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

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

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  • (PMID = 28839554.001).
  • [ISSN] 2041-4137
  • [Journal-full-title] Frontline gastroenterology
  • [ISO-abbreviation] Frontline Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
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2. Spechler SJ, Berta M, Patterson CO: Risk Stratification for Esophageal Adenocarcinoma Screening and Surveillance. Gastroenterol Hepatol (N Y); 2006 Nov;2(11):798-799

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

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  • (PMID = 28381948.001).
  • [ISSN] 1554-7914
  • [Journal-full-title] Gastroenterology & hepatology
  • [ISO-abbreviation] Gastroenterol Hepatol (N Y)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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3. Rastogi A, Sharma P: Short-Segment Barrett's Esophagus and Adenocarcinoma. Gastroenterol Hepatol (N Y); 2006 Feb;2(2):134-139

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

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  • (PMID = 28286441.001).
  • [ISSN] 1554-7914
  • [Journal-full-title] Gastroenterology & hepatology
  • [ISO-abbreviation] Gastroenterol Hepatol (N Y)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Barrett’s esophagus / adenocarcinoma / high-grade dysplasia / long-segment Barrett’s esophagus / low-grade dysplasia / short-segment Barrett’s esophagus
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4. Struijs B, de Bree R, van Groeningen CJ, Mooi WJ, Leemans CR: Tonsillar metastasis of oesophageal adenocarcinoma. Eur Arch Otorhinolaryngol; 2008 Jan;265(1):127-9
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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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  • (PMID = 17657505.001).
  • [ISSN] 0937-4477
  • [Journal-full-title] European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
  • [ISO-abbreviation] Eur Arch Otorhinolaryngol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2099162
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5. Huang Y, Peters CJ, Fitzgerald RC, Gjerset RA: Progressive silencing of p14ARF in oesophageal adenocarcinoma. J Cell Mol Med; 2009 Feb;13(2):398-409
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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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  • (PMID = 18410530.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA111868-02; United States / NCI NIH HHS / CA / R01 CA111868-03; United Kingdom / Medical Research Council / / MC/ U105365007; United States / NCI NIH HHS / CA / R01 CA111868-01; United States / NCI NIH HHS / CA / CA 111868; United Kingdom / Medical Research Council / / ; United States / NCI NIH HHS / CA / R01 CA111868-04; United States / NCI NIH HHS / CA / R01 CA111868-05; United States / NCI NIH HHS / CA / R01 CA111868; United States / NCI NIH HHS / CA / R01 CA111868-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Histones; 0 / Tumor Suppressor Protein p14ARF; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ NIHMS289834; NLM/ PMC3098888
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6. Haghdoost AA, Hosseini H, Chamani G, Zarei MR, Rad M, Hashemipoor M, Zahedi MJ, Darvish-Moghadam S: Rising incidence of adenocarcinoma of the esophagus in Kerman, Iran. Arch Iran Med; 2008 Jul;11(4):364-70
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rising incidence of adenocarcinoma of the esophagus in Kerman, Iran.
  • BACKGROUND: The fall in the incidence of esophageal squamous cell cancer and noncardia gastric cancers in western countries parallels a concomitant rise in the incidence of gastric cardia cancer and distal adenocarcinoma of the esophagus.
  • We aimed to investigate the incidence trend of different gastric and esophageal cancers in Kerman, southeast Iran.
  • METHODS: The information of all newly diagnosed patients with gastric and esophageal cancers were collected actively from all histopathology departments around the Kerman Province during 1991 - 2002 retrospectively.
  • RESULTS: The annual age standardized incidence risks of esophageal and gastric cancers in Kerman were 1.9 and 6.9 per 100,000 populations.
  • In average, the risks of gastric and esophageal squamous cell cancers were more or less constant, while the risk of adenocarcinoma of the esophagus increased around 11% annually.
  • The rising incidence of adenocarcinoma of the esophagus in Kerman parallels its temporal pattern in western countries.
  • [MeSH-major] Adenocarcinoma / epidemiology. Esophageal Neoplasms / epidemiology. Stomach Neoplasms / epidemiology

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  • (PMID = 18588366.001).
  • [ISSN] 1029-2977
  • [Journal-full-title] Archives of Iranian medicine
  • [ISO-abbreviation] Arch Iran Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Iran
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7. Rubenstein JH, Vakil N, Inadomi JM: The cost-effectiveness of biomarkers for predicting the development of oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2005 Jul 15;22(2):135-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The cost-effectiveness of biomarkers for predicting the development of oesophageal adenocarcinoma.
  • BACKGROUND: The recommended surveillance strategy for oesophageal adenocarcinoma may prevent as few as 50% of cancer deaths.
  • The population consisted of 50-year-old Caucasian men with gastro-oesophageal reflux, who were monitored until age 80.
  • CONCLUSIONS: Biomarkers predicting the development of oesophageal adenocarcinoma would need to be fairly accurate and inexpensive to be cost-effective.
  • These results should guide the development of biomarkers for oesophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Biomarkers / blood. Esophageal Neoplasms / diagnosis

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  • (PMID = 16011672.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 1 T32 DK062708
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers
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8. Long-term antacid use increases likelihood of oesophageal cancer. Nurs Stand; 2009 Apr 22;23(33):17

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

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  • (PMID = 27991114.001).
  • [ISSN] 2047-9018
  • [Journal-full-title] Nursing standard (Royal College of Nursing (Great Britain) : 1987)
  • [ISO-abbreviation] Nurs Stand
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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9. Lanas A, Alcedo González J: [Chemoprevention in adenocarcinoma of the esophagus]. Acta Gastroenterol Latinoam; 2007 Mar;37(1):37-48
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  • [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
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10. Gillen S, Feith M, Gertler R, Langer R, Massmann J, Sarbia M, Friess H: Testicular metastasis from adenocarcinoma of the esophagus. Ann Thorac Surg; 2009 Mar;87(3):957-9
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  • [Title] Testicular metastasis from adenocarcinoma of the esophagus.
  • We report the case of a 61-year-old patient, operated on for adenocarcinoma of the esophagus in 2002, who presented in 2007 with a hydrocele and palpable mass of the right testis.
  • Histopathology revealed a testicular and epididymidal metastasis from the esophageal adenocarcinoma.
  • No case of testicular metastasis from esophageal cancer, including Barrett's carcinoma has been reported.
  • [MeSH-major] Adenocarcinoma / secondary. Esophageal Neoplasms / pathology. Testicular Neoplasms / secondary

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  • (PMID = 19231438.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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11. Paterson AL, Fitzgerald RC: Biomarkers in Barrett's oesophagus and oesophageal adenocarcinoma. Expert Opin Med Diagn; 2007 Nov;1(3):363-76

  • [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
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12. Ilson D, Bains M, Rizk N, Rusch V, Flores R, Park B, Shah M, Kelsen D, Miron B, Goodman K: Phase II trial of preoperative bevacizumab (Bev), irinotecan (I), cisplatin (C), and radiation (RT) in esophageal adenocarcinoma: Preliminary safety analysis. J Clin Oncol; 2009 May 20;27(15_suppl):4573

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

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  • (PMID = 27963076.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Cheung WY, Zhai R, Kulke M, Heist R, Asomaning K, Ma C, Wang Z, Su L, Christiani D, Liu G: Epidermal growth factor (EGF) gene polymorphism, gastroesophageal reflux disease (GERD), and esophageal adenocarcinoma (EAC) risk. J Clin Oncol; 2009 May 20;27(15_suppl):11029

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

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  • (PMID = 27963962.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Yoon HH, Powell M, Murphy K, Montgomery EA, Hafez MJ, Liu G, Forastiere AA, Benson AB, Kleinberg LR, Gibson MK, ECOG E1201-T1 Study Group: Outcome prediction based on single nucleotide polymorphisms (SNPs) in DNA repair paths in patients (pts) with esophageal adenocarcinoma (EAC) treated with preoperative (preop) cisplatin (C)-based chemoradiation (CRT): Results from the Eastern Cooperative Oncology Group (ECOG). J Clin Oncol; 2009 May 20;27(15_suppl):4530

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

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

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

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

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

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  • (PMID = 27961883.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Capdevila J, Clive S, Tabernero J, Lardelli P, Soto-Matos A, Baselga J, Piera A, Pardos I, Rye R, Smyth JF: Phase I study of the novel anticancer drug PM00104 as a 24-hour IV infusion every 3 weeks (q3w) in patients (pts) with advanced solid tumors or lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):2568

  • [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
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18. Rousseau M, Guevremont P, Chasen M, Spicer J, Eckert E, Alcindor T, Ades S, Ferri LE: The management of dysphagia in esophageal cancer patients undergoing neoadjuvant chemotherapy: Is invasive tube feeding required? J Clin Oncol; 2009 May 20;27(15_suppl):9613

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

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  • (PMID = 27963863.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Lagergren J: Controversies surrounding body mass, reflux, and risk of oesophageal adenocarcinoma. Lancet Oncol; 2006 Apr;7(4):347-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Controversies surrounding body mass, reflux, and risk of oesophageal adenocarcinoma.
  • At first the association between body mass, reflux, and oesophageal adenocarcinoma might seem easily interpreted, but a more thorough assessment of the published work shows that several factors are missing.
  • Reflux and obesity are established risk factors for oesophageal adenocarcinoma, particularly when they occur in combination.
  • However, the interplay between these and other factors with regard to oesophageal adenocarcinoma is uncertain.
  • Moreover, the contribution of these risk factors in explaining the increasing incidence of oesophageal adenocarcinoma is unclear, because the trends in prevalence of reflux and obesity do not match those of incidence of oesophageal adenocarcinoma.
  • Moreover, none of these factors contribute strongly to the striking predominance of oesophageal adenocarcinoma in men.
  • Thus, several factors that can explain the development of oesophageal adenocarcinoma need to be addressed.
  • [MeSH-major] Adenocarcinoma / etiology. Body Mass Index. Esophageal Neoplasms / etiology. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / etiology

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  • (PMID = 16574550.001).
  • [ISSN] 1470-2045
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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20. Vial M, Grande L, Pera M: Epidemiology of adenocarcinoma of the esophagus, gastric cardia, and upper gastric third. Recent Results Cancer Res; 2010;182:1-17
The Lens. Cited by Patents in .

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

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  • (PMID = 20676867.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
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21. Westerterp M, Sloof GW, Hoekstra OS, Ten Kate FJ, Meijer GA, Reitsma JB, Boellaard R, van Lanschot JJ, Molthoff CF: 18FDG uptake in oesophageal adenocarcinoma: linking biology and outcome. J Cancer Res Clin Oncol; 2008 Feb;134(2):227-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 18FDG uptake in oesophageal adenocarcinoma: linking biology and outcome.
  • PURPOSE: Variable uptake of 18FDG has been noticed in positron emission tomography (PET) studies of patients with oesophageal adenocarcinoma.
  • The aim of the present study was to investigate biological parameters involved in 18FDG uptake in oesophageal adenocarcinoma for selection of patients with increased 18FDG uptake and prediction of prognostic value of 18FDG PET.
  • PATIENTS AND METHODS: Preoperative PET scans were performed in 26 patients with histologically proven oesophageal adenocarcinoma.
  • CONCLUSIONS: Glut-1 expression and tumour size seem parameters associated with 18FDG uptake in patients with biopsy proven oesophageal adenocarcinoma, and may be used to select oesophageal cancer patients in whom 18FDG-PET is of diagnostic value and may predict disease outcome.
  • [MeSH-major] Adenocarcinoma / metabolism. Esophageal Neoplasms / metabolism. Fluorodeoxyglucose F18 / pharmacokinetics. Radiopharmaceuticals / pharmacokinetics
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Esophagectomy. Esophagogastric Junction / diagnostic imaging. Female. Follow-Up Studies. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Positron-Emission Tomography. Preoperative Care. Tissue Array Analysis. Tissue Distribution. Treatment Outcome

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  • (PMID = 17653575.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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22. Wijnhoven BP, Hussey DJ, Watson DI, Tsykin A, Smith CM, Michael MZ, South Australian Oesophageal Research Group: MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma. Br J Surg; 2010 Jun;97(6):853-61
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma.
  • BACKGROUND: The genetic changes that drive metaplastic progression from squamous oesophageal mucosa toward intestinal metaplasia and adenocarcinoma are unclear.
  • The aberrant expression of microRNAs (miRNAs) is involved in the development of cancer.
  • This study examined whether miRNAs play a role in the development of oesophageal adenocarcinoma.
  • METHODS: RNA was extracted from mucosa of normal oesophageal squamous epithelium, normal gastric epithelium, Barrett's oesophagus with intestinal metaplasia and oesophageal adenocarcinoma obtained from 16 individuals.
  • Expression of miR-143, miR-145 and miR-215 was lower in oesophageal adenocarcinoma than in Barrett's oesophagus.
  • MiR-205 levels were lower in gastric epithelium than in both Barrett's oesophagus and adenocarcinoma.
  • CONCLUSION: Expression of miRNA might define disease states in oesophageal epithelium.
  • Dysregulation of specific miRNAs could contribute to metaplastic and neoplastic processes in the oesophageal mucosa.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. MicroRNAs / analysis. RNA, Messenger / analysis

