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[Title] The price of doubt is esophageal adenocarcinoma.

[MeSH-major] Adenocarcinoma / prevention & control. Esophageal Neoplasms / prevention & control. Gastroesophageal Reflux / surgery

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[CommentOn] Ann Surg. 2007 Jul;246(1):22-3 [17592285.001]

(PMID = 18376213.001).

[ISSN] 0003-4932

[Journal-full-title] Annals of surgery

[ISO-abbreviation] Ann. Surg.

[Language] eng

[Publication-type] Comment; Letter

[Publication-country] United States

   

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[Title] Potential role of NF-kappaB in esophageal adenocarcinoma: as an emerging molecular target.

Esophageal adenocarcinoma is increasing in incidence and arises in a background of reflux induced inflammation, metaplasia, and dysplasia.

Because a role for NF-kappaB has been implicated in the pathogenesis of esophageal cancer, this transcription factor has been the focus of the current research of this devastating disease.

Research efforts to improve the effect of chemotherapy have led to an improvement in patient survival but there is still a need for improvement, and NF-kappaB is a potential target for cancer drug development.

In this review, we have attempted to highlight the possible role of NF-kappaB in esophageal adenocarcinoma and discuss the anticancer strategy with NF-kappaB as a promising molecular target in esophageal cancer therapy.

[MeSH-major] Adenocarcinoma / metabolism. Esophageal Neoplasms / metabolism. NF-kappa B / biosynthesis

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(PMID = 18533190.001).

[ISSN] 1095-8673

[Journal-full-title] The Journal of surgical research

[ISO-abbreviation] J. Surg. Res.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Cytokines; 0 / NF-kappa B

[Number-of-references] 58

   

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[Title] XRCC1 and XPD polymorphisms and esophageal adenocarcinoma risk.

DNA damage is important in the pathogenesis of esophageal adenocarcinoma (EA).

[MeSH-major] Adenocarcinoma / genetics. DNA-Binding Proteins / genetics. Esophageal Neoplasms / genetics. Genetic Predisposition to Disease. Polymorphism, Genetic. Xeroderma Pigmentosum Group D Protein / genetics

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(PMID = 17264068.001).

[ISSN] 0143-3334

[Journal-full-title] Carcinogenesis

[ISO-abbreviation] Carcinogenesis

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA109193; United States / NCI NIH HHS / CA / CA110822; United States / NCI NIH HHS / CA / CA74386; United States / NCI NIH HHS / CA / ES/CA06409

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1; EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human

   

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[Title] Reflux, Barrett's, and adenocarcinoma of the esophagus: can we disrupt the pathway?

[MeSH-major] Adenocarcinoma / physiopathology. Barrett Esophagus / physiopathology. Esophageal Neoplasms / physiopathology. Esophagus / pathology. Gastroesophageal Reflux / physiopathology

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(PMID = 20094815.001).

[ISSN] 1873-4626

[Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract

[ISO-abbreviation] J. Gastrointest. Surg.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Update in the diagnosis of gastroesophageal reflux disease.

GERD is known to cause erosive esophagitis, Barrett esophagus and has been linked to the development of adenocarcinoma of the esophagus.

Currently upper gastrointestinal endoscopy is the main clinical tool for visualizing esophageal lesions.

Since the majority of GERD patients do not have endoscopic visible lesions other methods are required to document the abnormal acid exposure in the distal esophagus.

For many clinicians ambulatory esophageal pH monitoring is the gold standard in diagnosing GERD since it quantifies distal esophageal acid exposure and allows the evaluation of the relationship between symptoms and acid reflux.

[MeSH-major] Gastroesophageal Reflux / diagnosis

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(PMID = 17013449.001).

[ISSN] 1841-8724

[Journal-full-title] Journal of gastrointestinal and liver diseases : JGLD

[ISO-abbreviation] J Gastrointestin Liver Dis

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Romania

[Number-of-references] 20

   

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[Title] Role of obesity in Barrett's esophagus and cancer.

The incidence of esophageal adenocarcinoma (EAC) has increased dramatically in the western world, and there also appears to have been an increase in the incidence of Barrett's esophagus and gastroesophageal reflux disease in recent years.

This article reviews current evidence for the role that overweight/obesity and body fat distribution have in development of the esophagitis metaplasia-dysplasia-adenocarcinoma sequence.

[MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / etiology. Esophageal Neoplasms / etiology. Gastroesophageal Reflux / etiology. Obesity / complications

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(PMID = 19500735.001).

[ISSN] 1558-5042

[Journal-full-title] Surgical oncology clinics of North America

[ISO-abbreviation] Surg. Oncol. Clin. N. Am.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Adipokines; 0 / Ghrelin

[Number-of-references] 80

   

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[Title] Role of neoadjuvant therapy for esophageal adenocarcinoma.

This article examines the role of neoadjuvant therapy in the treatment of locally advanced esophageal adenocarcinoma.

Primary chemoradiotherapy is the accepted standard of care for medically inoperable patients, whereas adjuvant chemoradiotherapy may be considered for patients who undergo primary resection of lower esophageal/gastroesophageal junction tumors.

[MeSH-major] Adenocarcinoma / therapy. Esophageal Neoplasms / therapy. Neoadjuvant Therapy / methods

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(PMID = 19500742.001).

[ISSN] 1558-5042

[Journal-full-title] Surgical oncology clinics of North America

[ISO-abbreviation] Surg. Oncol. Clin. N. Am.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] Q20Q21Q62J / Cisplatin

[Number-of-references] 60

   

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BACKGROUND: Barrett esophagus is highly prevalent in the Western world; however, only a minority of affected individuals progress to esophageal adenocarcinoma.

Identifying simple, reliable, clinical, and endoscopic predictors of high-grade dysplasia and adenocarcinoma would be helpful for risk stratification in screening and surveillance programs.

METHODS: Clinical, endoscopic, and histologic data were reviewed for patients with a new Barrett diagnosis between 2002 and 2005.

