[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 24 of about 24
1. Maru DM, Singh RR, Hannah C, Albarracin CT, Li YX, Abraham R, Romans AM, Yao H, Luthra MG, Anandasabapathy S, Swisher SG, Hofstetter WL, Rashid A, Luthra R: MicroRNA-196a is a potential marker of progression during Barrett's metaplasia-dysplasia-invasive adenocarcinoma sequence in esophagus. Am J Pathol; 2009 May;174(5):1940-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA-196a is a potential marker of progression during Barrett's metaplasia-dysplasia-invasive adenocarcinoma sequence in esophagus.
  • Barrett's esophagus (BE)/Barrett's metaplasia (BM) is a recognized precursor of esophageal adenocarcinoma (EA) with an intermediary stage of dysplasia.
  • The low yield and high cost of endoscopic screening of patients with BE underscores the need for novel biomarkers, such as microRNA (miRNA), which have emerged as important players in neoplastic progression for risk assessment of developing dysplasia/adenocarcinoma.
  • Higher levels of miR-196a were observed in EA, BE, and dysplastic lesions compared with normal squamous mucosa, and in high-grade dysplasia compared with BE and low-grade dysplasia.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis. Esophagus / pathology. MicroRNAs / genetics
  • [MeSH-minor] Adult. Aged. Calgranulin B / genetics. Calgranulin B / metabolism. Cornified Envelope Proline-Rich Proteins / genetics. Cornified Envelope Proline-Rich Proteins / metabolism. DNA Primers / chemistry. Disease Progression. Female. Humans. Keratin-5 / genetics. Keratin-5 / metabolism. Male. Metaplasia. Middle Aged. Neoplasm Invasiveness. RNA, Messenger / genetics. RNA, Messenger / metabolism. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • 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
  • [Cites] Leukemia. 2007 May;21(5):912-6 [17330104.001]
  • [Cites] Clin Cancer Res. 2007 Feb 1;13(3):912-9 [17289885.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4553-5 [17510380.001]
  • [Cites] Oncogene. 2007 Jun 28;26(30):4442-52 [17237814.001]
  • [Cites] Nat Biotechnol. 2008 Apr;26(4):462-9 [18362881.001]
  • [Cites] Oncogene. 2008 Nov 6;27(52):6667-78 [18663355.001]
  • [Cites] Gastroenterology. 2000 Aug;119(2):333-8 [10930368.001]
  • [Cites] J Biol Chem. 2001 Jun 1;276(22):19231-7 [11279051.001]
  • [Cites] Am J Gastroenterol. 2001 Oct;96(10):2839-48 [11693316.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15149-54 [11742071.001]
  • [Cites] Oncogene. 2002 Jan 17;21(3):475-8 [11821959.001]
  • [Cites] Mamm Genome. 2003 Feb;14(2):140-8 [12584609.001]
  • [Cites] Gastrointest Endosc Clin N Am. 2003 Apr;13(2):369-97 [12916666.001]
  • [Cites] Cell Res. 2004 Feb;14(1):46-53 [15040889.001]
  • [Cites] World J Gastroenterol. 2004 Apr 15;10(8):1093-7 [15069705.001]
  • [Cites] Am J Surg. 1995 Jun;169(6):609-14 [7771626.001]
  • [Cites] Trends Biochem Sci. 1996 Apr;21(4):134-40 [8701470.001]
  • [Cites] Cancer. 1998 Nov 15;83(10):2049-53 [9827707.001]
  • [Cites] Nature. 2005 Feb 17;433(7027):769-73 [15685193.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3146-54 [15833844.001]
  • [Cites] Cell. 2005 Aug 26;122(4):553-63 [16122423.001]
  • [Cites] N Engl J Med. 2005 Oct 27;353(17):1768-71 [16251533.001]
  • [Cites] Nature. 2005 Dec 1;438(7068):671-4 [16319892.001]
  • [Cites] J Clin Oncol. 2006 Jan 10;24(2):259-67 [16344314.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Apr 7;342(2):465-71 [16487489.001]
  • [Cites] Nat Rev Cancer. 2006 Apr;6(4):259-69 [16557279.001]
  • [Cites] Science. 2006 Apr 7;312(5770):75-9 [16484454.001]
  • [Cites] Nat Rev Cancer. 2006 Nov;6(11):857-66 [17060945.001]
  • [Cites] JAMA. 2007 May 2;297(17):1901-8 [17473300.001]
  • (PMID = 19342367.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calgranulin B; 0 / Cornified Envelope Proline-Rich Proteins; 0 / DNA Primers; 0 / KRT5 protein, human; 0 / Keratin-5; 0 / MIRN196 microRNA, human; 0 / MicroRNAs; 0 / RNA, Messenger; 0 / SPRR2C protein, human
  • [Other-IDs] NLM/ PMC2671281
  •  go-up   go-down


2. Ong CA, Lao-Sirieix P, Fitzgerald RC: Biomarkers in Barrett's esophagus and esophageal adenocarcinoma: predictors of progression and prognosis. World J Gastroenterol; 2010 Dec 07;16(45):5669-81
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biomarkers in Barrett's esophagus and esophageal adenocarcinoma: predictors of progression and prognosis.
  • Barrett's esophagus is a well-known premalignant lesion of the lower esophagus that is characterized by intestinal metaplasia of the squamous epithelium.
  • It is clinically important due to the increased risk (0.5% per annum) of progression to esophageal adenocarcinoma (EA), which has a poor outcome unless diagnosed early.
  • The current clinical management of Barrett's esophagus is hampered by the lack of accurate predictors of progression.
  • Biomarkers have the potential to improve radically the clinical management of patients with Barrett's esophagus and EA but have not yet entered mainstream clinical practice.
  • This review aims to highlight the most promising predictive and prognostic biomarkers in Barrett's esophagus and EA and to discuss what is required to move the field forward towards clinical application.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Biomarkers, Tumor / analysis. Esophageal Neoplasms / diagnosis