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  • (PMID = 20301167.001).
  • [ISSN] 1365-2168
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Messenger
  • [Investigator] Wijnhoven BP; Hussey DJ; Watson DI; Smith CM; Mayne GC; Michael MZ; Astill D; Van der Hoek MB; Tsykin A; Tilanus HW; Wijnhoven BP
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23. Desai HG, Kamani PM: Factors responsible for the increasing incidence of oesophageal adenocarcinoma. J Assoc Physicians India; 2007 Jun;55:435-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Factors responsible for the increasing incidence of oesophageal adenocarcinoma.
  • Amongst white population of developed countries, the prevalence of oesophageal adenocarcinoma has dramatically increased during the last four decades.
  • During this period, the increased damage to the oesophageal mucosa with gastroesophageal reflux could result from increased acid output (due to absence of Helicobacter pylori in the gastric mucosa with excellent sanitation) and/or increased frequency of reflux due to an "epidemic" of overweight (65% of the population).
  • The most important environmental factors, responsible for the fastest increasing cancer in humans, are discussed.
  • [MeSH-major] Adenocarcinoma / epidemiology. Esophageal Neoplasms / epidemiology. Global Health. Helicobacter Infections / epidemiology

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  • (PMID = 17879499.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Number-of-references] 51
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24. Kubo A, Corley DA, Jensen CD, Kaur R: Dietary factors and the risks of oesophageal adenocarcinoma and Barrett's oesophagus. Nutr Res Rev; 2010 Dec;23(2):230-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dietary factors and the risks of oesophageal adenocarcinoma and Barrett's oesophagus.
  • Incidence rates for oesophageal adenocarcinoma have increased by over 500% during the past few decades without clear reasons.
  • Gastro-oesophageal reflux disease, obesity and smoking have been identified as risk factors, although the demographic distribution of these risk factors is not consistent with the demographic distribution of oesophageal adenocarcinoma, which is substantially more common among whites and males than any other demographic groups.
  • Numerous epidemiological studies have suggested associations between dietary factors and the risks of oesophageal adenocarcinoma and its precursor, Barrett's oesophagus, though a comprehensive review is lacking.
  • The main aim of the present review is to consider the evidence linking dietary factors with the risks of oesophageal adenocarcinoma, Barrett's oesophagus, and the progression from Barrett's oesophagus to oesophageal adenocarcinoma.
  • The existing epidemiological evidence is strongest for an inverse relationship between intake of vitamin C, β-carotene, fruits and vegetables, particularly raw fruits and vegetables and dark green, leafy and cruciferous vegetables, carbohydrates, fibre and Fe and the risk of oesophageal adenocarcinoma and Barrett's oesophagus.
  • Patients at higher risk for Barrett's oesophagus and oesophageal adenocarcinoma may benefit from increasing their consumption of fruits and vegetables and reducing their intake of red meat and other processed food items.
  • Further research is needed to evaluate the relationship between diet and the progression of Barrett's oesophagus to oesophageal adenocarcinoma.
  • Evidence from cohort studies will help determine whether randomised chemoprevention trials are warranted for the primary prevention of Barrett's oesophagus or its progression to cancer.

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  • (PMID = 20624335.001).
  • [ISSN] 1475-2700
  • [Journal-full-title] Nutrition research reviews
  • [ISO-abbreviation] Nutr Res Rev
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK081271-02; United States / NIDDK NIH HHS / DK / F32 DK081271; United States / NIDDK NIH HHS / DK / 5F32DK81271-2; United States / NIDDK NIH HHS / DK / F32 DK081271-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Micronutrients
  • [Other-IDs] NLM/ NIHMS223558; NLM/ PMC3062915
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25. Mehta S, Johnson IT, Rhodes M: Systematic review: the chemoprevention of oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2005 Nov 1;22(9):759-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systematic review: the chemoprevention of oesophageal adenocarcinoma.
  • The incidence of oesophageal adenocarcinoma is increasing in the UK faster than any other malignancy.
  • Despite its relatively poor prognosis and the limited success of existing treatments, there is enthusiasm that chemopreventive agents might be able to stem the transition from normal squamous epithelium to adenocarcinoma.
  • We discuss gastro-oesophageal reflux as the main risk factor for the development of Barrett's metaplasia, the only known precursor of oesophageal adenocarcinoma.
  • Treatment options for reflux disease are considered with regard to their effects on cancer risk.
  • Available treatments for reflux disease have not convincingly altered the likelihood of cancer development.
  • [MeSH-major] Adenocarcinoma / prevention & control. Esophageal Neoplasms / prevention & control
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Arachidonic Acid / metabolism. Barrett Esophagus / complications. Diet. Disease Progression. Fatty Acids, Omega-3 / metabolism. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / drug therapy. Humans. Nitric Oxide / metabolism. Oxidative Stress / physiology. Proton Pump Inhibitors

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  • (PMID = 16225483.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Fatty Acids, Omega-3; 0 / Proton Pump Inhibitors; 27YG812J1I / Arachidonic Acid; 31C4KY9ESH / Nitric Oxide
  • [Number-of-references] 96
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26. Bergman JJ: The endoscopic diagnosis and staging of oesophageal adenocarcinoma. Best Pract Res Clin Gastroenterol; 2006;20(5):843-66
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  • [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
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27. Rubenstein JH, Taylor JB: Meta-analysis: the association of oesophageal adenocarcinoma with symptoms of gastro-oesophageal reflux. Aliment Pharmacol Ther; 2010 Nov;32(10):1222-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Meta-analysis: the association of oesophageal adenocarcinoma with symptoms of gastro-oesophageal reflux.
  • BACKGROUND: Endoscopic screening has been proposed for patients with symptoms of gastro-oesophageal reflux disease (GERD) in the hope of reducing mortality from oesophageal adenocarcinoma.
  • Assessing the net benefits of such a strategy requires a precise understanding of the cancer risk in the screened population.
  • AIM: To estimate precisely the association between symptoms of GERD and oesophageal adenocarcinoma.
  • At least weekly symptoms of GERD increased the odds of oesophageal adenocarcinoma fivefold (odds ratio = 4.92; 95% confidence interval = 3.90, 6.22), and daily symptoms increased the odds sevenfold (random effects summary odds ratio = 7.40, 95% confidence interval = 4.94, 11.1), each compared with individuals without symptoms or less frequent symptoms.
  • Duration of symptoms was also associated with oesophageal adenocarcinoma, but with very heterogeneous results, and unclear thresholds.
  • CONCLUSIONS: Frequent GERD symptoms are strongly associated with oesophageal adenocarcinoma.
  • These results should be useful in developing epidemiological models of the development of oesophageal adenocarcinoma, and in models of interventions aimed at reducing mortality from this cancer.

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  • [Copyright] Published 2010. This article is a US Government work and is in the public domain in the USA.
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  • (PMID = 20955441.001).
  • [ISSN] 1365-2036
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K23 DK079291; United States / NIDDK NIH HHS / DK / K23DK079291
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS411964; NLM/ PMC3481544
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28. Lagergren J, Jansson C: Sex hormones and oesophageal adenocarcinoma: influence of childbearing? Br J Cancer; 2005 Oct 17;93(8):859-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sex hormones and oesophageal adenocarcinoma: influence of childbearing?
  • The male predominance of oesophageal adenocarcinoma might be explained by oestrogen protection in women.
  • The influence of childbearing on the risk of oesophageal adenocarcinoma was investigated in a Swedish population-based case (n=63) -control (n=141) study.
  • In conclusion, we found no inverse association between childbearing and oesophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / physiopathology. Esophageal Neoplasms / physiopathology. Estrogens / physiology. Infertility, Female / complications

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  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Oct;7(10):913-5 [9796637.001]
  • (PMID = 16189516.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Estrogens
  • [Other-IDs] NLM/ PMC2361653
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29. Lagergren J: Etiology and risk factors for oesophageal adenocarcinoma: possibilities for chemoprophylaxis? Best Pract Res Clin Gastroenterol; 2006;20(5):803-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Etiology and risk factors for oesophageal adenocarcinoma: possibilities for chemoprophylaxis?
  • The rapid increase in the incidence of oesophageal adenocarcinoma, particularly among white males, seems to be a true increase occurring in many parts of the industrialised world during the last few decades.
  • Barrett's oesophagus, gastrooesophageal reflux, high body mass, male sex, tobacco smoking, and high dietary intake of fruit and vegetables.
  • Several other potential risk factors have been studied for which the evidence is less clear, including medications that relax the lower oesophageal sphincter or diets high in fat or low in nutrients from plant foods.
  • Other factors have been found to be possibly inversely linked with the risk of oesophageal adenocarcinoma, including infection with Helicobacter pylori and anti-inflammatory drugs (such as aspirin and other non-steroidal anti-inflammatory drugs, including cyclo-oxygenase inhibitors).
  • The methodological problem of 'confounding by indication' makes it difficult to interpret the results of anti-inflammatory drugs, and currently such medication cannot be recommended for the prevention of oesophageal adenocarcinoma.
  • Similarly, since there is no strong evidence of a preventive effect of medical or surgical antireflux therapy with regard to risk of oesophageal adenocarcinoma, such therapy cannot be recommended in the prevention of this cancer.
  • Although some of the known risk factors might contribute to the increasing incidence of oesophageal adenocarcinoma, the explanation that can entirely explain this striking trend remains to be identified.
  • Oesophageal adenocarcinoma is a highly deadly cancer, but the overall prognosis and the prognosis after oesophageal cancer surgery has improved during recent years.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / prevention & control. Esophageal Neoplasms / etiology. Esophageal Neoplasms / prevention & control
  • [MeSH-minor] Age Factors. Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Barrett Esophagus / complications. Body Mass Index. Chemoprevention. Esophageal Sphincter, Lower / drug effects. Food Habits. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / therapy. Helicobacter Infections / complications. Helicobacter pylori. Humans. Incidence. Prognosis. Risk Factors. Smoking / adverse effects

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  • (PMID = 16997162.001).
  • [ISSN] 1521-6918
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
  • [Number-of-references] 69
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30. Fitzgerald RC: Genetics and prevention of oesophageal adenocarcinoma. Recent Results Cancer Res; 2005;166:35-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetics and prevention of oesophageal adenocarcinoma.
  • Gastric cancer has been declining for more than half a century, whereas the incidence of oesophageal cancer is increasing rapidly.
  • The histopathological subtype is also changing with a predominance of oesophageal adenocarcinoma compared with squamous carcinoma.
  • The reasons for these epidemiological changes are not clear, although population-based data have implicated gastro-oesophageal reflux disease as a risk factor.
  • In susceptible individuals reflux of duodeno-gastric contents can lead to the development of a columnar-lined oesophagus, commonly called Barrett's oesophagus.
  • This can then progress to adenocarcinoma via a metaplasia-dysplasia-carcinoma sequence.
  • At the current time, the mortality from oesophageal adenocarcinoma exceeds 80% at 5 years.
  • Therefore, endoscopic surveillance programmes have been generally recommended for patients with Barrett's oesophagus in an attempt to detect early, curable lesions.
  • There is mounting evidence that there is an underlying genetic susceptibility to Barrett's oesophagus and oesophageal adenocarcinoma.
  • Once patients are identified as having Barrett's oesophagus their chance for developing adenocarcinoma is in the order of 0.5%-1% per year.
  • The histological assessment of dysplasia as a predictor of cancer development is highly subjective.
  • We have demonstrated an increase in the expression of a novel proliferation marker, Mcm2, which occurs during the malignant progression of Barrett's oesophagus.
  • In view of the role of reflux components in the pathogenesis of Barrett's oesophagus the effect of acid and bile on the cell phenotype have been studied.
  • Given the epidemic increase in oesophageal adenocarcinoma and the dismal 5-year mortality rate, a radical approach is necessary to prevent cancer development in individuals with pre-malignant lesions.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / prevention & control. Esophageal Neoplasms / genetics. Esophageal Neoplasms / prevention & control. Neoplasm Proteins / genetics


31. Lagarde SM, ten Kate FJ, Reitsma JB, Busch OR, van Lanschot JJ: Prognostic factors in adenocarcinoma of the esophagus or gastroesophageal junction. J Clin Oncol; 2006 Sep 10;24(26):4347-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic factors in adenocarcinoma of the esophagus or gastroesophageal junction.
  • The incidence of adenocarcinoma of the esophagus is rising rapidly in Western Europe and North America.
  • TNM cancer staging systems predict survival on the basis of the anatomic extent of the tumor.
  • However, the adequacy of the current TNM staging system for adenocarcinoma of the esophagus or gastroesophageal junction (GEJ) is questioned repeatedly.
  • Furthermore, their potential application in the clinical setting in patients with adenocarcinoma of the esophagus or GEJ is discussed.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / therapy. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / therapy. Esophagogastric Junction. Stomach Neoplasms / diagnosis. Stomach Neoplasms / therapy
  • [MeSH-minor] Chemotherapy, Adjuvant. Diagnosis, Computer-Assisted. Humans. Lymphatic Metastasis. Neoadjuvant Therapy. Neoplasm Invasiveness. Neoplasm Staging / methods. Nomograms. Prognosis. Radiotherapy, Adjuvant. Risk Factors