Patients were classified, by an expert gastrointestinal pathologist, as having intestinal metaplasia, indefinite-for-dysplasia, low-grade dysplasia, high-grade dysplasia, and esophageal adenocarcinoma.

RESULTS: In all, 109 patients (26 women, 83 men, mean age: 58.8) were newly diagnosed with Barrett metaplasia (n = 39), indefinite/low-grade dysplasia (n = 35), and high-grade dysplasia/esophageal adenocarcinoma (n = 35) over a 3-year period.

CONCLUSIONS: Male gender, longstanding gastroesophageal reflux disease, hiatal hernia size, and segment length are strongly associated with higher grades of dysplasia at index diagnosis.

These factors along with H. pylori status warrant further prospective evaluation as predictors of risk for development of high-grade dysplasia and esophageal adenocarcinoma.

[MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagoscopy. Hernia, Hiatal / pathology

[MeSH-minor] Adult. Aged. Aged, 80 and over. Esophagus / pathology. Female. Gastroesophageal Reflux / epidemiology. Gastroesophageal Reflux / pathology. Humans. Male. Metaplasia / epidemiology. Metaplasia / pathology. Middle Aged. Precancerous Conditions / epidemiology. Precancerous Conditions / pathology. Prognosis. Risk Assessment

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(PMID = 17211862.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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Obesity is a well-established risk factor for the development and mortality from several cancers, including adenocarcinoma of the oesophagus, oesophago-gastric junction and colorectum.

Despite a large body of epidemiological evidence describing this relationship, the mechanisms relating obesity and cancer are only starting to be uncovered.

For each individual cancer, we examine and present the published data examining the role of leptin in both cell and animal models, the association between circulating leptin levels and cancer risk, and finally the expression of the leptin system in human gastro-intestinal tract tumours, in relation to tumour biology, stage and patient outcome.

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[Copyright] © 2010 The Authors. obesity reviews © 2010 International Association for the Study of Obesity.

(PMID = 20149119.001).

[ISSN] 1467-789X

[Journal-full-title] Obesity reviews : an official journal of the International Association for the Study of Obesity

[ISO-abbreviation] Obes Rev

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Leptin; 0 / Receptors, Leptin

   

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[Title] Introduction: esophagus, dysplasia, and early esophageal adenocarcinoma: managing the transition.

[MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology

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[Cites] J Natl Cancer Inst. 2005 Jan 19;97(2):142-6 [15657344.001]

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(PMID = 20162375.001).

[ISSN] 1873-4626

[Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract

[ISO-abbreviation] J. Gastrointest. Surg.

[Language] eng

[Publication-type] Introductory Journal Article

[Publication-country] United States

   

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[Title] Role of intraoperative sentinel lymph node mapping in the management of carcinoma of the esophagus.

BACKGROUND/AIM: Precise evaluation of lymph node status is one of the most important factors in determining clinical outcome in treating gastro-intestinal (GI) cancer.

Sentinel lymph node (SLN) mapping clearly has become highly feasible and accurate in staging GI cancer.

This study aims to investigate the feasibility and accuracy of detection of SLN using methylene blue dye in patients with carcinoma of the esophagus and assess its potential role in determining the rational extent of lymphadenectomy in esophageal cancer surgery.

MATERIALS AND METHODS: Thirty-two patients of esophageal cancer diagnosed on endoscopic biopsy were enrolled in this prospective study.

The SLNs of esophageal cancer were only found in N1 area in 21 (80.77%) cases, and in N2 or N3 area in only 19.33%.

SLN had a sensitivity of 85.71% in mid esophageal tumors and 93.33% in lower esophageal tumors.

The SLN biopsy had sensitivity of 87.5% in the case of squamous cell carcinoma and 92.86% in the cases of adenocarcinoma of the esophagus.

The accuracy of the procedure for squamous cell carcinoma and adenocarcinoma was 60% and 76.47%, respectively.

CONCLUSION: SLN mapping is an accurate diagnostic procedure for detecting lymph node metastasis in patients with esophageal cancer and may indicate rational extent of lymphadenectomy in these patients.

SLN mapping provides "right nodes" to the pathologists for detailed analysis and appropriate staging, thereby helping in individualizing the multi-modal treatment for esophageal cancer.

[MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / surgery. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Sentinel Lymph Node Biopsy

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(PMID = 20616411.001).

[ISSN] 1998-4049

[Journal-full-title] Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association

[ISO-abbreviation] Saudi J Gastroenterol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Saudi Arabia

[Chemical-registry-number] 0 / Enzyme Inhibitors; T42P99266K / Methylene Blue

[Other-IDs] NLM/ PMC3003219

   

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[Title] [Surgical therapy for esophageal carcinoma: a prospective 20-year analysis].

[Transliterated title] Chirurgische Therapie des Osophaguskarzinoms: Eine prospektive 20-Jahres-Analyse.

BACKGROUND: The aim of our study was the analysis of long-term developments in the surgical therapy for esophageal carcinoma at our hospital over a period of 20 years with a differentiated view on the two predominant histological tumour types.

PATIENTS AND METHODS: Between September 1985 and September 2005, esophageal resections were performed in 470 patients at our clinic on account of a malignant tumour of the esophagus.

The abdomino-thoracic resection with abdominal and extended mediastinal lymph node dissection as well as intrathoracic anastomosis was the standard treatment in the case of squamous cell carcinoma, whereas in adenocarcinoma a transhiatal resection with abdominal and dorsal mediastinal lymphadenectomy and cervical esophagogastrostomy was carried out.

A proportionally identical amount of transhiatal resections for squamous cell carcinoma was found in both intervals, whereas the transhiatal procedures for adenocarcinoma increased in the last decade (3.6 % in the period between 9 / 1985 and 9 / 1995, as compared with 23.6 % between 10 / 1995 and 9 / 2005) (p < 0.05).

While the overall prognosis for squamous cell carcinoma did not significantly differ in the two decades (p = 0.2040), patients with adenocarcinoma were found to have a significantly improved long-term survival (log-rank test: p = 0.0365) in the second decade.

