[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 719
1. Avissar NE, Toia L, Hu Y, Watson TJ, Jones C, Raymond DP, Matousek A, Peters JH: Bile acid alone, or in combination with acid, induces CDX2 expression through activation of the epidermal growth factor receptor (EGFR). J Gastrointest Surg; 2009 Feb;13(2):212-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Evidence suggests that Barrett's esophagus intestinal metaplasia may occur via induction of caudal homeobox gene 2 (CDX2).
  • [MeSH-major] Adenocarcinoma / metabolism. Deoxycholic Acid / pharmacology. Epithelial Cells / drug effects. Esophageal Neoplasms / metabolism. Homeodomain Proteins / metabolism. Receptor, Epidermal Growth Factor / drug effects

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DEOXYCHOLIC ACID .
  • 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] Biophys J. 2003 Oct;85(4):2732-45 [14507736.001]
  • [Cites] Oncogene. 2006 Dec 7;25(58):7565-76 [16785991.001]
  • [Cites] J Natl Cancer Inst. 2005 Jan 19;97(2):142-6 [15657344.001]
  • [Cites] Nature. 1970 Aug 15;227(5259):680-5 [5432063.001]
  • [Cites] J Biol Chem. 2001 May 11;276(19):16045-50 [11278982.001]
  • [Cites] Dis Esophagus. 2006;19(4):260-6 [16866857.001]
  • [Cites] Gastroenterology. 2005 Dec;129(6):2009-31 [16344068.001]
  • [Cites] Cell. 2006 Nov 3;127(3):635-48 [17081983.001]
  • [Cites] J Surg Res. 2005 May 15;125(2):189-212 [15854673.001]
  • [Cites] Gastroenterology. 2005 Apr;128(4):1042-55 [15825085.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 May 24;102(21):7565-70 [15894614.001]
  • [Cites] Scand J Gastroenterol. 2007 Dec;42(12 ):1460-5 [17852856.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Jul;7(7):505-16 [16829981.001]
  • [Cites] Carcinogenesis. 2007 Feb;28(2):488-96 [16990345.001]
  • [Cites] Gastroenterology. 2002 Apr;122(4):985-93 [11910351.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6500-5 [12438243.001]
  • [Cites] Am J Gastroenterol. 1999 Aug;94(8):2033-6 [10445524.001]
  • [Cites] Gut. 1992 Apr;33(4):439-43 [1582583.001]
  • [Cites] EMBO J. 2002 Feb 1;21(3):303-13 [11823423.001]
  • [Cites] Mod Pathol. 2004 Oct;17 (10 ):1282-8 [15167938.001]
  • [Cites] J Gastrointest Surg. 2007 Jul;11(7):827-34 [17458588.001]
  • [Cites] Surgery. 2005 Nov;138(5):924-31 [16291394.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2002 Nov;283(5):G1098-106 [12381523.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Mar 2;354(1):154-9 [17214962.001]
  • [Cites] Gastroenterology. 2004 Nov;127(5):1540-57 [15521021.001]
  • [Cites] Gastroenterology. 2006 Apr;130(4):1191-206 [16618413.001]
  • [Cites] J Cell Sci. 2003 Apr 15;116(Pt 8):1429-36 [12640028.001]
  • [Cites] EMBO J. 2002 Sep 16;21(18):4796-808 [12234920.001]
  • [Cites] Br J Cancer. 1999 Jun;80(7):1012-9 [10362109.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5380-94 [12101233.001]
  • [Cites] Prog Neurobiol. 1997 Jan;51(1):19-37 [9044427.001]
  • [Cites] Biochem Pharmacol. 2005 Oct 1;70(7):1035-47 [16139803.001]
  • [Cites] Gut. 2006 Jan;55(1):16-25 [16118348.001]
  • [Cites] J Cell Sci. 2001 Sep;114(Pt 17):3075-81 [11590234.001]
  • [Cites] Mol Biol Cell. 2001 Sep;12(9):2629-45 [11553704.001]
  • [Cites] J Biol Chem. 2000 Mar 31;275(13):9222-9 [10734059.001]
  • [Cites] Cancer Treat Rev. 2004 Feb;30(1):1-17 [14766123.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] J Biol Chem. 2002 Aug 23;277(34):31214-9 [12063263.001]
  • [Cites] Biochem Pharmacol. 2007 Apr 1;73(7):1001-12 [17222808.001]
  • [Cites] J Cell Sci. 2006 Feb 1;119(Pt 3):571-81 [16443754.001]
  • [Cites] J Biol Chem. 2006 May 26;281(21):14948-60 [16547009.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2003 Jul;285(1):G31-6 [12606307.001]
  • [Cites] J Cell Sci. 2001 Jun;114(Pt 11):2167-78 [11493652.001]
  • [Cites] Semin Oncol. 2007 Apr;34(2 Suppl 1):S2-6 [17449347.001]
  • [Cites] Hepatology. 2002 Feb;35(2):307-14 [11826403.001]
  • [Cites] Curr Opin Gastroenterol. 2004 Mar;20(2):70-6 [15703624.001]
  • [Cites] Surgery. 2005 Sep;138(3):415-21 [16213893.001]
  • (PMID = 18854960.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX2 Transcription Factor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Ligands; 0 / RNA, Messenger; 005990WHZZ / Deoxycholic Acid; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


2. Dvorak K, Watts GS, Ramsey L, Holubec H, Payne CM, Bernstein C, Jenkins GJ, Sampliner RE, Prasad A, Garewal HS, Bernstein H: Expression of bile acid transporting proteins in Barrett's esophagus and esophageal adenocarcinoma. Am J Gastroenterol; 2009 Feb;104(2):302-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of bile acid transporting proteins in Barrett's esophagus and esophageal adenocarcinoma.
  • Our major goal was to evaluate the expression of bile acid transporters in normal squamous epithelium, BE with different grades of dysplasia, and esophageal adenocarcinoma (EAC).

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19174784.001).
  • [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 / P30 CA023074; United States / NIEHS NIH HHS / ES / P30 ES006694; United States / NCI NIH HHS / CA / P50 CA095060
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Membrane Glycoproteins; 0 / Multidrug Resistance-Associated Proteins; 0 / Organic Anion Transporters, Sodium-Dependent; 0 / RNA, Messenger; 0 / Symporters; 0 / bile acid binding proteins; 0 / multidrug resistance-associated protein 3; 145420-23-1 / sodium-bile acid cotransporter
  • [Other-IDs] NLM/ NIHMS693533; NLM/ PMC4450811
  •  go-up   go-down


3. Xiao GQ, Burstein DE, Miller LK, Unger PD: Nephrogenic adenoma: immunohistochemical evaluation for its etiology and differentiation from prostatic adenocarcinoma. Arch Pathol Lab Med; 2006 Jun;130(6):805-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nephrogenic adenoma: immunohistochemical evaluation for its etiology and differentiation from prostatic adenocarcinoma.
  • Owing to its strong association with a history of urinary tract irritation, nephrogenic adenoma was initially thought to originate from urothelial metaplasia; however, no solid proof of this association has been found.
  • Prostatic adenocarcinoma tissue was positive for P504S and prostate-specific antigen, and normal prostatic gland tissue was positive for prostate-specific antigen and negative for P504S; p63-stained basal cells in normal prostatic gland tissue but did not react with prostatic adenocarcinoma tissue.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenoma / diagnosis. Immunohistochemistry / methods. Prostatic Neoplasms / diagnosis. Urologic Neoplasms / diagnosis
  • [MeSH-minor] Biomarkers, Tumor / analysis. Diagnosis, Differential. Humans. Male. Mucin-1 / analysis. Racemases and Epimerases / analysis. Urothelium / chemistry. Urothelium / pathology

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16740031.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mucin-1; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
  •  go-up   go-down


Advertisement
4. Alvarez H, Rojas PL, Yong KT, Ding H, Xu G, Prasad PN, Wang J, Canto M, Eshleman JR, Montgomery EA, Maitra A: Mesothelin is a specific biomarker of invasive cancer in the Barrett-associated adenocarcinoma progression model: translational implications for diagnosis and therapy. Nanomedicine; 2008 Dec;4(4):295-301
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mesothelin is a specific biomarker of invasive cancer in the Barrett-associated adenocarcinoma progression model: translational implications for diagnosis and therapy.
  • Esophageal adenocarcinoma arises in the backdrop of Barrett metaplasia-dysplasia sequence, with the vast majority of patients presenting with late-stage malignancy.
  • Mesothelin expression was assessed in esophageal tissue microarrays encompassing the entire histological spectrum of Barrett-associated dysplasia and adenocarcinoma.
  • Mesothelin was expressed in the esophageal adenocarcinoma cell line JH-EsoAd1 but not in primary human esophageal epithelial cells.
  • Anti-mesothelin antibody-conjugated nanoparticles can be useful for the diagnosis and therapy of mesothelin-overexpressing esophageal adenocarcinomas.

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Exp Med. 2004 Aug 2;200(3):297-306 [15289501.001]
  • [Cites] J Phys Chem B. 2007 Jun 28;111(25):6969-72 [17552555.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jan 9;93(1):136-40 [8552591.001]
  • [Cites] Gastroenterol Clin North Am. 1997 Sep;26(3):495-506 [9309400.001]
  • [Cites] Am J Surg Pathol. 2005 Mar;29(3):381-9 [15725808.001]
  • [Cites] Am J Surg Pathol. 2005 Mar;29(3):390-9 [15725809.001]
  • [Cites] Mod Pathol. 2005 Jun;18(6):752-61 [15696124.001]
  • [Cites] Am J Surg Pathol. 2005 Nov;29(11):1497-504 [16224217.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11631-8 [16357174.001]
  • [Cites] Am J Clin Pathol. 2005 Dec;124(6):838-45 [16416732.001]
  • [Cites] Mod Pathol. 2006 Mar;19(3):417-28 [16415794.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2006 Mar;14(1):24-30 [16540726.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 May;15(5):1014-20 [16702385.001]
  • [Cites] Cancer Detect Prev. 2006;30(2):180-7 [16647225.001]
  • [Cites] Am J Clin Pathol. 2006 Oct;126(4):572-9 [17019794.001]
  • [Cites] Semin Diagn Pathol. 2006 Feb;23(1):20-4 [17044192.001]
  • [Cites] Gene Ther. 2007 Aug;14(16):1189-98 [17581599.001]
  • [Cites] Gynecol Oncol. 2007 Sep;106(3):490-7 [17532030.001]
  • [Cites] Chest. 2007 Oct;132(4):1239-46 [17646232.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3214-24 [18451147.001]
  • [Cites] J Immunother. 2000 Jul-Aug;23(4):473-9 [10916757.001]
  • [Cites] Am J Gastroenterol. 2000 Aug;95(8):1888-93 [10950031.001]
  • [Cites] Cancer Res. 2000 Nov 15;60(22):6281-7 [11103784.001]
  • [Cites] Hum Pathol. 2001 Apr;32(4):379-88 [11331954.001]
  • [Cites] Clin Cancer Res. 2001 Dec;7(12):3862-8 [11751476.001]
  • [Cites] N Engl J Med. 2002 Mar 14;346(11):836-42 [11893796.001]
  • [Cites] Surg Oncol Clin N Am. 2002 Apr;11(2):235-56 [12424848.001]
  • [Cites] Mol Cancer Ther. 2002 Jun;1(8):595-600 [12479219.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2003 Sep;11(3):238-43 [12966350.001]
  • [Cites] Mod Pathol. 2003 Sep;16(9):902-12 [13679454.001]
  • [Cites] Am J Surg Pathol. 2003 Nov;27(11):1418-28 [14576474.001]
  • [Cites] Mol Biol Cell. 2003 Nov;14(11):4376-86 [12960427.001]
  • [Cites] N Engl J Med. 2003 Dec 4;349(23):2241-52 [14657432.001]
  • [Cites] Cancer Res. 2003 Dec 15;63(24):8614-22 [14695172.001]
  • [Cites] Methods Enzymol. 2003;373:507-28 [14714424.001]
  • [Cites] Hum Pathol. 2004 Mar;35(3):357-66 [15017593.001]
  • [Cites] Clin Cancer Res. 2004 Jun 15;10(12 Pt 1):3937-42 [15217923.001]
  • [Cites] Gastroenterology. 2004 Jul;127(1):310-30 [15236196.001]
  • [Cites] Cancer Cell. 2004 Jul;6(1):11-6 [15261138.001]
  • [Cites] Nat Biotechnol. 2004 Aug;22(8):969-76 [15258594.001]
  • [Cites] Vaccine. 2007 Jan 2;25(1):127-35 [16930783.001]
  • [Cites] Anticancer Res. 2006 Nov-Dec;26(6C):4721-8 [17214332.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] Int J Cancer. 2007 Apr 1;120(7):1511-7 [17192896.001]
  • [Cites] Nano Lett. 2007 Mar;7(3):761-5 [17288490.001]
  • [Cites] Int J Cancer. 1994 Apr 1;57(1):90-7 [8150545.001]
  • (PMID = 18691948.001).
  • [ISSN] 1549-9642
  • [Journal-full-title] Nanomedicine : nanotechnology, biology, and medicine
  • [ISO-abbreviation] Nanomedicine
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA119397-04; United States / NCI NIH HHS / CA / R01 CA119397; United States / NCI NIH HHS / CA / R01 CA119397-04; United States / NCI NIH HHS / CA / R01CA119397
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / mesothelin
  • [Other-IDs] NLM/ NIHMS79893; NLM/ PMC2606904
  •  go-up   go-down


5. Arici DS, Tuncer E, Ozer H, Simek G, Koyuncu A: Expression of retinoblastoma and cyclin D1 in gastric carcinoma. Neoplasma; 2009;56(1):63-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We investigated Rb and cyclin D1 expression in 43 patients (32 men, 11 women; mean age: 64) with primary gastric adenocarcinoma and compared the results with adjacent nonneoplastic mucosa.
  • Adjacent nonneoplastic mucosa consisted of atrophy, dysplasia, intestinal metaplasia and gastritis.
  • There were significant trends for increased expression of Rb and cyclinD1 from nonneoplastic mucosa including atrophy, dyplasia, intestinal metaplasia and gastritis to carcinoma.
  • Key words: Retinoblastoma, cyclin D1, gastric carcinoma, dysplasia, atrophy, intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / metabolism. Cyclin D1 / biosynthesis. Precancerous Conditions / metabolism. Retinoblastoma Protein / biosynthesis. Stomach Neoplasms / metabolism


6. Holmes K, Egan B, Swan N, O'Morain C: Genetic Mechanisms and Aberrant Gene Expression during the Development of Gastric Intestinal Metaplasia and Adenocarcinoma. Curr Genomics; 2007 Sep;8(6):379-97
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic Mechanisms and Aberrant Gene Expression during the Development of Gastric Intestinal Metaplasia and Adenocarcinoma.
  • Gastric adenocarcinoma occurs via a sequence of molecular events known as the Correa's Cascade which often progresses over many years.
  • Despite recent antibiotic intervention of H. pylori infections, gastric adenocarcinoma remains the second most common cause of cancer deaths worldwide.
  • Intestinal metaplasia is the next step along the carcinogenic sequence after gastritis and is considered to be a precursor lesion for gastric cancer; however, not all patients with intestinal metaplasia develop adenocarcinoma and little is known about the molecular and genetic events that trigger the progression of intestinal metaplasia into adenocarcinoma.
  • This review aims to highlight the progress to date in the genetic events involved in intestinal-type gastric adenocarcinoma and its precursor lesion, intestinal metaplasia.
  • The use of technologies such as whole genome microarray analysis, immunohistochemical analysis and DNA methylation analysis has allowed an insight into some of the events which occur in intestinal metaplasia and may be involved in carcinogenesis.

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2397-405 [15059891.001]
  • [Cites] Oncogene. 2004 Jun 3;23(26):4646-54 [15064707.001]
  • [Cites] Cancer Biol Ther. 2004 Jul;3(7):593-601 [15136761.001]
  • [Cites] Mod Pathol. 2004 Oct;17(10):1223-34 [15154009.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4336-40 [15156190.001]
  • [Cites] Gut. 2004 Aug;53(8):1082-9 [15247172.001]
  • [Cites] Oncogene. 2004 Sep 2;23(40):6830-44 [15273739.001]
  • [Cites] Gut. 2004 Oct;53(10):1416-23 [15361487.001]
  • [Cites] Gan. 1979 Apr;70(2):181-5 [467883.001]
  • [Cites] J Cancer Res Clin Oncol. 1979 Jun 8;94(2):201-6 [468906.001]
  • [Cites] Gastroenterology. 1978 Nov;75(5):796-9 [700322.001]
  • [Cites] Cancer Res. 1992 Dec 15;52(24):6735-40 [1458460.001]
  • [Cites] Cancer Res. 1991 Jun 15;51(12):3075-9 [2039987.001]
  • [Cites] Cancer Res. 1988 Jul 1;48(13):3554-60 [3288329.001]
  • [Cites] Mol Cancer. 2006;5:10 [16545139.001]
  • [Cites] Mod Pathol. 2006 Jun;19(6):854-63 [16575401.001]
  • [Cites] Cancer Lett. 2007 Jan 8;245(1-2):22-32 [16713672.001]
  • [Cites] J Gastroenterol. 2006 May;41(5):401-7 [16799880.001]
  • [Cites] Carcinogenesis. 2007 Jan;28(1):118-23 [16885196.001]
  • [Cites] Anticancer Res. 2006 Jul-Aug;26(4B):2909-14 [16886612.001]
  • [Cites] J Mol Med (Berl). 2006 Oct;84(10):872-82 [16924468.001]
  • [Cites] Dev Biol. 2007 Feb 1;302(1):1-12 [16989803.001]
  • [Cites] Oncogene. 2006 Oct 9;25(46):6176-87 [17028597.001]
  • [Cites] World J Gastroenterol. 2006 Oct 14;12(38):6207-11 [17036397.001]
  • [Cites] Cancer Res. 2002 May 1;62(9):2625-9 [11980659.001]
  • [Cites] Nat Rev Cancer. 2002 Mar;2(3):161-74 [11990853.001]
  • [Cites] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769.001]
  • [Cites] Helicobacter. 2002 Jun;7(3):192-8 [12047325.001]
  • [Cites] Cancer Res. 2002 Jun 15;62(12):3503-6 [12067995.001]
  • [Cites] J Pathol. 2002 May;197(1):37-43 [12081201.001]
  • [Cites] Int J Cancer. 2002 Dec 20;102(6):623-8 [12448005.001]
  • [Cites] Cancer Res. 2002 Dec 1;62(23):7012-7 [12460921.001]
  • [Cites] J Pathol. 2003 Jan;199(1):36-40 [12474224.001]
  • [Cites] Int J Surg Pathol. 2006 Jan;14(1):21-33 [16501831.001]
  • [Cites] Lab Invest. 2006 Jun;86(6):591-8 [16534497.001]
  • [Cites] World J Gastroenterol. 2006 Oct 21;12(39):6280-4 [17072949.001]
  • [Cites] World J Gastroenterol. 2006 Nov 21;12(43):6949-54 [17109515.001]
  • [Cites] Gut. 2006 Dec;55(12):1810-20 [17124160.001]
  • [Cites] Int J Cancer. 2007 Mar 1;120(5):953-60 [17163415.001]
  • [Cites] Br J Cancer. 2007 Jan 15;96(1):95-103 [17179985.001]
  • [Cites] Mol Carcinog. 2007 Feb;46(2):155-64 [17186543.001]
  • [Cites] Dig Dis Sci. 2007 Feb;52(2):536-42 [17226075.001]
  • [Cites] Helicobacter. 2007 Feb;12(1):1-15 [17241295.001]
  • [Cites] Histochem J. 1981 Nov;13(6):931-9 [7338482.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1995 Apr-May;4(3):223-31 [7606196.001]
  • [Cites] Cancer. 1995 Mar 15;75(6 Suppl):1460-6 [7889475.001]
  • [Cites] Cancer. 1994 Jul 15;74(2):556-64 [8033033.001]
  • [Cites] Am J Surg Pathol. 1996 Oct;20(10):1161-81 [8827022.001]
  • [Cites] Cancer Detect Prev. 1999;23(3):204-14 [10336999.001]
  • [Cites] Nature. 2000 Mar 23;404(6776):398-402 [10746728.001]
  • [Cites] Int J Cancer. 2000 Sep 1;87(5):654-8 [10925358.001]
  • [Cites] Curr Mol Med. 2007 Feb;7(1):15-28 [17311530.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2007;21(2):281-97 [17382277.001]
  • [Cites] Neoplasma. 2007;54(3):235-9 [17447856.001]
  • [Cites] World J Gastroenterol. 2007 Apr 21;13(15):2214-7 [17465504.001]
  • [Cites] Kurume Med J. 2000;47(3):199-203 [11059220.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2816-21 [11306450.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2847-51 [11306456.001]
  • [Cites] Oncogene. 2001 Jan 18;20(3):329-35 [11313962.001]
  • [Cites] Int J Cancer. 2001 Jun 15;92(6):832-8 [11351303.001]
  • [Cites] Pathol Int. 2001 Jun;51(6):445-51 [11422806.001]
  • [Cites] Cell. 2001 Aug 10;106(3):275-86 [11509177.001]
  • [Cites] Cancer Res. 2002 Jan 1;62(1):233-40 [11782383.001]
  • [Cites] World J Gastroenterol. 2001 Aug;7(4):522-6 [11819821.001]
  • [Cites] Gastroenterology. 2002 Mar;122(3):689-96 [11875002.001]
  • [Cites] Virchows Arch. 2002 Mar;440(3):311-7 [11889603.001]
  • [Cites] J Pathol. 2003 May;200(1):23-31 [12692837.001]
  • [Cites] Cancer Sci. 2003 Feb;94(2):135-41 [12708487.001]
  • [Cites] Gastroenterology. 2003 May;124(5):1193-201 [12730860.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2569-77 [12750281.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Apr;286(4):G515-20 [15010360.001]
  • [Cites] IARC Sci Publ. 2004;(157):327-49 [15055305.001]
  • [Cites] Pathol Int. 2002 Dec;52(12):764-8 [12588445.001]
  • [Cites] Am J Pathol. 2005 Aug;167(2):577-84 [16049341.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7127-36 [16103062.001]
  • [Cites] Gene. 2005 Oct 24;360(1):1-19 [16154715.001]
  • [Cites] J Exp Clin Cancer Res. 2005 Sep;24(3):405-14 [16270527.001]
  • [Cites] Cancer Sci. 2005 Nov;96(11):729-37 [16271066.001]
  • [Cites] J Pathol. 2005 Dec;207(4):396-401 [16278805.001]
  • [Cites] Cancer. 2006 Feb 1;106(3):483-93 [16362978.001]
  • [Cites] Cancer. 2006 Mar 15;106(6):1250-9 [16475210.001]
  • [Cites] World J Gastroenterol. 2006 Jan 14;12(2):192-8 [16482617.001]
  • [Cites] Cancer Sci. 2007 Mar;98(3):284-93 [17270017.001]
  • [Cites] Exp Oncol. 2006 Dec;28(4):263-9 [17285108.001]
  • [Cites] Gastric Cancer. 2007;10(1):45-51 [17334718.001]
  • [Cites] Gastroenterology. 2007 Mar;132(3):1066-76 [17383428.001]
  • [Cites] Oncogene. 2007 Apr 2;26(15):2202-11 [17401429.001]
  • [Cites] World J Gastroenterol. 2007 Mar 28;13(12):1794-7; discussion 1797-8 [17465468.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2006 Feb;290(2):G310-8 [16239403.001]
  • [Cites] World J Gastroenterol. 2005 Oct 14;11(38):5993-6 [16273612.001]
  • [Cites] Mod Pathol. 2006 Jan;19(1):141-8 [16357845.001]
  • [Cites] Clin Cancer Res. 2006 Feb 1;12(3 Pt 1):989-95 [16467114.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):281-7 [16492916.001]
  • [Cites] J Gastroenterol Hepatol. 2006 Feb;21(2):438-42 [16509871.001]
  • [Cites] Nat Rev Cancer. 2006 Apr;6(4):259-69 [16557279.001]
  • [Cites] BMC Cancer. 2006;6:91 [16608517.001]
  • [Cites] World J Gastroenterol. 2006 May 21;12(19):2979-90 [16718776.001]
  • [Cites] Gastroenterology. 2006 Jul;131(1):246-58 [16831607.001]
  • [Cites] Gastroenterology. 2006 Sep;131(3):925-33 [16952561.001]
  • [Cites] Oncogene. 2006 Oct 9;25(46):6188-96 [17028598.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Dec 1;350(4):825-33 [17049492.001]
  • [Cites] Clin Cancer Res. 2006 Nov 1;12(21):6386-94 [17085650.001]
  • [Cites] Cancer. 2007 Jan 15;109(2):188-97 [17149756.001]
  • [Cites] Histopathology. 2006 Dec;49(6):612-21 [17163846.001]
  • [Cites] Neoplasia. 2006 Dec;8(12):995-1002 [17217616.001]
  • [Cites] Int J Cancer. 2007 May 1;120(9):1914-21 [17236199.001]
  • [Cites] Dig Liver Dis. 2007 Mar;39(3):222-7 [17267315.001]
  • [Cites] Cancer Res. 2003 Jun 15;63(12):3309-16 [12810664.001]
  • [Cites] Br J Cancer. 1955 Sep;9(3):377-85 [13269635.001]
  • [Cites] Am J Pathol. 2003 Oct;163(4):1551-6 [14507661.001]
  • [Cites] Mol Pathol. 2003 Oct;56(5):293-8 [14514924.001]
  • [Cites] J Biol Chem. 2003 Dec 19;278(51):51549-56 [14525978.001]
  • [Cites] J Cancer Res Clin Oncol. 2004 Mar;130(3):135-45 [14655050.001]
  • [Cites] Br J Cancer. 2004 Jan 12;90(1):216-23 [14710232.001]
  • [Cites] Cancer Res. 2004 Jan 15;64(2):523-9 [14744765.001]
  • [Cites] Lab Invest. 2004 Apr;84(4):479-84 [14968123.001]
  • [Cites] Cancer Res. 2004 Feb 15;64(4):1255-65 [14973074.001]
  • [Cites] World J Gastroenterol. 2004 Oct 15;10(20):2936-9 [15378768.001]
  • [Cites] World J Gastroenterol. 2004 Nov 1;10(21):3194-6 [15457573.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):7740-7 [15520178.001]
  • [Cites] World J Gastroenterol. 2005 Jan 7;11(1):61-8 [15609398.001]
  • [Cites] Gastric Cancer. 2004;7(4):246-53 [15616773.001]
  • [Cites] Clin Cancer Res. 2005 Jan 15;11(2 Pt 1):473-82 [15701830.001]
  • [Cites] Int J Cancer. 2005 Jul 20;115(6):849-60 [15729716.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Feb;14(2):451-8 [15734972.001]
  • [Cites] Clin Lab Med. 2005 Mar;25(1):197-222 [15749238.001]
  • [Cites] Gastroenterology. 2005 Mar;128(3):642-53 [15765400.001]
  • [Cites] Cancer Res. 2005 Mar 15;65(6):2115-24 [15781621.001]
  • [Cites] World J Gastroenterol. 2005 Apr 28;11(16):2390-7 [15832406.001]
  • [Cites] Histopathology. 2005 May;46(5):505-14 [15842632.001]
  • [Cites] Infect Immun. 2005 May;73(5):2736-43 [15845476.001]
  • [Cites] J Clin Pathol. 2005 May;58(5):515-9 [15858124.001]
  • [Cites] J Surg Oncol. 2005 Jun 1;90(3):114-33; discussion 133 [15895459.001]
  • [Cites] Histopathology. 2005 Jun;46(6):649-58 [15910596.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):828-33 [15944707.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):839-43 [15944709.001]
  • (PMID = 19412438.001).
  • [ISSN] 1389-2029
  • [Journal-full-title] Current genomics
  • [ISO-abbreviation] Curr. Genomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC2671722
  • [Keywords] NOTNLM ; Intestinal metaplasia / aberrant gene expression / gastric cancer / genetic markers.
  •  go-up   go-down


7. Greengauz-Roberts O, Stöppler H, Nomura S, Yamaguchi H, Goldenring JR, Podolsky RH, Lee JR, Dynan WS: Saturation labeling with cysteine-reactive cyanine fluorescent dyes provides increased sensitivity for protein expression profiling of laser-microdissected clinical specimens. Proteomics; 2005 May;5(7):1746-57
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In an experiment comparing LCM clinical samples of gastric adenocarcinoma versus precancerous, spasmolytic polypeptide expressing metaplasia (SPEM) from the same patient, cysteine labeling allowed the identification of more than 1000 discrete protein spots in samples containing 5000 cells.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYSTEINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15761955.001).
  • [ISSN] 1615-9853
  • [Journal-full-title] Proteomics
  • [ISO-abbreviation] Proteomics
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA095941-01; United States / NCI NIH HHS / CA / R21 CA095941; United States / NCI NIH HHS / CA / 1 R21 CA 95941; United States / NCI NIH HHS / CA / R21 CA095941-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Carbocyanines; 0 / Fluorescent Dyes; K848JZ4886 / Cysteine
  •  go-up   go-down


8. Montgomery E, Mamelak AJ, Gibson M, Maitra A, Sheikh S, Amr SS, Yang S, Brock M, Forastiere A, Zhang S, Murphy KM, Berg KD: Overexpression of claudin proteins in esophageal adenocarcinoma and its precursor lesions. Appl Immunohistochem Mol Morphol; 2006 Mar;14(1):24-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of claudin proteins in esophageal adenocarcinoma and its precursor lesions.
  • The authors identified upregulation of Claudins 3, 4, and 7 in gastric adenocarcinoma using Affymetrix U-133 oligonucleotide microarrays and immunohistochemistry (IHC).
  • While normal gastric mucosa lacked Claudin 3, 4, and 7 expression, intestinal metaplasia and dysplasia showed these proteins.
  • The authors hypothesized that Claudins would be similarly overexpressed in Barrett's esophagus (BE)/adenocarcinoma.
  • IHC validation was performed using tissue microarrays constructed from esophageal resection specimens containing squamous (44 cases), gastric (40 cases), and non-dysplastic BE (16 cases), low-grade and high-grade dysplasia (16 and 26 cases), adenocarcinoma (58 cases), and nodal metastases (27 cases).
  • By IHC, Claudin 3 expression was 1+ in most (>95%) normal squamous or gastric tissues and 2+ to 4+ in more than 80% of high-grade dysplasia, adenocarcinoma, and metastases specimens.
  • Claudin 4 protein expression was 2+ or less in most squamous and gastric mucosa (>90%) but 3+ or 4+ in BE, low- and high-grade dysplasia, adenocarcinoma, and metastases specimens (>90%).
  • In high-grade dysplasia, adenocarcinoma, and metastases, Claudin 7 was less intense, with 60% to 70% staining 3+ or 4+ and 30% to 40% staining weakly (1+ or 2+).
  • The findings suggest that alterations in Claudin proteins are an early event in tumorigenesis and may provide targets for diagnosis and directed therapy for esophageal adenocarcinoma and its precursors.