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  • [CommentIn] J Clin Oncol. 2007 Mar 1;25(7):907-8; author reply 908-9 [17327616.001]
  • [CommentIn] J Clin Oncol. 2007 Mar 1;25(7):906-7; author reply 908-9 [17327615.001]
  • (PMID = 16963732.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 134
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32. Jeon J, Luebeck EG, Moolgavkar SH: Age effects and temporal trends in adenocarcinoma of the esophagus and gastric cardia (United States). Cancer Causes Control; 2006 Sep;17(7):971-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Age effects and temporal trends in adenocarcinoma of the esophagus and gastric cardia (United States).
  • A number of hypotheses have been advanced to explain the rapid increase of the incidence of esophageal adenocarcinoma in the US.
  • To address this problem, we have developed multi-stage carcinogenesis models that describe the age-specific incidence of adenocarcinoma of the esophagus and of the gastric cardia with separate adjustments for temporal trends.
  • These models explicitly incorporate important features of the cancers, such as the metaplastic conversion of normal esophagus to Barrett's esophagus (BE).
  • We fit these models separately to the incidence of adenocarcinoma of the esophagus and of the gastric cardia reported in the Surveillance Epidemiology and End Results (SEER) registry over the period 1973-2000.
  • [MeSH-major] Adenocarcinoma / epidemiology. Cardia. Esophageal Neoplasms / epidemiology. Stomach Neoplasms / epidemiology

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  • (PMID = 16841264.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA047658; United States / NCI NIH HHS / CA / R01 CA119224-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
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33. Gockel I, Heckhoff S, Messow CM, Kneist W, Junginger T: Transhiatal and transthoracic resection in adenocarcinoma of the esophagus: does the operative approach have an influence on the long-term prognosis? World J Surg Oncol; 2005 Jun 24;3:40

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

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  • [Cites] Lancet. 2002 May 18;359(9319):1727-33 [12049861.001]
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  • (PMID = 15978128.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1182399
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34. Jiménez P, Piazuelo E, Cebrian C, Ortego J, Strunk M, García-Gonzalez MA, Santander S, Alcedo J, Lanas A: Prostaglandin EP2 receptor expression is increased in Barrett's oesophagus and oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2010 Feb 1;31(3):440-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prostaglandin EP2 receptor expression is increased in Barrett's oesophagus and oesophageal adenocarcinoma.
  • BACKGROUND: Accumulating evidence suggests that cyclooxygenase-2 (COX-2)-derived prostaglandin E2 (PGE2) is involved in oesophageal adenocarcinogenesis.
  • AIM: To investigate which PGE2 receptor subtypes regulate PGE2 signals in the oesophageal adenocarcinoma sequence.
  • METHODS: Expression was determined in oesophageal biopsies from 85 patients with oesophagitis, Barrett's metaplasia, intraepithelial neoplasia, oesophageal adenocarcinoma and normal oesophagus.
  • Expression of EP receptors was also determined in response to acid and bile exposure in the Barrett's adenocarcinoma cell line OE33.
  • RESULTS: All four EP receptors subtypes were expressed in human oesophageal tissues.
  • COX-2 and, especially, EP2 were increased in the Barrett's metaplasia-intraepithelial neoplasia-adenocarcinoma sequence.
  • Expression of the EP4 receptor protein was increased in oesophageal adenocarcinoma.
  • CONCLUSIONS: Our data suggest that in addition to COX-2, EP2 and EP4 receptors could be a selective target in the prevention and/or treatment of the Barrett's-associated adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Cyclooxygenase 1 / metabolism. Esophageal Neoplasms / pathology. RNA, Messenger / metabolism. Receptors, Prostaglandin E / metabolism

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  • (PMID = 19843025.001).
  • [ISSN] 1365-2036
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / PTGER2 protein, human; 0 / RNA, Messenger; 0 / Receptors, Prostaglandin E; 0 / Receptors, Prostaglandin E, EP2 Subtype; EC 1.14.99.1 / Cyclooxygenase 1
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35. Barthel JS, Kucera ST, Lin JL, Hoffe SE, Strosberg JR, Ahmed I, Dilling TJ, Stevens CW: Does Barrett's esophagus respond to chemoradiation therapy for adenocarcinoma of the esophagus? Gastrointest Endosc; 2010 Feb;71(2):235-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does Barrett's esophagus respond to chemoradiation therapy for adenocarcinoma of the esophagus?
  • BACKGROUND: Adenocarcinoma of the esophagus is frequently associated with Barrett's esophagus (BE).
  • The response of esophageal adenocarcinoma to chemoradiation therapy is well described; however, the effect of chemoradiation on tumor-associated BE has not been specifically reported.
  • SETTING: A single National Cancer Institute Comprehensive Cancer Care Center experience.
  • PATIENTS: The study cohort consisted of 43 patients with stage I to IVA esophageal adenocarcinoma associated with BE who received either neoadjuvant or definitive chemoradiation therapy and underwent either esophagectomy or surveillance at our institution.
  • MAIN OUTCOME MEASUREMENT: The presence and extent of BE after chemoradiation therapy of esophageal adenocarcinoma associated with endoscopically documented pretreatment BE.
  • CONCLUSIONS: Chemoradiation therapy of esophageal adenocarcinoma does not eliminate tumor-associated BE, nor does it affect the length of the BE segment.
  • [MeSH-major] Adenocarcinoma / therapy. Barrett Esophagus / therapy. Esophageal Neoplasms / therapy. Esophagoscopy. Precancerous Conditions / pathology

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  • [Copyright] C
  • (PMID = 20003971.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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36. Barclay JY, Morris A, Nwokolo CU: Telomerase, hTERT and splice variants in Barrett's oesophagus and oesophageal adenocarcinoma. Eur J Gastroenterol Hepatol; 2005 Feb;17(2):221-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Telomerase, hTERT and splice variants in Barrett's oesophagus and oesophageal adenocarcinoma.
  • BACKGROUND AND OBJECTIVES: The enzyme telomerase is re-activated in most cancers but its mechanism of regulation in oesophageal carcinogenesis is unclear.
  • The aim of this study was to determine the roles of human telomerase reverse transcriptase (hTERT) mRNA expression and hTERT mRNA splicing in the regulation of telomerase enzyme activity in Barrett's oesophagus and oesophageal adenocarcinoma.
  • METHODS: Paired samples from oesophageal adenocarcinoma (n=21) and adjacent macroscopically normal mucosa, and paired samples from Barrett's oesophagus (n=16) and adjacent cardia mucosa were obtained.
  • RESULTS: In oesophageal adenocarcinoma, compared to adjacent mucosa, median telomerase activity increased significantly (from 5 to 229 total product generated (tpg), P=0.0002), but median hTERT mRNA levels were not significantly different.
  • Similarly, median telomerase activity was significantly higher in oesophageal adenocarcinoma compared to Barrett's oesophagus (229 vs 20 tpg, P=0.001), but hTERT mRNA levels were not significantly different.
  • There was no significant difference in telomerase activity and hTERT mRNA levels between Barrett's oesophagus and adjacent cardia.
  • The frequency of detection of all variants increased from cardia to Barrett's oesophagus to oesophageal adenocarcinoma (P<0.05).
  • CONCLUSIONS: A major increase in telomerase activity occurs after the Barrett's oesophagus stage in oesophageal carcinogenesis.
  • In this cancer, an important clinical diagnostic role for the transcripts of the telomerase gene is improbable.
  • [MeSH-major] Adenocarcinoma / enzymology. Barrett Esophagus / enzymology. Esophageal Neoplasms / enzymology. Gene Expression Regulation, Neoplastic. Telomerase / metabolism

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  • (PMID = 15674101.001).
  • [ISSN] 0954-691X
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.7.49 / Telomerase
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37. Zhang X, Watson DI, Jamieson GG: Lymph node metastases of adenocarcinoma of the esophagus and esophagogastric junction. Chin Med J (Engl); 2007 Dec 20;120(24):2268-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lymph node metastases of adenocarcinoma of the esophagus and esophagogastric junction.
  • BACKGROUND: Esophageal adenocarcinoma is becoming an increasingly important problem.
  • The aim of this study was to evaluate the relationship between tumor invasion depth and lymph node metastasis for adenocarcinoma of the esophagus and esophagogastric junction, and to analyze the impact of lymph node metastases on survival of the patients.
  • METHODS: The study group comprised 121 patients with adenocarcinoma of the esophagus or esophagogastric junction, who underwent esophagectomy between January 1985 and December 2003 at either the Royal Adelaide Hospital or the Flinders Medical Center, Australia.
  • RESULTS: The tumors were located entirely within the esophagus in 83 patients, and involved the gastro-esophageal junction in 38.
  • When tumor invasion was within mucosa or submucosa of the esophagus (T1), the lymph node metastasis rate was 22.2% (10/45), the mean number of metastatic lymph nodes was 0.3, and the proportion of more than 4 lymph nodes metastases was 0% (0/45).
  • When tumor invaded the adjacent structures of the esophagus (T4), the lymph node metastasis rate was 85.7% (6/7); the mean number of metastatic lymph nodes was 5.1, and the proportion of more than 4 lymph nodes metastases was 71.4% (5/7).
  • CONCLUSIONS: There is a close association between tumor invasion depth and lymph node metastasis for adenocarcinoma of the esophagus and esophagogastric junction.
  • Moreover, when the tumor invades deeper into the esophageal wall, the percentage of patients with more than 4 involved nodes increases.
  • [MeSH-major] Adenocarcinoma / pathology. Esophageal Neoplasms / pathology. Esophagogastric Junction / pathology. Stomach Neoplasms / pathology

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  • (PMID = 18167216.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
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38. Chak A, Ochs-Balcom H, Falk G, Grady WM, Kinnard M, Willis JE, Elston R, Eng C: Familiality in Barrett's esophagus, adenocarcinoma of the esophagus, and adenocarcinoma of the gastroesophageal junction. Cancer Epidemiol Biomarkers Prev; 2006 Sep;15(9):1668-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Familiality in Barrett's esophagus, adenocarcinoma of the esophagus, and adenocarcinoma of the gastroesophageal junction.
  • BACKGROUND AND AIM: The familial aggregation of Barrett's esophagus, adenocarcinoma of the esophagus, and adenocarcinoma of the gastroesophageal junction, jointly termed familial Barrett's esophagus, may represent a complex genetic trait.
  • The aim of this study was to determine the proportion of patients with these diseases who have familial Barrett's esophagus.
  • METHODS: Information on gastroesophageal reflux symptoms, known risk factors for Barrett's esophagus, and family history of Barrett's esophagus and cancers, was collected at six hospitals using a structured questionnaire from probands with either long-segment Barrett's esophagus, adenocarcinoma of the esophagus, or adenocarcinoma of the gastroesophageal junction.
  • Family history of Barrett's esophagus or esophageal cancer in a first- or second-degree relative was determined by reviewing medical records of all relatives reported to be affected.
  • Upon review of medical records of the reportedly affected relatives, familial Barrett's esophagus was definitively determined in the case of 30 (7.3%) probands comprising 17 of 276 (6.2%) with Barrett's esophagus, 11 of 116 (9.5%) with adenocarcinoma of the esophagus, and 2 of 21 (9.5%) with adenocarcinoma of the gastroesophageal junction.
  • The diagnosis in the relative reported by the proband to be affected was found not to be Barrett's esophagus or adenocarcinoma in 15 (3.6%) cases.
  • The diagnosis could not be determined in 26 (6.3%) cases in which the proband reported an affected relative.
  • There were no significant differences in age of disease onset, gender, race, or gastroesophageal reflux symptoms between definitive familial Barrett's esophagus probands and nonfamilial probands.
  • CONCLUSION: Familial Barrett's esophagus can be confirmed in 7.3% of persons presenting with Barrett's esophagus, adenocarcinoma of the esophagus, or adenocarcinoma of the gastroesophageal junction.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Esophagogastric Junction

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  • (PMID = 16985029.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA30722; United States / NIDDK NIH HHS / DK / DK002800; United States / NIDDK NIH HHS / DK / DK061426; United States / NIDDK NIH HHS / DK / DK070863; United States / NIGMS NIH HHS / GM / GM28356; United States / PHS HHS / / P30CAD43703; United States / NCI NIH HHS / CA / R25 CA094186
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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39. Anderson LA, Watson RG, Murphy SJ, Johnston BT, Comber H, Mc Guigan J, Reynolds JV, Murray LJ: Risk factors for Barrett's oesophagus and oesophageal adenocarcinoma: results from the FINBAR study. World J Gastroenterol; 2007 Mar 14;13(10):1585-94
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  • [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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  • (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
  •  go-up   go-down


