

[Cites] Med Clin North Am. 2000 Sep;84(5):1163-82, viii [11026923.001]

[Cites] Expert Opin Investig Drugs. 2001 Oct;10(10):1875-82 [11772293.001]

[Cites] J Clin Epidemiol. 2003 Oct;56(10):968-76 [14568628.001]

[Cites] Int J Cancer. 2004 Sep 10;111(4):633-9 [15239144.001]

[Cites] J Surg Oncol. 1983 Sep;24(1):83-7 [6887943.001]

[Cites] Gastroenterology. 1987 Nov;93(5):1009-13 [3653628.001]

[Cites] Am J Surg. 1989 Jan;157(1):175-9 [2535920.001]

[Cites] Bull World Health Organ. 1990;68(6):789-95 [2073716.001]

[Cites] Gastroenterology. 1991 Sep;101(3):635-9 [1650315.001]

[Cites] Ann Intern Med. 1991 Dec 15;115(12):952-4 [1659272.001]

[Cites] N Engl J Med. 1993 May 6;328(18):1313-6 [8385741.001]

[Cites] Ann Intern Med. 1993 Oct 15;119(8):836-43 [8379605.001]

[Cites] Adv Intern Med. 1994;39:123-47 [8140953.001]

(PMID = 16150858.001).

[ISSN] 0017-5749

[Journal-full-title] Gut

[ISO-abbreviation] Gut

[Language] eng

[Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 184SNS8VUH / Sulindac; K619IIG2R9 / sulindac sulfone

[Other-IDs] NLM/ PMC1856089

   

[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] Colorectal polyps on portal phase contrast-enhanced CT colonography: lesion attenuation and distinction from tagged feces.

OBJECTIVE: The purpose of our study was to determine the attenuation of colorectal polyps on portal phase contrast-enhanced CT colonography (CTC) and evaluate whether enhanced polyps can be clearly distinguished from tagged feces during CTC review.

Forty-eight colonoscopy-proven polyps (6-20 mm) and 41 polypoid tagged feces (6-19 mm) were selected from contrast-enhanced CTC performed without (n = 37 examinations) and with (n = 10 examinations) fecal tagging, respectively.

Attenuation of the polyps and tagged feces was measured.

Four independent blinded radiologists reviewed the polyps and tagged feces at both wide (width, 1,500 H; level -400 H) and soft-tissue (width, 400 H; level, 20 H) window settings to distinguish them by using subjective visual assessment.

RESULTS: Polyp attenuation on the portal phase was not correlated with size (R = -0.003; p = 0.99) and was not different between histologic types (p = 0.884).

Enhanced polyps (mean +/- SD, 119.9 +/- 25.3 H; range, 50-173 H) showed significantly lower attenuation than did tagged feces (1,521.4 +/- 683.6 H; range, 495-2,683 H) without any overlap (p < 0.0005).

An 8-mm sessile adenomatous polyp was misinterpreted as tagged feces by one reviewer.

CONCLUSION: Polyp attenuation on portal phase contrast-enhanced CTC ranges from 50 to 173 H.

Contrast-enhanced polyps are clearly and consistently distinguished from barium-tagged polypoid feces.

[MeSH-major] Colonic Polyps / radiography. Colonography, Computed Tomographic / methods. Contrast Media / administration & dosage. Feces. Radiographic Image Enhancement / methods. Rectal Diseases / radiography

MedlinePlus Health Information. consumer health - Bowel Movement.

MedlinePlus Health Information. consumer health - Colonic Polyps.

MedlinePlus Health Information. consumer health - Rectal Disorders.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17579149.001).

[ISSN] 1546-3141

[Journal-full-title] AJR. American journal of roentgenology

[ISO-abbreviation] AJR Am J Roentgenol

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Contrast Media

   

[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 describe a 58-year-old woman who was incidentally found to have gastric and colonic polyposis, hypoalbuminemia, cutaneous hyperpigmentation and onychodystrophy (Cronkhite-Canada syndrome).

Histology of polyps from the stomach showed features of juvenile or retention type (hamartomatous) polyps with Helicobacter pylori (H. pylori) infection.

The large pedunculated colonic polyps showed hamartomatous polyps with adenomatous component and polypectomy was performed.

After the treatment with H. pylori eradication and omeprazole, the gastric polyposis, hypoalbuminemia and anemia regressed, and endoscopic polypectomy of gastric polyps were performed.