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16540726.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CLDN3 protein, human; 0 / CLDN4 protein, human; 0 / CLDN7 protein, human; 0 / Claudin-3; 0 / Claudin-4; 0 / Claudins; 0 / Membrane Proteins; 0 / RNA, Messenger
  •  go-up   go-down


9. Tantipalakorn C, Khunamornpong S, Lertprasertsuke N, Tongsong T: Female genital tract tumors and gastrointestinal lesions in the Peutz-Jeghers syndrome. J Med Assoc Thai; 2009 Dec;92(12):1686-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • An ovarian microscopic cystadenoma was diagnosed together with a minimal deviation mucinous adenocarcinoma (MDA) of the uterine cervix and mucinous metaplasia in tubal mucosa and endometrium.
  • Pathological findings warranted a search for evidence of PJS Typical pigmentation at the hard palate and colonoscopic finding of hamartomatous polyps established the diagnosis of PJS.
  • The presented case suggests MDA and mucinous metaplasia warrant a search for PJS.
  • [MeSH-major] Gastrointestinal Neoplasms / diagnosis. Gastrointestinal Tract / pathology. Genital Neoplasms, Female / pathology. Genitalia, Female / pathology. Peutz-Jeghers Syndrome / diagnosis
  • [MeSH-minor] Adenocarcinoma, Mucinous / pathology. Adenocarcinoma, Mucinous / surgery. Cystadenoma / pathology. Cystadenoma / surgery. Female. Humans. Hysterectomy. Middle Aged. Ovarian Neoplasms / pathology. Ovarian Neoplasms / surgery. Ovariectomy. Risk Factors. Salpingectomy

  • Genetic Alliance. consumer health - Peutz Jeghers syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20043574.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Thailand
  •  go-up   go-down


10. Boult JK, Tanière P, Hallissey MT, Campbell MJ, Tselepis C: Oesophageal adenocarcinoma is associated with a deregulation in the MYC/MAX/MAD network. Br J Cancer; 2008 Jun 17;98(12):1985-92
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oesophageal adenocarcinoma is associated with a deregulation in the MYC/MAX/MAD network.
  • Oesophageal adenocarcinoma, which arises from an acquired columnar lesion, Barrett's metaplasia, is rising in incidence more rapidly than any other cancer in the Western world.
  • Elevated expression of c-MYC has been demonstrated in oesophageal adenocarcinoma; however, the expression of other members of the MYC/MAX/MAD network has not been addressed.
  • The aims of this work were to characterise the expression of c-MYC, MAX and the MAD family in adenocarcinoma development and assess the effects of overexpression on cellular behaviour. mRNA expression in samples of Barrett's metaplasia and oesophageal adenocarcinoma were examined by qRT-PCR.
  • Consistent with previous work expression of c-MYC was deregulated in oesophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / genetics. Esophageal Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Genes, myc. Repressor Proteins / genetics

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gut. 2005 Mar;54 Suppl 1:i1-5 [15711002.001]
  • [Cites] Oncogene. 1995 Jun 1;10(11):2195-205 [7784064.001]
  • [Cites] Int J Oncol. 2005 May;26(5):1369-75 [15809730.001]
  • [Cites] J Cell Biol. 2005 May 9;169(3):405-13 [15866886.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Apr 15;166(2):157-62 [16631473.001]
  • [Cites] Gut. 2006 Oct;55(10):1449-60 [16641131.001]
  • [Cites] Biomarkers. 2006 Nov-Dec;11(6):547-61 [17056474.001]
  • [Cites] Dis Esophagus. 2007;20(3):212-6 [17509117.001]
  • [Cites] Neoplasia. 2004 Sep-Oct;6(5):660-73 [15548375.001]
  • [Cites] Oncogene. 1999 Nov 18;18(48):6621-34 [10597267.001]
  • [Cites] Am J Pathol. 2000 Feb;156(2):555-66 [10666385.001]
  • [Cites] Curr Opin Genet Dev. 2000 Feb;10(1):100-5 [10679391.001]
  • [Cites] Cancer. 2000 Apr 1;88(7):1623-32 [10738221.001]
  • [Cites] Am J Respir Cell Mol Biol. 2000 Oct;23(4):560-5 [11017923.001]
  • [Cites] Annu Rev Cell Dev Biol. 2000;16:653-99 [11031250.001]
  • [Cites] Nucleic Acids Res. 2001 Jan 15;29(2):397-406 [11139609.001]
  • [Cites] Lancet. 2000 Dec 16;356(9247):2079-85 [11145505.001]
  • [Cites] Nucleic Acids Res. 1995 May 25;23(10):1686-90 [7784172.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Aug 29;92(18):8488-92 [7667316.001]
  • [Cites] Cancer Res. 1995 Nov 1;55(21):4800-3 [7585509.001]
  • [Cites] Nat Med. 1995 Jul;1(7):638-43 [7585143.001]
  • [Cites] EMBO J. 1995 Nov 15;14(22):5646-59 [8521822.001]
  • [Cites] Oncogene. 1995 Dec 21;11(12):2487-501 [8545105.001]
  • [Cites] Cancer Lett. 1996 Apr 19;102(1-2):73-6 [8603382.001]
  • [Cites] Br J Cancer. 1996 Jun;73(11):1347-55 [8645578.001]
  • [Cites] Curr Top Microbiol Immunol. 1997;224:149-58 [9308238.001]
  • [Cites] Cancer Res. 1997 Nov 1;57(21):4905-12 [9354456.001]
  • [Cites] Cancer Res. 1997 Dec 15;57(24):5571-8 [9407969.001]
  • [Cites] Oncogene. 1998 Feb 26;16(8):967-77 [9519870.001]
  • [Cites] Oncol Rep. 1998 Jan-Feb;5(1):213-6 [9458379.001]
  • [Cites] Mol Cell Biol. 1999 Jan;19(1):1-11 [9858526.001]
  • [Cites] EMBO J. 1999 Feb 1;18(3):717-26 [9927431.001]
  • [Cites] Mol Cell. 1999 May;3(5):565-77 [10360173.001]
  • [Cites] Oncogene. 1999 May 13;18(19):3004-16 [10378696.001]
  • [Cites] J Biol Chem. 1999 Oct 1;274(40):28794-802 [10497252.001]
  • [Cites] Nat Cell Biol. 2001 Jun;3(6):580-6 [11389443.001]
  • [Cites] Cancer. 2001 Aug 1;92(3):549-55 [11505399.001]
  • [Cites] Nat Rev Cancer. 2002 Oct;2(10):764-76 [12360279.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2002 Nov;14(11):1179-86 [12439111.001]
  • [Cites] Gut. 2003 Feb;52(2):174-80 [12524396.001]
  • [Cites] Anticancer Res. 2003 Jan-Feb;23(1A):161-5 [12680208.001]
  • [Cites] Gut. 2003 May;52(5):623-8 [12692043.001]
  • [Cites] Ann Oncol. 2003;14 Suppl 5:v61-118 [14684501.001]
  • [Cites] Gut. 2004 Aug;53(8):1070-4 [15247170.001]
  • [Cites] Clin Exp Rheumatol. 1990 Mar-Apr;8(2):145-50 [1692520.001]
  • [Cites] Science. 1991 Mar 8;251(4998):1211-7 [2006410.001]
  • [Cites] Oncogene. 1992 Apr;7(4):775-9 [1565473.001]
  • [Cites] J Pathol. 1992 Mar;166(3):225-33 [1381423.001]
  • [Cites] Cell. 1993 Jan 29;72(2):211-22 [8425218.001]
  • [Cites] Cell. 1993 Jan 29;72(2):223-32 [8425219.001]
  • [Cites] Oncogene. 1994 Apr;9(4):1247-52 [8134128.001]
  • [Cites] J Cell Biol. 1995 Mar;128(6):1197-208 [7896882.001]
  • [Cites] Scand J Gastroenterol. 2004 Dec;39(12):1175-9 [15742992.001]
  • (PMID = 18493233.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / MAX protein, human; 0 / MXD1 protein, human; 0 / Repressor Proteins
  • [Other-IDs] NLM/ PMC2441969
  •  go-up   go-down


11. Yap YL, So JB: Gastric adenocarcinoma occurring in a young patient with common variable immunodeficiency syndrome. Singapore Med J; 2009 Jun;50(6):e201-3
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gastric adenocarcinoma occurring in a young patient with common variable immunodeficiency syndrome.
  • Patients with common variable immunodeficiency syndrome (CVID) have an increased risk of gastric adenocarcinoma.
  • We describe a case of gastric adenocarcinoma in a 29-year-old man with CVID.
  • CVID is a predisposing factor for gastric adenocarcinoma.
  • Premalignant conditions like chronic atrophic gastritis, intestinal metaplasia and dysplasia require regular endoscopic surveillance in these high-risk patients.
  • [MeSH-major] Adenocarcinoma / complications. Adenocarcinoma / diagnosis. Common Variable Immunodeficiency / complications. Common Variable Immunodeficiency / diagnosis. Stomach Neoplasms / complications. Stomach Neoplasms / diagnosis
  • [MeSH-minor] Adult. Disease-Free Survival. Endoscopy. Humans. Male. Pyloric Stenosis / diagnosis. Tomography, X-Ray Computed / methods. Treatment Outcome


12. Villanacci V, Rossi E, Zambelli C, Galletti A, Cestari R, Missale G, Casa DD, Bassotti G: COX-2, CDX2, and CDC2 immunohistochemical assessment for dysplasia-carcinoma progression in Barrett's esophagus. Dig Liver Dis; 2007 Apr;39(4):305-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIMS: To assess the role of cyclooxygenase 2, caudal-type homeobox transcription factor 2 and cell division cycle 2/cyclin-dependent kinase 1 in the Barrett's metaplasia-dysplasia-adenocarcinoma sequence.
  • PATIENTS AND METHODS: Specimens from 46 patients with Barrett's esophagus (39% without dysplasia, 33% with dysplasia and 28% with adenocarcinoma) were stained for cyclooxygenase 2, caudal-type homeobox transcription factor 2 and cell division cycle 2.
  • Caudal-type homeobox transcription factor 2: Nuclear positivity decreased from Barrett's esophagus without dysplasia (71.6%), to Barrett's esophagus with low grade dysplasia (35.3%), to Barrett's esophagus with high grade dysplasia (17.14%); in adenocarcinoma these percentages were intermediate between high and low grade dysplasia (30.5%).
  • Cell division cycle 2: Expression on deeper glandular structures was 40% in Barrett's esophagus without dysplasia, 55.47% in Barrett's esophagus with dysplasia, and 63.84% in adenocarcinoma, with no statistical differences between groups.
  • A diffuse positivity was found in Barrett's esophagus with adenocarcinoma (p=0.0001 vs. no dysplasia and low grade dysplasia).
  • CONCLUSIONS: Further evaluation of cyclooxygenase 2, cell division cycle 2 and caudal-type homeobox transcription factor 2, in association with morphology, might help to improve the accuracy of diagnosis and be useful for the clinical-pathological assessment of patients with Barrett's esophagus.
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Biomarkers / metabolism. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Female. Humans. Immunohistochemistry. Male. Middle Aged. Precancerous Conditions / metabolism. Precancerous Conditions / pathology

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • 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 = 17307036.001).
  • [ISSN] 1590-8658
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.22 / CDC2 Protein Kinase
  •  go-up   go-down


13. Räsänen JV, Sihvo EI, Ahotupa MO, Färkkilä MA, Salo JA: The expression of 8-hydroxydeoxyguanosine in oesophageal tissues and tumours. Eur J Surg Oncol; 2007 Dec;33(10):1164-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the present study we investigated whether DNA damage linked to oxidative stress (as 8-OHdG) is present in Barrett's mucosa with or without associated adenocarcinoma or high-grade dysplasia and in normal controls' squamous mucosa.
  • EXPERIMENTAL DESIGN: We measured 8-OHdG in 51 patients (13 Barrett's metaplasia, six Barrett's oesophagus with high-grade dysplasia, 18 adenocarcinoma of the distal oesophagus/oesophagogastric junction and 14 normal controls).
  • RESULTS: Analysis revealed that 8-OHdG was present in both Barrett's metaplasia with and without dysplasia as well as in adenocarcinoma of the oesophagus/oesophagogastric junction.
  • Although the study group was small the amount of 8-OHdG was significantly increased in the distal oesophagus both in Barrett's epithelium 1.26 (0.08-29.47) and in high-grade dysplasia 1.35 (1.04-1.65) as well as in adenocarcinoma of oesophagus/oesophagogastric junction 1.08 (0.59-1.94) compared to controls 0.06 (0-4.08) (p=0.002, p=0.012, p=0.001, respectively).
  • CONCLUSIONS: Our results show the presence of oxidative DNA damage in the distal oesophagus of patients with Barrett's oesophagus and adenocarcinoma of the oesophagus/oesophagogastric junction.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. DNA Damage / physiology. Deoxyguanosine / analogs & derivatives. Esophageal Neoplasms / metabolism. Esophagus / metabolism

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17467227.001).
  • [ISSN] 1532-2157
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; G9481N71RO / Deoxyguanosine
  •  go-up   go-down


14. Schmidt MK, Meurer L, Volkweis BS, Edelweiss MI, Schirmer CC, Kruel CD, Gurski RR: c-Myc overexpression is strongly associated with metaplasia-dysplasia-adenocarcinoma sequence in the esophagus. Dis Esophagus; 2007;20(3):212-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] c-Myc overexpression is strongly associated with metaplasia-dysplasia-adenocarcinoma sequence in the esophagus.
  • We aim to determine the expression of the proto-oncogene c-Myc in patients with Barrett's esophagus (BE) and esophageal adenocarcinoma, and to evaluate the prevalence of such expression in relation to the metaplasia-dysplasia-adenocarcinoma sequence.
  • BE is a premalignant lesion and plays an important role in the development of esophageal adenocarcinoma.
  • The c-Myc protein expression was determined by immunohistochemical analysis in four different groups: 31 patients with normal tissue, 43 patients with BE without dysplasia, 11 patients with dysplasia in BE and 37 patients with esophageal adenocarcinoma.
  • Demographic and endoscopic data (sex, age, race and intestinal metaplasia extension), and morphologic and histopathologic tumor characteristics (deep tumor invasion, lymph node status, and tumor differentiation) were analyzed.
  • Overexpression of c-Myc was found in only 9.6% of normal tissue specimens, 37.2% of Barrett's esophagus, 45.5% of BE patients with dysplasia and 73% of adenocarcinoma samples, with significant statistical difference among these groups.
  • No correlation was identified when the c-Myc expression was compared with morphologic and histologic tumor features or endoscopic data.
  • However, linear correlation of c-Myc overexpression along the metaplasia-dysplasia-adenocarcinoma sequence was observed.
  • This study demonstrates a significant increase in the expression of c-Myc in Barrett's esophagus, dysplasia and adenocarcinoma in relation to the control group, as well as a linear progression of this gene expression in this sequence.
  • These results point out the importance of this marker in the development of esophageal adenocarcinoma from BE.

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17509117.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc
  •  go-up   go-down


15. Peters CJ, Fitzgerald RC: Systematic review: the application of molecular pathogenesis to prevention and treatment of oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2007 Jun 01;25(11):1253-69
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systematic review: the application of molecular pathogenesis to prevention and treatment of oesophageal adenocarcinoma.
  • BACKGROUND: Oesophageal adenocarcinoma is an increasingly common cancer with a poor prognosis.
  • It develops in a stepwise progression from Barrett's metaplasia to dysplasia, and then adenocarcinoma followed by metastasis.
  • AIM: To outline the key molecular changes in oesophageal adenocarcinoma and to summarize the chemopreventative and therapeutic strategies proposed.
  • Search terms included: Barrett's (o)esophagus, intestinal metaplasia, (o)esophageal adenocarcinoma, molecular changes, genetic changes, pathogenesis, chemoprevention, therapeutic strategies and treatment.
  • RESULTS: A large number of molecular changes have been identified in the progression from Barrett's oesophagus to oesophageal adenocarcinoma although there does not appear to be an obligate order of events.
  • In established adenocarcinoma, targeted treatments under evaluation include receptor tyrosine kinase inhibitors of EGFR and cyclin-dependent kinase inhibitors, which may benefit a subgroup of patients.
  • CONCLUSIONS: Advances in molecular methodology have led to a greater understanding of the oesophageal adenocarcinoma pathways, which provides opportunities for chemoprevention and therapeutic strategies with a mechanistic basis.
  • [MeSH-major] Adenocarcinoma / prevention & control. Angiogenesis Inhibitors / therapeutic use. Anti-Inflammatory Agents / therapeutic use. Antioxidants / therapeutic use. Esophageal Neoplasms / prevention & control

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17509094.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Anti-Inflammatory Agents; 0 / Antioxidants
  • [Number-of-references] 149
  •  go-up   go-down


16. Targa AC, César AC, Cury PM, Silva AE: Apoptosis in different gastric lesions and gastric cancer: relationship with Helicobacter pylori, overexpression of p53 and aneuploidy. Genet Mol Res; 2007;6(3):554-65
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Its deregulation is associated with the occurrence of lesions such as in atrophic gastritis, peptic ulcers, intestinal metaplasia, and stomach tumorigenesis.
  • Thus, the aim of the present study was to investigate the frequency of apoptotic cells (apoptotic index, AI) by using two different immunohistochemical techniques, TUNEL and anti-activated caspase-3 antibody (CPP32), in gastric dyspepsia [chronic gastritis (CG, N = 34), chronic atrophic gastritis (CAG, N = 11), gastric ulcer (GU, N = 17), and intestinal metaplasia (IM, N = 15)], normal gastric mucosae (NM, N = 8), and gastric adenocarcinoma (GC, N = 12).

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • 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 = 17985308.001).
  • [ISSN] 1676-5680
  • [Journal-full-title] Genetics and molecular research : GMR
  • [ISO-abbreviation] Genet. Mol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] EC 3.4.22.- / Caspase 3
  •  go-up   go-down


17. Hu Y, Williams VA, Gellersen O, Jones C, Watson TJ, Peters JH: The pathogenesis of Barrett's esophagus: secondary bile acids upregulate intestinal differentiation factor CDX2 expression in esophageal cells. J Gastrointest Surg; 2007 Jul;11(7):827-34
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Caudal-related homeobox 2 (CDX2) is a transcription factor recently implicated in early differentiation and maintenance of normal intestinal epithelium and is suggested to play a key role in the pathogenesis of intestinal metaplasia in Barrett's esophagus.
  • (2) adenocarcinoma (SEG-1); and (3) squamous cell carcinoma (HKESC-1 & HKESC-2), were exposed in cell culture for 1-24 h to 100-1,000 microM deoxycholic, chenodeoxycholic, and glycocholic acids.
  • The maximal induction of CDX2 expression was seen in SEG-1 adenocarcinoma cells.
  • Expression in Het-1A cells also increased significantly as did expression in HKESC-1,2 cells, although to a lesser extent than in adenocarcinoma.
  • They further support the role of bile acids in the pathogenesis of Barrett's esophagus and link the clinical evidence of a high prevalence of luminal bile acids in Barrett's to expression of the gene thought to be responsible for the phenotypic expression of intestinal metaplasia.

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • 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
  • [CommentIn] Arch Surg. 2008 Aug;143(8):807 [18711046.001]
  • [ErratumIn] J Gastrointest Surg. 2008 Feb;12(2):400 [18071834.001]
  • [Cites] Cancer Genet Cytogenet. 2002 Jun;135(2):120-7 [12127396.001]
  • [Cites] JAMA. 1993 Sep 15;270(11):1320 [8360967.001]
  • [Cites] Am J Surg Pathol. 2003 Nov;27(11):1442-7 [14576477.001]
  • [Cites] Cancer Genet Cytogenet. 2000 Apr 15;118(2):112-20 [10748291.001]
  • [Cites] J Gastroenterol. 2003;38(1):14-22 [12560917.001]
  • [Cites] Gastroenterology. 2002 Mar;122(3):689-96 [11875002.001]
  • [Cites] Int J Oncol. 2002 Oct;21(4):769-74 [12239615.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Jun 7;294(2):470-9 [12051735.001]
  • [Cites] Surgery. 1997 Nov;122(5):874-81 [9369886.001]
  • [Cites] Mod Pathol. 2004 Oct;17 (10 ):1282-8 [15167938.001]
  • [Cites] Surgery. 2005 Nov;138(5):924-31 [16291394.001]
  • [Cites] J Clin Pathol. 2004 Oct;57(10 ):1063-8 [15452161.001]
  • [Cites] Br J Cancer. 1999 Feb;79(3-4):595-603 [10027336.001]
  • [Cites] Cancer Res. 1991 Jan 1;51(1):365-71 [1703038.001]
  • [Cites] Gut. 2006 Jan;55(1):16-25 [16118348.001]
  • [Cites] Mol Cell Biol. 1996 Feb;16(2):619-25 [8552090.001]
  • [Cites] Arch Surg. 2004 Jul;139(7):712-6; discussion 716-7 [15249402.001]
  • (PMID = 17458588.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Duplicate Publication; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / CDX2 Transcription Factor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / MUC2 protein, human; 0 / Mucin-2; 0 / Mucins; 0 / RNA, Messenger
  •  go-up   go-down


18. Sung MT, Lopez-Beltran A, Eble JN, MacLennan GT, Tan PH, Montironi R, Jones TD, Ulbright TM, Blair JE, Cheng L: Divergent pathway of intestinal metaplasia and cystitis glandularis of the urinary bladder. Mod Pathol; 2006 Nov;19(11):1395-401
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Divergent pathway of intestinal metaplasia and cystitis glandularis of the urinary bladder.
  • Intestinal metaplasia has been proposed to be a precursor lesion of adenocarcinoma in the urinary bladder.
  • Hepatocyte-specific antigen (Hep) has also been shown to be a useful marker of intestinal metaplasia.
  • Tissues from 46 patients, including 22 cases of intestinal metaplasia of the urinary bladder, 11 cases of typical cystitis glandularis, and 13 cases containing both lesions, were selected and immunohistochemical stains for CDX2, Hep, cytokeratin 20 (CK20), and cytokeratin 7 (CK7) were performed.
  • Nuclear staining for CDX2 was observed in 29 of 35 (83%) cases of intestinal metaplasia of the urinary bladder.
  • CK20 was expressed in 28 of 35 (80%) cases of intestinal metaplasia, but was observed in only one of 24 (4%) cases of cystitis glandularis in 15% of cells.
  • CK7 was expressed in only six of 35 (17%) cases of intestinal metaplasia, whereas expression of CK7 was observed in all cases (100%) of typical cystitis glandularis with a mean percentage of positively staining cells of 63%.
  • The mean percentages of positively staining cells in intestinal metaplasia with CDX2, CK20, and CK7 were 55, 49, and 53%, respectively.
  • All examples of both intestinal metaplasia and typical cystitis glandularis were uniformly negative for Hep.
  • In the urinary bladder, intestinal metaplasia and typical cystitis glandularis have sharply contrasting immunoprofiles.
  • Additionally, the absence of Hep staining in intestinal metaplasia of the urinary bladder, despite its morphologic resemblance to normal colonic mucosa and intestinal metaplasia in other organs, may signify the presence of unique metaplastic pathways in the urinary bladder.
  • [MeSH-minor] Autoantigens / analysis. Cell Transformation, Neoplastic / pathology. Hepatocytes / immunology. Homeodomain Proteins / analysis. Humans. Immunohistochemistry. Keratin-20 / analysis. Keratin-7 / analysis. Metaplasia. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16951671.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantigens; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / KRT20 protein, human; 0 / KRT7 protein, human; 0 / Keratin-20; 0 / Keratin-7
  •  go-up   go-down


