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1. 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.
  • While there are now better estimates of some of the model inputs, such as cancer risk and quality of life, the revised values make it less likely that surveillance could prove cost effective.
  • 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.

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  • [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
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2. Spechler SJ, Berta M, Patterson CO: Risk Stratification for Esophageal Adenocarcinoma Screening and Surveillance. Gastroenterol Hepatol (N Y); 2006 Nov;2(11):798-799

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk Stratification for Esophageal Adenocarcinoma Screening and Surveillance.

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  • [Cites] Am J Gastroenterol. 2005 Apr;100(4):927-35 [15784042.001]
  • [Cites] Aliment Pharmacol Ther. 2004 Feb;19 Suppl 1:49-53 [14725579.001]
  • [Cites] Gastrointest Endosc. 2006 Aug;64(2):167-75 [16860063.001]
  • [Cites] Am J Gastroenterol. 2004 Dec;99(12):2295-6 [15571571.001]
  • [Cites] Clin Gastroenterol Hepatol. 2004 Sep;2(9):744-53 [15354274.001]
  • (PMID = 28381948.001).
  • [ISSN] 1554-7914
  • [Journal-full-title] Gastroenterology & hepatology
  • [ISO-abbreviation] Gastroenterol Hepatol (N Y)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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3. 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.

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  • [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
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4. Linares Torres P, Castañón López C, Llano Alonso C, Alvarez Posadilla M, Vivas Alegre S, Espinel Díez J, Ribas Arino MT: [Association of adenocarcinoma of esophagus and breast cancer in a male with Madelung' disease]. An Med Interna; 2006 Mar;23(3):133-5
MedlinePlus Health Information. consumer health - Male Breast Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Association of adenocarcinoma of esophagus and breast cancer in a male with Madelung' disease].
  • [Transliterated title] Asociación de adenocarcinoma de esófago y cáncer de mama en un varón con enfermedad de Madelung.
  • The development of a cancer of the esophagus in women who previously had received radiotherapy for breast cancer is a known although infrequent event.
  • We report a case of adenocarcinoma of the esophagus in a man diagnosed of benign symmetrical lipomatosis (Madelung' disease), who had received adjuvant radiotherapy three years before for breast cancer.
  • [MeSH-major] Adenocarcinoma / complications. Breast Neoplasms, Male / complications. Carcinoma, Ductal, Breast / complications. Esophageal Neoplasms / complications. Lipomatosis, Multiple Symmetrical / complications. Neoplasms, Radiation-Induced / etiology. Neoplasms, Second Primary / etiology. Radiotherapy, Adjuvant / adverse effects
  • [MeSH-minor] Aged. Alcohol Drinking / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Barrett Esophagus / complications. Chemotherapy, Adjuvant. Combined Modality Therapy. Deglutition Disorders / etiology. Fatal Outcome. Hematemesis / etiology. Humans. Lymph Node Excision. Male. Mastectomy, Modified Radical. Risk Factors. Smoking / adverse effects


5. Zare M, Jazii FR, Alivand MR, Nasseri NK, Malekzadeh R, Yazdanbod M: Qualitative analysis of Adenomatous Polyposis Coli promoter: hypermethylation, engagement and effects on survival of patients with esophageal cancer in a high risk region of the world, a potential molecular marker. BMC Cancer; 2009;9:24
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] Qualitative analysis of Adenomatous Polyposis Coli promoter: hypermethylation, engagement and effects on survival of patients with esophageal cancer in a high risk region of the world, a potential molecular marker.
  • BACKGROUND: Squamous cell carcinoma of esophagus (SCCE) occurs at a high incidence rate in certain parts of the world.
  • Adenomatous Polyposis Coli (APC) promoter hypermethylation has been shown to be a suitable marker for both serum and solid tumors of adenocarcinoma of esophagus.
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. DNA Methylation. Esophageal Neoplasms / genetics. Genes, APC. Promoter Regions, Genetic / genetics

  • Genetic Alliance. consumer health - Esophageal Cancer.
  • Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).
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  • [Cites] Int J Cancer. 1997 Jul 3;72(1):27-30 [9212218.001]
  • [Cites] Cell. 1997 Aug 22;90(4):707-16 [9288750.001]
  • [Cites] Biochem Mol Biol Int. 1998 Jan;44(1):157-63 [9503159.001]
  • [Cites] Cancer. 1998 Nov 15;83(10):2049-53 [9827707.001]
  • [Cites] Carcinogenesis. 1999 Jan;20(1):77-84 [9934853.001]
  • [Cites] Clin Cancer Res. 1999 May;5(5):1231-40 [10353761.001]
  • [Cites] Mol Biotechnol. 2005 Sep;31(1):81-4 [16118416.001]
  • [Cites] Cell. 2004 Jan 23;116(2):235-46 [14744434.001]
  • [Cites] Onkologie. 2004 Apr;27(2):200-6 [15138356.001]
  • [Cites] Science. 1972 Feb 25;175(4024):846-53 [5008604.001]
  • [Cites] Nucleic Acids Res. 1991 Jan 25;19(2):408 [2014181.001]
  • [Cites] Semin Cancer Biol. 2005 Dec;15(6):484-93 [16055342.001]
  • [Cites] Ann Oncol. 2005 Nov;16(11):1740-8 [15980157.001]
  • [Cites] Int J Cancer. 2006 Feb 15;118(4):924-31 [16108009.001]
  • [Cites] Oncogene. 2006 May 18;25(21):3084-92 [16407829.001]
  • [Cites] Clin Cancer Res. 2006 Aug 1;12(15):4515-22 [16899597.001]
  • [Cites] Asian Pac J Cancer Prev. 2006 Jul-Sep;7(3):375-80 [17059325.001]
  • [Cites] Gut. 2007 Jan;56(1):13-9 [16785283.001]
  • [Cites] Minerva Chir. 2002 Dec;57(6):767-80 [12592219.001]
  • [Cites] Lab Invest. 2003 Apr;83(4):519-26 [12695555.001]
  • [Cites] Methods Mol Biol. 2001;181:217-28 [12843453.001]
  • [Cites] Clin Cancer Res. 2003 Aug 1;9(8):2912-9 [12912936.001]
  • [Cites] Langenbecks Arch Chir Suppl Kongressbd. 1998;115(Suppl I):485-9 [14518303.001]
  • [Cites] Cancer Res. 1991 Aug 15;51(16):4495-9 [1868473.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Apr 15;89(8):3385-8 [1565631.001]
  • [Cites] Am J Hum Genet. 1992 Sep;51(3):478-85 [1496981.001]
  • [Cites] Cancer Res. 1992 Dec 1;52(23):6525-30 [1423299.001]
  • [Cites] Hum Genet. 1993 Feb;90(6):650-2 [8383094.001]
  • [Cites] Endoscopy. 1993 Nov;25(9):609-12 [8119215.001]
  • [Cites] Cancer Res. 1994 Apr 1;54(7):1638-40 [7907942.001]
  • [Cites] Cancer Res. 1994 Jun 1;54(11):3007-10 [8187090.001]
  • [Cites] Cancer Res. 1994 Jul 1;54(13):3396-7 [8012957.001]
  • [Cites] Virchows Arch. 1994;424(6):607-11 [8055154.001]
  • [Cites] Cancer Res. 1994 Dec 1;54(23):6094-6 [7954453.001]
  • [Cites] Hum Mol Genet. 2007 Apr 15;16 Spec No 1:R50-9 [17613547.001]
  • [Cites] Oncogene. 2007 Sep 20;26(43):6332-40 [17452981.001]
  • [Cites] J Urol. 2008 Jan;179(1):346-52 [18006010.001]
  • [Cites] World J Gastroenterol. 2008 Jan 14;14(2):203-10 [18186556.001]
  • [Cites] J Appl Genet. 2008;49(1):1-10 [18263964.001]
  • [Cites] N Engl J Med. 2008 Mar 13;358(11):1118-28 [18337602.001]
  • [Cites] Int J Cancer. 2008 Jun 1;122(11):2498-502 [18302152.001]
  • [Cites] Int J Cancer. 2008 Nov 1;123(9):2073-9 [18697202.001]
  • [Cites] Semin Oncol. 1999 Oct;26(5 Suppl 15):2-8 [10566604.001]
  • [Cites] J Clin Invest. 2000 Feb;105(4):401-7 [10683367.001]
  • [Cites] Oncogene. 2000 Jul 27;19(32):3642-6 [10951570.001]
  • [Cites] Cancer Res. 2000 Aug 15;60(16):4366-71 [10969779.001]
  • [Cites] Cancer Res. 2000 Sep 15;60(18):5021-6 [11016622.001]
  • [Cites] Br J Cancer. 2000 Nov;83(9):1249-54 [11027442.001]
  • [Cites] Mod Pathol. 2000 Oct;13(10):1055-9 [11048797.001]
  • [Cites] J Natl Cancer Inst. 2000 Nov 15;92(22):1805-11 [11078757.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):3119-23 [11306496.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3410-8 [11309301.001]
  • [Cites] Clin Cancer Res. 2001 Apr;7(4):883-91 [11309337.001]
  • [Cites] Am J Clin Pathol. 2000 Dec;114(6):890-5 [11338478.001]
  • [Cites] Oncogene. 2001 Jun 14;20(27):3528-32 [11429699.001]
  • [Cites] Nucleic Acids Res. 2001 Jul 1;29(13):E65-5 [11433041.001]
  • [Cites] Oncogene. 2001 Nov 1;20(50):7368-74 [11704866.001]
  • [Cites] Zhonghua Zhong Liu Za Zhi. 1999 Jan;21(1):16-8 [11776787.001]
  • [Cites] Carcinogenesis. 2002 Apr;23(4):645-55 [11960918.001]
  • [Cites] Cancer Res. 2002 Jul 1;62(13):3663-6 [12097272.001]
  • [Cites] Carcinogenesis. 2002 Oct;23(10):1713-20 [12376481.001]
  • [Cites] Dis Esophagus. 2002;15(3):214-8 [12444993.001]
  • [Cites] Gastroenterology. 1994 Dec;107(6):1759-63 [7958689.001]
  • [Cites] Cell. 1995 Apr 21;81(2):197-205 [7537636.001]
  • [Cites] Zhonghua Zhong Liu Za Zhi. 1995 Jan;17(1):9-12 [7656796.001]
  • [Cites] PCR Methods Appl. 1995 Apr;4(5):S185-94 [7580907.001]
  • [Cites] Cancer Res. 1996 May 1;56(9):1961-4 [8616831.001]
  • [Cites] Cancer Res. 1996 Feb 15;56(4):722-7 [8631003.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9821-6 [8790415.001]
  • [Cites] Nucleic Acids Res. 1996 Dec 15;24(24):5064-6 [9016686.001]
  • [Cites] Science. 1997 Mar 21;275(5307):1787-90 [9065402.001]
  • (PMID = 19149902.001).
  • [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] 0 / DNA Primers; 0 / Genetic Markers
  • [Other-IDs] NLM/ PMC2637891
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6. Long-term antacid use increases likelihood of oesophageal cancer. Nurs Stand; 2009 Apr 22;23(33):17

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term antacid use increases likelihood of oesophageal cancer.
  • : The risk of oesophageal adenocarcinoma is greater in people who take long-term over-the-counter (OTC) acid neutralising drugs when no upper gastrointestinal (GI) condition has been diagnosed.

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  • (PMID = 27991114.001).
  • [ISSN] 2047-9018
  • [Journal-full-title] Nursing standard (Royal College of Nursing (Great Britain) : 1987)
  • [ISO-abbreviation] Nurs Stand
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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7. Bashir M, Kirmani D, Bhat HF, Baba RA, Hamza R, Naqash S, Wani NA, Andrabi KI, Zargar MA, Khanday FA: P66shc and its downstream Eps8 and Rac1 proteins are upregulated in esophageal cancers. Cell Commun Signal; 2010;8:13
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] P66shc and its downstream Eps8 and Rac1 proteins are upregulated in esophageal cancers.
  • In the present study, the expression of p66shc and its associate targets namely Eps8 (epidermal pathway substrate 8), Rac1 (ras-related C3 botulinum toxin substrate1) and Grb2 (growth factor receptor bound protein 2) were examined in fresh tissue specimens from patients with esophageal squamous cell carcinoma and esophageal adenocarcinoma using western blot analysis.
  • A thorough analysis of both esophageal squamous cell carcinoma and adenocarcinoma showed p66shc expression to be significantly higher in both types of carcinomas as compared to the controls.
  • The controls of adenocarcinoma show a higher basal expression level of p66shc as compared to the controls of squamous cell carcinoma.
  • The expression level of downstream targets of p66shc i.e., eps8 and rac1 was also found to be consistently higher in human esophageal carcinomas, and hence correlated positively with p66shc expression.
  • However the expression of grb2 was found to be equal in both esophageal squamous cell carcinoma and adenocarcinoma.
  • From the results it is also suggestive that p66shc may have a role in the regulation of esophageal carcinomas and represents a possible mechanism of signaling for the development of squamous cell carcinoma and adenocarcinoma of esophagus.

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  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • [Cites] Nature. 1999 Nov 18;402(6759):309-13 [10580504.001]
  • [Cites] Int J Cancer. 1999 May 31;81(5):682-7 [10328216.001]
  • [Cites] Curr Opin Genet Dev. 2000 Dec;10(6):668-74 [11088019.001]
  • [Cites] Carcinogenesis. 2001 Aug;22(8):1119-29 [11470739.001]
  • [Cites] Laryngoscope. 2001 Jul;111(7):1285-9 [11568556.001]
  • [Cites] Oncogene. 2001 Oct 1;20(44):6322-30 [11607835.001]
  • [Cites] J Cell Biol. 2002 Jan 7;156(1):125-36 [11777939.001]
  • [Cites] Am J Gastroenterol. 2002 Jan;97(1):22-6 [11808965.001]
  • [Cites] Oncogene. 2002 May 30;21(24):3872-8 [12032825.001]
  • [Cites] Nat Rev Cancer. 2002 Feb;2(2):133-42 [12635176.001]
  • [Cites] Cancer Res. 2003 Oct 15;63(20):6772-83 [14583473.001]
  • [Cites] Int J Cancer. 2004 Feb 20;108(5):672-8 [14696093.001]
  • [Cites] Mol Cell Biol. 2004 Feb;24(4):1747-57 [14749389.001]
  • [Cites] Endocrinology. 2005 May;146(5):2473-80 [15705774.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 May 24;102(21):7589-94 [15897451.001]
  • [Cites] Oncogene. 2005 Nov 3;24(48):7203-12 [16170380.001]
  • [Cites] Mol Biol Cell. 2006 Jan;17(1):122-9 [16251354.001]
  • [Cites] J Cell Biol. 2006 Mar 13;172(6):817-22 [16520382.001]
  • [Cites] J Biol Chem. 2007 Jul 6;282(27):19399-409 [17496330.001]
  • [Cites] Clin Cancer Res. 2007 Oct 1;13(19):5798-804 [17908971.001]
  • [Cites] J Biol Chem. 2008 Mar 7;283(10):6110-7 [18174162.001]
  • [Cites] Endocr Relat Cancer. 2009 Mar;16(1):1-16 [19001530.001]
  • [Cites] Cell. 1992 Jul 10;70(1):93-104 [1623525.001]
  • [Cites] Mol Cell Biol. 1995 Jul;15(7):3805-12 [7791787.001]
  • [Cites] EMBO J. 1993 Oct;12(10):3799-808 [8404850.001]
  • [Cites] Science. 1993 May 28;260(5112):1338-43 [8493579.001]
  • [Cites] Mol Biol Cell. 1996 Sep;7(9):1429-42 [8885237.001]
  • [Cites] EMBO J. 1997 Feb 17;16(4):706-16 [9049300.001]
  • [Cites] J Biol Chem. 1997 Oct 31;272(44):28042-9 [9346957.001]
  • [Cites] Cancer Res. 2000 Sep 15;60(18):5171-8 [11016645.001]
  • (PMID = 20565814.001).
  • [ISSN] 1478-811X
  • [Journal-full-title] Cell communication and signaling : CCS
  • [ISO-abbreviation] Cell Commun. Signal
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2901305
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8. Novotna K, Trkova M, Pazdro A, Smejkal M, Soukupova A, Kodetova D, Smejkal P, Sedlacek Z: TP53 gene mutations are rare in nondysplastic Barrett's esophagus. Dig Dis Sci; 2006 Jan;51(1):110-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TP53 gene mutations are rare in nondysplastic Barrett's esophagus.
  • In search of potential prognostic markers, we analyzed a large series of tissues of Barrett's esophagus and samples of adenocarcinomas arising in the terrain of Barrett's esophagus for TP53 gene mutations by direct sequencing of exons 5 to 9 of the TP53 gene.
  • While 9 of 21 adenocarcinomas tested (42.9%) contained a TP53 mutation, none of 24 samples from Barrett's esophagus were mutated.
  • This observation suggests that TP53 gene mutation may be a relatively late event in the progression from nondysplastic Barrett's esophagus to adenocarcinoma of esophagus.
  • Therefore, TP53 gene mutations alone are not likely to represent a widely useful prognostic marker of the risk of progression to malignancy, at least not in Barrett's esophagus without dysplasia.
  • [MeSH-major] Barrett Esophagus / genetics. DNA / genetics. Genes, p53 / genetics. Mutation
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Biopsy. Disease Progression. Esophageal Neoplasms / genetics. Esophageal Neoplasms / pathology. Exons. Female. Genetic Markers. Humans. Male. Middle Aged. Polymerase Chain Reaction. Precancerous Conditions / genetics. Precancerous Conditions / pathology. Retrospective Studies. Risk Factors

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  • [CommentIn] Dig Dis Sci. 2007 Sep;52(9):2183-5 [17404881.001]
  • (PMID = 16416221.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; 9007-49-2 / DNA
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9. Sendler A: Metabolic response evaluation by PET during neoadjuvant treatment for adenocarcinoma of the esophagus and esophagogastric junction. Recent Results Cancer Res; 2010;182:167-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metabolic response evaluation by PET during neoadjuvant treatment for adenocarcinoma of the esophagus and esophagogastric junction.
  • Following several randomized trials, neoadjuvant therapy in adenocarcinoma of esophagus and the esophagogastric junction can be seen as an international standard.
  • So far, FDG-PET does not change treatment in esophageal and gastric cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Esophageal Neoplasms / metabolism. Esophagogastric Junction / radionuclide imaging. Fluorodeoxyglucose F18. Neoadjuvant Therapy. Positron-Emission Tomography / methods. Stomach Neoplasms / metabolism

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  • (PMID = 20676880.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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10. Liu L, Hofstetter WL, Rashid A, Swisher SG, Correa AM, Ajani JA, Hamilton SR, Wu TT: Significance of the depth of tumor invasion and lymph node metastasis in superficially invasive (T1) esophageal adenocarcinoma. Am J Surg Pathol; 2005 Aug;29(8):1079-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Significance of the depth of tumor invasion and lymph node metastasis in superficially invasive (T1) esophageal adenocarcinoma.
  • Superficially invasive esophageal adenocarcinomas are a heterogeneous group of tumors, including tumors invading into mucosa and submucosa.
  • We evaluated 90 consecutive patients with resected T1 adenocarcinoma of esophagus or esophagogastric junction.
  • Our study indicated evaluation of depth of tumor invasion, status of lymph nodes, and lymphovascular invasion is important in resected superficially invasive esophageal adenocarcinoma and may provide supportive information for the decision about postoperative adjuvant therapy.
  • [MeSH-major] Adenocarcinoma / pathology. Esophageal Neoplasms / pathology. Lymphatic Metastasis / pathology. Neoplasm Invasiveness / pathology

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  • (PMID = 16006804.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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11. Ilson D, Bains M, Rizk N, Rusch V, Flores R, Park B, Shah M, Kelsen D, Miron B, Goodman K: Phase II trial of preoperative bevacizumab (Bev), irinotecan (I), cisplatin (C), and radiation (RT) in esophageal adenocarcinoma: Preliminary safety analysis. J Clin Oncol; 2009 May 20;27(15_suppl):4573

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial of preoperative bevacizumab (Bev), irinotecan (I), cisplatin (C), and radiation (RT) in esophageal adenocarcinoma: Preliminary safety analysis.
  • Bev + chemo improves response rate (RR) and time to progression (TTP) when added to weekly I/C in advanced esophagogastric cancer but does not increase chemo toxicity [JCO 24: 5201; 2006].
  • We are now combining in a Phase II trial Bev/I/C with concurrent radiotherapy (RT) in esophageal adenocarcinoma (EA) with the primary endpoint of safety.

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  • (PMID = 27963076.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Ng T, DiPetrillo T, Suntharalingam M, Fontaine J, McNulty B, Akerman P, Chen W, Horiba MN, Burrows W, Safran H: Neoadjuvant paclitaxel poliglumex, cisplatin, and radiation for esophageal cancer: A phase II trial. J Clin Oncol; 2009 May 20;27(15_suppl):e15542

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neoadjuvant paclitaxel poliglumex, cisplatin, and radiation for esophageal cancer: A phase II trial.
  • The Brown University Oncology Group previously performed a phase I study establishing the dose of single agent PPX with radiation, and the combination of PPX, cisplatin and radiation for esophagogastric cancer.
  • A phase II study was therefore initiated to evaluate the pathologic response rate of neoadjuvant PPX, cisplatin and radiation for patients with esophageal cancer.
  • METHODS: Eligible patients had pathologically confirmed adenocarcinoma or squamous cell carcinoma of the esophagus or GE junction with no evidence of distant metastasis.

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  • (PMID = 27962301.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Kelsen D, Jhawer M, Ilson D, Tse A, Randazzo J, Robinson E, Capanu M, Shah MA: Analysis of survival with modified docetaxel, cisplatin, fluorouracil (mDCF), and bevacizumab (BEV) in patients with metastatic gastroesophageal (GE) adenocarcinoma: Results of a phase II clinical trial. J Clin Oncol; 2009 May 20;27(15_suppl):4512

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of survival with modified docetaxel, cisplatin, fluorouracil (mDCF), and bevacizumab (BEV) in patients with metastatic gastroesophageal (GE) adenocarcinoma: Results of a phase II clinical trial.
  • : 4512 Background: Metastatic GE cancer is an aggressive disease with poor patient (pt) outcomes.
  • The addition of BEV to chemotherapy has improved survival in several solid tumors, and has demonstrated encouraging activity in GE cancer (Shah et al, JCO 2006).
  • We report mature tolerability and efficacy results of mDCF+BEV in GE cancer, with an emphasis on prolonged pt survival.
  • RESULTS: Pt enrollment has completed: median age 57(range 29-74), median KPS 80% (70-100), M:F 32:12, gastric/GEJ/esophagus 22:17:5.

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  • (PMID = 27962705.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Cheung WY, Zhai R, Kulke M, Heist R, Asomaning K, Ma C, Wang Z, Su L, Christiani D, Liu G: Epidermal growth factor (EGF) gene polymorphism, gastroesophageal reflux disease (GERD), and esophageal adenocarcinoma (EAC) risk. J Clin Oncol; 2009 May 20;27(15_suppl):11029

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epidermal growth factor (EGF) gene polymorphism, gastroesophageal reflux disease (GERD), and esophageal adenocarcinoma (EAC) risk.
  • : 11029 Background: Single nucleotide polymorphisms (SNPs) of key cancer genes, such as EGF A61G, are associated with an elevated risk of EAC, but the lack of full penetrance indicates that the effects of these SNPs on esophageal carcinogenesis are modified by additional genetic or environmental variables.

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  • (PMID = 27963962.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Lurje G, Leers JM, Pohl A, Oezcelik A, Zhang W, Yang D, Hagen JA, DeMeester SR, DeMeester TR, Lenz HJ: Polymorphisms in epidermal growth factor (EGF) and proteinase activated receptor 1 (PAR-1) associated with tumor recurrence in localized adenocarcinoma (EA) of the esophagus treated with surgery alone. J Clin Oncol; 2009 May 20;27(15_suppl):4564

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polymorphisms in epidermal growth factor (EGF) and proteinase activated receptor 1 (PAR-1) associated with tumor recurrence in localized adenocarcinoma (EA) of the esophagus treated with surgery alone.
  • : 4564 Background: Tumor angiogenesis is a well-recognized aspect of human cancer biology and is mediated at least in part by EGF and PAR-1, which in turn may impact the process of tumor growth and progression.
  • Further, it is being increasingly recognized that esophageal squamous cell carcinoma and EA are separate and distinct disease groups and need to be considered individually.
  • METHODS: Between 1992 and 2005 normal esophageal tissue samples from 239 patients with localized EA treated with surgery alone were obtained at University of Southern California medical facilities.

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  • (PMID = 27963056.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Jhawer M, Kindler HL, Wainberg Z, Ford J, Kunz P, Tang L, McCallum S, Kallender H, Shah MA, MET111643 Investigators and GlaxoSmithKline: Assessment of two dosing schedules of GSK1363089 (GSK089), a dual MET/VEGFR2 inhibitor, in metastatic gastric cancer (GC): Interim results of a multicenter phase II study. J Clin Oncol; 2009 May 20;27(15_suppl):4502

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessment of two dosing schedules of GSK1363089 (GSK089), a dual MET/VEGFR2 inhibitor, in metastatic gastric cancer (GC): Interim results of a multicenter phase II study.
  • METHODS: Pts with distal esophagus, GE junction or stomach adenocarcinoma, 0-2 prior chemotherapy regimens, adequate organ function, measurable disease, and ECOG PS 0-2 are sequentially enrolled in 2 cohorts:.