The prognosis for adenocarcinoma, therefore, could be improved in the course of time with a 3-year survival rate of finally 40 % (as compared with 17.5 % in the first decade), and a 5-year survival rate of 25 % (as compared with 15 %).

CONCLUSION: Surgical therapy for esophageal carcinoma has undergone distinct changes over the past 20 years.

Especially with adenocarcinoma of the esophagus, these changes have led to a significantly more favourable long-term prognosis.

[MeSH-major] Adenocarcinoma / surgery. Carcinoma, Squamous Cell / surgery. Diffusion of Innovation. Esophageal Neoplasms / surgery. Thoracotomy / trends

[MeSH-minor] Adult. Aged. Anastomosis, Surgical. Diaphragm / surgery. Disease-Free Survival. Esophagus / surgery. Female. Follow-Up Studies. Humans. Lymph Node Excision. Male. Middle Aged. Neoplasm Staging. Prospective Studies. Stomach / surgery

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(PMID = 18563693.001).

[ISSN] 0044-409X

[Journal-full-title] Zentralblatt für Chirurgie

[ISO-abbreviation] Zentralbl Chir

[Language] ger

[Publication-type] Comparative Study; English Abstract; Journal Article

[Publication-country] Germany

   

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[Title] Rising incidence of adenocarcinoma of the esophagus in Kerman, Iran.

BACKGROUND: The fall in the incidence of esophageal squamous cell cancer and noncardia gastric cancers in western countries parallels a concomitant rise in the incidence of gastric cardia cancer and distal adenocarcinoma of the esophagus.

We aimed to investigate the incidence trend of different gastric and esophageal cancers in Kerman, southeast Iran.

METHODS: The information of all newly diagnosed patients with gastric and esophageal cancers were collected actively from all histopathology departments around the Kerman Province during 1991 - 2002 retrospectively.

RESULTS: The annual age standardized incidence risks of esophageal and gastric cancers in Kerman were 1.9 and 6.9 per 100,000 populations.

In average, the risks of gastric and esophageal squamous cell cancers were more or less constant, while the risk of adenocarcinoma of the esophagus increased around 11% annually.

The rising incidence of adenocarcinoma of the esophagus in Kerman parallels its temporal pattern in western countries.

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

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(PMID = 18588366.001).

[ISSN] 1029-2977

[Journal-full-title] Archives of Iranian medicine

[ISO-abbreviation] Arch Iran Med

[Language] eng

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

[Publication-country] Iran

   

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[Title] Obesity is not associated with adverse outcome following surgical resection of oesophageal adenocarcinoma.

OBJECTIVE: To study the impact of obesity on postoperative morbidity and outcome following surgical resection of primary oesophageal adenocarcinoma (EADC).

DFS and OS at 5 years were increased for patients who were obese at the time of oesophageal resection (P=0.008).

CONCLUSIONS: Obesity is not associated with increased postoperative complication rates or adverse outcome following oesophageal resection, and should therefore not be considered a relative contraindication to the surgical management of EADC.

The improved survival of obese patients who underwent oesophageal resection for EADC suggests that further investigation of the association between obesity and oesophageal malignancy is now warranted.

[MeSH-major] Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagectomy / adverse effects. Obesity / complications

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[Copyright] Copyright © 2010 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.

[ErratumIn] Eur J Cardiothorac Surg. 2010 Dec;38(6):820-1

(PMID = 20444616.001).

[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

[Grant] Canada / Canadian Institutes of Health Research / /

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

[Publication-country] Germany

   

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[Title] Helicobacter pylori and esophageal cancer risk: a meta-analysis.

We conducted this meta-analysis to examine the association between Helicobacter pylori and esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma.

Case-control or nested case-control studies were selected if they used serology or endoscopic methods to detect H. pylori in the stomach and if control subjects were not restricted to upper gastrointestinal tract cancer or peptic ulcer disease patients.

For esophageal squamous cell carcinoma, the summary OR (95% CI) was 1.10 (0.78-1.55).

[MeSH-major] Adenocarcinoma / etiology. Carcinoma, Squamous Cell / etiology. Esophageal Neoplasms / etiology. Helicobacter Infections / epidemiology. Helicobacter pylori / physiology

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[CommentIn] Cancer Prev Res (Phila). 2008 Oct;1(5):308-11 [19138974.001]

[CommentIn] Cancer Prev Res (Phila). 2009 Jan;2(1):94 [19139023.001]

(PMID = 19138977.001).

[ISSN] 1940-6215

[Journal-full-title] Cancer prevention research (Philadelphia, Pa.)

[ISO-abbreviation] Cancer Prev Res (Phila)

[Language] eng

[Grant] United States / Intramural NIH HHS / / Z99 CA999999

[Publication-type] Journal Article; Meta-Analysis; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Bacterial Proteins; 0 / cagA protein, Helicobacter pylori

[Other-IDs] NLM/ NIHMS419215; NLM/ PMC3501739

   

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[Title] [Surgical management of Barrett's esophagus].

[Transliterated title] Barrett-oesophagus sebészi kezelése.

Barrett's esophagus is a complication of gastroesophageal reflux disease in which metaplastic, intestinal-type epithelium containing mucin-producing goblet cells with characteristic staining on histology replaces the squamous epithelium normally found in the esophagus.

Different surgical procedures are suggested in dysplasia free patients, in low grade dysplasia, high grade dysplasia and adenocarcinoma.

Instead of the widely accepted surgical procedure with high grade dysplasia and early carcinoma we suggest an intervention which is oncologically radical, functionally adequate and less inconvenient and stressing for the patients: left side thoraco-laparotomy, distal esophageal and proximal (lesser curvature) gastric resection with adequate lymphadenectomy and reconstruction with esophago-jejuno-gastric interposition.