19. Zaky AH, Watari J, Tanabe H, Sato R, Moriichi K, Tanaka A, Maemoto A, Fujiya M, Ashida T, Kohgo Y: Clinicopathologic implications of genetic instability in intestinal-type gastric cancer and intestinal metaplasia as a precancerous lesion: proof of field cancerization in the stomach. Am J Clin Pathol; 2008 Apr;129(4):613-21
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinicopathologic implications of genetic instability in intestinal-type gastric cancer and intestinal metaplasia as a precancerous lesion: proof of field cancerization in the stomach.
  • To clarify field cancerization in the stomach by genetic alterations, we studied 83 cases of intestinal-type gastric cancer (GC) and paired intestinal metaplasia (IM) distant from GC and 39 cases of chronic gastritis with IM (CG-IM) for genetic instability (GIN).
  • [MeSH-major] Adenocarcinoma / genetics. Loss of Heterozygosity. Microsatellite Repeats. Precancerous Conditions / genetics. Stomach Neoplasms / genetics
  • [MeSH-minor] Aged. DNA, Neoplasm / analysis. Female. Humans. Lymph Nodes / pathology. Male. Metaplasia / genetics. Metaplasia / pathology

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18343789.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  •  go-up   go-down


20. Smith AK, Hansel DE, Jones JS: Role of cystitis cystica et glandularis and intestinal metaplasia in development of bladder carcinoma. Urology; 2008 May;71(5):915-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of cystitis cystica et glandularis and intestinal metaplasia in development of bladder carcinoma.
  • OBJECTIVES: Cystitis cystica et glandularis (CCEG) and intestinal metaplasia (IM) have been suggested to represent precursors of bladder adenocarcinoma.
  • The records and imaging findings of patients with a pathologic diagnosis of florid CCEG and/or IM were reviewed for a concurrent or future diagnosis of bladder carcinoma or pelvic lipomatosis.
  • Of the 117 patients with CCEG, a subset was identified with concurrent mucinous adenocarcinoma (n = 1; <1%), squamous cell carcinoma (n = 4; 3%), or urothelial carcinoma (n = 34; 29%) at diagnosis.
  • Pure IM was identified concurrently with adenocarcinoma in 2 (10%), urothelial carcinoma in 4 (21%), and urothelial carcinoma with glandular differentiation in 1 (5%) of 19 patients.
  • Although IM can be associated with a concurrent diagnosis of carcinoma, we found no evidence that it increases the future risk of malignancy and our findings do not support a recommendation for surveillance cystoscopy in such patients.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Metaplasia / complications. Middle Aged. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18455631.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


21. Kojima K, Kishimoto T, Nagai Y, Tanizawa T, Nakatani Y, Miyazaki M, Ishikura H: The expression of hepatocyte nuclear factor-4alpha, a developmental regulator of visceral endoderm, correlates with the intestinal phenotype of gastric adenocarcinomas. Pathology; 2006 Dec;38(6):548-54
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We investigated the possible involvement of HNF-4alpha in intestinal metaplasia and the intestinalisation of gastric adenocarcinomas.
  • METHODS: Thirty-five cases of adenocarcinomas and 46 cases of adjacent non-neoplastic mucosa with (22 lesions) or without (24 lesions) intestinal metaplasia were immunostained for HNF-4alpha.
  • RESULTS: The HNF-4alpha expression was exclusively seen in glandular cells with intestinal metaplasia, which was correlated with MUC2 expression (p<0.05) and inversely correlated with MUC5AC expression (p<0.05).
  • [MeSH-major] Adenocarcinoma / pathology. Endoderm / physiology. Hepatocyte Nuclear Factor 4 / metabolism. Intestines / pathology. Stomach Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Stomach 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 = 17393984.001).
  • [ISSN] 0031-3025
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HNF4A protein, human; 0 / Hepatocyte Nuclear Factor 4
  •  go-up   go-down


22. Bobryshev YV, Tran D, Killingsworth MC, Buckland M, Lord RV: Dendritic cells in Barrett's esophagus and esophageal adenocarcinoma. J Gastrointest Surg; 2009 Jan;13(1):44-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dendritic cells in Barrett's esophagus and esophageal adenocarcinoma.
  • A comprehensive literature search failed to find any report of the presence of dendritic cells in Barrett's intestinal metaplasia and esophageal adenocarcinoma and this prompted our study.
  • MATERIAL AND METHODS: We used immunohistochemical staining and electron microscopy to examine whether dendritic cells are present in Barrett's esophagus and esophageal adenocarcinoma.
  • Immunohistochemical staining with CD83, a specific marker for dendritic cells, was performed on paraffin-embedded sections of Barrett's intestinal metaplasia (IM, n = 12), dysplasia (n = 11) and adenocarcinoma (n = 14).
  • CONCLUSIONS: These findings demonstrate that dendritic cells are present in Barrett's tissues, with a significant increase in density in adenocarcinoma compared to benign Barrett's esophagus.
  • Dendritic cells may have a role in the pathogenesis and immunotherapy treatment of Barrett's esophagus and adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Dendritic Cells / ultrastructure. Esophageal Neoplasms / pathology

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Intern Med. 1999 Jun 1;130(11):883-90 [10375336.001]
  • [Cites] Immunol Rev. 2004 Jun;199:9-26 [15233723.001]
  • [Cites] Cancer Immunol Immunother. 2004 Nov;53(11):978-86 [15197496.001]
  • [Cites] Int J Cancer. 1996 Sep 27;68(1):1-7 [8895531.001]
  • [Cites] Cancer Immunol Immunother. 2007 Dec;56(12):1967-77 [17564704.001]
  • [Cites] J Natl Cancer Inst. 2005 Jan 19;97(2):142-6 [15657344.001]
  • [Cites] Pathology. 1996 Nov;28(4):321-7 [9007950.001]
  • [Cites] Br J Cancer. 2001 Aug 17;85(4):473-83 [11506482.001]
  • [Cites] Gut. 2004 Aug;53(8):1070-4 [15247170.001]
  • [Cites] Immunol Cell Biol. 2002 Dec;80(6):520-30 [12406385.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):1047-60 [10071300.001]
  • [Cites] Am J Clin Pathol. 1994 Jun;101(6):761-7 [8209866.001]
  • [Cites] Cardiovasc Res. 1998 Mar;37(3):799-810 [9659465.001]
  • [Cites] Biochim Biophys Acta. 2007 Sep;1776(1):10-21 [17618050.001]
  • [Cites] Gut. 2008 Feb;57(2):173-80 [17932103.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1813-21 [11748282.001]
  • [Cites] Immunol Rev. 2007 Dec;220:151-68 [17979845.001]
  • [Cites] J Gastroenterol Hepatol. 1998 Apr;13(4):356-62 [9641297.001]
  • [Cites] Clin Cancer Res. 1998 Mar;4(3):585-93 [9533525.001]
  • [Cites] Cancer. 2001 Jun 1;91(11):2136-47 [11391595.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1993;422(5):351-5 [8322450.001]
  • [Cites] Clin Cancer Res. 2000 May;6(5):1755-66 [10815894.001]
  • [Cites] Arch Histol Cytol. 1995 Aug;58(3):307-22 [8527238.001]
  • [Cites] Int Immunopharmacol. 2003 Aug;3(8):1061-71 [12860163.001]
  • [Cites] Cancer. 1988 Aug 1;62(3):534-40 [2455589.001]
  • [Cites] Virchows Arch B Cell Pathol Incl Mol Pathol. 1992;61(6):409-14 [1349780.001]
  • [Cites] Pathol Res Pract. 1991 May;187(4):496-502 [1876530.001]
  • [Cites] Clin Cancer Res. 1997 Mar;3(3):483-90 [9815709.001]
  • [Cites] Tohoku J Exp Med. 1993 Mar;169(3):187-95 [8248911.001]
  • [Cites] Physiol Rev. 2002 Jan;82(1):97-130 [11773610.001]
  • [Cites] Annu Rev Immunol. 2003;21:685-711 [12615891.001]
  • [Cites] J Exp Med. 1973 May 1;137(5):1142-62 [4573839.001]
  • [Cites] J Leukoc Biol. 1993 Jan;53(1):19-28 [8426088.001]
  • [Cites] Int Arch Allergy Immunol. 2002 Oct;129(2):113-8 [12403928.001]
  • [Cites] Int J Oncol. 1994 Aug;5(2):231-6 [21559580.001]
  • [Cites] Adv Cancer Res. 2002;84:231-76 [11883529.001]
  • [Cites] Cancer. 1989 Feb 1;63(3):496-503 [2912528.001]
  • [Cites] Immunobiology. 2002 Jul;205(3):231-46 [12182451.001]
  • [Cites] Am J Gastroenterol. 2006 Jun;101(6):1178-82 [16771933.001]
  • [Cites] Eur J Immunol. 2007 Mar;37(3):634-48 [17266176.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] Nature. 1998 Mar 19;392(6673):245-52 [9521319.001]
  • [Cites] Nat Rev Immunol. 2004 Dec;4(12):941-52 [15573129.001]
  • [Cites] J Pathol. 2005 Nov;207(3):269-76 [16177953.001]
  • [Cites] Nature. 2007 Sep 27;449(7161):419-26 [17898760.001]
  • [Cites] Cell. 2002 Mar 22;108(6):755-67 [11955430.001]
  • [Cites] Dig Dis Sci. 2008 Jul;53(7):1739-46 [18080193.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Apr;286(4):G515-20 [15010360.001]
  • [Cites] Springer Semin Immunopathol. 2005 Jan;26(3):289-307 [15609003.001]
  • [Cites] Immunol Invest. 2000 May;29(2):177-85 [10854187.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] Cancer Lett. 2000 Oct 16;159(1):103-8 [10974412.001]
  • [Cites] Cell Oncol. 2007;29(6):507-17 [18032827.001]
  • [Cites] Cancer Invest. 2004;22(3):417-34 [15493363.001]
  • (PMID = 18685901.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD83 antigen; 0 / Immunoglobulins; 0 / Membrane Glycoproteins
  •  go-up   go-down


23. Strauss BL, Bratthauer GL, Tavassoli FA: STAT 5a expression in the breast is maintained in secretory carcinoma, in contrast to other histologic types. Hum Pathol; 2006 May;37(5):586-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • No expression was seen in apocrine metaplasia or in other specialized breast carcinomas, such as mucinous or clear cell carcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Breast / metabolism. Breast Neoplasms / metabolism. STAT5 Transcription Factor / metabolism

  • Genetic Alliance. consumer health - Secretory breast carcinoma.
  • MedlinePlus Health Information. consumer health - Breast 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 = 16647957.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / STAT5 Transcription Factor; 0 / STAT5A protein, human; 0 / Tumor Suppressor Proteins
  •  go-up   go-down


24. Edelstein ZR, Farrow DC, Bronner MP, Rosen SN, Vaughan TL: Central adiposity and risk of Barrett's esophagus. Gastroenterology; 2007 Aug;133(2):403-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Washington residents newly diagnosed with specialized intestinal metaplasia on at least 1 of 4 esophageal biopsy specimens taken at community gastroenterology clinics (cases [n = 193]) were compared with matched population controls (n = 211).
  • CONCLUSIONS: These observations indicate the importance of identifying the mechanisms underlying obesity's role in BE and esophageal adenocarcinoma, and suggest that weight loss might be a fruitful approach to the prevention of these diseases.
  • [MeSH-minor] Adult. Aged. Body Mass Index. Case-Control Studies. Female. Humans. Male. Metaplasia. Middle Aged. Odds Ratio. Risk Assessment. Risk Factors. Smoking / adverse effects. Waist-Hip Ratio. Washington / epidemiology

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • MedlinePlus Health Information. consumer health - Obesity.
  • 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
  • (PMID = 17681161.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA091955; United States / NCI NIH HHS / CA / R01 CA72866
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  •  go-up   go-down


25. Grimm M, Lazariotou M, Kircher S, Stuermer L, Reiber C, Höfelmayr A, Gattenlöhner S, Otto C, Germer CT, von Rahden BH: MMP-1 is a (pre-)invasive factor in Barrett-associated esophageal adenocarcinomas and is associated with positive lymph node status. J Transl Med; 2010;8:99
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MMP-1 was co-labelled with Ki-67 (proliferation), Cdx-2 (marker for intestinal metaplasia, BE) and analyzed on mRNA level.
  • [MeSH-major] Adenocarcinoma / enzymology. Barrett Esophagus / pathology. Esophageal Neoplasms / enzymology. Lymphatic Metastasis. Matrix Metalloproteinase 1 / metabolism

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] Cancer Biomark. 2008;4(1):1-10 [18334729.001]
  • [Cites] Gut. 2000 Jul;47(1):50-6 [10861264.001]
  • [Cites] Arch Surg. 2000 Jul;135(7):831-5; discussion 836 [10896378.001]
  • [Cites] Br J Cancer. 2001 Jan;84(2):276-82 [11161388.001]
  • [Cites] J Clin Oncol. 2001 Feb 15;19(4):1118-27 [11181677.001]
  • [Cites] Br J Cancer. 2001 Aug 3;85(3):383-92 [11487270.001]
  • [Cites] J Cell Sci. 2001 Nov;114(Pt 21):3865-72 [11719553.001]
  • [Cites] N Engl J Med. 2002 Mar 14;346(11):836-42 [11893796.001]
  • [Cites] Gastroenterology. 2002 Aug;123(2):636-9 [12145816.001]
  • [Cites] J Clin Pathol. 2002 Oct;55(10):758-62 [12354802.001]
  • [Cites] Lancet. 2002 Nov 16;360(9345):1587-9 [12443613.001]
  • [Cites] Gastric Cancer. 2003;6(1):30-8 [12673424.001]
  • [Cites] Am J Pathol. 2003 Sep;163(3):1081-90 [12937148.001]
  • [Cites] Am J Surg Pathol. 2003 Nov;27(11):1442-7 [14576477.001]
  • [Cites] Br J Cancer. 2003 Dec 1;89(11):2116-21 [14647147.001]
  • [Cites] Anticancer Res. 2004 Jul-Aug;24(4):2579-83 [15330218.001]
  • [Cites] J Clin Pathol. 2004 Oct;57(10):1063-8 [15452161.001]
  • [Cites] Science. 1976 Oct 1;194(4260):23-8 [959840.001]
  • [Cites] Nature. 1980 Mar 6;284(5751):67-8 [6243750.001]
  • [Cites] Hepatology. 1997 Mar;25(3):580-4 [9049202.001]
  • [Cites] Biochem Cell Biol. 1996;74(6):759-75 [9164646.001]
  • [Cites] J Pathol. 1998 Jul;185(3):256-61 [9771478.001]
  • [Cites] Br J Surg. 1998 Nov;85(11):1457-9 [9823902.001]
  • [Cites] Int J Mol Med. 1999 Jul;4(1):73-7 [10373641.001]
  • [Cites] J Natl Cancer Inst. 2005 Jan 19;97(2):142-6 [15657344.001]
  • [Cites] World J Gastroenterol. 2005 Oct 28;11(40):6360-5 [16419166.001]
  • [Cites] World J Gastroenterol. 2007 Feb 7;13(5):676-82 [17278189.001]
  • [Cites] Br J Cancer. 2007 Mar 26;96(6):903-11 [17342087.001]
  • [Cites] Scand J Gastroenterol. 2007 Dec;42(12):1473-8 [17852862.001]
  • [Cites] Arch Oral Biol. 2008 Sep;53(9):810-8 [18571622.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2008 Aug;295(2):G211-8 [18556417.001]
  • [Cites] Nat Rev Cancer. 2008 Oct;8(10):755-68 [18784658.001]
  • [Cites] Folia Histochem Cytobiol. 2008;46(4):471-8 [19141401.001]
  • [Cites] Cancer Lett. 2009 Mar 18;275(2):170-7 [18703277.001]
  • [Cites] Carcinogenesis. 2009 May;30(5):793-8 [19321798.001]
  • [Cites] Dig Liver Dis. 2009 Oct;41(10):740-8 [19372066.001]
  • [Cites] Dis Esophagus. 2009;22(8):664-7 [19191857.001]
  • [Cites] Mol Biol Rep. 2010 Jan;37(1):197-205 [19562509.001]
  • [Cites] BMC Cancer. 2010;10:82 [20205946.001]
  • [Cites] Ann Surg. 2007 Jul;246(1):22-3 [17592285.001]
  • [Cites] Cell Cycle. 2007 Oct 1;6(19):2332-8 [17786053.001]
  • [Cites] J Gastroenterol Hepatol. 2007 Dec;22(12):2303-9 [18031395.001]
  • [Cites] Oncologist. 2000;5(2):108-14 [10794801.001]
  • (PMID = 20946664.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.24.7 / Matrix Metalloproteinase 1
  • [Other-IDs] NLM/ PMC2967517
  •  go-up   go-down


26. Thompson OM, Beresford SA, Kirk EA, Bronner MP, Vaughan TL: Serum leptin and adiponectin levels and risk of Barrett's esophagus and intestinal metaplasia of the gastroesophageal junction. Obesity (Silver Spring); 2010 Nov;18(11):2204-11
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum leptin and adiponectin levels and risk of Barrett's esophagus and intestinal metaplasia of the gastroesophageal junction.
  • Persons diagnosed with Barrett's esophagus (BE) are at increased risk of developing esophageal adenocarcinoma (EA).
  • The primary purposes of this study were to determine whether circulating levels of leptin and adiponectin, both of which are deregulated in obese states, predict risk of specialized intestinal metaplasia (SIM) occurring in the esophagus (BE) and/or gastroesophageal junction, and evaluate the extent to which they mediate the relationship between obesity and these conditions.

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • 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
  • [Cites] Mol Cell Endocrinol. 2007 Aug 15;274(1-2):60-8 [17618045.001]
  • [Cites] Gastroenterology. 2007 Jul;133(1):34-41; quiz 311 [17631128.001]
  • [Cites] Mol Cell Endocrinol. 2008 Mar 26;285(1-2):43-50 [18313838.001]
  • [Cites] Gut. 2008 Apr;57(4):448-54 [18178609.001]
  • [Cites] J Am Diet Assoc. 2006 Jun;106(6):822-8; quiz 829-30 [16720123.001]
  • [Cites] J Clin Endocrinol Metab. 2000 May;85(5):1954-62 [10843181.001]
  • [Cites] J Clin Endocrinol Metab. 2001 May;86(5):1930-5 [11344187.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2002 Aug;11(8):745-52 [12163328.001]
  • [Cites] Surg Oncol Clin N Am. 2002 Apr;11(2):235-56 [12424848.001]
  • [Cites] J Natl Cancer Inst. 2003 Sep 17;95(18):1404-13 [13130116.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Oct;88(10):4823-31 [14557461.001]
  • [Cites] World J Surg. 2004 Feb;28(2):148-54 [14727064.001]
  • [Cites] Am J Epidemiol. 1984 Jul;120(1):164-6 [6741917.001]
  • [Cites] Nature. 1994 Dec 1;372(6505):425-32 [7984236.001]
  • [Cites] Am J Public Health. 1995 Apr;85(4):555-7 [7702122.001]
  • [Cites] N Engl J Med. 1996 Feb 1;334(5):292-5 [8532024.001]
  • [Cites] Biochem Biophys Res Commun. 1996 Apr 16;221(2):286-9 [8619847.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Feb;82(2):579-84 [9024258.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Apr;82(4):1293-300 [9100610.001]
  • [Cites] Semin Gastrointest Dis. 1997 Apr;8(2):59-67 [9109693.001]
  • [Cites] Am J Gastroenterol. 1998 Nov;93(11):2303-4 [9820428.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Apr 2;257(1):79-83 [10092513.001]
  • [Cites] J Natl Cancer Inst. 2005 Jan 19;97(2):142-6 [15657344.001]
  • [Cites] Am J Gastroenterol. 2005 Oct;100(10):2151-6 [16181362.001]
  • [Cites] Aliment Pharmacol Ther. 2005 Nov 15;22(10):1005-10 [16268976.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Nov;14(11 Pt 1):2481-6 [16284367.001]
  • [Cites] J Cell Physiol. 2006 Apr;207(1):12-22 [16110483.001]
  • [Cites] Ann Epidemiol. 2006 Apr;16(4):299-304 [16242962.001]
  • [Cites] Br J Cancer. 2006 May 8;94(9):1221-5 [16570048.001]
  • [Cites] J Clin Oncol. 2006 May 10;24(14):2137-50 [16682732.001]
  • [Cites] Endocrinology. 2006 Sep;147(9):4505-16 [16740977.001]
  • [Cites] Dis Esophagus. 2006;19(5):321-8 [16984526.001]
  • [Cites] World J Gastroenterol. 2007 Mar 14;13(10):1585-94 [17461453.001]
  • [Cites] BMC Cancer. 2007;7:97 [17559672.001]
  • [Cites] Gut. 2008 Jan;57(1):16-24 [17761783.001]
  • (PMID = 20111023.001).
  • [ISSN] 1930-739X
  • [Journal-full-title] Obesity (Silver Spring, Md.)
  • [ISO-abbreviation] Obesity (Silver Spring)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA072866-04; United States / NCI NIH HHS / CA / R25 CA092408; United States / NCI NIH HHS / CA / K05 CA124911; United States / NCI NIH HHS / CA / R25 CA092408-06; United States / NCI NIH HHS / CA / CA124911-05; United States / NCI NIH HHS / CA / CA072866-04; United States / NCI NIH HHS / CA / 2R25CA092408-06; United States / NCI NIH HHS / CA / R01 CA72866; United States / NCI NIH HHS / CA / CA092408-06; United States / NCI NIH HHS / CA / K05 CA124911-05; United States / NCI NIH HHS / CA / R01 CA072866
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Leptin
  • [Other-IDs] NLM/ NIHMS299614; NLM/ PMC3125020
  •  go-up   go-down


27. Fine SW, Chan TY, Epstein JI: Inverted papillomas of the prostatic urethra. Am J Surg Pathol; 2006 Aug;30(8):975-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The remaining cases showed foci of squamous metaplasia with moderate atypia (n = 4), rare true papillary fronds in a classic inverted papilloma background (n = 2), or both (n = 1).
  • Eleven cases with prostatic tissue revealed adenocarcinoma of the prostate [n = 6; Gleason score 6 (n = 3) or 7 (n = 3)], high-grade prostatic intraepithelial neoplasia (n = 1), benign prostatic hypertrophy (n = 3), or adenosis (n = 1).
  • No patients had a prior history of either inverted papilloma or urothelial carcinoma, whereas 2 patients were diagnosed with high-grade urothelial carcinoma of the bladder synchronous with their inverted papilloma diagnosis.
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Humans. Incidental Findings. Male. Middle Aged. Neoplasms, Multiple Primary / pathology. Prognosis. Prostatic Neoplasms / pathology. Urinary Bladder Neoplasms / pathology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16861968.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


28. Nomura S, Nakajima A, Ishimine S, Matsuhashi N, Kadowaki T, Kaminishi M: Differential expression of peroxisome proliferator-activated receptor in histologically different human gastric cancer tissues. J Exp Clin Cancer Res; 2006 Sep;25(3):443-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Immunohistochemical staining for PPARgamma was performed using biopsy specimens of human gastric cancer of various histological types, gastric adenomas, and intestinal metaplasia.
  • All samples of intestinal metaplasia and most samples of gastric tumors, except for signet ring cell carcinoma, expressed PPARgamma in the epithelial cells.
  • All samples of intestinal metaplasia expressed PPARgamma only in the cytosol.
  • For adenoma, 90% was positive for PPARgamma in cytosol, and 40% was positive in nuclei, for well-differentiated adenocarcinoma, 80% was positive in cytosol, and 20% was positive in nuclei.
  • For moderately differentiated adenocarcinomas, 70% was positive for cytosol, and 80% was positive for nuclei; for poorly differentiated adenocarcinoma, 30% was positive in cytosol, and 70% was positive in nuclei.
  • The frequency of samples with positive cytosolic staining decreased as the differentiation stage turned from intestinal metaplasia to adenoma, well-, moderately-, and poorly-differentiated cancers.
  • Simultaneously, there was a tendency toward an increased frequency of samples with positive nuclear PPARgamma staining as the differentiation stage transformed from intestinal metaplasia to poorly-differentiated cancer.
  • The findings also supported an intestinal metaplasia-adenoma-well-differentiated gastric cancer sequence, and signet ring cell cancer was suggested to be of a different lineage from other types of gastric cancers.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenoma / metabolism. Carcinoma, Signet Ring Cell / metabolism. Intestinal Neoplasms / metabolism. Metaplasia / metabolism. PPAR gamma / metabolism. Stomach Neoplasms / metabolism

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17167986.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / PPAR gamma
  •  go-up   go-down


29. Castilloux J, Bouron-Dal Soglio D, Faure C: Endoscopic assessment of children with esophageal atresia: Lack of relationship of esophagitis and esophageal metaplasia to symptomatology. Can J Gastroenterol; 2010 May;24(5):312-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endoscopic assessment of children with esophageal atresia: Lack of relationship of esophagitis and esophageal metaplasia to symptomatology.
  • Endoscopy was considered normal if no esophagitis, intestinal metaplasia or gastric metaplasia (GM) was discerned.
  • No intestinal metaplasia or adenocarcinoma was detected.
  • [MeSH-major] Deglutition Disorders / etiology. Endoscopy, Gastrointestinal / methods. Esophageal Atresia / diagnosis. Esophagitis / diagnosis. Esophagus / pathology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Cross-Sectional Studies. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Infant. Male. Metaplasia / complications. Metaplasia / diagnosis. Retrospective Studies