40. Lagarde SM, ten Kate FJ, Richel DJ, Offerhaus GJ, van Lanschot JJ: Molecular prognostic factors in adenocarcinoma of the esophagus and gastroesophageal junction. Ann Surg Oncol; 2007 Feb;14(2):977-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular prognostic factors in adenocarcinoma of the esophagus and gastroesophageal junction.
  • OBJECTIVE: This review describes genetic and molecular changes related to adenocarcinoma of the esophagus and gastroesophageal junction (GEJ) with emphasis on prognostic value and possibilities for targeted therapy in clinical setting.
  • Adenocarcinoma of the esophagus or GEJ is an aggressive disease with early lymphatic and hematogenous dissemination.
  • Better knowledge of molecular bases may lead to new paradigms, improved prognostication, early diagnosis and individually tailored therapeutic options.
  • METHODS: A review of recent English literature (1990-October 2005) concerning esophageal adenocarcinoma was performed.
  • This review focuses on genetic and molecular changes as prognosticators of adenocarcinoma of the esophagus and GEJ.
  • CONCLUSIONS: Adenocarcinomas of the esophagus and GEJ show multiple genetic alterations, which indicate that progression of cancer is a multistep complex process with many different alterations.
  • Presumably, it is not one molecular factor that can predict the biological behavior of this cancer.
  • [MeSH-major] Adenocarcinoma / genetics. Biomarkers, Tumor / genetics. Esophageal Neoplasms / genetics. Esophagogastric Junction


41. Ladanchuk TC, Johnston BT, Murray LJ, Anderson LA, FINBAR study group: Risk of Barrett's oesophagus, oesophageal adenocarcinoma and reflux oesophagitis and the use of nitrates and asthma medications. Scand J Gastroenterol; 2010 Dec;45(12):1397-403
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  • [Title] Risk of Barrett's oesophagus, oesophageal adenocarcinoma and reflux oesophagitis and the use of nitrates and asthma medications.
  • OBJECTIVE: To investigate the relationship between use of asthma medication and nitrates and risk of reflux oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma.
  • MATERIAL AND METHODS: Data were collected on use of asthma medication and nitrates at least 1 year before interview from patients with reflux oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma.
  • Associations between use of asthma medications and nitrates and the risk of reflux oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma were estimated using multiple logistic regression.
  • RESULTS: Nine hundred and forty-one subjects were recruited: 230 reflux oesophagitis, 224 Barrett's oesophagus, 227 oesophageal adenocarcinoma patients and 260 population controls.
  • Barrett's oesophagus patients were more likely than controls to have had a diagnosis of asthma (odds ratio 2.15, 95% confidence interval 1.15-4.03) and to have used asthma medications (odds ratio 2.13, 95% confidence interval 1.09-4.16).
  • No significant associations were observed between use of asthma medication or nitrates and reflux oesophagitis or oesophageal adenocarcinoma.
  • CONCLUSIONS: Gastro-oesophageal reflux symptoms appear to confound the association between asthma medication use and Barrett's oesophagus.
  • However, it is possible that asthma medications may increase the risk of Barrett's oesophagus by other mechanisms.
  • [MeSH-major] Adenocarcinoma / chemically induced. Anti-Asthmatic Agents / adverse effects. Barrett Esophagus / chemically induced. Esophageal Neoplasms / chemically induced. Esophagitis, Peptic / chemically induced. Nitrates / adverse effects

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  • (PMID = 20626305.001).
  • [ISSN] 1502-7708
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Asthmatic Agents; 0 / Nitrates
  • [Investigator] Murray LJ; Anderson LA; Johnston BT; Watson RG; McGuigan J; Ferguson HR; Murphy SJ; Reynolds JV; Comber H
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42. Reid BJ, Li X, Galipeau PC, Vaughan TL: Barrett's oesophagus and oesophageal adenocarcinoma: time for a new synthesis. Nat Rev Cancer; 2010 Feb;10(2):87-101
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  • [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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  • (PMID = 20094044.001).
  • [ISSN] 1474-1768
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA124911-02; United States / NCI NIH HHS / CA / K05 CA124911; United States / NCI NIH HHS / CA / P01 CA091955; United States / NCI NIH HHS / CA / P01 CA091955-08; United States / NCI NIH HHS / CA / K05 CA124911-02
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 218
  • [Other-IDs] NLM/ NIHMS200752; NLM/ PMC2879265
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43. van Blankenstein M, Looman CW, Siersema PD, Kuipers EJ, Coebergh JW: Trends in the incidence of adenocarcinoma of the oesophagus and cardia in the Netherlands 1989-2003. Br J Cancer; 2007 Jun 4;96(11):1767-71
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  • [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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  • (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
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44. Kirkeleit J, Riise T, Bjørge T, Moen BE, Bråtveit M, Christiani DC: Increased risk of oesophageal adenocarcinoma among upstream petroleum workers. Occup Environ Med; 2010 May;67(5):335-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased risk of oesophageal adenocarcinoma among upstream petroleum workers.
  • OBJECTIVES: To investigate cancer risk, particularly oesophageal cancer, among male upstream petroleum workers offshore potentially exposed to various carcinogenic agents.
  • The historical cohort was linked to the Cancer Registry of Norway and the Norwegian Cause of Death Registry.
  • RESULTS: Male offshore workers had excess risk of oesophageal cancer (RR 2.6, 95% CI 1.4 to 4.8) compared with the reference population.
  • Only the adenocarcinoma type had a significantly increased risk (RR 2.7, 95% CI 1.0 to 7.0), mainly because of an increased risk among upstream operators (RR 4.3, 95% CI 1.3 to 14.5).
  • Upstream operators did not have significant excess of respiratory system or colon cancer or mortality from any other lifestyle-related diseases investigated.
  • CONCLUSION: We found a fourfold excess risk of oesophageal adenocarcinoma among male workers assumed to have had the most extensive contact with crude oil.
  • Due to the small number of cases, and a lack of detailed data on occupational exposure and lifestyle factors associated with oesophageal adenocarcinoma, the results must be interpreted with caution.
  • Nevertheless, given the low risk of lifestyle-related cancers and causes of death in this working group, the results add to the observations in other low-powered studies on oesophageal cancer, further suggesting that factors related to the petroleum stream or carcinogenic agents used in the production process might be associated with risk of oesophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / epidemiology. Esophageal Neoplasms / epidemiology. Occupational Diseases / epidemiology. Occupational Exposure / adverse effects. Petroleum / toxicity

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  • (PMID = 19858535.001).
  • [ISSN] 1470-7926
  • [Journal-full-title] Occupational and environmental medicine
  • [ISO-abbreviation] Occup Environ Med
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA074386; United States / NCI NIH HHS / CA / R01 CA074386-03; United States / NCI NIH HHS / CA / R01 CA074386-04; United States / NCI NIH HHS / CA / R01 CA074386-05; United States / NCI NIH HHS / CA / R01 CA074386-06A1; United States / NCI NIH HHS / CA / R01 CA074386-07; United States / NCI NIH HHS / CA / R01 CA074386-08; United States / NCI NIH HHS / CA / R01 CA074386-09; United States / NCI NIH HHS / CA / R01 CA074386-10
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Petroleum
  • [Other-IDs] NLM/ NIHMS493408; NLM/ PMC3728278
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45. Peters CJ, Fitzgerald RC: Systematic review: the application of molecular pathogenesis to prevention and treatment of oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2007 Jun 01;25(11):1253-69
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  • [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
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46. Lamb PJ, Griffin SM, Burt AD, Lloyd J, Karat D, Hayes N: Sentinel node biopsy to evaluate the metastatic dissemination of oesophageal adenocarcinoma. Br J Surg; 2005 Jan;92(1):60-7
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  • [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
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47. Goddeeris K, Verslype C, Wilms G, Van Cutsem E: Leptomeningeal carcinomatosis associated with oesophageal adenocarcinoma: two case reports and review of the literature. Acta Gastroenterol Belg; 2006 Oct-Dec;69(4):377-80
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  • [Title] Leptomeningeal carcinomatosis associated with oesophageal adenocarcinoma: two case reports and review of the literature.
  • We report two cases of leptomeningeal carcinomatosis in patients with oesophageal adenocarcinoma.
  • Diagnosis of LC can be overlooked without a high index of suspicion.
  • [MeSH-major] Adenocarcinoma / secondary. Esophageal Neoplasms / pathology. Meningeal Neoplasms / secondary

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  • (PMID = 17343079.001).
  • [ISSN] 1784-3227
  • [Journal-full-title] Acta gastro-enterologica Belgica
  • [ISO-abbreviation] Acta Gastroenterol. Belg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
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48. Lagarde SM, de Boer JD, ten Kate FJ, Busch OR, Obertop H, van Lanschot JJ: Postoperative complications after esophagectomy for adenocarcinoma of the esophagus are related to timing of death due to recurrence. Ann Surg; 2008 Jan;247(1):71-6
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  • [Title] Postoperative complications after esophagectomy for adenocarcinoma of the esophagus are related to timing of death due to recurrence.
  • After esophagectomy for adenocarcinoma of the distal esophagus and/or gastroesophageal junction, the majority of patients develops an early recurrence and dies within 2 years.
  • METHODS: A consecutive series of 351 patients who underwent esophagectomy for adenocarcinoma of the esophagus and gastroesophageal junction was reviewed.
  • RESULTS: Of the 351 included patients, 191 patients (54%) died due to recurrence of esophageal adenocarcinoma.
  • Multivariate Cox regression analysis demonstrated that T-stage, lymph node ratio >0.20, the presence of extracapsular lymph node involvement, but not complications were significant factors for the prediction of death due to cancer recurrence.
  • CONCLUSION: The relation between perioperative complications and cancer recurrence per se is not causal.
  • However, postoperative complications are independently associated with the early timing of death due to cancer recurrence.
  • [MeSH-major] Adenocarcinoma / mortality. Adenocarcinoma / surgery. Esophageal Neoplasms / mortality. Esophageal Neoplasms / surgery. Esophagectomy. Neoplasm Recurrence, Local / mortality. Postoperative Complications / mortality

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  • (PMID = 18156925.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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49. Shibata A, Matsuda T, Ajiki W, Sobue T: Trend in incidence of adenocarcinoma of the esophagus in Japan, 1993-2001. Jpn J Clin Oncol; 2008 Jul;38(7):464-8
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  • [Title] Trend in incidence of adenocarcinoma of the esophagus in Japan, 1993-2001.
  • BACKGROUND: Several studies with population-based cancer registry data have suggested that incidence of adenocarcinoma of the esophagus has been increasing since 1970 in some European and North American countries and Australia.
  • However, data from Asian countries with regard to the incidence of esophageal cancer by histological type based on the population-based cancer registry are lacking.
  • The aim of this study was to describe the incidence of esophageal cancer by histological type in a Japanese population.
  • METHODS: Cancer incidence data for 1993-2001 from 15 population-based cancer registries were collected by the Japan Cancer Surveillance Research Group in 2005.
  • RESULTS: Squamous cell carcinoma remains the predominant type in all esophageal cancers in Japan.
  • The ratio of squamous cell carcinoma to adenocarcinoma is 26:1.
  • For adenocarcinoma, estimated average annual percentage change was 4.7% (95% confidence interval: 0.7, 8.9) in men and 6.0% (2.4, 9.8) in women.
  • CONCLUSION: No dramatic increase in adenocarcinoma has occurred, and absolute incidence remains low in Japan.
  • [MeSH-major] Adenocarcinoma / epidemiology. Asian Continental Ancestry Group / statistics & numerical data. Esophageal Neoplasms / epidemiology

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  • (PMID = 18664481.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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50. Neale RE, Doecke JD, Pandeya N, Sadeghi S, Green AC, Webb PM, Whiteman DC, Australian Cancer Study: Does type 2 diabetes influence the risk of oesophageal adenocarcinoma? Br J Cancer; 2009 Mar 10;100(5):795-8
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  • [Title] Does type 2 diabetes influence the risk of oesophageal adenocarcinoma?
  • Since hyperinsulinaemia may promote obesity-linked cancers, we compared type 2 diabetes prevalence among oesophageal adenocarcinoma (OAC) patients and population controls.
  • [MeSH-major] Adenocarcinoma / etiology. Diabetes Mellitus, Type 2 / complications. Esophageal Neoplasms / etiology

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  • [Cites] Br J Cancer. 2000 Jul;83(1):127-32 [10883680.001]
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  • (PMID = 19190630.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2653775
  • [Investigator] Whiteman DC; Webb PM; Green AC; Hayward NK; Parsons PG; Purdie DM
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51. Mitchell EM, Pal N, Kalyan JP, Rhodes M, Lewis MP: Poor outcome of oesophageal adenocarcinoma after prior antireflux surgery. Int J Surg; 2009 Dec;7(6):566-9
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  • [Title] Poor outcome of oesophageal adenocarcinoma after prior antireflux surgery.
  • AIMS: Gastro-oesophageal reflux disease is an important risk factor for oesophageal adenocarcinoma, but abolishing reflux through surgery has not been shown to reduce this risk.
  • PATIENTS AND METHODS: Six hundred and forty three patients underwent surgical resection in our unit for oesophagogastric adenocarcinoma between 2000 and 2009.
  • CONCLUSIONS: Patients who have undergone antireflux surgery for chronic gastro-oesophageal reflux disease can develop adenocarcinoma and need to be monitored closely.
  • [MeSH-major] Adenocarcinoma / mortality. Adenocarcinoma / surgery. Cause of Death. Esophageal Neoplasms / mortality. Esophageal Neoplasms / surgery. Gastroesophageal Reflux / surgery