[MeSH-major] Anti-Ulcer Agents / therapeutic use. Helicobacter Infections / drug therapy. Helicobacter pylori. Omeprazole / therapeutic use. Polyps / complications. Stomach Neoplasms / complications

[MeSH-minor] Colonic Polyps / complications. Colonic Polyps / microbiology. Colonic Polyps / pathology. Female. Humans. Hyperpigmentation / pathology. Middle Aged. Nails, Malformed / pathology. Proton Pump Inhibitors. Syndrome

MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.

MedlinePlus Health Information. consumer health - Stomach Cancer.

Hazardous Substances Data Bank. OMEPRAZOLE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16434870.001).

[ISSN] 1598-9992

[Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi

[ISO-abbreviation] Korean J Gastroenterol

[Language] kor

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Korea (South)

[Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Proton Pump Inhibitors; KG60484QX9 / Omeprazole

   

[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

Genetic Alliance. consumer health - Acute Myelocytic Leukemia.

Genetic Alliance. consumer health - Medulloblastoma.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

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

(PMID = 17259933.001).

[ISSN] 1743-4262

[Journal-full-title] Nature clinical practice. Oncology

[ISO-abbreviation] Nat Clin Pract Oncol

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / G-T mismatch-binding protein

   

[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] Reduction of miss rates of colonic adenomas by zoom chromoendoscopy.

BACKGROUND AND AIMS: The aim of this study was to determine the detection rate of polyps using zoom chromoendoscopy (ZE) compared with standard video colonoscopy.

The second colonoscopy (C2) was done with a zoom colonoscope spraying the whole colon with indigocarmine (0.4%).

During C1, 56 lesions were detected in 26 of 50 patients (34 hyperplastic and 22 adenomatous).

During C2, 19 additional polyps were documented prior to ZE (15% tandem miss rate), and 20 further lesions were detected with ZE (21% additional polyp detection rate compared to C1 and C2 without ZE).

Of the 39 additional lesions removed during C2 after ZE, 29 were hyperplastic and 10 were adenomatous.

Most adenomas detected during the second investigation were found in patients in whom adenomatous polyps had already been removed during the initial colonoscopy (9 of 26 patients vs 1 of 24 patients, p<0.02).

The pit pattern classification allowed a correct differentiation between hyperplastic and adenomatous polyps (accuracy 93%, sensitivity 90%, specificity 97%).

CONCLUSION: Using zoom chromoendoscopy, the rate of detecting colonic polyps can be increased at the cost of a longer retrieval time.

[MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology. Colonoscopy / methods. Coloring Agents. Diagnostic Errors / prevention & control. Indigo Carmine

MedlinePlus Health Information. consumer health - Colonoscopy.

Hazardous Substances Data Bank. INDIGO .

Hazardous Substances Data Bank. Indigotindisulfonate sodium .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Gastroenterol. 2002 Jul;97(7):1696-700 [12135020.001]

[Cites] Endoscopy. 2001 Dec;33(12):1001-6 [11740641.001]

[Cites] Dis Colon Rectum. 1982 Oct;25(7):669-72 [7128368.001]

[Cites] J Clin Pathol. 1994 Oct;47(10):880-5 [7962600.001]

[Cites] Endoscopy. 2001 Apr;33(4):367-73 [11315901.001]

[Cites] N Engl J Med. 1993 Dec 30;329(27):1977-81 [8247072.001]

[Cites] Gastrointest Endosc. 2002 Sep;56(3):333-8 [12196768.001]

[Cites] Endoscopy. 2004 Dec;36(12):1109-14 [15578305.001]

[Cites] Endoscopy. 1998 Jun;30(5):437-43 [9693889.001]

[Cites] Endoscopy. 2001 Apr;33(4):306-10 [11315890.001]

[Cites] N Engl J Med. 1992 Mar 5;326(10):658-62 [1736104.001]

[Cites] J Natl Cancer Inst. 1992 Oct 21;84(20):1572-5 [1404450.001]

[Cites] Gastrointest Endosc. 1996 Jul;44(1):8-14 [8836710.001]

[Cites] N Engl J Med. 1992 Mar 5;326(10):653-7 [1736103.001]

[Cites] Am J Gastroenterol. 2002 Jul;97(7):1587-90 [12135005.001]

[Cites] Gastrointest Endosc. 1999 Mar;49(3 Pt 2):S63-6 [10049451.001]

[Cites] World J Surg. 1997 Sep;21(7):694-701 [9276699.001]

[Cites] Gut. 1996 Sep;39(3):449-56 [8949653.001]

[Cites] Gastrointest Endosc. 2002 May;55(6):687-94 [11979251.001]

[Cites] Dis Colon Rectum. 1987 Apr;30(4):247-50 [3829872.001]

[Cites] Am J Gastroenterol. 2001 Sep;96(9):2628-32 [11569686.001]

[Cites] Gastroenterology. 1997 Jan;112(1):24-8 [8978338.001]

[Cites] Gastroenterology. 1996 Apr;110(4):1253-8 [8613016.001]

[Cites] Endoscopy. 2001 Dec;33(12):1036-41 [11764766.001]

(PMID = 16283340.001).