  • 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] BMC Clin Pathol. 2005 Aug 12;5:7 [16095543.001]
  • [Cites] Cancer. 1995 Jan 15;75(2):423-9 [7812911.001]
  • [Cites] Cancer Invest. 2001;19(5):554-68 [11458821.001]
  • [Cites] J Natl Cancer Inst. 2001 Jul 18;93(14):1054-61 [11459866.001]
  • [Cites] J Clin Oncol. 2006 Jan 10;24(2):259-67 [16344314.001]
  • [Cites] BMJ. 2009;338:b604 [19336487.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jul 9;93(14):7081-4 [8692948.001]
  • [Cites] Oncogene. 2002 Jan 17;21(3):475-8 [11821959.001]
  • [Cites] Gastroenterology. 2000 Aug;119(2):333-8 [10930368.001]
  • [Cites] Methods Inf Med. 2001 Mar;40(1):1-5 [11310153.001]
  • [Cites] Am J Gastroenterol. 2008 Mar;103(3):788-97 [18341497.001]
  • [Cites] Hum Pathol. 2001 Apr;32(4):368-78 [11331953.001]
  • [Cites] Dis Esophagus. 2004;17(2):136-40 [15230726.001]
  • [Cites] Cancer Res. 2006 May 15;66(10):5021-8 [16707423.001]
  • [Cites] Gut. 2000 Aug;47(2):251-5 [10896917.001]
  • [Cites] Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):659-65 [17255290.001]
  • [Cites] Cancer Res. 1997 Mar 15;57(6):1030-4 [9067264.001]
  • [Cites] Mod Pathol. 2009 Jan;22(1):58-65 [18820669.001]
  • [Cites] Lancet. 2003 Nov 1;362(9394):1439-44 [14602436.001]
  • [Cites] Gut. 2006 Oct;55(10):1390-7 [16682429.001]
  • [Cites] Clin Cancer Res. 2004 Apr 15;10(8):2738-41 [15102678.001]
  • [Cites] BMJ. 2009;338:b375 [19237405.001]
  • [Cites] Br J Cancer. 2005 Aug 22;93(4):387-91 [16106245.001]
  • [Cites] Nucleic Acids Res. 1994 Aug 11;22(15):2990-7 [8065911.001]
  • [Cites] Cancer Res. 2000 Sep 15;60(18):5021-6 [11016622.001]
  • [Cites] PLoS Med. 2007 Feb;4(2):e67 [17326708.001]
  • [Cites] Clin Cancer Res. 2007 Feb 1;13(3):912-9 [17289885.001]
  • [Cites] Gut. 2009 Nov;58(11):1451-9 [19651633.001]
  • [Cites] Genome Res. 1999 May;9(5):482-91 [10330128.001]
  • [Cites] Nucleic Acids Res. 2002 Apr 1;30(7):e28 [11917034.001]
  • [Cites] Surg Endosc. 2010 May;24(5):1144-50 [19997751.001]
  • [Cites] BMC Cancer. 2008;8:254 [18778486.001]
  • [Cites] Gastroenterology. 2003 Dec;125(6):1670-7 [14724819.001]
  • [Cites] Nature. 2002 Jan 31;415(6871):530-6 [11823860.001]
  • [Cites] Clin Cancer Res. 2001 May;7(5):1118-26 [11350874.001]
  • [Cites] J Clin Oncol. 2006 Aug 10;24(23):3789-98 [16785472.001]
  • [Cites] Nat Rev Genet. 2010 Mar;11(3):191-203 [20125086.001]
  • [Cites] Ann Surg Oncol. 2008 Dec;15(12):3459-70 [18825457.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8284-9 [11719461.001]
  • [Cites] BMJ. 2009;338:b606 [19502216.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] J Clin Oncol. 2006 Feb 10;24(5):748-54 [16401681.001]
  • [Cites] Int J Cancer. 2005 Jun 20;115(3):351-8 [15688381.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Mar;15(3):509-16 [16537709.001]
  • [Cites] Gastrointest Endosc. 2005 Oct;62(4):488-98 [16185958.001]
  • [Cites] Am J Gastroenterol. 2001 Nov;96(11):3071-83 [11721752.001]
  • [Cites] Int J Cancer. 2007 May 1;120(9):1914-21 [17236199.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9523-7 [1946366.001]
  • [Cites] Am J Gastroenterol. 2010 Jul;105(7):1523-30 [20461069.001]
  • [Cites] Gastroenterology. 1996 Feb;110(2):614-21 [8566611.001]
  • [Cites] Dis Esophagus. 2008;21(2):97-102 [18269642.001]
  • [Cites] J Clin Oncol. 2007 Feb 20;25(6):698-707 [17308274.001]
  • [Cites] Clin Cancer Res. 2003 Aug 1;9(8):2912-9 [12912936.001]
  • [Cites] Lab Invest. 2007 May;87(5):466-72 [17310216.001]
  • [Cites] Gastroenterology. 2002 Aug;123(2):461-7 [12145799.001]
  • [Cites] Gastroenterology. 2010 Dec;139(6):1995-2004.e15 [20621683.001]
  • [Cites] N Engl J Med. 2006 Aug 10;355(6):560-9 [16899776.001]
  • [Cites] Lancet. 2005 Feb 5-11;365(9458):488-92 [15705458.001]
  • [Cites] Am J Gastroenterol. 2009 Sep;104(9):2153-60 [19584833.001]
  • [Cites] BMC Cancer. 2006;6:134 [16712734.001]
  • [Cites] Aliment Pharmacol Ther. 2006 Mar 1;23(5):587-93 [16480397.001]
  • [Cites] Int J Cancer. 2006 Jul 15;119(2):264-8 [16477636.001]
  • [Cites] Mol Pathol. 2003 Dec;56(6):313-7 [14645692.001]
  • [Cites] Genome Res. 2006 Aug;16(8):1046-55 [16809668.001]
  • [Cites] Scand J Gastroenterol. 2007 Nov;42(11):1271-4 [17852872.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Nov;1(6):413-23 [19138988.001]
  • [Cites] Dis Esophagus. 2003;16(1):17-23 [12581249.001]
  • [Cites] Clin Cancer Res. 1998 Jul;4(7):1755-63 [9676852.001]
  • [Cites] Am J Gastroenterol. 2000 Jul;95(7):1669-76 [10925966.001]
  • [Cites] Am J Gastroenterol. 2006 Jan;101(1):12-7 [16405528.001]
  • [Cites] Ann Surg Oncol. 2007 Dec;14(12):3602-9 [17896157.001]
  • [Cites] Cancer Res. 2009 May 15;69(10):4112-5 [19435894.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3410-8 [11309301.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2284-9 [9122186.001]
  • [Cites] Br J Cancer. 2000 Feb;82(4):865-70 [10732760.001]
  • [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] Gut. 2002 Mar;50(3):373-7 [11839717.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2560-6 [12855631.001]
  • [Cites] BMJ. 2009;338:b605 [19477892.001]
  • [Cites] Mol Carcinog. 2006 Oct;45(10):786-94 [16921482.001]
  • [Cites] Eur J Cancer. 2008 Mar;44(4):588-99 [18272361.001]
  • [Cites] Anticancer Res. 2004 Jul-Aug;24(4):2579-83 [15330218.001]
  • [Cites] Gut. 1998 Aug;43(2):216-22 [10189847.001]
  • [Cites] Am J Gastroenterol. 2004 Oct;99(10):1887-94 [15447746.001]
  • [Cites] Mol Cell Proteomics. 2002 Nov;1(11):845-67 [12488461.001]
  • [Cites] Scand J Gastroenterol. 2007 Jun;42(6):682-8 [17505989.001]
  • [Cites] Clin Cancer Res. 2010 Jan 1;16(1):330-7 [20028767.001]
  • [Cites] Gastroenterology. 2005 Dec;129(6):1825-31 [16344051.001]
  • [Cites] Gut. 2006 Apr;55(4):442 [16531521.001]
  • [Cites] Am J Gastroenterol. 2001 May;96(5):1355-62 [11374668.001]
  • [Cites] Anticancer Res. 2000 May-Jun;20(3B):1933-7 [10928129.001]
  • [Cites] Cancer. 2007 Feb 15;109(4):658-67 [17211865.001]
  • [Cites] Gut. 2006 Dec;55(12):1810-20 [17124160.001]
  • [Cites] Hum Pathol. 1988 Feb;19(2):166-78 [3343032.001]
  • [Cites] Am J Med. 2010 May;123(5):462-7 [20399324.001]
  • [Cites] Clin Cancer Res. 2008 Dec 15;14(24):8279-87 [19088045.001]
  • [Cites] Genome Res. 2006 Mar;16(3):383-93 [16449502.001]
  • [Cites] Clin Cancer Res. 2009 Oct 1;15(19):6192-200 [19789312.001]
  • [Cites] Oncogene. 2005 Jun 9;24(25):4138-48 [15824739.001]
  • [Cites] Nat Genet. 2005 Aug;37(8):853-62 [16007088.001]
  • [Cites] Cancer. 2008 May 15;112(10):2173-80 [18348304.001]
  • [Cites] Ann Surg Oncol. 2007 Feb;14(2):977-91 [17122988.001]
  • [Cites] Nat Rev Cancer. 2010 Feb;10(2):87-101 [20094044.001]
  • [Cites] Am J Gastroenterol. 2000 Aug;95(8):1888-93 [10950031.001]
  • [Cites] Gastroenterology. 2002 Jun;122(7):1800-7 [12055587.001]
  • [Cites] J Clin Pathol. 2006 Jun;59(6):631-4 [16731604.001]
  • [Cites] Am J Gastroenterol. 2009 May;104(5):1093-6 [19417749.001]
  • [Cites] Drug Discov Today. 2005 Jul 15;10(14):965-76 [16023055.001]
  • [Cites] Ann Thorac Surg. 2001 Sep;72(3):859-66 [11565671.001]
  • [Cites] Am J Gastroenterol. 2009 Oct;104(10):2588-94 [19623166.001]
  • [Cites] N Engl J Med. 1976 Aug 26;295(9):476-80 [940579.001]
  • [Cites] Hum Pathol. 2000 Jan;31(1):35-9 [10665910.001]
  • [Cites] Gastroenterology. 2001 Jun;120(7):1607-19 [11375943.001]
  • [Cites] Cancer Metastasis Rev. 2009 Dec;28(3-4):317-26 [19997771.001]
  • [Cites] Am J Gastroenterol. 2001 Oct;96(10):2839-48 [11693316.001]
  • [Cites] Am J Gastroenterol. 2009 Feb;104(2):502-13 [19174812.001]
  • [Cites] Hum Pathol. 2005 Sep;36(9):955-61 [16153457.001]
  • [Cites] J Natl Cancer Inst. 2000 Aug 16;92(16):1316-21 [10944553.001]
  • (PMID = 21128316.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Genetic Markers
  • [Other-IDs] NLM/ PMC2997982
  •  go-up   go-down


