[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 1128
1. Ferguson HR, Wild CP, Anderson LA, Murphy SJ, Johnston BT, Murray LJ, Watson RG, McGuigan J, Reynolds JV, Hardie LJ: No association between hOGG1, XRCC1, and XPD polymorphisms and risk of reflux esophagitis, Barrett's esophagus, or esophageal adenocarcinoma: results from the factors influencing the Barrett's adenocarcinoma relationship case-control study. Cancer Epidemiol Biomarkers Prev; 2008 Mar;17(3):736-9
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.
  • [Title] No association between hOGG1, XRCC1, and XPD polymorphisms and risk of reflux esophagitis, Barrett's esophagus, or esophageal adenocarcinoma: results from the factors influencing the Barrett's adenocarcinoma relationship case-control study.
  • Reflux of gastric contents can lead to development of reflux esophagitis and Barrett's esophagus.
  • Barrett's esophagus is a risk factor for esophageal adenocarcinoma.
  • Small studies have reported associations with XPD Lys 751 Gln and esophageal adenocarcinoma.
  • XRCC1 Arg 399 Gln has been linked to Barrett's esophagus and reflux esophagitis.
  • In a population-based case-control study, we examined associations of the hOGG1 Ser 326 Cys, XRCC1 Arg 399 Gln, and XPD Lys 751 Gln polymorphisms with risk of esophageal adenocarcinoma, Barrett's esophagus, and reflux esophagitis.
  • Genomic DNA was extracted from blood samples collected from cases of esophageal adenocarcinoma (n = 210), Barrett's esophagus (n = 212), reflux esophagitis (n = 230), and normal population controls frequency matched for age and sex (n = 248).
  • There were no statistically significant associations between these polymorphisms and risk of esophageal adenocarcinoma, Barrett's esophagus, or reflux esophagitis.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Esophagitis, Peptic / genetics. Polymorphism, Genetic

  • 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 = 18349297.001).
  • [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


2. Vissers KJ, Dinjens WN, Riegman PH, Tilanus HW, van Dekken H: Allelic imbalance on distal 7q (7q36.1-q36.3) in gastric cardia and oesophageal (Barrett's) adenocarcinoma. Anticancer Res; 2005 Mar-Apr;25(2A):913-6
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allelic imbalance on distal 7q (7q36.1-q36.3) in gastric cardia and oesophageal (Barrett's) adenocarcinoma.
  • BACKGROUND: Oesophageal (Barrett's) and gastric cardia adenocarcinomas are cancers arising at and around the gastro-oesophageal junction.
  • MATERIALS AND METHODS: We investigated the 7q region with a set of 5 polymorphic markers spanning 7q36.1-q36.3 in 33 Barrett-related carcinomas.
  • RESULTS: Overall, the number of allelic loss was higher in Barrett's cancers than in gastric cardia carcinomas (p=0.04).
  • In Barrett's adenocarcinomas, imbalance varied from 28% to 45% (of informative cases) with the highest prevalence at marker D7S483.
  • CONCLUSION: Marker D7S483 can aid in discriminating oesophageal (Barrett's) and gastric cardia carcinomas.
  • Further, this region possibly harbours cancer gene(s) involved in Barrett-related adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / genetics. Allelic Imbalance. Barrett Esophagus / genetics. Cardia / pathology. Chromosomes, Human, Pair 7 / genetics. Esophageal Neoplasms / genetics. Stomach Neoplasms / genetics

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15868927.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  •  go-up   go-down


3. Huang Q, Yu C, Zhang X, Goyal RK: Comparison of DNA histograms by standard flow cytometry and image cytometry on sections in Barrett's adenocarcinoma. BMC Clin Pathol; 2008 May 30;8:5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of DNA histograms by standard flow cytometry and image cytometry on sections in Barrett's adenocarcinoma.
  • BACKGROUND: The purpose of this study was to compare DNA histograms obtained by standard flow cytometry (FC) and high fidelity image cytometry on sections (ICS) in normal gastrointestinal mucosa and Barrett's adenocarcinoma (BAC).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Anal Cell Pathol. 1998;17(4):189-200 [10391371.001]
  • [Cites] Eur J Cancer. 1999 May;35(5):787-95 [10505041.001]
  • [Cites] Am J Pathol. 2000 Feb;156(2):555-66 [10666385.001]
  • [Cites] Anal Quant Cytol Histol. 2000 Jun;22(3):199-205 [10872035.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):3164-70 [11306503.001]
  • [Cites] Am J Gastroenterol. 2001 Nov;96(11):3071-83 [11721752.001]
  • [Cites] Onkologie. 2003 Feb;26(1):32-7 [12624515.001]
  • [Cites] Gastrointest Endosc Clin N Am. 2003 Apr;13(2):369-97 [12916666.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):904-9 [14871819.001]
  • [Cites] Am J Gastroenterol. 2004 Oct;99(10):1887-94 [15447746.001]
  • [Cites] Histopathology. 2004 Oct;45(4):312-34 [15469470.001]
  • [Cites] BMC Clin Pathol. 2005 Aug 12;5:7 [16095543.001]
  • [Cites] Lab Invest. 2007 May;87(5):466-72 [17310216.001]
  • [Cites] J Clin Pathol. 2007 Jun;60(6):649-55 [17557867.001]
  • [Cites] Gastroenterol Clin Biol. 1991;15(10):703-10 [1816011.001]
  • [Cites] Gastroenterology. 1991 Dec;101(6):1588-93 [1955124.001]
  • [Cites] Cytometry. 1990;11(3):431-7 [2340777.001]
  • [Cites] Ann Pathol. 1990;10(3):161-5 [2386598.001]
  • [Cites] Hum Pathol. 1989 Jun;20(6):518-27 [2470665.001]
  • [Cites] Semin Diagn Pathol. 1989 Feb;6(1):55-82 [2645625.001]
  • [Cites] Cytometry. 1989 May;10(3):326-33 [2714115.001]
  • [Cites] Anal Quant Cytol Histol. 1995 Jun;17(3):163-71 [7546050.001]
  • [Cites] Hum Pathol. 1994 Oct;25(10):982-93 [7927321.001]
  • [Cites] Mod Pathol. 1994 Aug;7(6):652-64 [7991524.001]
  • [Cites] Mod Pathol. 1993 May;6(3):270-5 [8346174.001]
  • [Cites] Cytometry. 1993;14(5):472-7 [8354117.001]
  • [Cites] Gastroenterology. 1993 Jul;105(1):119-29 [8514029.001]
  • [Cites] Hum Pathol. 1996 Jun;27(6):553-60 [8666364.001]
  • [Cites] Anal Cell Pathol. 1996 Aug;11(3):159-71 [8888952.001]
  • [Cites] J Clin Pathol. 1996 Nov;49(11):931-7 [8944615.001]
  • [Cites] Anal Quant Cytol Histol. 1998 Jun;20(3):178-86 [9642444.001]
  • [Cites] Cytometry. 1998 Dec 15;34(6):257-63 [9879642.001]
  • (PMID = 18513411.001).
  • [ISSN] 1472-6890
  • [Journal-full-title] BMC clinical pathology
  • [ISO-abbreviation] BMC Clin Pathol
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK062867
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2424056
  •  go-up   go-down


Advertisement
4. Sarbia M, zur Hausen A, Feith M, Geddert H, von Rahden BH, Langer R, von Weyhern C, Siewert JR, Höfler H, Stein HJ: Esophageal (Barrett's) adenocarcinoma is not associated with Epstein-Barr virus infection: an analysis of 162 cases. Int J Cancer; 2005 Nov 20;117(4):698-700
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] Esophageal (Barrett's) adenocarcinoma is not associated with Epstein-Barr virus infection: an analysis of 162 cases.
  • [MeSH-major] Adenocarcinoma / complications. Barrett Esophagus / complications. Epstein-Barr Virus Infections / complications. Esophageal Neoplasms / complications

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15929074.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


5. Somerville M, Pitt M: Surveillance of Barrett's oesophagus: do we yet know whether it is worthwhile? Frontline Gastroenterol; 2010 Jul;1(2):88-93

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surveillance of Barrett's oesophagus: do we yet know whether it is worthwhile?
  • In 2004, the Peninsula Technology Assessment Group developed an economic model to assess the effectiveness and cost effectiveness of surveillance of Barrett's oesophagus in preventing morbidity and mortality from oesophageal adenocarcinoma.
  • At present, there seems little reason to change our original conclusion that surveillance of Barrett's oesophagus is unlikely to be cost effective and a definitive answer may only be possible from clinical trials now in progress.
  • As newer endoscopic techniques for treating Barrett's oesophagus and adenocarcinoma become more widely used, however, conventional surveillance programmes may no longer be undertaken, and revised economic models will be needed to assess the cost effectiveness of the new clinical pathways.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Gastroenterol Hepatol. 2004 Oct;2(10):868-79 [15476150.001]
  • [Cites] Histopathology. 2009 Jun;54(7):814-9 [19635100.001]
  • [Cites] Endoscopy. 2009 May;41(5):400-8 [19418393.001]
  • [Cites] Lancet Oncol. 2009 May;10(5):501-7 [19410194.001]
  • [Cites] J Natl Cancer Inst. 2004 Jun 2;96(11):885-7; author reply 887 [15173278.001]
  • [Cites] Lancet. 2009 Mar 7;373(9666):850-61 [19269522.001]
  • [Cites] Am J Gastroenterol. 2008 Jun;103(6):1340-5 [18510606.001]
  • [Cites] Ann Intern Med. 2003 Feb 4;138(3):176-86 [12558356.001]
  • [Cites] Health Qual Life Outcomes. 2006 Nov 27;4:90 [17129380.001]
  • [Cites] Eur J Cancer. 2008 Mar;44(4):588-99 [18272361.001]
  • [Cites] Clin Gastroenterol Hepatol. 2009 Jun;7(6):613-23 [19281858.001]
  • [Cites] Health Technol Assess. 2006 Mar;10(8):1-142, iii-iv [16545207.001]
  • [Cites] Am J Epidemiol. 2008 Aug 1;168(3):237-49 [18550563.001]
  • [Cites] Am J Gastroenterol. 1999 Aug;94(8):2043-53 [10445526.001]
  • [Cites] Pharmacoeconomics. 1998 Apr;13(4):397-409 [10178664.001]
  • [Cites] Am J Gastroenterol. 2008 May;103(5):1079-89 [18445097.001]
  • (PMID = 28839554.001).
  • [ISSN] 2041-4137
  • [Journal-full-title] Frontline gastroenterology
  • [ISO-abbreviation] Frontline Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  •  go-up   go-down


6. Wiech T, Nikolopoulos E, Weis R, Langer R, Bartholomé K, Timmer J, Walch AK, Höfler H, Werner M: Genome-wide analysis of genetic alterations in Barrett's adenocarcinoma using single nucleotide polymorphism arrays. Lab Invest; 2009 Apr;89(4):385-97
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] Genome-wide analysis of genetic alterations in Barrett's adenocarcinoma using single nucleotide polymorphism arrays.
  • We performed genome-wide analysis of copy-number changes and loss of heterozygosity (LOH) in Barrett's esophageal adenocarcinoma by single nucleotide polymorphism (SNP) microarrays to identify associated genomic alterations.
  • Using this technique, we identified several novel genes and DNA regions associated with esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Polymorphism, Single Nucleotide

  • 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 = 18663352.001).
  • [ISSN] 1530-0307
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


7. Rastogi A, Sharma P: Short-Segment Barrett's Esophagus and Adenocarcinoma. Gastroenterol Hepatol (N Y); 2006 Feb;2(2):134-139

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Short-Segment Barrett's Esophagus and Adenocarcinoma.
  • Barrett's esophagus is a known risk factor for the development of adenocarcinoma of the esophagus and esophagogastric junction.
  • Based on the length of the columnar segment at endoscopy, Barrett's esophagus has been arbitrarily separated into two broad categories: long-segment and short-segment.
  • The rapid rise in the incidence of esophageal adenocarcinoma has generated sustained research interest in this lesion.
  • Studies have shown that although the prevalence of short-segment Barrett's esophagus is higher than that of long-segment Barrett's esophagus, the risk of developing dysplasia and adenocarcinoma may actually be lower in those patients with short segment Barrett's esophagus.
  • Nonetheless, both dysplasia and esophageal adenocarcinoma have been reported in patients with short-segment Barrett's esophagus, making this arbitrary distinction clinically unimportant.
  • The current surveillance guidelines remain the same for both short- and long-segment Barrett's esophagus.
  • Another key issue is differentiating short-segment Barrett's esophagus from intestinal metaplasia of the gastric cardia.
  • The latter is distinct from esophageal intestinal metaplasia (ie, Barrett's esophagus) and probably does not warrant surveillance.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gut. 1992 Jun;33(6):733-7 [1624150.001]
  • [Cites] J Natl Cancer Inst. 2005 Jan 19;97(2):142-6 [15657344.001]
  • [Cites] Gastroenterology. 1984 Oct;87(4):927-33 [6468881.001]
  • [Cites] Am J Gastroenterol. 1999 Dec;94(12):3413-9 [10606296.001]
  • [Cites] JAMA. 1993 Sep 15;270(11):1320 [8360967.001]
  • [Cites] Gut. 2003 Jan;52(1):24-7 [12477754.001]
  • [Cites] Gastroenterology. 1995 Nov;109(5):1541-6 [7557137.001]
  • [Cites] Am J Gastroenterol. 1997 Mar;92(3):414-8 [9068460.001]
  • [Cites] Dig Dis Sci. 2002 Sep;47(9):2108-11 [12353864.001]
  • [Cites] Gastroenterology. 1999 Feb;116(2):277-85 [9922307.001]
  • [Cites] Gastroenterology. 1989 May;96(5 Pt 1):1249-56 [2703113.001]
  • [Cites] Gastrointest Endosc. 2001 May;53(6):559-65 [11323579.001]
  • [Cites] Gastrointest Endosc. 1987 Dec;33(6):413-6 [3443258.001]
  • [Cites] Cancer. 1987 Sep 1;60(5):1094-8 [3607726.001]
  • [Cites] Am J Gastroenterol. 2002 Aug;97(8):1888-95 [12190150.001]
  • [Cites] Gastroenterology. 2003 Dec;125(6):1670-7 [14724819.001]
  • [Cites] Am J Gastroenterol. 1999 Apr;94(4):913-8 [10201456.001]
  • [Cites] Am J Gastroenterol. 2001 May;96(5):1378-82 [11374671.001]
  • [Cites] Gut. 1997 Nov;41(5):585-9 [9414961.001]
  • [Cites] Endoscopy. 1993 Nov;25(9):652-4 [8119225.001]
  • [Cites] Am J Gastroenterol. 2002 Aug;97(8):1930-6 [12190156.001]
  • [Cites] Ann Intern Med. 2000 Apr 18;132(8):612-20 [10766679.001]
  • [Cites] Dig Dis Sci. 1997 Mar;42(3):597-602 [9073145.001]
  • [Cites] N Engl J Med. 1986 Aug 7;315(6):362-71 [2874485.001]
  • [Cites] Gastroenterology. 2004 Jul;127(1):310-30 [15236196.001]
  • [Cites] J Gastroenterol. 2004 Jan;39(1):14-20 [14767729.001]
  • [Cites] Ann Surg. 1983 Oct;198(4):554-65 [6625723.001]
  • [Cites] Gut. 1997 Jun;40(6):710-5 [9245922.001]
  • [Cites] Am J Surg Pathol. 2001 Jan;25(1):87-94 [11145256.001]
  • [Cites] Lancet. 1994 Dec 3;344(8936):1533-6 [7983953.001]
  • [Cites] Gastroenterology. 2002 Aug;123(2):461-7 [12145799.001]
  • [Cites] Gut. 1996 Jul;39(1):5-8 [8881798.001]
  • [Cites] Am J Gastroenterol. 1996 Aug;91(8):1507-11 [8759651.001]
  • [Cites] Gut. 2000 Jan;46(1):9-13 [10601047.001]
  • [Cites] Hum Pathol. 1988 Aug;19(8):942-8 [3402983.001]
  • [Cites] Gastrointest Endosc. 1994 Jan-Feb;40(1):111 [8163114.001]
  • [Cites] Gut. 1998 Jul;43(1):17-21 [9771400.001]
  • [Cites] Gut. 1991 Dec;32(12):1441-6 [1773946.001]
  • [Cites] Gastrointest Endosc. 2001 Sep;54(3):289-93 [11522967.001]
  • [Cites] Dig Dis Sci. 1997 Mar;42(3):603-7 [9073146.001]
  • [Cites] Dig Dis Sci. 1992 Jan;37(1):137-43 [1728519.001]
  • [Cites] Br J Surg. 1988 Aug;75(8):760-3 [3167523.001]
  • [Cites] Am J Gastroenterol. 1994 May;89(5):670-80 [8172136.001]
  • [Cites] Gastrointest Endosc. 2005 Feb;61(2):226-31 [15729230.001]
  • [Cites] Cancer. 1993 Aug 15;72(4):1155-8 [8339208.001]
  • [Cites] Am J Gastroenterol. 1996 May;91(5):981-6 [8633592.001]
  • [Cites] Am J Gastroenterol. 1997 Nov;92(11):2012-6 [9362182.001]
  • [Cites] Am J Gastroenterol. 1997 Mar;92(3):407-13 [9068459.001]
  • [Cites] Histopathology. 2001 Apr;38(4):307-11 [11318895.001]
  • [Cites] Gut. 1998 May;42(5):659-62 [9659160.001]
  • [Cites] Am J Gastroenterol. 1998 Jul;93(7):1033-6 [9672325.001]
  • [Cites] Cancer. 1996 Oct 15;78(8):1820-8 [8859198.001]
  • [Cites] Am J Gastroenterol. 1999 Aug;94(8):2037-42 [10445525.001]
  • [Cites] Am J Gastroenterol. 2000 Aug;95(8):1888-93 [10950031.001]
  • [Cites] Gastroenterology. 1993 Feb;104(2):510-3 [8425693.001]
  • [Cites] Gastrointest Endosc. 2001 Sep;54(3):294-301 [11522968.001]
  • [Cites] Am J Gastroenterol. 1999 Apr;94(4):937-43 [10201460.001]
  • [Cites] Cancer. 1998 Nov 15;83(10):2049-53 [9827707.001]
  • [Cites] N Engl J Med. 1985 Oct 3;313(14):857-9 [4033716.001]
  • (PMID = 28286441.001).
  • [ISSN] 1554-7914
  • [Journal-full-title] Gastroenterology & hepatology
  • [ISO-abbreviation] Gastroenterol Hepatol (N Y)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Barrett’s esophagus / adenocarcinoma / high-grade dysplasia / long-segment Barrett’s esophagus / low-grade dysplasia / short-segment Barrett’s esophagus
  •  go-up   go-down


8. Jovanović I, Todorović V, Milosavljević T, Micev M, Pesko P, Bjelović M, Mouzas Y, Tzardi M: Expression of p53 protein in Barrett's adenocarcinoma and adenocarcinoma of the gastric cardia and antrum. Vojnosanit Pregl; 2005 Dec;62(12):879-85
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] Expression of p53 protein in Barrett's adenocarcinoma and adenocarcinoma of the gastric cardia and antrum.
  • METHODS: The material comprised 66 surgical specimens; 10 were Barrett's carcinomas, 25 adenocarcinomas of the gastric cardia (type II adenocarcinoma of the esophagogastric junction - EGJ), and 31 adenocarcinomas of the antrum.
  • There was, however, a significant difference observed in the depth of tumour invasion between Barrett's adenocarcinoma and adenocarcinoma of the cardia compared with the adenocarcinoma of the antrum.
  • Namely, at the time of surgery, both Barrett's adenocarcinomas and adenocarcinomas of the cardia, were significantly more advanced comparing with the adenocarcinomas of the antrum.
  • Overexpression of p53 was found in 40% (4/10) of Barrett's adenocarcinomas, 72% (18/25) of adenocarcinoma of the cardia and 65% (20/31) of adenocarcinoma of the antrum.
  • Patients with more advanced Barrett's adenocarcinoma and in the cases of lymph node invasion revealed tendency for the greater p53 positivity compared with the early forms and lymph node-negative cases; however, this difference was not significant according to the statistical analysis.
  • With regard to adenocarcinoma of the cardia, higher rates of p53 positivity were recorded in poorly differentiated, more advanced cases with lymph node invasion.
  • On the contrary, in the patients with adenocarcinoma of the antrum, greater p53 positivity was revealed in early forms without lymph node involvement, but the observed difference was not statistically significant.
  • CONCLUSION: No significant differences in p53 protein expression in terms of sex, type (Lauren) of tumour, depth of invasion, lymph node involvement, or tumour differentiation were observed in any of the analyzed groups of tumours (Barrett's adenocarcinoma, adenocarcinoma of the cardia and adenocarcinoma of the antrum).
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / complications. Cardia. Esophageal Neoplasms / metabolism. Pyloric Antrum. Stomach Neoplasms / metabolism. Tumor Suppressor Protein p53 / metabolism

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Vojnosanit Pregl. 2006 Jan;63(1):87-8; author reply 88-9 [16471255.001]
  • (PMID = 16375215.001).
  • [ISSN] 0042-8450
  • [Journal-full-title] Vojnosanitetski pregled
  • [ISO-abbreviation] Vojnosanit Pregl
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Serbia and Montenegro
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


9. Vona-Davis L, Frankenberry K, Cunningham C, Riggs DR, Jackson BJ, Szwerc MF, McFadden DW: MAPK and PI3K inhibition reduces proliferation of Barrett's adenocarcinoma in vitro. J Surg Res; 2005 Jul 1;127(1):53-8
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] MAPK and PI3K inhibition reduces proliferation of Barrett's adenocarcinoma in vitro.
  • BACKGROUND: Esophageal adenocarcinoma often arises from Barrett's esophagus.
  • We hypothesized that inhibition of these pathways in Barrett's adenocarcinoma would decrease cell proliferation and alter apoptosis in vitro.
  • MATERIALS AND METHODS: Two Barrett's-associated adenocarcinoma cell lines, SEG-1 (wild-type p53) and BIC-1 (mutant p53), were treated with MAPK (U0126) and PI3K (LY294002) inhibitors at 20 microm concentrations.
  • CONCLUSIONS: Herein, we report significant antiproliferative effects against Barrett's adenocarcinoma by MAPK and PI3K inhibition in vitro.
  • [MeSH-major] Barrett Esophagus / pathology. Butadienes / pharmacology. Chromones / pharmacology. Enzyme Inhibitors / pharmacology. Mitogen-Activated Protein Kinases / antagonists & inhibitors. Morpholines / pharmacology. Nitriles / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors
  • [MeSH-minor] Adenocarcinoma. Apoptosis / drug effects. Cell Division / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Esophageal Neoplasms. Humans. Necrosis

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15964304.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Butadienes; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / Nitriles; 0 / U 0126; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  •  go-up   go-down


10. Islam A, Banerjee S, Kambhampati S, Baranda J, Banerjee S, Weston AP, Saxena NK, Banerjee SK: Angiogenic switch in Barrett's adenocarcinoma: the role of vascular endothelial growth factor. Front Biosci; 2006;11:2336-48
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Angiogenic switch in Barrett's adenocarcinoma: the role of vascular endothelial growth factor.
  • In this article, we reviewed the role this troupe in the development of Barrett's adenocarcinoma and also discussed the possible remedies, which have the impact on blocking the function of this troupe.
  • [MeSH-major] Adenocarcinoma / physiopathology. Barrett Esophagus / physiopathology. Esophageal Neoplasms / physiopathology. Neovascularization, Pathologic / physiopathology. Vascular Endothelial Growth Factor A / physiology

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16720317.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 87680; United States / NCRR NIH HHS / RR / P20 RR015563
  • [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.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 123
  •  go-up   go-down


11. Goda K, Tajiri H, Ikegami M, Urashima M, Nakayoshi T, Kaise M: Usefulness of magnifying endoscopy with narrow band imaging for the detection of specialized intestinal metaplasia in columnar-lined esophagus and Barrett's adenocarcinoma. Gastrointest Endosc; 2007 Jan;65(1):36-46
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.
  • [Title] Usefulness of magnifying endoscopy with narrow band imaging for the detection of specialized intestinal metaplasia in columnar-lined esophagus and Barrett's adenocarcinoma.
  • BACKGROUND: Barrett's esophagus with specialized intestinal metaplasia (SIM) from columnar-lined esophagus is difficult to distinguish with routine endoscopy.
  • OBJECTIVE: To examine the values of fine mucosal patterns and the capillary patterns observed by magnifying endoscopy with narrow band imaging (MENBI) for the detection of SIM in columnar-lined esophagus and superficial Barrett's adenocarcinoma.
  • PATIENTS: Fifty-eight patients, including 4 with superficial Barrett's adenocarcinoma.
  • RESULTS: Upon observation, all 6 adenocarcinoma sites were classified as irregular patterns in both the fine mucosal patterns and capillary patterns.
  • The addition of capillary patterns to fine mucosal patterns appeared to improve the diagnostic value for detecting SIM and superficial Barrett's adenocarcinoma upon observation by MENBI.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Endoscopy, Gastrointestinal / methods. Esophageal Neoplasms / diagnosis. Esophagus / pathology. Intestinal Mucosa / pathology

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Gastrointest Endosc. 2007 Jan;65(1):47-9 [17185079.001]
  • (PMID = 17185078.001).
  • [ISSN] 0016-5107
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


12. Hara T, Kijima H, Yamamoto S, Kise Y, Hanashi T, Nishi T, Chino O, Shimada H, Tanaka M, Inokuchi S, Makuuchi H: Immunohistochemical expression of p63 in esophageal Barrett's adenocarcinoma. Mol Med Rep; 2008 Jul-Aug;1(4):473-7
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] Immunohistochemical expression of p63 in esophageal Barrett's adenocarcinoma.
  • We examined p63 expression patterns in esophageal Barrett's adenocarcinoma, including early-stage cancers, as well as its clinicopathological significance.
  • The role of the p63 gene is thought to be different in esophageal Barrett's adenocarcinoma compared with esophageal squamous cell carcinoma. p63 immunoreactivity was most useful as a predictor of lymph node metastasis.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21479434.001).
  • [ISSN] 1791-2997
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  •  go-up   go-down