[ISSN] 0179-1958

[Journal-full-title] International journal of colorectal disease

[ISO-abbreviation] Int J Colorectal Dis

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Coloring Agents; D3741U8K7L / Indigo Carmine

   

[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

   

[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.

We analyzed the DNA of various organs and lesions in Korean patients with Cowden syndrome, their family members, and patients with familial adenomatous polyposis for germline or somatic PTEN mutations.

METHODS: The 11 patients included in this study were 5 patients with Cowden syndrome, 4 of their family members, and 2 patients with familial adenomatous polyposis.

Deletions and mutations in exons 1 to 9 of the PTEN gene were evaluated by polymerase chain reaction-single strand conformation polymorphism and sequencing analysis in esophageal acanthosis, gastric polyps, colonic polyps, skin lesions, and peripheral blood mononuclear cells.

RESULTS: All patients with Cowden syndrome showed several to numerous polyps in the gastrointestinal tract.

Identical mutations were found in all tissue samples, including colonic polyps, from each patient.

No PTEN mutations were found in their family members or in any patient with familial adenomatous polyposis.

[MeSH-major] Adenomatous Polyposis Coli / genetics. Chromosomes, Human, Pair 10. Germ-Line Mutation. Hamartoma Syndrome, Multiple / genetics. Phosphoric Monoester Hydrolases / genetics. Tumor Suppressor Proteins / genetics

Genetic Alliance. consumer health - Cowden Syndrome.

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 = 16007494.001).

[ISSN] 0012-3706

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

[ISO-abbreviation] Dis. Colon Rectum

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase

   

[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

   

[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] Adenocarcinoma of the colon associated with hyperplastic polyposis.

[MeSH-major] Adenocarcinoma, Mucinous / pathology. Adenomatous Polyps / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Neoplasms, Multiple Primary / pathology. Neoplastic Syndromes, Hereditary / diagnosis

[MeSH-minor] Adenoma, Villous / pathology. Adenoma, Villous / surgery. Adenomatous Polyposis Coli / diagnosis. Adult. Colectomy. Colonoscopy. CpG Islands. DNA Methylation / genetics. Diagnosis, Differential. Female. Humans. Hyperplasia. Proto-Oncogene Proteins B-raf / genetics

MedlinePlus Health Information. consumer health - Colonic Polyps.

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 = 20363055.001).

[ISSN] 0210-5705

[Journal-full-title] Gastroenterología y hepatología

[ISO-abbreviation] Gastroenterol Hepatol

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] Spain

[Chemical-registry-number] EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf

   

[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

   

[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 polyps in carriers of the APC I1307K polymorphism.

The prevalence of polyps and adenomas in specimens of colorectal cancer who are carriers and noncarriers of the APC I1307K polymorphism is compared.

METHOD: Prevalence of adenomatous polyps in the pathology specimens of the study participants, stratified by their APC I1307K polymorphism status, was studied in 900 consecutive cases of colorectal cancer diagnosed in northern Israel between 1998 and 2002, within the framework of a population-based, case-controlled study (MECC Study).

Prevalence was higher among Ashkenazi Jews (11.2 percent) than among non-Ashkenazi Jews (2.7 percent) or Arabs (3.1 percent).

After adjustment for age, APC I1307K carriers were significantly more likely than noncarriers to have polyps in their surgical specimen (51.3 percent vs. 32.6 percent, P = 0.002).

Adenomas with a tubular component (either tubular adenomas or tubulovillous adenomas), but not villous adenomas, were significantly more frequent among carriers (37.2 percent vs. 23.6 percent, P = 0.005).

CONCLUSION: Together with former evidence of I1307K being a risk factor for colorectal cancer, these data suggest that colonoscopic surveillance for colorectal adenomas and cancer may be warranted in I1307K carriers, even in the absence of other identifiable risk factors.

[MeSH-major] Adenoma / genetics. Colonic Polyps / genetics. Colorectal Neoplasms / genetics. Genes, APC. Polymorphism, Genetic

MedlinePlus Health Information. consumer health - Colonic Polyps.

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 = 16228836.001).

[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

   

[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

   

[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] Manejo anestésico de un paciente con displasia arritmogénica de ventrículo derecho, ascitis y colitis ulcerosa para una cirugía abdominal mayor.