3. Cook MB, Wild CP, Everett SM, Hardie LJ, Bani-Hani KE, Martin IG, Forman D: Risk of mortality and cancer incidence in Barrett's esophagus. Cancer Epidemiol Biomarkers Prev; 2007 Oct;16(10):2090-6
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk of mortality and cancer incidence in Barrett's esophagus.
  • BACKGROUND: There are very few prospective follow-up studies of Barrett esophagus (BE) cohorts assessing the risk of extraesophageal cancer incidence or mortality.
  • RESULTS: All-cause mortality was found to be elevated in patients with BE [SMR, 1.21; 95% confidence interval (95% CI), 1.06, 1.37] and remained so after esophageal cancers were excluded (SMR, 1.16; 95% CI, 1.01-1.32).
  • Increased mortality risks were also found for malignant neoplasms of the esophagus (SMR, 7.26; 95% CI, 3.87-12.42) and diseases of the digestive system (SMR, 2.03; 95% CI, 1.11-3.40).
  • Circulatory disease mortality was borderline statistically significant (SMR, 1.24; 95% CI, 1.00-1.52; P = 0.053) for those with a specialized intestinal metaplasia diagnosis of BE.
  • In the cancer incidence analyses, esophageal malignancies (SIR, 8.66; 95% CI, 4.73-14.53) and esophageal adenocarcinomas (SIR, 14.29; 95% CI, 7.13-22.56) were found to be increased in BE.
  • CONCLUSIONS: This study has shown evidence of an increased risk of esophageal cancer incidence and mortality in BE.
  • It has also shown that those who have a histologic BE diagnosis may also have an increased risk of circulatory disease mortality.
  • [MeSH-major] Adenocarcinoma / mortality. Barrett Esophagus / mortality. Carcinoma, Squamous Cell / mortality. Esophageal Neoplasms / mortality. Neoplasms, Multiple Primary / mortality. Precancerous Conditions / mortality

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17890521.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


Advertisement
4. Allameh A, Rasmi Y, Nasseri-Moghaddam S, Tavangar SM, Sharifi R, Sadreddini M: Immunohistochemical analysis of selected molecular markers in esophagus precancerous, adenocarcinoma and squamous cell carcinoma in Iranian subjects. Cancer Epidemiol; 2009 Jul;33(1):79-84
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical analysis of selected molecular markers in esophagus precancerous, adenocarcinoma and squamous cell carcinoma in Iranian subjects.
  • AIM: To investigate changes in potential causative factors during progression of esophagus cancer in a population living in high-risk area in Iran.
  • SUBJECTS: Formalin-fixed, paraffin-embedded esophageal specimens (n=87) from patients with gastroesophageal reflux disease (GERD), Barrett's metaplasia, adenocarcinoma (ADC) and squamous cells carcinoma (SCC) were collected based on their pathological diagnosis.
  • RESULTS: P53 expression was not detected in esophageal tissues from normal and GERD samples, whereas it was found positive in Barrett's, ADC, and SCC samples.
  • CONCLUSION: The pathological changes in ADC and SCC samples which were associated with increasing frequency of NT and COX-2 provides further evidence for involvement of these inflammatory factors in progression of esophagus cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Precancerous Conditions / metabolism. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Barrett Esophagus / metabolism. Barrett Esophagus / pathology. Case-Control Studies. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclooxygenase 2 / metabolism. Disease Progression. Esophagus / metabolism. Esophagus / pathology. Female. Gastroesophageal Reflux / metabolism. Gastroesophageal Reflux / pathology. Glutathione S-Transferase pi / metabolism. Humans. Immunohistochemistry. Iran. Male. Middle Aged. Tumor Suppressor Protein p53 / metabolism. Tyrosine / analogs & derivatives. Tyrosine / metabolism. Young Adult


5. Buskens CJ, Hulscher JB, van Gulik TM, Ten Kate FJ, van Lanschot JJ: Histopathologic evaluation of an animal model for Barrett's esophagus and adenocarcinoma of the distal esophagus. J Surg Res; 2006 Oct;135(2):337-44
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histopathologic evaluation of an animal model for Barrett's esophagus and adenocarcinoma of the distal esophagus.
  • INTRODUCTION: Barrett's esophagus and adenocarcinoma of the esophagus are related to long-standing duodeno-gastroesophageal reflux.
  • The development of an animal model in which Barrett's esophagus and/or carcinoma is induced by duodeno-(gastro-)esophageal reflux could provide better understanding of the pathogenesis of the metaplasia-dysplasia-carcinoma sequence and would create the possibility of investigating new treatment strategies for this aggressive disease.
  • Sequential morphological changes (i.e., esophagitis, intestinal metaplasia, dysplasia, and carcinoma) were studied after 4, 6, and 12 months.
  • In these animals, extensive esophagitis with squamous cell hyperplasia was found.
  • After 1 year, 9 of the 10 animals had developed a glandular metaplastic segment (median length, 10 mm), which was histologically and immunohistologically characteristic for the specialized columnar epithelium of Barrett's esophagus without signs of dysplasia.
  • Finally, in seven animals a mucinous tumor with cytologic characteristics of a well-differentiated mucinous adenocarcinoma was found without infiltrative growth.
  • Although they showed cytological characteristics of malignancy, histopathologic evaluation was more suggestive of a reactive mucous producing lesion fitting the diagnosis "esophagitis cystica profunda."
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Disease Models, Animal. Esophageal Neoplasms / pathology. Gastrointestinal Tract / surgery


6. di Pietro M, Peters CJ, Fitzgerald RC: Clinical puzzle: Barrett's oesophagus. Dis Model Mech; 2008 Jul-Aug;1(1):26-31
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The incidence of oesophageal adenocarcinoma has increased dramatically in the Western world over the past two decades.
  • Owing to its dismal 5-year prognosis in advanced stages, early diagnosis is required in order to improve survival rates.
  • Barrett's is defined as the substitution of the normal stratified squamous epithelium of the oesophagus with a columnar cell lining with intestinal-type differentiation; a phenomenon commonly referred to as intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology
  • [MeSH-minor] Animals. Biomarkers / analysis. Cell Transformation, Neoplastic. Disease Progression. Early Diagnosis. Genetic Predisposition to Disease. Humans. Models, Biological