13. Watari J, Sakurai J, Morita T, Yamazaki T, Okugawa T, Toyoshima F, Tanaka J, Tomita T, Kim Y, Oshima T, Hori K, Moriichi K, Tanabe H, Fujiya M, Kohgo Y, Das KM, Matsumoto T, Miwa H: A case of early Barrett's adenocarcinoma repeatedly developing multiple metachronous lesions shortly after endoscopic therapy: an analysis for genetic and epigenetic alterations. Gastrointest Endosc; 2010 Dec;72(6):1303-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of early Barrett's adenocarcinoma repeatedly developing multiple metachronous lesions shortly after endoscopic therapy: an analysis for genetic and epigenetic alterations.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Barrett Esophagus / surgery. Epigenesis, Genetic. Esophageal Neoplasms / genetics. Esophageal Neoplasms / surgery. Esophagoscopy. Neoplasms, Second Primary / genetics. Neoplasms, Second Primary / surgery

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20650453.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / APC protein, human; 0 / Adenomatous Polyposis Coli Protein; 0 / Antibodies; 0 / DAS-1 protein, human
  •  go-up   go-down


14. Gatenby PA, Ramus JR, Caygill CP, Winslet MC, Watson A: Aspirin is not chemoprotective for Barrett's adenocarcinoma of the oesophagus in multicentre cohort. Eur J Cancer Prev; 2009 Sep;18(5):381-4
Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aspirin is not chemoprotective for Barrett's adenocarcinoma of the oesophagus in multicentre cohort.
  • Barrett's columnar-lined oesophagus is the precursor lesion for oesophageal adenocarcinoma.
  • The overall rate of progression to adenocarcinoma is 0.59% per annum.
  • A large prospective multicentre trial is recruiting to assess the role of aspirin as a chemoprotective agent in prevention of development of cancer as well as cardiovascular protection in patients with Barrett's oesophagus.
  • This retrospective analysis of the large UK National Barrett's Oesophagus Registry database seeks to analyse this question from within its large natural history study cohort.
  • End point was development of dysplasia or oesophageal adenocarcinoma.
  • Numbers of patients developing all grades of dysplasia and adenocarcinoma were: 13 aspirin (15.1%) and 97 no aspirin (14.9%) (hazard ratio 0.723, 95% confidence interval 0.410-1.310, P = 0.294), high-grade dysplasia and adenocarcinoma: five aspirin (5.8%) and 25 no aspirin (3.8%) (hazard ratio 0.898, 95% confidence interval 0.340-2.368, P = 0.827) and adenocarcinoma: four aspirin (4.7%) and 16 no aspirin (2.5%) (hazard ratio 1.092, 95% confidence interval 0.358-3.335, P = 0.877).
  • No significant difference was observed in hazard of developing dysplasia or adenocarcinoma between patients taking aspirin and those not taking aspirin during the course of follow-up of surveillance for columnar-lined oesophagus.
  • In conclusion, no difference in risk of development of dysplasia or adenocarcinoma was observed between patients taking aspirin and those not taking aspirin in this large cohort.
  • [MeSH-major] Adenocarcinoma / prevention & control. Anticarcinogenic Agents / therapeutic use. Aspirin / therapeutic use. Barrett Esophagus / drug therapy. Esophageal Neoplasms / prevention & control. Precancerous Conditions / drug therapy

  • 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 = 19620873.001).
  • [ISSN] 1473-5709
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; R16CO5Y76E / Aspirin
  •  go-up   go-down


15. Dunn LJ, Robertson AG, Immanuel A, Griffin SM: Barrett's adenocarcinoma 52 years after subtotal esophagectomy for pediatric peptic stricture. Ann Thorac Surg; 2010 Feb;89(2):604-6
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 adenocarcinoma 52 years after subtotal esophagectomy for pediatric peptic stricture.
  • Barrett's esophagus results from the long-term effects of both acid and bile reflux.
  • Development of Barrett's epithelium in the esophageal remnant has been reported.
  • Here we report the case of a man who was diagnosed with adenocarcinoma in his esophageal remnant on a background of Barrett's change 52 years after undergoing one of the first esophageal resections for benign disease as a child.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / surgery. Esophageal Neoplasms / surgery. Esophageal Stenosis / surgery. Esophagitis, Peptic / surgery. Postoperative Complications / surgery

  • MedlinePlus Health Information. consumer health - After Surgery.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2010 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20103354.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  •  go-up   go-down


21. Kawano T: [Barrett's epithelium and Barrett's adenocarcinoma from the viewpoint of surgery]. Nihon Shokakibyo Gakkai Zasshi; 2005 Feb;102(2):170-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Barrett's epithelium and Barrett's adenocarcinoma from the viewpoint of surgery].
  • [MeSH-major] Barrett Esophagus / surgery. Esophagoscopy
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / etiology. Epithelium. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / etiology. Esophagogastric Junction / pathology. Esophagus / pathology. Humans. Laser Coagulation. Metaplasia

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15747533.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


22. Konturek PC, Kania J, Burnat G, Hahn EG: NO-releasing aspirin exerts stronger growth inhibitory effect on Barrett's adenocarcinoma cells than traditional aspirin. J Physiol Pharmacol; 2006 Dec;57 Suppl 12:15-24
Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NO-releasing aspirin exerts stronger growth inhibitory effect on Barrett's adenocarcinoma cells than traditional aspirin.
  • Expression of cyclooxygenase-2 (COX-2) is involved in the chronic inflammation-related development of Barrett's adenocarcinoma and the use of selective COX-2 inhibitors (coxibs) might provide new chemoprevention strategy for Barrett's adenocarcinoma (BA).
  • The role of NO-ASA in the prevention of Barrett's adenocarcinoma (BA) has not been studied so far.
  • 2) to compare the effect of NO-ASA with that of ASA on proliferation rate in Barrett''s adenocarcinoma cell line (OE-33 cells);.
  • The expression of COX-2 was assessed in biopsies obtained from the Barrett's mucosa and normal squamous epithelial esophageal mucosa from 20 BE patients by RT-PCR and Western blot analysis, respectively.
  • In Barrett's mucosa a significant up-regulation of COX-2 was observed.
  • These results indicate that this compound may represent a promising chemopreventive agent for Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / drug therapy. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Aspirin / pharmacology. Cyclooxygenase 2 Inhibitors / pharmacology. Nitric Oxide / metabolism. Nitric Oxide Donors / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Barrett Esophagus / drug therapy. Barrett Esophagus / enzymology. Caspase 3 / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclooxygenase 2 / genetics. Cyclooxygenase 2 / metabolism. Dose-Response Relationship, Drug. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / enzymology. Gene Expression. Humans. In Vitro Techniques

  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17244951.001).
  • [ISSN] 1899-1505
  • [Journal-full-title] Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
  • [ISO-abbreviation] J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Nitric Oxide Donors; 31C4KY9ESH / Nitric Oxide; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.4.22.- / Caspase 3; R16CO5Y76E / Aspirin
  •  go-up   go-down


23. Tischoff I, Hengge UR, Vieth M, Ell C, Stolte M, Weber A, Schmidt WE, Tannapfel A: Methylation of SOCS-3 and SOCS-1 in the carcinogenesis of Barrett's adenocarcinoma. Gut; 2007 Aug;56(8):1047-53
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).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Methylation of SOCS-3 and SOCS-1 in the carcinogenesis of Barrett's adenocarcinoma.
  • AIMS: This study was performed to elucidate the role of SOCS-1 and SOCS-3 in Barrett's adenocarcinoma and its precursor lesions.
  • METHODS: DNA of specimens from 19 Barrett's adenocarcinomas, 56 Barrett's intraepithelial neoplasias (n = 29 low grade and n = 27 high grade), 30 Barrett's mucosa without neoplasia, 20 samples of normal squamous and gastric epithelium and four cell lines were studied using methylation specific PCR for the SOCS-1 and SOCS-3 promoter following microdissection.
  • RESULTS: In normal squamous epithelium and normal gastric mucosa, neither SOCS-3 nor SOCS-1 methylation was observed.
  • In Barrett's mucosa without intraepithelial neoplasia, SOCS-3 methylation occurred in 4/30 cases (13%) whereas SOCS-1 was unmethylated.
  • A hypermethylated SOCS-3 promoter was found in 14/19 Barrett's adenocarcinomas (74%) and in 20/29 high and 6/27 low grade intraepithelial neoplasias (69% and 22%, respectively).
  • CONCLUSIONS: These data indicate that promoter methylation and subsequent transcript downregulation of SOCS-3 transcripts and, to a much lesser extent, SOCS-1 are involved in the multistep carcinogenesis of Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Suppressor of Cytokine Signaling Proteins / genetics

  • 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. 2004 Dec 20;112(6):1003-9 [15386345.001]
  • [Cites] Dig Dis. 2004;22(2):126-33 [15383753.001]
  • [Cites] Gut. 2005 Mar;54 Suppl 1:i21-6 [15711004.001]
  • [Cites] Gut. 2005 Mar;54 Suppl 1:i6-12 [15711008.001]
  • [Cites] Oncogene. 2005 Oct 6;24(44):6699-708 [16007169.001]
  • [Cites] J Hepatol. 2005 Nov;43(5):757-63 [16083990.001]
  • [Cites] Nat Med. 2005 Dec;11(12):1314-21 [16288283.001]
  • [Cites] Biochem Pharmacol. 2006 Mar 14;71(6):713-21 [16426581.001]
  • [Cites] Gastroenterology. 2006 Apr;130(4):1117-28 [16618406.001]
  • [Cites] J Clin Invest. 2006 Jun;116(6):1571-81 [16710471.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6546-52 [16818626.001]
  • [Cites] Gastroenterology. 2006 Jul;131(1):179-93 [16831601.001]
  • [Cites] Gut. 2006 Sep;55(9):1263-9 [16682432.001]
  • [Cites] Shock. 2006 Sep;26(3):226-34 [16912647.001]
  • [Cites] Cancer Res. 1999 Oct 15;59(20):5059-63 [10537273.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):4227-32 [10760290.001]
  • [Cites] Nat Genet. 2001 May;28(1):29-35 [11326271.001]
  • [Cites] Nat Cell Biol. 2001 May;3(5):460-5 [11331873.001]
  • [Cites] Cancer Lett. 2002 Dec 1;186(1):59-65 [12183076.001]
  • [Cites] Science. 2002 Sep 13;297(5588):1807-8; discussion 1807-8 [12229925.001]
  • [Cites] Lancet. 2002 Nov 16;360(9345):1587-9 [12443613.001]
  • [Cites] J Hum Genet. 2003;48(2):65-9 [12601549.001]
  • [Cites] Blood. 2003 Apr 1;101(7):2784-8 [12456503.001]
  • [Cites] APMIS. 2002 Dec;110(12):833-44 [12645661.001]
  • [Cites] Oncogene. 2003 Jun 26;22(26):4134-42 [12821948.001]
  • [Cites] Br J Cancer. 2003 Jul 21;89(2):338-43 [12865927.001]
  • [Cites] Oncogene. 2003 Jul 24;22(30):4757-9 [12879021.001]
  • [Cites] Am J Pathol. 2003 Sep;163(3):1101-7 [12937151.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14133-8 [14617776.001]
  • [Cites] Trends Immunol. 2003 Dec;24(12):659-66 [14644140.001]
  • [Cites] J Biol Chem. 2003 Dec 26;278(52):52021-31 [14522994.001]
  • [Cites] Oncogene. 2004 Jan 15;23(2):554-8 [14724583.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9821-6 [8790415.001]
  • (PMID = 17376806.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / SOCS1 protein, human; 0 / SOCS3 protein, human; 0 / Suppressor of Cytokine Signaling Proteins
  • [Other-IDs] NLM/ PMC1955493
  •  go-up   go-down


24. Jenkins JT, Charles A, Mitchell KG, Fullarton GM: Photodynamic therapy for Barretts' adenocarcinoma associated with an Angelchik device. Photodiagnosis Photodyn Ther; 2005 Sep;2(3):197-200

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Photodynamic therapy for Barretts' adenocarcinoma associated with an Angelchik device.
  • We present a novel case of an elderly patient with a Barrett's adenocarcinoma in the presence of an Angelchik prosthesis.
  • We aim to draw attention to issues relating to metaplastic Barretts' oesphagus and its adenocarcinoma complications and highlight relevant issues in multimodal endoscopic management and palliation using photodynamic therapy in the presence of the device.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 25048770.001).
  • [ISSN] 1572-1000
  • [Journal-full-title] Photodiagnosis and photodynamic therapy
  • [ISO-abbreviation] Photodiagnosis Photodyn Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  •  go-up   go-down


25. Nishi T, Makuuchi H, Shimada H, Chino O, Yamamoto S, Hara T: [Present state and measures of Barrett's cancer in Japan]. Nihon Rinsho; 2005 Aug;63(8):1470-4
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] [Present state and measures of Barrett's cancer in Japan].
  • Barrett's adenocarcinoma is common esophageal cancer in western countries but very rare in Japan.
  • We reviewed 206 cases of Barrett's cancer in Japanese literature that issued from 2000 to 2004.
  • There was no mucosal Barrett's cancer with lymph nodes metastasis, therefore EMR (endoscopic mucosal resection) method is an appropriate way for mucosal cancer.
  • Barrett's cancer with submucosal invasion occur lymph nodes metastasis, so surgical operation should be applied for deeper invasion to submucosal cancer.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / therapy. Barrett Esophagus / complications. Esophageal Neoplasms / etiology. Esophageal Neoplasms / therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16101242.001).
  • [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
  • [Number-of-references] 7
  •  go-up   go-down


26. Hoshihara Y, Kogure T, Yamamoto T, Hashimoto M, Hoteya O: [Endoscopic diagnosis of Barrett's esophagus]. Nihon Rinsho; 2005 Aug;63(8):1394-8
Genetic Alliance. consumer health - Barrett's Esophagus.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Endoscopic diagnosis of Barrett's esophagus].
  • In Japan Barrett's mucosa is defined as columnar lined esophagus (CLE).
  • The prevalence of Barrett's esophagus and Barrett's adenocarcinoma is very low.
  • But in Western countries Barrett's mucosa is defined as CLE with intestinal metaplasia, and many cases of Barrett's esophagus and Barrett's adenocarcinoma are reported.
  • The definite endoscopic diagnosis of Barrett's mucosa cannot be so easy.
  • In no cases were the longitudinal vessels observed under the gastric mucosa beyond the esophageal hiatus.
  • When longitudinal vessels are found only under the columnar epithelium at the oral side over the esophageal hiatus from the stomach, this indicates Barrett's epithelium.
  • Thus the definite diagnosis of Barrett's epithelium can be made by endoscopy.
  • [MeSH-major] Barrett Esophagus / diagnosis. Barrett Esophagus / pathology. Endoscopy, Gastrointestinal

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16101228.001).
  • [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
  • [Number-of-references] 17
  •  go-up   go-down


27. Singh R, Ragunath K, Jankowski J: Barrett's Esophagus: Diagnosis, Screening, Surveillance, and Controversies. Gut Liver; 2007 Dec;1(2):93-100

  • [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.
  • Barrett's esophagus (BE) is a frequent complication of gastroesophageal reflux disease, an acquired condition resulting from persistent mucosal injury to the esophagus.
  • 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.
  • Whether adequate control of gastroesophageal reflux early in the disease alters the natural history of Barrett's change once it has developed remains unanswered.

  • [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


28. Werther M, Saure C, Pahl R, Schorr F, Rüschoff J, Alles JU, Heinmöller E: Molecular genetic analysis of surveillance biopsy samples from Barrett's mucosa--significance of sampling. Pathol Res Pract; 2008;204(5):285-94
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] Molecular genetic analysis of surveillance biopsy samples from Barrett's mucosa--significance of sampling.
  • Our aim was to determine the spectrum and accumulation of mutations in surveillance biopsies from Barrett's mucosa of individual patients during follow-up.
  • We performed loss of heterozygosity (LOH) analysis of six recently described tumor suppressor genes relevant for the carcinogenesis of Barrett's adenocarcinoma from laser-microdissected, paraffin-embedded biopsy samples of Barrett's mucosa without or with low-grade dysplastic change.
  • In two patients, Barrett's adenocarcinoma was diagnosed 6 months after the first diagnosis of Barrett's mucosa.
  • From our microsatellite marker panel, we were not able to define a single surrogate marker that could serve as a potential biomarker, indicating an increased risk of progression to Barrett's adenocarcinoma.
  • Our results raise important questions regarding the biological dynamics of mutations in Barrett's mucosa in addition to the influence of sampling, especially with regard to the number of biopsies taken from Barrett's mucosa.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Esophagus / pathology. Genes, Tumor Suppressor. Mutation. Precancerous Conditions / genetics

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18337019.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Germany
  •  go-up   go-down


29. Rugge M, Fassan M, Zaninotto G, Pizzi M, Giacomelli L, Battaglia G, Rizzetto C, Parente P, Ancona E: Aurora kinase A in Barrett's carcinogenesis. Hum Pathol; 2010 Oct;41(10):1380-6
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] Aurora kinase A in Barrett's carcinogenesis.
  • In Barrett's mucosa, both aneuploidy and TP53 mutations are consistently recognized as markers of an increased risk of Barrett's adenocarcinoma.
  • Eighty-seven esophageal biopsy samples representative of all the phenotypic lesions occurring in the multistep process of Barrett's carcinogenesis (gastric metaplasia in 25, intestinal metaplasia in 25, low-grade intraepithelial neoplasia in 16, high-grade intraepithelial neoplasia in 11, and Barrett's adenocarcinoma in 10) were obtained from long segments of Barrett's mucosa.
  • Twenty-five additional biopsy samples of native esophageal mucosa were used for control purposes.
  • Nine of 10 Barrett's adenocarcinomas showed AURKA immunostaining.
  • AURKA overexpression is significantly associated with Barrett's mucosa progressing to Barrett's adenocarcinoma and contributes to esophageal carcinogenesis via chromosome instability.
  • The identification of AURKA as a novel molecular target of cancer progression in Barrett's mucosa provides a lead for the development of new therapeutic approaches in Barrett's mucosa patients.
  • [MeSH-major] Adenocarcinoma / enzymology. Barrett Esophagus / enzymology. Cell Transformation, Neoplastic / metabolism. Esophageal Neoplasms / enzymology. Esophagus / enzymology. Protein-Serine-Threonine Kinases / biosynthesis
  • [MeSH-minor] Aurora Kinase A. Aurora Kinases. Carcinoma in Situ / enzymology. Carcinoma in Situ / pathology. Cell Nucleus Size. Gastric Mucosa / enzymology. Gastric Mucosa / pathology. Humans. Immunohistochemistry. Intestinal Mucosa / enzymology. Intestinal Mucosa / pathology. Metaplasia. Mucous Membrane / enzymology. Mucous Membrane / pathology. Oligonucleotide Array Sequence Analysis. Retrospective Studies. Tumor Suppressor Protein p53 / biosynthesis

  • 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 Elsevier Inc. All rights reserved.
  • (PMID = 20656315.001).
  • [ISSN] 1532-8392
  • [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 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.7.11.1 / AURKA protein, human; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  •  go-up   go-down


30. Al-Taie OH, Graf T, Illert B, Katzenberger T, Mörk H, Kraus MR, Barthelmes HU, Scheurlen M, Seufert J: Differential effects of PPARgamma activation by the oral antidiabetic agent pioglitazone in Barrett's carcinoma in vitro and in vivo. J Gastroenterol; 2009;44(9):919-29
Hazardous Substances Data Bank. PIOGLITAZONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential effects of PPARgamma activation by the oral antidiabetic agent pioglitazone in Barrett's carcinoma in vitro and in vivo.
  • We investigated the biological effects of PPARgamma activation by the oral antidiabetic agent pioglitazone in Barrett's adenocarcinoma cells in vitro and in vivo.
  • RESULTS: PPARgamma mRNA and protein were overexpressed in endoscopic biopsies of Barrett's epithelium and the human Barrett's adenocarcinoma cancer cell line OE33 as compared to normal esophagus and stomach and the esophageal squamous epithelium cancer cell line Kyse-180.
  • Effects of systemic PPARgamma activation by the thiazolidinedione pioglitazone on tumor cell proliferation and apoptosis were then assessed in vivo in nude mice bearing transplantable Barrett's adenocarcinomas derived from OE33 cells.
  • CONCLUSION: These results indicate that PPARgamma is involved in the molecular pathogenesis of Barrett's adenocarcinoma formation and growth.
  • However, activation of PPARgamma exerts differential effects on growth of Barrett's adenocarcinoma cells in vitro and in vivo emphasizing the importance of additional cell context specific factors and systemic metabolic status for the modulation of PPARgamma action in vivo.
  • [MeSH-major] Barrett Esophagus / drug therapy. Esophageal Neoplasms / drug therapy. PPAR gamma / drug effects. Thiazolidinediones / pharmacology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Humans. Hypoglycemic Agents / pharmacology. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. RNA, Messenger

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2001 Aug 15;61(16):6213-8 [11507074.001]
  • [Cites] Cancer. 2004 Oct 1;101(7):1569-74 [15468186.001]
  • [Cites] Nat Rev Immunol. 2002 Oct;2(10):748-59 [12360213.001]
  • [Cites] Nature. 1997 Mar 27;386(6623):407-10 [9121558.001]
  • [Cites] FEBS Lett. 1999 Jul 16;455(1-2):135-9 [10428487.001]
  • [Cites] Cell Growth Differ. 2000 Jan;11(1):49-61 [10672903.001]
  • [Cites] Nat Med. 1998 Sep;4(9):1053-7 [9734399.001]
  • [Cites] Oral Oncol. 2003 Dec;39(8):855-61 [13679209.001]
  • [Cites] Genes Chromosomes Cancer. 1998 Jan;21(1):49-60 [9443041.001]
  • [Cites] Clin Exp Metastasis. 2003;20(6):549-54 [14598889.001]
  • [Cites] Cell. 1995 Dec 1;83(5):803-12 [8521497.001]
  • [Cites] Oncogene. 2002 Sep 5;21(39):6071-81 [12203119.001]
  • [Cites] Cancer Res. 1998 Aug 1;58(15):3344-52 [9699665.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] Nat Med. 1998 Sep;4(9):1046-52 [9734398.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Sep 26;97(20):10990-5 [10984506.001]
  • [Cites] Cancer Res. 2000 Oct 1;60(19):5558-64 [11034103.001]
  • [Cites] Nat Med. 1998 Sep;4(9):1058-61 [9734400.001]
  • [Cites] Hepatology. 2001 May;33(5):1087-97 [11343236.001]
  • [Cites] Cell. 1995 Dec 1;83(5):813-9 [8521498.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jan 7;94(1):237-41 [8990192.001]
  • [Cites] Gastroenterology. 2003 Feb;124(2):361-7 [12557142.001]
  • [Cites] Cell. 1995 Dec 15;83(6):835-9 [8521507.001]
  • [Cites] Mol Cells. 2007 Oct 31;24(2):167-76 [17978568.001]
  • [Cites] Ann Surg. 2004 Apr;239(4):491-500 [15024310.001]
  • [Cites] Br J Cancer. 2003 Oct 20;89(8):1409-12 [14562008.001]
  • [Cites] Breast Cancer Res Treat. 2003 Jun;79(3):391-7 [12846423.001]
  • [Cites] Mol Cell. 1998 Feb;1(3):465-70 [9660931.001]
  • [Cites] Cell Cycle. 2007 Jul 1;6(13):1539-48 [17611413.001]
  • [Cites] Int J Cancer. 2001 Nov 1;94(3):370-6 [11745416.001]
  • [Cites] Br J Cancer. 2000 Nov;83(10):1394-400 [11044367.001]
  • [Cites] Gastroenterology. 1998 Nov;115(5):1049-55 [9797355.001]
  • [Cites] Anticancer Res. 2001 Mar-Apr;21(2A):825-9 [11396171.001]
  • [Cites] Nature. 1992 Jan 30;355(6359):446-9 [1310351.001]
  • [Cites] Cancer J. 2002 Sep-Oct;8(5):395-9 [12416897.001]
  • [Cites] Br J Pharmacol. 2004 Jan;141(1):9-14 [14662734.001]
  • [Cites] Endocrinology. 1994 Aug;135(2):798-800 [8033830.001]
  • [Cites] J Investig Med. 2001 Sep;49(5):413-20 [11523697.001]
  • [Cites] Diabetes. 1997 Aug;46(8):1319-27 [9231657.001]
  • [Cites] Clin Cancer Res. 2007 Jan 1;13(1):246-52 [17200362.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 29;94(9):4318-23 [9113987.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 21;95(15):8806-11 [9671760.001]
  • [Cites] J Biol Chem. 2000 Jul 21;275(29):22435-41 [10801895.001]
  • [Cites] Cancer. 2003 Nov 15;98(10):2251-6 [14601096.001]
  • [Cites] Cancer Res. 1999 Nov 15;59(22):5671-3 [10582681.001]
  • [Cites] Hepatology. 2003 Jul;38(1):167-77 [12829999.001]
  • [Cites] Genes Dev. 1997 Aug 1;11(15):1987-98 [9271121.001]
  • (PMID = 19506796.001).
  • [ISSN] 1435-5922
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Thiazolidinediones; X4OV71U42S / pioglitazone
  •  go-up   go-down