A 43-year-old man with ulcerative colitis was scheduled for pancolectomy owing to adenomatous transformation of polyps.

[MeSH-minor] Adenomatous Polyps / surgery. Adult. Analgesia, Epidural / methods. Atracurium / analogs & derivatives. Catheter Ablation. Colonic Neoplasms / surgery. Colonic Polyps / surgery. Defibrillators, Implantable. Equipment Failure. Fentanyl. Humans. Isoflurane. Male. Monitoring, Intraoperative. Pain, Postoperative / drug therapy. Postoperative Care. Postoperative Complications / surgery. Preanesthetic Medication. Respiration, Artificial. Thiopental

Genetic Alliance. consumer health - Ulcerative Colitis.

MedlinePlus Health Information. consumer health - Ulcerative Colitis.

Hazardous Substances Data Bank. Isoflurane .

Hazardous Substances Data Bank. FENTANYL .

Hazardous Substances Data Bank. Thiopental .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16435619.001).

[ISSN] 0034-9356

[Journal-full-title] Revista española de anestesiología y reanimación

[ISO-abbreviation] Rev Esp Anestesiol Reanim

[Language] spa

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Spain

[Chemical-registry-number] 64228-79-1 / Atracurium; 76-75-5 / Thiopental; CYS9AKD70P / Isoflurane; QX62KLI41N / cisatracurium; UF599785JZ / Fentanyl

   

[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 primary endpoint was the detection of patients having colon cancer or at least one adenoma.

Significantly more neoplastic (adenomatous and cancerous) lesions and more flat adenomas could be detected using high definition endoscopy with surface enhancement.

[MeSH-major] Adenoma / diagnosis. Colonic Polyps / diagnosis. Colonoscopy / methods. Colorectal Neoplasms / diagnosis. Image Enhancement / instrumentation. Image Enhancement / methods

MedlinePlus Health Information. consumer health - Colonic Polyps.

MedlinePlus Health Information. consumer health - Colonoscopy.

MedlinePlus Health Information. consumer health - Colorectal Cancer.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] © Georg Thieme Verlag KG Stuttgart · New York.

[CommentIn] Endoscopy. 2010 Oct;42(10):866-9 [20886407.001]

(PMID = 20803419.001).

[ISSN] 1438-8812

[Journal-full-title] Endoscopy

[ISO-abbreviation] Endoscopy

[Language] eng

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

[Publication-country] Germany

   

[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.

Physiologically relevant concentrations of desoxycholate (DOC) and chenodesoxycholate (CDC) upregulated expression of c-fos and COX-2 in a concentration- and time-dependent manner.

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

   

[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] [Emerging concepts in colorectal serrated polyps].

Colorectal serrated polyps are heterogeneous epithelial lesions characterized by a serrated architecture.

They include the classical hyperplastic polyps and the much rarer serrated adenomas and mixed polyps.

Whereas serrated adenomas are composed of an unequivocal adenomatous epithelium with architectural serrated, mixed polyps include two separate hyperplastic and adenomatous components.

During the past few years, another type of serrated polyp with only very subtle proliferation abnormalities has been described.

These atypical serrated polyps may occur either sporadically or in the context of colorectal polyposis.

Despite their close resemblance to traditional hyperplastic polyps, some authors argued that they should be regarded as authentically neoplastic lesions and have proposed to call them "sessile serrated adenomas".

This article reviews the histological features, the endoscopic appearance, the natural history and the molecular phenotype of the different categories of serrated polyps and introduces the concept of "serrated neoplastic pathway" in the development of colorectal cancer.

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

MedlinePlus Health Information. consumer health - Colonic Polyps.

MedlinePlus Health Information. consumer health - Colorectal Cancer.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17273130.001).

[ISSN] 0399-8320

[Journal-full-title] Gastroentérologie clinique et biologique

[ISO-abbreviation] Gastroenterol. Clin. Biol.

[Language] fre

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] France

[Number-of-references] 90

   

[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

   

[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 pathway and APC (conventional)-type colorectal polyps: molecular-morphologic correlations, genetic pathways, and implications for classification.

This review addresses the genetic mutations and cell signaling pathway alterations in colorectal premalignant polyps, focusing on the link between molecular changes and morphologic features.

Biallelic APC (adenomatous polyposis coli) mutations are directly responsible for the specific and characteristic cytologic features of dysplastic cells in conventional tubular adenomas.

Sessile serrated adenomas (SSAs) are the precursor lesions of the serrated neoplasia pathway.

Intracellular butyrate inhibits histone deacetylase, allowing histone hyperacetylation and, eventually, transcriptional activation of specific genes.