[MeSH-major] Barrett Esophagus / pathology. Barrett Esophagus / surgery

[MeSH-minor] Adenocarcinoma / etiology. Australia. Esophageal Neoplasms / etiology. Esophagectomy / methods. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / surgery. History, 20th Century. Humans. Intensive Care Units / history. Journalism, Medical. London. Societies, Medical. Surgery Department, Hospital / history. Thoracic Surgical Procedures / history

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(PMID = 16550796.001).

[ISSN] 0025-0295

[Journal-full-title] Magyar sebészet

[ISO-abbreviation] Magy Seb

[Language] hun

[Publication-type] Biography; English Abstract; Historical Article; Journal Article; Portraits; Review

[Publication-country] Hungary

[Number-of-references] 22

[Personal-name-as-subject] Barrett N

   

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[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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(PMID = 20626966.001).

[ISSN] 1478-7083

[Journal-full-title] Annals of the Royal College of Surgeons of England

[ISO-abbreviation] Ann R Coll Surg Engl

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

   

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[Title] Molecular mechanisms of acid exposure in Barrett's esophagus.

Esophageal adenocarcinoma is one of the most deadly gastrointestinal tumors.

Gastroesophageal reflux has been established as a major risk factor for esophageal adenocarcinoma and Barrett's esophagus, the condition in which the normal squamous cells of the esophagus are replaced by metaplastic, specialized intestinal cells that are predisposed to malignancy.

Data from ex vivo and in vitro model systems suggests that acid exposure has pro-proliferative and anti-apoptotic effects which may facilitate neoplastic progression of Barrett's esophagus.

However, it is not clear whether the effects of acid exposure on proliferation and apoptosis are a direct result of the acid exposure itself, or whether they result indirectly from the effects of acid on inducing esophageal inflammation.

Such distinction may help in optimizing the level of gastric acid suppression for the prevention of cancer in Barrett's esophagus.

This report describes the molecular mechanisms whereby acid exposure directly and indirectly, through inducing inflammation, may contribute to the neoplastic progression of Barrett's esophagus and the potential role for acid suppression as a chemopreventive strategy in patients with Barrett's esophagus.

[MeSH-major] Barrett Esophagus / complications. Esophageal Neoplasms / etiology. Gastroesophageal Reflux / complications

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(PMID = 19847948.001).

[ISSN] 0925-4692

[Journal-full-title] Inflammopharmacology

[ISO-abbreviation] Inflammopharmacology

[Language] eng

[Grant] United States / NIDDK NIH HHS / DK / DK63621

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Acids; 0 / Cytokines; 0 / NF-kappa B; 0 / Reactive Nitrogen Species; 0 / Reactive Oxygen Species

[Number-of-references] 53

   

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[Title] Genetic diversity during the development of Barrett's oesophagus-associated adenocarcinoma: how, when and why?

Recent investigations into Barrett's oesophagus at the level of individual crypts have found significant genetic heterogeneity within a single lesion.

Furthermore, this genetic diversity has been shown to predict cancer development.

In the present article, we review the genetic alterations implicated in disease progression in Barrett's oesophagus and discuss how genetic diversity could arise during tumorigenesis.

Suggestions are made for future research to distinguish which of these theories is the predominant mechanism in Barrett's oesophagus-associated tumorigenesis.

[MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Cell Transformation, Neoplastic / genetics. Esophageal Neoplasms / genetics. Genetic Variation / physiology

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(PMID = 20298186.001).

[ISSN] 1470-8752

[Journal-full-title] Biochemical Society transactions

[ISO-abbreviation] Biochem. Soc. Trans.

[Language] eng

[Grant] United Kingdom / Cancer Research UK / / ; United Kingdom / Medical Research Council / /

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

[Publication-country] England

[Number-of-references] 45

   

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[Title] The risk of oesophageal cancer is not affected by a diagnosis of breast cancer.

Oesophageal adenocarcinoma (OAC) is less common and develops at a later age in women compared with men.

A cohort of women with breast cancer, a tumour commonly treated with oestrogen antagonists, was examined to identify the subsequent risk of developing OAC.

Earlier studies have implicated radiotherapy in increasing oesophageal cancer (OC) risk among women with breast cancer.

West Midlands Cancer Intelligence Unit data recording cancer diagnosis and treatment information was examined to identify patients with a first malignant primary breast cancer during 1977-2004.

Patients were followed until diagnosis of a second primary cancer, death or end of the time period examined.

No difference was identified when examined by OC morphology.There was no association between breast cancer and a second primary OC.

Radiotherapy that avoids deep irradiation in the treatment of breast cancer, local nodes or recurrence was not associated with an increased risk of developing a second primary OC.

[MeSH-major] Breast Neoplasms / complications. Esophageal Neoplasms / etiology. Neoplasms, Second Primary / etiology

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(PMID = 20145541.001).

[ISSN] 1473-5709

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

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

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Estrogens

   

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[Title] Smoking cessation and the risk of oesophageal cancer: An overview of published studies.

The epidemiologic studies on oesophageal cancer and smoking cessation published before December 2005 were reviewed here.

The results from at least 10 cohort and 10 case-control studies indicated that former smokers had a lower risk of squamous-cell or unspecified oesophageal cancer than current smokers.

Most investigations showed that the risk of oesophageal cancer remains elevated many years (at least 10) after cessation of smoking, to decline by about 40% only thereafter.

A few studies investigated the effect of smoking cessation on adenocarcinoma, and did not report a clear reduction of risk.

Data on oesophageal adenocarcinoma are however too limited to provide adequate inference on the relation with time since smoking cessation.

In conclusion, cessation of smoking could have an appreciable impact in reducing (squamous-cell) oesophageal cancer, and represents an obvious priority for prevention and public-health purposes.

[MeSH-major] Esophageal Neoplasms / epidemiology. Smoking / adverse effects. Smoking Cessation

[MeSH-minor] Adenocarcinoma / epidemiology. Adenocarcinoma / etiology. Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / etiology. Case-Control Studies. Cohort Studies. Humans. Risk Factors

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(PMID = 16919996.001).