31. Kinoshita Y, Yuki T: [Medical treatment of Barrett's esophagus]. Nihon Rinsho; 2005 Aug;63(8):1449-53
Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Medical treatment of Barrett's esophagus].
  • In patients with Barrett's esophagus, medical treatment is necessary for the control of reflux symptom, healing of accompanying erosive esophagitis, and prevention of carcinogenesis.
  • The values of PPI and aspirin/NSAIDs for the prevention of Barrett's carcinoma are still under investigation all over the world.
  • Since many groups are actively working to find the appropriate methods for preventing carcinogenesis on the Barrett's esophagus, we will have an evidence-based strategy for the prevention of Barrett's adenocarcinoma in near future.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Barrett Esophagus / drug therapy. Cyclooxygenase Inhibitors / therapeutic use. Enzyme Inhibitors / therapeutic use
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / prevention & control. Animals. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Drug Therapy, Combination. Esophageal Neoplasms / etiology. Esophageal Neoplasms / prevention & control. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / drug therapy. Humans. Membrane Proteins. Prostaglandin-Endoperoxide Synthases / physiology. Proton Pump Inhibitors

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16101238.001).
  • [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 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Enzyme Inhibitors; 0 / Membrane Proteins; 0 / Proton Pump Inhibitors; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; R16CO5Y76E / Aspirin
  • [Number-of-references] 24
  •  go-up   go-down


32. Scheil-Bertram S, Lorenz D, Ell C, Sheremet E, Fisseler-Eckhoff A: Expression of alpha-methylacyl coenzyme A racemase in the dysplasia carcinoma sequence associated with Barrett's esophagus. Mod Pathol; 2008 Aug;21(8):961-7
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] Expression of alpha-methylacyl coenzyme A racemase in the dysplasia carcinoma sequence associated with Barrett's esophagus.
  • Two different studies demonstrated alpha-methylacyl coenzyme A racemase (AMACR) to be a highly specific marker in Barrett's neoplastic lesions.
  • We present a retrospective study of early Barrett's adenocarcinoma treated with surgery (2000-2005, n=29; M:F=5:1, median age 67 years).
  • Barrett's epithelium that was negative for dysplasia and columnar epithelial cell changes indefinite for dysplasia (n=30) did not demonstrate AMACR immunoreactivity.
  • AMACR immunoreactivity was demonstrated in 27% (8/30) of cases of Barrett's epithelium with columnar epithelial cell changes indefinite for dysplasia.
  • Altogether 91% of cases with low-grade dysplasia were AMACR-positive and 96% of cases with high-grade dysplasia and early Barrett's adenocarcinoma were positive for AMACR.
  • In summary, the sensitivity of AMACR expression in low-grade dysplasia and subsequent early Barrett's adenocarcinoma was significantly higher in our study compared with previous data.
  • This might be a new diagnostic marker for dysplasia carcinoma sequence in Barrett's low-grade neoplastic lesions.
  • [MeSH-major] Adenocarcinoma / enzymology. Barrett Esophagus / enzymology. Esophageal Neoplasms / enzymology. Precancerous Conditions / enzymology. Racemases and Epimerases / metabolism

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18500268.001).
  • [ISSN] 1530-0285
  • [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] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
  •  go-up   go-down


33. Beales IL, Ogunwobi O, Cameron E, El-Amin K, Mutungi G, Wilkinson M: Activation of Akt is increased in the dysplasia-carcinoma sequence in Barrett's oesophagus and contributes to increased proliferation and inhibition of apoptosis: a histopathological and functional study. BMC Cancer; 2007;7:97
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.
  • [Title] Activation of Akt is increased in the dysplasia-carcinoma sequence in Barrett's oesophagus and contributes to increased proliferation and inhibition of apoptosis: a histopathological and functional study.
  • BACKGROUND: The incidence of oesophageal adenocarcinoma is increasing rapidly in the developed world.
  • Therefore we have examined the activation of Akt in Barrett's oesophagus and oesophageal adenocarcinoma and the functional effects of Akt activation in vitro.
  • The functional effects of Akt were examined using Barrett's adenocarcinoma cells in culture.
  • RESULTS: In normal squamous oesophagus, erosive oesophagitis and non-dysplastic Barrett's oesophagus, phospho-Akt was limited to the basal 1/3 of the mucosa.
  • Image analysis confirmed that Akt activation was significantly increased in non-dysplastic Barrett's oesophagus compared to squamous epithelium and further significantly increased in high-grade dysplasia and adenocarcinoma.
  • In all cases of high grade dysplasia and adenocarcinoma Akt was activated in the luminal 1/3 of the epithelium.
  • CONCLUSION: Akt is abnormally activated in Barrett's oesophagus, high grade dysplasia and adenocarcinoma.
  • Akt activation promotes proliferation and inhibits apoptosis in Barrett's adenocarcinoma cells and both transient acid exposure and leptin stimulate Akt phosphorylation.
  • Activation of Akt in obesity and by reflux of gastric acid may be important in the pathogenesis of Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / enzymology. Barrett Esophagus / enzymology. Cell Transformation, Neoplastic / metabolism. Enzyme Activation / physiology. Esophageal Neoplasms / enzymology. Proto-Oncogene Proteins c-akt / metabolism

  • 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
  • [Cites] J Biol Chem. 2002 Aug 2;277(31):27613-21 [12000750.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2002 Aug;283(2):G327-34 [12121879.001]
  • [Cites] Gastroenterology. 2003 Mar;124(3):615-25 [12612900.001]
  • [Cites] J Surg Res. 2003 Jul;113(1):50-5 [12943810.001]
  • [Cites] J Biol Chem. 2003 Sep 12;278(37):34783-93 [12826665.001]
  • [Cites] J Natl Cancer Inst. 2003 Sep 17;95(18):1404-13 [13130116.001]
  • [Cites] Cancer Res. 2004 Mar 1;64(5):1561-9 [14996709.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):1915-9 [15026323.001]
  • [Cites] J Biol Chem. 2004 Apr 16;279(16):16495-502 [14752104.001]
  • [Cites] Br J Cancer. 2004 Aug 16;91(4):714-9 [15266314.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Oct 8;323(1):44-8 [15351698.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Oct;287(4):G743-8 [15231484.001]
  • [Cites] Life Sci. 2004 Nov 5;75(25):2983-95 [15474551.001]
  • [Cites] J Clin Oncol. 2004 Oct 15;22(20):4217-26 [15483033.001]
  • [Cites] Am J Clin Pathol. 1995 Mar;103(3):295-9 [7872251.001]
  • [Cites] N Engl J Med. 1996 Feb 1;334(5):292-5 [8532024.001]
  • [Cites] Gastroenterology. 1996 Jul;111(1):85-92 [8698230.001]
  • [Cites] J Clin Invest. 1996 Nov 1;98(9):2120-8 [8903332.001]
  • [Cites] Cell. 1997 Oct 17;91(2):231-41 [9346240.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] Cell. 1999 Mar 19;96(6):857-68 [10102273.001]
  • [Cites] J Biol Chem. 1999 Jun 11;274(24):16741-6 [10358014.001]
  • [Cites] Ann Intern Med. 1999 Jun 1;130(11):883-90 [10375336.001]
  • [Cites] Gastrointest Endosc. 1999 Jul;50(1):23-6 [10385717.001]
  • [Cites] Am J Gastroenterol. 1999 Aug;94(8):2043-53 [10445526.001]
  • [Cites] CA Cancer J Clin. 2005 Jan-Feb;55(1):10-30 [15661684.001]
  • [Cites] Gut. 2005 Mar;54 Suppl 1:i21-6 [15711004.001]
  • [Cites] Gut. 2005 Mar;54 Suppl 1:i27-32 [15711005.001]
  • [Cites] Gastroenterology. 2005 May;128(5):1471-505 [15887129.001]
  • [Cites] J Surg Res. 2005 Jul 1;127(1):53-8 [15964304.001]
  • [Cites] Nat Clin Pract Gastroenterol Hepatol. 2004 Dec;1(2):106-12 [16265072.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2005 Dec;289(6):G991-7 [16081761.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2006 Feb;290(2):G335-42 [16239404.001]
  • [Cites] Mol Cell Endocrinol. 2006 Mar 9;247(1-2):140-9 [16442704.001]
  • [Cites] Regul Pept. 2006 Mar 15;134(1):1-8 [16169610.001]
  • [Cites] Endocrinology. 2006 Sep;147(9):4505-16 [16740977.001]
  • [Cites] Int J Colorectal Dis. 2007 Apr;22(4):401-9 [16912864.001]
  • [Cites] Br J Surg. 2007 Mar;94(3):346-54 [17212381.001]
  • [Cites] Exp Cell Res. 1999 Nov 25;253(1):210-29 [10579924.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2001 Feb;280(2):G298-307 [11208554.001]
  • [Cites] Br J Cancer. 2001 Mar 23;84(6):748-53 [11259087.001]
  • [Cites] Gastroenterology. 2002 Feb;122(2):299-307 [11832445.001]
  • [Cites] Am J Gastroenterol. 2002 Jun;97(6):1319-27 [12094844.001]
  • [Cites] Am J Gastroenterol. 2002 Jun;97(6):1328-31 [12094845.001]
  • [Cites] Gut. 2003 Feb;52(2):174-80 [12524396.001]
  • (PMID = 17559672.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC1899509
  •  go-up   go-down


34. Pühringer-Oppermann FA, Stein HJ, Sarbia M: Lack of EGFR gene mutations in exons 19 and 21 in esophageal (Barrett's) adenocarcinomas. Dis Esophagus; 2007;20(1):9-11
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.
  • [Title] Lack of EGFR gene mutations in exons 19 and 21 in esophageal (Barrett's) adenocarcinomas.
  • We analyzed exons 19 and 21 coding for the receptor tyrosine kinase of the epidermal growth factor gene in 105 samples of esophageal (Barrett's) adenocarcinoma by denaturing high-pressure liquid chromatography.
  • In conclusion, mutations within the tyrosine kinase domain of EGFR associated with sensitivity of non-small cell lung cancer patients to gefitinib are not present in esophageal (Barrett's) adenocarcinoma.

  • 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 = 17227303.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Codon; 0 / Quinazolines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  •  go-up   go-down


35. Peng DF, Razvi M, Chen H, Washington K, Roessner A, Schneider-Stock R, El-Rifai W: DNA hypermethylation regulates the expression of members of the Mu-class glutathione S-transferases and glutathione peroxidases in Barrett's adenocarcinoma. Gut; 2009 Jan;58(1):5-15
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.
  • [Title] DNA hypermethylation regulates the expression of members of the Mu-class glutathione S-transferases and glutathione peroxidases in Barrett's adenocarcinoma.
  • BACKGROUND: The accumulation of reactive oxygen species and subsequent oxidative DNA damage underlie the development of Barrett's oesophagus (BO) and its progression to Barrett's dysplasia (BD) and adenocarcinoma (BAC).
  • CONCLUSION: Epigenetic inactivation of members of the glutathione pathway can be an important mechanism in Barrett's tumourigenesis.

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • COS Scholar Universe. author profiles.
  • GeneTex Inc. NCBI Redirect Page | Genetex Inc. (subscription/membership/fee required).
  • Hazardous Substances Data Bank. AZACITIDINE .
  • 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 .
  • 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] Cancer Res. 2005 Apr 1;65(7):2684-9 [15805266.001]
  • [Cites] Front Biosci. 2005;10:1881-96 [15769673.001]
  • [Cites] J Surg Oncol. 2005 Jun 1;90(3):139-46; discussion 146 [15895452.001]
  • [Cites] Oncogene. 2005 Jun 9;24(25):4138-48 [15824739.001]
  • [Cites] Nat Rev Genet. 2005 Aug;6(8):597-610 [16136652.001]
  • [Cites] J Pathol. 2006 Jan;208(1):100-7 [16278815.001]
  • [Cites] Nat Rev Cancer. 2006 Feb;6(2):107-16 [16491070.001]
  • [Cites] Carcinogenesis. 2006 Jun;27(6):1160-8 [16537562.001]
  • [Cites] Curr Mol Med. 2006 Jun;6(4):401-8 [16900663.001]
  • [Cites] Neoplasia. 2006 Oct;8(10):843-50 [17032501.001]
  • [Cites] Cancer Res. 2006 Nov 1;66(21):10517-24 [17079474.001]
  • [Cites] Biochim Biophys Acta. 2007 Jan;1775(1):138-62 [17045745.001]
  • [Cites] Urology. 2007 Jan;69(1):11-6 [17270599.001]
  • [Cites] Biochem Pharmacol. 2007 May 1;73(9):1297-307 [17276411.001]
  • [Cites] Gut. 2007 Jun;56(6):763-71 [17145738.001]
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5583-6 [17575120.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):8043-50 [17804715.001]
  • [Cites] Mol Cell Biochem. 2008 Feb;309(1-2):99-107 [18008142.001]
  • [Cites] Mol Cell Biol. 2008 May;28(10):3219-35 [18332107.001]
  • [Cites] Arch Toxicol. 2008 Sep;82(9):641-54 [18253720.001]
  • [Cites] Cancer Lett. 2005 Apr 28;221(2):123-9 [15808397.001]
  • [Cites] J Gastroenterol Hepatol. 2000 Oct;15 Suppl:G49-57 [11100994.001]
  • [Cites] Endoscopy. 2001 Feb;33(2):109-18 [11272213.001]
  • [Cites] Cytogenet Cell Genet. 2000;91(1-4):234-8 [11173863.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3225-9 [11309270.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3410-8 [11309301.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3573-7 [11325821.001]
  • [Cites] Mutat Res. 2001 Jun 2;477(1-2):7-21 [11376682.001]
  • [Cites] Mutat Res. 2001 Sep 1;480-481:189-200 [11506813.001]
  • [Cites] Gastroenterology. 2001 Sep;121(3):592-8 [11522743.001]
  • [Cites] Anticancer Res. 2002 Jan-Feb;22(1A):39-44 [12017320.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7025-9 [11585728.001]
  • [Cites] Mutat Res. 2001 Oct 1;482(1-2):21-6 [11535245.001]
  • [Cites] Oncogene. 2002 Aug 12;21(35):5358-60 [12154398.001]
  • [Cites] Cancer Res. 2002 Dec 1;62(23):6823-6 [12460893.001]
  • [Cites] Biol Chem. 2003 Apr;384(4):567-74 [12751786.001]
  • [Cites] Indian J Exp Biol. 2002 Nov;40(11):1213-32 [13677623.001]
  • [Cites] Am J Pathol. 2003 Oct;163(4):1551-6 [14507661.001]
  • [Cites] Carcinogenesis. 2003 Oct;24(10):1637-44 [12896903.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]
  • [Cites] Onkologie. 2004 Apr;27(2):200-6 [15138356.001]
  • [Cites] Cancer. 1989 Jul 15;64(2):526-30 [2736498.001]
  • [Cites] Semin Surg Oncol. 1990;6(5):274-8 [2237086.001]
  • [Cites] JAMA. 1993 Sep 15;270(11):1320 [8360967.001]
  • [Cites] Gut. 1995 Aug;37(2):168-73 [7557561.001]
  • [Cites] J Mol Med (Berl). 1996 Jun;74(6):297-312 [8862511.001]
  • [Cites] Dis Esophagus. 1997 Jan;10(1):29-32; discussion 33 [9079270.001]
  • [Cites] Carcinogenesis. 1997 Nov;18(11):2265-70 [9395230.001]
  • [Cites] Semin Liver Dis. 1998;18(4):345-58 [9875553.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):103-7 [9916800.001]
  • [Cites] Curr Med Chem. 1999 Apr;6(4):279-309 [10101214.001]
  • [Cites] Free Radic Res. 1999 Oct;31(4):261-72 [10517532.001]
  • [CommentIn] Gut. 2009 Jan;58(1):1-2 [19091824.001]
  • (PMID = 18664505.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA106176-06; United States / NCI NIH HHS / CA / R01 CA106176-06; United States / NCI NIH HHS / CA / R01 CA106176; United States / NCI NIH HHS / CA / CA106176-07A1; United States / NCI NIH HHS / CA / R01 CA106176-07A1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / DNA, Neoplasm; 0 / Hydroxamic Acids; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; EC 1.11.1.9 / Glutathione Peroxidase; EC 2.5.1.18 / Glutathione Transferase; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ NIHMS186959; NLM/ PMC2845391
  •  go-up   go-down


36. Sappati Biyyani RS, Chessler L, McCain E, Nelson K, Fahmy N, King J: Familial trends of inheritance in gastro esophageal reflux disease, Barrett's esophagus and Barrett's adenocarcinoma: 20 families. Dis Esophagus; 2007;20(1):53-7
MedlinePlus Health Information. consumer health - GERD.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Familial trends of inheritance in gastro esophageal reflux disease, Barrett's esophagus and Barrett's adenocarcinoma: 20 families.
  • We reported four families with familial Barrett's esophagus (FBE) in 1993.
  • This follow-up study includes an additional 16 families with FBE, gastroesophageal reflux disease (GERD) and BE-related adenocarcinoma (BEAC) highlighting the familial trends of inheritance.

  • 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
  • (PMID = 17227311.001).
  • [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
  •  go-up   go-down


37. Schauer M, Stein H, Lordick F, Feith M, Theisen J, Siewert JR: Results of a multimodal therapy in patients with stage IV Barrett's adenocarcinoma. World J Surg; 2008 Dec;32(12):2655-60
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] Results of a multimodal therapy in patients with stage IV Barrett's adenocarcinoma.
  • BACKGROUND: Locally advanced and metastatic Barrett's carcinomas account for the majority of this tumor entity at the time of diagnosis.
  • METHODS: A total of 178 patients with Barrett's carcinoma who underwent multimodal therapy with resection of the tumor were reviewed.
  • CONCLUSIONS: This is the first study to compare the outcome of a modern multimodal therapy concept in patients with metastatic Barrett's carcinoma in comparison to patients with the locally advanced form of the disease.
  • [MeSH-major] Adenocarcinoma / secondary. Adenocarcinoma / therapy. Antineoplastic Agents / therapeutic use. Barrett Esophagus / therapy. Esophageal Neoplasms / pathology. Esophageal Neoplasms / therapy. Esophagectomy

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] World J Surg. 2003 Sep;27(9):1067-74 [12934159.001]
  • [Cites] Cancer. 1999 Feb 1;85(3):520-8 [10091725.001]
  • [Cites] Cancer. 2003 Oct 1;98(7):1521-30 [14508841.001]
  • [Cites] Cancer. 1999 Apr 1;85(7):1484-9 [10193937.001]
  • [Cites] Chirurg. 1998 Apr;69(4):349-59 [9612616.001]
  • [Cites] Br J Surg. 2004 Aug;91(8):997-1003 [15286961.001]
  • [Cites] Gastroenterology. 2005 May;128(6):1554-66 [15887151.001]
  • [Cites] Clin Cancer Res. 2005 Apr 1;11(7):2478-85 [15814623.001]
  • [Cites] Ann Surg Oncol. 2006 Jan;13(1):12-30 [16378161.001]
  • [Cites] World J Surg. 2003 Sep;27(9):1062-6 [12917757.001]
  • [Cites] Br J Cancer. 1999 May;80(5-6):834-42 [10360663.001]
  • [Cites] Curr Treat Options Oncol. 2000 Dec;1(5):387-98 [12057146.001]
  • [Cites] World J Surg. 2003 Sep;27(9):1058-61 [12925905.001]
  • [Cites] World J Surg. 2003 Sep;27(9):1052-7 [12917758.001]
  • [Cites] Ann Thorac Surg. 2001 Dec;72(6):1918-24; discussion 1924-5 [11789772.001]
  • [Cites] Gastroenterol Clin North Am. 2002 Jun;31(2):441-60 [12134612.001]
  • [Cites] Cancer. 1998 Nov 15;83(10):2049-53 [9827707.001]
  • [Cites] J Exp Clin Cancer Res. 1999 Sep;18(3):289-94 [10606171.001]
  • [Cites] Eur J Surg Oncol. 2001 Aug;27(5):509-10 [11504525.001]
  • [Cites] Dis Esophagus. 2007;20(2):173-7 [17439603.001]
  • (PMID = 18802733.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


38. Zaninotto G, Minnei F, Guirroli E, Ceolin M, Battaglia G, Bellumat A, Betetto G, Bozzola L, Cassaro M, Cataudella G, Dal Bò N, Farinati F, Florea G, Furlanetto A, Galliani E, Germanà B, Guerini A, Macrì E, Marcon V, Mastropaolo G, Meggio A, Miori G, Morelli L, Murer B, Norberto L, Togni R, Valiante F, Rugge M: The Veneto Region's Barrett's Oesophagus Registry: aims, methods, preliminary results. Dig Liver Dis; 2007 Jan;39(1):18-25

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Veneto Region's Barrett's Oesophagus Registry: aims, methods, preliminary results.
  • BACKGROUND: The natural history of Barrett's Oeosphagus is not completely clarified and Barrett's Oeosphagus Registries are considered useful tools to expand our knowledge on this disease.
  • A Barrett's Oeosphagus Registry has been therefore established in the Veneto Region and neighbouring provinces.
  • AIMS: The aims of the Registry are to assess the demographical, endoscopical and histological characteristics of Barrett's Oeosphagus patients; the prevalence of non-invasive neoplasia and Barrett's Adenocarcinoma and the timing and incidence of Barrett's Oeosphagus progression to malignancy.
  • METHODS: An interdisciplinary committee of endoscopists, pathologists and information technology experts was established in 2004 to design a website-based Barrett's Oesophagus Registry for the Veneto Region and neighbouring north-eastern Italian provinces.
  • RESULTS: In the first 18 months, 397 patients with endoscopically visible and histologically proven Barrett's Oeosphagus were enrolled in the Registry; the median age of these patients was 66 years (male:female=3:1).
  • Most patients (75%) had a Short Segment of Barrett's Oesophagus (<or=3 cm) and only 1 in 4 had a Long Segment of Barrett's Oesophagus (>3 cm).
  • Long Segment of Barrett's Oesophagus patients were 5 years older than the Short Segment of Barrett's Oesophagus patients (p<0.05), suggesting a progression from Short Segment of Barrett's Oesophagus to Long Segment of Barrett's Oesophagus.
  • Though no data are available on the incidence of non-invasive neoplasia or Barrett's Adenocarcinoma (i.e., progression to cancer at least 12 months after enrolment), the prevalence of neoplastic lesions (found within 12 months of enrolment) was 5% for Short Segment of Barrett's Oesophagus and 19% for Long Segment of Barrett's Oesophagus, indicating that a careful multiple-biopsy endoscopic protocol is needed, especially when Long Segment of Barrett's Oesophagus are suspected at endoscopy.
  • The prevalence of Barrett's Adenocarcinoma among patients with non-invasive neoplasia was 1/17 cases of low-grade non-invasive neoplasia and 2/3 cases of high-grade non-invasive neoplasia, indicating that these patients require strict endoscopic and bioptic follow-up.
  • CONCLUSION: A regional Barrett's Oeosphagus Registry is feasible at a relatively low cost and enables significant data to be collected in a relatively short time.
  • [MeSH-major] Barrett Esophagus. Esophagoscopy. Precancerous Conditions / diagnosis. Prevalence. Registries

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17141593.001).
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  •  go-up   go-down


39. Jiménez P, Piazuelo E, Cebrian C, Ortego J, Strunk M, García-Gonzalez MA, Santander S, Alcedo J, Lanas A: Prostaglandin EP2 receptor expression is increased in Barrett's oesophagus and oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2010 Feb 1;31(3):440-51
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] Prostaglandin EP2 receptor expression is increased in Barrett's oesophagus and oesophageal adenocarcinoma.
  • AIM: To investigate which PGE2 receptor subtypes regulate PGE2 signals in the oesophageal adenocarcinoma sequence.
  • METHODS: Expression was determined in oesophageal biopsies from 85 patients with oesophagitis, Barrett's metaplasia, intraepithelial neoplasia, oesophageal adenocarcinoma and normal oesophagus.
  • Expression of EP receptors was also determined in response to acid and bile exposure in the Barrett's adenocarcinoma cell line OE33.
  • COX-2 and, especially, EP2 were increased in the Barrett's metaplasia-intraepithelial neoplasia-adenocarcinoma sequence.
  • Expression of the EP4 receptor protein was increased in oesophageal adenocarcinoma.
  • CONCLUSIONS: Our data suggest that in addition to COX-2, EP2 and EP4 receptors could be a selective target in the prevention and/or treatment of the Barrett's-associated adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Cyclooxygenase 1 / metabolism. Esophageal Neoplasms / pathology. RNA, Messenger / metabolism. Receptors, Prostaglandin E / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19843025.001).
  • [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
  • [Chemical-registry-number] 0 / PTGER2 protein, human; 0 / RNA, Messenger; 0 / Receptors, Prostaglandin E; 0 / Receptors, Prostaglandin E, EP2 Subtype; EC 1.14.99.1 / Cyclooxygenase 1
  •  go-up   go-down


40. Nguyen NT, Chang K, Nahidi T, Wilson SE, Luketich JD: Esophagectomy for Barrett's esophagus: indications, techniques, and outcome. Curr Treat Options Gastroenterol; 2006 Feb;9(1):85-92
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Esophagectomy for Barrett's esophagus: indications, techniques, and outcome.
  • Barrett's esophagus describes metaplastic changes from squamous mucosa to specialized columnar epithelium that can progress from low-grade dysplasia to high-grade dysplasia and even invasive carcinoma.
  • The treatment of Barrett's esophagus with low-grade dysplasia or Barrett's adenocarcinoma is relatively standardized; however, controversy remains regarding appropriate therapy for Barrett's esophagus with high-grade dysplasia.
  • In these patients, surgery is indicated, as esophagectomy can be curative for early stage adenocarcinoma in Barrett's esophagus.
  • In experienced centers, minimally invasive esophagectomy is now an attractive alternative for the treatment of Barrett's esophagus with high-grade dysplasia.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Arch Surg. 2000 Aug;135(8):920-5 [10922253.001]
  • [Cites] Ann Thorac Surg. 2000 Sep;70(3):906-11; discussion 911-2 [11016332.001]
  • [Cites] J Gastrointest Surg. 2003 Feb;7(2):164-70; discussion 170-1 [12600440.001]
  • [Cites] Surgery. 2000 Mar;127(3):284-90 [10715983.001]
  • [Cites] Surg Laparosc Endosc. 1995 Feb;5(1):1-5 [7735533.001]
  • [Cites] Br J Surg. 2000 Aug;87(8):1102-5 [10931058.001]
  • [Cites] Ann Thorac Surg. 2001 Aug;72(2):593-6 [11515902.001]
  • [Cites] JSLS. 1998 Jul-Sep;2(3):243-7 [9876747.001]
  • [Cites] Gut. 1998 Aug;43(2):216-22 [10189847.001]
  • [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]
  • (PMID = 16423317.001).
  • [ISSN] 1092-8472
  • [Journal-full-title] Current treatment options in gastroenterology
  • [ISO-abbreviation] Curr Treat Options Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