Progressive loss of cell cycle control and decreased and altered cytoplasmic differentiation produce the characteristic constellation of morphologic changes of SSAs and traditional serrated adenomas.

[MeSH-major] Adenomatous Polyposis Coli / pathology. Colonic Polyps / pathology

[MeSH-minor] Adaptor Proteins, Signal Transducing. Adenomatous Polyposis Coli Protein / physiology. Carrier Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Nuclear Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics

MedlinePlus Health Information. consumer health - Colonic Polyps.

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 = 16483003.001).

[ISSN] 0002-9173

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

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

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / CDKN1A protein, human; 0 / Carrier Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / MLH1 protein, human; 0 / Nuclear Proteins; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf

[Number-of-references] 123

   

[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] An anti-adenoma antibody, Adnab-9, may reflect the risk for neoplastic progression in familial hamartomatous polyposis syndromes.

Patients with the hamartomatous polyposis Peutz-Jeghers and familial juvenile polyposis syndromes are predisposed to colorectal cancer but lack early genetic alterations found in adenomatous premalignant lesions.

We studied hamartomatous polyps for the expression of an early preneoplastic colorectal neoplasia risk marker also found in familial adenomatous polyposis patients.

Retrospective, genetic, and hospital archival tissue immunohistochemistry using Adnab-9, a premalignant marker often found in Paneth-like cells (PCs), was performed on sections of polyps from eight patients with Peutz-Jeghers syndrome, eight patients with familial juvenile polyposis, and 36 hyperplastic polyp control sections.

Hamartomatous polyposis patients also underwent specific genetic analysis.

Eighty-nine percent of Peutz-Jeghers syndrome polyps labeled with Adnab-9 compared with 63% for AD5; 88% of familial juvenile polyposis sections also labeled with Adnab-9.

Of the 36 hyperplastic polyp sections, only four (11%) labeled with Adnab-9 and one (3%) with AD5.

Adnab-9 labeling of PCs in the epithelial elements of hamartomatous colonic lesions of hereditary hamartomatous syndrome patients reflects the predisposition to colorectal cancer, further justifying early intervention strategies.

[MeSH-major] Adenomatous Polyposis Coli / pathology. Antibodies, Monoclonal. Biomarkers, Tumor. Colon / pathology. Colonic Polyps / pathology. Peutz-Jeghers Syndrome / pathology

Genetic Alliance. consumer health - Familial Polyposis.

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

[Cites] Am J Gastroenterol. 2000 Mar;95(3):596-604 [10710046.001]

[Cites] Dig Dis Sci. 2003 Jan;48(1):223-9 [12645814.001]

[Cites] Am J Gastroenterol. 2003 Mar;98(3):671-8 [12650805.001]

[Cites] Scand J Gastroenterol. 1992 Sep;27(9):737-42 [1411278.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2003 Oct;12(10):1095-9 [14578149.001]

[Cites] J Histochem Cytochem. 1981 Apr;29(4):577-80 [6166661.001]

[Cites] Dig Dis Sci. 2002 Feb;47(2):317-21 [11855547.001]

[Cites] Scand J Gastroenterol. 1993 Dec;28(12):1025-34 [8303203.001]

[Cites] Ann Surg Oncol. 1998 Dec;5(8):751-6 [9869523.001]

[Cites] N Engl J Med. 1987 Jun 11;316(24):1511-4 [3587280.001]

[Cites] Front Biosci. 1999 Mar 15;4:D329-38 [10077546.001]

[Cites] Dig Dis Sci. 2002 Jun;47(6):1349-55 [12064812.001]

[Cites] Dig Dis Sci. 2005 Apr;50(4):708-13 [15844706.001]

[Cites] Am J Gastroenterol. 1999 Jan;94(1):257-61 [9934767.001]

[Cites] Clin Genet. 2002 Oct;62(4):282-7 [12372054.001]

[Cites] Gastroenterology. 1997 Apr;112(4):1398-403 [9098028.001]

[Cites] Clin Genet. 1999 Aug;56(2):136-41 [10517250.001]

[Cites] Int J Pancreatol. 2001;29(3):141-50 [12067217.001]

[Cites] Gut. 2001 Feb;48(2):176-85 [11156637.001]

[Cites] Hum Pathol. 1999 Apr;30(4):467-73 [10208470.001]

[Cites] Science. 1996 Jan 19;271(5247):350-3 [8553070.001]

[Cites] Clin Gastroenterol Hepatol. 2004 Mar;2(3):246-51 [15017609.001]

[Cites] Gastroenterology. 2004 Oct;127(4):1030-7 [15480979.001]

(PMID = 17934846.001).