[ISSN] 1368-8375

[Journal-full-title] Oral oncology

[ISO-abbreviation] Oral Oncol.

[Language] eng

[Grant] United Kingdom / Medical Research Council / / MC/ U137686859

[Publication-type] Journal Article; Review

[Publication-country] England

[Number-of-references] 29

   

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[Title] Preoperative and early postoperative quality of life predict survival in potentially curable patients with esophageal cancer.

BACKGROUND: In patients with esophageal cancer, evidence for prognostic significance of preoperative quality of life (QoL) is limited, while the prognostic significance of postoperative QoL has not been investigated at all.

AIM: To determine whether preoperative and postoperative QoL measurements can predict survival independently from clinical and pathological factors, in patients with potentially curable esophageal adenocarcinoma.

CONCLUSION: In the present paper the first large consecutive series of potentially curable esophageal cancer patients is presented in whom prospectively collected QoL data before and after potentially curative surgical resection were used to predict survival.

Both preoperative (physical symptoms) and postoperative (social functioning, pain, and activity level) QoL subscales are independent predictors of survival in potentially curable patients with esophageal adenocarcinoma.

[MeSH-major] Carcinoma, Squamous Cell / mortality. Esophageal Neoplasms / mortality. Quality of Life

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[CommentIn] Ann Surg Oncol. 2010 Jan;17(1):12-3 [19851809.001]

(PMID = 19830496.001).

[ISSN] 1534-4681

[Journal-full-title] Annals of surgical oncology

[ISO-abbreviation] Ann. Surg. Oncol.

[Language] eng

[Publication-type] Journal Article; Randomized Controlled Trial

[Publication-country] United States

[Other-IDs] NLM/ PMC2805800

   

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[Title] p53 in esophageal adenocarcinoma: a critical reassessment of mutation frequency and identification of 72Arg as the dominant allele.

p53 alterations have been implicated in the progression of Barrett's esophagus to esophageal adenocarcinoma.

However, the wide range of reported p53 alteration frequencies in esophageal adenocarcinoma makes using p53 as a marker of malignant transformation of Barrett's esophagus problematic.

To determine the utility of p53 in Barrett's esophagus monitoring, the frequency of p53 alteration was critically reassessed using esophagectomy specimens of 40 cases of esophageal adenocarcinoma, including 10 with Barrett's esophagus and high-grade dysplasia, 8 with low-grade dysplasia and 7 with no dysplasia.

Mutations in p53 were identified in 75% (30/40) of the esophageal adenocarcinoma. p53 protein overexpression, detected by immunohistochemistry, was found in 58% (23/40) of the esophageal adenocarcinoma, 60% (6/10) of Barrett's esophagus with high-grade dysplasia, 12% (1/8) of Barrett's esophagus with low-grade dysplasia, and 0% of Barrett's esophagus without dysplasia.

However, p53 appeared to be a late marker in the neoplastic transformation, and no p53 change was found in approximately 25% of the adenocarcinoma.

We concluded that p53 is insufficient as a single marker for Barrett's esophagus monitoring but may be useful as part of a panel due to its high specificity.

[MeSH-major] Adenocarcinoma / genetics. Alleles. Esophageal Neoplasms / genetics. Genes, p53. Mutation

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(PMID = 17982662.001).

[ISSN] 1019-6439

[Journal-full-title] International journal of oncology

[ISO-abbreviation] Int. J. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

[Chemical-registry-number] 0 / Tumor Suppressor Protein p53

   

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The columnar-lined esophagus (CLE) has remained an enigma for several decades.

Starting with the basics, the definition and diagnosis of Barrett's esophagus (BE) continues to be a point of major debate globally leading to definitions that have been restrictive (requiring histologically confirmed intestinal metaplasia) or all-encompassing (simply the presence of CLE at endoscopy).

The interest in intestinal metaplasia stems from studies that have consistently demonstrated intestinal metaplasia and dysplasia both adjacent to and remote from esophageal adenocarcinoma.

There is ample evidence that once a diagnosis of BE is made, it has significant implications on the financial, psychosocial, and insurance status of the patients.

We feel that an optimal, practical definition of BE requires clear, accepted, reproducible, and clinically relevant criteria with evidence of an increased risk of cancer--the most crucial consequence of the lesion--and discuss the pros and cons of the need for documenting intestinal metaplasia in the CLE.

[MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Biopsy. Diagnostic Imaging. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / pathology. Gastric Mucosa / pathology. Humans. Metaplasia. Precancerous Conditions / pathology

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[CommentOn] Am J Gastroenterol. 2007 Jun;102(6):1154-61 [17433019.001]

(PMID = 17531009.001).

[ISSN] 0002-9270

[Journal-full-title] The American journal of gastroenterology

[ISO-abbreviation] Am. J. Gastroenterol.

[Language] eng

[Publication-type] Comment; Editorial

[Publication-country] United States

   

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Although identification of epithelial dysplasia in Barrett's esophagus (BE) is critically important because of a significant risk of progression to invasive adenocarcinoma, the diagnosis of dysplasia may be challenging.

Among confounding factors are interobserver variability, tangential sectioning, and severe mucosal inflammation leading to architectural and cytologic atypia similar to that of dysplasia. alpha-methylacyl-coenzyme A racemase (AMACR) is an enzyme involved in beta-oxidation of branched fatty acids and an established marker of prostate cancer.

Ninety-six routinely processed biopsy and/or resection specimens (23 negative for dysplasia; 19, low-grade dysplasia; 22, high-grade dysplasia; 16, reactive atypia; and 16, esophageal adenocarcinoma) were immunostained using a monoclonal anti-AMACR antibody p504S.

Of 16 specimens, 12 (75%) showed positive staining for AMACR in the adenocarcinoma group.

[MeSH-major] Barrett Esophagus / enzymology. Racemases and Epimerases / biosynthesis

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(PMID = 16996568.001).