41. Nomura T, Yamashita K, Miyashita M, Tajiri T: [Argon plasma coagulation in Barrett's esophagus]. Nihon Rinsho; 2005 Aug;63(8):1458-62
Hazardous Substances Data Bank. Argon, Elemental .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Argon plasma coagulation in Barrett's esophagus].
  • Recently, it has been reported that Barrett's esophagus and Barrett's adenocarcinoma in situ could be successfully managed by APC.
  • The aims of this treatment are to prevent the developing of adenocarcinoma and to promote the restitution of normal squamous epithelium.
  • Shorter length of Barrett's epithelium and normalization in pH with PPI treatment were the independent predictors of sustained long-term restitution of squamous epithelium.
  • In patient with Barrett's esophagus, APC offers an effective, minimally invasive alternative to other treatments previously performed.
  • [MeSH-major] Argon / therapeutic use. Barrett Esophagus / surgery. Electrocoagulation / methods
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / prevention & control. Combined Modality Therapy. Enzyme Inhibitors / therapeutic use. Esophageal Neoplasms / etiology. Esophageal Neoplasms / prevention & control. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / surgery. Humans. Proton Pump Inhibitors

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16101240.001).
  • [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 / Enzyme Inhibitors; 0 / Proton Pump Inhibitors; 67XQY1V3KH / Argon
  • [Number-of-references] 15
  •  go-up   go-down


42. Yu C, Zhang X, Huang Q, Klein M, Goyal RK: High-fidelity DNA histograms in neoplastic progression in Barrett's esophagus. Lab Invest; 2007 May;87(5):466-72
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] High-fidelity DNA histograms in neoplastic progression in Barrett's esophagus.
  • This study describes the high-fidelity DNA histograms in different stages of neoplastic progression to Barrett's adenocarcinoma (BAC).
  • One hundred and eighty-seven cases, including 34 normal gastrointestinal mucosa (control), 66 Barrett's-specialized intestinal metaplasia (SIM), 22 low-grade dysplasia (LGD), 22 high-grade dysplasia (HGD) and 43 BAC were investigated.
  • The high-fidelity DNA histograms suggest that (1) Barrett's SIM may already be dysplastic in nature, and all BAC may be markedly aneuploid; and (2) elevated cellular DNA heterogeneity and 5N fractions may be markers of progressive chromosomal changes and 'unstable aneuploidy' that identifies progressive lesions.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. DNA, Neoplasm / analysis. Esophageal Neoplasms / genetics. Ploidies. Precancerous Conditions / genetics
  • [MeSH-minor] Chromosomal Instability. Disease Progression. Gastric Mucosa. Humans. Image Cytometry

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17310216.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK62867
  • [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 / DNA, Neoplasm
  •  go-up   go-down


43. Ling FC, Khochfar J, Baldus SE, Brabender J, Drebber U, Bollschweiler E, Hoelscher AH, Schneider PM: HIF-1alpha protein expression is associated with the environmental inflammatory reaction in Barrett's metaplasia. Dis Esophagus; 2009;22(8):694-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HIF-1alpha protein expression is associated with the environmental inflammatory reaction in Barrett's metaplasia.
  • We examined the protein expression of HIF-1alpha within the progression of Barrett's sequence as well as the type and degree of the environmental inflammatory reaction.
  • Squamous epithelium (SE), metaplastic, low- and high-grade dysplastic lesions, and tumor tissue of 57 resection specimens from patients with Barrett's adenocarcinoma were immunohistochemically analyzed.
  • HIF-1alpha protein expression increased significantly from SE to Barrett's metaplasia (BM) (P < 0.0001).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19302222.001).
  • [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 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit
  •  go-up   go-down


44. Kuester D, El-Rifai W, Peng D, Ruemmele P, Kroeckel I, Peters B, Moskaluk CA, Stolte M, Mönkemüller K, Meyer F, Schulz HU, Hartmann A, Roessner A, Schneider-Stock R: Silencing of MGMT expression by promoter hypermethylation in the metaplasia-dysplasia-carcinoma sequence of Barrett's esophagus. Cancer Lett; 2009 Mar 08;275(1):117-26
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] Silencing of MGMT expression by promoter hypermethylation in the metaplasia-dysplasia-carcinoma sequence of Barrett's esophagus.
  • To determine the relevance of MGMT in Barrett's carcinogenesis, we analyzed promotor hypermethylation and expression of MGMT in Barrett's adenocarcinomas and its paired precursor lesions from 133 patients using a methylation-specific PCR, real-time RT-PCR and immunohistochemistry.
  • Hypermethylation was detected in 78.9% of esophageal adenocarcinomas, in 100% of Barrett's intraepithelial neoplasia, in 88.9% of Barrett's metaplasia, but only in 21.4% of normal esophageal mucosa samples (P<0.001) and correlated significantly with downregulation of MGMT transcripts (P=0.048) and protein expression (P=0.02).
  • We conclude, that aberrant promoter methylation of MGMT is a frequent and early event during tumorigenesis of Barrett's esophagus.
  • High prevalence of MGMT hypermethylation may represent a candidate marker for improved diagnosis and targeted therapy in Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Carcinoma / metabolism. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Gene Silencing. Metaplasia / metabolism. Tumor Suppressor Proteins / genetics

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Carcinog. 2003 Jan;36(1):23-31 [12503076.001]
  • [Cites] Cancer Res. 2002 Jul 15;62(14):4061-4 [12124342.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):223-7 [12538473.001]
  • [Cites] Cancer Lett. 2003 Feb 20;190(2):125-33 [12565166.001]
  • [Cites] Br J Cancer. 2003 Feb 24;88(4):521-9 [12592365.001]
  • [Cites] Carcinogenesis. 2003 Jun;24(6):1039-44 [12807758.001]
  • [Cites] Gastric Cancer. 2003;6(2):86-95 [12861399.001]
  • [Cites] Adv Exp Med Biol. 2003;532:39-49 [12908548.001]
  • [Cites] Clin Cancer Res. 2003 Aug 1;9(8):2912-9 [12912936.001]
  • [Cites] Virchows Arch. 2003 Oct;443(4):518-23 [12920593.001]
  • [Cites] Clin Cancer Res. 2003 Nov 1;9(14):5306-12 [14614014.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Jun;13(6):967-75 [15184253.001]
  • [Cites] Dig Dis. 2004;22(2):126-33 [15383753.001]
  • [Cites] Carcinogenesis. 1983 Dec;4(12):1591-7 [6360407.001]
  • [Cites] Cancer Commun. 1990;2(1):13-20 [2369549.001]
  • [Cites] Cancer Res. 1990 Dec 15;50(24):7908-11 [2253230.001]
  • [Cites] Cancer Res. 1991 Aug 15;51(16):4131-4 [1868433.001]
  • [Cites] J Natl Cancer Inst. 1992 Mar 4;84(5):337-40 [1738185.001]
  • [Cites] Carcinogenesis. 1995 Sep;16(9):2255-7 [7554086.001]
  • [Cites] Cancer. 1998 Nov 15;83(10):2049-53 [9827707.001]
  • [Cites] Cancer Res. 1999 Feb 15;59(4):793-7 [10029064.001]
  • [Cites] Mol Carcinog. 1999 Feb;24(2):90-8 [10078936.001]
  • [Cites] Am J Pathol. 1999 Apr;154(4):965-73 [10233832.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):997-1003 [15758010.001]
  • [Cites] Int J Oncol. 2005 Jun;26(6):1493-500 [15870861.001]
  • [Cites] Ann Surg Oncol. 2005 May;12(5):354-63 [15915369.001]
  • [Cites] Oncogene. 2005 Jun 9;24(25):4138-48 [15824739.001]
  • [Cites] Int J Hematol. 2006 May;83(4):341-7 [16757436.001]
  • [Cites] Int J Cancer. 2006 Jul 15;119(2):264-8 [16477636.001]
  • [Cites] J Clin Oncol. 2006 Jul 20;24(21):3431-7 [16849758.001]
  • [Cites] Cancer Res. 2007 Sep 15;67(18):8952-9 [17875738.001]
  • [Cites] Mutat Res. 2000 Apr;462(2-3):83-100 [10767620.001]
  • [Cites] Cancer Res. 2000 May 1;60(9):2368-71 [10811111.001]
  • [Cites] Cancer Res. 2000 Sep 15;60(18):5021-6 [11016622.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3410-8 [11309301.001]
  • [Cites] Int J Oncol. 2001 Jun;18(6):1187-93 [11351250.001]
  • [Cites] Cancer Res. 2001 Jun 15;61(12):4689-92 [11406538.001]
  • [Cites] Int J Cancer. 2001 Sep15;93(6):805-9 [11519041.001]
  • [Cites] Carcinogenesis. 2001 Oct;22(10):1715-9 [11577014.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8113-7 [11719438.001]
  • [Cites] Cancer. 2001 Dec 1;92(11):2760-8 [11753949.001]
  • [Cites] Jpn J Cancer Res. 2002 Feb;93(2):184-9 [11856482.001]
  • [Cites] Lancet Oncol. 2003 Jan;4(1):37-44 [12517538.001]
  • (PMID = 19027227.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK067629; United States / NCI NIH HHS / CA / R01 CA106176; United States / NCI NIH HHS / CA / R01CA106176
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
  • [Other-IDs] NLM/ NIHMS576423; NLM/ PMC4028828
  •  go-up   go-down


45. Yoon HY, Kim HI, Kim CB: [Clinicopathologic characteristics of adenocarcinoma in cardia according to Siewert classification]. Korean J Gastroenterol; 2008 Nov;52(5):293-7
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinicopathologic characteristics of adenocarcinoma in cardia according to Siewert classification].
  • RESULTS: Barrett's adenocarcinoma was recognized in two patients so called type I.
  • [MeSH-major] Adenocarcinoma / pathology. Cardia. Stomach Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Barrett Esophagus / pathology. Barrett Esophagus / surgery. Esophageal Neoplasms / classification. Esophageal Neoplasms / mortality. Esophageal Neoplasms / pathology. Female. Humans. Kaplan-Meier Estimate. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19077475.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
  •  go-up   go-down


46. Segat D, Cassaro M, Dazzo E, Cavallini L, Romualdi C, Salvador R, Vitale MP, Vitiello L, Fassan M, Rugge M, Zaninotto G, Ancona E, Baroni MD: Pericentriolar material analyses in normal esophageal mucosa, Barrett's metaplasia and adenocarcinoma. Histol Histopathol; 2010 05;25(5):551-60
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] Pericentriolar material analyses in normal esophageal mucosa, Barrett's metaplasia and adenocarcinoma.
  • Barrett's esophagus metaplasia is a pre-cancerous condition caused by chronic esophagitis.
  • Chromosomal instability (CIN) is common in Barrett's cells: therefore, we investigated the possible presence of centrosomal aberrations (a main cause of CIN) by centrosomal protein immunostaining in paraffined esophageal samples of patients who developed a Barrett's adenocarcinoma.
  • The alterations could even be found in adjacent native squamous epithelium, Barrett's mucosa and submucosal gland cells, as well as in the basal/epibasal layers of the mucosa and submucosal gland duct, which are the regions hosting esophageal stem and progenitor cells.
  • Importantly, PCM altered signals in Barrett's mucosa and their apparent evolution in successive histopathological steps were correlated to adenocarcinoma aggressiveness, suggesting PCM as a possible prognostic marker for tumor relapse.
  • Extending our observations in a prospective study might help in the development of new prevention protocols for adenocarcinoma patients.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Centrosome / metabolism. Esophageal Neoplasms / metabolism. Esophagus / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20238294.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antigens; 0 / Tubulin; 0 / pericentrin
  •  go-up   go-down


47. Delgado JS, Mustafi R, Yee J, Cerda S, Chumsangsri A, Dougherty U, Lichtenstein L, Fichera A, Bissonnette M: Sorafenib triggers antiproliferative and pro-apoptotic signals in human esophageal adenocarcinoma cells. Dig Dis Sci; 2008 Dec;53(12):3055-64
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.
  • [Title] Sorafenib triggers antiproliferative and pro-apoptotic signals in human esophageal adenocarcinoma cells.
  • BACKGROUND AND PURPOSE: Current therapies offer scant benefit to patients with advanced esophageal adenocarcinoma.
  • We investigated the effects of Sorafenib, a multifunctional kinase inhibitor, on several growth regulatory pathways that control cell growth and survival in SEG-1 cells derived from Barrett's adenocarcinoma.
  • CONCLUSIONS: These results support a rational basis for future clinical studies to assess the therapeutic benefit of Sorafenib in esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Benzenesulfonates / pharmacology. Cell Proliferation / drug effects. Esophageal Neoplasms / pathology. Pyridines / pharmacology

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • Hazardous Substances Data Bank. NICOTINAMIDE .
  • 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] Biochem Pharmacol. 2007 May 1;73(9):1308-17 [17266941.001]
  • [Cites] Gut. 1989 Jan;30(1):14-8 [2920919.001]
  • [Cites] Clin Cancer Res. 2003 Oct 15;9(13):4819-25 [14581353.001]
  • [Cites] Gastroenterology. 1984 Oct;87(4):927-33 [6468881.001]
  • [Cites] ANZ J Surg. 2007 Jan-Feb;77(1-2):37-9 [17295818.001]
  • [Cites] Dis Esophagus. 2007;20(3):212-6 [17509117.001]
  • [Cites] Oncol Rep. 1999 Jul-Aug;6(4):877-82 [10373674.001]
  • [Cites] Gastroenterology. 2002 Feb;122(2):299-307 [11832445.001]
  • [Cites] Eur J Cancer. 2005 Mar;41(5):664-72 [15763640.001]
  • [Cites] Eur J Surg Oncol. 2007 Apr;33(3):307-13 [17123775.001]
  • [Cites] Oncogene. 2003 Oct 30;22(49):7809-18 [14586407.001]
  • [Cites] Histopathology. 2001 Dec;39(6):589-96 [11903577.001]
  • [Cites] Gut. 2005 Mar;54 Suppl 1:i6-12 [15711008.001]
  • [Cites] Br J Surg. 2002 Jul;89(7):824-37 [12081731.001]
  • [Cites] Surgery. 2004 Aug;136(2):160-8 [15300175.001]
  • [Cites] Oncogene. 2007 May 14;26(22):3291-310 [17496923.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2006 Jan;11(1):75-87 [16947086.001]
  • [Cites] J Clin Oncol. 2005 Sep 20;23(27):6771-90 [16170185.001]
  • [Cites] Clin Gastroenterol Hepatol. 2006 May;4(5):566-72 [16630761.001]
  • [Cites] Cancer Res. 2006 Jun 1;66(11):5656-64 [16740703.001]
  • [Cites] Anal Biochem. 2000 Oct 15;285(2):194-204 [11017702.001]
  • [Cites] EMBO J. 2000 Nov 1;19(21):5813-23 [11060032.001]
  • [Cites] Gut. 1991 Dec;32(12):1441-6 [1773946.001]
  • [Cites] Am J Gastroenterol. 1997 Feb;92(2):212-5 [9040193.001]
  • [Cites] Mol Cell Biol. 2000 May;20(10):3497-509 [10779339.001]
  • [Cites] BMC Cancer. 2007 Jun 08;7:97 [17559672.001]
  • [Cites] J Natl Med Assoc. 2007 Jun;99(6):620-6 [17595930.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Oct;287(4):G743-8 [15231484.001]
  • [Cites] Oncol Rep. 2007 Jun;17(6):1377-82 [17487394.001]
  • [Cites] Cancer Res. 2006 Mar 1;66(5):2544-52 [16510571.001]
  • [Cites] Dis Esophagus. 2008;21(6):514-21 [18840136.001]
  • [Cites] Aliment Pharmacol Ther. 2007 Feb 15;25(4):447-53 [17270000.001]
  • [Cites] Gut. 2003 Feb;52(2):174-80 [12524396.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2006 Feb;290(2):G335-42 [16239404.001]
  • [Cites] J Surg Res. 2005 Jul 1;127(1):53-8 [15964304.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] Nat Rev Drug Discov. 2006 Oct;5(10):835-44 [17016424.001]
  • [Cites] Am J Gastroenterol. 1998 Jul;93(7):1028-32 [9672324.001]
  • [Cites] Oncogene. 2007 May 14;26(22):3227-39 [17496918.001]
  • [Cites] JAMA. 2001 May 9;285(18):2331-8 [11343480.001]
  • [Cites] Cancer Res. 2006 Dec 15;66(24):11851-8 [17178882.001]
  • [Cites] Hum Pathol. 2001 Apr;32(4):379-88 [11331954.001]
  • [Cites] Clin Cancer Res. 2007 Sep 15;13(18 Pt 1):5305-13 [17875759.001]
  • [Cites] J Clin Pathol. 2006 Jun;59(6):631-4 [16731604.001]
  • [Cites] Semin Oncol. 2007 Apr;34(2 Suppl 1):S2-6 [17449347.001]
  • [Cites] Cochrane Database Syst Rev. 2006 Oct 18;(4):CD004063 [17054195.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] J Natl Cancer Inst. 2000 Aug 16;92(16):1316-21 [10944553.001]
  • (PMID = 18512153.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA036745; United States / NIDDK NIH HHS / DK / P30DK42086
  • [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 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Cyclin E; 0 / MYC protein, human; 0 / Phenylurea Compounds; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 0 / Pyridines; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 136601-57-5 / Cyclin D1; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  •  go-up   go-down


48. Kuester D, Dar AA, Moskaluk CC, Krueger S, Meyer F, Hartig R, Stolte M, Malfertheiner P, Lippert H, Roessner A, El-Rifai W, Schneider-Stock R: Early involvement of death-associated protein kinase promoter hypermethylation in the carcinogenesis of Barrett's esophageal adenocarcinoma and its association with clinical progression. Neoplasia; 2007 Mar;9(3):236-45
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] Early involvement of death-associated protein kinase promoter hypermethylation in the carcinogenesis of Barrett's esophageal adenocarcinoma and its association with clinical progression.
  • Esophageal Barrett's adenocarcinoma (BA) develops through a multistage process, which is associated with the transcriptional silencing of tumor-suppressor genes by promoter CpG island hypermethylation.
  • In this study, we explored the promoter hypermethylation and protein expression of proapoptotic death-associated protein kinase (DAPK) during the multistep Barrett's carcinogenesis cascade.
  • Hypermethylation of DAPK promoter was detected in 20% of normal mucosa, 50% of Barrett's metaplasia, 53% of dysplasia, and 60% of adenocarcinomas, and resulted in a marked decrease in DAPK protein expression (P < .01).
  • Thus, we consider DAPK inactivation by promoter hypermethylation as an early event in Barrett's carcinogenesis and suggest that a decreased protein expression of DAPK likely plays a role in the development and progression of BA.

  • 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] Nat Cell Biol. 2001 Jan;3(1):1-7 [11146619.001]
  • [Cites] Cancer Lett. 2006 Aug 18;240(1):69-75 [16246486.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2847-51 [11306456.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3225-9 [11309270.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3410-8 [11309301.001]
  • [Cites] Oncogene. 2001 Mar 29;20(14):1765-70 [11313923.001]
  • [Cites] Gastroenterology. 2002 Feb;122(2):590-1 [11845806.001]
  • [Cites] Gastroenterology. 2002 Apr;122(4):1113-21 [11910361.001]
  • [Cites] Clin Cancer Res. 2003 Aug 1;9(8):2912-9 [12912936.001]
  • [Cites] J Natl Cancer Inst. 2000 Sep 20;92(18):1511-6 [10995806.001]
  • [Cites] Cancer Res. 2000 Sep 15;60(18):5021-6 [11016622.001]
  • [Cites] Lancet. 2000 Dec 16;356(9247):2079-85 [11145505.001]
  • [Cites] Virchows Arch. 2004 Aug;445(2):135-41 [15185075.001]
  • [Cites] Dig Dis. 2004;22(2):126-33 [15383753.001]
  • [Cites] Dig Dis. 2004;22(2):196-201 [15383761.001]
  • [Cites] Cancer Sci. 2004 Sep;95(9):736-40 [15471559.001]
  • [Cites] Genes Dev. 1995 Jan 1;9(1):15-30 [7828849.001]
  • [Cites] EMBO J. 1997 Mar 3;16(5):998-1008 [9118961.001]
  • [Cites] Adv Cancer Res. 1998;72:141-96 [9338076.001]
  • [Cites] Nature. 1997 Nov 13;390(6656):180-4 [9367156.001]
  • [Cites] EMBO J. 1998 Apr 15;17(8):2426-35 [9545253.001]
  • [Cites] Cancer. 1998 Nov 15;83(10):2049-53 [9827707.001]
  • [Cites] Gastroenterology. 1998 Dec;115(6):1381-6 [9834265.001]
  • [Cites] Am J Pathol. 1999 Apr;154(4):965-73 [10233832.001]
  • [Cites] Gastroenterology. 1999 Jul;117(1):218-28 [10381931.001]
  • [Cites] J Cell Biol. 1999 Jul 12;146(1):141-8 [10402466.001]
  • [Cites] Int J Oncol. 2005 Jun;26(6):1493-500 [15870861.001]
  • [Cites] Oncogene. 2005 Jun 9;24(25):4138-48 [15824739.001]
  • [Cites] Neoplasia. 2005 Apr;7(4):331-5 [15967110.001]
  • [Cites] Int J Biochem Cell Biol. 2005 Sep;37(9):1763-7 [16009322.001]
  • [Cites] Clin Cancer Res. 2005 Sep 15;11(18):6544-9 [16166431.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Sep;14(9):2113-7 [16172218.001]
  • [Cites] Neoplasia. 2005 Sep;7(9):854-61 [16229808.001]
  • [Cites] J Cancer Res Clin Oncol. 2005 Nov;131(11):733-40 [16075282.001]
  • [Cites] J Pathol. 2006 May;209(1):95-105 [16575786.001]
  • [Cites] Cancer Res. 2001 Feb 1;61(3):939-42 [11221887.001]
  • (PMID = 17401463.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106176; United States / NCI NIH HHS / CA / CA106176
  • [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 / Apoptosis Regulatory Proteins; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
  • [Other-IDs] NLM/ PMC1838580
  •  go-up   go-down


49. Koike T, Ohara S, Inomata Y, Abe Y, Iijima K, Shimosegawa T: The prevalence of Helicobacter pylori infection and the status of gastric acid secretion in patients with gastroesophageal junction adenocarcinoma in Japan. Inflammopharmacology; 2007 Apr;15(2):61-4
The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for gastroesophageal junction adenocarcinoma .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The prevalence of Helicobacter pylori infection and the status of gastric acid secretion in patients with gastroesophageal junction adenocarcinoma in Japan.
  • We have previously reported that H. pylori infection prevents reflux esophagitis (RE) and Barrett's esophagus (BE) by decreasing gastric acid secretion.
  • Gastroesophageal (GE) junction adenocarcinoma, including Barrett's adenocarcinoma, has been thought to be a complication of gastroesophageal reflux disease.
  • However, the relationship between H. pylori infection, gastric acid secretion and GE junction adenocarcinoma had not yet been investigated in Japan.
  • We demonstrated that the status of gastric acid secretion was higher in patients with GE junction adenocarcinoma than in patients with early gastric cancer (EGC), and that the level was the same in patients with RE and those with BE.
  • We also found that the prevalence of H. pylori infection in patients with GE junction adenocarcinoma was significantly lower than that in patients with EGC, although not as low as that in patients with RE and BE, suggesting that preservation of gastric acid secretion may be important for the development of GE junction adenocarcinoma in Japanese people, regardless of the presence of H. pylori infection.
  • [MeSH-major] Adenocarcinoma / complications. Helicobacter Infections / complications. Helicobacter pylori. Stomach Neoplasms / complications

  • 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
  • (PMID = 17450443.001).
  • [ISSN] 0925-4692
  • [Journal-full-title] Inflammopharmacology
  • [ISO-abbreviation] Inflammopharmacology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 42
  •  go-up   go-down


50. Yoo C, Zhao J, Pal M, Hersberger K, Huber CG, Simeone DM, Beer DG, Lubman DM: Automated integration of monolith-based protein separation with on-plate digestion for mass spectrometric analysis of esophageal adenocarcinoma human epithelial samples. Electrophoresis; 2006 Sep;27(18):3643-51
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Automated integration of monolith-based protein separation with on-plate digestion for mass spectrometric analysis of esophageal adenocarcinoma human epithelial samples.
  • Proteins from primary esophageal Barrett's adenocarcinoma tissue were prefractionated by chromatofocusing and analyzed successfully by this automated configuration, obtaining rapid protein identifications through PMF and sequencing analyses with high sequence coverage.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Neoplasm Proteins / analysis. Proteome / analysis. Proteomics / methods

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16927349.001).
  • [ISSN] 0173-0835
  • [Journal-full-title] Electrophoresis
  • [ISO-abbreviation] Electrophoresis
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM 49500; United States / NCI NIH HHS / CA / R01CA106402
  • [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] Germany
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Proteome
  •  go-up   go-down