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  • (PMID = 19833239.001).
  • [ISSN] 1743-9159
  • [Journal-full-title] International journal of surgery (London, England)
  • [ISO-abbreviation] Int J Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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52. Rutegård M, Nordenstedt H, Lu Y, Lagergren J, Lagergren P: Sex-specific exposure prevalence of established risk factors for oesophageal adenocarcinoma. Br J Cancer; 2010 Aug 24;103(5):735-40
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  • [Title] Sex-specific exposure prevalence of established risk factors for oesophageal adenocarcinoma.
  • BACKGROUND: There is an unexplained male predominance in the incidence of oesophageal adenocarcinoma, and the sex-specific distribution of its risk factors in the general population is not known.
  • METHODS: A random sample of Swedish citizens aged 40-79 years completed a questionnaire for assessment of the prevalence of five risk factors for oesophageal adenocarcinoma: reflux symptoms, body mass index, tobacco smoking habits, socioeconomic status, and use of non-steroidal anti-inflammatory drugs (NSAIDs).
  • CONCLUSIONS: Exposure to some but not all established risk factors for oesophageal adenocarcinoma seems to be more common in men than in women, but the differences are small and unlikely to explain the male predominance of this tumour.
  • [MeSH-major] Adenocarcinoma / epidemiology. Esophageal Neoplasms / epidemiology

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  • (PMID = 20700121.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
  • [Other-IDs] NLM/ PMC2938252
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53. Witzig R, Schönberger B, Fink U, Busch R, Gundel H, Sendler A, Peschel C, Siewert JR, Lordick F: Delays in diagnosis and therapy of gastric cancer and esophageal adenocarcinoma. Endoscopy; 2006 Nov;38(11):1122-6
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  • [Title] Delays in diagnosis and therapy of gastric cancer and esophageal adenocarcinoma.
  • BACKGROUND AND STUDY AIMS: In the past, there were long delays in the diagnosis of patients with cancer of the stomach or esophagus.
  • The objective of this study was to describe current delays in the diagnosis and treatment of gastric and esophageal adenocarcinoma and to compare the findings with those from an historical control population treated at the same institutions 10 years earlier.
  • PATIENTS AND METHODS: Patients with biopsy-proven gastric cancer or esophageal adenocarcinoma who were treated at two academic medical centers in Germany between April and October 2003 were consecutively screened for eligibility to take part in the study.
  • RESULTS: The median total delay for patients with gastric cancer (n = 104) was 3.5 months (range 0.3 - 29.6), and in patients with esophageal adenocarcinoma (n = 22) the total delay was significantly shorter (median 2.2 months, range 1.2 - 11.7; P < 0.05).
  • Comparing these findings with those from an historic cohort of patients with gastric cancer (n = 100) revealed a significant decrease in the total delay (3.5 versus 8.0 months, P < 0.001).
  • CONCLUSIONS: The current findings indicate that delays in the diagnosis and treatment of gastric cancer have become significantly shorter within the last 10 years as our understanding of and ability to treat this form of cancer have improved.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / therapy. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / therapy. Stomach Neoplasms / diagnosis. Stomach Neoplasms / therapy


54. Smithers BM, Couper GC, Thomas JM, Wong D, Gotley DC, Martin I, Harvey JA, Thomson DB, Walpole ET, Watts N, Burmeister BH: Positron emission tomography and pathological evidence of response to neoadjuvant therapy in adenocarcinoma of the esophagus. Dis Esophagus; 2008;21(2):151-8
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  • [Title] Positron emission tomography and pathological evidence of response to neoadjuvant therapy in adenocarcinoma of the esophagus.
  • Our aim was to determine if fluorodeoxyglucose positron emission tomography (FDG-PET) could be correlated with a pathological response in patients with esophageal adenocarcinoma receiving neoadjuvant chemotherapy and/or chemoradiation therapy.
  • Patients with resectable, histologically proven adenocarcinoma of the esophagus were entered in the study.
  • Presently an FDG-PET scan performed 3-6 weeks after neoadjuvant therapy for adenocarcinoma of the esophagus should not be used as a marker of the potential result of the treatment.

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  • (PMID = 18269651.001).
  • [ISSN] 1442-2050
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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55. Miyashita T, Ohta T, Fujimura T, Ninomiya I, Fushida S, Hattori T, Miwa K: Duodenal juice stimulates oesophageal stem cells to induce Barrett's oesophagus and oesophageal adenocarcinoma in rats. Oncol Rep; 2006 Jun;15(6):1469-75
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  • [Title] Duodenal juice stimulates oesophageal stem cells to induce Barrett's oesophagus and oesophageal adenocarcinoma in rats.
  • the present study was performed to examine the sequential process of the development of Barrett's oesophagus (BE) and oesophageal adenocarcinoma (ADC) induced by duodeno-oesophageal reflux (DER) in rats.
  • Total gastrectomy was performed in male Wistar rats weighing approximately 250 g followed by reconstruction with oesophago-jejunostomy, which causes unavoidable DER without exposure to exogenous carcinogens.
  • On the 20th week, glandular structures that stained positively with Galactose oxidase-Schiff (foveolar metaplasia) were observed in the basal layer of the oesophageal squamous epithelium.
  • Persistent stimulation with DER can alter the stem cells in the squamous epithelial basal layer leading to the formation of columnar-lined cells and subsequent ADC.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / etiology. Duodenogastric Reflux / complications. Duodenum / secretion. Esophageal Neoplasms / etiology. Esophagus / pathology. Gastroesophageal Reflux / complications. Stem Cells / pathology

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  • (PMID = 16685381.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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56. Beales IL, Ogunwobi OO: Glycine-extended gastrin inhibits apoptosis in Barrett's oesophageal and oesophageal adenocarcinoma cells through JAK2/STAT3 activation. J Mol Endocrinol; 2009 Apr;42(4):305-18
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  • [Title] Glycine-extended gastrin inhibits apoptosis in Barrett's oesophageal and oesophageal adenocarcinoma cells through JAK2/STAT3 activation.
  • Barrett's oesophagus (BO) and oesophageal adenocarcinoma (OAC) are regarded as complications of gastro-oesophageal reflux disease, although all the factors that contribute to the development of these lesions are unknown.
  • We have examined the effects of glycine-extended gastrin (G-Gly), an alternative product of progastrin processing on apoptosis in the QhERT Barrett's oesophageal cell line and OE33 and BIC-1 OAC cells.
  • [MeSH-major] Adenocarcinoma / pathology. Apoptosis / drug effects. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Gastrins / pharmacology. Janus Kinase 2 / metabolism. STAT3 Transcription Factor / metabolism

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  • (PMID = 19153190.001).
  • [ISSN] 1479-6813
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Gastrins; 0 / RNA, Small Interfering; 0 / Receptors, Cholecystokinin; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / glycine-extended gastrin 17; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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57. Lerut T, Decker G, Coosemans W, De Leyn P, Decaluwé H, Nafteux P, Van Raemdonck D: Quality indicators of surgery for adenocarcinoma of the esophagus and gastroesophageal junction. Recent Results Cancer Res; 2010;182:127-42
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  • [Title] Quality indicators of surgery for adenocarcinoma of the esophagus and gastroesophageal junction.
  • Surgical treatment of adenocarcinoma of the esophagus and gastroesophageal junction is complex and challenging.
  • As a result there is disagreement on the selection of patients for surgery, type of surgical approach in particular in relation to the extent of lymph node dissection as well as the extent of esophageal and/or gastric resection.
  • [MeSH-major] Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagogastric Junction. Stomach Neoplasms / surgery

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  • (PMID = 20676877.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
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58. Tuynman JB, Lagarde SM, Ten Kate FJ, Richel DJ, van Lanschot JJ: Met expression is an independent prognostic risk factor in patients with oesophageal adenocarcinoma. Br J Cancer; 2008 Mar 25;98(6):1102-8
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  • [Title] Met expression is an independent prognostic risk factor in patients with oesophageal adenocarcinoma.
  • Oesophageal adenocarcinoma is an aggressive malignancy with propensity for early lymphatic and haematogenous dissemination.
  • Tumour sections from 145 consecutive patients undergoing intentionally curative surgery for oesophageal adenocarcinoma were immunohistochemically analysed for Met and COX-2 expression.
  • These findings support the importance of Met in oesophageal adenocarcinoma and support the concept of Met tyrosine kinase inhibition as (neo-) adjuvant treatment.
  • [MeSH-major] Adenocarcinoma / metabolism. Esophageal Neoplasms / metabolism. Proto-Oncogene Proteins c-met / metabolism

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  • (PMID = 18349821.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-met
  • [Other-IDs] NLM/ PMC2275481
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59. Boult JK, Tanière P, Hallissey MT, Campbell MJ, Tselepis C: Oesophageal adenocarcinoma is associated with a deregulation in the MYC/MAX/MAD network. Br J Cancer; 2008 Jun 17;98(12):1985-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oesophageal adenocarcinoma is associated with a deregulation in the MYC/MAX/MAD network.
  • Oesophageal adenocarcinoma, which arises from an acquired columnar lesion, Barrett's metaplasia, is rising in incidence more rapidly than any other cancer in the Western world.
  • Elevated expression of c-MYC has been demonstrated in oesophageal adenocarcinoma; however, the expression of other members of the MYC/MAX/MAD network has not been addressed.
  • The aims of this work were to characterise the expression of c-MYC, MAX and the MAD family in adenocarcinoma development and assess the effects of overexpression on cellular behaviour. mRNA expression in samples of Barrett's metaplasia and oesophageal adenocarcinoma were examined by qRT-PCR.
  • Consistent with previous work expression of c-MYC was deregulated in oesophageal adenocarcinoma.
  • In conclusion, the expression patterns of c-MYC, MAX and the MAD family were shown to be deregulated in the oesophageal cancer model.
  • [MeSH-major] Adenocarcinoma / genetics. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / genetics. Esophageal Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Genes, myc. Repressor Proteins / genetics

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  • (PMID = 18493233.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / MAX protein, human; 0 / MXD1 protein, human; 0 / Repressor Proteins
  • [Other-IDs] NLM/ PMC2441969
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60. Quera R, O'Sullivan K, Quigley EM: Surveillance in Barrett's oesophagus: will a strategy focused on a high-risk group reduce mortality from oesophageal adenocarcinoma? Endoscopy; 2006 Feb;38(2):162-9
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  • [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
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61. Sarbia M: The histological appearance of oesophageal adenocarcinoma--an analysis based on 215 resection specimens. Virchows Arch; 2006 May;448(5):532-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The histological appearance of oesophageal adenocarcinoma--an analysis based on 215 resection specimens.
  • The current study was performed to determine whether the histopathological appearance of oesophageal adenocarcinoma (AC) differs significantly from that of cardiac or gastric AC.
  • Therefore, HE-stained slides of 215 primarily resected oesophageal AC, 108 cardiac and 184 gastric AC were classified according to a variety of clinico-pathologic parameters.
  • According to Lauren's classification, oesophageal AC (1.4%) less frequently belonged to the diffuse type than cardiac (2.8%) and gastric AC (23.9%; p<0.0001).
  • Tubular and papillary AC, as defined by the WHO classification, were more frequent among oesophageal (94.4%) than among cardiac (87.0%) and gastric AC (59.2%; p<0.0001).
  • Solid carcinomas, according to Carneiro's classification, were less frequent among oesophageal (2.8%) than among cardiac (10.2%) and gastric AC (9.2%; p<0.0001).
  • Oesophageal AC were graded more frequently G1/G2 (53.9%) than cardiac (30.6%) and gastric AC (27.7%; p<0.0001).
  • Among oesophageal AC, Lauren's classification (p=0.0067), Carneiro's classification (p=0.0170), tumour grade (p=0.0005), lymphatic vessel invasion (p<0.0001) but not WHO classification were histological predictors of postoperative survival.
  • In conclusion, oesophageal AC displays the same histological spectrum as cardiac and gastric AC.
  • However, the relative proportion of differentiated, gland-forming carcinomas is significantly more frequent in the oesophagus than in the cardia and in the stomach.
  • [MeSH-major] Adenocarcinoma / classification. Adenocarcinoma / pathology. Esophageal Neoplasms / classification. Esophageal Neoplasms / pathology. Stomach Neoplasms / pathology

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  • (PMID = 16498532.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
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62. Brown LM, Devesa SS, Chow WH: Incidence of adenocarcinoma of the esophagus among white Americans by sex, stage, and age. J Natl Cancer Inst; 2008 Aug 20;100(16):1184-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence of adenocarcinoma of the esophagus among white Americans by sex, stage, and age.
  • Rapid increases in the incidence of adenocarcinoma of the esophagus have been reported among white men.
  • We identified 22,759 patients from January 1, 1975, through December 31, 2004, with esophageal cancer, of whom 9526 were diagnosed with adenocarcinoma of the esophagus.
  • Among white men, increases in the incidence of esophageal cancer were largely attributed to a 463% increase in the incidence of adenocarcinoma over this time period, from 1.01 per 100,000 person-years (95% confidence interval [CI] = 0.90 to 1.13) in 1975-1979 to 5.69 per 100,000 person-years (95% CI = 5.47 to 5.91) in 2000-2004.
  • A similar rapid increase was also apparent among white women, among whom the adenocarcinoma rate increased 335%, from 0.17 (95% CI = 0.13 to 0.21) to 0.74 per 100,000 person-years (95% CI = 0.67 to 0.81), over the same time period.
  • Adenocarcinoma rates rose among white men and women in all stage and age groups, indicating that these increases are real and not an artifact of surveillance.