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gastroenterology. 2005 Dec;129(6):2125-6; author reply 2126 [16344087.001]
  • [Cites] Gastroenterology. 2005 Dec;129(6):1825-31 [16344051.001]
  • [Cites] Aliment Pharmacol Ther. 2006 Mar 15;23(6):735-42 [16556175.001]
  • [Cites] Gut. 2006 Aug;55(8):1078-83 [16469795.001]
  • [Cites] Gut. 2006 Oct;55(10):1390-7 [16682429.001]
  • [Cites] Cancer Detect Prev. 2006;30(5):423-31 [17064856.001]
  • [Cites] Nature. 2006 Nov 23;444(7118):444-54 [17122850.001]
  • [Cites] Gut. 2006 Dec;55(12):1810-20 [17124160.001]
  • [Cites] Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):659-65 [17255290.001]
  • [Cites] Gastrointest Endosc. 2007 Feb;65(2):185-95 [17258973.001]
  • [Cites] Aliment Pharmacol Ther. 2007 Feb 15;25(4):447-53 [17270000.001]
  • [Cites] J Clin Oncol. 2007 Feb 20;25(6):698-707 [17308274.001]
  • [Cites] PLoS Med. 2007 Feb;4(2):e67 [17326708.001]
  • [Cites] Histopathology. 2007 Jun;50(7):920-7 [17543082.001]
  • [Cites] Gut. 2007 Jul;56(7):906-17 [17185354.001]
  • [Cites] Genet Med. 2007 Jun;9(6):341-7 [17575500.001]
  • [Cites] Nat Rev Cancer. 2007 Sep;7(9):645-58 [17687385.001]
  • [Cites] Genes Dev. 2007 Nov 1;21(21):2788-803 [17974918.001]
  • [Cites] Gut. 2008 Feb;57(2):167-72 [17965067.001]
  • [Cites] Nat Rev Cancer. 2008 Feb;8(2):94-107 [18202697.001]
  • [Cites] Gut. 2008 Aug;57(8):1041-8 [18305067.001]
  • [Cites] Gastroenterology. 2000 Mar;118(3):487-96 [10702199.001]
  • [Cites] J Clin Pathol. 2000 Feb;53(2):89-94 [10767821.001]
  • [Cites] Gastroenterology. 2000 Aug;119(2):333-8 [10930368.001]
  • [Cites] J Natl Cancer Inst. 2000 Aug 16;92(16):1316-21 [10944553.001]
  • [Cites] Gut. 2001 Mar;48(3):304-9 [11171817.001]
  • [Cites] Endoscopy. 2001 May;33(5):391-400 [11396755.001]
  • [Cites] J Natl Cancer Inst. 2001 Jul 18;93(14):1054-61 [11459866.001]
  • [Cites] Cancer. 2001 Aug 1;92(3):549-55 [11505399.001]
  • [Cites] J Natl Cancer Inst. 2002 Mar 20;94(6):422-9 [11904314.001]
  • [Cites] Gastroenterology. 2002 Apr;122(4):1101-12 [11910360.001]
  • [Cites] Eur J Cardiothorac Surg. 2002 Jul;22(1):1-6 [12103364.001]
  • [Cites] Am J Clin Pathol. 2002 Jul;118(1):60-6 [12109857.001]
  • [Cites] Gastroenterology. 2002 Aug;123(2):461-7 [12145799.001]
  • [Cites] Am J Gastroenterol. 2002 Aug;97(8):1888-95 [12190150.001]
  • [Cites] Int J Cancer. 2002 Dec 1;102(4):422-7 [12402314.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2560-6 [12855631.001]
  • [Cites] Gut. 2004 Aug;53(8):1070-4 [15247170.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1996 Jun;5(6):457-9 [8781742.001]
  • [Cites] Br J Clin Pract. 1996 Jul-Aug;50(5):245-8 [8794600.001]
  • [Cites] Dig Dis Sci. 1997 Apr;42(4):697-701 [9125634.001]
  • [Cites] In Vitro Cell Dev Biol Anim. 1998 Jan;34(1):46-52 [9542635.001]
  • [Cites] Oncogene. 2005 Jun 9;24(25):4138-48 [15824739.001]
  • [Cites] Cancer. 2005 Aug 15;104(4):730-9 [15971196.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2005 Dec;19(6):889-907 [16338648.001]
  • [Cites] Gut. 2006 Apr;55(4):442 [16531521.001]
  • (PMID = 19048049.001).
  • [ISSN] 1754-8411
  • [Journal-full-title] Disease models & mechanisms
  • [ISO-abbreviation] Dis Model Mech
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers
  • [Other-IDs] NLM/ PMC2561971
  •  go-up   go-down


7. Li M, Anastassiades CP, Joshi B, Komarck CM, Piraka C, Elmunzer BJ, Turgeon DK, Johnson TD, Appelman H, Beer DG, Wang TD: Affinity peptide for targeted detection of dysplasia in Barrett's esophagus. Gastroenterology; 2010 Nov;139(5):1472-80
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Affinity peptide for targeted detection of dysplasia in Barrett's esophagus.
  • BACKGROUND & AIMS: Dysplasia is a premalignant condition in Barrett's esophagus that is difficult to detect on endoscopy because of its flat architecture and patchy distribution.
  • We aim to select and validate an affinity peptide that binds to esophageal dysplasia for future clinical studies.
  • METHODS: Peptide selection was performed using phage display by removing nonspecific binders using Q-hTERT (intestinal metaplasia) cells and achieving specific binding against OE33 (esophageal adenocarcinoma) cells.
  • On esophageal specimens (n = 12), the fluorescence intensity (mean ± SEM) in 1-mm intervals classified histologically as squamous (n = 145), intestinal metaplasia (n = 83), dysplasia (n = 61), and gastric mucosa (n = 69) was 46.5 ± 1.6, 62.3 ± 5.8, 100.0 ± 9.0, and 42.4 ± 3.0 arb units, respectively.
  • CONCLUSIONS: The peptide sequence SNFYMPL binds specifically to dysplasia in Barrett's esophagus and can be fluorescence labeled to target premalignant mucosa on imaging.