51. Richert Z, Robaszkiewicz M: [Gastroesophageal reflux disease and malignancy]. Rev Prat; 2008 Sep 15;58(13):1414-5, 1417, 1419-20
MedlinePlus Health Information. consumer health - GERD.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Severe gastroesophageal reflux disease (GERD) predisposes to the development of Barrett's esophagus defined by the replacement of the squamous epithelium of the distal esophagus by a columnar epithelium.
  • Barrett's esophagus is a precancerous condition which has a risk of malignant transformation to adenocarcinoma.
  • Barrett's adenocarcinoma remains a relatively rare condition.
  • Its incidence among patients followed up for Barrett's esophagus is approximately 0.5% patients per year.
  • Besides GERD, obesity, male gender and age are the main risk factors for the development of Barrett's mucosa and esophageal adenocarcinoma.
  • Men above 50 presenting with ancient and frequent GERD symptoms could benefit from an upper-GI endoscopy to detect Barrett's esophagus.
  • Though still controversial, surveillance of Barrett's mucosa could allow detection of high grade dysplasia and esophageal adenocarcinoma at an early stage, enabling a curative treatment.
  • [MeSH-major] Barrett Esophagus / etiology. Gastroesophageal Reflux / complications

  • Genetic Alliance. consumer health - Gastroesophageal Reflux.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18924321.001).
  • [ISSN] 0035-2640
  • [Journal-full-title] La Revue du praticien
  • [ISO-abbreviation] Rev Prat
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


52. Konturek PC, Burnat G, Rau T, Hahn EG, Konturek S: Effect of adiponectin and ghrelin on apoptosis of Barrett adenocarcinoma cell line. Dig Dis Sci; 2008 Mar;53(3):597-605
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.
  • [Title] Effect of adiponectin and ghrelin on apoptosis of Barrett adenocarcinoma cell line.
  • BACKGROUND: Obesity is an important risk factor for Barrett adenocarcinoma.
  • However, the role of adiponectin (anti-inflammatory adipokine from adipose tissue) and ghrelin (orexigenic peptide gastric origin) on the progression of Barrett's carcinogenesis has not been investigated so far.
  • (1) to compare the expression of adiponectin and ghrelin receptors in Barrett's esophagus and in normal squamous epithelium;.
  • (2) to assess the effect of adiponectin and ghrelin on apoptosis in Barrett's adenocarcinoma cells in vitro; and (3) to investigate the effect of ghrelin on IL-1beta and COX-2 expression in OE-19 cells incubated with TNFalpha.
  • METHODS: The expression of ghrelin and adiponectin receptors (GHS-R1a, Adipo-R1, Adipo R-2) in biopsies from Barrett's esophagus and in Barrett's adenocarcinoma cell line OE-19 was assessed by quantitative RT-PCR (qRT-PCR).
  • At the mRNA level, the expression of adiponectin receptors (Adipo-R1, Adipo-R2) was decreased, and the expression of ghrelin receptor (GHS-R1a) was increased in Barrett's mucosa.
  • CONCLUSION: Adiponectin and ghrelin have an inhibitory effect on Barrett's carcinogenesis by two different mechanisms:.
  • The decrease in levels of these two peptides in obesity may explain the progression of Barrett's carcinoma in obese individuals.
  • [MeSH-major] Adenocarcinoma / metabolism. Apoptosis / physiology. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Receptors, Adiponectin / metabolism. Receptors, Ghrelin / metabolism

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • Hazardous Substances Data Bank. DEOXYCHOLIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Aliment Pharmacol Ther. 2005 Nov 15;22(10):1005-10 [16268976.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 24;101(8):2476-81 [14983034.001]
  • [Cites] Clin Cancer Res. 2005 Jan 15;11(2 Pt 1):466-72 [15701829.001]
  • [Cites] FASEB J. 2004 Mar;18(3):439-56 [15003990.001]
  • [Cites] Eur J Endocrinol. 2005 Sep;153(3):403-7 [16131603.001]
  • [Cites] Am J Gastroenterol. 2001 Feb;96(2):331-7 [11232672.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Jun 23;345(1):271-9 [16678125.001]
  • [Cites] Endocrinology. 2000 Nov;141(11):4255-61 [11089560.001]
  • [Cites] J Pharmacol Exp Ther. 2006 Oct;319(1):477-87 [16868036.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2006 Feb;2(2):80-8 [16932262.001]
  • [Cites] Regul Pept. 2006 May 15;134(2-3):105-13 [16529829.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Apr;92(4):1510-6 [17213279.001]
  • [Cites] Circulation. 2004 May 11;109(18):2221-6 [15117840.001]
  • [Cites] N Engl J Med. 2002 May 23;346(21):1623-30 [12023994.001]
  • [Cites] J Biol Chem. 2005 May 6;280(18):18341-7 [15734737.001]
  • [Cites] Lancet. 2000 Dec 16;356(9247):2079-85 [11145505.001]
  • [Cites] Curr Opin Gastroenterol. 2002 Jul;18(4):471-8 [17033323.001]
  • [Cites] Clin Cancer Res. 2005 May 15;11(10):3642-6 [15897559.001]
  • [Cites] Curr Atheroscler Rep. 2006 Sep;8(5):433-8 [16901415.001]
  • [Cites] Clin Sci (Lond). 2006 Mar;110(3):267-78 [16464169.001]
  • [Cites] J Clin Invest. 2004 Jul;114(1):57-66 [15232612.001]
  • [Cites] Endocr Rev. 2006 Dec;27(7):762-78 [17056740.001]
  • [Cites] Eur J Pharmacol. 2006 Apr 24;536(1-2):171-81 [16581065.001]
  • [Cites] Cancer. 2006 Jun 1;106(11):2376-81 [16639730.001]
  • [Cites] J Clin Invest. 2006 Jul;116(7):1784-92 [16823476.001]
  • [Cites] Gut. 2005 Mar;54 Suppl 1:i1-5 [15711002.001]
  • (PMID = 17763959.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Culture Media; 0 / Ghrelin; 0 / Interleukin-1beta; 0 / Receptors, Adiponectin; 0 / Receptors, Ghrelin; 0 / Tumor Necrosis Factor-alpha; 005990WHZZ / Deoxycholic Acid; EC 1.14.99.1 / Cyclooxygenase 2
  •  go-up   go-down


53. Möbius C, Stein HJ, Spiess C, Becker I, Feith M, Theisen J, Gais P, Jütting U, Siewert JR: COX2 expression, angiogenesis, proliferation and survival in Barrett's cancer. Eur J Surg Oncol; 2005 Sep;31(7):755-9
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.
  • [Title] COX2 expression, angiogenesis, proliferation and survival in Barrett's cancer.
  • OBJECTIVES: To examine COX2 expression and its relation to angiogenesis, Ki67 and Bcl2 expression in Barrett's cancer.
  • METHODS: Specimens from 48 R0-resected Barrett's adenocarcinoma were immunostained for cyclooxygenase 2 (COX2), CD 31 and alpha-sm actin to discriminate between mature and immature vessels, Mib-1 and Bcl2.
  • CONCLUSIONS: Elevated COX2 expression is associated with lymph-node metastases and reduced survival in Barrett's cancer.
  • [MeSH-major] Barrett Esophagus / genetics. Barrett Esophagus / physiopathology. Esophageal Neoplasms / genetics. Esophageal Neoplasms / physiopathology. Gene Expression Profiling. Neovascularization, Pathologic. Prostaglandin-Endoperoxide Synthases / biosynthesis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15979837.001).
  • [ISSN] 0748-7983
  • [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] 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  •  go-up   go-down


54. 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
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] Expression of survivin, p53, and caspase 3 in Barrett's esophagus carcinogenesis.
  • The regulation of apoptosis, as a distinctive form of programmed cell death, in multistep Barrett's esophagus (BE) carcinogenesis is poorly understood.
  • 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.
  • Cytoplasmic survivin location may indicate an initial antiapoptotic, more than proliferative, role in the early phases of Barrett carcinogenesis.
  • [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.
  • [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


55. 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
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] Association of COX-2 expression with corresponding active and chronic inflammatory reactions in Barrett's metaplasia and progression to cancer.
  • AIMS: Risk reduction for Barrett's cancer in individuals taking non-steroidal anti-inflammatory drugs has been reported.
  • Cyclooxygenase (COX)-2, one of the inhibited enzymes, is putatively involved in Barrett's cancer pathogenesis.
  • 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.
  • Within the Barrett's sequence, a significant progressive increase in COX-2 expression was identified (P < 0.0001).
  • 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.
  • This supports the potential of a chemoprevention strategy using COX-2 inhibitors independent of the extent and type of the inflammatory reaction in Barrett's oesophagus.
  • [MeSH-major] Barrett Esophagus / enzymology. Cyclooxygenase 2 / genetics. Esophageal Neoplasms / enzymology. Inflammation / enzymology. Membrane Proteins / genetics

  • [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


56. Konturek PC, Burnat G, Hahn EG: Inhibition of Barret's adenocarcinoma cell growth by simvastatin: involvement of COX-2 and apoptosis-related proteins. J Physiol Pharmacol; 2007 Aug;58 Suppl 3:141-8
Hazardous Substances Data Bank. SIMVASTATIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of Barret's adenocarcinoma cell growth by simvastatin: involvement of COX-2 and apoptosis-related proteins.
  • The role of statins in the prevention and therapy of Barrett's adenocarcinoma (BA) has not been investigated so far.
  • Clinical trial are necessary to prove the beneficial effects of statins on cancerogenesis in Barrett's esophagus.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cyclooxygenase 2 / metabolism. Esophageal Neoplasms / drug therapy. Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology. Simvastatin / pharmacology
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Barrett Esophagus / complications. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Gene Expression Regulation / drug effects. Humans. Proto-Oncogene Proteins c-bcl-2 / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. bcl-2-Associated X Protein / drug effects. bcl-2-Associated X Protein / metabolism

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Statins.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17901590.001).
  • [ISSN] 0867-5910
  • [Journal-full-title] Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
  • [ISO-abbreviation] J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; AGG2FN16EV / Simvastatin; EC 1.14.99.1 / Cyclooxygenase 2
  •  go-up   go-down


57. Stolte M, Kirtil T, Oellig F, Vogel C, Mueller H, May A, Ell C, Wittenberg R: The pattern of invasion of early carcinomas in Barrett's esophagus is dependent on the depth of infiltration. Pathol Res Pract; 2010 May 15;206(5):300-4
Genetic Alliance. consumer health - Barrett's Esophagus.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pattern of invasion of early carcinomas in Barrett's esophagus is dependent on the depth of infiltration.
  • The differential diagnosis "high-grade intraepithelial neoplasia" or "well-differentiated Barrett's adenocarcinoma limited to the mucosa" is controversial.
  • We investigated 277 endoscopically resected specimens of early Barrett's carcinoma.
  • Depth of infiltration was classified as follows: m 1=carcinoma limited to Barrett's mucosa; m 2=carcinoma infiltrating the neo-muscularis mucosae; m 3=infiltration of the original lamina propria of the esophageal mucosa; m 4=infiltration of the original muscularis mucosae; sm 1, sm 2, and sm 3=infiltration into the upper third, middle third, and lower third of the submucosa.
  • 74-96% of m 1-m 4 Barrett's carcinomas limited to the mucosa have a D 0-pattern.
  • Our study shows that the pattern of invasion in early cancer in Barrett's esophagus statistically significantly depends on depth of infiltration.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophagus / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2010 Elsevier GmbH. All rights reserved.
  • (PMID = 20188488.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


58. Pech O, Günter E, Dusemund F, Origer J, Lorenz D, Ell C: Accuracy of endoscopic ultrasound in preoperative staging of esophageal cancer: results from a referral center for early esophageal cancer. Endoscopy; 2010 Jun;42(6):456-61
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.
  • RESULTS: 179 consecutive patients (mean age 64.4 +/- 9.5 years; 142 men) underwent esophageal resection for Barrett's adenocarcinoma (n = 134) and squamous cell cancer (n = 45).
  • [MeSH-major] Adenocarcinoma / ultrasonography. Barrett Esophagus / ultrasonography. Carcinoma, Squamous Cell / ultrasonography. Endosonography. Esophageal Neoplasms / ultrasonography

  • Genetic Alliance. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Georg Thieme Verlag KG Stuttgart.New York.
  • (PMID = 20306385.001).
  • [ISSN] 1438-8812
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


59. Sud D, Zhong W, Beer DG, Mycek MA: Time-resolved optical imaging provides a molecular snapshot of altered metabolic function in living human cancer cell models. Opt Express; 2006 May 15;14(10):4412-26
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A fluorescence lifetime imaging microscopy (FLIM) method was developed and applied to investigate metabolic function in living human normal esophageal (HET-1) and Barrett's adenocarcinoma (SEG-1) cells.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19516593.001).
  • [ISSN] 1094-4087
  • [Journal-full-title] Optics express
  • [ISO-abbreviation] Opt Express
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


60. Lao-Sirieix P, Corovic A, Jankowski J, Lowe A, Triadafilopoulos G, Fitzgerald RC: Physiological and molecular analysis of acid loading mechanisms in squamous and columnar-lined esophagus. Dis Esophagus; 2008;21(6):529-38
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.
  • SUMMARY: Barrett's esophagus (BE) may be an adaptive cellular response to repeated acid exposure.
  • Barrett's adenocarcinoma cell lines TE7 and OE-33 were compared with a normal esophageal (NE) cell line OE-21.
  • The degree of acid loading is greater in BE than NE cells and it occurs via dual ion exchangers similar to gastric mucosa.
  • Only Barrett's epithelial cells can maintain a physiological pHi following prolonged and repeated reflux exposure, which may confer a teleological advantage.
  • [MeSH-major] Barrett Esophagus / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology. Esophageal pH Monitoring. Gastroesophageal Reflux / physiopathology

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - GERD.
  • 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 = 18840137.001).
  • [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
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Neoplasm
  •  go-up   go-down


61. Messmann H: [Barrett's esophagus carcinoma]. Praxis (Bern 1994); 2006 Jun 21;95(25-26):1029-35
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 esophagus carcinoma].
  • The incidence of Barrett's esophagus, long segment as well as short segment, has increased over the last few years.
  • However there is a simultaneous increase of Barrett's adenocarcinoma in the Western world, while the number of squamous epithelium cancer decreases.
  • Due to available data it is clear that the risk of Barrett's esophagus has been overestimated, mainly because of a publication bias.
  • The risk of a Barrett's esophagus carcinoma has been published with 0.5%/year.
  • The diagnosis of Barrett's esophagus is made endoscopically and histologically, this means 4 quadrant biopsies every 1-2 cm are gold standard.
  • In patients with proven Barrett's esophagus regular surveillance endoscopies depending on the presence of intraepithelial neoplasia are recommended.
  • While patients with Barrett's esophagus and no or with low grade intraepithelial neoplasia need only surveillance, those with high grade intraepithelial neoplasia should be treated.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16836063.001).
  • [ISSN] 1661-8157
  • [Journal-full-title] Praxis
  • [ISO-abbreviation] Praxis (Bern 1994)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


62. Murphy SJ, Hughes AE, Patterson CC, Anderson LA, Watson RG, Johnston BT, Comber H, McGuigan J, Reynolds JV, Murray LJ: A population-based association study of SNPs of GSTP1, MnSOD, GPX2 and Barrett's esophagus and esophageal adenocarcinoma. Carcinogenesis; 2007 Jun;28(6):1323-8
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.
  • [Title] A population-based association study of SNPs of GSTP1, MnSOD, GPX2 and Barrett's esophagus and esophageal adenocarcinoma.
  • Oxidative stress appears to be important in the pathogenesis of Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC).
  • The Factors Influencing the Barrett's Adenocarcinoma Relationship (FINBAR) study is a population-based, case-control study of BE and EAC in Ireland.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Glutathione Peroxidase / genetics. Glutathione S-Transferase pi / genetics. Polymorphism, Single Nucleotide. Superoxide Dismutase / genetics

  • 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
  • (PMID = 17277236.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.11.1.- / GPX2 protein, human; EC 1.11.1.9 / Glutathione Peroxidase; EC 1.15.1.1 / Superoxide Dismutase; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi
  •  go-up   go-down


63. Murphy SJ, Anderson LA, Ferguson HR, Johnston BT, Watson PR, McGuigan J, Comber H, Reynolds JV, Murray LJ, Cantwell MM: Dietary antioxidant and mineral intake in humans is associated with reduced risk of esophageal adenocarcinoma but not reflux esophagitis or Barrett's esophagus. J Nutr; 2010 Oct;140(10):1757-63
Hazardous Substances Data Bank. SELENIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dietary antioxidant and mineral intake in humans is associated with reduced risk of esophageal adenocarcinoma but not reflux esophagitis or Barrett's esophagus.
  • The role of antioxidants in the pathogenesis of reflux esophagitis (RE), Barrett's esophagus (BE), and esophageal adenocarcinoma (EAC) remains unknown.
  • We performed an assessment of dietary antioxidant intake in a case control study of RE (n = 219), BE (n = 220), EAC (n = 224), and matched population controls (n = 256) (the Factors Influencing the Barrett's Adenocarcinoma Relationship study) using a modification of a validated FFQ.
  • [MeSH-major] Adenocarcinoma / prevention & control. Antioxidants / administration & dosage. Barrett Esophagus / prevention & control. Diet. Gastroesophageal Reflux / prevention & control. Minerals / administration & dosage

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • MedlinePlus Health Information. consumer health - Antioxidants.
  • MedlinePlus Health Information. consumer health - GERD.
  • MedlinePlus Health Information. consumer health - Minerals.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Sodium ascorbate .
  • Hazardous Substances Data Bank. L-Ascorbic Acid .
  • Hazardous Substances Data Bank. COPPER, ELEMENTAL .
  • Hazardous Substances Data Bank. ZINC, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20702746.001).
  • [ISSN] 1541-6100
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Minerals; 1406-18-4 / Vitamin E; 36-88-4 / Carotenoids; 789U1901C5 / Copper; H6241UJ22B / Selenium; J41CSQ7QDS / Zinc; PQ6CK8PD0R / Ascorbic Acid
  •  go-up   go-down


64. Vieth M, Schubert B, Lang-Schwarz K, Stolte M: Frequency of Barrett's neoplasia after initial negative endoscopy with biopsy: a long-term histopathological follow-up study. Endoscopy; 2006 Dec;38(12):1201-5
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] Frequency of Barrett's neoplasia after initial negative endoscopy with biopsy: a long-term histopathological follow-up study.
  • BACKGROUND: Barrett's adenocarcinoma is being diagnosed increasingly.
  • We examine possible differences between long segment and short-segment Barrett esophagus (LSBE and SSBE) in long-term follow-up on the basis of our histopathology registry.
  • METHODS AND PATIENTS: All Barrett's esophagus patients diagnosed histologically between 1990 and 1995 (n = 1071) were selected.
  • Of the remaining 748 patients with follow up for more than 5 years, 315 had documented LSBE, 246 had SSBE, and 187 had no length of Barrett esophagus recorded (NLBE).
  • CONCLUSION: The yearly incidence of Barrett esophagus cancer varies between 0.4 % and 1.7 %.
  • Despite the limitations of this retrospective and pathology-based study, the observed risk of developing cancer in Barrett esophagus without neoplasia is comparable to that found in other studies, mainly from the US and the UK, and varies between 0.7 % and 1.0 % of yearly incidence.
  • [MeSH-major] Barrett Esophagus / epidemiology. Barrett Esophagus / pathology. Esophageal Neoplasms / epidemiology. Esophageal Neoplasms / pathology. Esophagoscopy / methods. Esophagus / pathology
  • [MeSH-minor] Adenocarcinoma / epidemiology. Adenocarcinoma / pathology. Biopsy / standards. Female. Follow-Up Studies. Humans. Incidence. Male. Middle Aged. Risk Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17163319.001).
  • [ISSN] 0013-726X
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


65. Marx AH, Zielinski M, Kowitz CM, Dancau AM, Thieltges S, Simon R, Choschzick M, Yekebas E, Kaifi JT, Mirlacher M, Atanackovic D, Brümmendorf TH, Fiedler W, Bokemeyer C, Izbicki JR, Sauter G: Homogeneous EGFR amplification defines a subset of aggressive Barrett's adenocarcinomas with poor prognosis. Histopathology; 2010 Sep;57(3):418-26
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.
  • [Title] Homogeneous EGFR amplification defines a subset of aggressive Barrett's adenocarcinomas with poor prognosis.
  • The aim of this study was performed to determine the potential impact of tumour heterogeneity on anti-EGFR therapy in Barrett's adenocarcinoma (BAC).
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Gene Amplification. Receptor, Epidermal Growth Factor / genetics

  • 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] © 2010 Blackwell Publishing Limited.
  • (PMID = 20840671.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


66. Fassan M, Pizzi M, Battaglia G, Giacomelli L, Parente P, Bocus P, Ancona E, Rugge M: Programmed cell death 4 (PDCD4) expression during multistep Barrett's carcinogenesis. J Clin Pathol; 2010 Aug;63(8):692-6
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] Programmed cell death 4 (PDCD4) expression during multistep Barrett's carcinogenesis.
  • AIM: To test the contribution of programmed cell death 4 (PDCD4) tumour suppressor gene in Barrett's carcinogenesis.
  • METHODS: PDCD4 immunohistochemical expression was assessed in 88 biopsy samples obtained from histologically proven long-segment Barrett's mucosa (BM; 25 non-intestinal columnar metaplasia, 25 intestinal metaplasia (IM), 16 low-grade intraepithelial neoplasia (LG-IEN), 12 high-grade IEN (HG-IEN) and 10 Barrett's adenocarcinoma (BAc)).
  • As controls, 25 additional samples of native oesophageal mucosa (N) were obtained from patients with dyspepsia.
  • Results PDCD4 immunostaining decreased progressively and significantly with the progression of the phenotypic changes occurring during Barrett's carcinogenesis (p<0.001).
  • Further efforts are needed to validate PDCD4 as a potential prognostic marker in patients with Barrett's oesophagus.
  • [MeSH-major] Apoptosis Regulatory Proteins / metabolism. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Precancerous Conditions / metabolism. RNA-Binding Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biopsy. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Disease Progression. Down-Regulation. Gene Expression Regulation, Neoplastic. Humans. MicroRNAs / genetics. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Oligonucleotide Array Sequence Analysis / methods. RNA, Neoplasm / genetics. Retrospective Studies

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pathol Int. 1999 Dec;49(12):1067-77 [10632927.001]
  • [Cites] Oncol Rep. 2010 Jul;24(1):135-9 [20514454.001]
  • [Cites] Lancet. 2000 Dec 16;356(9247):2079-85 [11145505.001]
  • [Cites] Am J Gastroenterol. 2002 Aug;97(8):1888-95 [12190150.001]
  • [Cites] Am J Pathol. 2003 Jan;162(1):255-61 [12507908.001]
  • [Cites] Oncogene. 2003 Jun 12;22(24):3712-20 [12802278.001]
  • [Cites] Oncogene. 2003 Jul 31;22(31):4905-10 [12894233.001]
  • [Cites] J Pathol. 2003 Aug;200(5):640-6 [12898601.001]
  • [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] Neoplasia. 2004 Jan-Feb;6(1):1-6 [15068665.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 22;101(25):9309-14 [15184677.001]
  • [Cites] Cancer Cell. 2004 Jul;6(1):11-6 [15261138.001]
  • [Cites] Oncogene. 2004 Sep 30;23(45):7484-93 [15334056.001]
  • [Cites] Oncogene. 2004 Oct 21;23(49):8135-45 [15361828.001]
  • [Cites] Am J Pathol. 1999 Apr;154(4):965-73 [10233832.001]
  • [Cites] Am J Physiol Cell Physiol. 2004 Dec;287(6):C1541-6 [15317660.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3146-54 [15833844.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6034-41 [16024603.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460.001]
  • [Cites] Oncogene. 2006 Jun 1;25(23):3346-56 [16449976.001]
  • [Cites] Gastroenterology. 2006 Sep;131(3):925-33 [16952561.001]
  • [Cites] Oncogene. 2006 Oct 5;25(45):6101-12 [16682950.001]
  • [Cites] Science. 2006 Oct 20;314(5798):467-71 [17053147.001]
  • [Cites] Gut. 2006 Dec;55(12):1810-20 [17124160.001]
  • [Cites] Dig Liver Dis. 2007 Jan;39(1):18-25 [17141593.001]
  • [Cites] Cancer. 2007 Oct 15;110(8):1697-707 [17849461.001]
  • [Cites] Clin Cancer Res. 2008 Jan 1;14(1):149-54 [18172265.001]
  • [Cites] J Biol Chem. 2008 Jan 11;283(2):1026-33 [17991735.001]
  • [Cites] J Thorac Cardiovasc Surg. 2008 Feb;135(2):255-60; discussion 260 [18242245.001]
  • [Cites] Oncogene. 2008 Mar 6;27(11):1527-35 [17828298.001]
  • [Cites] J Biol Chem. 2008 Mar 28;283(13):8601-10 [18223253.001]
  • [Cites] Oncogene. 2008 Apr 3;27(15):2128-36 [17968323.001]
  • [Cites] Oncogene. 2008 Jul 17;27(31):4373-9 [18372920.001]
  • [Cites] Oncogene. 2008 Aug 14;27(35):4820-9 [18427550.001]
  • [Cites] Oncogene. 2009 Jan 8;28(1):73-84 [18850008.001]
  • [Cites] Breast Cancer Res Treat. 2009 Mar;114(2):203-9 [18386173.001]
  • [Cites] Clin Cancer Res. 2009 Mar 15;15(6):1915-22 [19276261.001]
  • [Cites] Clin Cancer Res. 2009 Jun 15;15(12):4009-16 [19509156.001]
  • [Cites] CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49 [19474385.001]
  • [Cites] J Pathol. 2009 Oct;219(2):214-21 [19593777.001]
  • [ErratumIn] J Clin Pathol. 2011 Mar;64(3):274
  • (PMID = 20702469.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / MIRN21 microRNA, human; 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / PDCD4 protein, human; 0 / RNA, Neoplasm; 0 / RNA-Binding Proteins
  • [Other-IDs] NLM/ PMC2976066
  •  go-up   go-down


67. Wolfsen HC, Hemminger LL: Salvage photodynamic therapy for persistent esophageal cancer after chemoradiation therapy. Photodiagnosis Photodyn Ther; 2006 Mar;3(1):11-4
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.
  • RESULTS: Two patients had squamous carcinoma while five patients had Barrett's adenocarcinoma (Barrett's median segment length=8cm; range 5-10cm).
  • The other five patients treated for Barrett's carcinoma have remained disease free although one had died 33 months from metastatic colon cancer.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 25049021.001).
  • [ISSN] 1572-1000
  • [Journal-full-title] Photodiagnosis and photodynamic therapy
  • [ISO-abbreviation] Photodiagnosis Photodyn Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  •  go-up   go-down


68. Naritaka Y, Ogawa K, Shimakawa T, Wagatsuma Y, Isohata N, Asaka S, Miyaki A, Shiozawa S, Katsube T, Yoshimatsu K, Aiba M, Ide H: Collision carcinoma of the residual cervical esophagus 27 years after esophageal cancer surgery. Anticancer Res; 2007 Jan-Feb;27(1B):505-11
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.
  • A case of collision carcinoma (squamous cell carcinoma and Barrett's adenocarcinoma) in the residual cervical esophagus of a 68-year-old woman at 27 years after subtotal esophagectomy for thoracic esophageal carcinoma is reported.
  • Pathological examination showed squamous cell carcinoma on the esophageal side of the esophagogastric anastomosis and columnar epithelium with a tongue-shaped extension across the anastomotic line that included Barrett's epithelium, as well as adenocarcinoma, on the gastric tube side.
  • The squamous cell carcinoma and adenocarcinoma were contiguous, but there was a distinct border between them and no morphological transition.
  • Immunohistochemical staining showed positivity for p53 in the squamous carcinoma cells, while it was negative in the adenocarcinoma cells.
  • In contrast, HER2 (c-erb-2) was strongly positive in the adenocarcinoma cells, but negative in the squamous carcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology


69. Donnelly M, Anderson LA, Johnston BT, Watson RG, Murphy SJ, Comber H, McGuigan J, Reynolds JV, Murray LJ: Oesophageal cancer: caregiver mental health and strain. Psychooncology; 2008 Dec;17(12):1196-201
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Patients with oesophageal adenocarcinoma in Ireland were recruited into the FINBAR study (the main aim of which was to investigate factors influencing the Barrett's adenocarcinoma relationship).