  • Genetic Alliance. consumer health - Esophageal Atresia.
  • MedlinePlus Health Information. consumer health - Swallowing Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Pediatr Gastroenterol Nutr. 2001;32 Suppl 2:S1-31 [11525610.001]
  • [Cites] J Paediatr Child Health. 1997 Oct;33(5):388-93 [9401880.001]
  • [Cites] Gastroenterology. 2002 May;122(6):1569-91 [12016424.001]
  • [Cites] J Pediatr Surg. 2003 May;38(5):702-4 [12720174.001]
  • [Cites] J Pediatr Gastroenterol Nutr. 2005 Feb;40(2):210-5 [15699699.001]
  • [Cites] J Pediatr Surg. 2005 Apr;40(4):719-20 [15852288.001]
  • [Cites] J Pediatr Surg. 2005 Aug;40(8):1227-31 [16080923.001]
  • [Cites] J Pediatr Surg. 2005 Dec;40(12):e1-4 [16338286.001]
  • [Cites] J Pediatr Surg. 2006 Feb;41(2):331-4 [16481246.001]
  • [Cites] Am J Gastroenterol. 2006 Aug;101(8):1900-20; quiz 1943 [16928254.001]
  • [Cites] Dis Esophagus. 2006;19(5):366-72 [16984534.001]
  • [Cites] Am J Gastroenterol. 1998 Jul;93(7):1028-32 [9672324.001]
  • [Cites] J Pediatr Surg. 1998 Sep;33(9):1341-6 [9766349.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] Am J Gastroenterol. 1999 Oct;94(10):2825-8 [10520828.001]
  • [Cites] Gastroenterology. 2006 Nov;131(5):1392-9 [17101315.001]
  • [Cites] J Pediatr Surg. 2007 Feb;42(2):370-4 [17270551.001]
  • [Cites] Clin Gastroenterol Hepatol. 2007 Jun;5(6):702-6 [17544997.001]
  • [Cites] Am J Gastroenterol. 2008 Mar;103(3):788-97 [18341497.001]
  • [Cites] Pediatr Surg Int. 2008 May;24(5):531-6 [18351365.001]
  • [Cites] J Pediatr Gastroenterol Nutr. 2008 Jul;47(1):102-6 [18607277.001]
  • [Cites] Pediatr Surg Int. 2003 Apr;19(1-2):40-3 [12721721.001]
  • [Cites] Ann Surg. 2003 Nov;238(5):686-9 [14578730.001]
  • [Cites] Gastrointest Endosc. 2003 Nov;58(5):661-70 [14595298.001]
  • [Cites] Pediatr Surg Int. 2004 Jun;20(6):402-7 [15148615.001]
  • [Cites] Chest. 2004 Sep;126(3):915-25 [15364774.001]
  • [Cites] J Pediatr Surg. 1989 Aug;24(8):741-4 [2769539.001]
  • [Cites] J Pediatr Surg. 1993 Sep;28(9):1178-80 [8308687.001]
  • [Cites] J Pediatr Surg. 1994 Sep;29(9):1208-11 [7807346.001]
  • [Cites] Arch Surg. 1995 May;130(5):502-8; discussion 508-9 [7748088.001]
  • [Cites] Am J Gastroenterol. 1997 Jan;92(1):27-31 [8995932.001]
  • [Cites] Am J Gastroenterol. 1997 Feb;92(2):212-5 [9040193.001]
  • [Cites] Am J Gastroenterol. 1997 Aug;92(8):1293-7 [9260792.001]
  • [Cites] J Pediatr Surg. 1997 Nov;32(11):1570-4 [9396528.001]
  • [Cites] Gastroenterology. 2002 Feb;122(2):299-307 [11832445.001]
  • (PMID = 20485706.001).
  • [ISSN] 0835-7900
  • [Journal-full-title] Canadian journal of gastroenterology = Journal canadien de gastroenterologie
  • [ISO-abbreviation] Can. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC2886573
  •  go-up   go-down


30. Callacondo D, Ganoza-Salas A, Anicama-Lima W, Quispe-Mauricio A, Longacre TA: Primary squamous cell carcinoma of the stomach with paraneoplastic leukocytosis: a case report and review of literature. Hum Pathol; 2009 Oct;40(10):1494-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • No foci of squamous metaplasia or gland-forming elements were identified in the resection specimen, although there was marked chronic gastritis with intestinal metaplasia.
  • [MeSH-minor] Adenocarcinoma / pathology. Aged, 80 and over. Diabetes Mellitus, Type 2 / complications. Humans. Hypertension / complications. Immunohistochemistry. In Situ Hybridization. Male. Neoplasms, Multiple Primary / pathology. Prostatic Neoplasms / pathology

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • Genetic Alliance. consumer health - Stomach carcinoma.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Hum Pathol. 2010 Feb;41(2):307. Callacondo-Riva, David [corrected to Callacondo, David]
  • (PMID = 19467693.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


31. Rossi E, Grisanti S, Villanacci V, Della Casa D, Cengia P, Missale G, Minelli L, Buglione M, Cestari R, Bassotti G: HER-2 overexpression/amplification in Barrett's oesophagus predicts early transition from dysplasia to adenocarcinoma: a clinico-pathologic study. J Cell Mol Med; 2009 Sep;13(9B):3826-33
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HER-2 overexpression/amplification in Barrett's oesophagus predicts early transition from dysplasia to adenocarcinoma: a clinico-pathologic study.
  • Barrett's oesophagus (BO) is the primary precursor lesion for oesophageal adenocarcinoma (ADC).
  • The natural history of metaplasia-dysplasia-carcinoma sequence remains largely unknown.
  • We retrospectively evaluated by univariate analysis of single variables clinical records and histological specimens of 21 patients with a confirmed diagnosis of BO and/or oesophageal dysplasia.
  • Median age at diagnosis was 63 years (range 37-84).
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Gene Expression Regulation, Neoplastic. Receptor, ErbB-2 / metabolism

  • 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 = 19292734.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC4516530
  •  go-up   go-down


32. Li C, Rock KL, Woda BA, Jiang Z, Fraire AE, Dresser K: IMP3 is a novel biomarker for adenocarcinoma in situ of the uterine cervix: an immunohistochemical study in comparison with p16(INK4a) expression. Mod Pathol; 2007 Feb;20(2):242-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IMP3 is a novel biomarker for adenocarcinoma in situ of the uterine cervix: an immunohistochemical study in comparison with p16(INK4a) expression.
  • Adenocarcinoma in situ of the uterine cervix remains a diagnostic challenge in a small proportion of cases.
  • This suggests a need for biomarker that may be of help in establishing the diagnosis.
  • The aim of this study was to evaluate the potential of insulin-like growth factor-II mRNA-binding protein 3 and cyclin-dependent kinase inhibitor p16(INK4a) as biomarkers for adenocarcinoma in situ.
  • Forty-four samples of adenocarcinoma in situ from 40 patients and 23 control cases of benign uterine cervix were included in this study.
  • In addition to benign endocervical epithelium, 19 of these 23 control cases also showed focal tubal metaplasia.
  • Cytoplasmic immunoreactivity for insulin-like growth factor-II mRNA-binding protein 3 was identified in 41 (93%) adenocarcinoma in situ samples, among which, 29 (71%), 10 (24%), and 2 (5%) samples showed insulin-like growth factor-II mRNA-binding protein 3 positive staining in 50% or more, >5 to <50 and <5% of adenocarcinoma in situ lesional cells, respectively.
  • Immunohistochemical reaction intensity for insulin-like growth factor-II mRNA-binding protein 3 was found to be strong in 34 adenocarcinoma in situ samples, intermediate in five, and weak in two.
  • All 23 control cases were negative for insulin-like growth factor-II mRNA-binding protein 3. p16(INK4a) expression was identified in all of the adenocarcinoma in situ samples with intermediate staining intensity seen in seven samples and strong in the remainder.
  • Fourteen of 19 (74%) tubal metaplasia cases showed p16(INK4a) immunoreactivity in >50% of the tubal metaplastic epithelium with staining intensity ranging from weak to strong.
  • Our findings demonstrate significant expression of insulin-like growth factor-II mRNA-binding protein 3 and p16(INK4a) in adenocarcinoma in situ as compared to benign endocervical glands, suggesting that expression of these biomarkers may be helpful in the distinction of adenocarcinoma in situ from benign endocervical glands, particularly in difficult borderline cases.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Carcinoma in Situ / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Neoplasm Proteins / metabolism. RNA-Binding Proteins / metabolism. Uterine Cervical Neoplasms / metabolism


33. Chennat J, Waxman I: Endoscopic treatment of Barrett's esophagus: From metaplasia to intramucosal carcinoma. World J Gastroenterol; 2010 Aug 14;16(30):3780-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endoscopic treatment of Barrett's esophagus: From metaplasia to intramucosal carcinoma.
  • The annual incidence of adenocarcinoma arising from Barrett's esophagus (BE) is approximately 0.5%.
  • Through a process of gradual transformation from low-grade dysplasia to high-grade dysplasia (HGD), adenocarcinoma can develop in the setting of BE.
  • The clinical importance of appropriate identification and treatment of BE in its various stages, from intestinal metaplasia to intramucosal carcinoma (IMC) hinges on the dramatically different prognostic status between early neoplasia and more advanced stages.
  • Once a patient has symptoms of adenocarcinoma, there is usually locally advanced disease with an approximate 5-year survival rate of about 20%.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / surgery. Esophageal Neoplasms / surgery. Esophagoscopy. Esophagus / surgery. Precancerous Conditions / surgery
  • [MeSH-minor] Catheter Ablation. Cryosurgery. Disease Progression. Humans. Metaplasia. Mucous Membrane / pathology. Mucous Membrane / surgery. Photochemotherapy. Treatment Outcome

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gastrointest Endosc. 2000 Sep;52(3):328-32 [10968845.001]
  • [Cites] Gastrointest Endosc. 2001 Dec;54(6):682-8 [11726842.001]
  • [Cites] Br J Surg. 2002 Mar;89(3):344-8 [11872061.001]
  • [Cites] Endoscopy. 2002 Aug;34(8):604-10 [12173079.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2002 Oct;14(10):1085-91 [12362099.001]
  • [Cites] Gastrointest Endosc. 2003 Jun;57(7):854-9 [12776032.001]
  • [Cites] Gastrointest Endosc. 2003 Aug;58(2):183-8 [12872083.001]
  • [Cites] Gastrointest Endosc Clin N Am. 2003 Jul;13(3):505-12 [14629106.001]
  • [Cites] Br J Surg. 2004 Jan;91(1):90-8 [14716801.001]
  • [Cites] Gastroenterology. 1989 May;96(5 Pt 1):1249-56 [2703113.001]
  • [Cites] J Am Acad Dermatol. 1994 Dec;31(6):925-44; quiz 944-6 [7962774.001]
  • [Cites] Gut. 2000 Apr;46(4):574-7 [10716690.001]
  • [Cites] Gastroenterology. 2000 Apr;118(4):670-7 [10734018.001]
  • [Cites] J Gastrointest Surg. 2000 Mar-Apr;4(2):117-8 [10885954.001]
  • [Cites] Am J Gastroenterol. 1997 Feb;92(2):212-5 [9040193.001]
  • [Cites] J Thorac Cardiovasc Surg. 1997 Nov;114(5):824-9 [9375613.001]
  • [Cites] J Gastrointest Surg. 1998 Mar-Apr;2(2):186-92 [9834415.001]
  • [Cites] Gastrointest Endosc. 2004 Dec;60(6):1002-10 [15605025.001]
  • [Cites] Am J Surg Pathol. 2005 May;29(5):680-6 [15832094.001]
  • [Cites] Gastrointest Endosc. 2005 Jul;62(1):16-23 [15990814.001]
  • [Cites] Gastrointest Endosc. 2005 Jul;62(1):24-30 [15990815.001]
  • [Cites] Gastrointest Endosc. 2005 Oct;62(4):617-23 [16185985.001]
  • [Cites] Surg Endosc. 2006 Jan;20(1):125-30 [16333533.001]
  • [Cites] Am J Gastroenterol. 2006 Jul;101(7):1449-57 [16863545.001]
  • [Cites] Gastrointest Endosc. 2007 Jan;65(1):60-6 [17185080.001]
  • [Cites] Gastrointest Endosc. 2007 Feb;65(2):185-95 [17258973.001]
  • [Cites] J Clin Invest. 2007 Mar;117(3):524-9 [17332879.001]
  • [Cites] Surg Endosc. 2007 May;21(5):820-4 [17294308.001]
  • [Cites] Gastroenterology. 2007 Apr;132(4):1226-33 [17408660.001]
  • [Cites] Gastrointest Endosc. 2007 Sep;66(3):460-8 [17643436.001]
  • [Cites] Clin Gastroenterol Hepatol. 2008 Feb;6(2):159-64 [18096439.001]
  • [Cites] Gastrointest Endosc. 2008 Jul;68(1):35-40 [18355819.001]
  • [Cites] Gastrointest Endosc. 2008 Jul;68(1):11-8 [18577472.001]
  • [Cites] Gut. 2008 Sep;57(9):1200-6 [18460553.001]
  • [Cites] J Gastrointest Surg. 2008 Oct;12(10):1627-36; discussion 1636-7 [18704598.001]
  • [Cites] Gastrointest Endosc. 2008 Nov;68(5):867-76 [18561930.001]
  • [Cites] N Engl J Med. 2009 May 28;360(22):2277-88 [19474425.001]
  • [Cites] Am J Gastroenterol. 2009 Jun;104(6):1366-73 [19491850.001]
  • [Cites] Nat Rev Gastroenterol Hepatol. 2009 Jul;6(7):393-401 [19488071.001]
  • [Cites] Ann Surg. 2009 Sep;250(3):472-83 [19730178.001]
  • [Cites] Gastrointest Endosc. 2009 Oct;70(4):635-44 [19559428.001]
  • [Cites] Am J Gastroenterol. 2009 Nov;104(11):2684-92 [19690526.001]
  • [Cites] Gastrointest Endosc Clin N Am. 2010 Jan;20(1):35-53, vi [19951793.001]
  • [Cites] Clin Gastroenterol Hepatol. 2010 Jan;8(1):23-9 [19602454.001]
  • [Cites] Dis Esophagus. 2010 Jan;23(1):13-9 [19515183.001]
  • [Cites] J Gastrointest Surg. 2000 Mar-Apr;4(2):131-4 [10885959.001]
  • [Cites] Gastroenterology. 2000 Aug;119(2):333-8 [10930368.001]
  • (PMID = 20698040.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2921089
  •  go-up   go-down


34. Yamamichi N, Inada K, Ichinose M, Yamamichi-Nishina M, Mizutani T, Watanabe H, Shiogama K, Fujishiro M, Okazaki T, Yahagi N, Haraguchi T, Fujita S, Tsutsumi Y, Omata M, Iba H: Frequent loss of Brm expression in gastric cancer correlates with histologic features and differentiation state. Cancer Res; 2007 Nov 15;67(22):10727-35
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Loss of Brm is frequent in the major gastric cancer types (well- or moderately-differentiated tubular adenocarcinoma and poorly-differentiated adenocarcinoma) and positively correlates with the undifferentiated state.
  • Among the minor gastric cancer types, Brm expression persists in signet-ring cell carcinoma and mucinous adenocarcinoma, but a marked decrease is observed in papillary adenocarcinoma.
  • Intestinal metaplasia never shows decreased expression, indicating that Brm is a valid marker of gastric oncogenesis.
  • We further show that Brm is required for villin expression, a definitive marker of intestinal metaplasia and differentiation.
  • [MeSH-major] Adenocarcinoma / metabolism. Gene Expression Regulation, Neoplastic. Microfilament Proteins / biosynthesis. Stomach Neoplasms / metabolism. Transcription Factors / biosynthesis. Transcription Factors / genetics

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • 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 = 18006815.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Microfilament Proteins; 0 / SMARCA2 protein, human; 0 / Transcription Factors; 0 / villin
  •  go-up   go-down


35. Lee HW, Yang DH, Kim HK, Lee BH, Choi KC, Choi YH, Park YE: Expression of MUC2 in gastric carcinomas and background mucosae. J Gastroenterol Hepatol; 2007 Aug;22(8):1336-43
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: We analyzed the expression of MUC2 in gastric mucosa and intestinal metaplasia adjacent to the tumoral area and carcinomas (n = 98) using immunohistochemistry.
  • RESULTS: In the intestinal metaplasia adjacent to the tumoral area, MUC2 was detected in 76 (97.4%) of 78 intestinal metaplasia, and MUC2 expression was inversely associated with the depth of wall penetration (P = 0.026) and tumor stage (P = 0.021).
  • Although the expression rate of MUC2 antigens was higher in intestinal-type adenocarcinoma than in diffuse-type adenocarcinoma, a significant correlation with pathologic staging of the TNM system (pTNM staging) and MUC2 expression could not be found in each subtype of gastric carcinomas.
  • CONCLUSION: The expression of MUC2 in intestinal metaplasia was higher in tumors of earlier stages.
  • These findings suggest that increased MUC2 expression in intestinal metaplasia in the neighborhood of the carcinomas may play an important role in gastric carcinomas.

  • MedlinePlus Health Information. consumer health - Stomach 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 = 17559374.001).
  • [ISSN] 0815-9319
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / MUC2 protein, human; 0 / Mucin-2; 0 / Mucins
  •  go-up   go-down


36. Anderson MR, Harrison R, Atherfold PA, Campbell MJ, Darnton SJ, Obszynska J, Jankowski JA: Met receptor signaling: a key effector in esophageal adenocarcinoma. Clin Cancer Res; 2006 Oct 15;12(20 Pt 1):5936-43
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Met receptor signaling: a key effector in esophageal adenocarcinoma.
  • PURPOSE: The incidence of esophageal adenocarcinoma is rising, and survival rates remain poor.
  • We assessed the prognostic significance of Met expression in esophageal adenocarcinoma.
  • RESULTS: An increased expression of Met was seen along the metaplasia- adenocarcinoma sequence.
  • Inhibitors of Met may be effective treatment for esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / physiopathology. Esophageal Neoplasms / physiopathology. Proto-Oncogene Proteins / genetics. Receptors, Growth Factor / genetics

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17062664.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / DNA Primers; 0 / HGF protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Growth Factor; 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.10.1 / MET protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-met
  •  go-up   go-down


37. Mabrut JY, Collard JM, Baulieux J: [Duodenogastric and gastroesophageal bile reflux]. J Chir (Paris); 2006 Nov-Dec;143(6):355-65
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This study reviews current data regarding duodenogastric and gastroesophageal bile reflux-pathophysiology, clinical presentation, methods of diagnosis (namely, 24-hour intraluminal bile monitoring) and therapeutic management.
  • In patients with concomitant gastroesophageal reflux, the backwash of duodenal content into the lower esophagus can cause mixed (alkaline and acid) reflux esophagitis, and lead, in turn, to esophageal mucosal damage such as Barrett's metaplasia and adenocarcinoma.

  • Genetic Alliance. consumer health - Gastroesophageal Reflux.
  • MedlinePlus Health Information. consumer health - GERD.
  • Hazardous Substances Data Bank. CHOLESTYRAMINE RESIN .
  • Hazardous Substances Data Bank. SUCRALFATE .
  • Hazardous Substances Data Bank. CISAPRIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17285081.001).
  • [ISSN] 0021-7697
  • [Journal-full-title] Journal de chirurgie
  • [ISO-abbreviation] J Chir (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anion Exchange Resins; 0 / Anti-Ulcer Agents; 0 / Bile Acids and Salts; 0 / Gastrointestinal Agents; 0 / Proton Pump Inhibitors; 11041-12-6 / Cholestyramine Resin; 54182-58-0 / Sucralfate; UVL329170W / Cisapride
  • [Number-of-references] 182
  •  go-up   go-down


38. Biancone L, Calabrese E, Palmieri G, Petruzziello C, Onali S, Sica GS, Cossignani M, Condino G, Das KM, Pallone F: Ileal lesions in patients with ulcerative colitis after ileo-rectal anastomosis: relationship with colonic metaplasia. World J Gastroenterol; 2008 Sep 14;14(34):5290-300
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ileal lesions in patients with ulcerative colitis after ileo-rectal anastomosis: relationship with colonic metaplasia.
  • Possible relation between development of colonic metaplasia and ileal lesions was investigated.
  • RESULTS: Stenosing adenocarcinoma of the rectal stump was detected in 1 UC patient.
  • Ileal ulcers were detected in 7/10 UC, associated with colonic metaplasia in 4/7 (57.1%) and Das-1 and CG3 reactivity in 3/4 UC.
  • In controls, recurrence occurred in 4/6 CD, associated with colonic metaplasia in 3/4 and reactivity with Das-1 and CG3 in 2/3.
  • Changes of the ileal content after colectomy may contribute to the development of colonic metaplasia, leading to ileal lesions both in the pouch and in the neo-terminal ileum after IRA.
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Anastomosis, Surgical / adverse effects. Capsule Endoscopy. Case-Control Studies. Colectomy / adverse effects. Colon / pathology. Colon / surgery. Female. Humans. Male. Metaplasia. Middle Aged. Rectal Neoplasms / pathology. Rectum / surgery. Young Adult

  • Genetic Alliance. consumer health - Ulcerative Colitis.
  • MedlinePlus Health Information. consumer health - Ulcerative Colitis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Gastrointest Surg. 2003 Feb;7(2):246-53; discussion 253-4 [12600449.001]
  • [Cites] Gastroenterology. 2002 Oct;123(4):999-1005 [12360460.001]
  • [Cites] Ann Surg. 2003 Sep;238(3):433-41; discussion 442-5 [14501509.001]
  • [Cites] Gut. 2004 Jan;53(1):108-14 [14684584.001]
  • [Cites] Am J Gastroenterol. 2003 Dec;98(12):2719-26 [14687823.001]
  • [Cites] Gastroenterology. 2004 May;126(6):1611-9 [15168371.001]
  • [Cites] Gastroenterology. 1976 Mar;70(3):439-44 [1248701.001]
  • [Cites] Br J Surg. 1977 Feb;64(2):77-83 [890251.001]
  • [Cites] J Clin Invest. 1985 Jul;76(1):311-8 [4019782.001]
  • [Cites] Dis Colon Rectum. 1987 Jan;30(1):25-8 [3026757.001]
  • [Cites] J Cell Biol. 1988 Aug;107(2):563-72 [3047141.001]
  • [Cites] Dis Colon Rectum. 1989 Apr;32(4):323-6 [2538299.001]
  • [Cites] Dig Dis Sci. 1989 Oct;34(10):1505-10 [2791801.001]
  • [Cites] Gut. 1990 Mar;31(3):247-9 [2182398.001]
  • [Cites] Gastroenterology. 1990 Oct;99(4):956-63 [2394349.001]
  • [Cites] Neth J Med. 1989 Jun;35 Suppl 1:S54-66 [2702314.001]
  • [Cites] Dig Dis Sci. 1992 Dec;37(12):1882-9 [1335407.001]
  • [Cites] J Immunol. 1993 Mar 15;150(6):2487-93 [8450225.001]
  • [Cites] Surg Gynecol Obstet. 1993 Dec;177(6):565-72 [8266266.001]
  • [Cites] Mayo Clin Proc. 1994 May;69(5):409-15 [8170189.001]
  • [Cites] Gastroenterology. 1994 Aug;107(2):435-43 [8039620.001]
  • [Cites] Arch Surg. 1996 May;131(5):497-500; discussion 501-2 [8624195.001]
  • [Cites] Dig Dis. 1997 May-Jun;15(3):172-88 [9158926.001]
  • [Cites] Aliment Pharmacol Ther. 1997 Dec;11(6):1041-6 [9663827.001]
  • [Cites] Br J Surg. 1998 Jun;85(6):800-3 [9667712.001]
  • [Cites] Inflamm Bowel Dis. 1999 Feb;5(1):33-9 [10028447.001]
  • [Cites] Gut. 1999 Oct;45(4):542-5 [10486362.001]
  • [Cites] Lancet. 1956 Sep 15;271(6942):532-6 [13368449.001]
  • [Cites] Am J Gastroenterol. 2005 Jan;100(1):93-101 [15654787.001]
  • [Cites] Scand J Surg. 2005;94(1):40-2 [15865115.001]
  • [Cites] Am J Surg. 2005 Jul;190(1):39-42 [15972169.001]
  • [Cites] Am J Surg Pathol. 2005 Nov;29(11):1472-81 [16224214.001]
  • [Cites] Dis Colon Rectum. 2005 Nov;48(11):2038-46 [16175321.001]
  • [Cites] Am J Gastroenterol. 2005 Dec;100(12):2796-807 [16393238.001]
  • [Cites] Colorectal Dis. 2007 Jun;9(5):384-92 [17504334.001]
  • [Cites] Inflamm Bowel Dis. 2007 Oct;13(10):1256-65 [17577246.001]
  • [Cites] Clin Exp Immunol. 1999 Nov;118(2):219-27 [10540182.001]
  • [Cites] Nature. 2000 May 25;405(6785):417 [10839527.001]
  • [Cites] Nature. 2000 Jun 29;405(6790):1073-7 [10890451.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 1;97(16):8799-806 [10922038.001]
  • [Cites] Gastroenterology. 2000 Aug;119(2):305-9 [10930365.001]
  • [Cites] Gastroenterology. 2000 Dec;119(6):1454-60 [11113066.001]
  • [Cites] Gastroenterology. 2002 Feb;122(2):512-30 [11832465.001]
  • [Cites] Gastroenterology. 2003 May;124(5):1202-9 [12730861.001]
  • (PMID = 18785281.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2744059
  •  go-up   go-down


39. Ling FC, Baldus SE, Khochfar J, Xi H, Neiss S, Brabender J, Metzger R, Drebber U, Dienes HP, Bollschweiler E, Hoelscher AH, Schneider PM: Association of COX-2 expression with corresponding active and chronic inflammatory reactions in Barrett's metaplasia and progression to cancer. Histopathology; 2007 Jan;50(2):203-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of COX-2 expression with corresponding active and chronic inflammatory reactions in Barrett's metaplasia and progression to cancer.
  • The aim of this study was to examine a possible association between COX-2 protein expression and the development and progression of the Barrett's metaplasia-dysplasia-carcinoma sequence and the type and degree of associated inflammatory reaction.
  • METHODS AND RESULTS: Squamous epithelium, metaplastic, low-grade, high-grade dysplastic lesions and tumour tissue of 49 resection specimens from patients with Barrett's adenocarcinoma were immunohistochemically analysed.
  • The most significant differences were detected between squamous epithelium and Barrett's metaplasia (P < 0.001) and from low- to high-grade dysplasia (P < 0.0001).
  • Active and chronic inflammation were significantly different between squamous epithelium and Barrett's metaplasia (P < 0.0001), but not during further progression in the sequence.
  • CONCLUSIONS: Increasing COX-2 expression in Barrett's metaplasia is significantly associated with a change in the local inflammatory reaction, but not during further progression through dysplasia to cancer.

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Histopathology. 2007 Mar;50(4):531
  • (PMID = 17222248.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
  •  go-up   go-down


40. Vannella L, Lahner E, Osborn J, Bordi C, Miglione M, Delle Fave G, Annibale B: Risk factors for progression to gastric neoplastic lesions in patients with atrophic gastritis. Aliment Pharmacol Ther; 2010 May;31(9):1042-50
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • All patients had at least one follow-up gastroscopy/histology at an interval of at least 1 year after the atrophic gastritis diagnosis.
  • Cox-regression analysis identified the following risk factors: age over 50 years (HR 8.8, 95%CI 1.2-68.4), atrophic pangastritis (HR 4.5, 95% CI 1.5-14.1) and severe intestinal metaplasia in the gastric body (HR 4.0, 95% CI 1.3-11.8).
  • CONCLUSIONS: Atrophic pangastritis, severe body intestinal metaplasia and/or age over 50 years increase the risk for developing GNL in patients with atrophic gastritis.
  • [MeSH-major] Adenocarcinoma / pathology. Gastric Mucosa / pathology. Gastritis, Atrophic / pathology. Precancerous Conditions / pathology. Stomach Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20175768.001).
  • [ISSN] 1365-2036
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


41. Rantanen TK, Räsänen JV, Sihvo EI, Ahotupa MO, Färkkilä MA, Salo JA: The impact of antireflux surgery on oxidative stress of esophageal mucosa caused by gastroesophageal reflux disease: 4-yr follow-up study. Am J Gastroenterol; 2006 Feb;101(2):222-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND AND AIM: Oxidative stress to esophageal mucosa plays a key role in the pathogenesis of gastroesophageal reflux disease (GERD), Barrett's esophagus, and adenocarcinoma.
  • Preoperatively, 12 of the 20 had erosive esophagitis or Barrett's metaplasia.