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
  • [Cites] Am J Med. 2002 Oct 15;113(6):499-505 [12427500.001]
  • [Cites] Gastroenterology. 2002 Feb;122(2):406-14 [11832455.001]
  • [Cites] Clin Cancer Res. 2003 Oct 15;9(13):4819-25 [14581353.001]
  • [Cites] Gut. 2004 Aug;53(8):1070-4 [15247170.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):6247-51 [15342411.001]
  • [Cites] Int J Pept Protein Res. 1990 Mar;35(3):161-214 [2191922.001]
  • [Cites] Science. 1990 Jul 27;249(4967):386-90 [1696028.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Aug;87(16):6378-82 [2201029.001]
  • [Cites] Gastroenterology. 1993 Jul;105(1):40-50 [8514061.001]
  • [Cites] Br J Cancer. 1999 Feb;79(3-4):595-603 [10027336.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5907-16 [15994969.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1721-9 [16452232.001]
  • [Cites] Endoscopy. 2006 Sep;38(9):867-72 [16981102.001]
  • [Cites] Clin Cancer Res. 2007 Oct 15;13(20):6049-55 [17947467.001]
  • [Cites] Nat Med. 2008 Apr;14(4):454-8 [18345013.001]
  • [Cites] Gastroenterology. 2008 Jul;135(1):24-31 [18442484.001]
  • [Cites] Arch Pathol Lab Med. 2008 Oct;132(10):1577-85 [18834215.001]
  • [Cites] Leukemia. 2009 Feb;23(2):235-44 [19151784.001]
  • [Cites] Clin Exp Metastasis. 2009;26(2):105-19 [18975117.001]
  • [Cites] Lancet. 2009 Mar 7;373(9666):850-61 [19269522.001]
  • [Cites] Mol Biosyst. 2009 Nov;5(11):1279-91 [19823742.001]
  • [Cites] Am J Clin Pathol. 2009 Jul;132(1):94-100 [19864239.001]
  • [Cites] N Engl J Med. 2009 Dec 24;361(26):2548-56 [20032324.001]
  • [Cites] Gastroenterology. 2010 Feb;138(2):435-46 [19852961.001]
  • [Cites] J Natl Cancer Inst. 2010 Feb 24;102(4):271-4 [20075370.001]
  • [Cites] Gastroenterology. 2010 Mar;138(3):828-33.e1 [20096697.001]
  • [Cites] Carcinogenesis. 2003 Jul;24(7):1183-90 [12807723.001]
  • [Cites] Cancer Res. 2000 Mar 1;60(5):1341-7 [10728696.001]
  • [Cites] Cell Growth Differ. 2001 Apr;12(4):201-10 [11331249.001]
  • [CommentIn] Nat Rev Gastroenterol Hepatol. 2011 Jan;8(1):3 [21265056.001]
  • (PMID = 20637198.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U54 CA163059; United States / NCI NIH HHS / CA / U54 CA163059-01; United States / NCI NIH HHS / CA / U54 CA13642; United States / NCI NIH HHS / CA / U54 CA136429; United States / NCI NIH HHS / CA / U54 CA136429-01
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Affinity Labels; 0 / Carrier Proteins
  • [Other-IDs] NLM/ NIHMS365874; NLM/ PMC3319360
  •  go-up   go-down


8. 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
COS Scholar Universe. author profiles.

  • [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.
  • In contrast, normal squamous and cardiac mucosa, as well as noninvasive Barrett lesions, failed to label with mesothelin.
  • 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.
  • [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


9. Ormeci N, Savas B, Coban S, Palabiyikoğlu M, Ensari A, Kuzu I, Kursun N: The usefulness of chromoendoscopy with methylene blue in Barrett's metaplasia and early esophageal carcinoma. Surg Endosc; 2008 Mar;22(3):693-700
Hazardous Substances Data Bank. METHYLENE BLUE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The usefulness of chromoendoscopy with methylene blue in Barrett's metaplasia and early esophageal carcinoma.
  • BACKGROUND: Barrett's esophagus is a condition that is premalignant for adenocarcinoma of the esophagus and the esophagogastric junction.
  • Early detection of Barrett's metaplasia and dysplasia is very important to decrease the mortality and morbidity from esophageal adenocarcinoma cancer.
  • This study aimed to evaluate the effectiveness of methylene blue-targeted biopsies in the differential diagnosis of intestinal metaplasia, dysplasia, and superficial esophageal carcinoma.
  • The esophagus was stained with methylene blue, after which six biopsies were taken from stained and unstained areas.
  • However, there was no statistical difference between the two methods in the diagnosis of esophagitis or esophageal carcinoma (p > 0.05).
  • Stained biopsies were superior to unstained biopsies in terms of sensitivity for Barrett's epithelium and esophageal carcinoma (p < 0.001).
  • CONCLUSION: Chromoendoscopy is useful for delineating Barrett's epithelium and for indicating the correct location for securing biopsies where dysplasia or early esophageal cancer is suspected.
  • [MeSH-major] Barrett Esophagus / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology. Esophagoscopy / methods. Methylene Blue. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy, Needle. Cohort Studies. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Risk Assessment. Sensitivity and Specificity. Staining and Labeling / methods

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gastrointest Endosc. 1998 Jul;48(1):26-31 [9684660.001]
  • [Cites] Endoscopy. 2004 Jul;36(7):590-4 [15243880.001]
  • [Cites] Int J Epidemiol. 2000 Aug;29(4):645-54 [10922340.001]
  • [Cites] Endoscopy. 2005 Jan;37(1):8-18 [15657852.001]
  • [Cites] Gut. 2004 Aug;53(8):1070-4 [15247170.001]
  • [Cites] Gut. 2003 Jan;52(1):24-7 [12477754.001]
  • [Cites] Dig Dis Sci. 2002 Sep;47(9):2108-11 [12353864.001]
  • [Cites] Gastrointest Endosc. 2001 Sep;54(3):403-9 [11522995.001]
  • [Cites] Gastrointest Endosc. 2001 May;53(6):559-65 [11323579.001]
  • [Cites] Gastroenterol Clin North Am. 2002 Jun;31(2):461-79, ix [12134613.001]
  • [Cites] Crit Rev Oncol Hematol. 2003 May;46(2):187-206 [12711361.001]
  • [Cites] Endoscopy. 2005 Jun;37(6):583-6 [15933935.001]
  • [Cites] Endoscopy. 2005 Sep;37(9):879-920 [16116544.001]
  • [Cites] Gastroenterology. 2000 Apr;118(4):670-7 [10734018.001]
  • [Cites] Gut. 2005 Mar;54 Suppl 1:i6-12 [15711008.001]
  • [Cites] Gut. 2003 May;52(5):623-8 [12692043.001]
  • [Cites] Gastroenterology. 2004 Jul;127(1):310-30 [15236196.001]
  • [Cites] Scand J Gastroenterol. 1993 Mar;28(3):193-6 [8446842.001]
  • [Cites] Endoscopy. 2001 Nov;33(11):909-16 [11668398.001]
  • [Cites] Endoscopy. 2001 May;33(5):391-400 [11396755.001]
  • [Cites] Dig Dis Sci. 2000 Feb;45(2):225-9 [10711429.001]
  • [Cites] Ann Intern Med. 2003 Feb 4;138(3):176-86 [12558356.001]
  • [Cites] JAMA. 2002 Apr 17;287(15):1972-81 [11960540.001]
  • [Cites] Dig Dis Sci. 2005 Feb;50(2):389-93 [15745106.001]
  • [Cites] Gut. 2001 Mar;48(3):314-9 [11171819.001]
  • [Cites] Gut. 2003 Jan;52(1):28-33 [12477755.001]
  • [Cites] Gastrointest Endosc. 2001 Sep;54(3):289-93 [11522967.001]
  • [Cites] Am J Gastroenterol. 1997 Feb;92(2):212-5 [9040193.001]
  • [Cites] Gastrointest Endosc. 2000 May;51(5):560-8 [10805842.001]
  • [Cites] Lancet. 2003 Aug 2;362(9381):373-4 [12907012.001]
  • [Cites] Endoscopy. 2004 Feb;36(2):103-9 [14765307.001]
  • [Cites] Am J Med. 2001 Dec 3;111 Suppl 8A:130S-136S [11749938.001]
  • [Cites] Gastroenterology. 2001 Jan;120(1):7-12 [11208708.001]
  • [Cites] Gastroenterology. 2005 Dec;129(6):1825-31 [16344051.001]
  • [Cites] Gastroenterology. 2000 Sep;119(3):677-82 [10982761.001]
  • [Cites] Gastrointest Endosc. 1996 Jul;44(1):1-7 [8836709.001]
  • [Cites] Endoscopy. 1999 May;31(4):325-8 [10376462.001]
  • [Cites] Gastrointest Endosc. 2001 Jan;53(1):47-52 [11154488.001]
  • [Cites] Gastroenterol Clin North Am. 2002 Jun;31(2):441-60 [12134612.001]
  • [Cites] Gastrointest Endosc. 2001 Sep;54(3):294-301 [11522968.001]
  • [Cites] Gastrointest Endosc. 2001 Mar;53(3):333-5 [11231393.001]
  • [Cites] N Engl J Med. 2002 Mar 14;346(11):836-42 [11893796.001]
  • [Cites] Endoscopy. 2002 Aug;34(8):604-10 [12173079.001]
  • [Cites] Gut. 2003 Jan;52(1):18-23 [12477753.001]
  • (PMID = 17704887.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] T42P99266K / Methylene Blue
  •  go-up   go-down