  • MedlinePlus Health Information. consumer health - Caregivers.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Stress.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 John Wiley & Sons, Ltd.
  • (PMID = 18470954.001).
  • [ISSN] 1099-1611
  • [Journal-full-title] Psycho-oncology
  • [ISO-abbreviation] Psychooncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


70. Abdel-Latif MM, Windle H, Terres A, Eidhin DN, Kelleher D, Reynolds JV: Helicobacter pylori extract induces nuclear factor-kappa B, activator protein-1, and cyclooxygenase-2 in esophageal epithelial cells. J Gastrointest Surg; 2006 Apr;10(4):551-62
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.
  • Helicobacter pylori infection is recognized as the major cause of gastritis and gastric cancer; however, its role in the development of gastroesophageal reflux disease and Barrett's adenocarcinoma is unclear.
  • The induction of such transcription factors may play a role in the specific immune response within Barrett's mucosa and may indirectly cause inflammation of the gastric cardia and the distal esophagus.

  • Hazardous Substances Data Bank. Sodium ascorbate .
  • Hazardous Substances Data Bank. L-Ascorbic Acid .
  • 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 .
  • 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
  • [Cites] Aliment Pharmacol Ther. 1995 Apr;9(2):127-35 [7605852.001]
  • [Cites] Lancet. 1994 Feb 26;343(8896):508-10 [7906759.001]
  • [Cites] J Allergy Clin Immunol. 1998 Jun;101(6 Pt 1):825-31 [9648711.001]
  • [Cites] Nature. 1970 Aug 15;227(5259):680-5 [5432063.001]
  • [Cites] Annu Rev Immunol. 1994;12:141-79 [8011280.001]
  • [Cites] Hum Pathol. 1994 Sep;25(9):915-9 [8088767.001]
  • [Cites] Adv Immunol. 1995;58:1-27 [7741027.001]
  • [Cites] Digestion. 1996 Nov-Dec;57(6):433-45 [8913706.001]
  • [Cites] Am J Surg Pathol. 1997 Sep;21(9):1023-9 [9298878.001]
  • [Cites] Dig Dis Sci. 1994 Apr;39(4):770-5 [7512016.001]
  • [Cites] Cancer Res. 1998 Feb 15;58(4):588-90 [9485003.001]
  • [Cites] Gastroenterology. 1997 Dec;113(6):1983-91 [9394739.001]
  • [Cites] Gastroenterology. 1996 Dec;111(6):1524-33 [8942731.001]
  • [Cites] Scand J Gastroenterol. 1999 Jul;34(7):658-62 [10466875.001]
  • [Cites] Dis Esophagus. 1997 Jul;10(3):196-200 [9280079.001]
  • [Cites] Gut. 2001 Sep;49(3):364-71 [11511558.001]
  • [Cites] Dig Dis Sci. 2001 Oct;46(10 ):2277-84 [11680608.001]
  • [Cites] Ann Surg. 2004 Apr;239(4):491-500 [15024310.001]
  • [Cites] Scand J Gastroenterol. 1994 May;29(5):425-9 [8036458.001]
  • [Cites] J Gastrointest Surg. 2003 Jan;7(1):68-76 [12559187.001]
  • [Cites] Gastroenterology. 1997 Jul;113(1):15-24 [9207257.001]
  • [Cites] Gut. 1997 Sep;41(3):277-80 [9378377.001]
  • [Cites] Am J Gastroenterol. 1999 Nov;94(11):3175-80 [10566710.001]
  • [Cites] Gastroenterology. 1998 Apr;114(4):633-9 [9516382.001]
  • [Cites] Lancet. 1989 Jul 22;2(8656):187-9 [2568521.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Apr;86(7):2336-40 [2494664.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum. 1994;61:1-241 [7715068.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Gastroenterology. 1998 Jul;115(1):50-7 [9649458.001]
  • [Cites] J Appl Physiol. 1975 Sep;39(3):479-81 [1176415.001]
  • [Cites] Dig Dis Sci. 1995 Jun;40(6):1292-6 [7781450.001]
  • [Cites] Gut. 1998 Jul;43 Suppl 1:S6-9 [9764031.001]
  • [Cites] J Mol Med (Berl). 1996 Oct;74(10):589-607 [8912180.001]
  • [Cites] Gastroenterology. 1997 Oct;113(4):1099-109 [9322504.001]
  • (PMID = 16627221.001).
  • [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] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Antioxidants; 0 / Cell Extracts; 0 / Cyclooxygenase 2 Inhibitors; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Imidazoles; 0 / Interleukin-8; 0 / NF-kappa B; 0 / Pyridines; 0 / Transcription Factor AP-1; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 1; OU13V1EYWQ / SB 203580; PQ6CK8PD0R / Ascorbic Acid
  •  go-up   go-down


71. Takashima T, Fujiwara Y, Hamaguchi M, Sasaki E, Tominaga K, Watanabe T, Oshitani N, Higuchi K, Arakawa T: Relationship between peroxisome proliferator-activated receptor-gamma expression and differentiation of human esophageal squamous cell carcinoma. Oncol Rep; 2005 Apr;13(4):601-6
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.
  • We showed that PPAR-gamma is expressed in Barrett's adenocarcinoma cell lines and inhibited the growth of these lines through the induction of G1 cell cycle arrest and apoptosis.
  • [MeSH-major] Barrett Esophagus / metabolism. Carcinoma, Squamous Cell / metabolism. Esophageal Neoplasms / metabolism. PPAR gamma / biosynthesis

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15756430.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / 15-deoxyprostaglandin J2; 0 / Antibodies, Monoclonal; 0 / Chromans; 0 / Ligands; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Thiazolidinediones; 63231-63-0 / RNA; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; I66ZZ0ZN0E / troglitazone; LHQ7J5KV9B / Bisbenzimidazole; RXY07S6CZ2 / Prostaglandin D2; VC2W18DGKR / Thymidine
  •  go-up   go-down


72. Ruffato A, Mattioli S, Lugaresi ML, D'Ovidio F, Antonacci F, Di Simone MP: Long-term results after Heller-Dor operation for oesophageal achalasia. Eur J Cardiothorac Surg; 2006 Jun;29(6):914-9
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Seven out of 173 patients (4%), 6 of whom were pre-operatively classified as sigmoid achalasia, subsequently underwent oesophagectomy, 3 for epidermoid cancer, 1 for Barrett's adenocarcinoma, 2 for stasis oesophagitis and recurrent sepsis, 1 for severe dysphagia.

  • Genetic Alliance. consumer health - Achalasia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16675239.001).
  • [ISSN] 1010-7940
  • [Journal-full-title] European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
  • [ISO-abbreviation] Eur J Cardiothorac Surg
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


73. McFadden DW, Riggs DR, Jackson BJ, Cunningham C: Corn-derived carbohydrate inositol hexaphosphate inhibits Barrett's adenocarcinoma growth by pro-apoptotic mechanisms. Oncol Rep; 2008 Feb;19(2):563-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Corn-derived carbohydrate inositol hexaphosphate inhibits Barrett's adenocarcinoma growth by pro-apoptotic mechanisms.
  • We hypothesized that IP6 would inhibit the cell growth rate of Barrett's adenocarcinoma in vitro.
  • Two Barrett's-associated adenocarcinoma cell lines, SEG-1 and BIC-1, were treated with IP6 at 0.5, 1.0 and 5.0 mM concentrations.
  • Our findings suggest that IP6 has the potential to become an effective adjunct for Barrett's adenocarcinoma.
  • Further studies are needed to evaluate safety and clinical utility of this agent in patients with Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Antineoplastic Agents / pharmacology. Barrett Esophagus / pathology. Cell Proliferation / drug effects. Esophageal Neoplasms / pathology. Phytic Acid / pharmacology

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18202808.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbohydrates; 7IGF0S7R8I / Phytic Acid
  •  go-up   go-down


74. Cohen MC, Vergani P, Vigovich F, Thomson M, Taylor CJ, Hammond D: Investigation of genomic instability in paediatric Barrett's oesophagus using laser microdissection on paraffin-embedded endoscopic biopsies. J Pediatr Gastroenterol Nutr; 2007 Jul;45(1):44-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Investigation of genomic instability in paediatric Barrett's oesophagus using laser microdissection on paraffin-embedded endoscopic biopsies.
  • OBJECTIVES: To investigate the occurrence of microsatellite instability (MSI) in paediatric Barrett's oesophagus (BE) with the aim of identifying a potential marker for patients at risk for developing dysplasia or adenocarcinoma at a later stage.
  • DNA extracted from a formalin-fixed colonic adenocarcinoma known to have MSI was used as a positive control.
  • CONCLUSIONS: A single molecular marker that would allow recognition of those patients at risk for Barrett's adenocarcinoma has not yet been identified.
  • [MeSH-major] Barrett Esophagus / genetics. Esophagus / pathology. Microsatellite Instability

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17592363.001).
  • [ISSN] 1536-4801
  • [Journal-full-title] Journal of pediatric gastroenterology and nutrition
  • [ISO-abbreviation] J. Pediatr. Gastroenterol. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
  •  go-up   go-down


75. Abela JE, Going JJ, Mackenzie JF, McKernan M, O'Mahoney S, Stuart RC: Systematic four-quadrant biopsy detects Barrett's dysplasia in more patients than nonsystematic biopsy. Am J Gastroenterol; 2008 Apr;103(4):850-5
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.
  • [Title] Systematic four-quadrant biopsy detects Barrett's dysplasia in more patients than nonsystematic biopsy.
  • AIMS: To compare detection of Barrett's dysplasia and adenocarcinoma by systematic versus nonsystematic surveillance biopsy protocols.
  • The surgical team adopted annual systematic four-quadrant biopsy Barrett's surveillance in 1995.
  • The medical team continued annual Barrett's surveillance with nonsystematic biopsy until 2004.
  • We compare detection of Barrett's dysplasia and esophageal adenocarcinoma in unselected patients by these two biopsy strategies over 10 yr.
  • All patients had > or = 3 cm Barrett's esophagus and histological proof of intestinal metaplasia.
  • Patients referred for dysplasia management or with prevalent adenocarcinoma were excluded.
  • Two had intramucosal adenocarcinoma.
  • No cohort A patient developed advanced cancer but three cohort B patients developed and died of invasive Barrett's adenocarcinoma (0.6% per patient-year).
  • CONCLUSIONS: Patient age, gender, Barrett's segment length, and follow-up were similar (though not identical) in both cohorts, but confounding seems unlikely to account for a 13-fold difference in detection of prevalent dysplasia between the two groups.
  • Our data support the hypothesis that systematic four-quadrant biopsy is considerably more effective than nonsystematic biopsy sampling in detecting Barrett's dysplasia and early adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Biopsy / methods


76. Inomata Y, Koike T, Ohara S, Abe Y, Sekine H, Iijima K, Ariizumi K, Yamagishi H, Kitagawa Y, Imatani A, Shimosegawa T: Preservation of gastric acid secretion may be important for the development of gastroesophageal junction adenocarcinoma in Japanese people, irrespective of the H. pylori infection status. Am J Gastroenterol; 2006 May;101(5):926-33
MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preservation of gastric acid secretion may be important for the development of gastroesophageal junction adenocarcinoma in Japanese people, irrespective of the H. pylori infection status.
  • BACKGROUND: We have previously reported that Helicobacter pylori infection prevents reflux esophagitis (RE) and Barrett's esophagus (BE) by decreasing gastric acid secretion.
  • Gastroesophageal (GE) junction adenocarcinoma, including Barrett's adenocarcinoma, has been thought to be a complication of gastroesophageal reflux disease (GERD).
  • However, the relationship between H. pylori infection, gastric acid secretion, and GE junction adenocarcinoma has not yet been investigated in Japan.
  • METHODS: A total of 168 Japanese patients (RE alone: 80, short-segment BE (SSBE): 16, long-segment BE (LSBE): 20, GE junction adenocarcinoma: 12, distal early gastric cancer (EGC): 40; male/female = 106/62; mean age 61.5 yr) and 80 Japanese control subjects who had no localized lesions in the upper gastrointestinal tract (male/female = 43/37, mean age 58.1 yr) were enrolled for this study.
  • On the other hand, while the prevalence of H. pylori infection in patients with GE junction adenocarcinoma (58.3%) was significantly lower than that in patients with EGC (87.5%), it tended to be higher than that in patients with RE alone or BE.
  • The mean EGT value in patients with GE junction adenocarcinoma (3.94) was significantly higher than that in control subjects and patients with EGC (0.67), but it was comparable to that independent of the H. pylori infection status in patients with RE alone or BE.
  • CONCLUSION: Preservation of gastric acid secretion may be important for the development of GE junction adenocarcinoma in Japanese people, irrespective of the H. pylori infection status.
  • [MeSH-major] Adenocarcinoma / complications. Adenocarcinoma / physiopathology. Esophageal Neoplasms / complications. Esophageal Neoplasms / physiopathology. Esophagitis, Peptic / physiopathology. Esophagogastric Junction. Gastric Acid / secretion. Helicobacter Infections / complications. Helicobacter pylori
  • [MeSH-minor] Barrett Esophagus / complications. Barrett Esophagus / physiopathology. Female. Gastric Acidity Determination. Gastrins / analysis. Humans. Male. Middle Aged. Prevalence. Stomach Neoplasms / complications. Stomach Neoplasms / physiopathology

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Am J Gastroenterol. 2006 May;101(5):934-6 [16696780.001]
  • (PMID = 16573782.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gastrins
  •  go-up   go-down


77. Melzer E, Shtoyerman R, Appelman Z, Kashtan H: Familial Barrett's adenocarcinoma. Am J Gastroenterol; 2006 Mar;101(3):677
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] Familial Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyps / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16542304.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  •  go-up   go-down


78. Vallböhmer D, Peters JH, Oh D, Kuramochi H, Shimizu D, Demeester SR, Hagen JA, Chandrasoma PT, Danenberg KD, DeMeester TR, Danenberg P: Survivin, a potential biomarker in the development of Barrett's adenocarcinoma. Surgery; 2005 Oct;138(4):701-6; discussion 706-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survivin, a potential biomarker in the development of Barrett's adenocarcinoma.
  • The aim of this study was to measure survivin gene expression in normal squamous/columnar epithelium and in the various stages of development of Barrett's adenocarcinoma.
  • (2) antral tissue from patients with no evidence of Barrett's, dysplasia, or cancer (n = 29, antral control);.
  • (3) specialized intestinal metaplasia from patients with Barrett's esophagus (n = 16; Barrett's group);.
  • (4) low- or high-grade dysplasia (n = 12, dysplasia group), and (5) adenocarcinoma (n = 45 cancer group).
  • Expression in quiescent Barrett's epithelium was similar to both control tissues.
  • Expression levels in dysplastic epithelium were greater than in squamous control (P = .01) and Barrett's tissues (P = .04), but not higher than columnar control tissues, whereas expression in adenocarcinoma was greater than all tissues except dysplasia (P < .001).
  • CONCLUSIONS: Survivin expression may be a biomarker in the development of Barrett's adenocarcinoma that is able to distinguish between quiescent Barrett's, dysplastic Barrett's, and Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / complications. Barrett Esophagus / metabolism. Biomarkers, Tumor / metabolism. Esophageal Neoplasms / etiology. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16269299.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA84424-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [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
  •  go-up   go-down


79. Shammas MA, Koley H, Batchu RB, Bertheau RC, Protopopov A, Munshi NC, Goyal RK: Telomerase inhibition by siRNA causes senescence and apoptosis in Barrett's adenocarcinoma cells: mechanism and therapeutic potential. Mol Cancer; 2005 Jul 15;4:24
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.
  • [Title] Telomerase inhibition by siRNA causes senescence and apoptosis in Barrett's adenocarcinoma cells: mechanism and therapeutic potential.
  • RESULTS: We designed siRNAs against two different regions of telomerase gene and evaluated their effect on telomere length, proliferative potential, and gene expression in Barrett's adenocarcinoma SEG-1 cells.
  • Telomerase siRNAs may therefore be strong candidates for highly selective therapy for chemoprevention and treatment of Barrett's adenocarcinoma.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gastroenterology. 2004 May;126(5):1337-46 [15131795.001]
  • [Cites] Oncogene. 2004 Apr 12;23(16):2919-33 [15077154.001]
  • [Cites] N Engl J Med. 1986 Aug 7;315(6):362-71 [2874485.001]
  • [Cites] Nature. 1990 May 31;345(6274):458-60 [2342578.001]
  • [Cites] Annu Rev Biochem. 1992;61:113-29 [1497307.001]
  • [Cites] Science. 1994 Dec 23;266(5193):2011-5 [7605428.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Sep 26;92(20):9363-7 [7568133.001]
  • [Cites] Hum Mol Genet. 1996 May;5(5):685-91 [8733138.001]
  • [Cites] Br J Haematol. 1998 Sep;102(4):957-64 [9734646.001]
  • [Cites] Cancer. 1998 Nov 15;83(10):2049-53 [9827707.001]
  • [Cites] Nature. 1999 Jun 24;399(6738):806-9 [10391249.001]
  • [Cites] Carcinogenesis. 2005 May;26(5):867-74 [15471900.001]
  • [Cites] Oncogene. 1999 Nov 4;18(46):6191-200 [10597217.001]
  • [Cites] J Gastrointest Surg. 2000 Mar-Apr;4(2):135-42 [10675236.001]
  • [Cites] J Biol Chem. 2000 Dec 29;275(52):41082-6 [11053425.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jan 2;98(1):31-6 [11134512.001]
  • [Cites] Mol Cell. 2001 Jul;8(1):213-24 [11511374.001]
  • [Cites] Genome Biol. 2001;2(8):RESEARCH0032 [11532216.001]
  • [Cites] Apoptosis. 2001 Dec;6(6):447-52 [11595834.001]
  • [Cites] J Cell Sci. 2001 Dec;114(Pt 24):4557-65 [11792820.001]
  • [Cites] Oncogene. 2002 Jan 21;21(4):638-42 [11850790.001]
  • [Cites] Mech Ageing Dev. 2002 Apr 30;123(8):927-36 [12044941.001]
  • [Cites] Nat Med. 2003 Mar;9(3):347-51 [12579197.001]
  • [Cites] Bioorg Med Chem Lett. 2003 Apr 7;13(7):1333-6 [12657276.001]
  • [Cites] Nat Rev Cancer. 2003 Apr;3(4):286-95 [12671667.001]
  • [Cites] Mol Cancer Ther. 2003 Sep;2(9):825-33 [14555701.001]
  • [Cites] Clin Cancer Res. 2004 Feb 1;10(3):828-39 [14871958.001]
  • [Cites] Mol Cancer Ther. 2004 Oct;3(10):1201-6 [15486186.001]
  • (PMID = 16022731.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / PHS HHS / / P01-78378; United States / PHS HHS / / NIH-P50-100007; United States / NIDDK NIH HHS / DK / R01 DK031092; United States / PHS HHS / / P050-100007; United States / NIDDK NIH HHS / DK / DK031092
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Small Interfering; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC1187920
  •  go-up   go-down


80. Andreu Garcia M: [Esophageal adenoma-carcinoma and Barrett's esophagus. Gastric adenocarcinoma and Helicobacter pylori]. Gastroenterol Hepatol; 2008 Oct;31 Suppl 4:66-9
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Esophageal adenoma-carcinoma and Barrett's esophagus. Gastric adenocarcinoma and Helicobacter pylori].
  • [Transliterated title] Adenocarcinoma esfágico y esófago de Barrett. Adenocarcinoma gástrico y Helicobacter pylori.
  • In the meeting of the American Gastroenterological Association, notable among all the studies presented on the prevention and treatment of esophageal and gastric cancer were the following contributions: the use of clinical practice guidelines for the prevention and surveillance of Barrett's esophagus (BE) should be improved; treatment with proton pump inhibitors does not seem to reduce the risk of esophageal cancer; endoscopic therapy of intramucosal cancer through complete mucosal resection is effective; Helicobacter pylori eradication prevents the development of metachronous gastric cancer in patients treated for a first intramucosal adenocarcinoma through endoscopic resection; the risk of developing gastric cancer is 6 times higher in patients with mucosa-associated lymphoid tissue (MALT) lymphoma than in the general population; and photodynamic therapy may be an alternative for the treatment of "invisible" gastric adenocarcinoma, which should be followed-up endoscopically.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / complications. Esophageal Neoplasms / etiology. Helicobacter Infections / complications. Helicobacter pylori. Stomach Neoplasms / etiology


81. Song S, Krishnan K, Liu K, Bresalier RS: Polyphenon E inhibits the growth of human Barrett's and aerodigestive adenocarcinoma cells by suppressing cyclin D1 expression. Clin Cancer Res; 2009 Jan 15;15(2):622-31
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.
  • [Title] Polyphenon E inhibits the growth of human Barrett's and aerodigestive adenocarcinoma cells by suppressing cyclin D1 expression.
  • This study was designed to determine the effects of Poly E on the growth of human Barrett's and aerodigestive adenocarcinoma cells and the mechanisms involved in growth regulation by this agent.
  • EXPERIMENTAL DESIGN: Human adenocarcinoma cells and immortalized Barrett's epithelial cells were used as model systems.
  • RESULTS: Poly E inhibited the proliferation of immortalized Barrett's cells as well as various adenocarcinoma cells, and this was associated with the down-regulation of cyclin D1 protein expression.
  • These results provide insight into the mechanisms by which Poly E inhibits growth of Barrett's and adenocarcinoma cells, and provides a rationale for using this agent as a potential chemopreventive and therapeutic strategy for esophageal adenocarcinoma and its precursor, Barrett's esophagus.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Green tea .
  • 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] Life Sci. 2006 May 15;78(25):2889-97 [16378625.001]
  • [Cites] J Biol Chem. 2006 Apr 21;281(16):10865-75 [16495219.001]
  • [Cites] Gut. 2006 Dec;55(12):1810-20 [17124160.001]
  • [Cites] Am J Epidemiol. 2008 Jan 1;167(1):71-7 [17906295.001]
  • [Cites] Clin Cancer Res. 2000 May;6(5):1891-5 [10815912.001]
  • [Cites] J Biol Chem. 2001 Feb 9;276(6):4476-84 [11084038.001]
  • [Cites] Cancer Res. 2001 Jul 15;61(14):5389-95 [11454681.001]
  • [Cites] Clin Cancer Res. 2001 Dec;7(12):4220-9 [11751523.001]
  • [Cites] Int J Cancer. 2002 Mar 20;98(3):415-8 [11920593.001]
  • [Cites] Carcinogenesis. 2002 Aug;23(8):1307-13 [12151348.001]
  • [Cites] Int J Oncol. 2002 Dec;21(6):1275-83 [12429978.001]
  • [Cites] Oncogene. 2002 Dec 12;21(57):8852-61 [12483537.001]
  • [Cites] Carcinogenesis. 2003 Jul;24(7):1183-90 [12807723.001]
  • [Cites] World J Gastroenterol. 2004 Feb 15;10(4):476-80 [14966901.001]
  • [Cites] Cancer Res. 1994 Apr 1;54(7):1812-7 [8137296.001]
  • [Cites] Int J Cancer. 1994 May 1;57(3):353-61 [8168995.001]
  • [Cites] J Natl Cancer Inst. 1994 Jun 1;86(11):855-8 [8182766.001]
  • [Cites] Cancer Res. 1994 Jun 15;54(12):3107-10 [8205525.001]
  • [Cites] Nature. 1994 Jun 23;369(6482):669-71 [8208295.001]
  • [Cites] Int J Cancer. 1994 Aug 15;58(4):568-73 [8056453.001]
  • [Cites] Trends Biochem Sci. 1995 May;20(5):187-90 [7610482.001]
  • [Cites] Proc Assoc Am Physicians. 1995 Jul;107(2):181-6 [8624851.001]
  • [Cites] Int J Cancer. 1997 Jan 27;70(3):255-8 [9033623.001]
  • [Cites] Cancer Lett. 1997 Jan 30;112(2):141-7 [9066720.001]
  • [Cites] Genes Dev. 1997 Apr 15;11(8):957-72 [9136925.001]
  • [Cites] J Cell Biochem. 1997 Oct 1;67(1):55-65 [9328839.001]
  • [Cites] Br J Cancer. 1999 Feb;79(3-4):595-603 [10027336.001]
  • [Cites] Clin Cancer Res. 2005 Apr 1;11(7):2735-46 [15814656.001]
  • [Cites] Gastroenterology. 2005 May;128(6):1554-66 [15887151.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):8049-56 [16140980.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10623-31 [16288056.001]
  • [Cites] Gastroenterology. 2005 Dec;129(6):1825-31 [16344051.001]
  • [Cites] J Exp Ther Oncol. 2005;5(1):69-78 [16416603.001]
  • [Cites] Int J Oncol. 2006 Mar;28(3):715-22 [16465377.001]
  • [Cites] Neoplasia. 2006 Jan;8(1):52-8 [16533426.001]
  • [Cites] Radiother Oncol. 2006 Aug;80(2):185-91 [16905211.001]
  • (PMID = 19147768.001).
  • [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 / R01 CA069480-13; United States / NCI NIH HHS / CA / CA069480-13; United States / NIDDK NIH HHS / DK / P30 DK056338; United States / NCI NIH HHS / CA / R01CA69480; United States / NIDDK NIH HHS / DK / DK56338; United States / NCI NIH HHS / CA / R01 CA069480
  • [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 / Antineoplastic Agents; 0 / Tea; 0 / polyphenon E; 136601-57-5 / Cyclin D1; 8R1V1STN48 / Catechin; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 3.4.99.- / ATP dependent 26S protease
  • [Other-IDs] NLM/ NIHMS220918; NLM/ PMC2925407
  •  go-up   go-down