  • Genetic Alliance. consumer health - Gastroesophageal Reflux.
  • MedlinePlus Health Information. consumer health - GERD.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16454822.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; EC 1.11.1.7 / Peroxidase; EC 1.15.1.1 / Superoxide Dismutase; GAN16C9B8O / Glutathione
  •  go-up   go-down


42. Sharma P, Wani S, Bansal A: The quest for intestinal metaplasia--is it worth the effort? Am J Gastroenterol; 2007 Jun;102(6):1162-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The quest for intestinal metaplasia--is it worth the effort?
  • Starting with the basics, the definition and diagnosis of Barrett's esophagus (BE) continues to be a point of major debate globally leading to definitions that have been restrictive (requiring histologically confirmed intestinal metaplasia) or all-encompassing (simply the presence of CLE at endoscopy).
  • The interest in intestinal metaplasia stems from studies that have consistently demonstrated intestinal metaplasia and dysplasia both adjacent to and remote from esophageal adenocarcinoma.
  • The proponents of not requiring histology suggest that if a sufficient number of biopsies is obtained over an adequate period of time, intestinal metaplasia can usually be demonstrated in such cases and that the true neoplastic potential of the cardiac and fundic-type mucosa detected in the CLE has not been delineated.
  • The optimal number of biopsies required to detect intestinal metaplasia is largely unknown, and in this issue of The American Journal of Gastroenterology, Harrison et al. add to the limited data on this subject.
  • There is ample evidence that once a diagnosis of BE is made, it has significant implications on the financial, psychosocial, and insurance status of the patients.
  • We feel that an optimal, practical definition of BE requires clear, accepted, reproducible, and clinically relevant criteria with evidence of an increased risk of cancer--the most crucial consequence of the lesion--and discuss the pros and cons of the need for documenting intestinal metaplasia in the CLE.
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Biopsy. Diagnostic Imaging. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / pathology. Gastric Mucosa / pathology. Humans. Metaplasia. Precancerous Conditions / pathology

  • 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
  • [CommentOn] Am J Gastroenterol. 2007 Jun;102(6):1154-61 [17433019.001]
  • (PMID = 17531009.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] United States
  •  go-up   go-down


43. Sun JH, Das KK, Amenta PS, Yokota K, Watari J, Sato T, Kohgo Y, Das KM: Preferential expression of cyclooxygenase-2 in colonic-phenotype of gastric intestinal metaplasia: association with helicobacter pylori and gastric carcinoma. J Clin Gastroenterol; 2006 Feb;40(2):122-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preferential expression of cyclooxygenase-2 in colonic-phenotype of gastric intestinal metaplasia: association with helicobacter pylori and gastric carcinoma.
  • OBJECTIVES: Gastric intestinal metaplasia (GIM) associated with H. pylori (HP) has been considered a premalignant lesion.
  • [MeSH-major] Adenocarcinoma / metabolism. Cyclooxygenase 2 / metabolism. Gastric Mucosa / metabolism. Helicobacter Infections / metabolism. Helicobacter pylori / metabolism. Metaplasia / metabolism. Precancerous Conditions / metabolism. Stomach Neoplasms / metabolism

  • MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • 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 = 16394872.001).
  • [ISSN] 0192-0790
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Grant] United States / PHS HHS / / R01 47673
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / DAS-1 protein, human; EC 1.14.99.1 / Cyclooxygenase 2
  •  go-up   go-down


44. Yu M, Zheng H, Tsuneyama K, Takahashi H, Nomoto K, Xu H, Takano Y: Paradoxical expression of maspin in gastric carcinomas: correlation with carcinogenesis and progression. Hum Pathol; 2007 Aug;38(8):1248-55
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To clarify the role of maspin in the genesis and progression of gastric carcinomas, its expression pattern and level were studied by immunohistochemistry on tissue microarrays containing gastric carcinoma (n = 237), normal gastric mucosa (n = 23), intestinal metaplasia (n = 38), and adenoma (n = 42); and the findings were compared with clinicopathological parameters.
  • We found that cytoplasmic and nuclear maspin expression paralleled each other (P < .05) and decreased from intestinal metaplasia, adenoma, and carcinoma to normal gastric mucosa (P < .05).
  • [MeSH-major] Adenocarcinoma / secondary. Adenoma / pathology. Biomarkers, Tumor / metabolism. Precancerous Conditions / pathology. Serpins / metabolism. Stomach Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Nucleus / metabolism. Cell Nucleus / pathology. Cytoplasm / metabolism. Cytoplasm / pathology. Disease Progression. Female. Fluorescent Antibody Technique, Direct. Humans. Lymph Nodes / pathology. Male. Metaplasia. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Stomach / metabolism. Stomach / pathology. Survival Rate. Tissue Array Analysis

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17490717.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / SERPIN-B5; 0 / Serpins
  •  go-up   go-down


45. Menke V, van Es JH, de Lau W, van den Born M, Kuipers EJ, Siersema PD, de Bruin RW, Kusters JG, Clevers H: Conversion of metaplastic Barrett's epithelium into post-mitotic goblet cells by gamma-secretase inhibition. Dis Model Mech; 2010 Jan-Feb;3(1-2):104-10
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Barrett's esophagus (BE) affects approximately 2% of the Western population and progresses to esophageal adenocarcinoma (EAC) in 0.5% of these patients each year.
  • [MeSH-minor] Animals. Biopsy. Cell Line, Tumor. Cell Proliferation / drug effects. Colon / drug effects. Colon / metabolism. Colon / pathology. Dibenzazepines / pharmacology. Disease Models, Animal. Gene Expression Regulation / drug effects. Humans. Metaplasia. Rats. Receptors, Notch / antagonists & inhibitors. Receptors, Notch / genetics. Receptors, Notch / metabolism. Signal Transduction / drug effects

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20075383.001).
  • [ISSN] 1754-8411
  • [Journal-full-title] Disease models & mechanisms
  • [ISO-abbreviation] Dis Model Mech
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dibenzazepines; 0 / Receptors, Notch; 0 / dibenzazepine; EC 3.4.- / Amyloid Precursor Protein Secretases
  •  go-up   go-down


46. Morgner-Miehlke A, Koop H, Blum AL, Hermans ML, Miehlke S, Labenz J: [Symptom- versus endoscopy-based diagnosis and treatment of gastroesophageal reflux disease (GERD)]. Z Gastroenterol; 2006 May;44(5):399-410
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Symptom- versus endoscopy-based diagnosis and treatment of gastroesophageal reflux disease (GERD)].
  • The preference for one or the other strategy depends on the prevalence of so-called alarm symptoms, risk factors for a reflux carcinoma or Barrett's metaplasia, demographic factors, e. g., age and gender, patient's wish and initial response to empirical therapy with proton pump inhibitors (PPI).
  • [MeSH-major] Endoscopy, Digestive System. Esophagitis, Peptic / diagnosis. Gastroesophageal Reflux / diagnosis. Practice Guidelines as Topic
  • [MeSH-minor] Adenocarcinoma / diagnosis. Anti-Ulcer Agents / therapeutic use. Barrett Esophagus / diagnosis. Diagnosis, Differential. Disease Progression. Esophageal Neoplasms / diagnosis. Humans. Long-Term Care. Proton Pump Inhibitors. Risk Factors. Treatment Outcome

  • Genetic Alliance. consumer health - Gastroesophageal Reflux.
  • MedlinePlus Health Information. consumer health - GERD.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16688658.001).
  • [ISSN] 0044-2771
  • [Journal-full-title] Zeitschrift für Gastroenterologie
  • [ISO-abbreviation] Z Gastroenterol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Proton Pump Inhibitors
  •  go-up   go-down


47. Seder CW, Hartojo W, Lin L, Silvers AL, Wang Z, Thomas DG, Giordano TJ, Chen G, Chang AC, Orringer MB, Beer DG: INHBA overexpression promotes cell proliferation and may be epigenetically regulated in esophageal adenocarcinoma. J Thorac Oncol; 2009 Apr;4(4):455-62
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] INHBA overexpression promotes cell proliferation and may be epigenetically regulated in esophageal adenocarcinoma.
  • INTRODUCTION: The expression, mechanisms of regulation, and functional impact of activin (INHBA) in esophageal adenocarcinoma (EAC) have not been fully defined.
  • METHODS: INHBA expression was examined in 46 esophageal samples (nine Barrett's metaplasia (BM); seven BM/low-grade dysplasia; eight low-grade dysplasia; seven high-grade dysplasia; 15 EAC) using oligonucleotide microarrays and real-time reverse transcription-polymerase chain reaction (RT-PCR) and in 90 tissue samples (79 EAC; 8 dysplastic; 3 BM) using immunohistochemistry (IHC).
  • [MeSH-major] Adenocarcinoma / pathology. Epigenesis, Genetic. Esophageal Neoplasms / pathology. Inhibin-beta Subunits / physiology

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19240652.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 P30 CA46592
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Follistatin; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / inhibin beta A subunit; 104625-48-1 / Activins; 93443-12-0 / Inhibin-beta Subunits; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / histone acetyltransferase type B complex
  •  go-up   go-down


48. Kazakov DV, Calonje E, Zelger B, Luzar B, Belousova IE, Mukensnabl P, Michal M: Sebaceous carcinoma arising in nevus sebaceus of Jadassohn: a clinicopathological study of five cases. Am J Dermatopathol; 2007 Jun;29(3):242-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In three cases, prominent mucinous metaplasia of sweat ducts and glands was seen.
  • [MeSH-major] Adenocarcinoma, Sebaceous / pathology. Head and Neck Neoplasms / pathology. Neoplasms, Multiple Primary / pathology. Nevus / pathology. Sebaceous Gland Neoplasms / pathology

  • Genetic Alliance. consumer health - Nevus.
  • MedlinePlus Health Information. consumer health - Birthmarks.
  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • MedlinePlus Health Information. consumer health - Moles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17519621.001).
  • [ISSN] 0193-1091
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


49. Pavlakis K, Messini I, Athanassiadou S, Kyrodimou E, Pandazopoulou A, Vrekoussis T, Stathopoulos EN: Endocervical glandular lesions: a diagnostic approach combining a semi-quantitative scoring method to the expression of CEA, MIB-1 and p16. Gynecol Oncol; 2006 Dec;103(3):971-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: The hematoxylin and eosin-stained sections of 95 cervical biopsies were examined by 4 different observers and were grouped into three categories, benign, dysplasia and adenocarcinoma in situ, depending on the degree of nuclear stratification, nuclear atypia and the number of mitosis and apoptotic figures.
  • RESULTS: Using the semi-quantitative scoring system, most of the cases that were initially diagnosed as atypical hyperplasia or tuboendometrial metaplasia fell into the benign category.
  • This scoring system discriminates effectively (Kruskal-Wallis, p<0.001) between the three categories (benign, endocervical glandular dysplasia and adenocarcinoma in situ).
  • Ki-67, CEA and p16 failed to discriminate between tuboendometrial metaplasia and epithelial glandular dysplasia.
  • Nevertheless, the proportion of cases that were classified similarly to the prestudy diagnosis was higher when the combined score was used.
  • [MeSH-major] Uterine Cervical Neoplasms / diagnosis. Uterine Cervical Neoplasms / metabolism


50. She R, Szakacs J: Carcinosarcoma of the liver: a case report and review of the literature. Arch Pathol Lab Med; 2005 Jun;129(6):790-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hepatocellular carcinoma, fibrolamellar type, was accompanied by neuroendocrine carcinoma (neuron-specific enolase and synaptophysin positive) and adenocarcinoma (cytokeratin 7 and 20 positive).
  • Findings in this case support the view that metaplasia of carcinomatous cells gives rise to the sarcomatous elements.
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Benzamides. Carcinoma, Hepatocellular / diagnosis. Diagnosis, Differential. Fatal Outcome. Female. Hepatorenal Syndrome. Humans. Imatinib Mesylate. Middle Aged. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Sarcoma / diagnosis

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • 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 = 15913431.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  •  go-up   go-down


51. Roberts KJ, Harper E, Alderson D, Hallissey M: Long-term survival and cost analysis of an annual Barrett's surveillance programme. Eur J Gastroenterol Hepatol; 2010 Apr;22(4):399-403
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: Surveillance endoscopy aims to identify progression to high-grade dysplasia (HGD) or oesophageal adenocarcinoma (OA) at an early stage in patients with Barrett's metaplasia (BM).
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Endoscopy, Digestive System. Esophageal Neoplasms / pathology. Population Surveillance / methods. Survivors

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19858726.001).
  • [ISSN] 1473-5687
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  •  go-up   go-down


52. Zhang J, Parwani AV, Ali SZ: Hepatocyte paraffin 1 immunoexpression in esophageal brush samples. Cancer; 2005 Oct 25;105(5):304-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Intestinal metaplasia (IM) is often a component of Barrett esophagus (BE) and is characterized by a distinctive type of epithelium.
  • Because IM has the potential to progress to dysplasia or adenocarcinoma, an accurate identification of its presence is important clinically.
  • A cytopathologic diagnosis of IM on esophageal brushings by morphology alone can be difficult.
  • RESULTS: Among the samples of BE with IM, 9 of 11 samples (82%) were immunoreactive for Heppar-1, compared with 0 of 11 specimens of BE with only cardiac-type metaplasia.
  • [MeSH-major] Antigens / biosynthesis. Barrett Esophagus / diagnosis. Barrett Esophagus / pathology
  • [MeSH-minor] Adenocarcinoma / etiology. Aged. Aged, 80 and over. Antibodies, Monoclonal. Antibodies, Monoclonal, Humanized. Biomarkers / analysis. Cytological Techniques. Esophageal Neoplasms / etiology. Hepatocytes / metabolism. Humans. Immunoassay. Metaplasia. Middle Aged. Retrospective Studies. Sensitivity and Specificity

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Cancer. 2006 Feb 25;108(1):73-4; author reply 74-5 [16104041.001]
  • (PMID = 15918175.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens; 0 / Biomarkers; 0 / veltuzumab
  •  go-up   go-down


53. Abdo-Francis JM, Sobrino-Cossío S, Bernal-Sahagún F, Hernández-Guerrero A: [Prevalence of intestinal metaplasia of the gastric cardia and its relation with Helicobacter pylori strains cagA and vacA]. Cir Cir; 2010 Jul-Aug;78(4):315-21
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Prevalence of intestinal metaplasia of the gastric cardia and its relation with Helicobacter pylori strains cagA and vacA].
  • [Transliterated title] Prevalencia de metaplasia intestinal en el cardias gástrico y su relación con cepas virulentas de Helicobacter pylori cagA y vacA.
  • BACKGROUND: Esophageal metaplasia progression is a consequence of chronic gastroesophageal reflux (CGR).
  • In addition, they present an increased risk for the development of gastric adenocarcinoma.
  • We undertook this study to establish a relationship between the presence of pathogenic Helicobacter pylori strains and the presence of metaplasia progression in patients with CGR.
  • Cardiac intestinal metaplasia was observed in 35% of the patients.
  • A marked tendency was observed to develop cardiac intestinal metaplasia in those patients diagnosed with high-pathogenicity strains infected in both anatomic areas.
  • CONCLUSIONS: These results suggest that infection with Helicobacter pylori can be considered a risk factor for developing gastric cardiac intestinal metaplasia.
  • [MeSH-minor] Adult. Aged. Biopsy. Cross-Sectional Studies. Female. Gastroesophageal Reflux / complications. Gastroscopy. Humans. Male. Metaplasia / epidemiology. Metaplasia / etiology. Middle Aged. Neutrophils / pathology. Precancerous Conditions / epidemiology. Precancerous Conditions / etiology. Precancerous Conditions / microbiology. Precancerous Conditions / pathology. Prospective Studies. Species Specificity. Virulence. Young Adult

  • MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21167097.001).
  • [ISSN] 0009-7411
  • [Journal-full-title] Cirugía y cirujanos
  • [ISO-abbreviation] Cir Cir
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Bacterial Proteins; 0 / VacA protein, Helicobacter pylori; 0 / cagA protein, Helicobacter pylori
  •  go-up   go-down


54. Debruyne PR, Witek M, Gong L, Birbe R, Chervoneva I, Jin T, Domon-Cell C, Palazzo JP, Freund JN, Li P, Pitari GM, Schulz S, Waldman SA: Bile acids induce ectopic expression of intestinal guanylyl cyclase C Through nuclear factor-kappaB and Cdx2 in human esophageal cells. Gastroenterology; 2006 Apr;130(4):1191-206
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND & AIMS: Although progression to adenocarcinoma at the gastroesophageal junction reflects exposure to acid and bile acids associated with reflux, mechanisms mediating this transformation remain undefined.
  • CONCLUSIONS: Transformation associated with reflux at the gastroesophageal junction reflects activation by bile acid and acid of a transcriptional program involving NF-kappaB and Cdx2, which mediate intestinal metaplasia and ectopic expression of GC-C.
  • [MeSH-minor] Adenocarcinoma / enzymology. Cell Line, Tumor. Deoxycholic Acid / pharmacology. Esophageal Neoplasms / enzymology. Esophagogastric Junction / enzymology. Esophagogastric Junction / metabolism. Gene Expression. Humans. Promoter Regions, Genetic. RNA, Messenger / metabolism. Receptors, Guanylate Cyclase-Coupled. Tissue Distribution / drug effects. Transcription, Genetic / drug effects

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DEOXYCHOLIC ACID .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16618413.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA75123; United States / NCI NIH HHS / CA / CA79663; United States / NCI NIH HHS / CA / CA95026; United States / NHLBI NIH HHS / HL / K30 HL004522; United States / NIGMS NIH HHS / GM / T32 GM08562
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Receptors, Peptide; 005990WHZZ / Deoxycholic Acid; EC 4.6.1.2 / Guanylate Cyclase; EC 4.6.1.2 / Receptors, Guanylate Cyclase-Coupled; EC 4.6.1.2 / enterotoxin receptor
  •  go-up   go-down


55. Taneous M, Ramalingam P, Mode DG, Heiner JG, Terris MK, Lee JR: Primary mucinous adenocarcinoma in a defunctionalized urinary bladder: a case report. J Med Case Rep; 2009;3:9306
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary mucinous adenocarcinoma in a defunctionalized urinary bladder: a case report.
  • INTRODUCTION: Malignancies are rare in defunctionalized bladders and are thought to arise from metaplasia secondary to chronic inflammation.
  • Transitional cell and squamous cell carcinomas are the most common but there are three reported cases of mucinous adenocarcinoma.
  • CASE PRESENTATION: We report a 57-year-old Caucasian man presenting with penile discharge for 30 years following ileal conduit surgery for neurogenic bladder, and who was found to have primary mucinous adenocarcinoma of his defunctionalized bladder.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Urology. 1997 Sep;50(3):427-31 [9301710.001]
  • [Cites] Eur Urol. 1996;29(3):308-11 [8740037.001]
  • [Cites] Urology. 1995 Jul;46(1):107-10 [7604470.001]
  • [Cites] Ann Pathol. 1995;15(2):131-3 [7755802.001]
  • [Cites] J Urol. 2002 Apr;167(4):1782-3 [11912412.001]
  • [Cites] Scand J Urol Nephrol. 1985;19(4):303-4 [4089557.001]
  • [Cites] Urology. 1984 Aug;24(2):192-5 [6087535.001]
  • [Cites] JAMA. 1982 Dec 3;248(21):2885-6 [7143654.001]
  • [Cites] J Urol. 2004 Sep;172(3):831-8 [15310979.001]
  • [Cites] Urology. 1991 Apr;37(4):315-21 [2014595.001]
  • (PMID = 20062735.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2803829
  •  go-up   go-down


56. Gibson GR, Qian D, Ku JK, Lai LL: Metaplastic breast cancer: clinical features and outcomes. Am Surg; 2005 Sep;71(9):725-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • When stratified by stage, however, survival appears similar to that of adenocarcinoma of the breast, and these tumors should be treated as such.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Female. Humans. Mastectomy. Metaplasia. Middle Aged. Neoplasm Staging. Radiotherapy, Adjuvant. Retrospective Studies. Survival Analysis

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16468506.001).
  • [ISSN] 0003-1348
  • [Journal-full-title] The American surgeon
  • [ISO-abbreviation] Am Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


57. Fujiyama Y, Ishizuka I, Koyama S: [Histochemical diagnosis of short segment Barrett's esophagus]. Nihon Rinsho; 2005 Aug;63(8):1420-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Histochemical diagnosis of short segment Barrett's esophagus].
  • It is also reported that we have few frequent findings of typical Barrett's esophagus, long segment Barrett's esophagus (LSBE) which is seen predominantly in Europe and United States, however the frequency of finding of short segment Barrett's esophagus (SSBE) and adenocarcinoma derived from SSBE is gradually increasing in Japan.
  • So it is thought that precise diagnosis of SSBE and the evaluation of potential malignancy of SSBE are needed in the present medical management.
  • It is well known that Barrett's epithelium is categorized gastric fundic type, junctional type and specialized columnar epithelium, especially Barrett's mucosa is characterized by specialized columnar epithelium, e. g. incomplete epithelial type of intestinal metaplasia.
  • We have set up two characteristic groups, gastric mucin dominant and intestinal mucin dominant by using specific mucin staining for MUC2, MUC5AC, Con A and CD10.
  • [MeSH-minor] Adenocarcinoma / etiology. Cell Proliferation. Cell Transformation, Neoplastic / genetics. Esophageal Neoplasms / etiology. Esophagus / cytology. Esophagus / metabolism. Esophagus / pathology. Humans. Ki-67 Antigen / metabolism. Metaplasia / genetics. Metaplasia / pathology. Mucins / metabolism. Mucous Membrane / cytology. Mucous Membrane / metabolism. Mucous Membrane / pathology. Risk. Tumor Suppressor Protein p53 / metabolism

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16101233.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Mucins; 0 / Tumor Suppressor Protein p53
  • [Number-of-references] 22
  •  go-up   go-down


58. di Pietro M, Fitzgerald RC: Barrett's oesophagus: an ideal model to study cancer genetics. Hum Genet; 2009 Aug;126(2):233-46
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Patients with Barrett's oesophagus are at increased risk of oesophageal adenocarcinoma which occurs through dysplastic stages with increasing degree of cellular and architectural disorganization.
  • Here, we review the knowledge acquired so far on the genetic and molecular alterations along the oesophageal metaplasia-dysplasia-carcinoma sequence.
  • [MeSH-major] Barrett Esophagus / diagnosis. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics
  • [MeSH-minor] Carcinoma / diagnosis. Carcinoma / genetics. Cell Transformation, Neoplastic. Endoscopy / methods. Female. Gene Expression Regulation, Neoplastic. Genetic Predisposition to Disease. Humans. Male. Medical Oncology / methods. Metaplasia. Models, Biological. Prognosis