10. Gaddam S, Sharma P: Advances in endoscopic diagnosis and treatment of Barrett's esophagus. J Dig Dis; 2010 Dec;11(6):323-33
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advances in endoscopic diagnosis and treatment of Barrett's esophagus.
  • Barrett's esophagus (BE) is defined as abnormal specialized columnar metaplasia with intestinalization in place of the normal squamous esophageal epithelium.
  • Patients with high grade dysplasia (HGD) and early cancer have a high rate of progression to invasive adenocarcinoma and traditionally these patients were treated with esophagectomy.
  • [MeSH-major] Adenocarcinoma. Barrett Esophagus. Endoscopy, Digestive System / trends. Esophageal Neoplasms

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.
  • (PMID = 21091894.001).
  • [ISSN] 1751-2980
  • [Journal-full-title] Journal of digestive diseases
  • [ISO-abbreviation] J Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  •  go-up   go-down


11. 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
COS Scholar Universe. author profiles.

  • [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.
  • Claudins 3, 4, and 7 gene expression was analyzed by Affymetrix U-133 microarrays in three esophageal adenocarcinomas, one case of BE, and three normal esophagi.
  • 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 microarray analysis, Claudin 3 showed a marked increase in mRNA expression compared with normal esophagus (approximately 100-fold).
  • 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%).
  • Claudin 7 expression was minimal in squamous and gastric mucosa but strong (3+ to 4+) in BE and low-grade dysplasia.
  • 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.
  • [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


12. Jaquet Y, Pilloud R, Grosjean P, Radu A, Monnier P: Extended endoscopic mucosal resection in the esophagus and hypopharynx: a new rigid device. Eur Arch Otorhinolaryngol; 2007 Jan;264(1):57-62
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extended endoscopic mucosal resection in the esophagus and hypopharynx: a new rigid device.
  • We present a new device allowing for the diagnosis and treatment of extended superficial lesions of the esophagus and hypopharynx such as early squamous cell carcinoma, intestinal metaplasia with high grade intraepithelial neoplasia or early adenocarcinoma arising in Barrett's esophagus.
  • The deep resection margin was precisely located at the submucosal level, a prerequisite for a safe resection of superficial cancers of the esophagus and hypopharynx.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / surgery. Endoscopy / methods. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Hypopharyngeal Neoplasms / pathology. Hypopharyngeal Neoplasms / surgery. Minimally Invasive Surgical Procedures / instrumentation
  • [MeSH-minor] Barrett Esophagus / pathology. Barrett Esophagus / surgery. Early Diagnosis. Equipment Design. Humans. Mucous Membrane / pathology

  • MedlinePlus Health Information. consumer health - Endoscopy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Laryngoscope. 1999 Oct;109(10):1703-8 [10522946.001]
  • [Cites] Otolaryngol Head Neck Surg. 2001 Jan;124(1):58-67 [11228455.001]
  • [Cites] Endoscopy. 2000 Nov;32(11):836-44 [11085471.001]
  • [Cites] Ann Surg. 1999 Sep;230(3):433-8; discussion 438-40 [10493489.001]
  • [Cites] Endoscopy. 2004 Sep;36(9):782-7 [15326573.001]
  • [Cites] Endoscopy. 2004 Apr;36(4):298-305 [15057678.001]
  • [Cites] Gastrointest Endosc. 2004 Oct;60(4):623-7 [15472695.001]
  • [Cites] Endoscopy. 2004 Sep;36(9):788-801 [15326574.001]
  • [Cites] J Thorac Cardiovasc Surg. 2005 Nov;130(5):1399 [16256795.001]
  • [Cites] J Thorac Cardiovasc Surg. 1999 Jan;117(1):16-23; discussion 23-5 [9869753.001]
  • [Cites] Otolaryngol Head Neck Surg. 2001 Feb;124(2):208-12 [11226943.001]
  • [Cites] Mod Pathol. 2006 Mar;19(3):475-80 [16444191.001]
  • [Cites] Gastrointest Endosc. 2003 Aug;58(2):288-92 [12872107.001]
  • [Cites] Gastrointest Endosc. 2003 Jun;57(7):854-9 [12776032.001]
  • [Cites] Endoscopy. 1998 Mar;30(3):258-65 [9615874.001]
  • [Cites] J Clin Pathol. 1999 Jul;52(7):509-12 [10605403.001]
  • (PMID = 17043858.001).
  • [ISSN] 0937-4477
  • [Journal-full-title] European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
  • [ISO-abbreviation] Eur Arch Otorhinolaryngol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


13. Long KB, Hornick JL: SOX2 is highly expressed in squamous cell carcinomas of the gastrointestinal tract. Hum Pathol; 2009 Dec;40(12):1768-73
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] SOX2 is highly expressed in squamous cell carcinomas of the gastrointestinal tract.
  • SOX2 is a high-mobility group box embryonic stem cell transcription factor that is expressed in the developing foregut and normal gastric epithelium and is downregulated in intestinal metaplasia of the stomach and esophagus.
  • In addition, SOX2 colocalizes with p63 in the basal layer and plays a critical role in the maintenance of the stratified squamous epithelium of the esophagus.
  • SOX2 expression in squamous cell carcinomas of the gastrointestinal tract has not been previously evaluated.
  • The purpose of this study was to determine whether SOX2 is differentially expressed in squamous cell carcinomas versus adenocarcinomas of the esophagus and rectum/anal canal and to compare its expression to p63, cytokeratin 5/6, and CDX2.
  • In total, 93 tumors were evaluated: 26 esophageal squamous cell carcinomas, 23 esophageal adenocarcinomas, 21 squamous cell carcinomas of the anal canal, and 23 rectal adenocarcinomas.
  • SOX2 was expressed in 81% of esophageal squamous cell carcinomas and 91% of anal canal squamous cell carcinomas, compared to 13% and 17% of esophageal and rectal adenocarcinomas, respectively. p63 was expressed in 96% of esophageal squamous cell carcinomas and 100% of anal canal squamous cell carcinomas; the single squamous cell carcinoma negative for p63 was strongly positive for SOX2.
  • Cytokeratin 5/6 was expressed in most esophageal and anal canal squamous cell carcinomas, but was also positive in 43% of esophageal adenocarcinomas and 13% of rectal adenocarcinomas.
  • In summary, SOX2 is preferentially expressed in squamous cell carcinomas of the esophagus and anal canal compared to adenocarcinomas from these sites.
  • SOX2 may be useful in an immunohistochemical panel to differentiate between squamous cell carcinomas and adenocarcinomas of the gastrointestinal tract.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Squamous Cell / metabolism. Gastrointestinal Neoplasms / metabolism. SOXB1 Transcription Factors / biosynthesis
  • [MeSH-minor] Adenocarcinoma / metabolism. Diagnosis, Differential. Homeodomain Proteins / biosynthesis. Humans. Immunohistochemistry. Keratin-5 / biosynthesis. Keratin-6 / biosynthesis. Membrane Proteins / biosynthesis

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19716157.001).
  • [ISSN] 1532-8392
  • [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 / CDX2 protein, human; 0 / CKAP4 protein, human; 0 / Homeodomain Proteins; 0 / Keratin-5; 0 / Keratin-6; 0 / Membrane Proteins; 0 / SOX2 protein, human; 0 / SOXB1 Transcription Factors
  •  go-up   go-down