82. Pera M, Grande L, Iglesias M, Ramón JM, Conio M: [New advances in the diagnosis and treatment of early onset dysplasia and adenocarcinoma in Barrett's oesophagus]. Cir Esp; 2009 Jun;85(6):331-40
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] [New advances in the diagnosis and treatment of early onset dysplasia and adenocarcinoma in Barrett's oesophagus].
  • [Transliterated title] Nuevos avances en el diagnóstico y el tratamiento de la displasia y el adenocarcinoma precoz en el esófago de Barrett.
  • Periodic endoscopic follow-up is recommended after the diagnosis of Barrett's oesophagus, particularly in patients with dysplasia.
  • The new endoscopic techniques show promising results in identifying areas suspected of housing high grade dysplasia and adenocarcinoma.
  • Endoscopic resection of the mucosa has become a fundamental technique for the complete histological assessment of these lesions and is able to establish appropriate therapeutic decisions.
  • Likewise, this technique may be the therapeutic option in patients with high grade dysplasia and adenocarcinoma, although its application must be complemented with ablation techniques such as radiofrequency to eliminate the residual Barrett's metaplasia.
  • Oesophagectomy associated with lymphadenectomy is the option of choice in patients with submucosal adenocarcinoma.
  • The diagnosis and treatment of patients with early onset high grade dysplasia and adenocarcinoma must be carried out with multidisciplinary teams who can evaluate each case individually.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / surgery. Barrett Esophagus / complications. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / surgery. Esophagus / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19463990.001).
  • [ISSN] 0009-739X
  • [Journal-full-title] Cirugía española
  • [ISO-abbreviation] Cir Esp
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Number-of-references] 71
  •  go-up   go-down


83. de Faria PC Jr, Andreollo NA, Trevisan MA, Lopes LR: [Relationship of the sialomucins (Tn and Stn antigens) with adenocarcinoma in Barrett's esophagus]. Rev Assoc Med Bras (1992); 2007 Jul-Aug;53(4):360-4
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Relationship of the sialomucins (Tn and Stn antigens) with adenocarcinoma in Barrett's esophagus].
  • [Transliterated title] A inter-relação das sialomucinas (antígenos Tn e Stn) com o adenocarcinoma no esôfago de Barrett.
  • OBJECTIVE: Barrett's esophagus (BE) is a consequence of chronic gastroesophageal reflux and is considered a risk factor for adenocarcinoma.
  • This research aimed to analyze these antigens in patients with BE and in adenocarcinoma associated with BE.
  • METHODS: Utilizing immunohistochemistry tests, Tn and Stn antigens were studied in the endoscopic biopsies of 29 patients with BE and seven with adenocarcinoma in BE, as well as eight individuals with normal esophageal epithelium at upper digestive endoscopy.
  • However, in adenocarcinoma in BE, both antigens were 100% positive.
  • CONCLUSION: It is probable that the BE group in which the Tn antigens in the goblet cells are positive, similarly to the same antigen in the adenocarcinoma group, might indicate a higher susceptibility for potential occurrence of cancer.
  • In the future, trials with sialomucins could be used routinely, thereby contributing as a prognostic factor of adenocarcinoma in BE.
  • [MeSH-major] Adenocarcinoma / immunology. Barrett Esophagus / immunology. Esophageal Neoplasms / immunology. Sialomucins / analysis

  • 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
  • (PMID = 17823742.001).
  • [ISSN] 0104-4230
  • [Journal-full-title] Revista da Associação Médica Brasileira (1992)
  • [ISO-abbreviation] Rev Assoc Med Bras (1992)
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / Biomarkers, Tumor; 0 / Sialomucins; 0 / Tn antigen; 0 / sialosyl-Tn antigen
  •  go-up   go-down


84. Burnat G, Rau T, Elshimi E, Hahn EG, Konturek PC: Bile acids induce overexpression of homeobox gene CDX-2 and vascular endothelial growth factor (VEGF) in human Barrett's esophageal mucosa and adenocarcinoma cell line. Scand J Gastroenterol; 2007 Dec;42(12):1460-5
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] Bile acids induce overexpression of homeobox gene CDX-2 and vascular endothelial growth factor (VEGF) in human Barrett's esophageal mucosa and adenocarcinoma cell line.
  • OBJECTIVE: Barrett's esophagus (BE) is an acquired precancerous condition that develops from mucosal injury incurred after chronic gastroesophageal acid and bile reflux.
  • The aims of the present study were 1) to compare the mRNA and protein expression of CDX-2 in biopsies obtained from patients with BE and normal squamous epithelium and 2) to study the effect of two different bile salts, ursodeoxycholic acid (UDCA) and deoxycholic acid (DCA), on the mRNA expression of CDX-2 and vascular endothelial growth factor (VEGF) in Barrett's the adenocarcinoma cell line (OE-33).
  • MATERIAL AND METHODS: CDX-2 expression was measured in Barrett's mucosa and normal esophageal mucosa obtained from 15 patients with BE histologically diagnosed by immunohistochemistry, Western blot, and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR).
  • RESULTS: Both mRNA and protein expression of CDX-2 were significantly up-regulated in Barrett's mucosa as compared to normal esophageal mucosa.
  • DCA appears to be a stronger stimulant of the expression of VEGF than UDCA in the Barrett's carcinoma cell line, indicating a stronger carcinogenic potential of this bile salt.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Bile Acids and Salts / pharmacology. Esophageal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Homeodomain Proteins / genetics. Vascular Endothelial Growth Factor A / metabolism

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17852856.001).
  • [ISSN] 0036-5521
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A
  •  go-up   go-down


85. Szachnowicz S, Cecconello I, Iriya K, Marson AG, Takeda FR, Gama-Rodrigues JJ: Origin of adenocarcinoma in Barrett's esophagus: p53 and Ki67 expression and histopathologic background. Clinics (Sao Paulo); 2005 Apr;60(2):103-12
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] Origin of adenocarcinoma in Barrett's esophagus: p53 and Ki67 expression and histopathologic background.
  • Barrett's esophagus is the substitution of squamous epithelium of the distal esophagus by columnar epithelium.
  • Intestinal metaplasia in Barrett's esophagus is considered to be the main risk factor for the development of adenocarcinoma.
  • Diffuse adenocarcinoma and Barrett's esophagus without intestinal metaplasia are rare, and reports on the subject are scarce.
  • PURPOSE AND METHOD: To estimate the prevalence of adenocarcinoma in 297 patients with Barrett's esophagus, during the period of 1990 to 2002, and in 13 patients undergoing surgery, to conduct detailed macroscopic and microscopic analysis, with performance of immunohistochemical tests for p53 and Ki67, correlating the type of tumor with its adjacent epithelium.
  • RESULTS: In our patients with Barrett's esophagus, there was a prevalence of 5.7% of adenocarcinoma.
  • The tumors developed only when the Barrett's esophagus segment was long (>3.0 cm).
  • The histological study revealed 2 patients (15.4%) with Barrett's esophagus adjacent to a tumor with gastric metaplasia without the presence of intestinal metaplasia.
  • CONCLUSION: Adenocarcinoma develops from mixed columnar epithelium, either intestinal or gastric, showing both the gastric and the intestinal patterns; thus, tumors can also grow in columnar epithelium without intestinal metaplasia.
  • Barrett's esophagus should be followed up for the possibility of progression to malignancy, especially when the segment is longer than 3 cm.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Ki-67 Antigen / analysis. Tumor Suppressor Protein p53 / analysis

  • 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
  • (PMID = 15880245.001).
  • [ISSN] 1807-5932
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


86. Barritt AS 4th, Shaheen NJ: Should patients with Barrett's oesophagus be kept under surveillance? The case against. Best Pract Res Clin Gastroenterol; 2008;22(4):741-50

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Should patients with Barrett's oesophagus be kept under surveillance? The case against.
  • Barrett's oesophagus, or columnar metaplasia of the oesophagus, is a known risk factor for adenocarcinoma of the oesophagus.
  • Barrett's oesophagus is thought to be the result of longstanding gastro-oesophageal reflux disease, a very common diagnosis in the United States and other western countries.
  • Because Barrett's oesophagus is a transition state between a common complaint and a devastating illness, endoscopic screening and surveillance strategies are commonly employed.
  • However, neither screening nor surveillance strategies have been proven to reduce mortality from oesophageal adenocarcinoma.
  • We address the multifaceted case against surveillance for oesophageal adenocarcinoma.
  • The overall incidence of oesophageal adenocarcinoma is very low, especially compared to other cancers where surveillance is used.
  • The pace of progression from Barrett's to adenocarcinoma is not known.
  • There are drawbacks to endoscopic surveillance for dysplasia and adenocarcinoma in patients with established Barrett's oesophagus that include sampling error, inconsistent pathologic interpretation of biopsies, and cost.
  • Taken individually or together, these limitations make a strong case against surveillance endoscopy in Barrett's oesophagus.
  • [MeSH-major] Barrett Esophagus / diagnosis. Endoscopy, Gastrointestinal / contraindications. Mass Screening / methods. Population Surveillance / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Best Pract Res Clin Gastroenterol. 2008;22(4):721-39 [18656826.001]
  • (PMID = 18656827.001).
  • [ISSN] 1521-6918
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] eng
  • [Publication-type] Comment; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 29
  •  go-up   go-down


87. Kubo A, Corley DA, Jensen CD, Kaur R: Dietary factors and the risks of oesophageal adenocarcinoma and Barrett's oesophagus. Nutr Res Rev; 2010 Dec;23(2):230-46
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] Dietary factors and the risks of oesophageal adenocarcinoma and Barrett's oesophagus.
  • Incidence rates for oesophageal adenocarcinoma have increased by over 500% during the past few decades without clear reasons.
  • Gastro-oesophageal reflux disease, obesity and smoking have been identified as risk factors, although the demographic distribution of these risk factors is not consistent with the demographic distribution of oesophageal adenocarcinoma, which is substantially more common among whites and males than any other demographic groups.
  • Numerous epidemiological studies have suggested associations between dietary factors and the risks of oesophageal adenocarcinoma and its precursor, Barrett's oesophagus, though a comprehensive review is lacking.
  • The main aim of the present review is to consider the evidence linking dietary factors with the risks of oesophageal adenocarcinoma, Barrett's oesophagus, and the progression from Barrett's oesophagus to oesophageal adenocarcinoma.
  • The existing epidemiological evidence is strongest for an inverse relationship between intake of vitamin C, β-carotene, fruits and vegetables, particularly raw fruits and vegetables and dark green, leafy and cruciferous vegetables, carbohydrates, fibre and Fe and the risk of oesophageal adenocarcinoma and Barrett's oesophagus.
  • Patients at higher risk for Barrett's oesophagus and oesophageal adenocarcinoma may benefit from increasing their consumption of fruits and vegetables and reducing their intake of red meat and other processed food items.
  • Further research is needed to evaluate the relationship between diet and the progression of Barrett's oesophagus to oesophageal adenocarcinoma.
  • Evidence from cohort studies will help determine whether randomised chemoprevention trials are warranted for the primary prevention of Barrett's oesophagus or its progression to cancer.

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Vitamins.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Carcinogenesis. 1998 May;19(5):933-7 [9635885.001]
  • [Cites] Cancer Res. 1998 Jul 15;58(14):2929-34 [9679948.001]
  • [Cites] J Lab Clin Med. 1998 Aug;132(2):134-41 [9708574.001]
  • [Cites] Int J Oncol. 1998 Oct;13(4):855-64 [9735417.001]
  • [Cites] Cancer Res. 1998 Oct 1;58(19):4245-9 [9766645.001]
  • [Cites] Nutr Cancer. 1998;32(1):43-8 [9824856.001]
  • [Cites] Nat Genet. 1999 May;22(1):106-9 [10319873.001]
  • [Cites] Carcinogenesis. 1999 Sep;20(9):1801-8 [10469627.001]
  • [Cites] JPEN J Parenter Enteral Nutr. 1999 Sep-Oct;23(5 Suppl):S89-92 [10483904.001]
  • [Cites] Int J Cancer. 2005 Feb 20;113(5):825-8 [15499620.001]
  • [Cites] Clin Gastroenterol Hepatol. 2005 Jan;3(1):1-10 [15645398.001]
  • [Cites] Am J Gastroenterol. 2005 Jan;100(1):190-200 [15654800.001]
  • [Cites] Am J Gastroenterol. 2005 Mar;100(3):568-76 [15743353.001]
  • [Cites] Blood. 2005 Jul 15;106(2):740-5 [15790781.001]
  • [Cites] Cancer Sci. 2005 Sep;96(9):535-42 [16128738.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Oct;14(10):2377-83 [16214920.001]
  • [Cites] Genet Test. 2005 Fall;9(3):231-41 [16225403.001]
  • [Cites] Clin Gastroenterol Hepatol. 2005 Nov;3(11):1089-94 [16271339.001]
  • [Cites] Am J Gastroenterol. 2005 Nov;100(11):2599-600 [16279923.001]
  • [Cites] Gastroenterology. 2005 Dec;129(6):1825-31 [16344051.001]
  • [Cites] J Natl Cancer Inst. 2006 Jan 4;98(1):72-5 [16391374.001]
  • [Cites] J Natl Cancer Inst. 2006 Mar 1;98(5):345-54 [16507831.001]
  • [Cites] Int J Cancer. 2006 May 15;118(10):2559-66 [16380980.001]
  • [Cites] J Am Coll Nutr. 2006 Feb;25(1):64-9 [16522934.001]
  • [Cites] Am J Gastroenterol. 2008 Mar;103(3):555-61 [17986316.001]
  • [Cites] Am J Epidemiol. 2008 Apr 1;167(7):839-46 [18218607.001]
  • [Cites] Am J Clin Nutr. 2008 Apr;87(4):949-56 [18400718.001]
  • [Cites] Nutr Cancer. 2008;60(1):39-48 [18444134.001]
  • [Cites] Int J Cancer. 2008 Aug 15;123(4):852-60 [18537156.001]
  • [Cites] Cancer Causes Control. 2008 Aug;19(6):577-84 [18231869.001]
  • [Cites] Int J Occup Environ Health. 2008 Jul-Sep;14(3):193-7 [18686719.001]
  • [Cites] Am J Gastroenterol. 2008 Jul;103(7):1614-23; quiz 1624 [18494834.001]
  • [Cites] Nutrition. 2008 Oct;24(10):941-9 [18562168.001]
  • [Cites] Am J Gastroenterol. 2008 Dec;103(12):2997-3004 [18853987.001]
  • [Cites] Int J Cancer. 2009 Mar 15;124(6):1270-5 [19058177.001]
  • [Cites] Am J Clin Nutr. 2009 Mar;89(3):890-6 [19144726.001]
  • [Cites] Cancer Causes Control. 2009 Apr;20(3):279-88 [18839322.001]
  • [Cites] Gastroenterol Clin North Am. 2009 Mar;38(1):27-57, vii [19327566.001]
  • [Cites] Int J Cancer. 2009 Jul 1;125(1):165-70 [19326432.001]
  • [Cites] Arch Physiol Biochem. 2009 May;115(2):86-96 [19485704.001]
  • [Cites] Surg Oncol Clin N Am. 2009 Jul;18(3):469-85 [19500737.001]
  • [Cites] Int J Cancer. 2009 Sep 1;125(5):1147-54 [19444905.001]
  • [Cites] Nutr Cancer. 2009;61(4):437-46 [19838915.001]
  • [Cites] Nutr Cancer. 2009;61(5):607-16 [19838934.001]
  • [Cites] CA Cancer J Clin. 2009 Nov-Dec;59(6):352-65 [19897839.001]
  • [Cites] J Nutr. 2010 Feb;140(2):317-24 [20032488.001]
  • [Cites] Mol Carcinog. 2010 Mar;49(3):211-4 [20025073.001]
  • [Cites] Gastroenterology. 2010 May;138(5):1704-13 [20006613.001]
  • [Cites] Semin Oncol. 1999 Oct;26(5 Suppl 15):2-8 [10566604.001]
  • [Cites] Pharmacol Res. 2000 Feb;41(2):221-9 [10623490.001]
  • [Cites] Carcinogenesis. 2000 Feb;21(2):257-63 [10657966.001]
  • [Cites] J Gastrointest Surg. 2006 Jun;10(6):870-7 [16769544.001]
  • [Cites] World J Gastroenterol. 2006 Jul 21;12(27):4296-303 [16865769.001]
  • [Cites] Nutr Cancer. 2006;54(2):171-8 [16898861.001]
  • [Cites] J Natl Cancer Inst. 2006 Aug 16;98(16):1158-61 [16912268.001]
  • [Cites] Gastroenterology. 2006 Oct;131(4):1271-83 [17030196.001]
  • [Cites] World J Gastroenterol. 2007 Mar 14;13(10):1585-94 [17461453.001]
  • [Cites] Cancer Causes Control. 2007 Sep;18(7):713-22 [17562192.001]
  • [Cites] Epidemiol Rev. 2007;29:6-28 [17510091.001]
  • [Cites] Cancer Sci. 2007 Nov;98(11):1683-8 [17868414.001]
  • [Cites] Am J Gastroenterol. 2007 Oct;102(10):2323-30; quiz 2331 [17581269.001]
  • [Cites] Int J Cancer. 2007 Dec 15;121(12):2753-60 [17691111.001]
  • [Cites] Am J Prev Med. 2007 Dec;33(6 Suppl):S318-26 [18021906.001]
  • [Cites] Oncol Rep. 2008 Feb;19(2):563-6 [18202808.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Feb;17(2):352-8 [18268119.001]
  • [Cites] Br Med Bull. 1999;55(3):578-92 [10746348.001]
  • [Cites] Nutr Cancer. 2000;36(1):7-13 [10798210.001]
  • [Cites] Br J Cancer. 2000 Jul;83(1):127-32 [10883680.001]
  • [Cites] Am J Clin Nutr. 2000 Aug;72(2 Suppl):637S-46S [10919970.001]
  • [Cites] Int J Cancer. 2000 Sep 1;87(5):750-4 [10925371.001]
  • [Cites] Int J Cancer. 2000 Nov 1;88(3):336-41 [11054660.001]
  • [Cites] Gastroenterology. 2001 Feb;120(2):387-91 [11159879.001]
  • [Cites] Proc Nutr Soc. 2001 Feb;60(1):91-106 [11310428.001]
  • [Cites] Nutr Cancer. 2000;38(2):186-91 [11525596.001]
  • [Cites] Eur J Cancer Prev. 2001 Aug;10(4):365-9 [11535879.001]
  • [Cites] J Intern Med. 2001 Oct;250(4):280-90 [11576316.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2001 Oct;10(10):1055-62 [11588131.001]
  • [Cites] Am J Gastroenterol. 2001 Oct;96(10):2839-48 [11693316.001]
  • [Cites] Am J Clin Nutr. 2002 Jan;75(1):137-44 [11756071.001]
  • [Cites] Int J Cancer. 2002 Mar 10;98(2):241-56 [11857415.001]
  • [Cites] N Engl J Med. 2002 Mar 14;346(11):836-42 [11893796.001]
  • [Cites] Oncogene. 2002 Sep 5;21(39):6071-81 [12203119.001]
  • [Cites] Nutr Cancer. 2002;42(1):33-40 [12235648.001]
  • [Cites] J Cancer Res Clin Oncol. 2002 Oct;128(10):575-80 [12384802.001]
  • [Cites] Cancer. 2002 Nov 15;95(10):2096-102 [12412162.001]
  • [Cites] J Natl Cancer Inst. 2003 Sep 17;95(18):1404-13 [13130116.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 Sep;12(9):940-4 [14504209.001]
  • [Cites] Int J Cancer. 2003 Dec 20;107(6):873-7 [14601044.001]
  • [Cites] J Nutr. 2003 Nov;133(11 Suppl 1):3748S-3753S [14608109.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 Nov;12(11 Pt 1):1222-6 [14652285.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2004;44:239-67 [14744246.001]
  • [Cites] Am J Clin Nutr. 2004 Apr;79(4):606-12 [15051604.001]
  • [Cites] Am J Gastroenterol. 2004 Apr;99(4):582-8 [15089886.001]
  • [Cites] Lancet. 2004 Apr 24;363(9418):1346-53 [15110491.001]
  • [Cites] Dig Dis Sci. 2004 Jun;49(6):914-9 [15309877.001]
  • [Cites] Science. 1972 Jul 7;177(4043):65-8 [5041776.001]
  • [Cites] N C Med J. 1981 Jul;42(7):467-71 [6265811.001]
  • [Cites] Carcinogenesis. 1983;4(6):755-7 [6861279.001]
  • [Cites] Carcinogenesis. 1985 Dec;6(12):1679-81 [4064244.001]
  • [Cites] Gastroenterology. 1987 Jan;92(1):118-24 [3781178.001]
  • [Cites] JAMA. 1991 Mar 13;265(10):1287-9 [1995976.001]
  • [Cites] Cancer Causes Control. 1991 Nov;2(6):427-42 [1764568.001]
  • [Cites] Cancer Causes Control. 1993 Mar;4(2):123-32 [8481491.001]
  • [Cites] JAMA. 1993 Sep 15;270(11):1320 [8360967.001]
  • [Cites] Am J Physiol. 1994 Jun;266(6 Pt 1):G1090-8 [7912894.001]
  • [Cites] Ann Surg Oncol. 1994 May;1(3):252-61 [7842295.001]
  • [Cites] J Natl Cancer Inst. 1995 Jan 18;87(2):104-9 [7707381.001]
  • [Cites] Dig Dis Sci. 1995 Jun;40(6):1292-6 [7781450.001]
  • [Cites] Am J Surg. 1995 Dec;170(6):552-6; discussion 556-7 [7491999.001]
  • [Cites] Am J Gastroenterol. 1996 Aug;91(8):1507-11 [8759651.001]
  • [Cites] J Am Diet Assoc. 1996 Oct;96(10):1027-39 [8841165.001]
  • [Cites] Cancer. 1996 Oct 15;78(8):1820-8 [8859198.001]
  • [Cites] Int J Cancer. 1996 Nov 4;68(3):300-4 [8903470.001]
  • [Cites] Int J Cancer. 1997 Mar 28;71(1):14-9 [9096659.001]
  • [Cites] Nutr Cancer. 1997;27(3):298-309 [9101561.001]
  • (PMID = 20624335.001).
  • [ISSN] 1475-2700
  • [Journal-full-title] Nutrition research reviews
  • [ISO-abbreviation] Nutr Res Rev
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK081271-02; United States / NIDDK NIH HHS / DK / F32 DK081271; United States / NIDDK NIH HHS / DK / 5F32DK81271-2; United States / NIDDK NIH HHS / DK / F32 DK081271-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Micronutrients
  • [Other-IDs] NLM/ NIHMS223558; NLM/ PMC3062915
  •  go-up   go-down


88. Sayana H, Wani S, Sharma P: Esophageal adenocarcinoma and Barrett's esophagus. Minerva Gastroenterol Dietol; 2007 Jun;53(2):157-69
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] Esophageal adenocarcinoma and Barrett's esophagus.
  • Esophageal adenocarcinoma (EAC) is the most rapidly rising incidence cancer associated with a poor 5-year survival rate.
  • Barrett's esophagus (BE) is a well established premalignant condition for the development of EAC and hence it is imperative that patients with BE or at risk for developing BE should be identified and managed appropriately.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / etiology. Barrett Esophagus / complications. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / etiology

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17557044.001).
  • [ISSN] 1121-421X
  • [Journal-full-title] Minerva gastroenterologica e dietologica
  • [ISO-abbreviation] Minerva Gastroenterol Dietol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 95
  •  go-up   go-down


89. Tomizawa Y, Wang KK: Changes in screening, prognosis and therapy for esophageal adenocarcinoma in Barrett's esophagus. Curr Opin Gastroenterol; 2009 Jul;25(4):358-65
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] Changes in screening, prognosis and therapy for esophageal adenocarcinoma in Barrett's esophagus.
  • PURPOSE OF REVIEW: Significant changes in concepts of managing Barrett's esophagus have led to change in the recommendations concerning screening, surveillance, biomarkers, and therapies in this condition over the past several years.
  • RECENT FINDINGS: Narrow band imaging and esophageal capsule endoscopy are alternative methods to screen for Barrett's esophagus.
  • Research efforts are currently directed towards risk stratification of patients and biomarkers have been developed to predict development of esophageal adenocarcinoma.
  • Recent studies have reported that frequent loss of heterozygosity (LOH) as well as allelic imbalances in chromosomes in esophageal adenocarcinoma.
  • SUMMARY: Recent advances in screening; prognostication and therapy for esophageal adenocarcinoma in Barrett's esophagus have brought a significant new insight in clinical practices and will eventually ensure better patients outcomes.

