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[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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Adenocarcinoma of oesophagus: what exactly is the size of the problem and who is at risk?

The incidence of oesophageal adenocarcinoma is increasing and the prognosis is poor.

The established risk factors are Barrett's oesophagus, gastro-oesophageal reflux, and obesity.

Medications that relax the lower oesophageal sphincter might contribute to increasing the risk.

Among dietary factors, low intake of fruit, vegetables, and cereal fibres seem to increase the risk of oesophageal adenocarcinoma.

Endoscopic surveillance for oesophageal adenocarcinoma among persons with reflux and obesity is discussed, but presently there is no evidence that strongly supports such a strategy.

[MeSH-major] Adenocarcinoma / epidemiology. Esophageal Neoplasms / epidemiology

[MeSH-minor] Barrett Esophagus / complications. Esophageal Sphincter, Lower / drug effects. Female. Gastroesophageal Reflux / complications. Helicobacter Infections / complications. Helicobacter pylori. Humans. Incidence. Life Style. Male. Middle Aged. Risk Factors

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[Cites] Int J Cancer. 2000 Sep 1;87(5):750-4 [10925371.001]

[Cites] JAMA. 2000 Aug 23-30;284(8):961-2 [10944640.001]

[Cites] Cancer Res. 2000 Oct 15;60(20):5767-72 [11059772.001]

[Cites] Digestion. 2000;62(4):225-31 [11070405.001]

[Cites] Gastroenterology. 2001 Feb;120(2):387-91 [11159879.001]

[Cites] Int J Cancer. 2001 Jul 1;93(1):148-52 [11391635.001]

[Cites] Cancer. 2001 Aug 1;92(3):549-55 [11505399.001]

[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] Gastroenterology. 2001 Dec;121(6):1286-93 [11729107.001]

[Cites] Helicobacter. 2001 Dec;6(4):310-6 [11843963.001]

[Cites] Int J Cancer. 2002 Jun 10;99(5):751-4 [12115512.001]

[Cites] JAMA. 1995 Aug 9;274(6):474-7 [7629956.001]

[Cites] Cancer. 1995 Oct 1;76(7):1116-9 [8630885.001]

[Cites] Arch Surg. 1996 Jul;131(7):708-13 [8678768.001]

[Cites] Cancer Causes Control. 1996 May;7(3):322-7 [8734825.001]

[Cites] Am J Gastroenterol. 1996 Sep;91(9):1855-6 [8792715.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1996 Oct;5(10):761-8 [8896886.001]

[Cites] Int J Epidemiol. 1996 Oct;25(5):941-7 [8921478.001]

[Cites] Am J Gastroenterol. 1997 Feb;92(2):212-5 [9040193.001]

[Cites] Br J Surg. 1997 Jan;84(1):119-25 [9043475.001]

[Cites] Gastroenterology. 1997 May;112(5):1448-56 [9136821.001]

[Cites] Int J Cancer. 1997 May 2;71(3):340-4 [9139864.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1997 May;6(5):369-77 [9149898.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1997 Jul;6(7):481-5 [9232333.001]

[Cites] Br Med Bull. 1997;53(2):238-52 [9246834.001]

[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] 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] Cancer Res. 1998 Jul 15;58(14):2929-34 [9679948.001]

[Cites] Helicobacter. 1998 Sep;3(3):145-51 [9731983.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1998 Sep;7(9):749-56 [9752982.001]

[Cites] Am J Gastroenterol. 1998 Oct;93(10):1800-2 [9772034.001]

[Cites] Gut. 2002 Sep;51(3):323-8 [12171951.001]

[Cites] J Nutr. 2002 Nov;132(11 Suppl):3467S-3470S [12421872.001]

[Cites] Int J Cancer. 2003 Mar 1;103(6):815-21 [12516104.001]

[Cites] Ann Intern Med. 2003 Feb 4;138(3):176-86 [12558356.001]

[Cites] J Natl Cancer Inst. 2004 Mar 3;96(5):388-96 [14996860.001]

[Cites] Am J Dig Dis. 1976 Nov;21(11):953-6 [984016.001]

[Cites] Can Med Assoc J. 1982 Jan 1;126(1):46-8 [7059872.001]

[Cites] Gastroenterology. 1984 Oct;87(4):927-33 [6468881.001]

[Cites] Ann Intern Med. 1985 Jul;103(1):52-4 [4003988.001]

[Cites] N Engl J Med. 1985 Oct 3;313(14):857-9 [4033716.001]