[ISSN] 0163-2116

[Journal-full-title] Digestive diseases and sciences

[ISO-abbreviation] Dig. Dis. Sci.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Adnab-9; 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / alpha-Defensins; 0 / alpha-defensin 5, human; EC 2.7.1.- / STK11 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases

   

[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)

   

[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.

Hereditary CRC is conventionally divided into two major categories: hereditary non-polyposis colorectal cancer (HNPCC) and those related to polyposis syndromes including familial adenomatous polyposis (FAP), Peutz-Jegher syndrome (PJS), and juvenile polyposis (JP).

Germ-line mutation of the APC gene induces FAP, an autosomal dominant disorder, characterized by the development of hundreds to thousands of colonic adenomas.

Recently, a mutation on the MYH gene is increasingly being investigated in patients with multiple polyps, and autosomal recessive MYH polyposis is considered to be a new category of polyposis.

Although there is no polyposis, polyps seem to be more villous and dysplastic and appear to grow rapidly into CRCs.

PJS and JP are reported to be characterized by hamartomatous polyps throughout the GI tract and germ-line mutations in the STK11 gene (PJS) and the DPC4/BMPR1A gene (JP).

[MeSH-major] Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Intestinal Polyposis / genetics. Peutz-Jeghers Syndrome / genetics

Genetic Alliance. consumer health - Colorectal Cancer.

Genetic Alliance. consumer health - Hereditary Cancer.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15725711.001).

[ISSN] 1598-9992

[Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi

[ISO-abbreviation] Korean J Gastroenterol

[Language] kor

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Korea (South)

[Number-of-references] 40

   

[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

   

[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, hyperplastic and hyperplasia-like colorectal polyps].

The colorectal hyperplastic polyp has generally been considered a finding of no clinical significance.

Recent research has, however, called attention to the existence of some variants of hyperplastic polyp which are potentially malignant.

The term "advanced serrated polyp" has been coined for such cases, which comprise mixed hyperplastic/adenomatous tissue, serrated adenoma, and sessile serrated polyp, in contrast to the traditional hyperplastic polyp.

Since epithelial dysplasia is an integrated component of mixed hyperplastic/adenomatous polyp and of the serrated adenoma, such a diagnosis would dictate control colonoscopy comparable to the guidelines for subjects with conventional adenomas.

The cytology of the sessile serrated polyp is, however, closer to that of the traditional hyperplastic polyp, whereas the architecture mimics that of the serrated adenoma.

For this reason, a consensus regarding the optimal management of such patients has not been obtained, but if the polyp is sizeable and located in the right colon, control should be considered.

The small, usually left-sided traditional polyp as a rule needs no follow-up, but the context in which such a lesion is found and its morphology may influence the clinical decision.

Future large-scale investigations of serrated colorectal polyps, including interobserver studies, will be required to identify histological details of clinical utility which can be adopted in daily routine practice.

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

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 = 17125655.001).

[ISSN] 1603-6824

[Journal-full-title] Ugeskrift for laeger

[ISO-abbreviation] Ugeskr. Laeg.

[Language] dan

[Publication-type] Comparative Study; English Abstract; Journal Article; Review

[Publication-country] Denmark

[Number-of-references] 40

   

[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 loss of sarco/endoplasmic reticulum calcium transport ATPase 3 expression is an early event during the multistep process of colon carcinogenesis.

To better characterize the role of SERCA3 in colon carcinogenesis, its expression has been investigated in colonic epithelium, benign lesions, adenomas, and adenocarcinomas.

In addition, the regulation of SERCA3 expression was analyzed in the context of the adenomatous polyposis coli/beta-catenin/T-cell factor 4 (TCF4) pathway and of specificity protein 1 (Sp1)-like factor-dependent transcription.

We report that SERCA3 expression increased along the crypts as cells differentiated in normal colonic mucosa and in hyperplastic polyps, was moderately and heterogeneously expressed in colonic adenomas with expression levels inversely correlated with the degree of dysplasia, was barely detectable in well and moderately differentiated adenocarcinomas, and was absent in poorly differentiated tumors.

Inhibition of Sp1-like factor-dependent transcription blocked SERCA3 expression during cell differentiation, and SERCA3 expression was induced by the expression of dominant-negative TCF4 in colon cancer cells.

These data link SERCA3 expression to the state of differentiation of colonic epithelial cells, and relate SERCA3 expression, already decreased in adenomas, to enhanced adenomatous polyposis coli/beta-catenin/TCF4-dependent signaling and deficient Sp1-like factor-dependent transcription.