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • International Agency for Research on Cancer - Screening Group. diagnostics - Planning and Implementing Cervical Cancer Prevention and Control Programs: A Manual for Managers .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 2008 Nov 1;14(21):6988-95 [18980994.001]
  • [Cites] J Natl Cancer Inst. 2008 Aug 20;100(16):1184-7 [18695138.001]
  • [Cites] Gastroenterology. 2009 Jan;136(1):56-64; quiz 351-2 [18996379.001]
  • [Cites] Am J Pathol. 2000 Feb;156(2):555-66 [10666385.001]
  • [Cites] Recent Results Cancer Res. 2000;155:1-14 [10693234.001]
  • [Cites] Recent Results Cancer Res. 2000;155:29-41 [10693236.001]
  • [Cites] Cancer. 2000 Jun 1;88(11):2520-8 [10861428.001]
  • [Cites] J Gastrointest Surg. 2000 Mar-Apr;4(2):117-8 [10885954.001]
  • [Cites] Gastroenterology. 2000 Aug;119(2):333-8 [10930368.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):3164-70 [11306503.001]
  • [Cites] Am J Gastroenterol. 2001 Oct;96(10):2839-48 [11693316.001]
  • [Cites] N Engl J Med. 2002 Mar 14;346(11):836-42 [11893796.001]
  • [Cites] Gastroenterology. 2002 Apr;122(4):1113-21 [11910361.001]
  • [Cites] N Engl J Med. 2002 Apr 11;346(15):1128-37 [11948273.001]
  • [Cites] JAMA. 2002 Apr 17;287(15):1972-81 [11960540.001]
  • [Cites] Arch Surg. 2003 Jul;138(7):721-5; discussion 726 [12860752.001]
  • [Cites] Am J Gastroenterol. 2003 Sep;98(9):1931-9 [14499768.001]
  • [Cites] Cancer Res. 2004 Oct 15;64(20):7629-33 [15492292.001]
  • [Cites] Gastroenterology. 1993 Dec;105(6):1637-42 [8253340.001]
  • [Cites] Hum Pathol. 1994 Oct;25(10):982-93 [7927321.001]
  • [Cites] Am J Gastroenterol. 1997 Feb;92(2):212-5 [9040193.001]
  • [Cites] Gastrointest Endosc. 1999 Jan;49(1):1-7 [9869715.001]
  • [Cites] Am J Gastroenterol. 1999 Apr;94(4):937-43 [10201460.001]
  • [Cites] Am J Pathol. 1999 Apr;154(4):965-73 [10233832.001]
  • [Cites] Am J Gastroenterol. 1999 Aug;94(8):2037-42 [10445525.001]
  • [Cites] Cancer Lett. 2005 Jan 20;217(2):221-30 [15617840.001]
  • [Cites] Gastrointest Endosc. 2005 May;61(6):741-6 [15855985.001]
  • [Cites] Gastroenterology. 2005 May;128(6):1554-66 [15887151.001]
  • [Cites] Clin Gastroenterol Hepatol. 2005 Jun;3(6):529-37 [15952094.001]
  • [Cites] Clin Gastroenterol Hepatol. 2005 Jun;3(6):543-52 [15952096.001]
  • [Cites] Am J Surg Pathol. 2005 Aug;29(8):1079-85 [16006804.001]
  • [Cites] Cancer. 2005 Aug 15;104(4):730-9 [15971196.001]
  • [Cites] Gastrointest Endosc. 2005 Oct;62(4):488-98 [16185958.001]
  • [Cites] J Mol Diagn. 2006 May;8(2):260-7 [16645214.001]
  • [Cites] Gastrointest Endosc. 2006 Jun;63(7):927-32 [16733105.001]
  • [Cites] Gastrointest Endosc. 2006 Aug;64(2):155-66 [16860062.001]
  • [Cites] Gastrointest Endosc. 2006 Aug;64(2):167-75 [16860063.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2006;20(5):813-27 [16997163.001]
  • [Cites] Cancer. 2006 Nov 1;107(9):2160-6 [17019737.001]
  • [Cites] Am J Gastroenterol. 2006 Nov;101(11):2457-62 [17029609.001]
  • [Cites] Gastrointest Endosc. 2007 Feb;65(2):185-95 [17258973.001]
  • [Cites] Clin Gastroenterol Hepatol. 2007 Mar;5(3):312-8 [17368230.001]
  • [Cites] Clin Gastroenterol Hepatol. 2007 Mar;5(3):319-25 [17368231.001]
  • [Cites] Gastrointest Endosc. 2007 Apr;65(4):577-83 [17324414.001]
  • [Cites] Gastroenterology. 2007 Apr;132(4):1226-33 [17408660.001]
  • [Cites] Hum Pathol. 2007 Aug;38(8):1137-44 [17640552.001]
  • [Cites] Gastrointest Endosc. 2007 Sep;66(3):460-8 [17643436.001]
  • [Cites] Am J Gastroenterol. 2008 Mar;103(3):788-97 [18341497.001]
  • [Cites] Am J Gastroenterol. 2008 Mar;103(3):525-32 [17459025.001]
  • [Cites] Gastrointest Endosc. 2008 Jul;68(1):35-40 [18355819.001]
  • [Cites] Gastrointest Endosc. 2008 Jul;68(1):25-31 [18499107.001]
  • [Cites] Hum Pathol. 2008 Aug;39(8):1128-35 [18602665.001]
  • [Cites] Gastrointest Endosc. 2008 Nov;68(5):867-76 [18561930.001]
  • (PMID = 19461512.001).
  • [ISSN] 1531-7056
  • [Journal-full-title] Current opinion in gastroenterology
  • [ISO-abbreviation] Curr. Opin. Gastroenterol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21CA122426; United States / NCI NIH HHS / CA / R01CA097048; United States / NCI NIH HHS / CA / R01 CA097048-06A2; United States / NCI NIH HHS / CA / R01 CA111603; United States / NCI NIH HHS / CA / CA097048-06A2; United States / NCI NIH HHS / CA / R21 CA122426-02; United States / NCI NIH HHS / CA / CA122426-02; United States / NCI NIH HHS / CA / CA111603-05; United States / NCI NIH HHS / CA / R01 CA111603-05; United States / NCI NIH HHS / CA / R01 CA097048; United States / NCI NIH HHS / CA / R21 CA122426; United States / NCI NIH HHS / CA / R01CA111603
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Number-of-references] 54
  • [Other-IDs] NLM/ NIHMS181013; NLM/ PMC3762463
  •  go-up   go-down


90. 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
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] 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.
  • [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.
  • [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


91. Shaheen NJ: Advances in Barrett's esophagus and esophageal adenocarcinoma. Gastroenterology; 2005 May;128(6):1554-66
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advances in Barrett's esophagus and esophageal adenocarcinoma.
  • Despite advances in diagnosis and therapy, esophageal adenocarcinoma remains an aggressive and usually lethal tumor.
  • This review focuses on the epidemiology of esophageal adenocarcinoma and its presumed precursor lesion, Barrett's esophagus; the pathogenesis of the cancer; advances in treatment of adenocarcinoma and Barrett's esophagus; and strategies for cancer prevention.
  • Although the absolute number of cases of adenocarcinoma in the United States is still small, the incidence of this cancer has increased dramatically in the last 40 years, and adenocarcinoma is now the predominant form of esophageal cancer in this country.
  • Recent evidence suggests that Barrett's esophagus is more prevalent in asymptomatic individuals than previously appreciated.
  • The pathogenesis of Barrett's esophagus is poorly understood.
  • Given that some subjects will have repeated bouts of severe erosive esophagitis and never develop Barrett's esophagus, host factors must play an important role.
  • The utility of neoadjuvant radiation and chemotherapy in those with adenocarcinoma, although they are widely practiced, is not of clear benefit, and some authorities recommend against it.
  • The value of chemoprevention in subjects with dysplastic Barrett's esophagus by use of cyclooxygenase 2 inhibitors, nonsteroidal anti-inflammatory drugs, or proton pump inhibitors is unknown.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / therapy. Barrett Esophagus / pathology. Barrett Esophagus / therapy. Esophageal Neoplasms / pathology. Esophageal Neoplasms / therapy

  • 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
  • (PMID = 15887151.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K23DK59311-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Number-of-references] 130
  •  go-up   go-down


92. Wijnhoven BP, Hussey DJ, Watson DI, Tsykin A, Smith CM, Michael MZ, South Australian Oesophageal Research Group: MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma. Br J Surg; 2010 Jun;97(6):853-61
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] MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma.
  • BACKGROUND: The genetic changes that drive metaplastic progression from squamous oesophageal mucosa toward intestinal metaplasia and adenocarcinoma are unclear.
  • This study examined whether miRNAs play a role in the development of oesophageal adenocarcinoma.
  • METHODS: RNA was extracted from mucosa of normal oesophageal squamous epithelium, normal gastric epithelium, Barrett's oesophagus with intestinal metaplasia and oesophageal adenocarcinoma obtained from 16 individuals.
  • Expression of miR-143, miR-145 and miR-215 was lower in oesophageal adenocarcinoma than in Barrett's oesophagus.
  • MiR-205 levels were lower in gastric epithelium than in both Barrett's oesophagus and adenocarcinoma.
  • Dysregulation of specific miRNAs could contribute to metaplastic and neoplastic processes in the oesophageal mucosa.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. MicroRNAs / analysis. RNA, Messenger / analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20301167.001).
  • [ISSN] 1365-2168
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Messenger
  • [Investigator] Wijnhoven BP; Hussey DJ; Watson DI; Smith CM; Mayne GC; Michael MZ; Astill D; Van der Hoek MB; Tsykin A; Tilanus HW; Wijnhoven BP
  •  go-up   go-down


93. Sabo E, Beck AH, Montgomery EA, Bhattacharya B, Meitner P, Wang JY, Resnick MB: Computerized morphometry as an aid in determining the grade of dysplasia and progression to adenocarcinoma in Barrett's esophagus. Lab Invest; 2006 Dec;86(12):1261-71
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Computerized morphometry as an aid in determining the grade of dysplasia and progression to adenocarcinoma in Barrett's esophagus.
  • The aims of this study were to use computerized morphometry in order to differentiate between the degree of dysplasia and to predict progression to invasive adenocarcinoma in Barrett's esophagus (BE).
  • Moreover, histomorphometric quantification of nuclear texture is a powerful tool for predicting progression to invasive adenocarcinoma in patients with HGD.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / pathology. Esophageal Neoplasms / etiology. Image Interpretation, Computer-Assisted / methods. Precancerous Conditions / 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
  • (PMID = 17075582.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR17695
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
  •  go-up   go-down


94. Burnat G, Majka J, Konturek PC: Bile acids are multifunctional modulators of the Barrett's carcinogenesis. J Physiol Pharmacol; 2010 Apr;61(2):185-92
Hazardous Substances Data Bank. DEOXYCHOLIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bile acids are multifunctional modulators of the Barrett's carcinogenesis.
  • Bile salts play an important pathogenic role in the development of Barrett adenocarcinoma (BA).
  • The aim of the present study was to compare the effects of two different bile salts, deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA) on the expression of COX-2, CDX-2 and DNA repair enzymes (MUTYH, OGG-1) in the Barrett epithelial cancer cells (OE-19).
  • We conclude that bile salts are involved in the carcinogenesis of Barrett adenocarcinoma via inhibition of DNA repair enzymes and induction of COX-2 and this last effect is, at least partly, mediated by NF kappaB.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Barrett Esophagus / genetics. Barrett Esophagus / pathology. Cell Line, Tumor. Cyclooxygenase 2 / genetics. DNA Glycosylases / genetics. Down-Regulation. Homeodomain Proteins / genetics. Humans. NF-kappa B / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20436219.001).
  • [ISSN] 1899-1505
  • [Journal-full-title] Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
  • [ISO-abbreviation] J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / NF-kappa B; 0 / RNA, Messenger; 005990WHZZ / Deoxycholic Acid; 724L30Y2QR / Ursodeoxycholic Acid; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase; EC 3.2.2.- / oxoguanine glycosylase 1, human
  •  go-up   go-down


95. Colleypriest BJ, Ward SG, Tosh D: How does inflammation cause Barrett's metaplasia? Curr Opin Pharmacol; 2009 Dec;9(6):721-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How does inflammation cause Barrett's metaplasia?
  • Oesophageal adenocarcinoma conveys a poor prognosis and has a rapidly increasing incidence.
  • Similarly, Barrett's metaplasia (a precursor lesion for oesophageal adenocarcinoma) has an increasing incidence.
  • Both oesophageal adenocarcinoma and Barrett's metaplasia are more common in the context of inflammation as a result of acid and bile reflux.
  • The cytokine profile of Barrett's metaplasia is predominantly a T-helper 2 response that contrasts with the T-helper 1 response in normal and inflamed oesophagus and normal intestine.
  • A key transcription factor in the development of Barrett's metaplasia, CDX2, has recently been shown to be induced in response to inflammatory mediators.
  • Understanding the role of oesophageal inflammation will provide important insight into the development of Barrett's metaplasia and oesophageal cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / etiology. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Esophagitis / complications

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19828375.001).
  • [ISSN] 1471-4973
  • [Journal-full-title] Current opinion in pharmacology
  • [ISO-abbreviation] Curr Opin Pharmacol
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300415
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / NF-kappa B; EC 1.14.99.1 / Cyclooxygenase 2
  • [Number-of-references] 53
  •  go-up   go-down


96. Horváth OP, Kalmár K: Early-stage adenocarcinoma in Barrett's esophagus: aspects of surgical therapies. Dig Dis; 2009;27(1):45-53
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] Early-stage adenocarcinoma in Barrett's esophagus: aspects of surgical therapies.
  • Adenocarcinomas in Barrett's esophagus are increasingly diagnosed at early stages thanks to effective surveillance programs.
  • Subtotal esophagectomy with extended lymphadenectomy is considered the best curative treatment for patients with early adenocarcinoma of the esophagus.
  • An individualized strategy should be employed based on staging (tumor penetration into the mucosa/submucosa, presence of lymph node metastasis), multicentricity of tumor, length of the underlying Barrett's mucosa and risk factors of the affected patient.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / surgery. Esophageal Neoplasms / surgery. Esophagectomy. Esophagoscopy
  • [MeSH-minor] Ablation Techniques. Humans. Lymph Node Excision. Lymphatic Metastasis. Minimally Invasive Surgical Procedures. Neoplasm Recurrence, Local. Neoplasm Staging. Respiratory Mucosa / pathology. Respiratory Mucosa / surgery

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19439960.001).
  • [ISSN] 1421-9875
  • [Journal-full-title] Digestive diseases (Basel, Switzerland)
  • [ISO-abbreviation] Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 55
  •  go-up   go-down


97. Matono S, Fujita H, Sueyoshi S, Tanaka T, Yamana H, Shirouzu K: Long-term survival after three-field lymph-adenectomy for an adenocarcinoma in Barrett's esophagus with metastasis to Virchow's node. Jpn J Thorac Cardiovasc Surg; 2006 Jan;54(1):11-5
Hazardous Substances Data Bank. FLUOROURACIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term survival after three-field lymph-adenectomy for an adenocarcinoma in Barrett's esophagus with metastasis to Virchow's node.
  • Here, we report a case of long-term survival after resection of an adenocarcinoma in Barrett's esophagus with metastasis to Virchow's node.
  • They were pathologically found to be an adenocarcinoma in the esophagus which had metastasised to the lymph node.
  • The pathological diagnosis was adenocarcinoma in Barrett's esophagus with the UICC stage classification of pT1, pN1, pM1-LYM, Stage IVB.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / complications. Esophageal Neoplasms / surgery. Lymph Node Excision / methods

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] World J Surg. 2003 May;27(5):571-9 [12715226.001]
  • [Cites] J Thorac Cardiovasc Surg. 1998 Dec;116(6):954-9 [9832686.001]
  • [Cites] Ann Thorac Cardiovasc Surg. 2002 Dec;8(6):328-35 [12517291.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4592-6 [14673047.001]
  • [Cites] Dig Surg. 2003;20(3):229-35; discussion 236-7 [12759503.001]
  • [Cites] World J Surg. 1994 Mar-Apr;18(2):266-72 [8042333.001]
  • [Cites] World J Surg. 2003 Sep;27(9):1052-7 [12917758.001]
  • [Cites] Surgery. 1995 Nov;118(5):845-55 [7482272.001]
  • [Cites] Ann Surg. 2000 Sep;232(3):353-61 [10973385.001]
  • (PMID = 16482930.001).
  • [ISSN] 1344-4964
  • [Journal-full-title] The Japanese journal of thoracic and cardiovascular surgery : official publication of the Japanese Association for Thoracic Surgery = Nihon Kyobu Geka Gakkai zasshi
  • [ISO-abbreviation] Jpn. J. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
  •  go-up   go-down


98. Babar M, Ennis D, Abdel-Latif M, Byrne PJ, Ravi N, Reynolds JV: Differential molecular changes in patients with asymptomatic long-segment Barrett's esophagus treated by antireflux surgery or medical therapy. Am J Surg; 2010 Feb;199(2):137-43
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential molecular changes in patients with asymptomatic long-segment Barrett's esophagus treated by antireflux surgery or medical therapy.
  • BACKGROUND: The Barrett's to adenocarcinoma sequence is characterized by molecular changes including activation of nuclear factor-kappaB (NF-kappaB) and related cytokines.
  • METHODS: Asymptomatic patients with long-segment Barrett's esophagus had endoscopic biopsy specimens taken from 2 cm below the squamocolumnar junction for measurement of activated NF-kappaB and a panel of cytokines and growth factors.
  • There were no differences in the length of Barrett's segment and endoscopic and histopathologic features in both groups.
  • [MeSH-major] Adenocarcinoma / prevention & control. Barrett Esophagus / drug therapy. Barrett Esophagus / surgery. Biomarkers, Tumor / metabolism. Esophageal Neoplasms / prevention & control. Fundoplication. Gastroesophageal Reflux / drug therapy. Gastroesophageal Reflux / surgery. NF-kappa B / metabolism. Proton Pump Inhibitors / therapeutic use

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • 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
  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 19306979.001).
  • [ISSN] 1879-1883
  • [Journal-full-title] American journal of surgery
  • [ISO-abbreviation] Am. J. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cytokines; 0 / NF-kappa B; 0 / Proton Pump Inhibitors
  •  go-up   go-down


99. Miller RC, Atherton PJ, Kabat BF, Fredericksen MB, Geno DM, Deschamps C, Jatoi A, Sloan JA, Romero Y: Marital status and quality of life in patients with esophageal cancer or Barrett's esophagus: the mayo clinic esophageal adenocarcinoma and Barrett's esophagus registry study. Dig Dis Sci; 2010 Oct;55(10):2860-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Marital status and quality of life in patients with esophageal cancer or Barrett's esophagus: the mayo clinic esophageal adenocarcinoma and Barrett's esophagus registry study.
  • AIMS: To quantify the association of marital status and changes in QOL over time in patients with EC and patients with Barrett's esophagus (BE).
  • METHODS: Eligible patients in the Mayo Clinic Esophageal Adenocarcinoma and Barrett's Esophagus Registry completed QOL assessments at baseline and approximately 1 year later.
  • [MeSH-major] Adenocarcinoma / epidemiology. Barrett Esophagus / epidemiology. Esophageal Neoplasms / epidemiology. Marital Status / statistics & numerical data. Quality of Life

  • Genetic Alliance. consumer health - Esophageal Cancer.
  • 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] J Am Geriatr Soc. 1994 Apr;42(4):413-9 [8144827.001]
  • [Cites] Soc Sci Med. 2003 Dec;57(11):2137-47 [14512244.001]
  • [Cites] Oncology. 2006;70(6):391-402 [17259744.001]
  • [Cites] Qual Life Res. 1996 Oct;5(5):469-80 [8973126.001]
  • [Cites] Breast Cancer Res. 2007;9(4):R44 [17640330.001]
  • [Cites] Gut. 1995 Oct;37(4):505-8 [7489936.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2004 Apr 1;58(5):1394-404 [15050315.001]
  • [Cites] Br J Surg. 2008 Sep;95(9):1121-6 [18581441.001]
  • [Cites] J Urol. 1996 Nov;156(5):1696-70 [8863573.001]
  • [Cites] J Clin Oncol. 2004 Jun 15;22(12):2395-403 [15197201.001]
  • [Cites] Ann Thorac Surg. 2002 Jun;73(6):1697-702; discussion 1702-3 [12078755.001]
  • [Cites] Eur J Cancer Care (Engl). 2003 Jun;12(2):183-93 [12787017.001]
  • [Cites] Cancer. 2005 May 1;103(9):1819-25 [15795905.001]
  • [Cites] Ann Epidemiol. 2000 May;10(4):224-38 [10854957.001]
  • [Cites] Arch Surg. 1989 Aug;124(8):925-7; discussion 928 [2474286.001]
  • [Cites] J Clin Epidemiol. 2008 Aug;61(8):788-95 [18359194.001]
  • [Cites] Urol Oncol. 2009 May-Jun;27(3):263-7 [18625568.001]
  • [Cites] Ann Epidemiol. 2007 Jul;17(7):540-7 [17434751.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2008 May 1;71(1):160-6 [18164846.001]
  • [Cites] Lancet. 1989 Oct 14;2(8668):888-91 [2571815.001]
  • [Cites] Res Nurs Health. 1990 Aug;13(4):227-36 [2197679.001]
  • [Cites] Cancer. 2000 Apr 15;88(8):1781-7 [10760752.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2006 Jul 1;65(3):830-5 [16564646.001]
  • [Cites] Qual Life Res. 1996 Feb;5(1):65-72 [8901368.001]
  • [Cites] Ann Oncol. 2005 May;16(5):805-16 [15817599.001]
  • [Cites] Clin Pharmacol Ther. 1983 Aug;34(2):234-9 [6872418.001]
  • [Cites] Gut. 1996 Apr;38(4):481-6 [8707073.001]
  • [Cites] JAMA. 1987 Dec 4;258(21):3125-30 [3669259.001]
  • [Cites] Soc Sci Med. 2001 Feb;52(3):357-68 [11330771.001]
  • [Cites] Oncologist. 2007 Dec;12(12):1456-63 [18165623.001]
  • [Cites] Cancer. 1991 Jun 15;67(12):3131-5 [1710541.001]
  • [Cites] Health Psychol. 2000 May;19(3):274-82 [10868772.001]
  • [Cites] Int J Behav Med. 1999;6(2):150-76 [16250685.001]
  • [Cites] Qual Life Res. 1996 Dec;5(6):521-31 [8993098.001]
  • (PMID = 20094784.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


100. Zou H, Molina JR, Harrington JJ, Osborn NK, Klatt KK, Romero Y, Burgart LJ, Ahlquist DA: Aberrant methylation of secreted frizzled-related protein genes in esophageal adenocarcinoma and Barrett's esophagus. Int J Cancer; 2005 Sep 10;116(4):584-91
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] Aberrant methylation of secreted frizzled-related protein genes in esophageal adenocarcinoma and Barrett's esophagus.
  • Hypermethylation of secreted frizzled-related proteins (SFRP) genes frequently occurs with several cancers but has not been studied in esophageal adenocarcinoma or its precursor-Barrett's esophagus.
  • To explore the role of SFRP methylation in the neoplastic progression of Barrett's esophagus and to evaluate methylated SFRP genes as biomarkers for Barrett's esophagus and cancer, methylation of SFRP genes was determined in esophageal adenocarcinomas, Barrett's esophagus and normal epithelia using methylation-specific PCR.
  • The mRNA expression of SFRP genes was quantified by real-time reverse-transcription PCR in esophageal adenocarcinoma cell lines with and without demethylation by 5-aza-2'deoxycytidine and inhibition of deacetylation by trichostatin A treatment.
  • Hypermethylation of SFRP1, 2, 4 and 5 was detected in 93%, 83%, 73% and 85% of 40 cancers; 81%, 89%, 78% and 73% of 37 Barrett's epithelia; 25%, 64%, 32% and 21% of 28 adjacent normal epithelia from Barrett's patients; and 10%, 67%, 0% and 13% of 30 normal esophagogastric epithelia from healthy individuals, respectively (p < 0.001 for SFRP1, 4 and 5; p < 0.05 for SFRP2).
  • Thus, hypermethylation of SFRP genes is a common early event in the evolution of esophageal adenocarcinoma, and methylation of SFRP1, 4 and 5 might serve as biomarkers for Barrett's neoplasia.
  • Aberrant promoter methylation appears to functionally silence SFRP gene expression in esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Barrett Esophagus / genetics. Barrett Esophagus / pathology. DNA Methylation. Esophageal Neoplasms / genetics. Esophageal Neoplasms / pathology. Eye Proteins / genetics. Eye Proteins / metabolism. Gene Expression Profiling. Intercellular Signaling Peptides and Proteins / genetics. Intercellular Signaling Peptides and Proteins / metabolism. Membrane Proteins / genetics. Membrane Proteins / metabolism. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15825175.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Eye Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / SFRP1 protein, human; 0 / SFRP4 protein, human; 0 / SFRP5 protein, human
  •  go-up   go-down






Advertisement