[Cites] Hepatogastroenterology. 1986 Apr;33(2):86-7 [3721391.001]

[Cites] N Engl J Med. 1986 Aug 7;315(6):362-71 [2874485.001]

[Cites] Cancer. 1988 Feb 1;61(3):612-7 [3338027.001]

[Cites] Ugeskr Laeger. 1987 Jul 6;149(28):1904-9 [3433407.001]

[Cites] Br J Surg. 1988 Aug;75(8):760-3 [3167523.001]

[Cites] Gut. 1989 Jan;30(1):14-8 [2920919.001]

[Cites] Gastroenterology. 1989 May;96(5 Pt 1):1249-56 [2703113.001]

[Cites] Int J Cancer. 1989 May 15;43(5):755-61 [2714880.001]

[Cites] Cancer. 1989 Jul 15;64(2):526-30 [2736498.001]

[Cites] Dig Dis Sci. 1989 Sep;34(9):1336-9 [2766899.001]

[Cites] Cancer Res. 1990 May 1;50(9):2569-76 [2328485.001]

[Cites] Int J Cancer. 1990 May 15;45(5):852-4 [2335388.001]

[Cites] Semin Surg Oncol. 1990;6(5):274-8 [2237086.001]

[Cites] JAMA. 1991 Mar 13;265(10):1287-9 [1995976.001]

[Cites] Gastroenterology. 1992 Apr;102(4 Pt 1):1400-2 [1551547.001]

[Cites] Eur J Cancer Prev. 1992 Apr;1(3):265-9 [1467772.001]

[Cites] Gastroenterology. 1993 Feb;104(2):510-3 [8425693.001]

[Cites] Cancer Res. 1993 Mar 15;53(6):1322-7 [8443812.001]

[Cites] Cancer Causes Control. 1993 Mar;4(2):123-32 [8481491.001]

[Cites] JAMA. 1994 Jul 20;272(3):205-11 [8022039.001]

[Cites] Int J Cancer. 1994 Jul 15;58(2):192-6 [8026880.001]

[Cites] Cancer Causes Control. 1994 Jul;5(4):333-40 [8080945.001]

[Cites] Cancer. 1995 Jan 1;75(1 Suppl):154-70 [8000994.001]

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

[Cites] J Natl Cancer Inst. 1998 Nov 4;90(21):1609-20 [9811310.001]

[Cites] Cancer. 1998 Nov 15;83(10):2049-53 [9827707.001]

[Cites] Gut. 1998 Sep;43(3):327-33 [9863476.001]

[Cites] Cancer Res. 1999 Jan 1;59(1):198-204 [9892207.001]

[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] Int J Cancer. 1993 May 28;54(3):402-7 [8509215.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1993 Jul-Aug;2(4):397-9 [8348064.001]

[Cites] Cancer Causes Control. 1994 Jan;5(1):88-9 [8123782.001]

[Cites] Int J Cancer. 2000 Feb 1;85(3):340-6 [10652424.001]

[Cites] Am J Gastroenterol. 2000 Feb;95(2):387-94 [10685740.001]

[Cites] Gastroenterology. 2000 Mar;118(3):487-96 [10702199.001]

[Cites] Cancer Causes Control. 2000 Mar;11(3):231-8 [10782657.001]

[Cites] Ann Intern Med. 2000 Aug 1;133(3):165-75 [10906830.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2000 Jul;9(7):757-60 [10919748.001]

(PMID = 15711002.001).

[ISSN] 0017-5749

[Journal-full-title] Gut

[ISO-abbreviation] Gut

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Number-of-references] 89

[Other-IDs] NLM/ PMC1867797

   

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[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Obesity and cancer].

[Transliterated title] Obésité et cancer.

Some systematic review and meta-analyses assessed the strength of associations between body mass index and common cancers such as breast, endometrial, colon and adenocarcinoma of oesophagus.

The inflammation associated with visceral adiposity is another factor which promotes cancer.

However, a regular physical activity and a limited caloric intake are probably safe in healthy subject to prevent cancer and also in cancer survivors.

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(PMID = 19524333.001).

[ISSN] 0248-8663

[Journal-full-title] La Revue de medecine interne

[ISO-abbreviation] Rev Med Interne

[Language] FRE

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

[Publication-country] France

[Chemical-registry-number] 0 / Biomarkers; 67763-96-6 / Insulin-Like Growth Factor I

[Number-of-references] 53

   

[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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Fruit and vegetable intake and the risk of stomach and oesophagus adenocarcinoma in the European Prospective Investigation into Cancer and Nutrition (EPIC-EURGAST).