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  • (PMID = 27962690.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. De Vita F, Orditura M, Innocente R, Vecchione L, Pinto C, Chiarion Sileni V, Martinelli E, Ruol A, Catalano G, Ciardiello F: A multicenter phase II study of induction CT with FOLFOX-4 and cetuximab followed by RT and cetuximab in locally advanced esophageal cancer (LAEC). J Clin Oncol; 2009 May 20;27(15_suppl):4546

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A multicenter phase II study of induction CT with FOLFOX-4 and cetuximab followed by RT and cetuximab in locally advanced esophageal cancer (LAEC).
  • METHODS: Eligibility criteria: resectable, locally advanced (uT3 or uN1, T4 if deemed resectable) squamous cell carcinoma (SCC) or adenocarcinoma (AC) of the esophagus; staged by EUS, CT and PET scan; age 18-70y; PS <2; normal organ functions.All pts received induction treatment with C at a starting dose of 400 mg/m<sup>2</sup> and further weekly infusion at a maintenance dose of 250 mg/m<sup>2</sup> and 4 cycles of FOLFOX-4 every two weeks.

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  • (PMID = 27963011.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Yoon HH, Powell M, Murphy K, Montgomery EA, Hafez MJ, Liu G, Forastiere AA, Benson AB, Kleinberg LR, Gibson MK, ECOG E1201-T1 Study Group: Outcome prediction based on single nucleotide polymorphisms (SNPs) in DNA repair paths in patients (pts) with esophageal adenocarcinoma (EAC) treated with preoperative (preop) cisplatin (C)-based chemoradiation (CRT): Results from the Eastern Cooperative Oncology Group (ECOG). J Clin Oncol; 2009 May 20;27(15_suppl):4530

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcome prediction based on single nucleotide polymorphisms (SNPs) in DNA repair paths in patients (pts) with esophageal adenocarcinoma (EAC) treated with preoperative (preop) cisplatin (C)-based chemoradiation (CRT): Results from the Eastern Cooperative Oncology Group (ECOG).

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  • (PMID = 27962996.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Leichman L, Goldman BH, Benedetti JK, Billingsley KG, Thomas CR, Iqbal S, Lenz H, Blanke C, Gold PJ, Corless CL: Oxaliplatin (OXP) plus protracted infusion 5-fluorouracil (PIFU) and external beam radiation (EBRT) prior to surgery (S) for potentially curable esophageal adenocarcinoma (EA): A Southwest Oncology Group (SWOG) phase II trial with molecular correlates (S0356). J Clin Oncol; 2009 May 20;27(15_suppl):4513

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oxaliplatin (OXP) plus protracted infusion 5-fluorouracil (PIFU) and external beam radiation (EBRT) prior to surgery (S) for potentially curable esophageal adenocarcinoma (EA): A Southwest Oncology Group (SWOG) phase II trial with molecular correlates (S0356).
  • 9 PTS (10%) had in-situ cancer or T1N0M0.

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  • (PMID = 27962704.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Kristeleit R, Calvert H, Arkenau H, Olmos D, Adam J, Plummer ER, Lock V, Squires M, Fazal L, Judson I: A phase I study of AT9283, an aurora kinase inhibitor, in patients with refractory solid tumors. J Clin Oncol; 2009 May 20;27(15_suppl):2566

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • An additional 4 patients received at least six cycles of therapy (squamous cell carcinoma of the lung, adenocarcinoma of the esophagus and colorectal carcinoma [2]) with a best response of stable disease.

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  • (PMID = 27961883.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Sekine I, Sumi M, Ito Y, Nokihara H, Yamamoto N, Kunitoh H, Ohe Y, Tamura T: Phase I study of concurrent high-dose three-dimensional conformal radiotherapy (3D-CRT) without elective nodal irradiation with chemotherapy using cisplatin and vinorelbine for unresectable stage III non-small cell lung cancer (NSCLC). J Clin Oncol; 2009 May 20;27(15_suppl):7546

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I study of concurrent high-dose three-dimensional conformal radiotherapy (3D-CRT) without elective nodal irradiation with chemotherapy using cisplatin and vinorelbine for unresectable stage III non-small cell lung cancer (NSCLC).
  • A total of 26 patients were excluded because of V<sub>20</sub> > 30% (n=10), overdose to the esophagus (n=8) and brachial plexus (n=2), comorbidity (n=3), or patient refusal (n=3).
  • Of these, 23 (74%) had adenocarcinoma and 20 (65%) had stage IIIA disease.

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  • (PMID = 27963322.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Ruhstaller T, Pless M, Schuller JC, Kranzbühler H, von Moos R, Moosmann P, Rauch D, Montemurro M, Schneider PM, Hess V: Cetuximab in combination with chemoradiotherapy prior to surgery in patients with resectable, locally advanced esophageal carcinoma: A prospective, multicenter phase lb-ll trial of the Swiss Group for Clinical Cancer Research (SAKK 75/06). J Clin Oncol; 2009 May 20;27(15_suppl):4570

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cetuximab in combination with chemoradiotherapy prior to surgery in patients with resectable, locally advanced esophageal carcinoma: A prospective, multicenter phase lb-ll trial of the Swiss Group for Clinical Cancer Research (SAKK 75/06).
  • : 4570 Background: Cetuximab significantly enhances efficacy of radiotherapy and chemotherapy in head and neck cancer.
  • We investigated the safety and feasibility of adding cetuximab to neoadjuvant chemoradiation of locally advanced esophageal cancer.
  • METHODS: Pts with resectable, locally advanced squamous cell carcinoma (SCC) or adenocarcinoma (AC) of the thoracic esophagus or gastroesophageal junction (staged by EUS, CT and PET scan) were treated with 2 cycles of induction chemotherapy (docetaxel 75mg/m2, cisplatin 75mg/m2 q3w and weekly cetuximab 250mg/m2), followed by concomitant chemo- immuno-radiation therapy (CIRT: docetaxel 20mg/m2, cisplatin 25mg/m2 and cetuximab 250mg/m2 weekly five times concomitant with 45 Gy radiotherapy in 25 fractions); followed by surgery 4-8 weeks later.
  • CONCLUSIONS: Adding cetuximab to preoperative chemoradiation for esophageal cancer is safe and feasible in a community-based multicenter setting.

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  • (PMID = 27963079.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Horgan AM, Darling G, Wong R, Visbal A, Guindi M, Jonker D, Liu G, Hornby J, Xu W, Knox JJ: Adjuvant sunitinib following chemoradiotherapy (CRT) and surgery for esophageal cancer: A phase II trial. J Clin Oncol; 2009 May 20;27(15_suppl):e15550

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adjuvant sunitinib following chemoradiotherapy (CRT) and surgery for esophageal cancer: A phase II trial.
  • : e15550 Background: Locally advanced esophageal cancer (LAEC) has a 5-year survival of < 30 %.
  • METHODS: Pts with LAEC of the thoracic esophagus or gastroesophageal junction, ECOG PS 0,1 and surgical candidates treated with: preoperative Irinotecan (65mg/m<sup>2</sup> initially, ammended to 50mg/m<sup>2</sup>) + Cisplatin (30mg/m<sup>2</sup>) on weeks 1,2,4,5,7,8 + concurrent conformal radiotherapy (50Gy/25 fractions) on weeks 4-8.
  • Median age 64 yr (43-71), male: 22, adenocarcinoma: squamous 22:6; 10 pts stage IIA, 5 IIB and 13 III.

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  • (PMID = 27962341.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Rousseau M, Guevremont P, Chasen M, Spicer J, Eckert E, Alcindor T, Ades S, Ferri LE: The management of dysphagia in esophageal cancer patients undergoing neoadjuvant chemotherapy: Is invasive tube feeding required? J Clin Oncol; 2009 May 20;27(15_suppl):9613

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The management of dysphagia in esophageal cancer patients undergoing neoadjuvant chemotherapy: Is invasive tube feeding required?
  • : 9613 Background: The dysphagia commonly associated with esophageal cancer often interferes with patient tolerance of neo-adjuvant chemotherapy.
  • METHODS: Pts undergoing neoadjuvant chemotherapy (TAX/CDDP/5FU Q3 weeks x3) for esophageal or GEJ adenocarcinoma at a single institution from 3/07-7/08 were identified from a prospective database.
  • CONCLUSIONS: Appropriately timed neoadjuvant chemotherapy with a highly effective regimen rapidly restores normal swallowing, maintains nutritional status, and obviates the need for ITF in patients with significant dysphagia from esophageal adenocarcinoma.

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  • (PMID = 27963863.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Capdevila J, Clive S, Tabernero J, Lardelli P, Soto-Matos A, Baselga J, Piera A, Pardos I, Rye R, Smyth JF: Phase I study of the novel anticancer drug PM00104 as a 24-hour IV infusion every 3 weeks (q3w) in patients (pts) with advanced solid tumors or lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):2568

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  • No objective responses were seen but 3 pts with pancreatic adenocarcinoma, hepatocarcinoma and lower esophagus adenocarcinoma presented stable disease lasting >3 months.

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  • (PMID = 27961881.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA008748
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Loaeza-del Castillo A, Villalobos-Pérez JJ: [Study of 30 years on the change in the frequency of esophageal squamous cell carcinoma, esophageal adenocarcinoma and adenocarcinoma of the esophagogastric union]. Rev Gastroenterol Mex; 2008 Jan-Mar;73(1):11-6
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  • [Title] [Study of 30 years on the change in the frequency of esophageal squamous cell carcinoma, esophageal adenocarcinoma and adenocarcinoma of the esophagogastric union].
  • [Transliterated title] Estudio de 30 años sobre el cambio en la frecuencia de carcinoma epidermoide esofágico, adenocarcinoma esofágico y adenocarcinoma de la unión esofagogástrica.
  • Esophageal cancer mortality is high and the incidence of this neoplasm is increasing.
  • OBJECTIVE: Our aim was to compare the frequency of esophageal adenocarcinoma cases (EA) and squamous cell carcinoma (SCC) cases in two study periods (1977-1988 vs. 1989-2006).
  • METHOD: Patients with esophageal cancer or adenocarcinoma of gastroesophageal junction (AGEJ) referred to the Nation al Institute of Medical Sciences and Nutrition "Salvador Zubirán" during 1989-2006 were included.
  • Risk factors for esophageal cancer and AGEJ were investigated.
  • The association between Barrett's esophagus and EA (OR 14; CI 95% 1.65-119.2, P = 0.0035) and for GEJC (RM 13.6; IC 95% 1.6-116, P = 0.004) was significant.
  • CONCLUSION: There has been an increase in EA, being now the predominant hystologic type of esophageal cancer.
  • [MeSH-major] Adenocarcinoma / epidemiology. Carcinoma, Squamous Cell / epidemiology. Esophageal Neoplasms / epidemiology. Esophagogastric Junction

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  • (PMID = 18792668.001).
  • [ISSN] 0375-0906
  • [Journal-full-title] Revista de gastroenterología de México
  • [ISO-abbreviation] Rev Gastroenterol Mex
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Mexico
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27. Lanas A, Alcedo González J: [Chemoprevention in adenocarcinoma of the esophagus]. Acta Gastroenterol Latinoam; 2007 Mar;37(1):37-48
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  • [Title] [Chemoprevention in adenocarcinoma of the esophagus].
  • [Transliterated title] Quimioprevención en adenocarcinoma de esófago.
  • The incidence of the adenocarcinoma of the esophagus (ACE) has dramatically for the last decades in western countries, which has been associated with a parallel increase in the incidence and prevalence of symptoms associated with gastroesophageal reflux diseases (GERD) and Barrett's esophagus (BE).
  • Different pathways, including overexpression of cyclooxygenase (COX) isoenzymes, has been proposed to explain the carcinogenic process leading from normal esophagus to esophagitis, BE and ACE.
  • The current therapy with protom pump inhibitors (PPI) is effective to reduce the esophageal acid exposure, to improve reflux symptoms, and to heal inflammatory injuries, but probably is not enough to avoid the dysplastic progression of the metaplastic epithelium.
  • [MeSH-major] Adenocarcinoma / prevention & control. Barrett Esophagus / drug therapy. Esophageal Neoplasms / prevention & control. Gastroesophageal Reflux / drug therapy

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  • (PMID = 17486744.001).
  • [ISSN] 0300-9033
  • [Journal-full-title] Acta gastroenterologica Latinoamericana
  • [ISO-abbreviation] Acta Gastroenterol. Latinoam.
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Argentina
  • [Number-of-references] 93
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28. Gillen S, Feith M, Gertler R, Langer R, Massmann J, Sarbia M, Friess H: Testicular metastasis from adenocarcinoma of the esophagus. Ann Thorac Surg; 2009 Mar;87(3):957-9
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  • [Title] Testicular metastasis from adenocarcinoma of the esophagus.
  • We report the case of a 61-year-old patient, operated on for adenocarcinoma of the esophagus in 2002, who presented in 2007 with a hydrocele and palpable mass of the right testis.
  • Histopathology revealed a testicular and epididymidal metastasis from the esophageal adenocarcinoma.
  • No case of testicular metastasis from esophageal cancer, including Barrett's carcinoma has been reported.
  • [MeSH-major] Adenocarcinoma / secondary. Esophageal Neoplasms / pathology. Testicular Neoplasms / secondary

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  • (PMID = 19231438.001).
  • [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
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29. Vial M, Grande L, Pera M: Epidemiology of adenocarcinoma of the esophagus, gastric cardia, and upper gastric third. Recent Results Cancer Res; 2010;182:1-17
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  • [Title] Epidemiology of adenocarcinoma of the esophagus, gastric cardia, and upper gastric third.
  • The incidence of adenocarcinoma of the esophagus and esophagogastric junction (gastric cardia) has risen rapidly over the past three decades in the United States and northern Europe.
  • The majority of these cancers arise from Barrett's esophagus.
  • However, less than 10% of the patients with esophageal adenocarcinoma were known to have Barrett's esophagus before.
  • Current evidence indicates that gastroesophageal reflux and obesity are major risk factors for adenocarcinoma of the esophagus.
  • Abdominal obesity, more prevalent in males, and independent of body mass index, seems to be associated with an increased risk of esophageal adenocarcinoma but not of cardia adenocarcinoma.
  • This observation may explain the high male:female ratio observed in esophageal adenocarcinoma.
  • Tobacco use has also been found as a possible risk factor for adenocarcinoma of the esophagus and gastric cardia.
  • On the other hand, low intake of fruits, vegetables, and cereal fibers seem to increase the risk of esophageal adenocarcinoma.
  • Currently, there is no evidence that strongly supports any specific strategy to screen a subgroup of the population at risk for adenocarcinoma of the esophagus or esophagogastric junction.
  • Future strategies to decrease obesity and tobacco use might help to reduce the burden of esophageal adenocarcinoma at least partially.
  • [MeSH-major] Adenocarcinoma / epidemiology. Cardia. Esophageal Neoplasms / epidemiology. Stomach Neoplasms / epidemiology
  • [MeSH-minor] Barrett Esophagus / complications. Esophagogastric Junction. Female. Gastroesophageal Reflux / complications. Helicobacter Infections / complications. Helicobacter pylori. Humans. Male. Obesity / complications

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  • (PMID = 20676867.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
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30. Barthel JS, Kucera ST, Lin JL, Hoffe SE, Strosberg JR, Ahmed I, Dilling TJ, Stevens CW: Does Barrett's esophagus respond to chemoradiation therapy for adenocarcinoma of the esophagus? Gastrointest Endosc; 2010 Feb;71(2):235-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does Barrett's esophagus respond to chemoradiation therapy for adenocarcinoma of the esophagus?
  • BACKGROUND: Adenocarcinoma of the esophagus is frequently associated with Barrett's esophagus (BE).
  • The response of esophageal adenocarcinoma to chemoradiation therapy is well described; however, the effect of chemoradiation on tumor-associated BE has not been specifically reported.
  • SETTING: A single National Cancer Institute Comprehensive Cancer Care Center experience.
  • PATIENTS: The study cohort consisted of 43 patients with stage I to IVA esophageal adenocarcinoma associated with BE who received either neoadjuvant or definitive chemoradiation therapy and underwent either esophagectomy or surveillance at our institution.
  • MAIN OUTCOME MEASUREMENT: The presence and extent of BE after chemoradiation therapy of esophageal adenocarcinoma associated with endoscopically documented pretreatment BE.
  • CONCLUSIONS: Chemoradiation therapy of esophageal adenocarcinoma does not eliminate tumor-associated BE, nor does it affect the length of the BE segment.
  • [MeSH-major] Adenocarcinoma / therapy. Barrett Esophagus / therapy. Esophageal Neoplasms / therapy. Esophagoscopy. Precancerous Conditions / pathology

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  • (PMID = 20003971.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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31. Zhang X, Watson DI, Jamieson GG: Lymph node metastases of adenocarcinoma of the esophagus and esophagogastric junction. Chin Med J (Engl); 2007 Dec 20;120(24):2268-70
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  • [Title] Lymph node metastases of adenocarcinoma of the esophagus and esophagogastric junction.
  • BACKGROUND: Esophageal adenocarcinoma is becoming an increasingly important problem.
  • The aim of this study was to evaluate the relationship between tumor invasion depth and lymph node metastasis for adenocarcinoma of the esophagus and esophagogastric junction, and to analyze the impact of lymph node metastases on survival of the patients.
  • METHODS: The study group comprised 121 patients with adenocarcinoma of the esophagus or esophagogastric junction, who underwent esophagectomy between January 1985 and December 2003 at either the Royal Adelaide Hospital or the Flinders Medical Center, Australia.
  • RESULTS: The tumors were located entirely within the esophagus in 83 patients, and involved the gastro-esophageal junction in 38.
  • When tumor invasion was within mucosa or submucosa of the esophagus (T1), the lymph node metastasis rate was 22.2% (10/45), the mean number of metastatic lymph nodes was 0.3, and the proportion of more than 4 lymph nodes metastases was 0% (0/45).
  • When tumor invaded the adjacent structures of the esophagus (T4), the lymph node metastasis rate was 85.7% (6/7); the mean number of metastatic lymph nodes was 5.1, and the proportion of more than 4 lymph nodes metastases was 71.4% (5/7).
  • CONCLUSIONS: There is a close association between tumor invasion depth and lymph node metastasis for adenocarcinoma of the esophagus and esophagogastric junction.
  • Moreover, when the tumor invades deeper into the esophageal wall, the percentage of patients with more than 4 involved nodes increases.
  • [MeSH-major] Adenocarcinoma / pathology. Esophageal Neoplasms / pathology. Esophagogastric Junction / pathology. Stomach Neoplasms / pathology

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  • (PMID = 18167216.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
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32. Lagarde SM, ten Kate FJ, Richel DJ, Offerhaus GJ, van Lanschot JJ: Molecular prognostic factors in adenocarcinoma of the esophagus and gastroesophageal junction. Ann Surg Oncol; 2007 Feb;14(2):977-91
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  • [Title] Molecular prognostic factors in adenocarcinoma of the esophagus and gastroesophageal junction.
  • OBJECTIVE: This review describes genetic and molecular changes related to adenocarcinoma of the esophagus and gastroesophageal junction (GEJ) with emphasis on prognostic value and possibilities for targeted therapy in clinical setting.
  • Adenocarcinoma of the esophagus or GEJ is an aggressive disease with early lymphatic and hematogenous dissemination.
  • Better knowledge of molecular bases may lead to new paradigms, improved prognostication, early diagnosis and individually tailored therapeutic options.
  • METHODS: A review of recent English literature (1990-October 2005) concerning esophageal adenocarcinoma was performed.
  • This review focuses on genetic and molecular changes as prognosticators of adenocarcinoma of the esophagus and GEJ.
  • CONCLUSIONS: Adenocarcinomas of the esophagus and GEJ show multiple genetic alterations, which indicate that progression of cancer is a multistep complex process with many different alterations.
  • Presumably, it is not one molecular factor that can predict the biological behavior of this cancer.
  • [MeSH-major] Adenocarcinoma / genetics. Biomarkers, Tumor / genetics. Esophageal Neoplasms / genetics. Esophagogastric Junction


33. Jeon J, Luebeck EG, Moolgavkar SH: Age effects and temporal trends in adenocarcinoma of the esophagus and gastric cardia (United States). Cancer Causes Control; 2006 Sep;17(7):971-81
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  • [Title] Age effects and temporal trends in adenocarcinoma of the esophagus and gastric cardia (United States).
  • A number of hypotheses have been advanced to explain the rapid increase of the incidence of esophageal adenocarcinoma in the US.
  • To address this problem, we have developed multi-stage carcinogenesis models that describe the age-specific incidence of adenocarcinoma of the esophagus and of the gastric cardia with separate adjustments for temporal trends.
  • These models explicitly incorporate important features of the cancers, such as the metaplastic conversion of normal esophagus to Barrett's esophagus (BE).
  • We fit these models separately to the incidence of adenocarcinoma of the esophagus and of the gastric cardia reported in the Surveillance Epidemiology and End Results (SEER) registry over the period 1973-2000.
  • [MeSH-major] Adenocarcinoma / epidemiology. Cardia. Esophageal Neoplasms / epidemiology. Stomach Neoplasms / epidemiology

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  • (PMID = 16841264.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA047658; United States / NCI NIH HHS / CA / R01 CA119224-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
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34. Lagarde SM, de Boer JD, ten Kate FJ, Busch OR, Obertop H, van Lanschot JJ: Postoperative complications after esophagectomy for adenocarcinoma of the esophagus are related to timing of death due to recurrence. Ann Surg; 2008 Jan;247(1):71-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Postoperative complications after esophagectomy for adenocarcinoma of the esophagus are related to timing of death due to recurrence.
  • After esophagectomy for adenocarcinoma of the distal esophagus and/or gastroesophageal junction, the majority of patients develops an early recurrence and dies within 2 years.
  • METHODS: A consecutive series of 351 patients who underwent esophagectomy for adenocarcinoma of the esophagus and gastroesophageal junction was reviewed.
  • RESULTS: Of the 351 included patients, 191 patients (54%) died due to recurrence of esophageal adenocarcinoma.
  • Multivariate Cox regression analysis demonstrated that T-stage, lymph node ratio >0.20, the presence of extracapsular lymph node involvement, but not complications were significant factors for the prediction of death due to cancer recurrence.
  • CONCLUSION: The relation between perioperative complications and cancer recurrence per se is not causal.
  • However, postoperative complications are independently associated with the early timing of death due to cancer recurrence.
  • [MeSH-major] Adenocarcinoma / mortality. Adenocarcinoma / surgery. Esophageal Neoplasms / mortality. Esophageal Neoplasms / surgery. Esophagectomy. Neoplasm Recurrence, Local / mortality. Postoperative Complications / mortality

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  • (PMID = 18156925.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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35. Smithers BM, Couper GC, Thomas JM, Wong D, Gotley DC, Martin I, Harvey JA, Thomson DB, Walpole ET, Watts N, Burmeister BH: Positron emission tomography and pathological evidence of response to neoadjuvant therapy in adenocarcinoma of the esophagus. Dis Esophagus; 2008;21(2):151-8
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  • [Title] Positron emission tomography and pathological evidence of response to neoadjuvant therapy in adenocarcinoma of the esophagus.
  • Our aim was to determine if fluorodeoxyglucose positron emission tomography (FDG-PET) could be correlated with a pathological response in patients with esophageal adenocarcinoma receiving neoadjuvant chemotherapy and/or chemoradiation therapy.
  • Patients with resectable, histologically proven adenocarcinoma of the esophagus were entered in the study.
  • Presently an FDG-PET scan performed 3-6 weeks after neoadjuvant therapy for adenocarcinoma of the esophagus should not be used as a marker of the potential result of the treatment.