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Cancer. 2007 Nov 15;121(10):2132-9 [17594693.001]
  • [Cites] Gut. 2007 Jul;56(7):906-17 [17185354.001]
  • [Cites] Am J Gastroenterol. 2004 Oct;99(10):1884-6 [15447745.001]
  • [Cites] Clin Cancer Res. 2003 Oct 15;9(13):4819-25 [14581353.001]
  • [Cites] Gastroenterology. 2007 Jul;133(1):34-41; quiz 311 [17631128.001]
  • [Cites] Genet Res. 1974 Feb;23(1):23-35 [4407212.001]
  • [Cites] J Natl Cancer Inst. 2005 Jan 19;97(2):142-6 [15657344.001]
  • [Cites] Am J Clin Pathol. 1978 Jul;70(1):1-5 [696666.001]
  • [Cites] Gastroenterology. 2000 Aug;119(2):333-8 [10930368.001]
  • [Cites] Am J Gastroenterol. 2002 Jan;97(1):22-6 [11808965.001]
  • [Cites] Gut. 2006 Jun;55(6):764-74 [16368780.001]
  • [Cites] Gut. 2004 Oct;53(10 ):1394-6 [15361482.001]
  • [Cites] Gastroenterology. 2000 Mar;118(3):487-96 [10702199.001]
  • [Cites] Cancer Lett. 2009 Mar 8;275(1):117-26 [19027227.001]
  • [Cites] Am J Gastroenterol. 2008 Mar;103(3):788-97 [18341497.001]
  • [Cites] Transl Res. 2007 Jul;150(1):3-17 [17585859.001]
  • [Cites] Dis Esophagus. 2006;19(5):366-72 [16984534.001]
  • [Cites] Gastroenterology. 2007 Jun;132(7):2412-21 [17570215.001]
  • [Cites] Am J Pathol. 1998 Jan;152(1):135-44 [9422531.001]
  • [Cites] Int J Cancer. 2008 Mar 15;122(6):1303-10 [18000824.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1996 Jun;5(6):457-9 [8781742.001]
  • [Cites] Aliment Pharmacol Ther. 2007 Jun 1;25(11):1253-69 [17509094.001]
  • [Cites] Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):659-65 [17255290.001]
  • [Cites] Am J Clin Pathol. 2002 Apr;117(4):558-66 [11939730.001]
  • [Cites] Am J Gastroenterol. 2007 Sep;102(9):1853-61 [17509033.001]
  • [Cites] Eur J Cancer. 2007 Mar;43(5):947-54 [17236756.001]
  • [Cites] Gut. 2006 Oct;55(10):1390-7 [16682429.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 May 24;102(21):7565-70 [15894614.001]
  • [Cites] Gastroenterology. 1992 Apr;102(4 Pt 1):1400-2 [1551547.001]
  • [Cites] Cancer. 2005 Aug 15;104(4):730-9 [15971196.001]
  • [Cites] Carcinogenesis. 2007 Feb;28(2):488-96 [16990345.001]
  • [Cites] J Gastroenterol. 2003;38(1):14-22 [12560917.001]
  • [Cites] Cancer Detect Prev. 2006;30(5):423-31 [17064856.001]
  • [Cites] PLoS Med. 2007 Feb;4(2):e67 [17326708.001]
  • [Cites] Gut. 2007 Dec;56(12):1678-84 [17785370.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):551-4 [12576417.001]
  • [Cites] Scand J Gastroenterol. 2008;43(5):524-30 [18415743.001]
  • [Cites] Carcinogenesis. 2007 Jan;28(1):136-42 [16905748.001]
  • [Cites] Gastroenterology. 1994 Jun;106(6):1589-95 [8194706.001]
  • [Cites] Cancer Genet Cytogenet. 1989 Oct 15;42(2):281-6 [2790761.001]
  • [Cites] World J Gastroenterol. 2008 Feb 21;14 (7):1044-52 [18286686.001]
  • [Cites] Br J Cancer. 2008 Mar 25;98(6):1102-8 [18349821.001]
  • [Cites] Int J Cancer. 2001 Jul 20;95(4):240-6 [11400117.001]
  • [Cites] Carcinogenesis. 2005 Sep;26(9):1536-41 [15878910.001]
  • [Cites] Int J Cancer. 2008 Jul 1;123(1):174-80 [18386788.001]
  • [Cites] Gut. 2007 Jun;56(6):763-71 [17145738.001]
  • [Cites] Cancer Res. 2004 Mar 1;64(5):1561-9 [14996709.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8284-9 [11719461.001]
  • [Cites] Gastroenterology. 1996 Nov;111(5):1200-5 [8898633.001]
  • [Cites] Gastroenterology. 2005 Oct;129(4):1274-81 [16230080.001]
  • [Cites] Dis Esophagus. 2007;20(1):36-41 [17227308.001]
  • [Cites] Mutagenesis. 2004 Jul;19(4):319-24 [15215332.001]
  • [Cites] Gut. 2008 Jun;57(6):727-33 [17895354.001]
  • [Cites] Am J Gastroenterol. 1999 May;94(5):1172-8 [10235188.001]
  • [Cites] Carcinogenesis. 2007 Jun;28(6):1254-8 [17264068.001]
  • [Cites] Lancet Oncol. 2001 Mar;2(3):149-56 [11902565.001]
  • [Cites] Gastroenterology. 2002 May;122(6):1569-91 [12016424.001]
  • [Cites] J Natl Cancer Inst. 1999 Dec 15;91(24):2087-95 [10601379.001]
  • [Cites] Gastroenterology. 2003 Mar;124(3):615-25 [12612900.001]
  • [Cites] Oncogene. 1999 Nov 22;18(49):6853-66 [10602461.001]
  • [Cites] Clin Cancer Res. 2005 Apr 1;11(7):2478-85 [15814623.001]
  • [Cites] Am J Gastroenterol. 2004 Nov;99(11):2107-14 [15554988.001]
  • [Cites] Front Biosci. 2006 Sep 01;11:2336-48 [16720317.001]
  • [Cites] Int J Cancer. 2004 Aug 20;111(2):224-8 [15197775.001]
  • [Cites] Endoscopy. 2008 Dec;40(12):1008-15 [19065484.001]
  • [Cites] J Cell Mol Med. 2009 Feb;13(2):398-409 [18410530.001]
  • [Cites] Clin Gastroenterol Hepatol. 2005 Jan;3(1):1-10 [15645398.001]
  • [Cites] Gastroenterology. 1996 Feb;110(2):614-21 [8566611.001]
  • [Cites] BMC Public Health. 2008 Jun 05;8:200 [18533989.001]
  • [Cites] Cell. 2004 Jan 23;116(2):235-46 [14744434.001]
  • [Cites] Am J Gastroenterol. 2008 Feb;103(2):443-9 [17925001.001]
  • [Cites] Nat Genet. 1999 May;22(1):106-9 [10319873.001]
  • [Cites] Nat Genet. 1998 Sep;20(1):58-61 [9731532.001]
  • [Cites] Dis Esophagus. 2004;17(4):322-7 [15569371.001]
  • [Cites] Gut. 2006 Nov;55(11):1538-44 [16785284.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3414-27 [15150093.001]
  • [Cites] Am J Gastroenterol. 2007 Nov;102(11):2373-9 [17581270.001]
  • [Cites] Cancer Lett. 2004 Aug 30;212(2):241-51 [15279904.001]
  • [Cites] Gastroenterology. 2001 Jun;120(7):1630-9 [11375945.001]
  • [Cites] Int J Cancer. 2006 Jul 15;119(2):264-8 [16477636.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1993 Jul-Aug;2(4):397-9 [8348064.001]
  • [Cites] Gastroenterology. 1998 Jul;115(1):19-27 [9649454.001]
  • [Cites] Cancer Res. 1992 May 15;52(10):2946-50 [1581911.001]
  • [Cites] Dev Biol. 2006 Nov 15;299(2):478-88 [16982047.001]
  • [Cites] Eur J Surg Oncol. 2005 Sep;31(7):755-9 [15979837.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 21;102(25):8905-9 [15956212.001]
  • [Cites] Hum Pathol. 1988 Aug;19(8):942-8 [3402983.001]
  • [Cites] Am J Gastroenterol. 2000 Jul;95(7):1669-76 [10925966.001]
  • [Cites] Nat Rev Genet. 2007 Apr;8(4):286-98 [17339880.001]
  • [Cites] Gastroenterology. 1997 Aug;113(2):478-86 [9247467.001]
  • [Cites] Dev Biol. 2005 Mar 1;279(1):125-41 [15708563.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2007 Jul;293(1):G45-53 [17615180.001]
  • [Cites] Gastroenterology. 2006 Apr;130(4):1191-206 [16618413.001]
  • [Cites] Clin Cancer Res. 2004 Jul 15;10(14):4784-92 [15269153.001]
  • [Cites] J Hum Genet. 2007;52(6):527-34 [17476458.001]
  • [Cites] Gut. 2005 May;54(5):710-7 [15831922.001]
  • [Cites] Gastroenterology. 2007 Aug;133(2):403-11 [17681161.001]
  • [Cites] J Natl Cancer Inst. 2000 Nov 15;92(22):1805-11 [11078757.001]
  • [Cites] Gut. 2008 Aug;57(8):1041-8 [18305067.001]
  • [Cites] J Cell Sci. 2003 Apr 15;116(Pt 8):1429-36 [12640028.001]
  • [Cites] Histopathology. 2000 Sep;37(3):241-9 [10971700.001]
  • [Cites] Gastroenterology. 2002 Apr;122(4):1101-12 [11910360.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2560-6 [12855631.001]
  • [Cites] Biomarkers. 2003 Nov-Dec;8(6):509-21 [15195681.001]
  • [Cites] Ann Intern Med. 1985 Jul;103(1):52-4 [4003988.001]
  • [Cites] J Cell Sci. 2002 May 1;115(Pt 9):1783-9 [11956310.001]
  • [Cites] Mol Carcinog. 2006 Oct;45(10):786-94 [16921482.001]
  • [Cites] Gastroenterology. 2001 Dec;121(6):1286-93 [11729107.001]
  • [Cites] Hum Pathol. 2003 Oct;34(10):965-7 [14608528.001]
  • [Cites] Gastrointest Endosc. 2007 Aug;66(2):219-24 [17643692.001]
  • [Cites] Genes Dev. 2005 Apr 15;19(8):877-90 [15833914.001]
  • [Cites] Differentiation. 2006 Sep;74(7):422-37 [16916379.001]
  • [Cites] Carcinogenesis. 2003 Dec;24(12):1951-60 [12970071.001]
  • [Cites] Cancer Res. 1992 Dec 15;52(24):6735-40 [1458460.001]
  • [Cites] J Anat. 1952 Oct;86(4):431-42 [12999645.001]
  • [Cites] Eur J Cancer. 2007 Oct;43(15):2144-52 [17764928.001]
  • [Cites] J Biol Chem. 1995 Dec 29;270(52):31315-20 [8537402.001]
  • [Cites] J Pediatr Surg. 2003 Jan;38(1):29-36; discussion 29-36 [12592614.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3221-5 [8475062.001]
  • [Cites] Gut. 2008 Apr;57(4):448-54 [18178609.001]
  • [Cites] Cancer Genet Cytogenet. 1998 Oct 1;106(1):11-7 [9772903.001]
  • [Cites] Int J Cancer. 2008 Nov 15;123(10):2331-6 [18729198.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2008 Aug;295(2):G211-8 [18556417.001]
  • [Cites] Gut. 2005 Nov;54(11):1527-35 [16227357.001]
  • [Cites] Clin Cancer Res. 2006 Oct 15;12(20 Pt 1):5936-43 [17062664.001]
  • [Cites] J Natl Cancer Inst. 2003 May 21;95(10):750-7 [12759393.001]
  • [Cites] J Clin Oncol. 2002 Jul 1;20(13):2971-9 [12089227.001]
  • [Cites] Gastroenterology. 2005 Dec;129(6):1825-31 [16344051.001]
  • [Cites] Gut. 2006 Jan;55(1):16-25 [16118348.001]
  • [Cites] Nat Genet. 2007 Feb;39(2):232-6 [17200670.001]
  • [Cites] Gastroenterology. 2008 Aug;135(2):370-9 [18538141.001]
  • [Cites] PLoS One. 2008;3(10):e3534 [18953412.001]
  • [Cites] Mol Carcinog. 2008 Apr;47(4):275-85 [17849424.001]
  • [Cites] Carcinogenesis. 2007 Jun;28(6):1323-8 [17277236.001]
  • [Cites] Surg Endosc. 2006 Feb;20(2):235-8 [16391958.001]
  • [Cites] Gut. 2006 Apr;55(4):442 [16531521.001]
  • [Cites] Int J Cancer. 2002 Dec 20;102(6):551-5 [12447994.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Sep;15(9):1668-73 [16985029.001]
  • [Cites] Oncogene. 2008 Nov 24;27(55):6920-9 [19029934.001]
  • [Cites] J Natl Cancer Inst. 2008 Aug 20;100(16):1184-7 [18695138.001]
  • [Cites] Oncogene. 2006 Jun 1;25(23):3346-56 [16449976.001]
  • [Cites] Int J Cancer. 2007 Sep 1;121(5):929-37 [17582597.001]
  • [Cites] Thorax. 1973 Jul;28(4):511-4 [4741456.001]
  • [Cites] Cancer Sci. 2008 Jan;99(1):46-53 [18005197.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] Am J Epidemiol. 2008 Aug 1;168(3):237-49 [18550563.001]
  • [Cites] J Med Genet. 2003 Sep;40(9):651-6 [12960209.001]
  • [Cites] Gastroenterology. 2007 Oct;133(4):1198-209 [17919494.001]
  • [Cites] Clin Cancer Res. 2008 Oct 15;14(20):6440-8 [18927283.001]
  • [Cites] Neoplasia. 2006 Nov;8(11):949-55 [17132227.001]
  • [Cites] Gut. 2002 Sep;51(3):323-8 [12171951.001]
  • [Cites] Oncogene. 2006 May 18;25(21):3084-92 [16407829.001]
  • [Cites] DNA Repair (Amst). 2007 Aug 1;6(8):1079-99 [17485253.001]
  • [Cites] Int J Cancer. 1996 Mar 28;66(1):48-54 [8608965.001]
  • [Cites] Gut. 2007 Nov;56(11):1512-21 [17604323.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Feb;157(1):82-6 [15676154.001]
  • [Cites] Oncogene. 2005 Jun 9;24(25):4138-48 [15824739.001]
  • [Cites] Nat Clin Pract Gastroenterol Hepatol. 2005 Jul;2(7):323-30 [16265286.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2007 Jul;293(1):G19-24 [17395902.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Mar;17(3):727-31 [18349295.001]
  • [Cites] Am J Gastroenterol. 2003 Jul;98(7):1627-33 [12873590.001]
  • [Cites] Am J Gastroenterol. 2001 Apr;96(4):990-6 [11316217.001]
  • [Cites] Cancer Res. 2006 Oct 1;66(19):9583-90 [17018615.001]
  • [Cites] Gastroenterology. 1997 Nov;113(5):1449-56 [9352846.001]
  • [Cites] Aliment Pharmacol Ther. 2004 Oct;20 Suppl 5:48-54; discussion 61-2 [15456464.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Aug;15(8):1451-7 [16896031.001]
  • [Cites] Gut. 2003 Aug;52(8):1085-9 [12865263.001]
  • [Cites] Ann N Y Acad Sci. 2002 Apr;959:24-9 [11976182.001]
  • [Cites] Gastroenterology. 1999 Mar;116(3):702-31 [10029630.001]
  • [Cites] Virchows Arch. 2011 Dec;459(6):581-6 [22081106.001]
  • [Cites] Cell Stem Cell. 2008 Jan 10;2(1):72-82 [18371423.001]
  • [Cites] Gastroenterology. 2001 Jun;120(7):1607-19 [11375943.001]
  • [Cites] Anticancer Res. 2007 May-Jun;27(3A):1285-94 [17593621.001]
  • [Cites] Gut. 2005 Jun;54(6):875-84 [15888799.001]
  • [Cites] Gastroenterology. 1996 Nov;111(5):1192-9 [8898632.001]
  • [Cites] Hum Pathol. 2009 Jan;40(1):65-74 [18755496.001]
  • [Cites] Hum Pathol. 1999 Dec;30(12):1508-14 [10667431.001]
  • [Cites] J Natl Cancer Inst. 2000 Aug 16;92(16):1316-21 [10944553.001]
  • [Cites] Gastroenterology. 2002 Jan;122(1):55-9 [11781280.001]
  • (PMID = 19365640.001).
  • [ISSN] 1432-1203
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 220
  •  go-up   go-down


59. Chang SC, Liao JW, Wong ML, Lai YS, Liu CI: Mammary carcinoma with sebaceous differentiation in a dog. Vet Pathol; 2007 Jul;44(4):525-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Microscopically, the tumors were composed of two distinctive neoplastic components, intraductal papillary adenocarcinoma and sebaceous carcinoma.
  • The cells with abundant foamy cytoplasm that resembled sebaceous cells were also found within the intraductal papillary-like nests of mammary carcinoma, providing evidence of sebaceous metaplasia.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17606516.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


60. Roa I, de Aretxabala X, Araya JC, Roa J: Preneoplastic lesions in gallbladder cancer. J Surg Oncol; 2006 Jun 15;93(8):615-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Metaplasia, dysplasia, and CIS are present in the mucosa adjacent to the cancer in 66%, 81.3%, and 69%, respectively.
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Carcinoma / pathology. Cell Transformation, Neoplastic / pathology. Disease Progression. Female. Humans. Hyperplasia. Male. Metaplasia. Middle Aged

  • MedlinePlus Health Information. consumer health - Gallbladder Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16724345.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 86
  •  go-up   go-down


61. Abiko K, Baba T, Ogawa M, Mikami Y, Koyama T, Mandai M, Konishi I: Minimal deviation mucinous adenocarcinoma ('adenoma malignum') of the uterine corpus. Pathol Int; 2010 Jan;60(1):42-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Minimal deviation mucinous adenocarcinoma ('adenoma malignum') of the uterine corpus.
  • Primary mucinous adenocarcinomas of the uterine corpus are typically low grade and frequently associated with endometrial hyperplasia and/or ordinary endometrioid adenocarcinoma, but may appear as a heterogeneous group of neoplasms.
  • Microscopic examination of hysterectomy specimens indicated highly differentiated mucinous adenocarcinoma diffusely infiltrating the portion of adenomyosis of the corpus.
  • In some areas endometrial glands of adenomyosis were replaced by benign-looking mucinous metaplasia.
  • HIK1083 and MUC6 immunohistochemistry indicated a gastric phenotype of the tumor, as seen in cases of prototypical minimal deviation adenocarcinoma (MDA) of the cervix.
  • In summary, mucinous endometrial adenocarcinoma rarely shows features similar to MDA of the cervix.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Uterine Cervical Neoplasms / pathology. Uterine Neoplasms / pathology


62. McElholm AR, McKnight AJ, Patterson CC, Johnston BT, Hardie LJ, Murray LJ, Finbar Group: A population-based study of IGF axis polymorphisms and the esophageal inflammation, metaplasia, adenocarcinoma sequence. Gastroenterology; 2010 Jul;139(1):204-12.e3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A population-based study of IGF axis polymorphisms and the esophageal inflammation, metaplasia, adenocarcinoma sequence.
  • Few studies have examined the relationship between genetic variation of this axis and esophageal adenocarcinoma (EAC) or its precursors.
  • [MeSH-major] Adenocarcinoma / genetics. Esophageal Neoplasms / genetics. Esophagitis / genetics. Esophagus / pathology. Polymorphism, Single Nucleotide
  • [MeSH-minor] Female. Humans. Insulin-Like Growth Factor I / genetics. Male. Metaplasia. Middle Aged

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20403354.001).
  • [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] 67763-96-6 / Insulin-Like Growth Factor I
  •  go-up   go-down


63. Bao H, Boussioutas A, Reynolds J, Russell S, Gu M: Imaging of goblet cells as a marker for intestinal metaplasia of the stomach by one-photon and two-photon fluorescence endomicroscopy. J Biomed Opt; 2009 Nov-Dec;14(6):064031
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imaging of goblet cells as a marker for intestinal metaplasia of the stomach by one-photon and two-photon fluorescence endomicroscopy.
  • Goblet cells are a requirement for the diagnosis of intestinal metaplasia of the stomach.
  • The appearance of goblet cells in gastric epithelium is an indicator of potential malignant progression toward adenocarcinoma.
  • Therefore, in vivo three-dimensional imaging of goblet cells is essential for diagnoses of a premalignant stage of gastric cancers called intestinal metaplasia.
  • We used mouse intestine, which has goblet cells, as a model of intestinal metaplasia.
  • [MeSH-minor] Animals. Fluorescein. Imaging, Three-Dimensional / methods. Metaplasia / pathology. Mice. Precancerous Conditions / pathology. Stomach Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Endoscopy.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUORESCEIN .
  • Hazardous Substances Data Bank. D&C Yellow No. 8 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20059269.001).
  • [ISSN] 1560-2281
  • [Journal-full-title] Journal of biomedical optics
  • [ISO-abbreviation] J Biomed Opt
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] TPY09G7XIR / Fluorescein
  •  go-up   go-down


64. Singh R, Ragunath K, Jankowski J: Barrett's Esophagus: Diagnosis, Screening, Surveillance, and Controversies. Gut Liver; 2007 Dec;1(2):93-100
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Barrett's Esophagus: Diagnosis, Screening, Surveillance, and Controversies.
  • The incidence of Barrett's metaplasia and Barrett's adenocarcinoma has been increasing, but the prognosis of Barrett's adenocarcinoma is worse because individuals present at a late stage.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Aliment Pharmacol Ther. 2007 Aug 1;26(3):501-7 [17635385.001]
  • [Cites] Gastrointest Endosc. 2006 Aug;64(2):167-75 [16860063.001]
  • [Cites] Gastroenterology. 1988 Jan;94(1):81-90 [3335302.001]
  • [Cites] J Thorac Cardiovasc Surg. 1994 Nov;108(5):813-21; discussion 821-2 [7967662.001]
  • [Cites] J Thorac Cardiovasc Surg. 1993 Mar;105(3):383-7; discussion 387-8 [8445916.001]
  • [Cites] Gut. 1996 Jul;39(1):5-8 [8881798.001]
  • [Cites] Cancer. 1998 Nov 15;83(10):2049-53 [9827707.001]
  • [Cites] Gastrointest Endosc. 1999 Mar;49(3 Pt 2):S12-6 [10049441.001]
  • [Cites] Am J Gastroenterol. 1999 Aug;94(8):2043-53 [10445526.001]
  • [Cites] Am J Gastroenterol. 2000 Dec;95(12):3383-7 [11151865.001]
  • [Cites] Am J Gastroenterol. 2007 Jan;102(1):21-3 [17266685.001]
  • [Cites] Hum Pathol. 2001 Apr;32(4):368-78 [11331953.001]
  • [Cites] Am J Gastroenterol. 2001 May;96(5):1355-62 [11374668.001]
  • [Cites] Gastroenterology. 2001 Jun;120(7):1630-9 [11375945.001]
  • [Cites] Gastrointest Endosc. 2001 Sep;54(3):294-301 [11522968.001]
  • [Cites] Gastrointest Endosc. 2002 May;55(6):641-7 [11979244.001]
  • [Cites] Gastrointest Endosc. 2002 Oct;56(4):479-87 [12297761.001]
  • [Cites] Lasers Surg Med. 2003;32(1):10-6 [12516065.001]
  • [Cites] Endoscopy. 2003 Dec;35(12):998-1003 [14648410.001]
  • [Cites] J Biomed Opt. 2004 May-Jun;9(3):568-77 [15189095.001]
  • [Cites] Gastrointest Endosc. 2005 May;61(6):671-8 [15855970.001]
  • [Cites] Gastroenterology. 2005 May;128(5):1468-70 [15887128.001]
  • [Cites] Endoscopy. 2005 Oct;37(10):929-36 [16189764.001]
  • [Cites] Gut. 2006 Apr;55(4):442 [16531521.001]
  • [Cites] Gastrointest Endosc. 2006 Aug;64(2):155-66 [16860062.001]
  • [Cites] Gastroenterology. 2006 Nov;131(5):1392-9 [17101315.001]
  • [Cites] Gastrointest Endosc. 2007 Jan;65(1):36-46 [17185078.001]
  • [Cites] Am J Gastroenterol. 2007 Jun;102(6):1154-61 [17433019.001]
  • [Cites] Gastroenterology. 1990 Oct;99(4):918-22 [2394347.001]
  • [Cites] Gastrointest Endosc. 1994 Nov-Dec;40(6):747-9 [7859976.001]
  • [Cites] Gastrointest Endosc. 1996 Jul;44(1):1-7 [8836709.001]
  • [Cites] Am J Gastroenterol. 1998 Jul;93(7):1028-32 [9672324.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] Am J Gastroenterol. 2000 Jul;95(7):1669-76 [10925966.001]
  • [Cites] Gastrointest Endosc. 2001 Jan;53(1):47-52 [11154488.001]
  • [Cites] Gastroenterology. 2001 Jun;120(7):1607-19 [11375943.001]
  • [Cites] Gastrointest Endosc. 2001 Sep;54(3):289-93 [11522967.001]
  • [Cites] Am J Gastroenterol. 2002 Aug;97(8):1888-95 [12190150.001]
  • [Cites] Gut. 2003 Jan;52(1):24-7 [12477754.001]
  • [Cites] Aliment Pharmacol Ther. 2003 May 15;17(10):1319-24 [12755845.001]
  • [Cites] Arch Pathol Lab Med. 2005 Feb;129(2):177-80 [15679415.001]
  • [Cites] Gastrointest Endosc. 2005 May;61(6):679-85 [15855971.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2005 Dec;19(6):889-907 [16338648.001]
  • [Cites] Aliment Pharmacol Ther. 2006 Mar 15;23(6):735-42 [16556175.001]
  • [Cites] Gastrointest Endosc. 1989 Nov-Dec;35(6):541-4 [2480927.001]
  • (PMID = 20485625.001).
  • [ISSN] 2005-1212
  • [Journal-full-title] Gut and liver
  • [ISO-abbreviation] Gut Liver
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2871632
  • [Keywords] NOTNLM ; Barrett's esophagus / Gastroesophageal reflux
  •  go-up   go-down


65. Parenti A, Leo G, Porzionato A, Zaninotto G, Rosato A, Ninfo V: Expression of survivin, p53, and caspase 3 in Barrett's esophagus carcinogenesis. Hum Pathol; 2006 Jan;37(1):16-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The aim of this study was to investigate, in the intestinal metaplasia-dysplasia-carcinoma sequence, the role of survivin, an inhibitor of apoptosis; the p53 protein, a tumor suppressor gene involved in cell cycle control; and caspase 3, a protease-inducing apoptosis and inhibited by survivin.
  • Immunohistochemical expression was tested in 40 cases of BE, including 11 low-grade and 19 high-grade dysplasias (HGD), and samples were obtained from 40 surgical specimens of esophagectomy performed for HGD or Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Caspases / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Tumor Suppressor Protein p53 / metabolism

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16360411.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
  •  go-up   go-down


66. McGowan CE, Lagares-Garcia JA, Bhattacharya B: Retained capsule endoscope leading to the identification of small bowel adenocarcinoma in a patient with undiagnosed Crohn disease. Ann Diagn Pathol; 2009 Dec;13(6):390-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Retained capsule endoscope leading to the identification of small bowel adenocarcinoma in a patient with undiagnosed Crohn disease.
  • Subsequent laparoscopy led to the identification of severe, active Crohn disease with strictures, ulcers, crypt abscesses, pyloric metaplasia, and transmural inflammation.
  • Extensive flat and polypoid high- and low-grade dysplasia were present, as well as an area of well-differentiated adenocarcinoma invading into the muscularis propria.
  • We discuss the epidemiology, pathogenesis, and diagnosis of small bowel malignancy.
  • [MeSH-major] Adenocarcinoma / diagnosis. Capsule Endoscopy. Crohn Disease / diagnosis. Ileal Neoplasms / diagnosis
  • [MeSH-minor] Abdominal Pain / diagnosis. Abdominal Pain / etiology. Aged. Humans. Male. Neoplasm Staging. Staining and Labeling. Treatment Outcome


67. Cameselle-Teijeiro J, Alberte-Lista L, Chiarelli S, Buriticá C, Gonçalves L, González-Cámpora R, Nogales FF: CD10 is a characteristic marker of tumours forming morules with biotin-rich, optically clear nuclei that occur in different organs. Histopathology; 2008 Feb;52(3):389-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adenocarcinoma, Papillary / chemistry. Adenocarcinoma, Papillary / pathology. Female. Humans. Lung Neoplasms / chemistry. Lung Neoplasms / pathology. Metaplasia / pathology. Pancreatic Neoplasms / chemistry. Pancreatic Neoplasms / pathology. Pulmonary Blastoma / chemistry. Pulmonary Blastoma / pathology. Thyroid Neoplasms / chemistry. Thyroid Neoplasms / pathology

  • Hazardous Substances Data Bank. BIOTIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18081818.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 6SO6U10H04 / Biotin; EC 3.4.24.11 / Neprilysin
  •  go-up   go-down


68. Resnick MB, Gavilanez M, Newton E, Konkin T, Bhattacharya B, Britt DE, Sabo E, Moss SF: Claudin expression in gastric adenocarcinomas: a tissue microarray study with prognostic correlation. Hum Pathol; 2005 Aug;36(8):886-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In addition, cores of normal mucosa and intestinal metaplasia were taken from most cases.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biomarkers, Tumor / analysis. Membrane Proteins / biosynthesis. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16112005.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 5 P20 RR017596-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / Phosphoproteins; 0 / TJP1 protein, human; 0 / Zonula Occludens-1 Protein
  •  go-up   go-down


69. Ogawa M, Nomura S, Varro A, Wang TC, Goldenring JR: Altered metaplastic response of waved-2 EGF receptor mutant mice to acute oxyntic atrophy. Am J Physiol Gastrointest Liver Physiol; 2006 Apr;290(4):G793-804
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Metaplastic cell lineages are putative precursors for the development of gastric adenocarcinoma.
  • The loss of parietal cells (oxyntic atrophy) is the initiating step in the evolution of gastric fundic mucosal lineage changes including metaplasia and hyperplasia.
  • DMP-777 elicits a rapid loss of parietal cells followed by the emergence of foveolar hyperplasia and spasmolytic polypeptide (SP)-expressing metaplasia (SPEM).
  • These results suggest that SP/TFF2 does not impact on the development of metaplasia after the induction of parietal cell loss.
  • The results support a role for EGF receptor ligands in the regulation of gastric metaplasia.

  • 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 .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16306133.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1-P50-CA-95103
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; 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 / Azetidines; 0 / DMP 777; 0 / Mucins; 0 / Muscle Proteins; 0 / Peptides; 0 / Piperazines; 0 / TFF2 protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


70. Miller CT, Lin L, Casper AM, Lim J, Thomas DG, Orringer MB, Chang AC, Chambers AF, Giordano TJ, Glover TW, Beer DG: Genomic amplification of MET with boundaries within fragile site FRA7G and upregulation of MET pathways in esophageal adenocarcinoma. Oncogene; 2006 Jan 19;25(3):409-18
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic amplification of MET with boundaries within fragile site FRA7G and upregulation of MET pathways in esophageal adenocarcinoma.
  • Esophageal adenocarcinoma (EA) is characterized by a poor prognosis making the identification of clinically targetable proteins essential for improving patient outcome.
  • Microarray analysis of Barrett's metaplasia, dysplasia, and EA revealed overexpression of the MET oncogene in EAs but only those with MET gene amplification.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosome Fragile Sites. Esophageal Neoplasms / genetics. Gene Amplification. Proto-Oncogene Proteins / genetics. Receptors, Growth Factor / genetics. Up-Regulation


71. Varela JE: Barrett's esophagus: a late complication of laparoscopic adjustable gastric banding. Obes Surg; 2010 Feb;20(2):244-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Barrett's esophagus or esophageal intestinal metaplasia is a known complication of chronic gastro-esophageal reflux disease that, in rare occasions, progresses to dysplasia and esophageal adenocarcinoma.