It is considered that fruit and vegetable (F&V) protect against oesophagus and gastric cancer (GC).

No evidence exists from cohort studies about adenocarcinoma of oesophagus (ACO).

[MeSH-major] Adenocarcinoma / prevention & control. Esophageal Neoplasms / prevention & control. Fruit. Stomach Neoplasms / prevention & control. Vegetables

MedlinePlus Health Information. consumer health - Esophageal Cancer.

MedlinePlus Health Information. consumer health - Stomach Cancer.

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[Copyright] Copyright (c) 2005 Wiley-Liss, Inc.

[CommentIn] Int J Cancer. 2006 Dec 15;119(12):2991; author reply 2992 [17016826.001]

(PMID = 16380980.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Grant] United Kingdom / Wellcome Trust / /

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

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The expression of 8-hydroxydeoxyguanosine in oesophageal tissues and tumours.

In the present study we investigated whether DNA damage linked to oxidative stress (as 8-OHdG) is present in Barrett's mucosa with or without associated adenocarcinoma or high-grade dysplasia and in normal controls' squamous mucosa.

EXPERIMENTAL DESIGN: We measured 8-OHdG in 51 patients (13 Barrett's metaplasia, six Barrett's oesophagus with high-grade dysplasia, 18 adenocarcinoma of the distal oesophagus/oesophagogastric junction and 14 normal controls).

The amount of DNA damage was determined by high-performance liquid chromatography in oesophagus samples obtained either from endoscopy or as samples from surgery.

RESULTS: Analysis revealed that 8-OHdG was present in both Barrett's metaplasia with and without dysplasia as well as in adenocarcinoma of the oesophagus/oesophagogastric junction.

Although the study group was small the amount of 8-OHdG was significantly increased in the distal oesophagus both in Barrett's epithelium 1.26 (0.08-29.47) and in high-grade dysplasia 1.35 (1.04-1.65) as well as in adenocarcinoma of oesophagus/oesophagogastric junction 1.08 (0.59-1.94) compared to controls 0.06 (0-4.08) (p=0.002, p=0.012, p=0.001, respectively).

Barrett's patients had no significant difference in 8-OHdG levels between their distal and proximal oesophageal samples.

CONCLUSIONS: Our results show the presence of oxidative DNA damage in the distal oesophagus of patients with Barrett's oesophagus and adenocarcinoma of the oesophagus/oesophagogastric junction.

This may have a connection to carcinogenesis in Barrett's oesophagus.

[MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. DNA Damage / physiology. Deoxyguanosine / analogs & derivatives. Esophageal Neoplasms / metabolism. Esophagus / metabolism

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(PMID = 17467227.001).

[ISSN] 1532-2157

[Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology

[ISO-abbreviation] Eur J Surg Oncol

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; G9481N71RO / Deoxyguanosine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[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

   

[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

   

[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

   

[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

   

[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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[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

   

[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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Trends in the incidence of adenocarcinoma of the oesophagus and cardia in the Netherlands 1989-2003.

Over the 15-year period 1989-2003, the incidence of oesophagus-cardia adenocarcinoma in the Netherlands rose annually by 2.6% for males and 1.2% for females.

This was the net outcome of annual increases in the incidence of adenocarcinoma of the oesophagus (ACO) of 7.2% for males and 3.5% for females and annual declines in the incidence of adenocarcinoma of the gastric cardia (AGC) of more than 1% for both genders.

[MeSH-major] Adenocarcinoma / epidemiology. Cardia. Esophageal Neoplasms / epidemiology. Stomach Neoplasms / epidemiology

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[Cites] Int J Epidemiol. 2001 Dec;30(6):1415-25 [11821356.001]

[Cites] Clin Ther. 2001 Dec;23(12):1984-98 [11813933.001]

[Cites] Bull World Health Organ. 2002;80(1):26-32 [11884970.001]

[Cites] Gastroenterology. 2002 Apr;122(4):1101-12 [11910360.001]

[Cites] Gastroenterology. 2002 May;122(5):1518-20 [11984536.001]

[Cites] Gastroenterology. 2002 Jul;123(1):60-7 [12105834.001]

[Cites] Gastroenterol Clin North Am. 2002 Jun;31(2):421-40, viii [12134611.001]

[Cites] Int J Obes Relat Metab Disord. 2002 Sep;26(9):1218-24 [12187399.001]

[Cites] Int J Cancer. 2003 Mar 1;103(6):815-21 [12516104.001]