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  • (PMID = 18269651.001).
  • [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 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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36. Haghdoost AA, Hosseini H, Chamani G, Zarei MR, Rad M, Hashemipoor M, Zahedi MJ, Darvish-Moghadam S: Rising incidence of adenocarcinoma of the esophagus in Kerman, Iran. Arch Iran Med; 2008 Jul;11(4):364-70
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  • [Title] Rising incidence of adenocarcinoma of the esophagus in Kerman, Iran.
  • BACKGROUND: The fall in the incidence of esophageal squamous cell cancer and noncardia gastric cancers in western countries parallels a concomitant rise in the incidence of gastric cardia cancer and distal adenocarcinoma of the esophagus.
  • We aimed to investigate the incidence trend of different gastric and esophageal cancers in Kerman, southeast Iran.
  • METHODS: The information of all newly diagnosed patients with gastric and esophageal cancers were collected actively from all histopathology departments around the Kerman Province during 1991 - 2002 retrospectively.
  • RESULTS: The annual age standardized incidence risks of esophageal and gastric cancers in Kerman were 1.9 and 6.9 per 100,000 populations.
  • In average, the risks of gastric and esophageal squamous cell cancers were more or less constant, while the risk of adenocarcinoma of the esophagus increased around 11% annually.
  • The rising incidence of adenocarcinoma of the esophagus in Kerman parallels its temporal pattern in western countries.
  • [MeSH-major] Adenocarcinoma / epidemiology. Esophageal Neoplasms / epidemiology. Stomach Neoplasms / epidemiology

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  • (PMID = 18588366.001).
  • [ISSN] 1029-2977
  • [Journal-full-title] Archives of Iranian medicine
  • [ISO-abbreviation] Arch Iran Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Iran
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37. Chak A, Ochs-Balcom H, Falk G, Grady WM, Kinnard M, Willis JE, Elston R, Eng C: Familiality in Barrett's esophagus, adenocarcinoma of the esophagus, and adenocarcinoma of the gastroesophageal junction. Cancer Epidemiol Biomarkers Prev; 2006 Sep;15(9):1668-73
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  • [Title] Familiality in Barrett's esophagus, adenocarcinoma of the esophagus, and adenocarcinoma of the gastroesophageal junction.
  • BACKGROUND AND AIM: The familial aggregation of Barrett's esophagus, adenocarcinoma of the esophagus, and adenocarcinoma of the gastroesophageal junction, jointly termed familial Barrett's esophagus, may represent a complex genetic trait.
  • The aim of this study was to determine the proportion of patients with these diseases who have familial Barrett's esophagus.
  • METHODS: Information on gastroesophageal reflux symptoms, known risk factors for Barrett's esophagus, and family history of Barrett's esophagus and cancers, was collected at six hospitals using a structured questionnaire from probands with either long-segment Barrett's esophagus, adenocarcinoma of the esophagus, or adenocarcinoma of the gastroesophageal junction.
  • Family history of Barrett's esophagus or esophageal cancer in a first- or second-degree relative was determined by reviewing medical records of all relatives reported to be affected.
  • Upon review of medical records of the reportedly affected relatives, familial Barrett's esophagus was definitively determined in the case of 30 (7.3%) probands comprising 17 of 276 (6.2%) with Barrett's esophagus, 11 of 116 (9.5%) with adenocarcinoma of the esophagus, and 2 of 21 (9.5%) with adenocarcinoma of the gastroesophageal junction.
  • The diagnosis in the relative reported by the proband to be affected was found not to be Barrett's esophagus or adenocarcinoma in 15 (3.6%) cases.
  • The diagnosis could not be determined in 26 (6.3%) cases in which the proband reported an affected relative.
  • There were no significant differences in age of disease onset, gender, race, or gastroesophageal reflux symptoms between definitive familial Barrett's esophagus probands and nonfamilial probands.
  • CONCLUSION: Familial Barrett's esophagus can be confirmed in 7.3% of persons presenting with Barrett's esophagus, adenocarcinoma of the esophagus, or adenocarcinoma of the gastroesophageal junction.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Esophagogastric Junction

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  • (PMID = 16985029.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / CA30722; United States / NIDDK NIH HHS / DK / DK002800; United States / NIDDK NIH HHS / DK / DK061426; United States / NIDDK NIH HHS / DK / DK070863; United States / NIGMS NIH HHS / GM / GM28356; United States / PHS HHS / / P30CAD43703; United States / NCI NIH HHS / CA / R25 CA094186
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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38. Lozoya-González D, Farca-Belsaguy A, Peláez-Luna M, Vázquez-Ballesteros E, González-Galeote E, Salceda-Otero JC: [Endoscopic mucosal resection due to adenocarcinoma of the esophagus caused by Barrett's esophagus.]. Rev Gastroenterol Mex; 2009 Oct-Dec;74(4):383-6
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  • [Title] [Endoscopic mucosal resection due to adenocarcinoma of the esophagus caused by Barrett's esophagus.].
  • [Transliterated title] Resección endoscópica de la mucosa debido a adenocarcinoma de esófago originado en un esófago de Barrett.
  • The endoscopic therapy has been used in the treatment of early stage neoplastic esophageal lesions with great success.
  • The staging accuracy of esophageal cancer with endoscopic ultrasound reaches 80% for T stage and 77% for N stage.
  • We present a case of a patient with high surgical risk, who underwent an upper endoscopy because of long history of gastroesophageal reflux disease and uncontrollable hiccup with successful endoscopic mucosal resection with plastic cap and polipectomy loop of an early stage esophageal adenocarcinoma derived of Barrett s esophagus.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / surgery. Esophageal Neoplasms / etiology. Esophageal Neoplasms / surgery. Esophagoscopy. Esophagus / surgery
  • [MeSH-minor] Aged. Barrett Esophagus / complications. Endosonography. Humans. Male. Mucous Membrane / surgery

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  • (PMID = 20423774.001).
  • [ISSN] 0375-0906
  • [Journal-full-title] Revista de gastroenterología de México
  • [ISO-abbreviation] Rev Gastroenterol Mex
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Mexico
  • [Chemical-registry-number] Adenocarcinoma Of Esophagus
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39. Struijs B, de Bree R, van Groeningen CJ, Mooi WJ, Leemans CR: Tonsillar metastasis of oesophageal adenocarcinoma. Eur Arch Otorhinolaryngol; 2008 Jan;265(1):127-9
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  • [Title] Tonsillar metastasis of oesophageal adenocarcinoma.
  • Tonsillar metastasis of adenocarcinoma of the oesophagus has not been reported previously.
  • We report a case of a 57-year-old male with a primary adenocarcinoma of the distal esophagus with a metastasis in the right palatine tonsil.
  • [MeSH-major] Adenocarcinoma / secondary. Esophageal Neoplasms / pathology. Tonsillar Neoplasms / secondary

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  • [Cites] Med Oral Patol Oral Cir Bucal. 2005 May-Jul;10(3):252-7 [15876970.001]
  • [Cites] World J Surg. 2003 Sep;27(9):1052-7 [12917758.001]
  • [Cites] Z Laryngol Rhinol Otol. 1966 Jun;45(6):389-94 [5985937.001]
  • [Cites] Otolaryngol Clin North Am. 1979 Feb;12(1):29-43 [220581.001]
  • [Cites] Ann Otol Rhinol Laryngol. 1979 Mar-Apr;88(2 Pt 1):235-40 [443718.001]
  • [Cites] Head Neck. 1992 Jan-Feb;14(1):55-7 [1624294.001]
  • [Cites] J Natl Cancer Inst. 1996 Apr 17;88(8):530-5 [8606381.001]
  • [Cites] Eur J Surg Oncol. 2001 Apr;27(3):328-30 [11373114.001]
  • [Cites] J Laryngol Otol. 1996 Mar;110(3):291-3 [8730375.001]
  • (PMID = 17657505.001).
  • [ISSN] 0937-4477
  • [Journal-full-title] European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
  • [ISO-abbreviation] Eur Arch Otorhinolaryngol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2099162
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40. Huang Y, Peters CJ, Fitzgerald RC, Gjerset RA: Progressive silencing of p14ARF in oesophageal adenocarcinoma. J Cell Mol Med; 2009 Feb;13(2):398-409
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Progressive silencing of p14ARF in oesophageal adenocarcinoma.
  • The frequency of oesophageal adenocarcinoma is increasing in Western countries for unknown reasons, and correlates with a corresponding increase in the pre-malignant condition, Barrett's Oesophagus, which raises the risk of adenocarcinoma by some 40- to 125-fold.
  • We have examined how disease progression correlates with changes in expression of the p14ARF (ARF) tumour suppressor, a key regulator of the p53 tumour suppressor pathway that is silenced in some 30% of cancers overall, but for which a role in oesophageal cancer is unclear.
  • We have used quantitative PCR, RT-PCR, methylation-specific PCR and chromatin-immunoprecipitation to examine the regulation and function of ARF in oesophageal adenocarcinoma tissue specimens and cell lines.
  • We find highly significant reductions (P< 0.001) in ARF expression during disease progression from normal oesophageal epithelium to Barrett's Oesophagus to adenocarcinoma, with 57/76 (75%) adenocarcinomas displaying undetectable levels of ARF expression.
  • Retention of ARF expression in adenocarcinoma is a highly significant indicator of increased survival (P< 0.001) and outperforms all clinical variables in a multivariate model.
  • CpG methylation as well as histone H3 methylation of lysines 9 and 27 contribute independently to ARF gene silencing in adenocarcinoma cell lines and can be reversed by 5-aza-2'-deoxycytidine.
  • The results suggest that silencing of ARF is involved in the pathogenesis of oesophageal adenocarcinoma and show that either DNA or histone methylation can provide the primary mechanism for ARF gene silencing.
  • [MeSH-major] Adenocarcinoma / genetics. Esophageal Neoplasms / genetics. Gene Silencing. Tumor Suppressor Protein p14ARF
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antimetabolites, Antineoplastic / metabolism. Azacitidine / analogs & derivatives. Azacitidine / metabolism. Barrett Esophagus / genetics. Barrett Esophagus / pathology. Base Sequence. Cell Line. Disease Progression. Epithelial Cells / cytology. Epithelial Cells / metabolism. Female. Histones / metabolism. Humans. Male. Methylation. Middle Aged. Molecular Sequence Data. Survival Rate

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  • [Cites] Oncogene. 2004 Jun 10;23(27):4780-8 [15107828.001]
  • [Cites] Virchows Arch. 2004 Aug;445(2):135-41 [15185075.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):6867-73 [15466175.001]
  • [Cites] Cancer Res. 2004 Oct 15;64(20):7629-33 [15492292.001]
  • [Cites] Science. 1994 Apr 15;264(5157):436-40 [8153634.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jul 9;93(14):7081-4 [8692948.001]
  • [Cites] Leukemia. 1997 Jan;11(1):1-5 [9001409.001]
  • [Cites] Br J Cancer. 1997;75(2):258-63 [9010035.001]
  • [Cites] Cancer Res. 1998 Feb 15;58(4):591-3 [9485004.001]
  • [Cites] Cell. 1998 Mar 20;92(6):713-23 [9529248.001]
  • [Cites] Cell. 1998 Mar 20;92(6):725-34 [9529249.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8292-7 [9653180.001]
  • [Cites] Cancer Res. 1998 Sep 1;58(17):3926-31 [9731504.001]
  • [Cites] Genes Dev. 1998 Oct 1;12(19):2984-91 [9765200.001]
  • [Cites] Mol Cell Biol. 1998 Nov;18(11):6457-73 [9774662.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8681-6 [10411935.001]
  • [Cites] Dis Esophagus. 2006;19(1):10-4 [16364037.001]
  • [Cites] Nat Genet. 2006 Apr;38(4):468-73 [16565718.001]
  • [Cites] Med Sci (Paris). 2006 May;22(5):519-24 [16687121.001]
  • [Cites] Cancer Res. 2006 Jun 1;66(11):5582-91 [16740693.001]
  • [Cites] Int J Biochem Cell Biol. 2006;38(10):1637-41 [16600663.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 2005;70:129-37 [16869746.001]
  • [Cites] Nat Genet. 2006 Dec;38(12):1386-96 [17099711.001]
  • [Cites] Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):659-65 [17255290.001]
  • [Cites] Nat Genet. 2007 Feb;39(2):232-6 [17200670.001]
  • [Cites] PLoS Med. 2007 Feb;4(2):e67 [17326708.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):7996-8001 [17804709.001]
  • [Cites] J Nutr. 2007 Dec;137(12):2622-8 [18029474.001]
  • [Cites] Oncogene. 1999 Oct 21;18(43):5843-9 [10557071.001]
  • [Cites] Cancer Res. 2000 Jan 1;60(1):129-33 [10646864.001]
  • [Cites] Clin Cancer Res. 2000 Aug;6(8):3153-8 [10955797.001]
  • [Cites] Genes Dev. 2000 Sep 15;14(18):2358-65 [10995391.001]
  • [Cites] Carcinogenesis. 2000 Nov;21(11):2057-64 [11062168.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2816-21 [11306450.001]
  • [Cites] Oral Oncol. 2001 Jun;37(4):341-4 [11337265.001]
  • [Cites] Oncogene. 2001 Aug 16;20(36):5025-32 [11526487.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Nov 9;288(4):921-6 [11688997.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8284-9 [11719461.001]
  • [Cites] Am J Gastroenterol. 2001 Nov;96(11):3071-83 [11721752.001]
  • [Cites] JAMA. 2002 Apr 17;287(15):1972-81 [11960540.001]
  • [Cites] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769.001]
  • [Cites] Virchows Arch. 2002 Aug;441(2):133-42 [12189502.001]
  • [Cites] Cancer Gene Ther. 2002 Oct;9(10):830-9 [12224024.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6456-61 [12438235.001]
  • [Cites] Pathol Res Pract. 2002;198(12):785-94 [12608655.001]
  • [Cites] Int J Cancer. 2003 May 20;105(1):98-100 [12672037.001]
  • [Cites] J Gastroenterol Hepatol. 2003 Jun;18(6):683-9 [12753151.001]
  • [Cites] Cancer Res. 2003 Jul 15;63(14):4211-7 [12874028.001]
  • (PMID = 18410530.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA111868-02; United States / NCI NIH HHS / CA / R01 CA111868-03; United Kingdom / Medical Research Council / / MC/ U105365007; United States / NCI NIH HHS / CA / R01 CA111868-01; United States / NCI NIH HHS / CA / CA 111868; United Kingdom / Medical Research Council / / ; United States / NCI NIH HHS / CA / R01 CA111868-04; United States / NCI NIH HHS / CA / R01 CA111868-05; United States / NCI NIH HHS / CA / R01 CA111868; United States / NCI NIH HHS / CA / R01 CA111868-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Histones; 0 / Tumor Suppressor Protein p14ARF; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ NIHMS289834; NLM/ PMC3098888
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41. Lagarde SM, ten Kate FJ, Reitsma JB, Busch OR, van Lanschot JJ: Prognostic factors in adenocarcinoma of the esophagus or gastroesophageal junction. J Clin Oncol; 2006 Sep 10;24(26):4347-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic factors in adenocarcinoma of the esophagus or gastroesophageal junction.
  • The incidence of adenocarcinoma of the esophagus is rising rapidly in Western Europe and North America.
  • TNM cancer staging systems predict survival on the basis of the anatomic extent of the tumor.
  • However, the adequacy of the current TNM staging system for adenocarcinoma of the esophagus or gastroesophageal junction (GEJ) is questioned repeatedly.
  • Furthermore, their potential application in the clinical setting in patients with adenocarcinoma of the esophagus or GEJ is discussed.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / therapy. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / therapy. Esophagogastric Junction. Stomach Neoplasms / diagnosis. Stomach Neoplasms / therapy
  • [MeSH-minor] Chemotherapy, Adjuvant. Diagnosis, Computer-Assisted. Humans. Lymphatic Metastasis. Neoadjuvant Therapy. Neoplasm Invasiveness. Neoplasm Staging / methods. Nomograms. Prognosis. Radiotherapy, Adjuvant. Risk Factors

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  • [CommentIn] J Clin Oncol. 2007 Mar 1;25(7):907-8; author reply 908-9 [17327616.001]
  • [CommentIn] J Clin Oncol. 2007 Mar 1;25(7):906-7; author reply 908-9 [17327615.001]
  • (PMID = 16963732.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 134
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42. Gockel I, Heckhoff S, Messow CM, Kneist W, Junginger T: Transhiatal and transthoracic resection in adenocarcinoma of the esophagus: does the operative approach have an influence on the long-term prognosis? World J Surg Oncol; 2005 Jun 24;3:40

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transhiatal and transthoracic resection in adenocarcinoma of the esophagus: does the operative approach have an influence on the long-term prognosis?
  • BACKGROUND: The goal of the present analysis was to investigate the long-term prognosis for adenocarcinoma of the esophagus treated with either the transhiatal (TH) or the transthoracic (TT) operative approach.
  • METHODS: Between September 1985 and March 2004, esophageal resection due to carcinoma was performed on a total of 424 patients.
  • This manuscript takes into account the 150 patients suffering from adenocarcinoma of the esophagus in whom a transhiatal resection of the esophagus was performed.
  • RESULTS: The transthoracic resection of the esophagus demonstrated a higher rate of general complications (p = 0.011) as well as a higher mortality rate (p = 0.011).
  • Considering all of the 150 patients with adenocarcinoma, as well as only those patients who had undergone curative resections (R0), the transhiatal approach was seen to demonstrate a better five-year survival rate of 32.1% versus 35.1%, with a median survival time of 24 versus 28 months, as compared with those who had undergone a transthoracic approach with a five-year survival rate of 13.6% (all patients) versus 17.7% (R0 resection) with a median survival time of 16 versus 17 months (p < 0.05).
  • CONCLUSION: The prognosis in patients with adenocarcinoma of the esophagus is influenced by the depth of the tumor (pT) and the pM-category, as shown in the multivariate analysis.
  • It is questionable, if a more extensive mediastinal lymph node dissection, in addition to the clearance of abdominal lymph nodes, offers prognostic advantages in adenocarcinoma of the esophagus.

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  • [Cites] Lancet. 2002 May 18;359(9319):1727-33 [12049861.001]
  • [Cites] Eur J Cardiothorac Surg. 1997 Jan;11(1):32-7 [9030787.001]
  • [Cites] World J Surg. 1996 May;20(4):507-10 discussion 511 [8662143.001]
  • [Cites] Br J Surg. 1993 Mar;80(3):367-70 [8472154.001]
  • [Cites] Eur J Cardiothorac Surg. 1999 Jun;15(6):769-73 [10431857.001]
  • [Cites] Langenbecks Arch Surg. 1999 Apr;384(2):141-8 [10328167.001]
  • [Cites] Am Surg. 1999 Dec;65(12):1137-41; discussion 1141-2 [10597061.001]
  • [Cites] Onkologie. 2001 Jun;24(3):278-82 [11455222.001]
  • [Cites] Ann Thorac Surg. 2001 Jul;72(1):306-13 [11465217.001]
  • [Cites] Ann Thorac Cardiovasc Surg. 2001 Dec;7(6):325-9 [11888470.001]
  • [Cites] Am J Surg. 1997 Sep;174(3):320-4 [9324146.001]
  • [Cites] N Engl J Med. 2002 Nov 21;347(21):1662-9 [12444180.001]
  • [Cites] Br J Surg. 1990 Aug;77(8):845-57 [2203505.001]
  • [Cites] Am J Surg. 1989 Nov;158(5):414-9 [2817222.001]
  • [Cites] Ann Surg. 1994 Sep;220(3):364-72; discussion 372-3 [8092902.001]
  • [Cites] Br J Surg. 1994 Mar;81(3):410-3 [8173915.001]
  • [Cites] J Thorac Cardiovasc Surg. 1993 Aug;106(2):205-9 [8341062.001]
  • [Cites] J Thorac Cardiovasc Surg. 1993 Feb;105(2):265-76; discussion 276-7 [8429654.001]
  • (PMID = 15978128.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1182399
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43. 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
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  • [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.
  • The aberrant expression of microRNAs (miRNAs) is involved in the development of cancer.
  • 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.
  • CONCLUSION: Expression of miRNA might define disease states in oesophageal epithelium.
  • 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

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  • (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
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44. Shibata A, Matsuda T, Ajiki W, Sobue T: Trend in incidence of adenocarcinoma of the esophagus in Japan, 1993-2001. Jpn J Clin Oncol; 2008 Jul;38(7):464-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trend in incidence of adenocarcinoma of the esophagus in Japan, 1993-2001.
  • BACKGROUND: Several studies with population-based cancer registry data have suggested that incidence of adenocarcinoma of the esophagus has been increasing since 1970 in some European and North American countries and Australia.
  • However, data from Asian countries with regard to the incidence of esophageal cancer by histological type based on the population-based cancer registry are lacking.
  • The aim of this study was to describe the incidence of esophageal cancer by histological type in a Japanese population.
  • METHODS: Cancer incidence data for 1993-2001 from 15 population-based cancer registries were collected by the Japan Cancer Surveillance Research Group in 2005.
  • RESULTS: Squamous cell carcinoma remains the predominant type in all esophageal cancers in Japan.
  • The ratio of squamous cell carcinoma to adenocarcinoma is 26:1.
  • For adenocarcinoma, estimated average annual percentage change was 4.7% (95% confidence interval: 0.7, 8.9) in men and 6.0% (2.4, 9.8) in women.
  • CONCLUSION: No dramatic increase in adenocarcinoma has occurred, and absolute incidence remains low in Japan.
  • [MeSH-major] Adenocarcinoma / epidemiology. Asian Continental Ancestry Group / statistics & numerical data. Esophageal Neoplasms / epidemiology

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  • (PMID = 18664481.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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45. Lerut T, Decker G, Coosemans W, De Leyn P, Decaluwé H, Nafteux P, Van Raemdonck D: Quality indicators of surgery for adenocarcinoma of the esophagus and gastroesophageal junction. Recent Results Cancer Res; 2010;182:127-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quality indicators of surgery for adenocarcinoma of the esophagus and gastroesophageal junction.
  • Surgical treatment of adenocarcinoma of the esophagus and gastroesophageal junction is complex and challenging.
  • As a result there is disagreement on the selection of patients for surgery, type of surgical approach in particular in relation to the extent of lymph node dissection as well as the extent of esophageal and/or gastric resection.
  • [MeSH-major] Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagogastric Junction. Stomach Neoplasms / surgery

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  • (PMID = 20676877.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
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46. Solomon NL, Cheung MC, Byrne MM, Zhuge Y, Franceschi D, Livingstone AS, Koniaris LG: Does chemoradiotherapy improve outcomes for surgically resected adenocarcinoma of the stomach or esophagus? Ann Surg Oncol; 2010 Jan;17(1):98-108
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does chemoradiotherapy improve outcomes for surgically resected adenocarcinoma of the stomach or esophagus?
  • BACKGROUND: To use a population-based registry to evaluate the effect of chemotherapy or radiation on survival for patients undergoing curative-intent surgery for adenocarcinoma of the esophagus or stomach.
  • METHODS: A linked data set between the Florida Cancer Data System and the Florida Agency for Health Care Administration from 1998 to 2003 was queried.
  • RESULTS: Overall, 3,378 patients underwent surgical extirpation with curative intent, 636 patients had esophageal adenocarcinoma (EAC), and 2,742 patients had gastric adenocarcinoma (GAC).
  • CONCLUSIONS: Patients with regional adenocarcinoma of the esophagus or stomach, but not those with localized disease, derive a statistically significant survival benefit from the addition of chemotherapy and radiation to surgical resection.
  • [MeSH-major] Adenocarcinoma / therapy. Esophageal Neoplasms / therapy. Stomach Neoplasms / therapy

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  • [CommentIn] Ann Surg Oncol. 2010 Jun;17(6):1715-6; author reply 1717 [20339949.001]
  • (PMID = 19777191.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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47. Mehta S, Johnson IT, Rhodes M: Systematic review: the chemoprevention of oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2005 Nov 1;22(9):759-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systematic review: the chemoprevention of oesophageal adenocarcinoma.
  • The incidence of oesophageal adenocarcinoma is increasing in the UK faster than any other malignancy.
  • Despite its relatively poor prognosis and the limited success of existing treatments, there is enthusiasm that chemopreventive agents might be able to stem the transition from normal squamous epithelium to adenocarcinoma.
  • We discuss gastro-oesophageal reflux as the main risk factor for the development of Barrett's metaplasia, the only known precursor of oesophageal adenocarcinoma.
  • Treatment options for reflux disease are considered with regard to their effects on cancer risk.
  • Available treatments for reflux disease have not convincingly altered the likelihood of cancer development.
  • [MeSH-major] Adenocarcinoma / prevention & control. Esophageal Neoplasms / prevention & control
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Arachidonic Acid / metabolism. Barrett Esophagus / complications. Diet. Disease Progression. Fatty Acids, Omega-3 / metabolism. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / drug therapy. Humans. Nitric Oxide / metabolism. Oxidative Stress / physiology. Proton Pump Inhibitors

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  • (PMID = 16225483.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Fatty Acids, Omega-3; 0 / Proton Pump Inhibitors; 27YG812J1I / Arachidonic Acid; 31C4KY9ESH / Nitric Oxide
  • [Number-of-references] 96
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48. Bergman JJ: The endoscopic diagnosis and staging of oesophageal adenocarcinoma. Best Pract Res Clin Gastroenterol; 2006;20(5):843-66
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  • [Title] The endoscopic diagnosis and staging of oesophageal adenocarcinoma.
  • The endoscopic evaluation of patients with oesophageal adenocarcinoma does not only serve the purpose of diagnosing the lesion and obtaining biopsies for histological evaluation: a systematic description of advanced lesions is also required to guide further therapeutic decisions.
  • New endoscopic imaging modalities hold the promise of better endoscopic detection of early cancer and its precursor lesions in Barrett's oesophagus.
  • Endoscopic ultrasonography (EUS) is superior to any other imaging modality in the assessment of local tumour infiltration of oesophageal adenocarcinoma and locoregional lymph nodes status.
  • EUS may also play a role in the selection of patients for local endoscopic treatment of early oesophageal cancer.
  • [MeSH-major] Adenocarcinoma / pathology. Esophageal Neoplasms / pathology. Esophagoscopy
  • [MeSH-minor] Barrett Esophagus / complications. Barrett Esophagus / diagnosis. Barrett Esophagus / pathology. Barrett Esophagus / therapy. Biopsy, Fine-Needle. Endosonography. Humans. Neoadjuvant Therapy. Neoplasm Staging. Sensitivity and Specificity

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  • (PMID = 16997165.001).
  • [ISSN] 1521-6918
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 70
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49. 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
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  • [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.

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  • [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
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50. Bahmanyar S, Ye W: Dietary patterns and risk of squamous-cell carcinoma and adenocarcinoma of the esophagus and adenocarcinoma of the gastric cardia: a population-based case-control study in Sweden. Nutr Cancer; 2006;54(2):171-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dietary patterns and risk of squamous-cell carcinoma and adenocarcinoma of the esophagus and adenocarcinoma of the gastric cardia: a population-based case-control study in Sweden.
  • We conducted a large population-based case-control study in Sweden to examine the association of dietary patterns and the development of cancers from the esophagus or gastroesophageal junction.
  • In total 185 patients with esophageal adenocarcinoma, 165 with esophageal squamous-cell carcinoma, 258 with gastric cardia adenocarcinoma, and 815 randomly selected population controls underwent face-to-face interviews.
  • A high score of Western diet was associated with increased risks of gastric cardia adenocarcinoma (high 3rd tertile vs. low 1st quartile, OR = 1.8, 95% CI = 1.1-2.9, P for trend = 0.04) and esophageal adenocarcinoma (high 3rd tertile vs. low 1st tertile, OR = 1.6, 95% CI = 0.9-3.1, P for trend = 0.13), whereas a dietary pattern characterized by high beer and liquor intake (alcohol drinker) significantly increased the risk of squamous-cell carcinoma of the esophagus (3rd tertile vs. low 1st tertile, OR = 3.5, 95% CI = 1.9-6.3, P for trend < 0.0001).
  • Our study confirms the important role of diet in the carcinogenesis of esophageal and cardia cancer.
  • [MeSH-major] Adenocarcinoma / epidemiology. Carcinoma, Squamous Cell / epidemiology. Esophageal Neoplasms / epidemiology. Food Habits. Stomach Neoplasms / epidemiology

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  • (PMID = 16898861.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA57947-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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51. Brown LM, Devesa SS, Chow WH: Incidence of adenocarcinoma of the esophagus among white Americans by sex, stage, and age. J Natl Cancer Inst; 2008 Aug 20;100(16):1184-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence of adenocarcinoma of the esophagus among white Americans by sex, stage, and age.
  • Rapid increases in the incidence of adenocarcinoma of the esophagus have been reported among white men.
  • We identified 22,759 patients from January 1, 1975, through December 31, 2004, with esophageal cancer, of whom 9526 were diagnosed with adenocarcinoma of the esophagus.
  • Among white men, increases in the incidence of esophageal cancer were largely attributed to a 463% increase in the incidence of adenocarcinoma over this time period, from 1.01 per 100,000 person-years (95% confidence interval [CI] = 0.90 to 1.13) in 1975-1979 to 5.69 per 100,000 person-years (95% CI = 5.47 to 5.91) in 2000-2004.
  • A similar rapid increase was also apparent among white women, among whom the adenocarcinoma rate increased 335%, from 0.17 (95% CI = 0.13 to 0.21) to 0.74 per 100,000 person-years (95% CI = 0.67 to 0.81), over the same time period.
  • Adenocarcinoma rates rose among white men and women in all stage and age groups, indicating that these increases are real and not an artifact of surveillance.