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • MedlinePlus Health Information. consumer health - GERD.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Surg Obes Relat Dis. 2009 Mar-Apr;5(2):150-5 [18849200.001]
  • [Cites] Dis Esophagus. 2000;13(1):5-11 [11005324.001]
  • [Cites] Surg Obes Relat Dis. 2008 Jan-Feb;4(1):1-4; discussion 4-5 [18069070.001]
  • [Cites] Obes Surg. 2005 May;15(5):710-2 [15946466.001]
  • [Cites] Ann Thorac Surg. 2006 Nov;82(5):1910-3 [17062279.001]
  • [Cites] Surg Obes Relat Dis. 2009 Jan-Feb;5(1):72-6 [19161936.001]
  • [Cites] Arch Surg. 2005 Jul;140(7):639-43 [16027327.001]
  • [Cites] Obes Surg. 1996 Apr;6(2):155-158 [10729857.001]
  • [Cites] J Gastrointest Surg. 2006 Feb;10(2):259-64 [16455459.001]
  • [Cites] Surg Obes Relat Dis. 2008 Nov-Dec;4(6):735-9 [18586570.001]
  • [Cites] Surg Endosc. 2004 Jan;18(1):60-3 [14625728.001]
  • [Cites] Surg Obes Relat Dis. 2008 Nov-Dec;4(6):740-7 [18539539.001]
  • (PMID = 19997783.001).
  • [ISSN] 1708-0428
  • [Journal-full-title] Obesity surgery
  • [ISO-abbreviation] Obes Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


72. Nakanuma Y, Zen Y, Harada K, Ikeda H, Sato Y, Uehara T, Sasaki M: Tumorigenesis and phenotypic characteristics of mucin-producing bile duct tumors: an immunohistochemical approach. J Hepatobiliary Pancreat Sci; 2010 May;17(3):211-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Aberrant expression of CDX2 with MUC2 and CK20 is related to the development of intestinal metaplasia.
  • Decreased expression of membranous beta-catenin and E-cadherin and aberrant expression of MMP-7 and -9 and of MUC1 are related to invasion of IPNB with tubular adenocarcinoma, whereas MUC2 is involved in the invasion of IPNB with mucinous carcinoma.
  • [MeSH-minor] Adenocarcinoma, Mucinous / pathology. Cadherins / metabolism. Cholangiocarcinoma. Cyclin D1 / metabolism. Disease Progression. Homeodomain Proteins / metabolism. Humans. Immunohistochemistry. Keratin-20 / metabolism. Matrix Metalloproteinase 7 / metabolism. Matrix Metalloproteinase 9 / metabolism. Mucin-1 / metabolism. Mucin-2 / metabolism. Neoplasm Invasiveness / pathology. Pancreatic Neoplasms / pathology. Phenotype. beta Catenin / metabolism

  • MedlinePlus Health Information. consumer health - Bile Duct Cancer.
  • COS Scholar Universe. author profiles.
  • 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 .
  • 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 = 19680592.001).
  • [ISSN] 1868-6982
  • [Journal-full-title] Journal of hepato-biliary-pancreatic sciences
  • [ISO-abbreviation] J Hepatobiliary Pancreat Sci
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Cadherins; 0 / Homeodomain Proteins; 0 / Keratin-20; 0 / MUC1 protein, human; 0 / MUC2 protein, human; 0 / Mucin-1; 0 / Mucin-2; 0 / Mucins; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 3.4.24.23 / Matrix Metalloproteinase 7; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Number-of-references] 56
  •  go-up   go-down


73. Ponsot P: [Barrett's oesophagus: endoscopic diagnosis and follow-up]. Ann Chir; 2006 Jan;131(1):3-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Barrett's oesophagus: endoscopic diagnosis and follow-up].
  • Barrett's oesophagus (BO), or replacement of the squamous mucosa by a specialized intestinal metaplasia due to gastro-oesophageal reflux disease (GORD), predisposes to adenocarcinoma.
  • Macroscopic diagnosis of BO is sometimes difficult and, in case of doubt, endoscopy should be redone after a period of efficient anti-secretory treatment.
  • Diagnosis of BO is histological and should be confirmed by biopsies.
  • The incidence of adenocarcinoma is globally estimated at 0.5% patient by year of follow-up, and exists for both short and long BO.
  • Due to this low incidence, screening for BO is only justified in patients at high risk for adenocarcinoma (male gender, age > 50 ans, old GORD in a young patient).
  • Low-grade dysplasia (LGD) then high-grade dysplasia (HGD) precedes adenocarcinoma.
  • Histological diagnosis of LGD is difficult: the main cause of confusion is inflammation so diagnosis of LGD must be confirmed after a 3-month high-dose anti-secretory treatment.
  • Diagnosis of HGD is easier but multiple biopsies are needed to determine the focal or multifocal disposition of HGD.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / diagnosis. Endoscopy, Gastrointestinal. Esophageal Neoplasms / etiology
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Gastroesophageal Reflux / complications. Humans. Prognosis. Risk Factors

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16376849.001).
  • [ISSN] 0003-3944
  • [Journal-full-title] Annales de chirurgie
  • [ISO-abbreviation] Ann Chir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 16
  •  go-up   go-down


74. Futagami S, Hiratsuka T, Shindo T, Horie A, Hamamoto T, Suzuki K, Kusunoki M, Miyake K, Gudis K, Crowe SE, Tsukui T, Sakamoto C: Expression of apurinic/apyrimidinic endonuclease-1 (APE-1) in H. pylori-associated gastritis, gastric adenoma, and gastric cancer. Helicobacter; 2008 Jun;13(3):209-18
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: APE-1 mRNA and protein expression were determined in H. pylori (CagA+) water-extract protein (HPWEP)-stimulated MKN-28 cells, gastric adenocarcinoma cell-line (AGS) cells, and human peripheral macrophages by real-time polymerase chain reaction and Western blot analysis.
  • In human tissues, APE-1 expression in H. pylori-infected gastritis without goblet cell metaplasia was significantly increased as compared to that in tissues from uninfected subjects.

  • MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • 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 = 18466396.001).
  • [ISSN] 1523-5378
  • [Journal-full-title] Helicobacter
  • [ISO-abbreviation] Helicobacter
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK061769
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 4.2.99.18 / APEX1 protein, human; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase
  •  go-up   go-down


75. Takubo K, Vieth M, Aida J, Sawabe M, Kumagai Y, Hoshihara Y, Arai T: Differences in the definitions used for esophageal and gastric diseases in different countries: endoscopic definition of the esophagogastric junction, the precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus, and histologic criteria for mucosal adenocarcinoma or high-grade dysplasia. Digestion; 2009;80(4):248-57
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences in the definitions used for esophageal and gastric diseases in different countries: endoscopic definition of the esophagogastric junction, the precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus, and histologic criteria for mucosal adenocarcinoma or high-grade dysplasia.
  • METHODS: Here we discuss four such important differences: the definition of the esophagogastric junction (EGJ), the possible precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus (BE), and the histologic criteria for mucosal adenocarcinoma.
  • If an area of columnar-lined esophagus (CLE) is only partially involved by intestinal metaplasia, then the latter cannot always be demonstrated in biopsy specimens.
  • Therefore, we do not think that a definition of BE as CLE with histologic intestinal metaplasia is practical.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis. Gastroenterology / standards. Precancerous Conditions / diagnosis. Terminology as Topic
  • [MeSH-minor] Esophagogastric Junction / pathology. Esophagoscopy. Gastroscopy. Humans. Stomach Neoplasms / diagnosis


76. Trakál E, Guidi A, Butti AL, Trakál JJ, Sambuelli R, Zárate FE: Detection of the risk of adenocarcinoma in Barrett's esophagus by means of tumor markers (p53 and Ki67). Acta Gastroenterol Latinoam; 2010 Sep;40(3):211-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of the risk of adenocarcinoma in Barrett's esophagus by means of tumor markers (p53 and Ki67).
  • The rising incidence of adenocarcinoma in Barrett's esophagus has intensified the research into methods of early recognition of cancer risk, detecting cytological and architectural changes (dysplasia) or using biomarkers as predictive tests.
  • The aim of this paper is to evaluate the involvement of two tumor markers: p53 (tumor suppressor gene) and Ki67 (proliferation marker), by means of immunohistochemical analysis with monoclonal antibodies designed for the specific localization of p53 and Ki67 antigens, in esophageal biopsies with columnar metaplasia of patients with and without dysplasia and adenocarcinoma, and to anticipate which ones are liable to suffer it in the future.
  • Both markers were positive in all intestinal metaplasia patients with high-grade dysplasia and adenocarcinoma, and even in some cases with low grade or without dysplasia.
  • In contrast, in those who have gastric metaplasia, tumor markers were negative.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Biomarkers, Tumor / analysis. Esophageal Neoplasms / pathology. Ki-67 Antigen / analysis. Precancerous Conditions / pathology. Tumor Suppressor Protein p53 / analysis

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • MedlinePlus Health Information. consumer health - Esophageal 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 = 21049770.001).
  • [ISSN] 0300-9033
  • [Journal-full-title] Acta gastroenterologica Latinoamericana
  • [ISO-abbreviation] Acta Gastroenterol. Latinoam.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Argentina
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


77. Fleischer DE, Overholt BF, Sharma VK, Reymunde A, Kimmey MB, Chuttani R, Chang KJ, Lightdale CJ, Santiago N, Pleskow DK, Dean PJ, Wang KK: Endoscopic ablation of Barrett's esophagus: a multicenter study with 2.5-year follow-up. Gastrointest Endosc; 2008 Nov;68(5):867-76
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: For patients with Barrett's esophagus (BE), life-long surveillance endoscopy is recommended because of an elevated risk for developing dysplasia and esophageal adenocarcinoma.
  • PATIENTS: Seventy subjects with 2 to 6 cm of BE and histologic evidence of intestinal metaplasia (IM).

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Gastroenterology. 2009 Jun;136(7):2399-401; discussion 2401-2 [19406136.001]
  • (PMID = 18561930.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00489268
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


78. Bobryshev YV, Tran D, Killingsworth MC, Buckland M, Lord RV: Dendritic cell-associated immune inflammation of cardiac mucosa: a possible factor in the formation of Barrett's esophagus. J Gastrointest Surg; 2009 Mar;13(3):442-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The development of Barrett's esophagus is poorly understood, but it has been suggested that cardiac mucosa is a precursor of intestinal type metaplasia and that inflammation of cardiac mucosa may play a role in the formation of Barrett's esophagus.
  • MATERIAL AND METHODS: Endoscopic biopsy specimens were obtained from 12 patients with cardiac mucosa without Barrett's esophagus or adenocarcinoma and from 21 patients with Barrett's esophagus without dysplasia (intestinal metaplasia).
  • In the Barrett's esophagus specimens that contained cardiac type glands, computerized CD83 expression quantitation revealed that there were more dendritic cells in cardiac mucosa than in intestinal metaplasia.
  • The finding of a larger number of dendritic cells in areas of cardiac mucosa in Barrett's esophagus biopsies suggests that the immune inflammation of cardiac mucosa might play a role in modifying the local tissue environment to promote the development of specialized intestinal type metaplasia.

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Immunol Rev. 2004 Jun;199:9-26 [15233723.001]
  • [Cites] Mod Pathol. 2003 Apr;16(4):316-24 [12692197.001]
  • [Cites] Br J Cancer. 2001 Aug 17;85(4):473-83 [11506482.001]
  • [Cites] Cardiovasc Res. 1998 Mar;37(3):799-810 [9659465.001]
  • [Cites] Biochim Biophys Acta. 2007 Sep;1776(1):10-21 [17618050.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1813-21 [11748282.001]
  • [Cites] Ann Surg. 1997 Dec;226(6):725-33; discussion 733-5 [9409571.001]
  • [Cites] Dis Esophagus. 2007;20(1):36-41 [17227308.001]
  • [Cites] Cell. 2000 Mar 3;100(5):575-85 [10721994.001]
  • [Cites] Arch Histol Cytol. 1995 Aug;58(3):307-22 [8527238.001]
  • [Cites] Immunobiology. 2006;211(6-8):627-32 [16920501.001]
  • [Cites] Trends Immunol. 2008 May;29(5):242-9 [18372215.001]
  • [Cites] J Immunol. 2002 Mar 1;168(5):2118-26 [11859097.001]
  • [Cites] Ann Surg. 1997 Oct;226(4):522-30; discussion 530-2 [9351720.001]
  • [Cites] Mod Pathol. 2004 Oct;17 (10 ):1282-8 [15167938.001]
  • [Cites] Physiol Rev. 2002 Jan;82(1):97-130 [11773610.001]
  • [Cites] Crit Rev Immunol. 2007;27(5):463-83 [18197808.001]
  • [Cites] Adv Cancer Res. 2008;99:363-407 [18037410.001]
  • [Cites] J Leukoc Biol. 1993 Jan;53(1):19-28 [8426088.001]
  • [Cites] Int Arch Allergy Immunol. 2002 Oct;129(2):113-8 [12403928.001]
  • [Cites] Surgery. 2004 Sep;136(3):633-40 [15349112.001]
  • [Cites] J Gastrointest Surg. 2009 Jan;13(1):44-53 [18685901.001]
  • [Cites] Am J Gastroenterol. 2002 Oct;97(10):2514-23 [12385432.001]
  • [Cites] Am J Surg Pathol. 2001 Feb;25(2):245-52 [11176074.001]
  • [Cites] Eur Heart J. 2005 Sep;26(17):1700-4 [15855191.001]
  • [Cites] Br J Cancer. 2005 Mar 14;92(5):888-90 [15756258.001]
  • [Cites] Immunobiology. 2002 Jul;205(3):231-46 [12182451.001]
  • [Cites] Eur J Immunol. 2007 Mar;37(3):634-48 [17266176.001]
  • [Cites] Nature. 1998 Mar 19;392(6673):245-52 [9521319.001]
  • [Cites] J Pathol. 2005 Nov;207(3):269-76 [16177953.001]
  • [Cites] Nature. 2007 Sep 27;449(7161):419-26 [17898760.001]
  • [Cites] Cell. 2002 Mar 22;108(6):755-67 [11955430.001]
  • [Cites] Semin Thorac Cardiovasc Surg. 1997 Jul;9(3):270-8 [9263345.001]
  • [Cites] Nature. 2008 Jul 24;454(7203):436-44 [18650914.001]
  • [Cites] Ann Surg. 2000 Mar;231(3):303-21 [10714623.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Apr;286(4):G515-20 [15010360.001]
  • [Cites] Cell Oncol. 2007;29(6):507-17 [18032827.001]
  • (PMID = 19015928.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


79. Bobryshev YV, Freeman AK, Botelho NK, Tran D, Levert-Mignon AJ, Lord RV: Expression of the putative stem cell marker Musashi-1 in Barrett's esophagus and esophageal adenocarcinoma. Dis Esophagus; 2010 Sep;23(7):580-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of the putative stem cell marker Musashi-1 in Barrett's esophagus and esophageal adenocarcinoma.
  • Cancer stem cells have been identified in several solid tumors, but stem cells in normal human esophagus or in Barrett's esophagus or adenocarcinoma have not been reported.
  • The present study investigated whether Musashi-1 is expressed in the esophagus and its relation to immune inflammation of the mucosa in Barrett's esophagus and esophageal adenocarcinoma.
  • Of these, 15 were esophageal adenocarcinoma, 17 were Barrett's esophagus (10 intestinal metaplasia and 7 dysplasia), and 9 were normal squamous esophagus tissue specimens from patients without esophageal pathology.
  • Musashi-1 expression was present in Barrett's intestinal metaplasia and in dysplastic Barrett's in which the majority of epithelial cells in individual glands expressed this antigen.
  • Expression of Musashi-1 was highest in esophageal adenocarcinoma, where it was most intense in glands that displayed features of early stages of adenocarcinoma formation.
  • In contrast, Musashi-1 staining level was weaker in glands that displayed features of advanced adenocarcinoma.
  • Musashi-1 mRNA expression levels were significantly higher in esophageal adenocarcinoma than in normal esophagus or Barrett's esophagus tissues.
  • Dendritic cell-specific intercellular molecule-3 (ICAM-3)-grabbing nonintegrin (DC-SIGN) mRNA expression levels were significantly increased in both Barrett's tissues and adenocarcinoma tissues.
  • Expression of the putative stem cell marker Musashi-1 is absent in normal squamous epithelium, weak in esophageal cardiac-type glands and Barrett's esophagus, and markedly increased in adenocarcinoma, especially in glands displaying features of early cancer development.
  • Musashi-1 expressing cells may be significant in the etiology of Barrett's esophagus and adenocarcinoma, and perhaps even a cell of origin for this disease.

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 Copyright the Authors. Journal compilation © 2010, Wiley Periodicals, Inc. and the International Society for Diseases of the Esophagus.
  • (PMID = 20459440.001).
  • [ISSN] 1442-2050
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MSI1 protein, human; 0 / Nerve Tissue Proteins; 0 / RNA-Binding Proteins
  •  go-up   go-down


80. Song JH, Kim SG, Jung SA, Lee MK, Jung HC, Song IS: The interleukin-8-251 AA genotype is associated with angiogenesis in gastric carcinogenesis in Helicobacter pylori-infected Koreans. Cytokine; 2010 Aug;51(2):158-65
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Helicobacter pylori (H. pylori) is an important risk factor of gastric adenocarcinoma.
  • Host susceptibility may help to predict H. pylori-infected individuals with a higher risk of gastric adenocarcinoma.
  • The IL-8-251A/T polymorphism was genotyped by PCR-RFLP from a total of 395 subjects; 92 normal controls, 87 H. pylori-infected controls, 108 chronic atrophic gastritis and/or intestinal metaplasia and 108 adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Helicobacter Infections / pathology. Helicobacter pylori. Interleukin-8 / genetics. Neovascularization, Pathologic / genetics. Polymorphism, Genetic. Stomach Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Angiopoietin-1 / metabolism. Asian Continental Ancestry Group / genetics. Disease Progression. Female. Gastric Mucosa / metabolism. Gastritis, Atrophic / genetics. Genetic Predisposition to Disease. Humans. Korea. Male. Matrix Metalloproteinase 9 / metabolism. Metaplasia / pathology. Middle Aged. Vascular Endothelial Growth Factor A / metabolism

  • MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20621718.001).
  • [ISSN] 1096-0023
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANGPT1 protein, human; 0 / Angiopoietin-1; 0 / Interleukin-8; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


81. Sanati S, Huettner P, Ylagan LR: Role of ProExC: a novel immunoperoxidase marker in the evaluation of dysplastic squamous and glandular lesions in cervical specimens. Int J Gynecol Pathol; 2010 Jan;29(1):79-87
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Nine low-grade squamous intraepithelial lesion, 35 high-grade squamous intraepithelial lesion, 23 squamous metaplasia, and 14 adenocarcinoma in situ specimens were retrieved from our hospital files.
  • ProExC had sensitivity, specificity, and positive and negative predictive value of 89%, 100%, 100%, and 82%, respectively, for distinguishing high-grade squamous intraepithelial lesion from squamous metaplasia, and 93%, 100%, 100%, and 98%, respectively, for distinguishing adenocarcinoma in situ from reactive benign endocervix.
  • ProExC is a valuable marker for distinguishing dysplastic squamous and endocervical lesions of the cervix from squamous metaplasia in histologic sections.
  • ProExC may eventually be used in conjunction with morphologic and human papillomavirus evaluation for better classification of indeterminate cervical lesions in Papanicolaou smears.
  • [MeSH-major] Biomarkers, Tumor / analysis. Cervical Intraepithelial Neoplasia / diagnosis. Immunoenzyme Techniques. Uterine Cervical Dysplasia / diagnosis. Uterine Cervical Neoplasms / diagnosis

  • MedlinePlus Health Information. consumer health - Cervical Cancer.
  • International Agency for Research on Cancer - Screening Group. diagnostics - A practical manual on visual screening for cervical neoplasia .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19952938.001).
  • [ISSN] 1538-7151
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; EC 3.6.4.12 / MCM2 protein, human; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 2; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  •  go-up   go-down


82. Shearer CJ, Going JJ, Neilson LJ, Stuart RC: Modified classification for adenocarcinoma of the gastro-oesophageal junction. ANZ J Surg; 2007 Jul;77(7):544-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modified classification for adenocarcinoma of the gastro-oesophageal junction.
  • BACKGROUND: Incidence of the gastro-oesophageal junction adenocarcinoma is increasing.
  • Cytokeratin (CK) 7 and 20 immunophenotypes differentiate Barrett's intestinal metaplasia (IM) from gastric IM.
  • METHODS: In this experimental study, 57 patients with gastro-oesophageal junction adenocarcinoma were subdivided endoscopically into 15 type 1, 26 type 2 and 16 type 3 adenocarcinomas.
  • RESULTS: Intestinal metaplasia was associated with type 1 adenocarcinoma in 12 of 15 patients, 80%; with type 2 in 13 of 26 patients, 50% and type 3 in 6 of 16 patients, 37.5%.
  • Immunostaining within the adenocarcinoma was variable.
  • CK immunostaining may refine Siewert's classification into oesophageal type 1 or gastric type 2 adenocarcinoma with IM.
  • [MeSH-major] Adenocarcinoma / classification. Esophageal Neoplasms / classification. Esophagogastric Junction

  • MedlinePlus Health Information. consumer health - Esophageal 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 = 17610690.001).
  • [ISSN] 1445-1433
  • [Journal-full-title] ANZ journal of surgery
  • [ISO-abbreviation] ANZ J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Keratin-20; 0 / Keratin-7
  •  go-up   go-down


83. Anjarwalla S, Rollason TP, Rooney N, Hirschowitz L: Atypical mucinous metaplasia and intraepithelial neoplasia of the female genital tract--a case report and review of the literature. Int J Gynecol Cancer; 2007 Sep-Oct;17(5):1147-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical mucinous metaplasia and intraepithelial neoplasia of the female genital tract--a case report and review of the literature.
  • Müllerian metaplasia of the female genital tract is usually of limited extent and subtype.
  • Although müllerian metaplasia is well recognized at different sites within the female genital tract, this highly unusual finding of multiple metaplastic epithelial subtypes and dysplasia involving the mucinous metaplastic epithelium along the entire genital tract and pelvic serosal surface has not, to the best of our knowledge, been reported previously in the absence of Peutz-Jeghers syndrome.
  • [MeSH-major] Adenocarcinoma, Mucinous / diagnosis. Genital Neoplasms, Female / diagnosis
  • [MeSH-minor] Female. Humans. Metaplasia / diagnosis. Metaplasia / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17433059.001).
  • [ISSN] 1048-891X
  • [Journal-full-title] International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
  • [ISO-abbreviation] Int. J. Gynecol. Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 16
  •  go-up   go-down


84. Inci K, Edebo A, Olbe L, Casselbrant A: Expression of protease-activated-receptor 2 (PAR-2) in human esophageal mucosa. Scand J Gastroenterol; 2009;44(6):664-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MATERIAL AND METHODS: Distal biopsies taken from healthy controls, patients with erosive reflux disease (ERD), patients with specialized intestinal metaplasia (SIM) and adenocarcinoma were analyzed for the PAR-2 receptor with reverse-transcription polymerase chain reaction (RT-PCR), Western blotting and immunohistochemistry.
  • [MeSH-major] Adenocarcinoma / genetics. Esophageal Neoplasms / genetics. Esophagus / metabolism. Gastroesophageal Reflux / genetics. Mucous Membrane / metabolism. Receptor, PAR-2 / biosynthesis
  • [MeSH-minor] Female. Gene Expression. Humans. Male. Metaplasia / genetics. Metaplasia / pathology. Middle Aged

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - GERD.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19263271.001).
  • [ISSN] 1502-7708
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Receptor, PAR-2
  •  go-up   go-down


85. Lewis JT, Talwalkar JA, Rosen CB, Smyrk TC, Abraham SC: Prevalence and risk factors for gallbladder neoplasia in patients with primary sclerosing cholangitis: evidence for a metaplasia-dysplasia-carcinoma sequence. Am J Surg Pathol; 2007 Jun;31(6):907-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence and risk factors for gallbladder neoplasia in patients with primary sclerosing cholangitis: evidence for a metaplasia-dysplasia-carcinoma sequence.
  • We evaluated the following histologic features: presence of diffuse lymphoplasmacytic chronic cholecystitis, pyloric metaplasia, intestinal metaplasia, dysplasia (low-grade or high-grade), and adenocarcinoma.
  • Gallbladder dysplasia and adenocarcinoma were correlated with several clinicopathologic parameters using Fisher exact test and t test, including:.
  • Lymphoplasmacytic chronic cholecystitis was present in 35 (49%), pyloric metaplasia in 69 (96%), intestinal metaplasia in 36 (50%), dysplasia in 27 (37%; low-grade in 12 and high-grade in 15), and adenocarcinoma in 10 (14%; 2 with lamina propria invasion and 8 with invasion into muscularis or adventitia).
  • The strong correlation between gallbladder dysplasia/adenocarcinoma and bile duct dysplasia/CC supports the concept of a neoplastic "field effect" along the intrahepatic and extrahepatic biliary tract in PSC.
  • [MeSH-major] Adenocarcinoma / epidemiology. Adenocarcinoma / etiology. Cholangitis, Sclerosing / complications. Gallbladder Neoplasms / epidemiology. Gallbladder Neoplasms / etiology

  • Genetic Alliance. consumer health - Primary sclerosing cholangitis.
  • MedlinePlus Health Information. consumer health - Gallbladder Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17527079.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


86. Lurje G, Vallbohmer D, Collet PH, Xi H, Baldus SE, Brabender J, Metzger R, Heitmann M, Neiss S, Drebber U, Holscher AH, Schneider PM: COX-2 mRNA expression is significantly increased in acid-exposed compared to nonexposed squamous epithelium in gastroesophageal reflux disease. J Gastrointest Surg; 2007 Sep;11(9):1105-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Little is known about the role of cyclooxygenase (COX)-2 in gastroesophageal reflux disease (GERD) and the development of Barrett's metaplasia.
  • RESULTS: COX-2 mRNA is progressively upregulated within the metaplasia-dysplasia-adenocarcinoma (MDA) sequence (p = 0.001).
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Cyclooxygenase 2 / metabolism. Esophageal Neoplasms / metabolism. Gastroesophageal Reflux / metabolism