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  • (PMID = 18695138.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS53143; NLM/ PMC2518165
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63. Van Blankenstein M, Looman CW, Kruijshaar ME, Siersema PD, Kuipers EJ, Bytzer P: Modelling a population with Barrett's oesophagus from oesophageal adenocarcinoma incidence data. Scand J Gastroenterol; 2007 Mar;42(3):308-17
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  • [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
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64. Lukić M, Segec A, Segeca I, Pinotić L, Pinotić K, Atalić B, Solić K, Vcev A: The role of the nutrition in the pathogenesis of gastroesophageal reflux disease, Barrett's oesophagus and oesophageal adenocarcinoma. Coll Antropol; 2010 Sep;34(3):905-9
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  • [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


65. Onwuegbusi BA, Rees JR, Lao-Sirieix P, Fitzgerald RC: Selective loss of TGFbeta Smad-dependent signalling prevents cell cycle arrest and promotes invasion in oesophageal adenocarcinoma cell lines. PLoS One; 2007 Jan 31;2(1):e177
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective loss of TGFbeta Smad-dependent signalling prevents cell cycle arrest and promotes invasion in oesophageal adenocarcinoma cell lines.
  • In cancer, Transforming Growth Factor beta (TGFbeta) increases proliferation and promotes invasion via selective loss of signalling pathways.
  • Oesophageal adenocarcinoma arises from Barrett's oesophagus, progresses rapidly and is usually fatal.
  • We therefore investigated the role of TGFbeta in Barrett's associated oesophageal adenocarcinoma using a panel of cell lines (OE33, TE7, SEG, BIC, FLO).
  • 4/5 adenocarcinoma cell lines failed to cell cycle arrest, down-regulate c-Myc or induce p21 in response to TGFbeta, and modulation of a Smad3/4 specific promoter was inhibited.
  • These hyperproliferative adenocarcinoma cell lines displayed a TGFbeta induced increase in the expression of the extracellular matrix degrading proteinases, urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor 1 (PAI-1), which correlated with an invasive cell phenotype as measured by in vitro migration, invasion and cell scattering assays.
  • These data would support a dual role for TGFbeta in oesophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Signal Transduction / physiology. Smad3 Protein / metabolism. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Barrett Esophagus / complications. Cell Cycle / physiology. Cell Line, Tumor. Cell Proliferation. Enzyme Activation. Enzyme Inhibitors / metabolism. Extracellular Matrix / metabolism. Extracellular Signal-Regulated MAP Kinases / genetics. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression Regulation. Humans. JNK Mitogen-Activated Protein Kinases / genetics. JNK Mitogen-Activated Protein Kinases / metabolism. Neoplasm Invasiveness. Phosphatidylinositol 3-Kinases / genetics. Phosphatidylinositol 3-Kinases / metabolism. Transcription, Genetic

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  • (PMID = 17264880.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Smad3 Protein; 0 / Transforming Growth Factor beta; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1766472
  • [General-notes] NLM/ Original DateCompleted: 20070723
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66. Loaeza-del Castillo A, Villalobos-Pérez JJ: [Study of 30 years on the change in the frequency of esophageal squamous cell carcinoma, esophageal adenocarcinoma and adenocarcinoma of the esophagogastric union]. Rev Gastroenterol Mex; 2008 Jan-Mar;73(1):11-6
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  • [Title] [Study of 30 years on the change in the frequency of esophageal squamous cell carcinoma, esophageal adenocarcinoma and adenocarcinoma of the esophagogastric union].
  • [Transliterated title] Estudio de 30 años sobre el cambio en la frecuencia de carcinoma epidermoide esofágico, adenocarcinoma esofágico y adenocarcinoma de la unión esofagogástrica.
  • Esophageal cancer mortality is high and the incidence of this neoplasm is increasing.
  • OBJECTIVE: Our aim was to compare the frequency of esophageal adenocarcinoma cases (EA) and squamous cell carcinoma (SCC) cases in two study periods (1977-1988 vs. 1989-2006).
  • METHOD: Patients with esophageal cancer or adenocarcinoma of gastroesophageal junction (AGEJ) referred to the Nation al Institute of Medical Sciences and Nutrition "Salvador Zubirán" during 1989-2006 were included.
  • Risk factors for esophageal cancer and AGEJ were investigated.
  • The association between Barrett's esophagus and EA (OR 14; CI 95% 1.65-119.2, P = 0.0035) and for GEJC (RM 13.6; IC 95% 1.6-116, P = 0.004) was significant.
  • CONCLUSION: There has been an increase in EA, being now the predominant hystologic type of esophageal cancer.
  • [MeSH-major] Adenocarcinoma / epidemiology. Carcinoma, Squamous Cell / epidemiology. Esophageal Neoplasms / epidemiology. Esophagogastric Junction

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  • (PMID = 18792668.001).
  • [ISSN] 0375-0906
  • [Journal-full-title] Revista de gastroenterología de México
  • [ISO-abbreviation] Rev Gastroenterol Mex
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Mexico
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67. Song S, Guha S, Liu K, Buttar NS, Bresalier RS: COX-2 induction by unconjugated bile acids involves reactive oxygen species-mediated signalling pathways in Barrett's oesophagus and oesophageal adenocarcinoma. Gut; 2007 Nov;56(11):1512-21
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  • [Title] COX-2 induction by unconjugated bile acids involves reactive oxygen species-mediated signalling pathways in Barrett's oesophagus and oesophageal adenocarcinoma.
  • OBJECTIVES: Bile reflux contributes to oesophageal injury and neoplasia.
  • COX-2 is involved in both inflammation and carcinogenesis; however, the precise mechanisms by which bile acids promote COX-2 expression in the oesophagus are largely unknown.
  • We analysed the molecular mechanisms that govern bile acid-mediated expression of COX-2 in Barrett's oesophagus and oesophageal adenocarcinoma (OA).
  • DESIGN: The effects of bile acids on COX-2 expression were analysed in immortalised Barrett's oesophagus and OA cells using immunoblotting and transient transfections.
  • Immunohistochemistry was performed on oesophageal mucosa obtained from an established rat model of bile reflux.
  • CONCLUSIONS: Unconjugated bile acids induce CREB and AP-1-dependent COX-2 expression in Barrett's oesophagus and OA through ROS-mediated activation of PI3K/AKT and ERK1/2.
  • This study enhances our understanding of the molecular mechanisms by which bile acids promote the development of oesophageal adenocarcinoma.

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  • (PMID = 17604323.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA069480; United States / NCI NIH HHS / CA / R01CA69480
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / Reactive Oxygen Species; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.3.1.48 / CREB-Binding Protein; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ PMC2095641
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68. Van Soest EM, Dieleman JP, Sturkenboom MC, Siersema PD, Kuipers EJ: Gastro-oesophageal reflux, medical resource utilization and upper gastrointestinal endoscopy in patients at risk of oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2008 Jul;28(1):137-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gastro-oesophageal reflux, medical resource utilization and upper gastrointestinal endoscopy in patients at risk of oesophageal adenocarcinoma.
  • BACKGROUND: Early identification of patients at risk of oesophageal adenocarcinoma (OAC) might improve survival.
  • AIM: To assess the medical resource utilization in the 3 years before OAC diagnosis as potential markers for early identification and intervention.
  • CONCLUSIONS: Only a minority of all OAC patients used acid inhibitors before diagnosis.
  • The use of medical care between cases and controls differed only in the final year before OAC diagnosis.
  • [MeSH-major] Adenocarcinoma / mortality. Endoscopy, Gastrointestinal / utilization. Esophageal Neoplasms / mortality. Gastroesophageal Reflux / mortality. Resource Allocation / trends
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Barrett Esophagus / diagnosis. Barrett Esophagus / mortality. Case-Control Studies. Female. Humans. Male. Middle Aged. Risk Factors. Survival Rate

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  • (PMID = 18373635.001).
  • [ISSN] 1365-2036
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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69. Sendler A: Metabolic response evaluation by PET during neoadjuvant treatment for adenocarcinoma of the esophagus and esophagogastric junction. Recent Results Cancer Res; 2010;182:167-77
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  • [Title] Metabolic response evaluation by PET during neoadjuvant treatment for adenocarcinoma of the esophagus and esophagogastric junction.
  • Following several randomized trials, neoadjuvant therapy in adenocarcinoma of esophagus and the esophagogastric junction can be seen as an international standard.
  • So far, FDG-PET does not change treatment in esophageal and gastric cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Esophageal Neoplasms / metabolism. Esophagogastric Junction / radionuclide imaging. Fluorodeoxyglucose F18. Neoadjuvant Therapy. Positron-Emission Tomography / methods. Stomach Neoplasms / metabolism

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  • (PMID = 20676880.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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70. Hong J, Behar J, Wands J, Resnick M, Wang LJ, DeLellis RA, Lambeth D, Souza RF, Spechler SJ, Cao W: Role of a novel bile acid receptor TGR5 in the development of oesophageal adenocarcinoma. Gut; 2010 Feb;59(2):170-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of a novel bile acid receptor TGR5 in the development of oesophageal adenocarcinoma.
  • BACKGROUND AND AIMS: Mechanisms of the progression from Barrett's oesophagus to oesophageal adenocarcinoma (OA) are not fully understood.
  • TGR5 mRNA and protein levels were significantly higher in OA tissues than in normal oesophageal mucosa or Barrett's mucosa.

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  • (PMID = 19926617.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK080703-01A1; United States / NIDDK NIH HHS / DK / R01 DK080703; United States / NIDDK NIH HHS / DK / DK073327-02; United States / NIDDK NIH HHS / DK / R21 DK073327-02; United States / NIDDK NIH HHS / DK / R21 DK073327; United States / NIDDK NIH HHS / DK / DK080703-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cholagogues and Choleretics; 0 / GPBAR1 protein, human; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Receptors, G-Protein-Coupled; 516-50-7 / Taurodeoxycholic Acid; EC 1.6.- / NOX5 protein, human; EC 1.6.3.1 / NADPH Oxidase; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gq-G11
  • [Other-IDs] NLM/ NIHMS182037; NLM/ PMC3049934
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71. Keld R, Guo B, Downey P, Gulmann C, Ang YS, Sharrocks AD: The ERK MAP kinase-PEA3/ETV4-MMP-1 axis is operative in oesophageal adenocarcinoma. Mol Cancer; 2010 Dec 09;9:313
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  • [Title] The ERK MAP kinase-PEA3/ETV4-MMP-1 axis is operative in oesophageal adenocarcinoma.
  • RESULTS: Here, we have studied the expression of the PEA3 subfamily members PEA3/ETV4 and ER81/ETV1 in oesophageal adenocarcinomas and determined their role in oesophageal adenocarcinoma cell function.
  • PEA3 plays an important role in controlling both the proliferation and invasive properties of OE33 oesophageal adenocarcinoma cells.
  • Enhanced ERK signaling is also more prevalent in late stage oesophageal adenocarcinomas.
  • CONCLUSIONS: This study shows that the ERK-PEA3-MMP-1 axis is upregulated in oesophageal adenocarcinoma cells and is a potentially important driver of the metastatic progression of oesophageal adenocarcinomas.