In conclusion, intracellular calcium homeostasis becomes progressively anomalous during colon carcinogenesis as reflected by deficient SERCA3 expression.

[MeSH-major] Biomarkers, Tumor / analysis. Calcium / metabolism. Calcium-Transporting ATPases / biosynthesis. Colonic Neoplasms / enzymology. Intestinal Mucosa / metabolism

[MeSH-minor] Adenomatous Polyposis Coli Protein / genetics. Blotting, Western. Cell Line, Tumor. Cell Transformation, Neoplastic. Colonic Polyps / enzymology. Cytoskeletal Proteins / genetics. DNA-Binding Proteins. Endoplasmic Reticulum / metabolism. Humans. Immunohistochemistry. Sarcoplasmic Reticulum Calcium-Transporting ATPases. TCF Transcription Factors. Trans-Activators / genetics. Transcription Factor 7-Like 2 Protein. Transcription Factors. Transfection. Transgenes. beta Catenin

Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .

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] Blood. 1999 Jun 15;93(12):4395-405 [10361138.001]

[Cites] J Immunol. 1999 Jul 1;163(1):82-92 [10384103.001]

[Cites] Annu Rev Nutr. 1999;19:545-86 [10448536.001]

[Cites] Cancer Res. 1999 Sep 1;59(17):4266-70 [10485470.001]

[Cites] Cancer Res. 1994 Nov 1;54(21):5523-6 [7923189.001]

[Cites] Gene. 1999 Nov 29;240(2):261-7 [10580145.001]

[Cites] J Biol Chem. 1992 Jul 15;267(20):14483-9 [1385815.001]

[Cites] Am J Physiol. 1992 Sep;263(3 Pt 1):G371-9 [1415549.001]

[Cites] Cell Calcium. 1993 Jul;14(7):531-8 [8402836.001]

[Cites] J Clin Invest. 1993 Dec;92(6):2916-21 [7504695.001]

[Cites] Am J Med Sci. 1994 Mar;307(3):167-72 [8160706.001]

[Cites] J Mol Recognit. 1994 Sep;7(3):189-97 [7880543.001]

[Cites] Gastroenterology. 1995 Nov;109(5):1468-74 [7557127.001]

[Cites] Southeast Asian J Trop Med Public Health. 1995;26 Suppl 1:190-6 [8629105.001]

[Cites] Biosci Rep. 1995 Oct;15(5):299-306 [8825032.001]

[Cites] J Biol Chem. 1996 Nov 8;271(45):28220-8 [8910439.001]

[Cites] Biochem Biophys Res Commun. 1997 Mar 6;232(1):80-3 [9125156.001]

[Cites] J Biol Chem. 1997 Apr 18;272(16):10746-50 [9099725.001]

[Cites] J Biol Chem. 1997 Aug 29;272(35):22199-206 [9268365.001]

[Cites] Virchows Arch. 1997 Aug;431(2):111-7 [9293892.001]

[Cites] Cytokines Mol Ther. 1996 Jun;2(2):111-4 [9384695.001]

[Cites] Biochem Biophys Res Commun. 1997 Dec 8;241(1):142-50 [9405248.001]

[Cites] J Biol Chem. 2000 Jan 14;275(2):1371-6 [10625687.001]

[Cites] Ann N Y Acad Sci. 1999;886:195-9 [10667218.001]

[Cites] Science. 2000 Apr 14;288(5464):331-3 [10764645.001]

[Cites] Nucleic Acids Res. 2000 Aug 1;28(15):2969-76 [10908361.001]

[Cites] FEBS Lett. 2000 Jul 7;476(3):203-7 [10913614.001]

[Cites] Biol Pharm Bull. 2000 Aug;23(8):926-9 [10963297.001]

[Cites] Leuk Res. 2000 Oct;24(10):795-804 [10996197.001]

[Cites] Am J Physiol Gastrointest Liver Physiol. 2000 Oct;279(4):G806-14 [11005769.001]

[Cites] Lancet. 2000 Oct 14;356(9238):1300-6 [11073017.001]

[Cites] Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12625-30 [11035797.001]

[Cites] Hepatogastroenterology. 2000 Sep-Oct;47(35):1291-7 [11100335.001]

[Cites] Cancer Res. 2001 Jan 15;61(2):570-6 [11212251.001]

[Cites] Mol Cell Biol. 2001 Apr;21(7):2413-22 [11259590.001]

[Cites] Biol Chem. 2001 Feb;382(2):329-42 [11308031.001]

[Cites] J Cell Physiol. 2001 Aug;188(2):143-60 [11424081.001]

[Cites] J Biol Chem. 2001 Jul 13;276(28):25742-52 [11337508.001]