  • Genetic Alliance. consumer health - Gastroesophageal Reflux.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - GERD.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Natl Cancer Inst. 2005 Jan 19;97(2):142-6 [15657344.001]
  • [Cites] Gastroenterology. 2000 Mar;118(3):487-96 [10702199.001]
  • [Cites] Langenbecks Arch Chir. 1978 Nov;347:267-70 [732426.001]
  • [Cites] J Gastrointest Surg. 2004 Dec;8(8):1007-16; discussion 1016-7 [15585388.001]
  • [Cites] Histopathology. 2007 Jan;50(2):203-9 [17222248.001]
  • [Cites] Gastroenterology. 2002 May;122(5):1500-11 [11984534.001]
  • [Cites] J Gastrointest Surg. 2004 Jan;8(1):1-17 [14746830.001]
  • [Cites] Clin Cancer Res. 2005 Dec 1;11(23):8341-7 [16322294.001]
  • [Cites] Cancer. 1995 Oct 1;76(7):1116-9 [8630885.001]
  • [Cites] Br J Cancer. 2003 Oct 20;89(8):1508-12 [14562024.001]
  • [Cites] J Surg Res. 2004 Mar;117(1):114-20 [15013721.001]
  • [Cites] Scand J Gastroenterol Suppl. 2003;(239):87-93 [14743889.001]
  • [Cites] Lancet Oncol. 2001 Sep;2(9):544-51 [11905709.001]
  • [Cites] Scand J Gastroenterol. 2001 Sep;36(9):897-903 [11521977.001]
  • [Cites] Gastroenterology. 2002 Apr;122(4):1101-12 [11910360.001]
  • [Cites] Ann Surg. 2001 Mar;233(3):322-37 [11224619.001]
  • [Cites] Am J Gastroenterol. 1974 Oct;62(4):325-32 [4432845.001]
  • [Cites] J Natl Cancer Inst. 1998 Oct 21;90(20):1529-36 [9790545.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] Arch Surg. 2004 Jul;139(7):712-6; discussion 716-7 [15249402.001]
  • [Cites] Carcinogenesis. 2005 Mar;26(3):565-70 [15564290.001]
  • [Cites] Cancer Res. 1998 Jul 15;58(14):2929-34 [9679948.001]
  • (PMID = 17619937.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 1.14.99.1 / Cyclooxygenase 2
  •  go-up   go-down


87. Barnes PJ, Boutilier R, Chiasson D, Rayson D: Metaplastic breast carcinoma: clinical-pathologic characteristics and HER2/neu expression. Breast Cancer Res Treat; 2005 May;91(2):173-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • They can be classified as monophasic spindle cell (sarcomatoid) carcinoma, biphasic carcinosarcoma, adenocarcinoma with divergent stromal differentiation (osseous, chondroid and rarely rhabdoid) as well as adenosquamous and pure squamous cell carcinomas.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. Metaplasia. Middle Aged. Nova Scotia / epidemiology

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • 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 = 15868445.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


88. Lennerz JK, Kim SH, Oates EL, Huh WJ, Doherty JM, Tian X, Bredemeyer AJ, Goldenring JR, Lauwers GY, Shin YK, Mills JC: The transcription factor MIST1 is a novel human gastric chief cell marker whose expression is lost in metaplasia, dysplasia, and carcinoma. Am J Pathol; 2010 Sep;177(3):1514-33
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The transcription factor MIST1 is a novel human gastric chief cell marker whose expression is lost in metaplasia, dysplasia, and carcinoma.
  • Recognized precursor lesions for gastric adenocarcinoma are intestinal metaplasia and spasmolytic polypeptide expressing metaplasia (SPEM), defined here by ectopic CDX2 and TFF2 expression, respectively.
  • In mice, expression of the bHLH transcription factor MIST1, normally restricted to mature chief cells, is down-regulated as chief cells undergo experimentally induced metaplasia.
  • Co-visualization of MIST1 and CDX2 shows similar progressive loss of MIST1 with a transitional, CDX2(+)/MIST1(-) hybrid-intestinal metaplasia stage.
  • Our findings implicate MIST1 as a reliable marker of mature, healthy chief cells, and we provide the first evidence that metaplasia in humans arises at least in part from the chief cell lineage.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hum Pathol. 2006 Sep;37(9):1162-8 [16938521.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2006 Dec;291(6):G999-1004 [17090722.001]
  • [Cites] Development. 2007 Jan;134(1):211-22 [17164426.001]
  • [Cites] Am J Surg Pathol. 2007 Jan;31(1):44-57 [17197918.001]
  • [Cites] J Clin Pathol. 2007 Feb;60(2):160-6 [16963467.001]
  • [Cites] Am J Gastroenterol. 2007 Mar;102(3):483-93; quiz 694 [17338734.001]
  • [Cites] Gastroenterology. 2007 May;132(5):1804-19 [17484876.001]
  • [Cites] Gene Expr. 2007;13(4-5):241-53 [17605298.001]
  • [Cites] Pathol Int. 2007 Aug;57(8):517-22 [17610477.001]
  • [Cites] Toxicol Pathol. 2007 Aug;35(5):636-48 [17654405.001]
  • [Cites] Gastroenterol Clin North Am. 2007 Dec;36(4):813-29, vi [17996792.001]
  • [Cites] Lab Invest. 2007 Dec;87(12):1265-76 [18004396.001]
  • [Cites] J Comp Neurol. 2008 Mar 20;507(3):1277-99 [18186028.001]
  • [Cites] Gastroenterology. 2008 Feb;134(2):500-10 [18242216.001]
  • [Cites] Gastroenterology. 2008 Feb;134(2):511-22 [18242217.001]
  • [Cites] Actas Urol Esp. 2007 Oct;31(9):1009-24 [18257370.001]
  • [Cites] Am J Surg Pathol. 2008 Apr;32(4):524-33 [18300795.001]
  • [Cites] J Clin Invest. 2008 Jul;118(7):2459-70 [18535670.001]
  • [Cites] Arch Pathol Lab Med. 2008 Oct;132(10):1577-85 [18834215.001]
  • [Cites] Nature. 2008 Nov 13;456(7219):259-63 [18849966.001]
  • [Cites] Gastroenterology. 2000 Jan;118(1):36-47 [10611152.001]
  • [Cites] Am J Gastroenterol. 2000 Jan;95(1):114-21 [10638568.001]
  • [Cites] Cancer. 2000 Feb 15;88(4):921-32 [10679663.001]
  • [Cites] Anat Rec. 2000 Jun 1;259(2):157-67 [10820318.001]
  • [Cites] Gastroenterology. 2000 Oct;119(4):961-71 [11040183.001]
  • [Cites] Histopathology. 2000 Dec;37(6):513-22 [11122433.001]
  • [Cites] Am J Surg Pathol. 2001 Aug;25(8):1054-60 [11474290.001]
  • [Cites] J Cell Biol. 2001 Nov 12;155(4):519-30 [11696558.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13687-92 [11717430.001]
  • [Cites] J Pathol. 2001 Dec;195(5):563-70 [11745692.001]
  • [Cites] Mod Pathol. 2002 Feb;15(2):102-9 [11850538.001]
  • [Cites] Gastroenterology. 2002 Mar;122(3):689-96 [11875002.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Jun 7;294(2):470-9 [12051735.001]
  • [Cites] Am J Surg Pathol. 2002 Sep;26(9):1161-8 [12218572.001]
  • [Cites] J Pathol. 2003 Apr;199(4):436-46 [12635134.001]
  • [Cites] Gut. 2003 Jun;52(6):807-12 [12740335.001]
  • [Cites] Stem Cells. 2003;21(3):322-36 [12743327.001]
  • [Cites] Mech Dev. 2002 Dec;119 Suppl 1:S285-91 [14516699.001]
  • [Cites] Dev Biol. 2009 Jan 1;325(1):211-24 [19013146.001]
  • [Cites] Dig Dis Sci. 2009 Mar;54(3):614-20 [18709553.001]
  • [Cites] Nature. 2009 Feb 5;457(7230):722-5 [18978771.001]
  • [Cites] Gastroenterology. 2009 Apr;136(4):1368-78 [19249398.001]
  • [Cites] Physiol Genomics. 2009 Apr 10;37(2):67-78 [19208773.001]
  • [Cites] Am J Surg Pathol. 2009 Jun;33(6):886-93 [19194279.001]
  • [Cites] Arch Pathol Lab Med. 2009 Nov;133(11):1763-74 [19886710.001]
  • [Cites] Lab Invest. 2009 Dec;89(12):1410-22 [19841619.001]
  • [Cites] Gastric Cancer. 2009;12(4):189-97 [20047123.001]
  • [Cites] Mod Pathol. 2010 Jan;23(1):54-61 [19820687.001]
  • [Cites] Mod Pathol. 2010 Jan;23(1):1-11 [19838164.001]
  • [Cites] Cell Stem Cell. 2010 Jan 8;6(1):25-36 [20085740.001]
  • [Cites] Gastroenterology. 2010 Feb;138(2):562-72, 572.e1-2 [19883649.001]
  • [Cites] Gastroenterology. 2010 Feb;138(2):550-61, 561.e1-8 [19909751.001]
  • [Cites] Mol Cell Biol. 2010 Mar;30(5):1269-84 [20038531.001]
  • [Cites] Arch Pathol Lab Med. 2010 Mar;134(3):427-43 [20196670.001]
  • [Cites] Mod Pathol. 2010 Jun;23(6):834-43 [20228780.001]
  • [Cites] Gastroenterology. 2010 Jun;138(7):2207-10, 2210.e1 [20450866.001]
  • [Cites] Gastroenterology. 2010 Jul;139(1):213-25.e3 [20398667.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2010 Aug;299(2):G368-80 [20413717.001]
  • [Cites] Mol Cell Biol. 2004 Apr;24(7):2673-81 [15024058.001]
  • [Cites] Peptides. 2004 May;25(5):779-83 [15177872.001]
  • [Cites] Gastroenterology. 2004 Aug;127(2):582-94 [15300590.001]
  • [Cites] J Mol Histol. 2004 May;35(4):403-8 [15503814.001]
  • [Cites] J Mol Histol. 2004 May;35(4):409-16 [15503815.001]
  • [Cites] J Natl Cancer Inst. 1968 Sep;41(3):627-34 [4175677.001]
  • [Cites] Scand J Gastroenterol. 1976;11(7):705-12 [792981.001]
  • [Cites] Pathol Res Pract. 1979 Jan;164(3):224-37 [461230.001]
  • [Cites] Lancet. 1984 Jun 16;1(8390):1311-5 [6145023.001]
  • [Cites] Cancer. 1986 Apr 15;57(8):1528-34 [2418943.001]
  • [Cites] Appl Pathol. 1985;3(3):159-63 [3915949.001]
  • [Cites] Cancer Res. 1988 Jul 1;48(13):3554-60 [3288329.001]
  • [Cites] Differentiation. 1991 Apr;46(3):209-21 [1833254.001]
  • [Cites] Gastroenterology. 1992 Jan;102(1):76-87 [1309362.001]
  • [Cites] Cancer Res. 1992 Dec 15;52(24):6735-40 [1458460.001]
  • [Cites] J Cell Biol. 1993 Apr;121(2):283-93 [8385670.001]
  • [Cites] Anat Rec. 1993 Jun;236(2):297-313 [8338234.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Mar 15;91(6):2216-20 [8134376.001]
  • [Cites] Int J Cancer. 1994 May 1;57(3):324-9 [8168991.001]
  • [Cites] Histochem J. 1994 Aug;26(8):644-7 [7982789.001]
  • [Cites] J Biol Chem. 1996 Feb 16;271(7):3671-6 [8631979.001]
  • [Cites] Eur J Cancer B Oral Oncol. 1996 Jul;32B(4):251-9 [8776422.001]
  • [Cites] Am J Surg Pathol. 1996 Oct;20(10):1161-81 [8827022.001]
  • [Cites] J Anat. 1996 Oct;189 ( Pt 2):303-13 [8886952.001]
  • [Cites] Int J Cancer. 1997 Feb 20;74(1):35-44 [9036867.001]
  • [Cites] Dev Biol. 1997 Feb 1;182(1):101-13 [9073453.001]
  • [Cites] Cell Tissue Res. 1998 Jul;293(1):121-31 [9634604.001]
  • [Cites] Cancer Res. 1999 Mar 1;59(5):1003-7 [10070955.001]
  • [Cites] Lab Invest. 1999 Jun;79(6):639-46 [10378506.001]
  • [Cites] Br J Cancer. 1999 Jan;79(1):65-71 [10408695.001]
  • [Cites] J Pathol. 1999 Feb;187(3):331-7 [10398088.001]
  • [Cites] Acta Pathol Microbiol Scand. 1951;29(1):26-44 [14902458.001]
  • [Cites] Br J Cancer. 1955 Sep;9(3):377-85 [13269635.001]
  • [Cites] Science. 2004 Nov 26;306(5701):1568-71 [15567866.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2005 Feb;288(2):G362-75 [15647607.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Am J Surg Pathol. 2005 May;29(5):579-87 [15832080.001]
  • [Cites] Clin Cancer Res. 2005 May 15;11(10):3766-72 [15897574.001]
  • [Cites] Protein Expr Purif. 2005 May;41(1):207-34 [15915565.001]
  • [Cites] Histopathology. 2005 Oct;47(4):357-67 [16178890.001]
  • [Cites] Gastroenterology. 2005 Nov;129(5):1807-8 [16285989.001]
  • [Cites] Nat Biotechnol. 2005 Dec;23(12):1534-41 [16258519.001]
  • [Cites] Semin Diagn Pathol. 2005 Feb;22(1):88-104 [16512601.001]
  • [Cites] Mod Pathol. 2006 May;19(5):675-83 [16528374.001]
  • (PMID = 20709804.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK079798-01A2; United States / NIDDK NIH HHS / DK / DK079798-02; United States / NIDDK NIH HHS / DK / R01 DK079798-02; United States / NIDDK NIH HHS / DK / R01 DK071590; United States / NIDDK NIH HHS / DK / R01 DK-079798-01; United States / NCI NIH HHS / CA / T32 CA009547; United States / NIDDK NIH HHS / DK / K08 DK066062; United States / NIDDK NIH HHS / DK / R01 DK079798; United States / NIAID NIH HHS / AI / T32 AI007172; United States / NIDDK NIH HHS / DK / R01 DK079798-01A2; United States / NCI NIH HHS / CA / T32-CA009547; United States / NIDDK NIH HHS / DK / K08 DK066062-05; United States / NIDDK NIH HHS / DK / P30 DK52574; United States / NIAID NIH HHS / AI / T32-AI007172; United States / NIDDK NIH HHS / DK / DK066062-05; United States / NIDDK NIH HHS / DK / P30 DK052574
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; 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 / Adaptor Proteins, Signal Transducing; 0 / CLNK protein, human
  • [Other-IDs] NLM/ PMC2928982
  •  go-up   go-down


89. Helm J, Enkemann SA, Coppola D, Barthel JS, Kelley ST, Yeatman TJ: Dedifferentiation precedes invasion in the progression from Barrett's metaplasia to esophageal adenocarcinoma. Clin Cancer Res; 2005 Apr 1;11(7):2478-85
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dedifferentiation precedes invasion in the progression from Barrett's metaplasia to esophageal adenocarcinoma.
  • PURPOSE: Adenocarcinoma arises in Barrett's esophagus by progression from metaplasia to cancer through grades of dysplasia.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Gene Expression Profiling
  • [MeSH-minor] Cell Differentiation / genetics. Cluster Analysis. Disease Progression. Epithelium / metabolism. Epithelium / pathology. Gene Expression Regulation, Neoplastic / genetics. Humans. Metaplasia / genetics. Models, Biological. Neoplasm Invasiveness / genetics. Oligonucleotide Array Sequence Analysis. Prognosis

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15814623.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K24-CA85429-04; United States / NCI NIH HHS / CA / R01-CA098522-01; United States / NCI NIH HHS / CA / RZ1-CA101355-01-A1; United States / NCI NIH HHS / CA / U01-CA85052-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  •  go-up   go-down


90. Ingravallo G, Dall'Olmo L, Segat D, Fassan M, Mescoli C, Dazzo E, Castoro C, Polimeno L, Rizzetto C, Baroni MD, Zaninotto G, Ancona E, Rugge M: CDX2 hox gene product in a rat model of esophageal cancer. J Exp Clin Cancer Res; 2009;28:108
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Barrett's mucosa is the precursor of esophageal adenocarcinoma.
  • De novo Cdx2 expression was consistently documented in the proliferative zone of the squamous epithelium close to reflux ulcers (Group A: 68%; Group B: 64%; Group C: 80%), multilayered epithelium and intestinal metaplasia (Group A: 9%; Group B: 41%; Group C: 60%), and esophageal adenocarcinomas (Group B: 36%; Group C: 35%).
  • CONCLUSION: De novo expression of Cdx2 is an early event in the spectrum of the lesions induced by experimental gastro-esophageal reflux and should be considered as a key step in the morphogenesis of esophageal adenocarcinoma.

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Carcinogenesis. 2000 Feb;21(2):257-63 [10657966.001]
  • [Cites] J Surg Res. 2006 Oct;135(2):337-44 [16926029.001]
  • [Cites] Gastroenterology. 2000 Aug;119(2):333-8 [10930368.001]
  • [Cites] Am J Surg Pathol. 2001 May;25(5):569-78 [11342767.001]
  • [Cites] Gastroenterology. 2002 Feb;122(2):588-90 [11845805.001]
  • [Cites] Anticancer Res. 2002 Jan-Feb;22(1A):39-44 [12017320.001]
  • [Cites] Am J Gastroenterol. 2002 Aug;97(8):1888-95 [12190150.001]
  • [Cites] J Cell Sci. 2003 Apr 15;116(Pt 8):1429-36 [12640028.001]
  • [Cites] J Exp Clin Cancer Res. 2003 Jun;22(2):273-8 [12866578.001]
  • [Cites] Scand J Gastroenterol. 2003 Jul;38(7):687-92 [12889552.001]
  • [Cites] Am J Gastroenterol. 2003 Sep;98(9):1931-9 [14499768.001]
  • [Cites] N Engl J Med. 2003 Dec 4;349(23):2241-52 [14657432.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 18;101(20):7641-5 [15136723.001]
  • [Cites] Lab Invest. 2004 Jun;84(6):753-65 [15094711.001]
  • [Cites] Ann Surg. 2004 Jul;240(1):57-67 [15213619.001]
  • [Cites] Cancer Cell. 2004 Jul;6(1):11-6 [15261138.001]
  • [Cites] Mod Pathol. 2004 Oct;17(10):1282-8 [15167938.001]
  • [Cites] J Clin Pathol. 2004 Oct;57(10):1063-8 [15452161.001]
  • [Cites] Br J Cancer. 1994 Aug;70(2):185-9 [8054264.001]
  • [Cites] Ann Surg Oncol. 1994 May;1(3):252-61 [7842295.001]
  • [Cites] Int J Cancer. 1996 Jul 17;67(2):269-74 [8760598.001]
  • [Cites] Carcinogenesis. 1997 Nov;18(11):2265-70 [9395230.001]
  • [Cites] J Gastrointest Surg. 1998 May-Jun;2(3):260-8 [9841983.001]
  • [Cites] Carcinogenesis. 1999 Sep;20(9):1801-8 [10469627.001]
  • [Cites] Br J Surg. 1950 Oct;38(150):175-82 [14791960.001]
  • [Cites] Dig Dis Sci. 2005 Mar;50(3):425-31 [15810620.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 May 24;102(21):7565-70 [15894614.001]
  • [Cites] Gut. 2006 Dec;55(12):1810-20 [17124160.001]
  • [Cites] J Exp Clin Cancer Res. 2006 Sep;25(3):297-302 [17167967.001]
  • [Cites] J Gastrointest Surg. 2007 Jul;11(7):869-74 [17440788.001]
  • [Cites] Dis Esophagus. 2007;20(5):372-8 [17760649.001]
  • [Cites] BMC Gastroenterol. 2008;8:1 [18190713.001]
  • [Cites] PLoS One. 2008;3(10):e3534 [18953412.001]
  • [Cites] Gut. 2009 May;58(5):620-8 [19136512.001]
  • [Cites] J Exp Clin Cancer Res. 2009;28:68 [19470182.001]
  • [Cites] Carcinogenesis. 2000 Aug;21(8):1587-91 [10910963.001]
  • (PMID = 19664209.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cdx2 protein, rat; 0 / Homeodomain Proteins; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC3225830
  •  go-up   go-down


91. Hao Z, Li X, Qiao T, Li S, Lv Y, Fan D: Downregulated expression of CIAPIN1 may contribute to gastric carcinogenesis by accelerating cell proliferation and promoting cell cycle progression. Cancer Biol Ther; 2009 Jun;8(11):1064-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Expression of CIAPIN1 in normal, inflammatory gastric mucosa, gastric precancerous lesions and gastric adenocarcinoma was detected by immunohistochemistry and western blotting and, influence of CIAPIN1 on the proliferation of gastric cancer cells was investigated by ectopic expression of CIAPIN1 and RNA interference (RNAi).
  • Our immunohistochemical results demonstrated that the expression of CIAPIN1 in gastric antral mucosa was progressively reduced along the sequence of normal/inflammatory gastric mucosa-atrophy-intestinal metaplasia-dysplasia-adenocarcinoma.

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19471113.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CIAPIN1 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering
  •  go-up   go-down


92. Jin Z, Olaru A, Yang J, Sato F, Cheng Y, Kan T, Mori Y, Mantzur C, Paun B, Hamilton JP, Ito T, Wang S, David S, Agarwal R, Beer DG, Abraham JM, Meltzer SJ: Hypermethylation of tachykinin-1 is a potential biomarker in human esophageal cancer. Clin Cancer Res; 2007 Nov 1;13(21):6293-300
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: TAC1 hypermethylation in tissue samples showed highly discriminative receiver-operator characteristic curve profiles, clearly distinguishing esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) from normal esophagus (P < 0.0001).
  • Both frequencies and normalized methylation values of TAC1 tissue methylation were significantly higher in Barrett's metaplasia (BE), dysplastic Barrett's esophagus, EAC, and ESCC than in normal esophagus (P < 0.01).
  • The frequency of TAC1 hypermethylation increased dramatically and early during neoplastic progression, from 7.5% in normal esophagus to 55.6% in BE from patients with Barrett's metaplasia alone, 57.5% in dysplastic Barrett's esophagus, and 61.2% in EAC.
  • Circulating methylated TAC1 promoter DNA also offers potential as a biomarker for the diagnosis of EAC.

  • Genetic Alliance. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17975140.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK067872; United States / NCI NIH HHS / CA / CA001808; United States / NCI NIH HHS / CA / CA085069; United States / NCI NIH HHS / CA / CA106763
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / Tachykinins; 63231-63-0 / RNA; 9007-49-2 / DNA
  •  go-up   go-down


93. Omori M, Hashi A, Ishii Y, Yuminamochi T, Nara M, Kondo T, Hirata S, Katoh R, Hoshi K: Clinical impact of preoperative screening for gastric mucin secretion in cervical discharge by HIK1083-labeled latex agglutination test. Am J Clin Pathol; 2008 Oct;130(4):585-94
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Glandular lesions with a gastric phenotype were identified histologically in all 26 cases positive for the HIK1083 latex test, such as minimal deviation adenocarcinoma, lobular endocervical glandular hyperplasia (LEGH), and pyloric gland metaplasia, but not in negative cases.
  • In 2 cases of LEGH, adenocarcinoma in situ was identified.
  • Screening of gastric mucin in cervical discharge may facilitate preoperative detection of some early cervical adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Antibodies, Monoclonal. Gastric Mucins / analysis. Latex Fixation Tests. Uterine Cervical Neoplasms / diagnosis. Vaginal Discharge / diagnosis
  • [MeSH-minor] Adult. Aged. Female. Humans. Immunohistochemistry. Mass Screening / methods. Middle Aged. Precancerous Conditions / diagnosis. Preoperative Care

  • MedlinePlus Health Information. consumer health - Cervical Cancer.
  • International Agency for Research on Cancer - Screening Group. diagnostics - A practical manual on visual screening for cervical neoplasia .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18794052.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Gastric Mucins
  •  go-up   go-down


94. Ito R, Oue N, Yoshida K, Kunimitsu K, Nakayama H, Nakachi K, Yasui W: Clinicopathological significant and prognostic influence of cadherin-17 expression in gastric cancer. Virchows Arch; 2005 Oct;447(4):717-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CDH17 expression was detected in 63/94 (67%) of gastric adenocarcinomas in addition to intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / analysis. Cadherins / biosynthesis. Stomach Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gastroenterology. 2002 Nov;123(5):1565-77 [12404231.001]
  • [Cites] Pathol Int. 2004 Jun;54(6):392-400 [15144397.001]
  • [Cites] J Cell Biol. 1994 Jun;125(6):1353-69 [8207063.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Jun 25;319(2):562-8 [15178443.001]
  • [Cites] Cancer Sci. 2003 May;94(5):425-30 [12824888.001]
  • [Cites] Int J Cancer. 2001 Sep;93(6):805-9 [11519041.001]
  • [Cites] Carcinogenesis. 2005 Jan;26(1):193-200 [15498792.001]
  • [Cites] Gastroenterology. 2000 Oct;119(4):961-71 [11040183.001]
  • [Cites] Acta Pathol Microbiol Scand. 1965;64:31-49 [14320675.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Nov 21;311(3):618-24 [14623315.001]
  • [Cites] Dev Dyn. 2001 Jun;221(2):182-93 [11376485.001]
  • [Cites] Cancer Res. 1993 Apr 1;53(7):1690-5 [8453643.001]
  • [Cites] Science. 1994 Apr 15;264(5157):430-3 [8153632.001]
  • [Cites] Int J Cancer. 1993 Apr 22;54(1):49-52 [8478147.001]
  • [Cites] J Cell Biol. 1997 Mar 10;136(5):1109-21 [9060475.001]
  • [Cites] J Clin Invest. 2002 Apr;109(8):987-91 [11956233.001]
  • [Cites] J Pathol. 2005 Apr;205(5):615-22 [15732140.001]
  • [Cites] Cancer Sci. 2004 May;95(5):385-92 [15132764.001]
  • [Cites] Ann N Y Acad Sci. 2000;915:136-43 [11193569.001]
  • (PMID = 16044349.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDH17 protein, human; 0 / CDX2 Transcription Factor; 0 / CDX2 protein, human; 0 / Cadherins; 0 / Homeodomain Proteins
  •  go-up   go-down


95. Kim CG, Choi IJ, Lee JY, Cho SJ, Nam BH, Kook MC, Hong EK, Kim YW: Biopsy site for detecting Helicobacter pylori infection in patients with gastric cancer. J Gastroenterol Hepatol; 2009 Mar;24(3):469-74
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MATERIALS AND METHODS: Consecutive patients (194) with gastric adenocarcinoma were prospectively enrolled.
  • Sensitivities of histology decreased in correlation with increasing severity of atrophy and intestinal metaplasia (both P < 0.001 using the chi-square test for trend).
  • The proportions of moderate to marked atrophy/intestinal metaplasia at UBGC (12.8%/14.7%) were significantly lower than those at antrum (50.0%/57.8%, P < 0.001 respectively) or UBLC (40.0%/48.9%, P < 0.001 respectively).
  • CONCLUSIONS: The UBGC side is the most sensitive and specific biopsy site to detect H. pylori in gastric cancer patients due to less frequent atrophy and intestinal metaplasia than at the antrum or UBLC side.
  • [MeSH-major] Adenocarcinoma / microbiology. Biopsy / methods. Gastroscopy. Helicobacter Infections / diagnosis. Helicobacter pylori / isolation & purification. Stomach / microbiology. Stomach Neoplasms / microbiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Bacterial / blood. Atrophy. Breath Tests. Female. Humans. Male. Metaplasia. Middle Aged. Predictive Value of Tests. Prospective Studies. Sensitivity and Specificity. Urease / analysis