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  • (PMID = 21143918.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenovirus E1A Proteins; 0 / ETV4 protein, human; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 0 / transcription factor PEA3; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.24.7 / Matrix Metalloproteinase 1
  • [Other-IDs] NLM/ PMC3009708
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72. Langer R, Ott K, Feith M, Lordick F, Specht K, Becker K, Hofler H: High pretherapeutic thymidylate synthetase and MRP-1 protein levels are associated with nonresponse to neoadjuvant chemotherapy in oesophageal adenocarcinoma patients. J Surg Oncol; 2010 Oct 1;102(5):503-8
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  • [Title] High pretherapeutic thymidylate synthetase and MRP-1 protein levels are associated with nonresponse to neoadjuvant chemotherapy in oesophageal adenocarcinoma patients.
  • BACKGROUND: The aim of this study was to determine whether pretherapeutic protein expression levels of the excision repair cross-complementing (ERCC1) enzyme, thymidylate synthetase (TS), multidrug-resistance protein 1 (MRP-1) and P-glycoprotein (P-gp) are associated with tumour response to cisplatin and fluorouracil (5-FU)-based neoadjuvant chemotherapy in oesophageal adenocarcinomas.
  • METHODS: The expression levels of ERCC1, TS, MDR-1 and P-gp were determined immunohistochemically in pretherapeutic tumour biopsies from 40 oesophageal adenocarcinoma patients and were correlated with histopathological tumour regression and with patient survival.
  • CONCLUSIONS: The pattern of pretherapeutic expression of TS and MRP-1 is related to chemotherapy response in oesophageal adenocarcinoma patients.
  • [MeSH-major] Adenocarcinoma / drug therapy. Esophageal Neoplasms / drug therapy. Neoplasm Proteins / metabolism. P-Glycoprotein / metabolism. Thymidylate Synthase / metabolism

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  • [Copyright] J. Surg. Oncol. 2010;102:503-508. © 2010 Wiley-Liss, Inc.
  • (PMID = 20589706.001).
  • [ISSN] 1096-9098
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / P-Glycoprotein; EC 2.1.1.45 / Thymidylate Synthase; EC 3.1.- / ERCC1 protein, human; EC 3.1.- / Endonucleases; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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73. Lagergren J, Jansson C, Viklund P: Chewing gum and risk of oesophageal adenocarcinoma: a new hypothesis tested in a population-based study. Eur J Cancer; 2006 Sep;42(14):2359-62
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  • [Title] Chewing gum and risk of oesophageal adenocarcinoma: a new hypothesis tested in a population-based study.
  • The aim of this study was to test the hypothesis that chewing gum is associated with risk of oesophageal and cardia adenocarcinoma.
  • All patients were prospectively and uniformly documented and classified shortly after diagnosis.
  • In all, 189 and 262 patients with oesophageal and cardia adenocarcinoma, respectively, and 820 population-based control subjects were interviewed.
  • Regular users of chewing gum (P3 times/week for P6 months) were not at increased risk of oesophageal adenocarcinoma (OR 1.0, 95% CI 0.6-2.2), and no duration-response relation was observed (P = 0.38).
  • No association between regular gum chewing and cardia adenocarcinoma was found (OR 1.0, 95% CI 0.6-1.7), irrespective of duration of use (P = 0.56).
  • In conclusion, with regard to risk of oesophageal or cardia adenocarcinoma, gum chewing seems harmless.
  • [MeSH-major] Adenocarcinoma / etiology. Cardia. Chewing Gum / adverse effects. Esophageal Neoplasms / etiology. Stomach Neoplasms / etiology

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  • (PMID = 16890425.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chewing Gum
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74. Jones RJ, Hawkins RE, Eatock MM, Ferry DR, Eskens FA, Wilke H, Evans TR: A phase II open-label study of DHA-paclitaxel (Taxoprexin) by 2-h intravenous infusion in previously untreated patients with locally advanced or metastatic gastric or oesophageal adenocarcinoma. Cancer Chemother Pharmacol; 2008 Mar;61(3):435-41
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  • [Title] A phase II open-label study of DHA-paclitaxel (Taxoprexin) by 2-h intravenous infusion in previously untreated patients with locally advanced or metastatic gastric or oesophageal adenocarcinoma.
  • PURPOSE: Combination chemotherapy regimens can improve survival in patients with advanced gastric and oesophageal adenocarcinoma.
  • PATIENTS AND METHODS: In this single arm, phase II study of DHA-paclitaxel, eligible patients with previously untreated, inoperable locally advanced or metastatic adenocarcinoma of the oesophagus, oesophago-gastric junction or stomach were treated with DHA-paclitaxel (1,100 mg/m(2)) administered by 2-h intravenous infusion every 21 days.
  • CONCLUSIONS: DHA-paclitaxel has modest activity in patients with oesophago-gastric cancer and with haematological toxicity that is comparable to paclitaxel and docetaxel.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents, Phytogenic / therapeutic use. Esophageal Neoplasms / drug therapy. Paclitaxel / analogs & derivatives. Stomach Neoplasms / drug therapy

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  • (PMID = 17440725.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / docosahexaenoyl-paclitaxel; P88XT4IS4D / Paclitaxel
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75. Tougeron D, Di Fiore F, Hamidou H, Rigal O, Paillot B, Michel P: Response to definitive chemoradiotherapy and survival in patients with an oesophageal adenocarcinoma versus squamous cell carcinoma: a matched-pair analysis. Oncology; 2007;73(5-6):328-34
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  • [Title] Response to definitive chemoradiotherapy and survival in patients with an oesophageal adenocarcinoma versus squamous cell carcinoma: a matched-pair analysis.
  • OBJECTIVES: The impact of the histological tumour type in patients treated with definitive chemoradiotherapy (CRT) for an oesophageal cancer is not well established.
  • METHODS: Fifty-seven patients with an oesophageal adenocarcinoma (ADC) were matched according to the tumour stage and the WHO performance as well as the CRT regimen status including 57 patients with an oesophageal squamous cell carcinoma (SCC).
  • Further studies are required to confirm this difference in response rate to definitive CRT according to histological type of the tumour in oesophageal cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / radiotherapy. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / radiotherapy. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / radiotherapy


76. Merry AH, Schouten LJ, Goldbohm RA, van den Brandt PA: Body mass index, height and risk of adenocarcinoma of the oesophagus and gastric cardia: a prospective cohort study. Gut; 2007 Nov;56(11):1503-11
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  • [Title] Body mass index, height and risk of adenocarcinoma of the oesophagus and gastric cardia: a prospective cohort study.
  • BACKGROUND: In the last decades, the incidence of oesophageal and gastric cardia adenocarcinoma has increased rapidly in the Western world.
  • We investigated the association between body mass index (BMI), height and risk of oesophageal and gastric cardia adenocarcinoma.
  • Cases were identified through annual record linkage with the Netherlands Cancer Registry.
  • After 13.3 years of follow-up, excluding the first follow-up year, complete data from 4552 subcohort members, 133 oesophageal and 163 gastric cardia adenocarcinomas were available for case-cohort analyses.
  • RESULTS: The RRs (95% CI) of oesophageal adenocarcinoma were 1.40 (0.95 to 2.04) and 3.96 (2.27 to 6.88) for overweight (BMI 25.0-29.9 kg/m(2)) and obese subjects (BMI >or=30.0 kg/m(2)), respectively, compared to subjects with normal weight (BMI 20.0-24.9 kg/m(2)).
  • For gastric cardia adenocarcinoma, these RRs were 1.32 (0.94 to 1.85) and 2.73 (1.56 to 4.79).
  • Also change in BMI during adulthood was positively associated with the risk of oesophageal and gastric cardia adenocarcinoma (p trend 0.001 and 0.02, respectively), while no association was found with BMI in early adulthood (p trend 0.17 and 0.17, respectively).
  • CONCLUSIONS: These results confirm higher risks of oesophageal and gastric cardia adenocarcinoma with increasing BMI.
  • This implies that the increasing prevalence of obesity may be one of the explanations for the rising incidence of oesophageal and gastric cardia adenocarcinoma in the Western world.
  • [MeSH-major] Adenocarcinoma / etiology. Body Height / physiology. Cardia. Esophageal Neoplasms / etiology. Obesity / complications. Stomach Neoplasms / etiology

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  • (PMID = 17337464.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2095659
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77. Liu JF, Jamieson GG, Wu TC, Zhu GJ, Drew PA: A preliminary study on the postoperative survival of patients given aspirin after resection for squamous cell carcinoma of the esophagus or adenocarcinoma of the cardia. Ann Surg Oncol; 2009 May;16(5):1397-402
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  • [Title] A preliminary study on the postoperative survival of patients given aspirin after resection for squamous cell carcinoma of the esophagus or adenocarcinoma of the cardia.
  • BACKGROUND: We examined the effect of aspirin on survival following resection for squamous cell carcinoma (SCC) of the esophagus or adenocarcinoma of the gastric cardia.
  • There was a significant improvement in survival for patients with adenocarcinoma of the cardia on aspirin compared with the two control groups combined (P = 0.029).
  • However, there was no significant difference between the survival curves for T2N0M0 adenocarcinoma patients on aspirin (21) and the two control groups combined (65) (P = 0.29).
  • [MeSH-major] Adenocarcinoma / drug therapy. Aspirin / administration & dosage. Carcinoma, Squamous Cell / drug therapy. Cyclooxygenase 2 Inhibitors / administration & dosage. Esophageal Neoplasms / drug therapy. Stomach Neoplasms / drug therapy

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  • (PMID = 19241108.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin; R16CO5Y76E / Aspirin; U3P01618RT / Fluorouracil
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78. Jenkins GJ, Mikhail J, Alhamdani A, Brown TH, Caplin S, Manson JM, Bowden R, Toffazal N, Griffiths AP, Parry JM, Baxter JN: Immunohistochemical study of nuclear factor-kappaB activity and interleukin-8 abundance in oesophageal adenocarcinoma; a useful strategy for monitoring these biomarkers. J Clin Pathol; 2007 Nov;60(11):1232-7
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  • [Title] Immunohistochemical study of nuclear factor-kappaB activity and interleukin-8 abundance in oesophageal adenocarcinoma; a useful strategy for monitoring these biomarkers.
  • AIMS: To determine if immunohistochemistry (IHC) could be used to monitor nuclear factor-kappaB (NF-kappaB) activity in oesophageal adenocarcinoma and pre-malignant (Barrett's) oesophageal tissues, relative to normal oesophageal mucosa.
  • The pro-inflammatory cytokine interleukin-8 (IL-8), a transcriptional target of NF-kappaB, was also studied to better understand NF-kappaB functionality; its RNA and protein levels were assessed in oesophageal tissues.
  • I-kappaB (another NF-kappaB target) showed down-regulation in dysplastic and adenocarcinoma tissues.
  • CONCLUSION: IHC, using antibodies against the NLS of p65, may be useful in monitoring overall NF-kappaB activity in oesophageal tissues.
  • As IHC is amenable to high-throughput screening (whereas traditional electrophoretic mobility shift assay methods are not), this may lead to the development of a better screening tool for early cancer risk.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Esophageal Neoplasms / metabolism. Interleukin-8 / metabolism. NF-kappa B / metabolism
  • [MeSH-minor] Barrett Esophagus / metabolism. Carrier Proteins / metabolism. Disease Progression. Humans. Polymerase Chain Reaction / methods. Precancerous Conditions / metabolism. Transcription Factor RelA / metabolism. Up-Regulation

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  • (PMID = 17220207.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / Interleukin-8; 0 / NF-kappa B; 0 / Transcription Factor RelA
  • [Other-IDs] NLM/ PMC2095472
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79. Milano F, Jorritsma T, Rygiel AM, Bergman JJ, Sondermeijer C, Ten Brinke A, vanHam SM, Krishnadath KK: Expression pattern of immune suppressive cytokines and growth factors in oesophageal adenocarcinoma reveal a tumour immune escape-promoting microenvironment. Scand J Immunol; 2008 Dec;68(6):616-23
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  • [Title] Expression pattern of immune suppressive cytokines and growth factors in oesophageal adenocarcinoma reveal a tumour immune escape-promoting microenvironment.
  • Immunotherapy for solid cancers, such as oesophageal adenocarcinoma (OAC), is generally hampered by an unfavourable immunological tumour microenvironment.
  • The OAC microenvironment is characterized by a lack of cytokines and factors that normally would enhance anti-cancer responses, such as IFN-gamma and GrB, and by a high expression of several immuno-suppressive factors, such as COX-2, VEGF and IL-8.
  • [MeSH-major] Adenocarcinoma / immunology. Cyclooxygenase 2 / metabolism. Cytokines / metabolism. Esophageal Neoplasms / immunology. Tumor Escape. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 19055699.001).
  • [ISSN] 1365-3083
  • [Journal-full-title] Scandinavian journal of immunology
  • [ISO-abbreviation] Scand. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Vascular Endothelial Growth Factor A; 63231-63-0 / RNA; EC 1.14.99.1 / Cyclooxygenase 2
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80. Madani K, Zhao R, Lim HJ, Casson AG: Prognostic value of p53 mutations in oesophageal adenocarcinoma: final results of a 15-year prospective study. Eur J Cardiothorac Surg; 2010 Jun;37(6):1427-32
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  • [Title] Prognostic value of p53 mutations in oesophageal adenocarcinoma: final results of a 15-year prospective study.
  • OBJECTIVE: This study evaluates the clinical significance of p53 mutations in oesophageal adenocarcinoma (EADC).
  • METHODS: Between February 1991 and February 2006, 142 consecutive patients with EADC underwent potentially curative oesophageal resection.
  • Strict clinicopathologic criteria were used to define primary EADC (Type I), excluding gastric cardia adenocarcinoma (Type II).
  • Genomic DNA was extracted from oesophageal tumours, each with matched histologically normal oesophageal epithelium (internal control) from the resection margin.
  • No p53 mutations were found in normal oesophageal epithelia.
  • [MeSH-major] Adenocarcinoma / genetics. Esophageal Neoplasms / genetics. Genes, p53. Mutation

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  • [Copyright] Copyright 2009 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20227286.001).
  • [ISSN] 1873-734X
  • [Journal-full-title] European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
  • [ISO-abbreviation] Eur J Cardiothorac Surg
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Protein p53
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81. Kaechele V, Moehler M, Lutz MP, von Wichert G, Eisele M, Klaus J, Galle PR, Adler G, Seufferlein T: A phase I/II study of oxaliplatin and paclitaxel in patients with non-resectable cancer of the oesophagus and adenocarcinoma of the gastro-oesophageal junction: a study of the Arbeitsgemeinschaft Internistische Onkologie. Cancer Chemother Pharmacol; 2010 May;66(1):191-5
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  • [Title] A phase I/II study of oxaliplatin and paclitaxel in patients with non-resectable cancer of the oesophagus and adenocarcinoma of the gastro-oesophageal junction: a study of the Arbeitsgemeinschaft Internistische Onkologie.
  • PURPOSE: To assess the efficacy and toxicity of paclitaxel and oxaliplatin in patients with non-resectable cancer of the oesophagus and adenocarcinoma of the gastro-oesophageal junction.
  • Patients with a non-resectable cancer of the oesophagus and/or adenocarcinoma of the gastro-oesophageal junction were eligible.
  • There were 5 patients (19%) with adenocarcinoma of the gastro-oesophageal junction and 21 patients (81%) with oesophageal cancer; 19 (73%) had a squamous cell cancer and 7 (27%) had an adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Esophageal Neoplasms / drug therapy. Esophagogastric Junction. Organoplatinum Compounds / administration & dosage. Paclitaxel / administration & dosage. Stomach Neoplasms / drug therapy