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  • [Cites] Epidemiol Rev. 2001;23(1):3-13 [11588851.001]
  • [Cites] Surg Oncol Clin N Am. 2002 Apr;11(2):235-56 [12424848.001]
  • [Cites] Int J Cancer. 2003 May 20;105(1):101-7 [12672038.001]
  • [Cites] J Natl Cancer Inst. 1989 Oct 18;81(20):1568-71 [2795682.001]
  • [Cites] JAMA. 1991 Mar 13;265(10):1287-9 [1995976.001]
  • [Cites] JAMA. 1993 Sep 15;270(11):1320 [8360967.001]
  • [Cites] Am J Epidemiol. 1995 Feb 15;141(4):300-4 [7840107.001]
  • [Cites] Cancer. 1998 Nov 15;83(10):2049-53 [9827707.001]
  • [Cites] J Infect Dis. 2005 Mar 1;191(5):761-7 [15688293.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 May;15(5):872-8 [16702363.001]
  • [Cites] Cancer Causes Control. 2006 Sep;17(7):971-81 [16841264.001]
  • [Cites] Scand J Gastroenterol. 2007 Jan;42(1):17-22 [17190757.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Feb;17(2):352-8 [18268119.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Gut. 2008 Jun;57(6):727-33 [17895354.001]
  • [CommentIn] J Natl Cancer Inst. 2009 Oct 21;101(20):1428; author reply 1429 [19724025.001]
  • (PMID = 18695138.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS53143; NLM/ PMC2518165
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52. Lagergren J: Etiology and risk factors for oesophageal adenocarcinoma: possibilities for chemoprophylaxis? Best Pract Res Clin Gastroenterol; 2006;20(5):803-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Etiology and risk factors for oesophageal adenocarcinoma: possibilities for chemoprophylaxis?
  • The rapid increase in the incidence of oesophageal adenocarcinoma, particularly among white males, seems to be a true increase occurring in many parts of the industrialised world during the last few decades.
  • Barrett's oesophagus, gastrooesophageal reflux, high body mass, male sex, tobacco smoking, and high dietary intake of fruit and vegetables.
  • Several other potential risk factors have been studied for which the evidence is less clear, including medications that relax the lower oesophageal sphincter or diets high in fat or low in nutrients from plant foods.
  • Other factors have been found to be possibly inversely linked with the risk of oesophageal adenocarcinoma, including infection with Helicobacter pylori and anti-inflammatory drugs (such as aspirin and other non-steroidal anti-inflammatory drugs, including cyclo-oxygenase inhibitors).
  • The methodological problem of 'confounding by indication' makes it difficult to interpret the results of anti-inflammatory drugs, and currently such medication cannot be recommended for the prevention of oesophageal adenocarcinoma.
  • Similarly, since there is no strong evidence of a preventive effect of medical or surgical antireflux therapy with regard to risk of oesophageal adenocarcinoma, such therapy cannot be recommended in the prevention of this cancer.
  • Although some of the known risk factors might contribute to the increasing incidence of oesophageal adenocarcinoma, the explanation that can entirely explain this striking trend remains to be identified.
  • Oesophageal adenocarcinoma is a highly deadly cancer, but the overall prognosis and the prognosis after oesophageal cancer surgery has improved during recent years.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / prevention & control. Esophageal Neoplasms / etiology. Esophageal Neoplasms / prevention & control
  • [MeSH-minor] Age Factors. Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Barrett Esophagus / complications. Body Mass Index. Chemoprevention. Esophageal Sphincter, Lower / drug effects. Food Habits. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / therapy. Helicobacter Infections / complications. Helicobacter pylori. Humans. Incidence. Prognosis. Risk Factors. Smoking / adverse effects

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  • (PMID = 16997162.001).
  • [ISSN] 1521-6918
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
  • [Number-of-references] 69
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53. 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.
  • BACKGROUND: Accumulating evidence suggests that cyclooxygenase-2 (COX-2)-derived prostaglandin E2 (PGE2) is involved in oesophageal adenocarcinogenesis.
  • 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.
  • RESULTS: All four EP receptors subtypes were expressed in human oesophageal tissues.
  • 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

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  • (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
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54. Barclay JY, Morris A, Nwokolo CU: Telomerase, hTERT and splice variants in Barrett's oesophagus and oesophageal adenocarcinoma. Eur J Gastroenterol Hepatol; 2005 Feb;17(2):221-7
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] Telomerase, hTERT and splice variants in Barrett's oesophagus and oesophageal adenocarcinoma.
  • BACKGROUND AND OBJECTIVES: The enzyme telomerase is re-activated in most cancers but its mechanism of regulation in oesophageal carcinogenesis is unclear.
  • The aim of this study was to determine the roles of human telomerase reverse transcriptase (hTERT) mRNA expression and hTERT mRNA splicing in the regulation of telomerase enzyme activity in Barrett's oesophagus and oesophageal adenocarcinoma.
  • METHODS: Paired samples from oesophageal adenocarcinoma (n=21) and adjacent macroscopically normal mucosa, and paired samples from Barrett's oesophagus (n=16) and adjacent cardia mucosa were obtained.
  • RESULTS: In oesophageal adenocarcinoma, compared to adjacent mucosa, median telomerase activity increased significantly (from 5 to 229 total product generated (tpg), P=0.0002), but median hTERT mRNA levels were not significantly different.
  • Similarly, median telomerase activity was significantly higher in oesophageal adenocarcinoma compared to Barrett's oesophagus (229 vs 20 tpg, P=0.001), but hTERT mRNA levels were not significantly different.
  • There was no significant difference in telomerase activity and hTERT mRNA levels between Barrett's oesophagus and adjacent cardia.
  • The frequency of detection of all variants increased from cardia to Barrett's oesophagus to oesophageal adenocarcinoma (P<0.05).
  • CONCLUSIONS: A major increase in telomerase activity occurs after the Barrett's oesophagus stage in oesophageal carcinogenesis.
  • In this cancer, an important clinical diagnostic role for the transcripts of the telomerase gene is improbable.
  • [MeSH-major] Adenocarcinoma / enzymology. Barrett Esophagus / enzymology. Esophageal Neoplasms / enzymology. Gene Expression Regulation, Neoplastic. Telomerase / metabolism

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  • (PMID = 15674101.001).
  • [ISSN] 0954-691X
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.7.49 / Telomerase
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55. Lagergren J, Jansson C: Use of tight belts and risk of esophageal adenocarcinoma. Int J Cancer; 2006 Nov 15;119(10):2464-6
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  • [Title] Use of tight belts and risk of esophageal adenocarcinoma.
  • It has recently been hypothesized that the general shift in use from suspenders to belts among men might be a factor that could promote reflux, particularly among overweight men, and thereby contribute to the alarmingly increasing incidence of esophageal and cardia adenocarcinoma.
  • Included were 189 patients with esophageal adenocarcinoma and 262 patients with cardia adenocarcinoma, who were compared with 167 patients with esophageal squamous cell carcinoma and 820 population-based control participants.
  • Daily use of tight belts 20 years earlier did not entail an increased risk of adenocarcinoma of the esophagus (OR 1.1, 95% CI 0.7-1.8) or cardia (OR 0.8, 95% CI 0.5-1.3) compared to never use.
  • No association with esophageal squamous cell carcinoma was found.
  • In conclusion, this study provided no support for the hypothesis that use of tight belts is associated with an increased risk of developing esophageal or cardia adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / epidemiology. Carcinoma, Squamous Cell / epidemiology. Clothing / adverse effects. Esophageal Neoplasms / epidemiology. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / etiology

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  • (PMID = 16894563.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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56. Ladanchuk TC, Johnston BT, Murray LJ, Anderson LA, FINBAR study group: Risk of Barrett's oesophagus, oesophageal adenocarcinoma and reflux oesophagitis and the use of nitrates and asthma medications. Scand J Gastroenterol; 2010 Dec;45(12):1397-403
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  • [Title] Risk of Barrett's oesophagus, oesophageal adenocarcinoma and reflux oesophagitis and the use of nitrates and asthma medications.
  • OBJECTIVE: To investigate the relationship between use of asthma medication and nitrates and risk of reflux oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma.
  • MATERIAL AND METHODS: Data were collected on use of asthma medication and nitrates at least 1 year before interview from patients with reflux oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma.
  • Associations between use of asthma medications and nitrates and the risk of reflux oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma were estimated using multiple logistic regression.
  • RESULTS: Nine hundred and forty-one subjects were recruited: 230 reflux oesophagitis, 224 Barrett's oesophagus, 227 oesophageal adenocarcinoma patients and 260 population controls.
  • Barrett's oesophagus patients were more likely than controls to have had a diagnosis of asthma (odds ratio 2.15, 95% confidence interval 1.15-4.03) and to have used asthma medications (odds ratio 2.13, 95% confidence interval 1.09-4.16).
  • No significant associations were observed between use of asthma medication or nitrates and reflux oesophagitis or oesophageal adenocarcinoma.
  • CONCLUSIONS: Gastro-oesophageal reflux symptoms appear to confound the association between asthma medication use and Barrett's oesophagus.
  • However, it is possible that asthma medications may increase the risk of Barrett's oesophagus by other mechanisms.
  • [MeSH-major] Adenocarcinoma / chemically induced. Anti-Asthmatic Agents / adverse effects. Barrett Esophagus / chemically induced. Esophageal Neoplasms / chemically induced. Esophagitis, Peptic / chemically induced. Nitrates / adverse effects

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  • (PMID = 20626305.001).
  • [ISSN] 1502-7708
  • [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] England
  • [Chemical-registry-number] 0 / Anti-Asthmatic Agents; 0 / Nitrates
  • [Investigator] Murray LJ; Anderson LA; Johnston BT; Watson RG; McGuigan J; Ferguson HR; Murphy SJ; Reynolds JV; Comber H
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57. Anderson LA, Watson RG, Murphy SJ, Johnston BT, Comber H, Mc Guigan J, Reynolds JV, Murray LJ: Risk factors for Barrett's oesophagus and oesophageal adenocarcinoma: results from the FINBAR study. World J Gastroenterol; 2007 Mar 14;13(10):1585-94
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  • [Title] Risk factors for Barrett's oesophagus and oesophageal adenocarcinoma: results from the FINBAR study.
  • AIM: To investigate risk factors associated with Barrett's oesophagus and oesophageal adenocarcinoma.
  • METHODS: This all-Ireland population-based case-control study recruited 224 Barrett's oesophagus patients, 227 oesophageal adenocarcinoma patients and 260 controls.
  • RESULTS: Gastro-oesophageal reflux was associated with Barrett's [OR 12.0 (95% CI 7.64-18.7)] and oesophageal adenocarcinoma [OR 3.48 (95% CI 2.25-5.41)].
  • Oesophageal adenocarcinoma patients were more likely than controls to be ex- or current smokers [OR 1.72 (95% CI 1.06-2.81) and OR 4.84 (95% CI 2.72-8.61) respectively] and to have a high body mass index [OR 2.69 (95% CI 1.62-4.46)].
  • No significant associations were observed between these risk factors and Barrett's oesophagus.
  • Fruit but not vegetables were negatively associated with oesophageal adenocarcinoma [OR 0.50 (95% CI 0.30-0.86)].
  • CONCLUSION: A high body mass index, a diet low in fruit and cigarette smoking may be involved in the progression from Barrett's oesophagus to oesophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / epidemiology. Barrett Esophagus / epidemiology. Esophageal Neoplasms / epidemiology

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  • [Cites] Eur J Cancer Prev. 1995 Dec;4(6):459-68 [8580781.001]
  • [Cites] World Health Organ Tech Rep Ser. 1995;854:1-452 [8594834.001]
  • [Cites] Int J Cancer. 1996 Nov 4;68(3):295-9 [8903469.001]
  • [Cites] Int J Cancer. 1996 Nov 4;68(3):300-4 [8903470.001]
  • [Cites] Am J Gastroenterol. 1997 Feb;92(2):212-5 [9040193.001]
  • [Cites] Am J Gastroenterol. 1997 Aug;92(8):1293-7 [9260792.001]
  • [Cites] Neurology. 1997 Aug;49(2):507-11 [9270586.001]
  • [Cites] J Natl Cancer Inst. 1997 Sep 3;89(17):1277-84 [9293918.001]
  • [Cites] J Natl Cancer Inst. 1998 Jan 21;90(2):150-5 [9450576.001]
  • [Cites] Am J Gastroenterol. 1998 Apr;93(4):536-41 [9576444.001]
  • [Cites] Am J Gastroenterol. 1999 Jan;94(1):86-91 [9934736.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] Ann Intern Med. 1999 Jun 1;130(11):883-90 [10375336.001]
  • [Cites] Am J Med. 1999 Jun;106(6):642-9 [10378622.001]
  • [Cites] Gastroenterology. 2002 Aug;123(2):461-7 [12145799.001]
  • [Cites] Nutr Cancer. 2002;42(1):33-40 [12235648.001]
  • [Cites] JAMA. 2002 Oct 9;288(14):1723-7 [12365955.001]
  • [Cites] J Cancer Res Clin Oncol. 2002 Oct;128(10):575-80 [12384802.001]
  • [Cites] J Nutr. 2002 Nov;132(11 Suppl):3467S-3470S [12421872.001]
  • [Cites] IARC Sci Publ. 2002;156:123-5 [12484143.001]
  • [Cites] JAMA. 2003 Jul 2;290(1):66-72 [12837713.001]
  • [Cites] Int J Epidemiol. 2003 Aug;32(4):645-50 [12913045.001]
  • [Cites] Am J Clin Nutr. 2003 Sep;78(3 Suppl):559S-569S [12936950.001]
  • [Cites] Cancer. 2003 Sep 1;98(5):940-8 [12942560.001]
  • [Cites] BMJ. 2003 Sep 6;327(7414):534-5 [12958113.001]
  • [Cites] J Natl Cancer Inst. 2003 Sep 17;95(18):1404-13 [13130116.001]
  • [Cites] World J Surg. 2003 Sep;27(9):999-1008; discussion 1006-8 [12917764.001]
  • [Cites] Hum Pathol. 2003 Oct;34(10):975-82 [14608530.001]
  • [Cites] Ann Surg. 2004 Jun;239(6):849-56; discussion 856-8 [15166964.001]
  • [Cites] Biomarkers. 2003 Nov-Dec;8(6):509-21 [15195681.001]
  • [Cites] Nat Rev Cancer. 2004 Aug;4(8):579-91 [15286738.001]
  • [Cites] Dig Dis Sci. 2004 Jun;49(6):914-9 [15309877.001]
  • [Cites] Am J Gastroenterol. 1999 Aug;94(8):2037-42 [10445525.001]
  • [Cites] Br J Cancer. 1999 Jul;80 Suppl 1:95-103 [10466767.001]
  • [Cites] Anticancer Res. 2004 Sep-Oct;24(5A):3029-34 [15517912.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4975-82 [16651456.001]
  • [Cites] Dis Esophagus. 2000;13(1):28-31 [11005328.001]
  • [Cites] Hepatogastroenterology. 2000 Jul-Aug;47(34):962-6 [11020858.001]
  • [Cites] Eur J Cancer Prev. 2001 Aug;10(4):365-9 [11535879.001]
  • [Cites] Cancer Causes Control. 2001 Oct;12(8):721-32 [11562112.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2001 Oct;10(10):1055-62 [11588131.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):620-5 [15767340.001]
  • [Cites] Rom J Gastroenterol. 2005 Jun;14(2):117-21 [15990929.001]
  • [Cites] Am J Gastroenterol. 2005 Oct;100(10):2151-6 [16181362.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Nov;14(11 Pt 1):2481-6 [16284367.001]
  • [Cites] Int J Cancer. 2006 May 15;118(10):2559-66 [16380980.001]
  • [Cites] JAMA. 1999 Oct 27;282(16):1519-22 [10546690.001]
  • [Cites] Semin Oncol. 1999 Oct;26(5 Suppl 15):2-8 [10566604.001]
  • [Cites] Int J Cancer. 2000 Feb 1;85(3):340-6 [10652424.001]
  • [Cites] Cancer Causes Control. 2000 Mar;11(3):231-8 [10782657.001]
  • [Cites] Cancer. 2000 Jun 1;88(11):2520-8 [10861428.001]
  • [Cites] Br J Cancer. 2000 Jul;83(1):127-32 [10883680.001]
  • [Cites] Int J Epidemiol. 2000 Aug;29(4):645-54 [10922340.001]
  • [Cites] Int J Cancer. 2000 Sep 1;87(5):750-4 [10925371.001]
  • [Cites] Am J Clin Nutr. 2002 Jan;75(1):137-44 [11756071.001]
  • [Cites] Int J Cancer. 2002 Jan 10;97(2):225-9 [11774268.001]
  • [Cites] Gastroenterology. 2002 Jan;122(1):26-33 [11781277.001]
  • [Cites] Public Health Nutr. 2001 Oct;4(5A):1037-42 [11820916.001]
  • [Cites] Public Health Nutr. 2001 Oct;4(5A):1099-106 [11820923.001]
  • [Cites] Surg Endosc. 2002 Apr;16(4):671-3 [11972212.001]
  • [Cites] Proc Nutr Soc. 2002 Feb;61(1):3-7 [12002792.001]
  • [Cites] Am J Gastroenterol. 2002 Jun;97(6):1328-31 [12094845.001]
  • [Cites] Obes Rev. 2002 Feb;3(1):9-15 [12119661.001]
  • [Cites] Oncogene. 2004 Aug 23;23(38):6365-78 [15322511.001]
  • [Cites] Br Med J. 1972 Sep 30;3(5830):793-5 [5076250.001]
  • [Cites] N Engl J Med. 1985 Oct 3;313(14):857-9 [4033716.001]
  • [Cites] Am J Gastroenterol. 1989 Dec;84(12):1494-6 [2596449.001]
  • [Cites] Gut. 1990 Jan;31(1):4-10 [2318431.001]
  • [Cites] Gastroenterology. 1990 Oct;99(4):918-22 [2394347.001]
  • [Cites] Cancer Res. 1990 Dec 1;50(23):7415-21 [2174724.001]
  • [Cites] Eur J Cancer Prev. 1992 Feb;1(2):159-64 [1463978.001]
  • [Cites] Eur J Cancer Prev. 1992 Apr;1(3):265-9 [1467772.001]
  • [Cites] Cancer Causes Control. 1993 Mar;4(2):123-32 [8481491.001]
  • [Cites] Int J Cancer. 1993 May 28;54(3):402-7 [8509215.001]
  • [Cites] Cancer Causes Control. 1994 Jul;5(4):333-40 [8080945.001]
  • [Cites] J Natl Cancer Inst. 1995 Jan 18;87(2):104-9 [7707381.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1995 Mar;4(2):85-92 [7742727.001]
  • [Cites] JAMA. 1995 Aug 9;274(6):474-7 [7629956.001]
  • (PMID = 17461453.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC4146903
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58. Peters CJ, Fitzgerald RC: Systematic review: the application of molecular pathogenesis to prevention and treatment of oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2007 Jun 01;25(11):1253-69
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  • [Title] Systematic review: the application of molecular pathogenesis to prevention and treatment of oesophageal adenocarcinoma.
  • BACKGROUND: Oesophageal adenocarcinoma is an increasingly common cancer with a poor prognosis.
  • It develops in a stepwise progression from Barrett's metaplasia to dysplasia, and then adenocarcinoma followed by metastasis.
  • AIM: To outline the key molecular changes in oesophageal adenocarcinoma and to summarize the chemopreventative and therapeutic strategies proposed.
  • Search terms included: Barrett's (o)esophagus, intestinal metaplasia, (o)esophageal adenocarcinoma, molecular changes, genetic changes, pathogenesis, chemoprevention, therapeutic strategies and treatment.
  • RESULTS: A large number of molecular changes have been identified in the progression from Barrett's oesophagus to oesophageal adenocarcinoma although there does not appear to be an obligate order of events.
  • In established adenocarcinoma, targeted treatments under evaluation include receptor tyrosine kinase inhibitors of EGFR and cyclin-dependent kinase inhibitors, which may benefit a subgroup of patients.
  • CONCLUSIONS: Advances in molecular methodology have led to a greater understanding of the oesophageal adenocarcinoma pathways, which provides opportunities for chemoprevention and therapeutic strategies with a mechanistic basis.
  • [MeSH-major] Adenocarcinoma / prevention & control. Angiogenesis Inhibitors / therapeutic use. Anti-Inflammatory Agents / therapeutic use. Antioxidants / therapeutic use. Esophageal Neoplasms / prevention & control

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  • (PMID = 17509094.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Anti-Inflammatory Agents; 0 / Antioxidants
  • [Number-of-references] 149
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59. Witzig R, Schönberger B, Fink U, Busch R, Gundel H, Sendler A, Peschel C, Siewert JR, Lordick F: Delays in diagnosis and therapy of gastric cancer and esophageal adenocarcinoma. Endoscopy; 2006 Nov;38(11):1122-6
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  • [Title] Delays in diagnosis and therapy of gastric cancer and esophageal adenocarcinoma.
  • BACKGROUND AND STUDY AIMS: In the past, there were long delays in the diagnosis of patients with cancer of the stomach or esophagus.
  • The objective of this study was to describe current delays in the diagnosis and treatment of gastric and esophageal adenocarcinoma and to compare the findings with those from an historical control population treated at the same institutions 10 years earlier.
  • PATIENTS AND METHODS: Patients with biopsy-proven gastric cancer or esophageal adenocarcinoma who were treated at two academic medical centers in Germany between April and October 2003 were consecutively screened for eligibility to take part in the study.
  • RESULTS: The median total delay for patients with gastric cancer (n = 104) was 3.5 months (range 0.3 - 29.6), and in patients with esophageal adenocarcinoma (n = 22) the total delay was significantly shorter (median 2.2 months, range 1.2 - 11.7; P < 0.05).
  • Comparing these findings with those from an historic cohort of patients with gastric cancer (n = 100) revealed a significant decrease in the total delay (3.5 versus 8.0 months, P < 0.001).
  • CONCLUSIONS: The current findings indicate that delays in the diagnosis and treatment of gastric cancer have become significantly shorter within the last 10 years as our understanding of and ability to treat this form of cancer have improved.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / therapy. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / therapy. Stomach Neoplasms / diagnosis. Stomach Neoplasms / therapy


60. Miyashita T, Ohta T, Fujimura T, Ninomiya I, Fushida S, Hattori T, Miwa K: Duodenal juice stimulates oesophageal stem cells to induce Barrett's oesophagus and oesophageal adenocarcinoma in rats. Oncol Rep; 2006 Jun;15(6):1469-75
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  • [Title] Duodenal juice stimulates oesophageal stem cells to induce Barrett's oesophagus and oesophageal adenocarcinoma in rats.
  • the present study was performed to examine the sequential process of the development of Barrett's oesophagus (BE) and oesophageal adenocarcinoma (ADC) induced by duodeno-oesophageal reflux (DER) in rats.
  • Total gastrectomy was performed in male Wistar rats weighing approximately 250 g followed by reconstruction with oesophago-jejunostomy, which causes unavoidable DER without exposure to exogenous carcinogens.
  • On the 20th week, glandular structures that stained positively with Galactose oxidase-Schiff (foveolar metaplasia) were observed in the basal layer of the oesophageal squamous epithelium.
  • Persistent stimulation with DER can alter the stem cells in the squamous epithelial basal layer leading to the formation of columnar-lined cells and subsequent ADC.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / etiology. Duodenogastric Reflux / complications. Duodenum / secretion. Esophageal Neoplasms / etiology. Esophagus / pathology. Gastroesophageal Reflux / complications. Stem Cells / pathology

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  • (PMID = 16685381.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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61. Reid BJ, Li X, Galipeau PC, Vaughan TL: Barrett's oesophagus and oesophageal adenocarcinoma: time for a new synthesis. Nat Rev Cancer; 2010 Feb;10(2):87-101
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  • [Title] Barrett's oesophagus and oesophageal adenocarcinoma: time for a new synthesis.
  • The public health importance of Barrett's oesophagus lies in its association with oesophageal adenocarcinoma.
  • The incidence of oesophageal adenocarcinoma has risen at an alarming rate over the past four decades in many regions of the Western world, and there are indications that the incidence of this disease is on the rise in Asian populations in which it has been rare.
  • Much has been learned of host and environmental risk factors that affect the incidence of oesophageal adenocarcinoma, and data indicate that patients with Barrett's oesophagus rarely develop oesophageal adenocarcinoma.
  • Given that 95% of oesophageal adenocarcinomas arise in individuals without a prior diagnosis of Barrett's oesophagus, what strategies can be used to reduce late diagnosis of oesophageal adenocarcinoma?