[ISSN] 0046-8177

[Journal-full-title] Human pathology

[ISO-abbreviation] Hum. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase

   

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EXPERIMENTAL DESIGN: EphB2 protein expression was analyzed by immunohistochemistry on tissue microarrays that included 76 different normal tissues, >4,000 samples from 138 different cancer types, and 1,476 samples of colon cancer with clinical follow-up data.

RESULTS: We found most prominent EphB2 expression in the intestinal epithelium (colonic crypts) with cancer of the colorectum displaying the highest EphB2 positivity of all tumors.

EphB2 expression was also observed in 75 tumor categories, including serous carcinoma of the endometrium (34.8%), adenocarcinoma of the esophagus (33.3%), intestinal adenocarcinoma of the stomach (30.2%), and adenocarcinoma of the small intestine (70%).

The occasional finding of strong EphB2 positivity in tumors without EphB2 positivity in the corresponding normal cells [adenocarcinoma of the lung (4%) and pancreas (2.2%)] suggests that deregulation of EphB2 signaling may involve up-regulation of the protein expression.

Deregulated EphB2 expression may play a role in several cancer types with loss of EphB2 expression serving as an indicator of the possible pathogenetic role of EphB2 signaling in the maintenance of tissue architecture of colon epithelium.

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(PMID = 16166419.001).

[ISSN] 1078-0432

[Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research

[ISO-abbreviation] Clin. Cancer Res.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] EC 2.7.10.1 / Receptor, EphB2

   

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[Title] Characterization of Barrett esophagus and esophageal adenocarcinoma by Fourier-transform infrared microscopy.

The objective of this exploratory study was to evaluate the feasibility of using Fourier-Transform Infrared (FTIR) spectromicroscopy to characterize formalin-fixed, paraffin-embedded human esophageal tissues.

Matched histologically normal esophageal squamous epithelium (NS), premalignant Barrett esophagus (BE), and primary esophageal adenocarcinoma (EADC) tissues, each defined according to strict clinicopathologic criteria, were obtained from patients who underwent esophageal resection.

Normal esophageal epithelia were characterized by a few well defined regions, mostly of large size (tens of contiguous pixels), which correlated with tissue histology, specifically the basal cell layer.

The technical feasibility of using FTIR to characterize formalin-fixed, paraffin-embedded human esophageal tissues demonstrates the potential of this technique to study archival human BE tissue specimens via automated screening techniques.

[MeSH-major] Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Spectroscopy, Fourier Transform Infrared / methods

[MeSH-minor] Adenocarcinoma / pathology. Cluster Analysis. Goblet Cells / cytology. Goblet Cells / pathology. Humans. Intestines / pathology. Light. Metaplasia / pathology. Microscopy. Synchrotrons

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(PMID = 19475154.001).

[ISSN] 1364-5528

[Journal-full-title] The Analyst

[ISO-abbreviation] Analyst

[Language] eng

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

[Publication-country] England

   

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[Title] Palliation of malignant dysphagia in esophageal cancer: a literature-based review.

Esophageal cancer is a lethal malignancy and adenocarcinoma of the esophagus is increasing in incidence.

The 5-year survival rate of patients with esophageal cancer is < 20%.

Palliation is an important goal of esophageal cancer therapy.

Investigation of dysphagia includes radiographic studies such as barium or Gastrografin swallow, esophagogastroduodenoscopy, endoscopic ultrasonography, and other staging studies for esophageal cancer.

Current management options for the palliation of dysphagia include esophageal dilatation, intraluminal stents, Nd:YAG laser therapy, photodynamic therapy, argon laser, systemic chemotherapy, external beam radiation therapy, brachytherapy, and combined chemoradiation therapy.

[MeSH-major] Adenocarcinoma / complications. Adenocarcinoma / therapy. Deglutition Disorders / etiology. Deglutition Disorders / therapy. Esophageal Neoplasms / complications. Esophageal Neoplasms / therapy. Palliative Care / methods

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[CommentIn] J Support Oncol. 2006 Sep;4(8):377 [17004509.001]

[CommentIn] J Support Oncol. 2006 Sep;4(8):378-9 [17004510.001]

(PMID = 17004508.001).

[ISSN] 1544-6794

[Journal-full-title] The journal of supportive oncology

[ISO-abbreviation] J Support Oncol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 94

   

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[Title] Esophageal adenocarcinoma: treatment modalities in the era of targeted therapy.

Esophageal adenocarcinoma is an aggressive malignancy with a poor outcome, and its incidence continues to rise at an alarming rate.

Multiple molecular pathways including the epidermal growth factor receptor, vascular endothelial growth factor, v-erb-b2 erythroblastic leukemia viral oncogene homolog (ERBB2), and Aurora kinase pathways are activated in many esophageal adenocarcinomas.

[MeSH-major] Adenocarcinoma / drug therapy. Esophageal Neoplasms / drug therapy. Molecular Targeted Therapy

[MeSH-minor] Angiogenesis Inhibitors / pharmacology. Antineoplastic Agents / pharmacology. Aurora Kinases. Barrett Esophagus / pathology. Clinical Trials as Topic. Combined Modality Therapy. Disease Progression. Esophagectomy. Humans. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / drug effects. Receptor, Epidermal Growth Factor / physiology. Treatment Outcome

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(PMID = 20300841.001).

[ISSN] 1573-2568

[Journal-full-title] Digestive diseases and sciences

[ISO-abbreviation] Dig. Dis. Sci.