[Cites] Eur J Clin Pharmacol. 2003 Sep;59(5-6):477-82 [12937872.001]

[Cites] Eur J Cancer. 2003 Nov;39(17):2487-94 [14602134.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2004 Jan;13(1):34-9 [14744730.001]

[Cites] Int J Cancer. 2000 Feb 1;85(3):340-6 [10652424.001]

[Cites] Cancer Res. 2000 Oct 15;60(20):5767-72 [11059772.001]

[Cites] Eur J Gastroenterol Hepatol. 2004 Jan;16(1):69-74 [15095855.001]

[Cites] Eur J Gastroenterol Hepatol. 2004 Sep;16(9):903-9 [15316416.001]

[Cites] Aliment Pharmacol Ther. 2004 Sep 15;20(6):645-55 [15352913.001]

[Cites] Clin Gastroenterol Hepatol. 2004 Oct;2(10):880-7 [15476151.001]

[Cites] J Thorac Cardiovasc Surg. 1975 Nov;70(5):826-35 [1186274.001]

[Cites] Am J Clin Pathol. 1978 Jul;70(1):1-5 [696666.001]

[Cites] Stat Med. 1987 Jun;6(4):449-67 [3629047.001]

[Cites] Stat Med. 1987 Jun;6(4):469-81 [3629048.001]

[Cites] J Thorac Cardiovasc Surg. 1996 Jul;112(1):130-6 [8691857.001]

[Cites] Am J Gastroenterol. 1997 Sep;92(9):1480-2 [9317067.001]

[Cites] Am J Gastroenterol. 1998 Oct;93(10):1800-2 [9772034.001]

[Cites] Br J Surg. 1998 Nov;85(11):1457-9 [9823902.001]

[Cites] Am J Gastroenterol. 1999 Jan;94(1):86-91 [9934736.001]

[Cites] Br J Surg. 1999 Apr;86(4):529-35 [10215831.001]

[Cites] Scand J Gastroenterol. 1999 Apr;34(4):353-60 [10365894.001]

[Cites] Int J Epidemiol. 1999 Jun;28(3):391-5 [10405839.001]

[Cites] Br J Cancer. 1952 Jun;6(2):127-30 [14954081.001]

[Cites] Gut. 2005 Jan;54(1):1-3 [15591495.001]

[Cites] Am J Gastroenterol. 2005 Apr;100(4):766-74 [15784017.001]

[Cites] Gut. 2005 Aug;54(8):1062-6 [15857935.001]

[Cites] Ann Intern Med. 2005 Aug 2;143(3):199-211 [16061918.001]

[Cites] Am J Gastroenterol. 2005 Oct;100(10):2151-6 [16181362.001]

[Cites] Gut. 2005 Nov;54(11):1527-35 [16227357.001]

[Cites] CA Cancer J Clin. 2005 Nov-Dec;55(6):334-51 [16282279.001]

[Cites] Lancet Oncol. 2005 Dec;6(12):945-52 [16321762.001]

[Cites] Ned Tijdschr Geneeskd. 2005 Dec 10;149(50):2775-82 [16385829.001]

[Cites] Best Pract Res Clin Gastroenterol. 2006;20(4):687-96 [16997153.001]

[Cites] Cancer. 2001 Aug 1;92(3):549-55 [11505399.001]

[Cites] Gut. 2002 Mar;50(3):368-72 [11839716.001]

(PMID = 17505507.001).

[ISSN] 0007-0920

[Journal-full-title] British journal of cancer

[ISO-abbreviation] Br. J. Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2359916

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

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(PMID = 20977081.001).

[ISSN] 0350-6134

[Journal-full-title] Collegium antropologicum

[ISO-abbreviation] Coll Antropol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Croatia

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[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

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(PMID = 15648181.001).

[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] 0 / Genetic Markers; 0 / Neoplasm Proteins

[Number-of-references] 59

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Sentinel node biopsy to evaluate the metastatic dissemination of oesophageal adenocarcinoma.

BACKGROUND: The aim of this study was to determine the feasibility and accuracy of sentinel lymph node (SLN) biopsy for oesophageal adenocarcinoma.

METHODS: Fifty-seven patients with adenocarcinoma of the lower oesophagus (n = 40) or gastric cardia (n = 17) underwent endoscopic peritumoral injection of (99m)Tc-radiolabelled nanocolloid before en bloc resection with extended lymphadenectomy.