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  • [Cites] Clin Cancer Res. 2009 May 15;15(10):3305-14 [19417022.001]
  • [Cites] N Engl J Med. 2009 May 28;360(22):2277-88 [19474425.001]
  • [Cites] Am J Gastroenterol. 2009 Jun;104(6):1356-62 [19491849.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Jul;18(7):2079-89 [19567501.001]
  • [Cites] Histopathology. 2009 Jun;54(7):814-9 [19635100.001]
  • [Cites] Am J Gastroenterol. 2009 Sep;104(9):2153-60 [19584833.001]
  • [Cites] BMC Fam Pract. 2009;10:59 [19706198.001]
  • [Cites] Nat Rev Cancer. 2009 Oct;9(10):701-13 [19693097.001]
  • [Cites] Gut. 2009 Nov;58(11):1451-9 [19651633.001]
  • [Cites] Clin Gastroenterol Hepatol. 2009 Dec;7(12):1299-304 [19523538.001]
  • [Cites] Dis Esophagus. 2009;22(8):676-81 [19222529.001]
  • [Cites] Biomarkers. 2006 Nov-Dec;11(6):547-61 [17056474.001]
  • [Cites] Am J Gastroenterol. 2006 Nov;101(11):2619-28 [16952280.001]
  • [Cites] Gut. 2006 Dec;55(12):1810-20 [17124160.001]
  • [Cites] Semin Radiat Oncol. 2007 Jan;17(1):2-9 [17185192.001]
  • [Cites] Scand J Gastroenterol. 2007 Jan;42(1):23-7 [17190758.001]
  • [Cites] Am J Gastroenterol. 2007 Jan;102(1):10-20 [17266684.001]
  • [Cites] PLoS Med. 2007 Feb;4(2):e67 [17326708.001]
  • [Cites] Am J Gastroenterol. 2007 Mar;102(3):483-93; quiz 694 [17338734.001]
  • [Cites] J Natl Cancer Inst. 2007 Apr 4;99(7):545-57 [17405999.001]
  • [Cites] World J Gastroenterol. 2007 Mar 14;13(10):1585-94 [17461453.001]
  • [Cites] Cancer Causes Control. 2007 Nov;18(9):1039-46 [17665311.001]
  • [Cites] Cancer Detect Prev. 2007;31(3):233-6 [17646057.001]
  • [Cites] Int J Cancer. 2007 Oct 15;121(8):1643-58 [17674367.001]
  • [Cites] Gastrointest Endosc. 2007 Sep;66(3):460-8 [17643436.001]
  • [Cites] Int J Pediatr Obes. 2006;1(2):109-13 [17907323.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Oct;16(10):2090-6 [17890521.001]
  • [Cites] Am J Gastroenterol. 2007 Nov;102(11):2373-9 [17581270.001]
  • [Cites] Aliment Pharmacol Ther. 2007 Dec;26(11-12):1465-77 [17900269.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2007 Dec;293(6):G1106-13 [17932229.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Dec;16(12):2637-40 [18086768.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Dec;16(12):2649-55 [18086770.001]
  • [Cites] Gut. 2008 Feb;57(2):173-80 [17932103.001]
  • [Cites] Int J Cancer. 2008 Jul 1;123(1):174-80 [18386788.001]
  • [Cites] Am J Gastroenterol. 2008 May;103(5):1079-89 [18445097.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 May;17(5):1169-78 [18483339.001]
  • [Cites] Cancer Res. 2008 Jun 1;68(11):4163-72 [18519675.001]
  • [Cites] Arch Iran Med. 2008 Jul;11(4):364-70 [18588366.001]
  • [Cites] Gut. 2008 Aug;57(8):1041-8 [18305067.001]
  • [Cites] Am J Epidemiol. 2008 Aug 1;168(3):237-49 [18550563.001]
  • [Cites] J Clin Gastroenterol. 2008 Aug;42(7):806-9 [18385604.001]
  • [Cites] Hum Pathol. 2008 Aug;39(8):1128-35 [18602665.001]
  • [Cites] Jpn J Clin Oncol. 2008 Jul;38(7):464-8 [18664481.001]
  • [Cites] Am J Gastroenterol. 2008 Jul;103(7):1614-23; quiz 1624 [18494834.001]
  • [Cites] J Natl Cancer Inst. 2008 Aug 20;100(16):1184-7 [18695138.001]
  • [Cites] Genome Res. 2008 Sep;18(9):1518-29 [18577705.001]
  • [Cites] Mutagenesis. 2008 Sep;23(5):399-405 [18515815.001]
  • [Cites] BMC Genomics. 2008;9:394 [18717985.001]
  • [Cites] Gut. 2008 Oct;57(10):1354-9 [18424568.001]
  • [Cites] J Gastrointest Surg. 2008 Oct;12(10):1627-36; discussion 1636-7 [18704598.001]
  • [Cites] Dis Esophagus. 2008;21(6):529-38 [18840137.001]
  • [Cites] Mol Cancer. 2008;7:75 [18831746.001]
  • [Cites] Gastroenterology. 2008 Oct;135(4):1392-1413, 1413.e1-5 [18801365.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2008 Aug;22(4):659-69 [18971125.001]
  • [Cites] Clin Cancer Res. 2008 Nov 1;14(21):6988-95 [18980994.001]
  • [Cites] Gastrointest Endosc. 2008 Nov;68(5):849-55 [18547567.001]
  • [Cites] Contemp Clin Trials. 2009 Jan;30(1):2-7 [19013259.001]
  • [Cites] J Gastroenterol Hepatol. 2008 Dec;23(12):1785-93 [19120871.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Oct;1(5):308-11 [19138974.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Oct;1(5):329-38 [19138977.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Nov;1(6):413-23 [19138988.001]
  • [Cites] Nat Genet. 2009 Feb;41(2):178-86 [19151715.001]
  • [Cites] Br J Cancer. 2009 Feb 10;100(3):551-7 [19156150.001]
  • [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] Cancer Res. 2004 Oct 15;64(20):7629-33 [15492292.001]
  • [Cites] Nature. 1975 May 15;255(5505):197-200 [1143315.001]
  • [Cites] J Thorac Cardiovasc Surg. 1975 Nov;70(5):826-35 [1186274.001]
  • [Cites] Science. 1976 Oct 1;194(4260):23-8 [959840.001]
  • [Cites] Hum Pathol. 1988 Feb;19(2):166-78 [3343032.001]
  • [Cites] Gastroenterology. 1989 Feb;96(2 Pt 1):355-67 [2910757.001]
  • [Cites] Stat Med. 1989 Apr;8(4):431-40 [2727467.001]
  • [Cites] J Thorac Cardiovasc Surg. 1993 Mar;105(3):383-7; discussion 387-8 [8445916.001]
  • [Cites] Stat Med. 1994 May 15;13(9):955-68 [8047747.001]
  • [Cites] J Thorac Cardiovasc Surg. 1994 Nov;108(5):813-21; discussion 821-2 [7967662.001]
  • [Cites] Cancer Causes Control. 2009 Apr;20(3):303-11 [18853262.001]
  • [Cites] Gastroenterology. 2009 Mar;136(3):799-805 [19162028.001]
  • [Cites] Cell Cycle. 2009 Mar 15;8(6):809-17 [19229128.001]
  • [Cites] Gastroenterology. 2009 Apr;136(4):1215-24, e1-2 [19250648.001]
  • [Cites] Am J Gastroenterol. 2009 Apr;104(4):834-42 [19319131.001]
  • [Cites] Lancet. 2009 Apr 11;373(9671):1301-9 [19328542.001]
  • [Cites] Cancer Biomark. 2009;5(3):143-58 [19407369.001]
  • [Cites] Cancer Prev Res (Phila). 2009 May;2(5):459-65 [19401529.001]
  • [Cites] Histopathology. 2009 May;54(6):699-712 [19438745.001]
  • [Cites] Cancer Res. 2009 May 15;69(10):4112-5 [19435894.001]
  • [Cites] Am J Gastroenterol. 1999 Jan;94(1):86-91 [9934736.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] Gut. 1998 Aug;43(2):216-22 [10189847.001]
  • [Cites] Cancer Res. 1999 Apr 15;59(8):1837-9 [10213488.001]
  • [Cites] Nat Genet. 1999 May;22(1):106-9 [10319873.001]
  • [Cites] Gastroenterology. 1999 Aug;117(2):327-35 [10419913.001]
  • [Cites] Br J Surg. 1950 Oct;38(150):175-82 [14791960.001]
  • [Cites] Thorax. 1953 Jun;8(2):87-101 [13077502.001]
  • [Cites] Am J Gastroenterol. 2004 Nov;99(11):2107-14 [15554988.001]
  • [Cites] Semin Cancer Biol. 2005 Feb;15(1):51-60 [15613288.001]
  • [Cites] J Infect Dis. 2005 Mar 1;191(5):761-7 [15688293.001]
  • [Cites] Scand J Gastroenterol. 2004 Dec;39(12):1175-9 [15742992.001]
  • [Cites] Gastroenterology. 2005 Mar;128(3):771-8 [15765412.001]
  • [Cites] Am J Gastroenterol. 2005 Apr;100(4):775-83 [15784018.001]
  • [Cites] Clin Cancer Res. 2005 Apr 1;11(7):2478-85 [15814623.001]
  • [Cites] J Gastroenterol Hepatol. 2005 Apr;20(4):633-6 [15836715.001]
  • [Cites] JAMA. 2005 May 4;293(17):2095-101 [15870412.001]
  • [Cites] Cancer Causes Control. 2005 Apr;16(3):285-94 [15947880.001]
  • [Cites] Clin Gastroenterol Hepatol. 2005 Jun;3(6):529-37 [15952094.001]
  • [Cites] J Gastroenterol Hepatol. 2005 Jul;20(7):995-1001 [15955205.001]
  • [Cites] Ann Intern Med. 2005 Aug 2;143(3):199-211 [16061918.001]
  • [Cites] Int J Cancer. 2006 May 15;118(10):2628-31 [16353151.001]
  • [Cites] Aliment Pharmacol Ther. 2006 Mar 15;23(6):727-33 [16556174.001]
  • [Cites] Gastrointest Endosc. 2006 Apr;63(4):570-80 [16564854.001]
  • [Cites] Nat Genet. 2006 Apr;38(4):468-73 [16565718.001]
  • [Cites] JAMA. 2006 Apr 5;295(13):1549-55 [16595758.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4975-82 [16651456.001]
  • [Cites] Clin Gastroenterol Hepatol. 2006 May;4(5):566-72 [16630761.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 May;15(5):872-8 [16702363.001]
  • [Cites] J Natl Cancer Inst. 2006 Jun 7;98(11):748-56 [16757699.001]
  • [Cites] J Nutr. 2006 Jul;136(7 Suppl):1935S-1939S [16772463.001]
  • [Cites] Clin Cancer Res. 2006 Jun 15;12(12):3661-97 [16778094.001]
  • [Cites] BMJ. 2006 Jun 24;332(7556):1512 [16793832.001]
  • [Cites] Scand J Gastroenterol. 2006 Aug;41(8):887-91 [16803686.001]
  • [Cites] Cancer Causes Control. 2006 Sep;17(7):901-9 [16841257.001]
  • [Cites] Cancer Causes Control. 2006 Sep;17(7):971-81 [16841264.001]
  • [Cites] Am J Gastroenterol. 2006 Jul;101(7):1430-6 [16863543.001]
  • [Cites] Aging Cell. 2006 Aug;5(4):325-30 [16913878.001]
  • [Cites] Carcinogenesis. 2006 Sep;27(9):1835-41 [16571649.001]
  • [Cites] Am J Gastroenterol. 2006 Aug;101(8):1900-20; quiz 1943 [16928254.001]
  • [Cites] Anal Chem. 2006 Sep 1;78(17):5977-86 [16944874.001]
  • [Cites] Gut. 2006 Oct;55(10):1390-7 [16682429.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Sep;15(9):1668-73 [16985029.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Oct;15(10):1935-40 [17035402.001]
  • [Cites] Br J Surg. 2002 Jul;89(7):824-37 [12081731.001]
  • [Cites] Trends Biochem Sci. 2002 Jul;27(7):339-44 [12114022.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2002 Aug;11(8):745-52 [12163328.001]
  • [Cites] Gut. 2002 Sep;51(3):323-8 [12171951.001]
  • [Cites] Int J Cancer. 2002 Dec 20;102(6):551-5 [12447994.001]
  • [Cites] Gastroenterology. 2003 Jan;124(1):47-56 [12512029.001]
  • [Cites] Int J Cancer. 2003 May 20;105(1):98-100 [12672037.001]
  • [Cites] Gastroenterology. 2003 May;124(5):1193-201 [12730860.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2560-6 [12855631.001]
  • [Cites] Lancet. 2005 Aug 20-26;366(9486):662-4 [16112303.001]
  • [Cites] Genes Chromosomes Cancer. 2007 Jun;46(6):532-42 [17330261.001]
  • [Cites] Carcinogenesis. 2007 Jun;28(6):1323-8 [17277236.001]
  • [Cites] Mol Cell Proteomics. 2007 Jun;6(6):987-99 [16829691.001]
  • [Cites] Genet Med. 2007 Jun;9(6):341-7 [17575500.001]
  • [Cites] Cancer Causes Control. 2007 Sep;18(7):713-22 [17562192.001]
  • [Cites] Transl Res. 2007 Jul;150(1):3-17 [17585859.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2007 Jul;293(1):G264-70 [17431220.001]
  • [Cites] Gastroenterology. 2007 Jul;133(1):34-41; quiz 311 [17631128.001]
  • [Cites] J Mol Med (Berl). 2007 Jul;85(7):733-43 [17415542.001]
  • [Cites] Gastroenterology. 2007 Aug;133(2):403-11 [17681161.001]
  • [Cites] Carcinogenesis. 2005 Sep;26(9):1536-41 [15878910.001]
  • [Cites] Am J Gastroenterol. 2005 Oct;100(10):2151-6 [16181362.001]
  • [Cites] Gastrointest Endosc. 2005 Oct;62(4):488-98 [16185958.001]
  • [Cites] Scand J Gastroenterol. 2005 Sep;40(9):1127-8 [16211720.001]
  • [Cites] Gastroenterology. 2005 Oct;129(4):1274-81 [16230080.001]
  • [Cites] Lancet Oncol. 2005 Dec;6(12):945-52 [16321762.001]
  • [Cites] Am J Gastroenterol. 2005 Dec;100(12):2616-21 [16393209.001]
  • [Cites] J Urol. 2006 Feb;175(2):425-31 [16406965.001]
  • [Cites] Cancer Causes Control. 2000 Mar;11(3):231-8 [10782657.001]
  • [Cites] Aliment Pharmacol Ther. 2000 Apr;14 Suppl 1:3-9 [10807397.001]
  • [Cites] Am J Gastroenterol. 2000 Jul;95(7):1669-76 [10925966.001]
  • [Cites] J Natl Cancer Inst. 2000 Aug 16;92(16):1316-21 [10944553.001]
  • [Cites] Am J Gastroenterol. 2000 Oct;95(10):2946-52 [11051373.001]
  • [Cites] Gut. 2001 Mar;48(3):304-9 [11171817.001]
  • [Cites] Ann Surg. 2001 Mar;233(3):322-37 [11224619.001]
  • [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):1607-19 [11375943.001]
  • [Cites] Gastroenterology. 2001 Jun;120(7):1630-9 [11375945.001]
  • [Cites] Cancer. 2001 Aug 1;92(3):549-55 [11505399.001]
  • [Cites] Cancer Causes Control. 2001 Oct;12(8):721-32 [11562112.001]
  • [Cites] Am J Gastroenterol. 2001 Sep;96(9):2575-83 [11569678.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2001 Oct;10(10):1055-62 [11588131.001]
  • [Cites] Gastroenterology. 2002 Jan;122(1):26-33 [11781277.001]
  • [Cites] Gastroenterology. 2002 Jan;122(1):55-9 [11781280.001]
  • [Cites] Gastroenterology. 2002 Mar;122(3):633-40 [11874995.001]
  • [Cites] Neoplasia. 2002 Mar-Apr;4(2):121-8 [11896567.001]
  • [Cites] Gastroenterology. 2002 Apr;122(4):1101-12 [11910360.001]
  • [Cites] JAMA. 2002 Apr 17;287(15):1972-81 [11960540.001]
  • [Cites] Surg Endosc. 2002 Feb;16(2):263-6 [11967675.001]
  • [Cites] J Gastrointest Surg. 2002 Jan-Feb;6(1):29-35; discussion 36 [11986015.001]
  • [Cites] J Mol Diagn. 2008 Jan;10(1):67-77 [18083688.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Jan;17(1):126-34 [18187391.001]
  • [Cites] Aliment Pharmacol Ther. 2008 Feb 15;27(4):316-20 [18062791.001]
  • [Cites] Cell Oncol. 2008;30(1):63-75 [18219111.001]
  • [Cites] Int J Cancer. 2008 Mar 15;122(6):1303-10 [18000824.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Feb;17(2):352-8 [18268119.001]
  • [Cites] Gut. 2008 Apr;57(4):448-54 [18178609.001]
  • [Cites] Am J Gastroenterol. 2008 Mar;103(3):788-97 [18341497.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Mar;17(3):727-31 [18349295.001]
  • [Cites] Gut. 2003 Aug;52(8):1081-4 [12865262.001]
  • [Cites] Gut. 2003 Aug;52(8):1085-9 [12865263.001]
  • [Cites] Cancer. 2003 Sep 1;98(5):940-8 [12942560.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):695-701 [12951588.001]
  • [Cites] J Med Genet. 2003 Sep;40(9):651-6 [12960209.001]
  • [Cites] J Natl Cancer Inst. 2003 Sep 17;95(18):1404-13 [13130116.001]
  • [Cites] Am J Gastroenterol. 2003 Sep;98(9):1931-9 [14499768.001]
  • [Cites] Nature. 2004 Feb 26;427(6977):787 [14985739.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3414-27 [15150093.001]
  • [Cites] Gastroenterology. 2004 Jul;127(1):310-30 [15236196.001]
  • [Cites] Cancer Cell. 2004 Jul;6(1):11-6 [15261138.001]
  • [Cites] Br J Surg. 2004 Aug;91(8):997-1003 [15286961.001]
  • [Cites] Nat Rev Cancer. 2004 Aug;4(8):579-91 [15286738.001]
  • [Cites] Cancer Causes Control. 2004 Oct;15(8):837-43 [15456997.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1995 Mar;4(2):85-92 [7742727.001]
  • [Cites] Am J Gastroenterol. 1996 Sep;91(9):1855-6 [8792715.001]
  • [Cites] Am J Gastroenterol. 1997 Apr;92(4):586-91 [9128304.001]
  • [Cites] J Natl Cancer Inst. 1997 Sep 3;89(17):1277-84 [9293918.001]
  • [Cites] Gastroenterology. 1997 Nov;113(5):1449-56 [9352846.001]
  • [Cites] Gut. 1997 Sep;41(3):303-7 [9378382.001]
  • [Cites] J Natl Cancer Inst. 1998 Jan 21;90(2):150-5 [9450576.001]
  • [Cites] Cancer Res. 1998 Feb 15;58(4):588-90 [9485003.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Feb;7(2):97-102 [9488582.001]
  • [Cites] Am J Gastroenterol. 1998 Jul;93(7):1028-32 [9672324.001]
  • (PMID = 20094044.001).
  • [ISSN] 1474-1768
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA124911-02; United States / NCI NIH HHS / CA / K05 CA124911; United States / NCI NIH HHS / CA / P01 CA091955; United States / NCI NIH HHS / CA / P01 CA091955-08; United States / NCI NIH HHS / CA / K05 CA124911-02
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 218
  • [Other-IDs] NLM/ NIHMS200752; NLM/ PMC2879265
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62. Beales IL, Ogunwobi OO: Glycine-extended gastrin inhibits apoptosis in Barrett's oesophageal and oesophageal adenocarcinoma cells through JAK2/STAT3 activation. J Mol Endocrinol; 2009 Apr;42(4):305-18
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  • [Title] Glycine-extended gastrin inhibits apoptosis in Barrett's oesophageal and oesophageal adenocarcinoma cells through JAK2/STAT3 activation.
  • Barrett's oesophagus (BO) and oesophageal adenocarcinoma (OAC) are regarded as complications of gastro-oesophageal reflux disease, although all the factors that contribute to the development of these lesions are unknown.
  • We have examined the effects of glycine-extended gastrin (G-Gly), an alternative product of progastrin processing on apoptosis in the QhERT Barrett's oesophageal cell line and OE33 and BIC-1 OAC cells.
  • [MeSH-major] Adenocarcinoma / pathology. Apoptosis / drug effects. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Gastrins / pharmacology. Janus Kinase 2 / metabolism. STAT3 Transcription Factor / metabolism

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  • (PMID = 19153190.001).
  • [ISSN] 1479-6813
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Gastrins; 0 / RNA, Small Interfering; 0 / Receptors, Cholecystokinin; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / glycine-extended gastrin 17; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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63. Reynolds JV, Murphy TJ, Ravi N: Multimodality therapy for adenocarcinoma of the esophagus, gastric cardia, and upper gastric third. Recent Results Cancer Res; 2010;182:155-66
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  • [Title] Multimodality therapy for adenocarcinoma of the esophagus, gastric cardia, and upper gastric third.
  • There is considerable controversy over the level of recommendations from randomized trials underpinning management decisions for patients presenting with localized adenocarcinoma of the esophagus and esophagogastric junction.
  • Despite a paucity of Level 1 recommendations compared with other gastrointestinal sites, in particular rectal cancer, there is an emerging consensus in practice to consider multimodal approaches in all cases that present with T3 or node-positive disease.
  • [MeSH-major] Adenocarcinoma / therapy. Cardia. Esophageal Neoplasms / therapy. Stomach Neoplasms / therapy

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  • (PMID = 20676879.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
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64. Leers J, Bollschweiler E, Hölscher AH: [Symptoms in patients with adenocarcinoma of the esophagus]. Z Gastroenterol; 2005 Mar;43(3):275-80
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  • [Title] [Symptoms in patients with adenocarcinoma of the esophagus].
  • [Transliterated title] Refluxanamnese von Patienten mit Adenokarzinom der Speiseröhre.
  • INTRODUCTION: Gastroesophageal reflux (GER) is the main risk factor for the development of adenocarcinoma of the esophagus (AC).
  • In 21 % of the patients the reflux symptoms stopped (median) three years (range two months -- 30 years) before the diagnosis of the carcinoma.
  • Only 55 % of all patients had one or more esophago-gastroscopy examinations before the diagnosis of AC.
  • These patients showed significantly more often earlier tumour stages than those patients without an endoscopy before diagnosis.
  • CONCLUSIONS: 15 % of the patients with adenocarcinoma of the esophagus show no, and in addition 25 % only discrete, heartburn; 1. an endoscopy due to heartburn was done in half of all cases, and 2. the medications do not fulfil the therapeutic standard; 3.patients with endoscopy had significantly more frequently an earlier tumour stage.
  • [MeSH-major] Adenocarcinoma / diagnosis. Esophageal Neoplasms / diagnosis. Gastroesophageal Reflux / complications
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Alcohol Drinking. Barrett Esophagus / complications. Body Mass Index. Chi-Square Distribution. Confidence Intervals. Esophagectomy. Esophagoscopy. Female. Gastroscopy. Humans. Male. Middle Aged. Occupations. Prospective Studies. Risk Factors. Smoking / adverse effects. Surveys and Questionnaires. Time Factors

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  • (PMID = 15765300.001).
  • [ISSN] 0044-2771
  • [Journal-full-title] Zeitschrift für Gastroenterologie
  • [ISO-abbreviation] Z Gastroenterol
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Germany
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65. Paterson AL, Fitzgerald RC: Biomarkers in Barrett's oesophagus and oesophageal adenocarcinoma. Expert Opin Med Diagn; 2007 Nov;1(3):363-76

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  • [Title] Biomarkers in Barrett's oesophagus and oesophageal adenocarcinoma.
  • Barrett's oesophagus is a well-recognised premalignant lesion for oesophageal adenocarcinoma.
  • It is present in 1 - 2% of the general population, and 2 - 5% of those with gastro-oesophageal reflux disease.
  • The majority of Barrett's cases within the population are undiagnosed, consequently most cases of oesophageal adenocarcinoma arise de novo.
  • The incidence of oesophageal adenocarcinoma has increased by more than sixfold in the last 30 years.
  • However, most patients with Barrett's oesophagus will not develop oesophageal adenocarcinoma.
  • The major focus of biomarker research in Barrett's oesophagus is to find a marker that is able to identify patients at the highest risk of progressing to adenocarcinoma.
  • Other potential roles include increasing the sensitivity of minimally invasive screening tests to identify patients with Barrett's oesophagus and predicting which patients are most likely to benefit from chemoprevention and endoscopic therapies.
  • In established oesophageal adenocarcinoma, biomarkers would be able to individualise patient management by providing valuable information on patient prognosis and their suitability for novel targeted therapies.
  • This review aims to explore the potential roles of biomarkers in Barrett's oesophagus and oesophageal adenocarcinoma, focusing on the most extensively studied candidates and future novel developments.