[Language] eng

[Grant] United States / NCRR NIH HHS / RR / 1 UL1 RR024975; United States / NCI NIH HHS / CA / T32 CA106183-04; United States / NCI NIH HHS / CA / T32 CA106183; United States / NCRR NIH HHS / RR / TL1 RR024978; United States / NCRR NIH HHS / RR / KL2 RR024977; United States / NCI NIH HHS / CA / R01 CA133738-01A2; United States / NCI NIH HHS / CA / R01 CA106176-07A1; United States / NCI NIH HHS / CA / CA133738; United States / NCI NIH HHS / CA / CA131225; United States / NCI NIH HHS / CA / R01 CA131225-01A2; United States / NCI NIH HHS / CA / R01 CA133738; United States / NCI NIH HHS / CA / R01 CA106176; United States / NCI NIH HHS / CA / R01 CA131225; United States / NCI NIH HHS / CA / T32 CA106183-05; United States / NCRR NIH HHS / RR / UL1 RR024975; United States / NCRR NIH HHS / RR / UL1 RR024975-03

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases

[Other-IDs] NLM/ NIHMS183809; NLM/ PMC2890301

   

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[Title] Successful evaluation of a new animal model using mice for esophageal adenocarcinoma.

INTRODUCTION: For the better understanding of the pathophysiological events occurring in the sequence inflammation-metaplasia-carcinoma in esophageal adenocarcinoma, an animal model would be desirable.

Some demonstrated a sequence similar to the human situation whereas others failed to initiate true esophageal adenocarcinoma or even Barrett's metaplasia.

Intestinal metaplasia could be found in 60% of the animals after 4 months and esophageal adenocarcinoma in 55% after 5 months.

CONCLUSION: After a certain learning curve esophagojejunostomy is feasible in mice with an acceptable mortality rate and leads to esophageal adenocarcinoma.

[MeSH-major] Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagus / surgery. Jejunum / surgery

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(PMID = 20300770.001).

[ISSN] 1435-2451

[Journal-full-title] Langenbeck's archives of surgery

[ISO-abbreviation] Langenbecks Arch Surg

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

   

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[Title] Targeted agents and esophageal cancer--the next step?

Esophageal cancer (EC) is an aggressive cancer and is a leading cause of cancer-related death worldwide.

In the United States and Western Europe, there has been a decline in the incidence of squamous cell carcinomas coupled with a rapid rise in incidence of adenocarcinoma of the esophagus and gastroesophageal junction.

[MeSH-major] Esophageal Neoplasms / drug therapy

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(PMID = 17185199.001).

[ISSN] 1053-4296

[Journal-full-title] Seminars in radiation oncology

[ISO-abbreviation] Semin Radiat Oncol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptor, Epidermal Growth Factor

[Number-of-references] 85

   

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[Title] [Barrett's esophagus: contemporary diagnostic and therapeutic approaches].

The author considers the modern concepts of the epidemiology, pathophysiology, clinical manifestations, and diagnostics of Barrett's esophagus (BE).

Special attention is paid to the evaluation of BE as precancer elevating the risk of esophageal adenocarcinoma, as well as the issues of the treatment and regular medical check-up of such patients.

[MeSH-major] Barrett Esophagus. Endoscopy, Gastrointestinal / methods. Enzyme Inhibitors / therapeutic use. Esophagectomy / methods. Histamine H2 Antagonists / therapeutic use. Proton Pump Inhibitors

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(PMID = 17243606.001).

[ISSN] 0023-2149

[Journal-full-title] Klinicheskaia meditsina

[ISO-abbreviation] Klin Med (Mosk)

[Language] rus

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

[Publication-country] Russia (Federation)

[Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Histamine H2 Antagonists; 0 / Proton Pump Inhibitors

[Number-of-references] 39

   

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[Title] PET detection of solitary distant skeletal muscle metastasis of esophageal adenocarcinoma.

A 67-year-old man with progressive dysphagia was recently diagnosed with a gastroesophageal junction adenocarcinoma.

Needle biopsy was performed and confirmed metastatic esophageal adenocarcinoma.

A case of skeletal muscle metastases from late-stage (IV) gastroesophageal adenocarcinoma was previously reported.

The case supports the previous report that PET is superior in detecting distant metastases for initial staging of esophageal carcinoma over CT.

[MeSH-major] Adenocarcinoma / radionuclide imaging. Adenocarcinoma / secondary. Esophageal Neoplasms / radionuclide imaging. Fluorodeoxyglucose F18. Muscle Neoplasms / radionuclide imaging. Muscle Neoplasms / secondary. Positron-Emission Tomography / methods

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(PMID = 15827406.001).

[ISSN] 0363-9762

[Journal-full-title] Clinical nuclear medicine

[ISO-abbreviation] Clin Nucl Med

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18

   

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[Title] Male predominance of upper gastrointestinal adenocarcinoma cannot be explained by differences in tobacco smoking in men versus women.

Incident UGI adenocarcinomas were identified by linkage to state cancer registries.

We present age-standardised cancer incidence rates per 100,000-person years and male/female ratios (M/F) calculated from age-adjusted Cox proportional hazards models, both with 95% confidence intervals (CI).

RESULTS: After 2013,142-person years follow-up, 338 adenocarcinomas of the oesophagus, 261 of gastric cardia and 222 of gastric non-cardia occurred in men.

In women, 23 tumours of oesophagus, 36 of gastric cardia and 88 of gastric non-cardia occurred in 1351,958-person years follow-up.

The age-standardised incidence rate of all adenocarcinoma sites was 40.5 (37.8-43.3) and 11.0 (9.2-12.8) in men and women, respectively.

Among smokers, the M/F of all UGI adenocarcinomas was 3.4 (2.7-4.1), with a M/F of 7.3 (4.6-11.7) for tumours in oesophagus, 3.7 (2.5-5.4) for gastric cardia and 1.7 (1.2-2.3) for gastric non-cardia.

In non-smokers, M/F ratios were 14.2 (5.1-39.5) for oesophagus, 6.1 (2.6-14.7) for gastric cardia and 1.3 (0.8-2.0) for gastric non-cardia.

CONCLUSION: The male predominance was similar in smokers and non-smokers for these cancer sites.

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

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[Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.

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(PMID = 20605442.001).