14. Maezato K, Nishimaki T, Oshiro M, Yamashiro T, Sasaki H, Sashida Y: Signet-ring cell carcinoma of the esophagus associated with Barrett's epithelium: report of a case. Surg Today; 2007;37(12):1096-101
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Signet-ring cell carcinoma of the esophagus associated with Barrett's epithelium: report of a case.
  • We herein report a case of infiltrative esophageal signet-ring cell carcinoma resembling gastric signet-ring cell carcinoma.
  • Grossly, the tumor was a diffusely infiltrative carcinoma involving the lower esophagus measuring 11 cm in diameter.
  • Histologically, the tumor was signet-ring cell carcinoma covered with normal squamous epithelium.
  • However, the most superficial part of the tumor center contained a region of Barrett's mucosa with incomplete-type intestinal metaplasia and a well-differentiated adenocarcinoma component with goblet cells.
  • The expression of cytokeratins 7 and 20 also indicated that both the Barrett's mucosa and the signet-ring cell carcinoma had an esophageal origin.
  • Esophageal signet-ring cell carcinoma with diffuse infiltrative growth is quite rare, and may need a special treatment strategy because of its highly aggressive behavior and poor treatment outcome.
  • [MeSH-major] Barrett Esophagus / complications. Carcinoma, Signet Ring Cell / pathology. Esophageal Neoplasms / pathology
  • [MeSH-minor] Aged. Biopsy. Diagnosis, Differential. Esophagectomy. Fatal Outcome. Humans. Male

  • Genetic Alliance. consumer health - Signet ring cell carcinoma.
  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 1996 Aug 15;335(7):462-7 [8672151.001]
  • [Cites] J Surg Oncol. 1999 May;71(1):54-7 [10362093.001]
  • [Cites] World J Surg. 2002 Sep;26(9):1155-9 [12209246.001]
  • [Cites] Nihon Shokakibyo Gakkai Zasshi. 1996 Sep;93(9):644-9 [8905971.001]
  • [Cites] Jpn J Surg. 1980 Jun;10(2):137-41 [7431687.001]
  • [Cites] Hum Pathol. 1999 Mar;30(3):288-94 [10088547.001]
  • [Cites] Gastric Cancer. 2003;6(3):159-67 [14520529.001]
  • [Cites] J Gastroenterol. 2001 Jun;36(6):410-4 [11428588.001]
  • [Cites] Gastric Cancer. 2006;9(2):51-66 [16767357.001]
  • [Cites] J Gastrointest Surg. 1998 May-Jun;2(3):244-9 [9841981.001]
  • [Cites] Lancet. 2002 May 18;359(9319):1727-33 [12049861.001]
  • [Cites] Clin Cancer Res. 2005 Mar 15;11(6):2229-36 [15788671.001]
  • [Cites] Endoscopy. 2004 Sep;36(9):776-81 [15326572.001]
  • [Cites] Int J Cancer. 2002 Jun 20;99(6):860-8 [12115489.001]
  • [Cites] Dis Esophagus. 2002;15(3):219-25 [12444994.001]
  • (PMID = 18030574.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


15. Ponsot P: [Barrett's oesophagus: endoscopic diagnosis and follow-up]. Ann Chir; 2006 Jan;131(1):3-6
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [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

  • [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


16. Chandrasoma P, Wijetunge S, Demeester SR, Hagen J, Demeester TR: The histologic squamo-oxyntic gap: an accurate and reproducible diagnostic marker of gastroesophageal reflux disease. Am J Surg Pathol; 2010 Nov;34(11):1574-81
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This study provides a method to develop a histologic definition of GERD based on biopsies obtained from the affected esophagus.
  • Biopsies were obtained from the esophagus, around the gastroesophageal junction and the stomach: proximal, body, and antrum.
  • Patients who had oxyntocardiac±cardiac±intestinal epithelia between the squamous epithelium proximally and the proximal limit of gastric oxyntic mucosa distally were defined as having a squamo-oxyntic gap.
  • Only oxyntocardiac epithelium was seen in 190 (11.5%) of the patients, oxyntocardiac and cardiac epithelia in 898 (54.3%), and intestinal metaplasia in addition to the other 2 epithelial types in 567 (34.2%).
  • The prevalence of intestinal metaplasia was directly proportional to length of the squamo-oxyntic gap, being 24.3% (340/1399) when the length was <1 cm, and 83.5% (147/176) with length 1 to 5 cm.
  • All patients with a length more than 5 cm had intestinal metaplasia.
  • The distribution of the 3 epithelia was constant irrespective of the length of the squamocolumnar gap; intestinal metaplasia, when present, was seen maximally in the proximal region of the gap, cardiac epithelium intermediate and oxyntocardiac epithelium in the most distal segment of the gap.
  • The squamo-oxyntic gap started in a dilated region distal to the end of the tubular esophagus and distal to the proximal limit of the rugal folds and extended into the tubular esophagus.
  • Distal gastric biopsies showed no evidence of significant inflammation, intestinal metaplasia or Helicobacter pylori infection in 1543 (93.2%) of the patients, indicating that the squamo-oxyntic gap was largely independent of gastric pathology.
  • We provide evidence that the squamo-oxyntic gap is equivalent to the columnar-lined esophagus.
  • The presence of intestinal metaplasia within the squamo-oxyntic gap is the most accurate risk indicator for esophageal adenocarcinoma and defines Barrett esophagus.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Epithelial Cells / pathology. Esophageal Neoplasms / diagnosis. Esophagus / pathology. Gastroesophageal Reflux / diagnosis. Parietal Cells, Gastric / pathology. Precancerous Conditions / diagnosis
  • [MeSH-minor] Biopsy. California. Endoscopy, Gastrointestinal. Humans. Metaplasia. Predictive Value of Tests. Reproducibility of Results. Retrospective Studies. Risk Assessment. Risk Factors. Severity of Illness Index

  • Genetic Alliance. consumer health - Gastroesophageal Reflux.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - GERD.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Am J Surg Pathol. 2011 May;35(5):773; author reply 773-4 [21502913.001]
  • (PMID = 20871393.001).
  • [ISSN] 1532-0979
  • [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


17. Micev M, Cosić-Micev M: [Pathology and pathobiology of the oesophageal carcinoma]. Acta Chir Iugosl; 2010;57(2):15-26
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Identification of dysplasia in mucosal biopsies is the most reliable pathologic indicator of an increased risk of development of squamous cell carcinoma and passes through the sequence of chronic esophagitis, low-grade and high-grade dysplasia and invasive carcinoma.
  • Although Barrett's esophagus is a precursor to esophageal adenocarcinoma and have a well described sequence of carcinogenesis: the Barrett's metaplasia-dysplasia-adenocarcinoma sequence, not all patients with this disorder require intensive surveillance.
  • More studies are needed to define other early nonmorphologic biomarkers for risk of squamous cell carcinoma.
  • [MeSH-major] Esophageal Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Barrett Esophagus / complications. Barrett Esophagus / pathology. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / pathology. Humans

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20954310.001).
  • [ISSN] 0354-950X
  • [Journal-full-title] Acta chirurgica Iugoslavica
  • [ISO-abbreviation] Acta Chir Iugosl
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Serbia
  •  go-up   go-down