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  • (PMID = 23489356.001).
  • [ISSN] 1753-0059
  • [Journal-full-title] Expert opinion on medical diagnostics
  • [ISO-abbreviation] Expert Opin Med Diagn
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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66. Quera R, O'Sullivan K, Quigley EM: Surveillance in Barrett's oesophagus: will a strategy focused on a high-risk group reduce mortality from oesophageal adenocarcinoma? Endoscopy; 2006 Feb;38(2):162-9
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  • [Title] Surveillance in Barrett's oesophagus: will a strategy focused on a high-risk group reduce mortality from oesophageal adenocarcinoma?
  • BACKGROUND AND STUDY AIMS: The incidence of oesophageal adenocarcinoma has increased significantly in recent years.
  • While surveillance of people with Barrett's oesophagus, its usual precursor, has been advocated in order to detect dysplasia and early cancer in those considered to be at greatest risk, the impact of such a strategy on survival from oesophageal adenocarcinoma is unclear.
  • This study aimed to determine the effect of surveillance on mortality from oesophageal adenocarcinoma in a group of patients considered to be at high risk of developing Barrett's oesophagus and adenocarcinoma.
  • PATIENTS AND METHODS: After performing a Medline search of the literature published between 1985 and 2004 for studies on gastro-oesophageal reflux disease, Barrett's oesophagus and adenocarcinoma, we examined the impact of surveillance on mortality from oesophageal adenocarcinoma in a hypothetical sample of 100 high-risk patients (men aged over 50 with Barrett's oesophagus but without high-grade dysplasia at entry).
  • RESULTS: Four patients in this high-risk group developed adenocarcinoma during surveillance, with survival rates of 78.9% (95%CI 64.9%-88.5%) at 2 years and 78.6% (95%CI 62.8%-89.2%) at 5 years.
  • Meanwhile, between 515 and 2060 patients with Barrett's oesophagus were not detected or surveyed by this strategy and between 16 and 61 of these developed adenocarcinoma, with much lower survival rates of 37.1% (95%CI 25.4%-50.3%) at 2 years and 16.7% (95%CI 9%-28.3%) at 5 years.
  • Although surveillance in the high-risk group resulted in the long-term survival of three patients who would not otherwise have survived, this gain was dramatically offset by the 13 to 51 patients, excluded from surveillance by this strategy, who died from oesophageal adenocarcinoma.
  • CONCLUSIONS: A surveillance programme based on current concepts of risk cannot have an impact on mortality from oesophageal adenocarcinoma.
  • To be effective, it will be necessary for surveillance programmes to utilise more precise methods for the identification of those who are most at risk of progression to adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / mortality. Barrett Esophagus / epidemiology. Esophageal Neoplasms / mortality. Population Surveillance. Precancerous Conditions / epidemiology

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  • (PMID = 16479424.001).
  • [ISSN] 0013-726X
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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67. Lagergren J: Controversies surrounding body mass, reflux, and risk of oesophageal adenocarcinoma. Lancet Oncol; 2006 Apr;7(4):347-9
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  • [Title] Controversies surrounding body mass, reflux, and risk of oesophageal adenocarcinoma.
  • At first the association between body mass, reflux, and oesophageal adenocarcinoma might seem easily interpreted, but a more thorough assessment of the published work shows that several factors are missing.
  • Reflux and obesity are established risk factors for oesophageal adenocarcinoma, particularly when they occur in combination.
  • However, the interplay between these and other factors with regard to oesophageal adenocarcinoma is uncertain.
  • Moreover, the contribution of these risk factors in explaining the increasing incidence of oesophageal adenocarcinoma is unclear, because the trends in prevalence of reflux and obesity do not match those of incidence of oesophageal adenocarcinoma.
  • Moreover, none of these factors contribute strongly to the striking predominance of oesophageal adenocarcinoma in men.
  • Thus, several factors that can explain the development of oesophageal adenocarcinoma need to be addressed.
  • [MeSH-major] Adenocarcinoma / etiology. Body Mass Index. Esophageal Neoplasms / etiology. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / etiology

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  • (PMID = 16574550.001).
  • [ISSN] 1470-2045
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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68. Lehmann K, Schneider PM: Differences in the molecular biology of adenocarcinoma of the esophagus, gastric cardia, and upper gastric third. Recent Results Cancer Res; 2010;182:65-72
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  • [Title] Differences in the molecular biology of adenocarcinoma of the esophagus, gastric cardia, and upper gastric third.
  • Adenocarcinoma of the distal esophagus, gastric cardia, and upper gastric third are grouped in type I-III by the Siewert classification.
  • [MeSH-major] Adenocarcinoma / genetics. Cardia. Esophageal Neoplasms / genetics. Stomach Neoplasms / genetics

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  • (PMID = 20676871.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
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69. Boult JK, Tanière P, Hallissey MT, Campbell MJ, Tselepis C: Oesophageal adenocarcinoma is associated with a deregulation in the MYC/MAX/MAD network. Br J Cancer; 2008 Jun 17;98(12):1985-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oesophageal adenocarcinoma is associated with a deregulation in the MYC/MAX/MAD network.
  • Oesophageal adenocarcinoma, which arises from an acquired columnar lesion, Barrett's metaplasia, is rising in incidence more rapidly than any other cancer in the Western world.
  • Elevated expression of c-MYC has been demonstrated in oesophageal adenocarcinoma; however, the expression of other members of the MYC/MAX/MAD network has not been addressed.
  • The aims of this work were to characterise the expression of c-MYC, MAX and the MAD family in adenocarcinoma development and assess the effects of overexpression on cellular behaviour. mRNA expression in samples of Barrett's metaplasia and oesophageal adenocarcinoma were examined by qRT-PCR.
  • Consistent with previous work expression of c-MYC was deregulated in oesophageal adenocarcinoma.
  • In conclusion, the expression patterns of c-MYC, MAX and the MAD family were shown to be deregulated in the oesophageal cancer model.
  • [MeSH-major] Adenocarcinoma / genetics. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / genetics. Esophageal Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Genes, myc. Repressor Proteins / genetics

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  • [Cites] Gut. 2005 Mar;54 Suppl 1:i1-5 [15711002.001]
  • [Cites] Oncogene. 1995 Jun 1;10(11):2195-205 [7784064.001]
  • [Cites] Int J Oncol. 2005 May;26(5):1369-75 [15809730.001]
  • [Cites] J Cell Biol. 2005 May 9;169(3):405-13 [15866886.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Apr 15;166(2):157-62 [16631473.001]
  • [Cites] Gut. 2006 Oct;55(10):1449-60 [16641131.001]
  • [Cites] Biomarkers. 2006 Nov-Dec;11(6):547-61 [17056474.001]
  • [Cites] Dis Esophagus. 2007;20(3):212-6 [17509117.001]
  • [Cites] Neoplasia. 2004 Sep-Oct;6(5):660-73 [15548375.001]
  • [Cites] Oncogene. 1999 Nov 18;18(48):6621-34 [10597267.001]
  • [Cites] Am J Pathol. 2000 Feb;156(2):555-66 [10666385.001]
  • [Cites] Curr Opin Genet Dev. 2000 Feb;10(1):100-5 [10679391.001]
  • [Cites] Cancer. 2000 Apr 1;88(7):1623-32 [10738221.001]
  • [Cites] Am J Respir Cell Mol Biol. 2000 Oct;23(4):560-5 [11017923.001]
  • [Cites] Annu Rev Cell Dev Biol. 2000;16:653-99 [11031250.001]
  • [Cites] Nucleic Acids Res. 2001 Jan 15;29(2):397-406 [11139609.001]
  • [Cites] Lancet. 2000 Dec 16;356(9247):2079-85 [11145505.001]
  • [Cites] Nucleic Acids Res. 1995 May 25;23(10):1686-90 [7784172.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Aug 29;92(18):8488-92 [7667316.001]
  • [Cites] Cancer Res. 1995 Nov 1;55(21):4800-3 [7585509.001]
  • [Cites] Nat Med. 1995 Jul;1(7):638-43 [7585143.001]
  • [Cites] EMBO J. 1995 Nov 15;14(22):5646-59 [8521822.001]
  • [Cites] Oncogene. 1995 Dec 21;11(12):2487-501 [8545105.001]
  • [Cites] Cancer Lett. 1996 Apr 19;102(1-2):73-6 [8603382.001]
  • [Cites] Br J Cancer. 1996 Jun;73(11):1347-55 [8645578.001]
  • [Cites] Curr Top Microbiol Immunol. 1997;224:149-58 [9308238.001]
  • [Cites] Cancer Res. 1997 Nov 1;57(21):4905-12 [9354456.001]
  • [Cites] Cancer Res. 1997 Dec 15;57(24):5571-8 [9407969.001]
  • [Cites] Oncogene. 1998 Feb 26;16(8):967-77 [9519870.001]
  • [Cites] Oncol Rep. 1998 Jan-Feb;5(1):213-6 [9458379.001]
  • [Cites] Mol Cell Biol. 1999 Jan;19(1):1-11 [9858526.001]
  • [Cites] EMBO J. 1999 Feb 1;18(3):717-26 [9927431.001]
  • [Cites] Mol Cell. 1999 May;3(5):565-77 [10360173.001]
  • [Cites] Oncogene. 1999 May 13;18(19):3004-16 [10378696.001]
  • [Cites] J Biol Chem. 1999 Oct 1;274(40):28794-802 [10497252.001]
  • [Cites] Nat Cell Biol. 2001 Jun;3(6):580-6 [11389443.001]
  • [Cites] Cancer. 2001 Aug 1;92(3):549-55 [11505399.001]
  • [Cites] Nat Rev Cancer. 2002 Oct;2(10):764-76 [12360279.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2002 Nov;14(11):1179-86 [12439111.001]
  • [Cites] Gut. 2003 Feb;52(2):174-80 [12524396.001]
  • [Cites] Anticancer Res. 2003 Jan-Feb;23(1A):161-5 [12680208.001]
  • [Cites] Gut. 2003 May;52(5):623-8 [12692043.001]
  • [Cites] Ann Oncol. 2003;14 Suppl 5:v61-118 [14684501.001]
  • [Cites] Gut. 2004 Aug;53(8):1070-4 [15247170.001]
  • [Cites] Clin Exp Rheumatol. 1990 Mar-Apr;8(2):145-50 [1692520.001]
  • [Cites] Science. 1991 Mar 8;251(4998):1211-7 [2006410.001]
  • [Cites] Oncogene. 1992 Apr;7(4):775-9 [1565473.001]
  • [Cites] J Pathol. 1992 Mar;166(3):225-33 [1381423.001]
  • [Cites] Cell. 1993 Jan 29;72(2):211-22 [8425218.001]
  • [Cites] Cell. 1993 Jan 29;72(2):223-32 [8425219.001]
  • [Cites] Oncogene. 1994 Apr;9(4):1247-52 [8134128.001]
  • [Cites] J Cell Biol. 1995 Mar;128(6):1197-208 [7896882.001]
  • [Cites] Scand J Gastroenterol. 2004 Dec;39(12):1175-9 [15742992.001]
  • (PMID = 18493233.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / MAX protein, human; 0 / MXD1 protein, human; 0 / Repressor Proteins
  • [Other-IDs] NLM/ PMC2441969
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70. Westerterp M, Sloof GW, Hoekstra OS, Ten Kate FJ, Meijer GA, Reitsma JB, Boellaard R, van Lanschot JJ, Molthoff CF: 18FDG uptake in oesophageal adenocarcinoma: linking biology and outcome. J Cancer Res Clin Oncol; 2008 Feb;134(2):227-36
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  • [Title] 18FDG uptake in oesophageal adenocarcinoma: linking biology and outcome.
  • PURPOSE: Variable uptake of 18FDG has been noticed in positron emission tomography (PET) studies of patients with oesophageal adenocarcinoma.
  • The aim of the present study was to investigate biological parameters involved in 18FDG uptake in oesophageal adenocarcinoma for selection of patients with increased 18FDG uptake and prediction of prognostic value of 18FDG PET.
  • PATIENTS AND METHODS: Preoperative PET scans were performed in 26 patients with histologically proven oesophageal adenocarcinoma.
  • CONCLUSIONS: Glut-1 expression and tumour size seem parameters associated with 18FDG uptake in patients with biopsy proven oesophageal adenocarcinoma, and may be used to select oesophageal cancer patients in whom 18FDG-PET is of diagnostic value and may predict disease outcome.
  • [MeSH-major] Adenocarcinoma / metabolism. Esophageal Neoplasms / metabolism. Fluorodeoxyglucose F18 / pharmacokinetics. Radiopharmaceuticals / pharmacokinetics
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Esophagectomy. Esophagogastric Junction / diagnostic imaging. Female. Follow-Up Studies. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Positron-Emission Tomography. Preoperative Care. Tissue Array Analysis. Tissue Distribution. Treatment Outcome

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  • [Cites] Eur J Nucl Med. 2001 Dec;28(12 ):1845-9 [11734925.001]
  • [Cites] Eur J Nucl Med. 1999 Jun;26(6):599-605 [10369945.001]
  • [Cites] Anticancer Res. 2003 Jul-Aug;23 (4):3263-72 [12926062.001]
  • [Cites] J Nucl Med. 2004 Sep;45(9):1519-27 [15347719.001]
  • [Cites] Langenbecks Arch Surg. 2004 Aug;389(4):283-8 [15197549.001]
  • [Cites] AJR Am J Roentgenol. 2005 Aug;185(2):436-40 [16037517.001]
  • [Cites] Cancer. 1998 Sep 1;83(5):918-24 [9731895.001]
  • [Cites] Biochem Biophys Res Commun. 1990 Jul 16;170(1):223-30 [2372287.001]
  • [Cites] J Nucl Med. 2001 Jan;42(1):9-16 [11197987.001]
  • [Cites] J Nucl Med. 2004 Jun;45(6):930-2 [15181126.001]
  • [Cites] J Clin Oncol. 2004 Sep 15;22(18):3805-12 [15365078.001]
  • [Cites] J Clin Oncol. 2000 Sep 15;18(18):3202-10 [10986052.001]
  • [Cites] Arch Otolaryngol Head Neck Surg. 2004 Dec;130(12 ):1361-7 [15611393.001]
  • [Cites] J Nucl Med. 1991 Aug;32(8):1508-12 [1869970.001]
  • [Cites] Clin Radiol. 1998 Sep;53(9):659-65 [9766719.001]
  • [Cites] J Bone Joint Surg Am. 2004 Dec;86-A(12 ):2677-85 [15590853.001]
  • [Cites] J Gastrointest Surg. 2005 Jan;9(1):54-61 [15623445.001]
  • [Cites] Ann Surg. 2005 Feb;241(2):286-94 [15650639.001]
  • [Cites] Nuklearmedizin. 2003 Jun;42(3):90-3 [12802470.001]
  • [Cites] J Clin Oncol. 2006 Oct 10;24(29):4692-8 [16966684.001]
  • [Cites] Neurology. 1982 Dec;32(12 ):1323-9 [6983044.001]
  • [Cites] Cancer. 1988 May 1;61(9):1776-81 [3355975.001]
  • [Cites] Ann Thorac Surg. 2006 Aug;82(2):391-4; discussion 394-5 [16863735.001]
  • [Cites] Ann Thorac Surg. 1999 Oct;68(4):1133-6; discussion 1136-7 [10543468.001]
  • [Cites] Cancer. 1998 Jun 1;82(11):2227-34 [9610703.001]
  • [Cites] Am J Physiol. 1980 Jan;238(1):E69-82 [6965568.001]
  • [Cites] J Cell Physiol. 2005 Mar;202(3):654-62 [15389572.001]
  • [Cites] Br J Cancer. 2004 Jan 12;90(1):224-9 [14710233.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2005 Mar;32(3):294-301 [15791438.001]
  • [Cites] J Biol Chem. 1997 Sep 5;272(36):22776-80 [9278438.001]
  • [Cites] Eur J Nucl Med. 2000 Dec;27(12):1778-85 [24578007.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2004 Jun;31 Suppl 1:S80-7 [15127240.001]
  • [Cites] J Nucl Med. 2002 Jan;43(1):39-45 [11801701.001]
  • [Cites] Ann Thorac Surg. 2006 Mar;81(3):1076-81 [16488726.001]
  • [Cites] Cancer Res. 1999 Sep 15;59(18):4709-14 [10493529.001]
  • [Cites] J Surg Oncol. 2004 Aug 1;87(2):95-104 [15282704.001]
  • [Cites] Eur J Nucl Med. 2001 Nov;28(11):1690-6 [11702112.001]
  • [Cites] J Nucl Med. 2004 Oct;45(10 ):1632-9 [15471826.001]
  • [Cites] J Nucl Med. 2004 Nov;45(11):1843-50 [15534053.001]
  • [Cites] J Nucl Med. 1996 Jun;37(6):1042-7 [8683298.001]
  • [Cites] Hepatogastroenterology. 2005 Mar-Apr;52(62):486-90 [15816463.001]
  • [Cites] J Clin Oncol. 1999 Oct;17 (10 ):3201-6 [10506619.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Jan;90(1):328-34 [15509640.001]
  • [Cites] Radiology. 2003 Jun;227(3):764-70 [12773680.001]
  • [Cites] Br J Cancer. 2002 May 6;86(9):1391-5 [11986769.001]
  • [Cites] J Clin Oncol. 2002 Jan 15;20(2):379-87 [11786564.001]
  • [Cites] Eur J Nucl Med. 1998 Oct;25(10 ):1429-34 [9818284.001]
  • [Cites] J Nucl Med. 1995 Oct;36(10 ):1836-9 [7562051.001]
  • [Cites] J Nucl Med. 2002 Feb;43(2):173-80 [11850481.001]
  • [Cites] J Nucl Med. 1993 Mar;34(3):414-9 [8441032.001]
  • [Cites] Clin Cancer Res. 2002 Nov;8(11):3315-23 [12429617.001]
  • [Cites] Clin Nucl Med. 2000 Nov;25(11):882-7 [11079584.001]
  • [Cites] Biol Res. 2002;35(1):9-26 [12125211.001]
  • [Cites] Br J Biomed Sci. 2000;57(2):170-8 [10912295.001]
  • [Cites] J Nucl Med. 1997 Oct;38(10 ):1614-23 [9379202.001]
  • [Cites] Eur J Cardiothorac Surg. 2000 Oct;18(4):425-8 [11024379.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2007 Mar;34(3):392-404 [17033848.001]
  • [Cites] Surg Oncol. 2001 Nov;10(3):81-90 [11750227.001]
  • (PMID = 17653575.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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71. Tuynman JB, Buskens CJ, Kemper K, ten Kate FJ, Offerhaus GJ, Richel DJ, van Lanschot JJ: Neoadjuvant selective COX-2 inhibition down-regulates important oncogenic pathways in patients with esophageal adenocarcinoma. Ann Surg; 2005 Dec;242(6):840-9, discussion 849-50
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  • [Title] Neoadjuvant selective COX-2 inhibition down-regulates important oncogenic pathways in patients with esophageal adenocarcinoma.
  • OBJECTIVES: To evaluate the effects of neoadjuvant therapy with the selective cyclooxygenase-2 (COX-2) inhibitor celecoxib in vitro and in patients with esophageal adenocarcinoma on COX-2 and MET expression.
  • SUMMARY BACKGROUND DATA: High COX-2 and/or MET expression levels are negative prognostic factors for adenocarcinoma of the esophagus.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors exert anticancer mechanisms as is evident from epidemiologic studies and from experimental models for esophageal cancer.
  • The mechanisms and the significance of these findings in patients with adenocarcinoma of the esophagus are unknown.
  • METHODS: Esophageal adenocarcinoma cell lines were used to asses the effects in vitro.
  • To study the clinical effects 12 patients with esophageal adenocarcinoma were included for neoadjuvant treatment (4 weeks) with celecoxib at 400 mg twice daily.
  • CONCLUSIONS: This is the first study to show in vitro and in patients with esophageal adenocarcinoma that selective COX-2 inhibition down-regulates COX-2 and MET expression, both important proteins involved in cancer progression and dissemination.
  • Therefore, (neo)adjuvant therapy with celecoxib might have clinical potential for patients with esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cyclooxygenase Inhibitors / pharmacology. Cyclooxygenase Inhibitors / therapeutic use. Esophageal Neoplasms / drug therapy. Pyrazoles / pharmacology. Pyrazoles / therapeutic use. Sulfonamides / pharmacology. Sulfonamides / therapeutic use

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  • [Cites] Gut. 1999 Dec;45(6):822-8 [10562579.001]
  • [Cites] Nature. 2005 Mar 17;434(7031):396-400 [15772665.001]
  • [Cites] Cancer Res. 2000 Oct 15;60(20):5767-72 [11059772.001]
  • [Cites] Br J Surg. 2001 Mar;88(3):338-56 [11260097.001]
  • [Cites] Am J Gastroenterol. 2001 Apr;96(4):990-6 [11316217.001]
  • [Cites] Cancer Res. 2001 Aug 1;61(15):5911-8 [11479233.001]
  • [Cites] Clin Cancer Res. 2001 Nov;7(11):3519-25 [11705871.001]
  • [Cites] Int J Cancer. 2002 Mar 1;98(1):8-13 [11857377.001]
  • [Cites] Am J Pathol. 2002 Mar;160(3):963-72 [11891194.001]
  • [Cites] Hepatology. 2002 May;35(5):1117-24 [11981761.001]
  • [Cites] Nat Rev Cancer. 2002 Apr;2(4):289-300 [12001990.001]
  • [Cites] Gastroenterology. 2002 Jun;122(7):1800-7 [12055587.001]
  • [Cites] Gastroenterology. 2002 Jul;123(1):60-7 [12105834.001]
  • [Cites] Eur J Clin Invest. 2002 Nov;32(11):838-46 [12423325.001]
  • [Cites] N Engl J Med. 2002 Nov 21;347(21):1662-9 [12444180.001]
  • [Cites] Gastroenterology. 2003 Jan;124(1):246-8 [12512047.001]
  • [Cites] Neurosci Lett. 2003 Mar 13;339(1):62-6 [12618301.001]
  • [Cites] FASEB J. 2003 Sep;17(12):1640-7 [12958170.001]
  • [Cites] N Engl J Med. 2003 Dec 4;349(23):2241-52 [14657432.001]
  • [Cites] Cancer Res. 2003 Dec 1;63(23):8351-9 [14678996.001]
  • [Cites] Nat Rev Mol Cell Biol. 2003 Dec;4(12):915-25 [14685170.001]
  • [Cites] J Surg Res. 2004 Mar;117(1):44-51 [15013713.001]
  • [Cites] Clin Cancer Res. 2004 May 1;10(9):3069-75 [15131045.001]
  • [Cites] J Surg Res. 2004 Jun 15;119(2):143-8 [15145696.001]
  • [Cites] Cancer Cell. 2004 Jul;6(1):5-6 [15261136.001]
  • [Cites] Cancer Cell. 2004 Jul;6(1):61-73 [15261142.001]
  • [Cites] Oncogene. 2004 Aug 19;23(37):6199-208 [15221009.001]
  • [Cites] Carcinogenesis. 2004 Oct;25(10):1945-52 [15155531.001]
  • [Cites] Crit Rev Oncol Hematol. 2004 Nov;52(2):81-101 [15501074.001]
  • [Cites] J Immunol Methods. 1983 Dec 16;65(1-2):55-63 [6606682.001]
  • [Cites] Br J Cancer. 1997;75(2):258-63 [9010035.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 1998;38:97-120 [9597150.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):7962-70 [15520203.001]
  • [Cites] Int J Cancer. 2005 Feb 10;113(4):678-82 [15455388.001]
  • [Cites] Lancet. 2004 Dec 4-10;364(9450):2021-9 [15582059.001]
  • [Cites] Crit Rev Oncol Hematol. 2005 Jan;53(1):35-69 [15607934.001]
  • [Cites] Carcinogenesis. 2005 Mar;26(3):565-70 [15564290.001]
  • [Cites] J Am Coll Surg. 2000 May;190(5):562-72; discussion 572-3 [10801023.001]
  • (PMID = 16327494.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; JCX84Q7J1L / Celecoxib
  • [Other-IDs] NLM/ PMC1409886
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72. Desai HG, Kamani PM: Factors responsible for the increasing incidence of oesophageal adenocarcinoma. J Assoc Physicians India; 2007 Jun;55:435-7
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  • [Title] Factors responsible for the increasing incidence of oesophageal adenocarcinoma.
  • Amongst white population of developed countries, the prevalence of oesophageal adenocarcinoma has dramatically increased during the last four decades.
  • During this period, the increased damage to the oesophageal mucosa with gastroesophageal reflux could result from increased acid output (due to absence of Helicobacter pylori in the gastric mucosa with excellent sanitation) and/or increased frequency of reflux due to an "epidemic" of overweight (65% of the population).
  • The most important environmental factors, responsible for the fastest increasing cancer in humans, are discussed.
  • [MeSH-major] Adenocarcinoma / epidemiology. Esophageal Neoplasms / epidemiology. Global Health. Helicobacter Infections / epidemiology

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  • (PMID = 17879499.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Number-of-references] 51
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73. Schauer M, Janssen KP, Rimkus C, Raggi M, Feith M, Friess H, Theisen J: Microarray-based response prediction in esophageal adenocarcinoma. Clin Cancer Res; 2010 Jan 1;16(1):330-7
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  • [Title] Microarray-based response prediction in esophageal adenocarcinoma.
  • PURPOSE: In locally advanced (uT(3), N(+)) adenocarcinomas of the esophagus, neoadjuvant chemotherapy improves patient outcome.
  • EXPERIMENTAL DESIGN: Biopsies of 47 patients with locally advanced (uT(3), N(+)) adenocarcinoma of the esophagus were obtained during primary staging.
  • All patients underwent neoadjuvant chemotherapy with cisplatin, 5-fluorouracil, and leucovorin and subsequent resection of the esophagus.
  • RESULTS: A total of 86 genes were at least 2-fold differentially regulated comparing responding with nonresponding adenocarcinomas of the esophagus.
  • CONCLUSIONS: There were significant differences in the gene profile between patients with adenocarcinoma of the esophagus responding to neoadjuvant chemotherapy compared with nonresponding patients.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / genetics. Neoadjuvant Therapy. Tissue Array Analysis

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  • (PMID = 20028767.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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74. Liu JF, Jamieson GG, Wu TC, Zhu GJ, Drew PA: A preliminary study on the postoperative survival of patients given aspirin after resection for squamous cell carcinoma of the esophagus or adenocarcinoma of the cardia. Ann Surg Oncol; 2009 May;16(5):1397-402
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  • [Title] A preliminary study on the postoperative survival of patients given aspirin after resection for squamous cell carcinoma of the esophagus or adenocarcinoma of the cardia.
  • BACKGROUND: We examined the effect of aspirin on survival following resection for squamous cell carcinoma (SCC) of the esophagus or adenocarcinoma of the gastric cardia.
  • There was a significant improvement in survival for patients with adenocarcinoma of the cardia on aspirin compared with the two control groups combined (P = 0.029).
  • However, there was no significant difference between the survival curves for T2N0M0 adenocarcinoma patients on aspirin (21) and the two control groups combined (65) (P = 0.29).
  • [MeSH-major] Adenocarcinoma / drug therapy. Aspirin / administration & dosage. Carcinoma, Squamous Cell / drug therapy. Cyclooxygenase 2 Inhibitors / administration & dosage. Esophageal Neoplasms / drug therapy. Stomach Neoplasms / drug therapy