[Cites] Am J Surg Pathol. 2002 Feb;26(2):249-56 [11812948.001]

[Cites] FEBS Lett. 2002 Mar 13;514(2-3):122-8 [11943137.001]

[Cites] J Biol Chem. 2002 May 10;277(19):16673-81 [11872750.001]

[Cites] J Biol Chem. 2002 Jul 19;277(29):26310-20 [11986315.001]

[Cites] Biochem Pharmacol. 2002 Jul 15;64(2):307-15 [12123752.001]

[Cites] J Biol Chem. 2002 Sep 27;277(39):36471-8 [12119294.001]

[Cites] FEBS Lett. 2002 Oct 23;530(1-3):147-52 [12387883.001]

[Cites] Diabetes. 2002 Nov;51(11):3245-53 [12401716.001]

[Cites] Cell. 2002 Oct 18;111(2):241-50 [12408868.001]

[Cites] J Biol Chem. 2002 Nov 22;277(47):45579-91 [12207029.001]

[Cites] Cancer Res. 2003 Jan 1;63(1):67-71 [12517779.001]

[Cites] Cell Calcium. 2002 Nov-Dec;32(5-6):269-78 [12543089.001]

[Cites] Cell Calcium. 2002 Nov-Dec;32(5-6):279-305 [12543090.001]

[Cites] Cell Calcium. 2002 Nov-Dec;32(5-6):405-11 [12543099.001]

[Cites] J Mol Biol. 2003 Feb 21;326(3):665-77 [12581631.001]

[Cites] Eur J Surg Oncol. 2003 Mar;29(2):107-17 [12633551.001]

[Cites] Blood. 2003 Apr 15;101(8):3220-8 [12515718.001]

[Cites] J Cell Sci. 2003 May 15;116(Pt 10):1861-2 [12692187.001]

[Cites] Biochem Biophys Res Commun. 2003 May 9;304(3):445-54 [12729578.001]

[Cites] J Biol Chem. 2003 May 16;278(20):17785-91 [12624107.001]

[Cites] J Mol Endocrinol. 2003 Jun;30(3):399-409 [12790808.001]

[Cites] Oncogene. 2003 Sep 4;22(38):6023-31 [12955081.001]

[Cites] J Biol Chem. 2003 Sep 12;278(37):35775-80 [12837748.001]

[Cites] J Biol Chem. 2003 Nov 28;278(48):47877-89 [12975374.001]

[Cites] Oncogene. 2003 Nov 24;22(53):8608-18 [14634622.001]

[Cites] Nat Cell Biol. 2003 Dec;5(12):1041-3 [14647298.001]

[Cites] Biochem Biophys Res Commun. 2004 Apr 23;317(1):235-43 [15047174.001]

[Cites] Curr Mol Med. 2004 May;4(3):313-22 [15101688.001]

[Cites] Annu Rev Biochem. 2004;73:437-65 [15189149.001]

[Cites] Biochem Biophys Res Commun. 2004 Oct 1;322(4):1223-36 [15336970.001]

[Cites] Arch Pathol. 1970 Apr;89(4):349-54 [5435674.001]

[Cites] Gastroenterology. 1974 Mar;66(3):347-56 [4813500.001]

[Cites] Am J Surg Pathol. 1984 Sep;8(9):687-98 [6476197.001]

[Cites] Am J Med Sci. 1987 Nov;294(5):388-94 [2962490.001]

[Cites] Nihon Ketsueki Gakkai Zasshi. 1988 Jul;51(4):746-51 [3144112.001]

[Cites] Nucleic Acids Res. 1989 Jul 25;17(14):5447-59 [2548163.001]

[Cites] Blood. 1990 Dec 15;76(12):2483-92 [1702327.001]

[Cites] J Biol Chem. 1998 May 29;273(22):13982-94 [9593748.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):9855-60 [9707565.001]

[Cites] Biochim Biophys Acta. 1999 Jan 18;1444(1):85-91 [9931450.001]

[Cites] Nutr Rev. 1999 Apr;57(4):124-6 [10228349.001]

[Cites] Biochem Cell Biol. 1998;76(5):779-85 [10353711.001]

(PMID = 15972967.001).

[ISSN] 0002-9440

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

[ISO-abbreviation] Am. J. Pathol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Trans-Activators; 0 / Transcription Factor 7-Like 2 Protein; 0 / Transcription Factors; 0 / beta Catenin; EC 3.6.3.8 / ATP2A3 protein, human; EC 3.6.3.8 / Calcium-Transporting ATPases; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; SY7Q814VUP / Calcium

[Other-IDs] NLM/ PMC1603437