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  • (PMID = 20354701.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Organoplatinum Compounds; 04ZR38536J / oxaliplatin; P88XT4IS4D / Paclitaxel
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82. Eisenberger CF, Stoecklein NH, Jazra S, Hosch SB, Peiper M, Scheunemann P, Am Esch JS, Knoefel WT: The detection of oesophageal adenocarcinoma by serum microsatellite analysis. Eur J Surg Oncol; 2006 Nov;32(9):954-60
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  • [Title] The detection of oesophageal adenocarcinoma by serum microsatellite analysis.
  • BACKGROUND AND AIMS: Organ-confined oesophageal cancer in an early stage can be cured in many patients, whereas more extensive lesions have a poor prognosis.
  • We sought to develop a non-invasive test for cancer detection and evaluation of the prognosis of the patients by using a novel molecular approach.
  • MATERIAL AND METHODS: Matched normal-, tumour- and serum-samples were obtained from 32 patients with adenocarcinoma of the oesophagus.
  • CONCLUSION: These data suggest that microsatellite DNA analysis in serum specimens might provide a potentially valuable tool for early detection of oesophageal cancer.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / genetics. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / genetics. Microsatellite Repeats / genetics

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  • (PMID = 16584865.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm
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83. Langer R, Von Rahden BH, Nahrig J, Von Weyhern C, Reiter R, Feith M, Stein HJ, Siewert JR, Höfler H, Sarbia M: Prognostic significance of expression patterns of c-erbB-2, p53, p16INK4A, p27KIP1, cyclin D1 and epidermal growth factor receptor in oesophageal adenocarcinoma: a tissue microarray study. J Clin Pathol; 2006 Jun;59(6):631-4
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  • [Title] Prognostic significance of expression patterns of c-erbB-2, p53, p16INK4A, p27KIP1, cyclin D1 and epidermal growth factor receptor in oesophageal adenocarcinoma: a tissue microarray study.
  • AIMS: To correlate immunohistochemical expression patterns and prognosis in oesophageal adenocarcinoma.
  • METHODS: The expression of c-erbB-2, p53, p16INK4A, p27KIP1, cyclin D1 and epidermal growth factor receptor (EGFR) was studied in a series of 137 primarily resected oesophageal adenocarcinoma samples.
  • CONCLUSION: The immunohistochemical expression of c-erbB-2 oncoprotein, cylin D1, p16INK4A, p27KIP1, p53 and EGFR in most oesophageal adenocarcinomas suggests their implication in the pathogenesis of this entity.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Esophageal Neoplasms / metabolism. Neoplasm Proteins / metabolism

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  • (PMID = 16731604.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53; 136601-57-5 / Cyclin D1; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC1860401
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84. Lagergren J, Jansson C: Use of tight belts and risk of esophageal adenocarcinoma. Int J Cancer; 2006 Nov 15;119(10):2464-6
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  • [Title] Use of tight belts and risk of esophageal adenocarcinoma.
  • It has recently been hypothesized that the general shift in use from suspenders to belts among men might be a factor that could promote reflux, particularly among overweight men, and thereby contribute to the alarmingly increasing incidence of esophageal and cardia adenocarcinoma.
  • Included were 189 patients with esophageal adenocarcinoma and 262 patients with cardia adenocarcinoma, who were compared with 167 patients with esophageal squamous cell carcinoma and 820 population-based control participants.
  • Daily use of tight belts 20 years earlier did not entail an increased risk of adenocarcinoma of the esophagus (OR 1.1, 95% CI 0.7-1.8) or cardia (OR 0.8, 95% CI 0.5-1.3) compared to never use.
  • No association with esophageal squamous cell carcinoma was found.
  • In conclusion, this study provided no support for the hypothesis that use of tight belts is associated with an increased risk of developing esophageal or cardia adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / epidemiology. Carcinoma, Squamous Cell / epidemiology. Clothing / adverse effects. Esophageal Neoplasms / epidemiology. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / etiology

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  • (PMID = 16894563.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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85. Tuynman JB, Buskens CJ, Kemper K, ten Kate FJ, Offerhaus GJ, Richel DJ, van Lanschot JJ: Neoadjuvant selective COX-2 inhibition down-regulates important oncogenic pathways in patients with esophageal adenocarcinoma. Ann Surg; 2005 Dec;242(6):840-9, discussion 849-50
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  • [Title] Neoadjuvant selective COX-2 inhibition down-regulates important oncogenic pathways in patients with esophageal adenocarcinoma.
  • OBJECTIVES: To evaluate the effects of neoadjuvant therapy with the selective cyclooxygenase-2 (COX-2) inhibitor celecoxib in vitro and in patients with esophageal adenocarcinoma on COX-2 and MET expression.
  • SUMMARY BACKGROUND DATA: High COX-2 and/or MET expression levels are negative prognostic factors for adenocarcinoma of the esophagus.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors exert anticancer mechanisms as is evident from epidemiologic studies and from experimental models for esophageal cancer.
  • The mechanisms and the significance of these findings in patients with adenocarcinoma of the esophagus are unknown.
  • METHODS: Esophageal adenocarcinoma cell lines were used to asses the effects in vitro.
  • To study the clinical effects 12 patients with esophageal adenocarcinoma were included for neoadjuvant treatment (4 weeks) with celecoxib at 400 mg twice daily.
  • CONCLUSIONS: This is the first study to show in vitro and in patients with esophageal adenocarcinoma that selective COX-2 inhibition down-regulates COX-2 and MET expression, both important proteins involved in cancer progression and dissemination.
  • Therefore, (neo)adjuvant therapy with celecoxib might have clinical potential for patients with esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cyclooxygenase Inhibitors / pharmacology. Cyclooxygenase Inhibitors / therapeutic use. Esophageal Neoplasms / drug therapy. Pyrazoles / pharmacology. Pyrazoles / therapeutic use. Sulfonamides / pharmacology. Sulfonamides / therapeutic use

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  • (PMID = 16327494.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; JCX84Q7J1L / Celecoxib
  • [Other-IDs] NLM/ PMC1409886
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86. Reynolds JV, Murphy TJ, Ravi N: Multimodality therapy for adenocarcinoma of the esophagus, gastric cardia, and upper gastric third. Recent Results Cancer Res; 2010;182:155-66
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  • [Title] Multimodality therapy for adenocarcinoma of the esophagus, gastric cardia, and upper gastric third.
  • There is considerable controversy over the level of recommendations from randomized trials underpinning management decisions for patients presenting with localized adenocarcinoma of the esophagus and esophagogastric junction.
  • Despite a paucity of Level 1 recommendations compared with other gastrointestinal sites, in particular rectal cancer, there is an emerging consensus in practice to consider multimodal approaches in all cases that present with T3 or node-positive disease.
  • [MeSH-major] Adenocarcinoma / therapy. Cardia. Esophageal Neoplasms / therapy. Stomach Neoplasms / therapy

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  • (PMID = 20676879.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
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87. Pierini R, Kroon PA, Guyot S, Ivory K, Johnson IT, Belshaw NJ: Procyanidin effects on oesophageal adenocarcinoma cells strongly depend on flavan-3-ol degree of polymerization. Mol Nutr Food Res; 2008 Dec;52(12):1399-407
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  • [Title] Procyanidin effects on oesophageal adenocarcinoma cells strongly depend on flavan-3-ol degree of polymerization.
  • Epidemiological studies have shown that the risk of developing oesophageal adenocarcinoma (OA) is inversely correlated to consumption of fruits and vegetables.
  • [MeSH-major] Adenocarcinoma / drug therapy. Biflavonoids / pharmacology. Catechin / pharmacology. Esophageal Neoplasms / drug therapy. Flavonoids / pharmacology. Malus / chemistry. Polymers / chemistry. Proanthocyanidins / pharmacology

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  • (PMID = 18683822.001).
  • [ISSN] 1613-4133
  • [Journal-full-title] Molecular nutrition & food research
  • [ISO-abbreviation] Mol Nutr Food Res
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biflavonoids; 0 / Flavonoids; 0 / Polymers; 0 / Proanthocyanidins; 0 / flavan-3-ol; 4852-22-6 / procyanidin; 8R1V1STN48 / Catechin
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88. Löfdahl HE, Lu Y, Lagergren J: Sex-specific risk factor profile in oesophageal adenocarcinoma. Br J Cancer; 2008 Nov 4;99(9):1506-10
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  • [Title] Sex-specific risk factor profile in oesophageal adenocarcinoma.
  • A nationwide Swedish case-control study of 388 men and 63 women with adenocarcinoma of the oesophagus and gastro-oesophageal function and 676 men controls and 140 women investigated whether sex differences in aetiology contribute to male predominance.

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  • (PMID = 18841152.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI057947; United States / NCI NIH HHS / CA / R01 CA57947-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2579703
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89. Früh M, Zhou W, Zhai R, Su L, Heist RS, Wain JC, Nishioka NS, Lynch TJ, Shepherd FA, Christiani DC, Liu G: Polymorphisms of inflammatory and metalloproteinase genes, Helicobacter pylori infection and the risk of oesophageal adenocarcinoma. Br J Cancer; 2008 Feb 26;98(4):689-92
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  • [Title] Polymorphisms of inflammatory and metalloproteinase genes, Helicobacter pylori infection and the risk of oesophageal adenocarcinoma.
  • Helicobacter pylori (HP) infection appears protective against oesophageal adenocarcinoma (EA) risk.
  • [MeSH-major] Adenocarcinoma / genetics. Esophageal Neoplasms / genetics. Helicobacter Infections / genetics. Helicobacter pylori / genetics. Matrix Metalloproteinase 2 / genetics. Polymorphism, Genetic / genetics

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  • (PMID = 18253117.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109193; United States / NCI NIH HHS / CA / R03 CA110822
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.24.17 / Matrix Metalloproteinase 3; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.65 / Matrix Metalloproteinase 12; EC 3.4.24.7 / Matrix Metalloproteinase 1
  • [Other-IDs] NLM/ PMC2259195
  •  go-up   go-down


90. Murray L, Sedo A, Scott M, McManus D, Sloan JM, Hardie LJ, Forman D, Wild CP: TP53 and progression from Barrett's metaplasia to oesophageal adenocarcinoma in a UK population cohort. Gut; 2006 Oct;55(10):1390-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TP53 and progression from Barrett's metaplasia to oesophageal adenocarcinoma in a UK population cohort.
  • BACKGROUND AND AIMS: Oesophageal adenocarcinoma frequently develops on a background of metaplastic Barrett's epithelium.
  • Incident oesophageal malignancies and high grade dysplasias were identified.
  • For each case up to five controls were matched on age, sex, and year of diagnosis.
  • Biopsies from the time of diagnosis of Barrett's epithelium were stained immunohistochemically for TP53, cyclin D1, cyclooxygenase 2 (COX-2), and beta-catenin proteins.
  • RESULTS: Twenty nine incident oesophageal malignancies and six cases of high grade dysplasia were identified.
  • The odds of diffuse or intense TP53 staining were substantially elevated in biopsies from patients who developed oesophageal adenocarcinoma compared with controls (odds ratio (OR) 11.7 (95% confidence interval (CI) 1.93, 71.4)).
  • CONCLUSIONS: Immunohistochemical detection of TP53 expression is a biomarker of malignant progression in Barrett's oesophagus but sensitivity is too low to act as a criterion to inform endoscopic surveillance strategies.
  • Additional biomarkers are required which when combined with TP53 will identify, with adequate sensitivity and specificity, Barrett's patients who are at risk of developing cancer.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / pathology. Esophageal Neoplasms / diagnosis. Esophagus / pathology. Tumor Suppressor Protein p53 / metabolism


91. Shetty VD, Thrumurthy SG, Pursnani KG, Ward JB, Mughal MM: Angelchik prosthesis with oesophageal adenocarcinoma: our surgical approach. Ann R Coll Surg Engl; 2010 Jul;92(5):W64-8
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Angelchik prosthesis with oesophageal adenocarcinoma: our surgical approach.
  • The Angelchik prosthesis is an incomplete doughnut-shaped device composed of silicone elastomer used in the treatment of gastro-oesophageal reflux disease (GORD).
  • It is used to encircle the lower oesophagus at the gastro-oesophageal junction (GOJ).
  • Development of adenocarcinoma in patients with Angelchik prosthesis is a rare occurrence.
  • This article describes two patients who developed adenocarcinoma above their prosthesis and whose cardio-oesophagectomy was technically challenging due to the formation of a dense inflammatory capsule around the prosthesis.
  • Our surgical approach to curative oesophageal resection with the Angelchik prosthesis in situ is also discussed.
  • [MeSH-major] Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Prostheses and Implants / adverse effects

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