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  • (PMID = 19241108.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin; R16CO5Y76E / Aspirin; U3P01618RT / Fluorouracil
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75. Lukić M, Segec A, Segeca I, Pinotić L, Pinotić K, Atalić B, Solić K, Vcev A: The role of the nutrition in the pathogenesis of gastroesophageal reflux disease, Barrett's oesophagus and oesophageal adenocarcinoma. Coll Antropol; 2010 Sep;34(3):905-9
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  • [Title] The role of the nutrition in the pathogenesis of gastroesophageal reflux disease, Barrett's oesophagus and oesophageal adenocarcinoma.
  • This paper aims at evaluating the role of improper nutrition in the pathogenesis of gastroesophageal reflux disease (GERD), Barrett's oesophagus (BE), and oesophageal adenocarcinoma (EADC).
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / etiology. Esophageal Neoplasms / etiology. Gastroesophageal Reflux / etiology. Nutritional Physiological Phenomena


76. Chak A, Faulx A, Eng C, Grady W, Kinnard M, Ochs-Balcom H, Falk G: Gastroesophageal reflux symptoms in patients with adenocarcinoma of the esophagus or cardia. Cancer; 2006 Nov 1;107(9):2160-6
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  • [Title] Gastroesophageal reflux symptoms in patients with adenocarcinoma of the esophagus or cardia.
  • BACKGROUND: The efficacy of endoscopic screening for chronic gastroesophageal reflux symptoms of heartburn and regurgitation in adult subjects depends on the sensitivity of this strategy for detecting Barrett esophagus in subjects before the development of adenocarcinoma of the esophagus or cardia.
  • The aim of the current study was to determine what proportion of patients with cancer of the esophagus or cardia would have been candidates for a screening endoscopy before their cancer diagnosis based on the presence and duration of preceding reflux symptoms.
  • METHODS: All patients with adenocarcinoma of the esophagus, adenocarcinoma of the cardia, or long-segment Barrett esophagus presenting for endoscopy at 4 tertiary care and 2 Veterans Affairs (VA) hospitals were given a previously validated questionnaire to determine their recall of common gastroesophageal reflux symptoms.
  • Only 67 of 110 patients (61%) with adenocarcinoma of the esophagus and 8 of 21 patients (38%) with adenocarcinoma of the cardia recalled symptoms of heartburn or regurgitation being present for >5 years before their diagnosis of cancer.
  • Only 40 of 110 patients (36%) with adenocarcinoma of the esophagus and 5 of 21 patients (24%) with adenocarcinoma of the cardia recalled weekly symptoms being present for >5 years before their cancer diagnosis.
  • Of the 244 patients with Barrett esophagus, 170 (70%) recalled heartburn or regurgitation for >5 years and 89 patients (37%) recalled weekly symptoms for >5 years.
  • CONCLUSIONS: Current practice, which uses a screening strategy of performing endoscopy in patients with >5 years of heartburn or regurgitation, can detect Barrett epithelium in only a limited proportion of those patients at risk for developing adenocarcinoma of the esophagus or adenocarcinoma of the cardia.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Cardia / pathology. Esophageal Neoplasms / diagnosis. Gastroesophageal Reflux / diagnosis. Stomach Neoplasms / diagnosis

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  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 17019737.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK002800; United States / NIDDK NIH HHS / DK / DK061426; United States / NIDDK NIH HHS / DK / DK070863
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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77. Van Blankenstein M, Looman CW, Kruijshaar ME, Siersema PD, Kuipers EJ, Bytzer P: Modelling a population with Barrett's oesophagus from oesophageal adenocarcinoma incidence data. Scand J Gastroenterol; 2007 Mar;42(3):308-17
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  • [Title] Modelling a population with Barrett's oesophagus from oesophageal adenocarcinoma incidence data.
  • OBJECTIVE: A recent study of adenocarcinoma of the oesophagus (ACO) incidence rates in Denmark showed a steep fall in the over-80 population, interpreted as the result of a decline in the prevalence of Barrett's oesophagus (BO) in this age group, for which three hypotheses were advanced: the specific mortality from ACO and, superimposed, either excess mortality from causes of death unrelated to ACO or a birth cohort effect.
  • [MeSH-major] Adenocarcinoma / epidemiology. Barrett Esophagus / epidemiology. Esophageal Neoplasms / epidemiology. Models, Statistical

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  • (PMID = 17354109.001).
  • [ISSN] 0036-5521
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Norway
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78. Rubenstein JH, Vakil N, Inadomi JM: The cost-effectiveness of biomarkers for predicting the development of oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2005 Jul 15;22(2):135-46
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  • [Title] The cost-effectiveness of biomarkers for predicting the development of oesophageal adenocarcinoma.
  • BACKGROUND: The recommended surveillance strategy for oesophageal adenocarcinoma may prevent as few as 50% of cancer deaths.
  • The population consisted of 50-year-old Caucasian men with gastro-oesophageal reflux, who were monitored until age 80.
  • CONCLUSIONS: Biomarkers predicting the development of oesophageal adenocarcinoma would need to be fairly accurate and inexpensive to be cost-effective.
  • These results should guide the development of biomarkers for oesophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Biomarkers / blood. Esophageal Neoplasms / diagnosis

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  • (PMID = 16011672.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 1 T32 DK062708
  • [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 / Biomarkers
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79. Lagarde SM, Reitsma JB, Ten Kate FJ, Busch OR, Obertop H, Zwinderman AH, Moons J, van Lanschot JJ, Lerut T: Predicting individual survival after potentially curative esophagectomy for adenocarcinoma of the esophagus or gastroesophageal junction. Ann Surg; 2008 Dec;248(6):1006-13
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  • [Title] Predicting individual survival after potentially curative esophagectomy for adenocarcinoma of the esophagus or gastroesophageal junction.
  • INTRODUCTION: Even after potentially curative esophagectomy, the majority of patients with adenocarcinoma of the esophagus or gastroesophageal junction die due to cancer recurrence.
  • The median esophageal cancer-specific survival was 38 months.
  • [MeSH-major] Adenocarcinoma / mortality. Esophageal Neoplasms / mortality. Esophagectomy / mortality. Esophagogastric Junction. Nomograms

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  • (PMID = 19092345.001).
  • [ISSN] 1528-1140
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
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80. Onwuegbusi BA, Rees JR, Lao-Sirieix P, Fitzgerald RC: Selective loss of TGFbeta Smad-dependent signalling prevents cell cycle arrest and promotes invasion in oesophageal adenocarcinoma cell lines. PLoS One; 2007 Jan 31;2(1):e177
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  • [Title] Selective loss of TGFbeta Smad-dependent signalling prevents cell cycle arrest and promotes invasion in oesophageal adenocarcinoma cell lines.
  • In cancer, Transforming Growth Factor beta (TGFbeta) increases proliferation and promotes invasion via selective loss of signalling pathways.
  • Oesophageal adenocarcinoma arises from Barrett's oesophagus, progresses rapidly and is usually fatal.
  • We therefore investigated the role of TGFbeta in Barrett's associated oesophageal adenocarcinoma using a panel of cell lines (OE33, TE7, SEG, BIC, FLO).
  • 4/5 adenocarcinoma cell lines failed to cell cycle arrest, down-regulate c-Myc or induce p21 in response to TGFbeta, and modulation of a Smad3/4 specific promoter was inhibited.
  • These hyperproliferative adenocarcinoma cell lines displayed a TGFbeta induced increase in the expression of the extracellular matrix degrading proteinases, urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor 1 (PAI-1), which correlated with an invasive cell phenotype as measured by in vitro migration, invasion and cell scattering assays.
  • These data would support a dual role for TGFbeta in oesophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Signal Transduction / physiology. Smad3 Protein / metabolism. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Barrett Esophagus / complications. Cell Cycle / physiology. Cell Line, Tumor. Cell Proliferation. Enzyme Activation. Enzyme Inhibitors / metabolism. Extracellular Matrix / metabolism. Extracellular Signal-Regulated MAP Kinases / genetics. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression Regulation. Humans. JNK Mitogen-Activated Protein Kinases / genetics. JNK Mitogen-Activated Protein Kinases / metabolism. Neoplasm Invasiveness. Phosphatidylinositol 3-Kinases / genetics. Phosphatidylinositol 3-Kinases / metabolism. Transcription, Genetic

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  • [Cites] J Cell Physiol. 2000 Feb;182(2):269-80 [10623891.001]
  • [Cites] Gut. 2006 Jun;55(6):764-74 [16368780.001]
  • [Cites] Nat Cell Biol. 2001 Apr;3(4):400-8 [11283614.001]
  • [Cites] Ann Surg. 2001 Aug;234(2):172-80 [11505062.001]
  • [Cites] Trends Cell Biol. 2001 Nov;11(11):S44-51 [11684442.001]
  • [Cites] J Cell Sci. 2001 Nov;114(Pt 21):3905-14 [11719557.001]
  • [Cites] Am J Pathol. 2002 Jan;160(1):237-46 [11786417.001]
  • [Cites] J Biol Chem. 2002 Feb 1;277(5):3150-7 [11689575.001]
  • [Cites] Clin Cancer Res. 2002 Feb;8(2):314-46 [11839647.001]
  • [Cites] Biochem Soc Trans. 2002 Apr;30(2):207-10 [12023852.001]
  • [Cites] EMBO J. 2002 Jul 15;21(14):3749-59 [12110587.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):391-401 [12538493.001]
  • [Cites] J Biol Chem. 2003 Feb 21;278(8):5941-6 [12493778.001]
  • [Cites] Nature. 2003 Oct 9;425(6958):577-84 [14534577.001]
  • [Cites] Oncogene. 2004 Aug 5;23(35):5978-85 [15184866.001]
  • [Cites] Surgery. 2004 Aug;136(2):310-6 [15300196.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2438-42 [2871553.001]
  • [Cites] J Biol Chem. 1991 Jan 15;266(2):1092-100 [1985937.001]
  • [Cites] Oncogene. 1991 Sep;6(9):1583-92 [1923525.001]
  • [Cites] J Biol Chem. 1991 Dec 5;266(34):23048-52 [1744101.001]
  • [Cites] J Biol Chem. 1992 Mar 15;267(8):5029-31 [1544886.001]
  • [Cites] Cancer. 1994 Apr 1;73(7):1785-94 [7907940.001]
  • [Cites] J Biol Chem. 1995 Mar 31;270(13):7117-24 [7706248.001]
  • [Cites] J Biol Chem. 1995 Sep 29;270(39):23007-12 [7559439.001]
  • [Cites] Br J Surg. 1996 Aug;83(8):1152-5 [8869332.001]
  • [Cites] Eur J Biochem. 1996 Oct 15;241(2):393-402 [8917435.001]
  • [Cites] Int J Cancer. 1997 Jul 3;72(1):1-22 [9212216.001]
  • [Cites] Genes Dev. 1997 Dec 1;11(23):3157-67 [9389648.001]
  • [Cites] Am J Pathol. 1998 Jan;152(1):135-44 [9422531.001]
  • [Cites] Int J Cancer. 1998 Mar 2;75(5):721-30 [9495240.001]
  • [Cites] Nat Med. 1998 Aug;4(8):923-8 [9701244.001]
  • [Cites] Nature. 1998 Aug 27;394(6696):909-13 [9732876.001]
  • [Cites] Clin Exp Metastasis. 1999 Feb;17(1):77-85 [10390151.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4782-8 [15930298.001]
  • [Cites] Int J Cancer. 2000 Feb 1;85(3):407-15 [10652434.001]
  • (PMID = 17264880.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Smad3 Protein; 0 / Transforming Growth Factor beta; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1766472
  • [General-notes] NLM/ Original DateCompleted: 20070723
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81. Kaijser M, Akre O, Cnattingius S, Ekbom A: Preterm birth, low birth weight, and risk for esophageal adenocarcinoma. Gastroenterology; 2005 Mar;128(3):607-9
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  • [Title] Preterm birth, low birth weight, and risk for esophageal adenocarcinoma.
  • BACKGROUND & AIMS: Gastroesophageal reflux is common among preterm infants and those who are small for gestational age, and it is a strong risk factor for adenocarcinoma of the esophagus.
  • METHODS: In a cohort of 3364 individuals born preterm and/or small for gestational age between 1925 and 1949, we assessed the long-term risk for esophageal cancer.
  • RESULTS: The standardized incidence rate ratio for esophageal adenocarcinoma was increased more than 7-fold in the cohort (standardized incidence rate ratio, 7.27; 95% confidence interval, 1.98-18.62), and a birth weight <2000 g was associated with a more than 11-fold increase in risk (standardized incidence rate ratio, 11.5; 95% confidence interval, 1.39-41.5).
  • [MeSH-major] Adenocarcinoma / etiology. Esophageal Neoplasms / etiology. Infant, Low Birth Weight. Premature Birth / complications

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  • (PMID = 15765396.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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82. Van Soest EM, Dieleman JP, Sturkenboom MC, Siersema PD, Kuipers EJ: Gastro-oesophageal reflux, medical resource utilization and upper gastrointestinal endoscopy in patients at risk of oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2008 Jul;28(1):137-43
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  • [Title] Gastro-oesophageal reflux, medical resource utilization and upper gastrointestinal endoscopy in patients at risk of oesophageal adenocarcinoma.
  • BACKGROUND: Early identification of patients at risk of oesophageal adenocarcinoma (OAC) might improve survival.
  • AIM: To assess the medical resource utilization in the 3 years before OAC diagnosis as potential markers for early identification and intervention.
  • CONCLUSIONS: Only a minority of all OAC patients used acid inhibitors before diagnosis.
  • The use of medical care between cases and controls differed only in the final year before OAC diagnosis.
  • [MeSH-major] Adenocarcinoma / mortality. Endoscopy, Gastrointestinal / utilization. Esophageal Neoplasms / mortality. Gastroesophageal Reflux / mortality. Resource Allocation / trends
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Barrett Esophagus / diagnosis. Barrett Esophagus / mortality. Case-Control Studies. Female. Humans. Male. Middle Aged. Risk Factors. Survival Rate

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  • (PMID = 18373635.001).
  • [ISSN] 1365-2036
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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83. Rubenstein JH, Taylor JB: Meta-analysis: the association of oesophageal adenocarcinoma with symptoms of gastro-oesophageal reflux. Aliment Pharmacol Ther; 2010 Nov;32(10):1222-7
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  • [Title] Meta-analysis: the association of oesophageal adenocarcinoma with symptoms of gastro-oesophageal reflux.
  • BACKGROUND: Endoscopic screening has been proposed for patients with symptoms of gastro-oesophageal reflux disease (GERD) in the hope of reducing mortality from oesophageal adenocarcinoma.
  • Assessing the net benefits of such a strategy requires a precise understanding of the cancer risk in the screened population.
  • AIM: To estimate precisely the association between symptoms of GERD and oesophageal adenocarcinoma.
  • At least weekly symptoms of GERD increased the odds of oesophageal adenocarcinoma fivefold (odds ratio = 4.92; 95% confidence interval = 3.90, 6.22), and daily symptoms increased the odds sevenfold (random effects summary odds ratio = 7.40, 95% confidence interval = 4.94, 11.1), each compared with individuals without symptoms or less frequent symptoms.
  • Duration of symptoms was also associated with oesophageal adenocarcinoma, but with very heterogeneous results, and unclear thresholds.
  • CONCLUSIONS: Frequent GERD symptoms are strongly associated with oesophageal adenocarcinoma.
  • These results should be useful in developing epidemiological models of the development of oesophageal adenocarcinoma, and in models of interventions aimed at reducing mortality from this cancer.

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  • [Copyright] Published 2010. This article is a US Government work and is in the public domain in the USA.
  • [Cites] Cancer Causes Control. 2000 Mar;11(3):231-8 [10782657.001]
  • [Cites] Gastroenterology. 2010 Jul;139(1):204-12.e3 [20403354.001]
  • [Cites] Am J Gastroenterol. 2002 Aug;97(8):1888-95 [12190150.001]
  • [Cites] Cancer. 2003 Sep 1;98(5):940-8 [12942560.001]
  • [Cites] JAMA. 1995 Aug 9;274(6):474-7 [7629956.001]
  • [Cites] J Natl Cancer Inst. 1998 Jan 21;90(2):150-5 [9450576.001]
  • [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] Can J Gastroenterol. 2005 Jan;19(1):15-35 [15685294.001]
  • [Cites] Gastroenterology. 2005 May;128(5):1471-505 [15887129.001]
  • [Cites] BMC Med Res Methodol. 2006;6:50 [17038197.001]
  • [Cites] World J Gastroenterol. 2007 Mar 14;13(10):1585-94 [17461453.001]
  • [Cites] Am J Gastroenterol. 2007 Aug;102(8):1596-602 [17459024.001]
  • [Cites] Gut. 2008 Feb;57(2):173-80 [17932103.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Feb;17(2):352-8 [18268119.001]
  • [Cites] Gut. 2008 Apr;57(4):448-54 [18178609.001]
  • [Cites] Am J Gastroenterol. 2008 Mar;103(3):788-97 [18341497.001]
  • [Cites] Br J Cancer. 2009 Mar 10;100(5):795-8 [19190630.001]
  • [Cites] Cancer Epidemiol. 2009 Jul;33(1):37-40 [19679045.001]
  • [Cites] Gut. 2009 Dec;58(12):1583-9 [19570765.001]
  • [Cites] Cancer. 2001 Aug 1;92(3):549-55 [11505399.001]
  • (PMID = 20955441.001).
  • [ISSN] 1365-2036
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K23 DK079291; United States / NIDDK NIH HHS / DK / K23DK079291
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS411964; NLM/ PMC3481544
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84. Lagergren J, Jansson C: Sex hormones and oesophageal adenocarcinoma: influence of childbearing? Br J Cancer; 2005 Oct 17;93(8):859-61
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  • [Title] Sex hormones and oesophageal adenocarcinoma: influence of childbearing?
  • The male predominance of oesophageal adenocarcinoma might be explained by oestrogen protection in women.
  • The influence of childbearing on the risk of oesophageal adenocarcinoma was investigated in a Swedish population-based case (n=63) -control (n=141) study.
  • In conclusion, we found no inverse association between childbearing and oesophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / physiopathology. Esophageal Neoplasms / physiopathology. Estrogens / physiology. Infertility, Female / complications

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  • [Cites] Br J Cancer. 2000 Jul;83(1):127-32 [10883680.001]
  • [Cites] Anticancer Res. 2002 May-Jun;22(3):1459-61 [12168823.001]
  • [Cites] Gut. 2005 Mar;54 Suppl 1:i1-5 [15711002.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] Clin Gastroenterol Hepatol. 2005 Jan;3(1):1-10 [15645398.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Oct;7(10):913-5 [9796637.001]
  • (PMID = 16189516.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Estrogens
  • [Other-IDs] NLM/ PMC2361653
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85. Fitzgerald RC: Genetics and prevention of oesophageal adenocarcinoma. Recent Results Cancer Res; 2005;166:35-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetics and prevention of oesophageal adenocarcinoma.
  • Gastric cancer has been declining for more than half a century, whereas the incidence of oesophageal cancer is increasing rapidly.
  • The histopathological subtype is also changing with a predominance of oesophageal adenocarcinoma compared with squamous carcinoma.
  • The reasons for these epidemiological changes are not clear, although population-based data have implicated gastro-oesophageal reflux disease as a risk factor.
  • In susceptible individuals reflux of duodeno-gastric contents can lead to the development of a columnar-lined oesophagus, commonly called Barrett's oesophagus.
  • This can then progress to adenocarcinoma via a metaplasia-dysplasia-carcinoma sequence.
  • At the current time, the mortality from oesophageal adenocarcinoma exceeds 80% at 5 years.
  • Therefore, endoscopic surveillance programmes have been generally recommended for patients with Barrett's oesophagus in an attempt to detect early, curable lesions.
  • There is mounting evidence that there is an underlying genetic susceptibility to Barrett's oesophagus and oesophageal adenocarcinoma.
  • Once patients are identified as having Barrett's oesophagus their chance for developing adenocarcinoma is in the order of 0.5%-1% per year.
  • The histological assessment of dysplasia as a predictor of cancer development is highly subjective.
  • We have demonstrated an increase in the expression of a novel proliferation marker, Mcm2, which occurs during the malignant progression of Barrett's oesophagus.
  • In view of the role of reflux components in the pathogenesis of Barrett's oesophagus the effect of acid and bile on the cell phenotype have been studied.
  • Given the epidemic increase in oesophageal adenocarcinoma and the dismal 5-year mortality rate, a radical approach is necessary to prevent cancer development in individuals with pre-malignant lesions.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / prevention & control. Esophageal Neoplasms / genetics. Esophageal Neoplasms / prevention & control. Neoplasm Proteins / genetics


86. Mal F, Perniceni T, Levard H, Denet C, Validire P, Gayet B: Pre-operative predictive factors of early recurrence after resection of adenocarcinoma of the esophagus and cardia. Gastroenterol Clin Biol; 2005 Dec;29(12):1275-8
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  • [Title] Pre-operative predictive factors of early recurrence after resection of adenocarcinoma of the esophagus and cardia.
  • OBJECTIVES: To determine pre-operative predictive factors of early recurrence in patients with esophageal and cardial adenocarcinoma.
  • PATIENTS AND METHODS: We retrospectively analyzed consecutive patients who underwent resection for esophageal and cardial adenocarcinoma in our institution between October 1992 and October 2001.
  • Tumor was located in lower esophagus in 71 cases and at the cardia in 29 cases.
  • CONCLUSION: Important weight loss could be a pre-operative predictive factor of early recurrence after resection of esophageal and cardial adenocarcinoma and surgery as first line treatment could be avoided in these patients.
  • [MeSH-major] Adenocarcinoma / surgery. Cardia / surgery. Esophageal Neoplasms / surgery. Neoplasm Recurrence, Local / epidemiology. Stomach Neoplasms / surgery

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  • (PMID = 16518287.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
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87. Dellon ES, Shaheen NJ: Does screening for Barrett's esophagus and adenocarcinoma of the esophagus prolong survival? J Clin Oncol; 2005 Jul 10;23(20):4478-82
International Agency for Research on Cancer - Screening Group. diagnostics - Planning and Implementing Cervical Cancer Prevention and Control Programs: A Manual for Managers .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does screening for Barrett's esophagus and adenocarcinoma of the esophagus prolong survival?
  • Despite the paucity of data supporting its use, screening upper endoscopy for patients with chronic gastroesophageal reflux disease symptoms to assess for Barrett's esophagus and esophageal adenocarcinoma has become a widely accepted practice.
  • We apply the principles of screening to Barrett's esophagus and esophageal adenocarcinoma.
  • The major fault with screening for Barrett's esophagus is that the at-risk population is too broadly characterized and that too many cancers occur outside of this risk pool.
  • Efforts may be better directed at further research identifying groups at risk for esophageal adenocarcinoma, developing more accurate and less-invasive methods of diagnosis, and discovering the underlying factors which continue to drive the increased incidence of this disease.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus. Esophageal Neoplasms / etiology. Gastroesophageal Reflux / complications. Mass Screening / economics

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  • (PMID = 16002837.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 39
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88. Song S, Guha S, Liu K, Buttar NS, Bresalier RS: COX-2 induction by unconjugated bile acids involves reactive oxygen species-mediated signalling pathways in Barrett's oesophagus and oesophageal adenocarcinoma. Gut; 2007 Nov;56(11):1512-21
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] COX-2 induction by unconjugated bile acids involves reactive oxygen species-mediated signalling pathways in Barrett's oesophagus and oesophageal adenocarcinoma.
  • OBJECTIVES: Bile reflux contributes to oesophageal injury and neoplasia.
  • COX-2 is involved in both inflammation and carcinogenesis; however, the precise mechanisms by which bile acids promote COX-2 expression in the oesophagus are largely unknown.
  • We analysed the molecular mechanisms that govern bile acid-mediated expression of COX-2 in Barrett's oesophagus and oesophageal adenocarcinoma (OA).
  • DESIGN: The effects of bile acids on COX-2 expression were analysed in immortalised Barrett's oesophagus and OA cells using immunoblotting and transient transfections.
  • Immunohistochemistry was performed on oesophageal mucosa obtained from an established rat model of bile reflux.
  • CONCLUSIONS: Unconjugated bile acids induce CREB and AP-1-dependent COX-2 expression in Barrett's oesophagus and OA through ROS-mediated activation of PI3K/AKT and ERK1/2.
  • This study enhances our understanding of the molecular mechanisms by which bile acids promote the development of oesophageal adenocarcinoma.