Lower oesophageal tumours had a greater proportion of SLNs (P = 0.018), radioactive uptake (P < 0.001) and malignant nodes (P = 0.004) in the mediastinum than gastric cardia tumours.

CONCLUSION: The sentinel node concept is applicable to oesophageal adenocarcinoma and could be used to tailor the extent of lymphadenectomy.

There is a close relationship between patterns of radioactive uptake and lymphatic tumour dissemination, which differ for lower oesophageal and gastric cardia tumours.

[MeSH-major] Adenocarcinoma / secondary. Esophageal Neoplasms / pathology. Sentinel Lymph Node Biopsy / methods. Stomach Neoplasms / pathology

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(PMID = 15584066.001).

[ISSN] 0007-1323

[Journal-full-title] The British journal of surgery

[ISO-abbreviation] Br J Surg

[Language] eng

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

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Systematic review: the application of molecular pathogenesis to prevention and treatment of oesophageal adenocarcinoma.

BACKGROUND: Oesophageal adenocarcinoma is an increasingly common cancer with a poor prognosis.

It develops in a stepwise progression from Barrett's metaplasia to dysplasia, and then adenocarcinoma followed by metastasis.

AIM: To outline the key molecular changes in oesophageal adenocarcinoma and to summarize the chemopreventative and therapeutic strategies proposed.

Search terms included: Barrett's (o)esophagus, intestinal metaplasia, (o)esophageal adenocarcinoma, molecular changes, genetic changes, pathogenesis, chemoprevention, therapeutic strategies and treatment.

RESULTS: A large number of molecular changes have been identified in the progression from Barrett's oesophagus to oesophageal adenocarcinoma although there does not appear to be an obligate order of events.

In established adenocarcinoma, targeted treatments under evaluation include receptor tyrosine kinase inhibitors of EGFR and cyclin-dependent kinase inhibitors, which may benefit a subgroup of patients.

CONCLUSIONS: Advances in molecular methodology have led to a greater understanding of the oesophageal adenocarcinoma pathways, which provides opportunities for chemoprevention and therapeutic strategies with a mechanistic basis.

[MeSH-major] Adenocarcinoma / prevention & control. Angiogenesis Inhibitors / therapeutic use. Anti-Inflammatory Agents / therapeutic use. Antioxidants / therapeutic use. Esophageal Neoplasms / prevention & control

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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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Aspirin is not chemoprotective for Barrett's adenocarcinoma of the oesophagus in multicentre cohort.

Barrett's columnar-lined oesophagus is the precursor lesion for oesophageal adenocarcinoma.

The overall rate of progression to adenocarcinoma is 0.59% per annum.

A large prospective multicentre trial is recruiting to assess the role of aspirin as a chemoprotective agent in prevention of development of cancer as well as cardiovascular protection in patients with Barrett's oesophagus.

This retrospective analysis of the large UK National Barrett's Oesophagus Registry database seeks to analyse this question from within its large natural history study cohort.

Multicentre UK retrospective cohort compared patients known to have been taking aspirin with those who did not take aspirin during the course of surveillance for columnar-lined oesophagus.

End point was development of dysplasia or oesophageal adenocarcinoma.

Numbers of patients developing all grades of dysplasia and adenocarcinoma were: 13 aspirin (15.1%) and 97 no aspirin (14.9%) (hazard ratio 0.723, 95% confidence interval 0.410-1.310, P = 0.294), high-grade dysplasia and adenocarcinoma: five aspirin (5.8%) and 25 no aspirin (3.8%) (hazard ratio 0.898, 95% confidence interval 0.340-2.368, P = 0.827) and adenocarcinoma: four aspirin (4.7%) and 16 no aspirin (2.5%) (hazard ratio 1.092, 95% confidence interval 0.358-3.335, P = 0.877).

No significant difference was observed in hazard of developing dysplasia or adenocarcinoma between patients taking aspirin and those not taking aspirin during the course of follow-up of surveillance for columnar-lined oesophagus.

In conclusion, no difference in risk of development of dysplasia or adenocarcinoma was observed between patients taking aspirin and those not taking aspirin in this large cohort.

[MeSH-major] Adenocarcinoma / prevention & control. Anticarcinogenic Agents / therapeutic use. Aspirin / therapeutic use. Barrett Esophagus / drug therapy. Esophageal Neoplasms / prevention & control. Precancerous Conditions / drug therapy

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(PMID = 19620873.001).

[ISSN] 1473-5709

[Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)

[ISO-abbreviation] Eur. J. Cancer Prev.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Anticarcinogenic Agents; R16CO5Y76E / Aspirin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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