18. Dias Pereira A, Suspiro A, Chaves P: Cancer risk in Barrett's oesophagus. Eur J Gastroenterol Hepatol; 2007 Nov;19(11):915-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • )Barrett's oesophagus results from the replacement of the normal squamous lining of the oesophagus by a columnar epithelium.
  • It is the sole known premalignant condition for oesophageal adenocarcinoma.
  • The prerequisite of the presence of intestinal metaplasia for the diagnosis of Barrett's oesophagus, although widely accepted, is questioned by some authors.
  • How adenocarcinoma incidence is influenced by requiring or not intestinal metaplasia for Barrett's oesophagus diagnosis is unknown.
  • Data on adenocarcinoma incidence in short segments (<3 cm) are very scarce, but it is believed to be lower than in long segments.
  • Frequently, therapeutic intervention is performed when high-grade dysplasia is diagnosed, preventing progression to adenocarcinoma.
  • [MeSH-major] Barrett Esophagus / pathology. Esophagus / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Disease Progression. Esophageal Neoplasms / pathology. Esophagoscopy. Humans. Incidence. Intestines / pathology. Metaplasia. Risk

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18049157.001).
  • [ISSN] 0954-691X
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


19. Punia RS, Arya S, Mohan H, Duseja A, Bal A: Spectrum of clinico-pathological changes in Barrett oesophagus. J Assoc Physicians India; 2006 Mar;54:187-9
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: Barrett oesophagus is replacement of squamous epithelium to specialised intestinal metaplasia.
  • It is associated with an increased risk for adenocarcinoma which develops through dysplasia.
  • On histology examination, in 6 cases, squamous epithelium was replaced by intestinal epithelium containing goblet cells and in 7 cases it was replaced by gastric epithelium.
  • Associated dysplasia was not seen in any of the case, while one case showed associated adenocarcinoma.
  • There is a paucity of patients with pure dysplasia in Barrett metaplasia.
  • Despite the fact that there are a number of patients presenting with Barrett esophagus and carcinoma, very few patients present with dysplasia, indicating that Barrett oesophagus is a silent disease presenting later as a carcinoma.
  • [MeSH-major] Barrett Esophagus / diagnosis. Barrett Esophagus / pathology. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / pathology
  • [MeSH-minor] Adult. Age Factors. Aged. Biopsy. Esophagoscopy. Female. Humans. India. Male. Metaplasia. Middle Aged. Retrospective Studies. Sex Factors. Staining and Labeling

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16800342.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  •  go-up   go-down


20. Chandrasoma P: Controversies of the cardiac mucosa and Barrett's oesophagus. Histopathology; 2005 Apr;46(4):361-73
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Confusion regarding the diagnosis of Barrett's oesophagus exists because of a false dogma that cardiac mucosa is normally present in the gastro-oesophageal junctional region.
  • Recent data indicate that the only normal epithelia in the oesophagus and proximal stomach are squamous epithelium and gastric oxyntic mucosa.
  • When this fact is recognized, it becomes easy to develop precise histological definitions for the normal state (presence of only squamous and oxyntic mucosa), metaplastic oesophageal columnar epithelium (cardiac mucosa with and without intestinal metaplasia, and oxynto-cardiac mucosa), the gastro-oesophageal junction (the proximal limit of gastric oxyntic mucosa), the oesophagus (that part of the foregut lined by squamous and metaplastic columnar epithelium), reflux disease (the presence of metaplastic columnar epithelium), and Barrett's oesophagus (cardiac mucosa with intestinal metaplasia).
  • It is also possible to assess accurately the severity of reflux which is directly proportional to the amount of metaplastic columnar epithelium, and the risk of adenocarcinoma which is related to the amount of dysplasia in intestinal metaplastic epithelium present within the columnar lined segment of the oesophagus.
  • Histopathological precision cannot be matched by any other modality and can convert the confusion that exists regarding diagnosis of Barrett's oesophagus to complete lucidity in a manner that is simple, accurate, and reproducible.
  • [MeSH-major] Barrett Esophagus / pathology. Cardia / pathology. Gastric Mucosa / pathology
  • [MeSH-minor] Esophagogastric Junction / pathology. Humans. Metaplasia

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Histopathology. 2006 Jul;49(1):97-8; author reply 98 [16842257.001]
  • (PMID = 15810947.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 48
  •  go-up   go-down


21. Basseri B, Conklin JL, Mertens RB, Lo SK, Bellack GS, Shaye OA: Heterotopic gastric mucosa (inlet patch) in a patient with laryngopharyngeal reflux (LPR) and laryngeal carcinoma: a case report and review of literature. Dis Esophagus; 2009;22(4):E1-5
MedlinePlus Health Information. consumer health - GERD.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The inlet patch is an area of heterotopic gastric mucosa most commonly located in the postcricoid portion of the esophagus at, or just below, the level of the upper esophageal sphincter.
  • Esophageal and supraesophageal symptoms are commonly associated with inlet patch, while esophageal adenocarcinoma rarely complicates it.
  • Laryngeal adenocarcinoma associated with inlet patch is not described in the literature.
  • Upper endoscopy at our institution revealed an upper esophageal stricture and a 1 cm inlet patch.
  • Biopsies showed columnar mucosa (predominantly gastric cardiac/fundic type) consistent with inlet patch, with focal intestinal metaplasia.
  • Dysphagia and regurgitation were improved by serial dilatations of the upper esophageal stricture.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19473208.001).
  • [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] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 30
  •  go-up   go-down


22. di Pietro M, Fitzgerald RC: Barrett's oesophagus: an ideal model to study cancer genetics. Hum Genet; 2009 Aug;126(2):233-46
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Chronic gastro-oesophageal reflux disease can induce a metaplastic change of the distal oesophagus called Barrett's oesophagus whereby the normal squamous epithelium is substituted by a columnar epithelium.
  • 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

  • [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


23. Chlumská A, Boudová L, Benes Z, Zámecník M: Histopathologic changes in gastroesophageal reflux disease. A study of 126 bioptic and autoptic cases. Cesk Patol; 2007 Oct;43(4):142-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The histologic diagnosis of reflux esophagitis is still complicated by the lack of a consensus opinion on what is the normal mucosa in the area of the gastroesophageal junction (GEJ).
  • Most authors consider GEJ as the junction between the squamous and the cardiac epithelium.
  • These glands are in fact indistinguishable from metaplastic mucosa that arises in the distal esophagus in consequence of gastroesophageal reflux (GER).
  • In our series of 120 endoscopic biopsies of the GEJ and distal esophagus the cardia type mucosa (CM) was always present.
  • In 17 cases, CM displayed intestinal metaplasia (IM) predominantly of incomplete type and no dysplasia.
  • In one specimen of esophagus resected for adenocarcinoma, CM with incomplete IM was found in the vicinity of the tumor.
  • Squamous metaplastic epithelium was often seen near the orifices of submucosal esophageal glands in these areas, indicating the metaplastic nature of the glandular mucosa in the distal esophagus.
  • [MeSH-minor] Adult. Cardia / pathology. Esophagogastric Junction / pathology. Esophagus / pathology. Female. Humans. Male. Middle Aged

  • Genetic Alliance. consumer health - Gastroesophageal Reflux.
  • 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 = 18188921.001).
  • [ISSN] 1210-7875
  • [Journal-full-title] Československá patologie
  • [ISO-abbreviation] Cesk Patol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Czech Republic
  •  go-up   go-down


24. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypermethylation of tachykinin-1 is a potential biomarker in human esophageal cancer.
  • PURPOSE: Our aim was to investigate whether and at what stage hypermethylation of the tachykinin-1 (TAC1) gene is associated with human esophageal neoplastic transformation.
  • EXPERIMENTAL DESIGN: TAC1 promoter hypermethylation was examined by real-time methylation-specific PCR in 258 human esophageal specimens and 126 plasma samples from patients or tissues at various stages of neoplastic evolution.
  • 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.
  • CONCLUSIONS: TAC1 promoter hypermethylation is a common event in both major histologic types of human esophageal carcinoma, occurs early, correlates with other progression risk factors in esophageal adenocarcinogenesis, and is a tissue biomarker of a poor prognosis in ESCC.
  • 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.
  • [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






Advertisement