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  • [Cites] Gastroenterology. 2001 Dec;121(6):1286-93 [11729107.001]
  • [Cites] J Biol Chem. 2001 Jan 5;276(1):413-20 [11020383.001]
  • [Cites] Carcinogenesis. 2002 Jan;23(1):73-9 [11756226.001]
  • [Cites] Gastroenterology. 2002 Feb;122(2):299-307 [11832445.001]
  • [Cites] Gastroenterology. 2002 Apr;122(4):985-93 [11910351.001]
  • [Cites] Gastroenterology. 2002 Apr;122(4):1101-12 [11910360.001]
  • [Cites] J Biol Chem. 2002 May 24;277(21):18649-57 [11901151.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2002 Aug;283(2):G327-34 [12121879.001]
  • [Cites] Mol Cell Biol. 2003 May;23(9):3052-66 [12697808.001]
  • [Cites] Laryngoscope. 2003 Jun;113(6):1059-63 [12782823.001]
  • [Cites] Carcinogenesis. 2003 Jul;24(7):1183-90 [12807723.001]
  • [Cites] Nutr Cancer. 2003;46(1):82-92 [12925308.001]
  • [Cites] Gut. 2003 Dec;52(12):1678-83 [14633942.001]
  • [Cites] Gut. 2004 Jan;53(1):27-33 [14684572.001]
  • [Cites] Carcinogenesis. 2004 Mar;25(3):419-23 [14656949.001]
  • [Cites] Leuk Lymphoma. 2004 Feb;45(2):265-70 [15101710.001]
  • [Cites] Mol Biol Cell. 2004 May;15(5):2156-63 [15004225.001]
  • [Cites] Ann Surg. 2004 Jul;240(1):57-67 [15213619.001]
  • [Cites] J Immunol. 2004 Aug 1;173(3):2011-22 [15265936.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Oct;287(4):G743-8 [15231484.001]
  • [Cites] Hepatology. 2004 Oct;40(4):961-71 [15382121.001]
  • [Cites] Endoscopy. 1979 May;11(2):121-6 [446424.001]
  • [Cites] J Clin Invest. 1986 Mar;77(3):850-9 [3005368.001]
  • [Cites] J Clin Invest. 1987 Feb;79(2):532-41 [3027128.001]
  • [Cites] Br J Surg. 1988 Jun;75(6):540-3 [3395818.001]
  • [Cites] Oncogene. 1994 Mar;9(3):791-9 [8108121.001]
  • [Cites] Eur J Biochem. 1994 May 1;221(3):889-97 [8181472.001]
  • [Cites] Carcinogenesis. 1994 Sep;15(9):1911-5 [7923585.001]
  • [Cites] Carcinogenesis. 1996 Mar;17(3):427-33 [8631127.001]
  • [Cites] Am J Gastroenterol. 2001 Apr;96(4):990-6 [11316217.001]
  • [Cites] Mutat Res. 2001 Sep 1;480-481:359-69 [11506828.001]
  • [Cites] Cell Growth Differ. 1997 Mar;8(3):283-91 [9056670.001]
  • [Cites] J Biol Chem. 1998 Jan 23;273(4):2424-8 [9442092.001]
  • [Cites] Gastroenterology. 1998 Feb;114(2):295-304 [9453489.001]
  • [Cites] J Gastrointest Surg. 1998 May-Jun;2(3):260-8 [9841983.001]
  • [Cites] J Gastrointest Surg. 1998 Jul-Aug;2(4):333-41 [9841990.001]
  • [Cites] Br J Cancer. 1999 Feb;79(3-4):595-603 [10027336.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] Gut. 1999 May;44(5):598-602 [10205192.001]
  • [Cites] Food Chem Toxicol. 2005 Jan;43(1):87-93 [15582199.001]
  • [Cites] Ann Surg. 2005 Jan;241(1):63-8 [15621992.001]
  • [Cites] Mutat Res. 2005 Jan;589(1):47-65 [15652226.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3462-9 [15833882.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):351-62 [15837624.001]
  • [Cites] J Biol Chem. 2005 Jun 3;280(22):21237-45 [15767259.001]
  • [Cites] J Gastroenterol. 2005 Jul;40(7):690-7 [16082585.001]
  • [Cites] Free Radic Biol Med. 2005 Sep 15;39(6):769-80 [16109307.001]
  • [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] Mol Biol Cell. 2005 Dec;16(12):5579-91 [16195339.001]
  • [Cites] Oncogene. 2005 Dec 15;24(56):8268-76 [16170369.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2006 Feb;290(2):G335-42 [16239404.001]
  • [Cites] Cancer. 2006 Jan 15;106(2):287-96 [16353199.001]
  • [Cites] Gut. 2006 Apr;55(4):450-6 [16210398.001]
  • [Cites] Oncogene. 2006 Apr 6;25(15):2170-80 [16301994.001]
  • [Cites] Cell Signal. 2006 Aug;18(8):1101-7 [16516442.001]
  • [Cites] Int J Cancer. 2006 Aug 15;119(4):771-82 [16557574.001]
  • [Cites] Gastroenterology. 2000 Mar;118(3):487-96 [10702199.001]
  • [Cites] J Biol Chem. 2000 May 19;275(20):15090-8 [10748108.001]
  • [Cites] J Gastrointest Surg. 2000 Mar-Apr;4(2):124-8 [10885957.001]
  • [Cites] Gastroenterology. 2001 Dec;121(6):1391-9 [11729118.001]
  • (PMID = 17604323.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA069480; United States / NCI NIH HHS / CA / R01CA69480
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / Reactive Oxygen Species; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.3.1.48 / CREB-Binding Protein; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ PMC2095641
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89. DeMeester SR: Endoscopic mucosal resection and vagal-sparing esophagectomy for high-grade dysplasia and adenocarcinoma of the esophagus. Semin Thorac Cardiovasc Surg; 2005;17(4):320-5
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] Endoscopic mucosal resection and vagal-sparing esophagectomy for high-grade dysplasia and adenocarcinoma of the esophagus.
  • Once a rare tumor, adenocarcinoma of the esophagus is currently the cancer with the fastest rising incidence in America.
  • In addition to the increasing prevalence of the disease, surveillance programs for patients with Barrett's have led to the identification of increasing numbers of patients with high-grade dysplasia or early-stage esophageal adenocarcinomas.
  • Endoscopic mucosal resection allows precise determination of the depth of tumor invasion and facilitates accurate local staging of early esophageal cancers.
  • A vagal-sparing esophagectomy accomplishes the goal of removing the diseased esophagus while minimizing the physiologic impact of an esophagectomy in patients with early-stage esophageal cancer.
  • [MeSH-major] Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagectomy / methods. Esophagoscopy. Esophagus / pathology. Precancerous Conditions / surgery

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  • (PMID = 16428038.001).
  • [ISSN] 1043-0679
  • [Journal-full-title] Seminars in thoracic and cardiovascular surgery
  • [ISO-abbreviation] Semin. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 28
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90. Hong J, Behar J, Wands J, Resnick M, Wang LJ, DeLellis RA, Lambeth D, Souza RF, Spechler SJ, Cao W: Role of a novel bile acid receptor TGR5 in the development of oesophageal adenocarcinoma. Gut; 2010 Feb;59(2):170-80
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] Role of a novel bile acid receptor TGR5 in the development of oesophageal adenocarcinoma.
  • BACKGROUND AND AIMS: Mechanisms of the progression from Barrett's oesophagus to oesophageal adenocarcinoma (OA) are not fully understood.
  • TGR5 mRNA and protein levels were significantly higher in OA tissues than in normal oesophageal mucosa or Barrett's mucosa.

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  • [Cites] BMC Cancer. 2009;9:190 [19534809.001]
  • [Cites] BMC Cancer. 2008;8:333 [19014523.001]
  • [Cites] Gene. 2001 May 16;269(1-2):131-40 [11376945.001]
  • [Cites] Aliment Pharmacol Ther. 2001 Aug;15(8):1087-100 [11472311.001]
  • [Cites] Am J Gastroenterol. 2002 Jan;97(1):22-6 [11808965.001]
  • [Cites] Gastroenterology. 2002 Feb;122(2):299-307 [11832445.001]
  • [Cites] Am J Physiol Cell Physiol. 2002 Jun;282(6):C1212-24 [11997235.001]
  • [Cites] Gastroenterology. 2002 Jun;122(7):1800-7 [12055587.001]
  • [Cites] Dis Esophagus. 2002;15(1):5-9 [12060036.001]
  • [Cites] Cell Mol Life Sci. 2002 Sep;59(9):1428-59 [12440767.001]
  • [Cites] Gut. 2003 Feb;52(2):174-80 [12524396.001]
  • [Cites] J Pediatr Gastroenterol Nutr. 2003 Feb;36(2):172-4 [12548050.001]
  • [Cites] J Biol Chem. 2003 Mar 14;278(11):9435-40 [12524422.001]
  • [Cites] Gut. 2003 Jun;52(6):775-83 [12740330.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2003 Jul;285(1):G86-95 [12799309.001]
  • [Cites] Am J Physiol Cell Physiol. 2003 Aug;285(2):C353-69 [12686516.001]
  • [Cites] Arch Biochem Biophys. 2003 Sep 1;417(1):3-11 [12921773.001]
  • [Cites] J Thorac Cardiovasc Surg. 2003 Dec;126(6):1952-7 [14688711.001]
  • [Cites] Surgery. 2004 Feb;135(2):215-21 [14739857.001]
  • [Cites] Nat Rev Immunol. 2004 Mar;4(3):181-9 [15039755.001]
  • [Cites] Am J Gastroenterol. 2004 Oct;99(10):1877-83 [15447744.001]
  • [Cites] Aliment Pharmacol Ther. 2004 Oct;20 Suppl 5:71-80; discussion 95-6 [15456468.001]
  • [Cites] Surgery. 1992 May;111(5):503-10 [1598670.001]
  • [Cites] Ann Surg Oncol. 1994 May;1(3):252-61 [7842295.001]
  • [Cites] Gut. 1995 Aug;37(2):168-73 [7557561.001]
  • [Cites] Ann Surg. 1996 Sep;224(3):358-70; discussion 370-1 [8813264.001]
  • [Cites] J Clin Invest. 1996 Nov 1;98(9):2120-8 [8903332.001]
  • [Cites] Dis Esophagus. 1997 Jan;10(1):29-32; discussion 33 [9079270.001]
  • [Cites] Cancer Res. 1997 Dec 15;57(24):5571-8 [9407969.001]
  • [Cites] Gastroenterology. 1998 Oct;115(4):919-28 [9753495.001]
  • [Cites] J Gastrointest Surg. 1998 May-Jun;2(3):260-8 [9841983.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] Gut. 1999 May;44(5):598-602 [10205192.001]
  • [Cites] Gastroenterology. 1999 Aug;117(2):327-35 [10419913.001]
  • [Cites] Nature. 1999 Sep 2;401(6748):79-82 [10485709.001]
  • [Cites] Dig Dis Sci. 2004 Oct;49(10):1664-71 [15573924.001]
  • [Cites] Mutat Res. 2005 Jan;589(1):47-65 [15652226.001]
  • [Cites] J Natl Cancer Inst. 2005 Jan 19;97(2):142-6 [15657344.001]
  • [Cites] Gut. 2005 Mar;54 Suppl 1:i21-6 [15711004.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Apr 1;329(1):386-90 [15721318.001]
  • [Cites] Thorac Surg Clin. 2005 Aug;15(3):335-40 [16104124.001]
  • [Cites] Nature. 2006 Jan 26;439(7075):484-9 [16400329.001]
  • [Cites] EMBO J. 2006 Apr 5;25(7):1419-25 [16541101.001]
  • [Cites] J Biol Chem. 2006 Jul 21;281(29):20368-82 [16707484.001]
  • [Cites] Carcinogenesis. 2007 Jan;28(1):136-42 [16905748.001]
  • [Cites] Dis Esophagus. 2007;20(3):256-64 [17509124.001]
  • [Cites] J Biol Chem. 2007 Jun 1;282(22):16244-55 [17403674.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Sep 14;361(1):156-61 [17659258.001]
  • [Cites] Lab Invest. 2008 Jun;88(6):643-51 [18427553.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Jul 18;372(1):78-84 [18468513.001]
  • [Cites] Science. 2000 Jan 7;287(5450):138-42 [10615049.001]
  • (PMID = 19926617.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK080703-01A1; United States / NIDDK NIH HHS / DK / R01 DK080703; United States / NIDDK NIH HHS / DK / DK073327-02; United States / NIDDK NIH HHS / DK / R21 DK073327-02; United States / NIDDK NIH HHS / DK / R21 DK073327; United States / NIDDK NIH HHS / DK / DK080703-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cholagogues and Choleretics; 0 / GPBAR1 protein, human; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Receptors, G-Protein-Coupled; 516-50-7 / Taurodeoxycholic Acid; EC 1.6.- / NOX5 protein, human; EC 1.6.3.1 / NADPH Oxidase; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gq-G11
  • [Other-IDs] NLM/ NIHMS182037; NLM/ PMC3049934
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91. Heyer CM, Rduch GJ, Zgoura P, Stachetzki U, Voigt E, Nicolas V: Metastasis to skeletal muscle from esophageal adenocarcinoma. Scand J Gastroenterol; 2005 Aug;40(8):1000-4
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  • [Title] Metastasis to skeletal muscle from esophageal adenocarcinoma.
  • Diagnosis of an adenocarcinoma of the esophagus was established by endosonography-guided biopsy.
  • [MeSH-major] Adenocarcinoma / secondary. Esophageal Neoplasms / pathology. Muscle Neoplasms / secondary. Muscle, Skeletal
  • [MeSH-minor] Biopsy. Combined Modality Therapy. Diagnosis, Differential. Esophagoscopy. Humans. Leg. Magnetic Resonance Imaging. Male. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 16165713.001).
  • [ISSN] 0036-5521
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Norway
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92. Bobryshev YV, Tran D, Killingsworth MC, Buckland M, Lord RV: Dendritic cells in Barrett's esophagus and esophageal adenocarcinoma. J Gastrointest Surg; 2009 Jan;13(1):44-53
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  • [Title] Dendritic cells in Barrett's esophagus and esophageal adenocarcinoma.
  • BACKGROUND: Like other premalignant conditions that develop in the presence of chronic inflammation, the development and progression of Barrett's esophagus is associated with the development of an immune response, but how this immune response is regulated is poorly understood.
  • A comprehensive literature search failed to find any report of the presence of dendritic cells in Barrett's intestinal metaplasia and esophageal adenocarcinoma and this prompted our study.
  • MATERIAL AND METHODS: We used immunohistochemical staining and electron microscopy to examine whether dendritic cells are present in Barrett's esophagus and esophageal adenocarcinoma.
  • Immunohistochemical staining with CD83, a specific marker for dendritic cells, was performed on paraffin-embedded sections of Barrett's intestinal metaplasia (IM, n = 12), dysplasia (n = 11) and adenocarcinoma (n = 14).
  • RESULTS: CD83+ cells were identified in the lamina propria surrounding intestinal type glands in Barrett's IM, dysplasia, and cancer tissues.
  • Computerized quantitative analysis showed that the numbers of dendritic cells were significantly higher in cancer tissues.
  • Double immunostaining with CD83, CD20, and CD3, and electron microscopy demonstrated that dendritic cells are present in Barrett's esophagus and form clusters with T cells and B cells directly within the lamina propria.
  • CONCLUSIONS: These findings demonstrate that dendritic cells are present in Barrett's tissues, with a significant increase in density in adenocarcinoma compared to benign Barrett's esophagus.
  • Dendritic cells may have a role in the pathogenesis and immunotherapy treatment of Barrett's esophagus and adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Dendritic Cells / ultrastructure. Esophageal Neoplasms / pathology

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  • (PMID = 18685901.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD83 antigen; 0 / Immunoglobulins; 0 / Membrane Glycoproteins
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93. Pera M, Manterola C, Vidal O, Grande L: Epidemiology of esophageal adenocarcinoma. J Surg Oncol; 2005 Dec 1;92(3):151-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epidemiology of esophageal adenocarcinoma.
  • The incidence of esophageal adenocarcinoma has risen rapidly over the past 25 years in the United States as well as in several Western European countries.
  • The majority of these cancers arise from a background of premalignant Barrett esophagus.
  • However, less than 10% of the patients with esophageal adenocarcinoma were known to have Barrett esophagus previously.
  • It is uncertain which risk factors contribute to the increasing incidence of esophageal adenocarcinoma, although gastroesophageal reflux disease, cigarette smoking, and obesity have been implicated.
  • Whereas infection with Helicobacter pylori and use of non-steroidal anti-inflammatory drugs are associated with reduced risk, low intakes of fruit, vegetables, and cereal fibers seem to increase the risk of esophageal adenocarcinoma.
  • Presently there is no evidence that strongly supports any specific strategy to screen a subgroup of the population at risk for Barrett esophagus and adenocarcinoma of the esophagus.
  • [MeSH-major] Adenocarcinoma / epidemiology. Esophageal Neoplasms / epidemiology. Esophagogastric Junction
  • [MeSH-minor] Alcohol Drinking / adverse effects. Barrett Esophagus / complications. Cardia. Diet. Europe / epidemiology. Female. Gastroesophageal Reflux / complications. Helicobacter Infections / complications. Helicobacter pylori. Humans. Incidence. Male. Obesity / complications. Risk Factors. Smoking / adverse effects. Survival Rate. United States / epidemiology

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16299786.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 92
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94. Malik V, Lucey JA, Duffy GJ, Wilson L, McNamara L, Keogan M, Gillham C, Reynolds JV: Early repeated 18F-FDG PET scans during neoadjuvant chemoradiation fail to predict histopathologic response or survival benefit in adenocarcinoma of the esophagus. J Nucl Med; 2010 Dec;51(12):1863-9
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  • [Title] Early repeated 18F-FDG PET scans during neoadjuvant chemoradiation fail to predict histopathologic response or survival benefit in adenocarcinoma of the esophagus.
  • This study evaluated the role of (18)F-FDG PET as an early predictor of histopathologic response to neoadjuvant chemoradiotherapy and overall survival in patients with adenocarcinoma of the esophagus undergoing multimodal therapy.
  • METHODS: Thirty-seven patients with locally advanced adenocarcinoma of the esophagus underwent pretreatment and an intratreatment (18)F-FDG PET scan in the second week of a 6-wk regimen of neoadjuvant chemoradiotherapy.
  • Our results show that, in contrast to published reports on neoadjuvant chemotherapy, combined chemoradiotherapy in patients with adenocarcinoma of the esophagus lowers the predictive accuracy of early repeated (18)F-FDG PET in identifying histopathologic responders and those with chances for increased survival below clinically applicable levels.
  • [MeSH-major] Adenocarcinoma / radionuclide imaging. Adenocarcinoma / therapy. Esophageal Neoplasms / radionuclide imaging. Esophageal Neoplasms / therapy. Fluorodeoxyglucose F18. Neoadjuvant Therapy. Radiopharmaceuticals

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  • (PMID = 21078796.001).
  • [ISSN] 1535-5667
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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95. Möbius C, Freire J, Becker I, Feith M, Brücher BL, Hennig M, Siewert JR, Stein HJ: VEGF-C expression in squamous cell carcinoma and adenocarcinoma of the esophagus. World J Surg; 2007 Sep;31(9):1768-72; discussion 1773-4
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  • [Title] VEGF-C expression in squamous cell carcinoma and adenocarcinoma of the esophagus.
  • In esophageal cancer the histologic tumor type and lymph node metastasis are independent predictors of recurrence and poor outcome.
  • To evaluate the rule of VEGF-C expression in esophageal cancer, we investigated 113 specimens, 59 squamous cell and 54 adenocarcinomas of the esophagus.
  • METHODS: The expression of VEGF-C was evaluated using immunohistochemistry (IHC) on 59 paraffin-embedded archival specimens from patients with squamous cell esophageal carcinomas and 54 paraffin-embedded archival specimens of patients with esophageal adenocarcinomas arising in Barrett's mucosa.
  • RESULTS: The expression of VEGF-C was significantly different between the two histological types of esophageal tumors.
  • In patients with adenocarcinoma of the esophagus there was no correlation between VEGF-C expression and clinicopathological parameters.
  • High VEGF-C expression tended to be correlated with poor survival in squamous cell cancer but not in adenocarcinoma of the esophagus.
  • CONCLUSIONS: The present study indicates that VEGF-C may play a role in tumor progression via lymphangiogenesis in squamous cell carcinoma of the esophagus.
  • This seems not to be true for the adenocarcinoma of the esophagus.
  • These data could help with the understanding of the different onset and characteristics of lymph node metastasis in squamous cell carcinoma and adenocarcinoma of the esophagus.
  • [MeSH-major] Adenocarcinoma / chemistry. Adenocarcinoma / pathology. Biomarkers, Tumor / analysis. Carcinoma, Squamous Cell / chemistry. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / chemistry. Esophageal Neoplasms / pathology. Vascular Endothelial Growth Factor C / analysis

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  • [Cites] Development. 1996 Dec;122(12):3829-37 [9012504.001]
  • [Cites] Cancer. 2000 Nov 1;89(9):1874-82 [11064343.001]
  • [Cites] Oncogene. 2000 Nov 20;19(49):5598-605 [11114740.001]
  • [Cites] Cancer. 1998 Sep 1;83(5):858-66 [9731887.001]
  • [Cites] Cancer. 2002 May 1;94(9):2511-6 [12015777.001]
  • [Cites] Oncol Rep. 2002 Sep-Oct;9(5):995-9 [12168062.001]
  • [Cites] Br J Cancer. 2001 Jul 20;85(2):255-60 [11461086.001]
  • [Cites] Eur J Cancer. 2001 May;37(7):918-23 [11313181.001]
  • [Cites] Int J Cancer. 2001 Sep 1;93(5):662-6 [11477575.001]
  • [Cites] J Mol Med (Berl). 1999 Jul;77(7):527-43 [10494799.001]
  • [Cites] Ann Surg. 2001 Sep;234(3):360-7; discussion 368-9 [11524589.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):1786-90 [11280723.001]
  • [Cites] Ann Surg. 2000 Sep;232(3):353-61 [10973385.001]
  • (PMID = 17354029.001).
  • [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 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factor C
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96. Heinrich H, Bauerfeind P: Endoscopic mucosal resection for staging and therapy of adenocarcinoma of the esophagus, gastric cardia, and upper gastric third. Recent Results Cancer Res; 2010;182:85-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endoscopic mucosal resection for staging and therapy of adenocarcinoma of the esophagus, gastric cardia, and upper gastric third.
  • Minamally invasive endoscopic resection techniques allow definitive histological staging for dysplasia and early cancer and in many cases curative treatment.
  • In Barrett's esophagus with High Grade Dysplasia (HGD) or early mucosal cancer, endoscopic mucosal resection (EMR) should be considered both as diagnostic and therapeutic first line procedure, with the possibility to repeat the procedure in case of residual Barrett's dysplasia or mucosal cancer.
  • In early cancer of the the submucosa, surgical resection should be discussed.
  • Endoscopic submucosal dissection (ESD) is a useful therapeutic option for HGD or early cancer in the squamous epithelium of the esophagus or in the stomach when en bloc resection is needed in large lesions.
  • [MeSH-major] Adenocarcinoma / pathology. Cardia. Esophageal Neoplasms / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Barrett Esophagus / pathology. Endoscopy. Esophagogastric Junction / pathology. Humans. Mucous Membrane / pathology. Mucous Membrane / surgery. Neoplasm Staging

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  • (PMID = 20676873.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
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97. Weiler-Bisig D, Ettlin G, Brink T, Arnold W, Glatz-Krieger K, Fischer A: Henoch-schonlein purpura associated with esophagus carcinoma and adenocarcinoma of the lung. Clin Nephrol; 2005 Apr;63(4):302-4
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  • [Title] Henoch-schonlein purpura associated with esophagus carcinoma and adenocarcinoma of the lung.
  • Henoch-Schönlein purpura (HSP) is known to exist in association with a variety of malignant diseases including squamous and small cell lung cancer and hematological malignancies.
  • We report the first cases of HSP associated with carcinoma of the esophagus and adenocarcinoma of the lung, respectively.
  • [MeSH-major] Adenocarcinoma / complications. Carcinoma, Squamous Cell / complications. Esophageal Neoplasms / complications. Lung Neoplasms / complications. Purpura, Schoenlein-Henoch / etiology

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  • (PMID = 15847258.001).
  • [ISSN] 0301-0430
  • [Journal-full-title] Clinical nephrology
  • [ISO-abbreviation] Clin. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Immunoglobulin A
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98. Lurje G, Lenz HJ: Molecular response prediction in multimodality treatment for adenocarcinoma of the esophagus and esophagogastric junction. Recent Results Cancer Res; 2010;182:179-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular response prediction in multimodality treatment for adenocarcinoma of the esophagus and esophagogastric junction.
  • Cancers arising from the esophagus are becoming more common in the United States and Europe.
  • Esophageal cancer is currently the most rapidly increasing cancer in the western world and is coinciding with a shift in histological type and primary tumor location.
  • Despite recent improvements in the detection, surgical resection, and (radio-) chemotherapy, the overall survival (OS) of esophageal cancer remains relatively poor.
  • [MeSH-major] Adenocarcinoma / therapy. Esophageal Neoplasms / therapy. Esophagogastric Junction. Stomach Neoplasms / therapy

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  • (PMID = 20676881.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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99. Healy LA, Ryan AM, Gopinath B, Rowley S, Byrne PJ, Reynolds JV: Impact of obesity on outcomes in the management of localized adenocarcinoma of the esophagus and esophagogastric junction. J Thorac Cardiovasc Surg; 2007 Nov;134(5):1284-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of obesity on outcomes in the management of localized adenocarcinoma of the esophagus and esophagogastric junction.
  • OBJECTIVE: Obesity trends in the Western world parallel the increased incidence of adenocarcinoma of the esophagus and esophagogastric junction.
  • The implications of obesity on standard outcomes in the management of localized adenocarcinoma, particularly operative risks, have not been systematically addressed.
  • These outcomes suggest that the added risks of obesity on standard outcomes in esophageal cancer surgery are modest and should not independently have a significant impact on risk assessment in esophageal cancer management.
  • [MeSH-major] Adenocarcinoma / therapy. Esophageal Neoplasms / therapy. Esophagogastric Junction. Obesity / complications

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  • (PMID = 17976464.001).
  • [ISSN] 1097-685X
  • [Journal-full-title] The Journal of thoracic and cardiovascular surgery
  • [ISO-abbreviation] J. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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100. Biondi A, Migliore M, Strano G, Vadala S, Tropea A, Basile F: Clinical biomarkers in esophageal adenocarcinoma. Front Biosci (Elite Ed); 2010;2:489-94
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  • [Title] Clinical biomarkers in esophageal adenocarcinoma.
  • This review describes genetic and molecular changes related to adenocarcinoma of the esophagus and gastroesophageal junction (GEJ) with emphasis on prognostic value and possibilities for targeted therapy in clinical setting.
  • The progression of Barrett's esophagus to adenocarcinoma has been the focus of particular scrutiny, and a number of potential tissue and serum-based disease biomarkers have emerged.
  • Tissue biomarkers allowing risk stratification of Barrett's are reviewed as well as strategies currently being used to discover novel biomarkers that will facilitate the early detection of esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis

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  • (PMID = 20036895.001).
  • [ISSN] 1945-0508
  • [Journal-full-title] Frontiers in bioscience (Elite edition)
  • [ISO-abbreviation] Front Biosci (Elite Ed)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers
  • [Number-of-references] 45
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