[ISSN] 1879-0852

[Journal-full-title] European journal of cancer (Oxford, England : 1990)

[ISO-abbreviation] Eur. J. Cancer

[Language] eng

[Grant] United Kingdom / Chief Scientist Office / / CZB/4/709; United States / Intramural NIH HHS / / ZIA CP000185-08

[Publication-type] Journal Article; Multicenter Study

[Publication-country] England

[Other-IDs] NLM/ NIHMS414823; NLM/ PMC3514413

   

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[Title] Multiple forms of genetic instability within a 2-Mb chromosomal segment of 3q26.3-q27 are associated with development of esophageal adenocarcinoma.

Gene amplification is one of the mechanisms to activate oncogenes in many cancers, including esophageal adenocarcinoma (EA).

[MeSH-major] Adenocarcinoma / genetics. Chromosomes, Human, Pair 3. Esophageal Neoplasms / genetics

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NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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(PMID = 16320248.001).

[ISSN] 1045-2257

[Journal-full-title] Genes, chromosomes & cancer

[ISO-abbreviation] Genes Chromosomes Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA71606

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / 5' Untranslated Regions

   

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[Title] Mucin pattern reflects the origin of the adenocarcinoma in Barrett's esophagus: a retrospective clinical and laboratorial study.

BACKGROUND: Mucin immunoexpression in adenocarcinoma arising in Barrett's esophagus (BE) may indicate the carcinogenesis pathway.

The aim of this study was to evaluate resected specimens of adenocarcinoma in BE for the pattern of mucins and to correlate to the histologic classification.

METHODS: Specimens were retrospectively collected from thirteen patients who underwent esophageal resection due to adenocarcinoma in BE.

CONCLUSION: Barrett's esophagus adenocarcinoma shows either gastric or intestinal type pattern of mucin expression.

The two types of tumors developed in Barrett's esophagus may reflect the original cell type involved in the malignant transformation.

[MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / complications. Esophageal Neoplasms / etiology. Mucin 5AC / analysis. Mucin-2 / analysis

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(PMID = 19272137.001).

[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

[Chemical-registry-number] 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / Mucin 5AC; 0 / Mucin-2

[Other-IDs] NLM/ PMC2662840

   

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[Title] Induction chemotherapy in Barrett cancer: influence on surgical risk and outcome.

OBJECTIVE: To study the impact of induction chemotherapy on surgical risk and outcome in locally advanced Barrett cancer.

BACKGROUND: Induction chemotherapy has become an accepted choice for the treatment of locally advanced adenocarcinoma of the esophagus and the esophagogastric junction.

CONCLUSIONS: Induction chemotherapy and early metabolic response assessment is a new concept in the treatment of locally advanced Barrett cancer.

[MeSH-major] Adenocarcinoma / surgery. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Barrett Esophagus / surgery. Esophageal Neoplasms / surgery. Neoadjuvant Therapy

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[CommentIn] Ann Surg. 2008 Jun;247(6):1080-1; author reply 1081 [18520245.001]

(PMID = 17893499.001).

[ISSN] 0003-4932

[Journal-full-title] Annals of surgery

[ISO-abbreviation] Ann. Surg.

[Language] eng

[Publication-type] Comparative Study; 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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[Title] Early events during neoplastic progression in Barrett's esophagus.

Barrett's esophagus is a condition in which the stratified squamous epithelium of the distal esophagus is replaced by specialized intestinal metaplasia.

Clinical management of Barrett's esophagus, like many other "premalignant" conditions, is characterized by overdiagnosis of benign early changes that will not cause death or suffering during the lifetime of an individual and underdiagnosis of life-threatening early disease.

Recent studies of a number of different types of cancer have revealed much greater genomic complexity than was previously suspected.

This genomic complexity could create challenges for early detection and prevention if it develops in premalignant epithelia prior to cancer.

Neoplastic progression unfolds in space and time, and Barrett's esophagus provides one of the best models for rapid advances, including "gold standard" cohort studies, to distinguish individuals who do and do not progress to cancer.

A large body of evidence accumulated over several decades implicates chromosome instability in neoplastic progression from Barrett's esophagus to esophageal adenocarcinoma.

Small, spatial scale studies have been used to infer the temporal order in which genomic abnormalities develop during neoplastic progression in Barrett's esophagus.

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(PMID = 22112482.001).

[ISSN] 1875-8592

[Journal-full-title] Cancer biomarkers : section A of Disease markers

[ISO-abbreviation] Cancer Biomark

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P01 CA091955; United States / NCI NIH HHS / CA / P01CA91955

[Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Biomarkers, Tumor

[Other-IDs] NLM/ NIHMS578448; NLM/ PMC4026269

   

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[Title] Body size and composition and the risk of gastric and oesophageal adenocarcinoma.

Although evidence has been mounting that obesity may be related to the increased incidence of oesophageal and gastric cardia malignancies, these reports (mainly case-control studies) have relied on imperfect measures of obesity such as body mass index (BMI), and generally have not clearly distinguished between anatomical subsites within the oesophagus and stomach.

Among 41,295 people followed on average for 11.3 years, 30 cases with cancers in the gastric cardia or lower third of the oesophagus and 68 cases with noncardia gastric adenocarcinomas were ascertained via the population cancer registry.

The risk of adenocarcinoma of the lower oesophagus and gastric cardia was positively associated with BMI with a hazards ratio (HR) and (95% confidence interval) for people with BMI>or=30 kg/m2 compared with those<25 kg/m2, of 3.7 (1.1-12.4), an HR per 10 cm increase in waist circumference of 1.46 (1.05-2.04), and a HR per 10 kg increase on fat-free mass of 2.06 (1.15-3.69).

Noncardia gastric adenocarcinoma showed little relationship with body size.

We observed an increased risk of adenocarcinoma of the lower oesophagus and gastric cardia associated with increased BMI, central adiposity and the nonfat component of weight, but found no association with noncardia gastric adenocarcinoma.

An increasing prevalence of obesity may be associated with the increasing incidence of gastro-oesophageal cancer observed in many populations.

[MeSH-major] Adenocarcinoma / etiology. Body Composition. Body Mass Index. Cardia. Esophageal Neoplasms / etiology. Stomach Neoplasms / etiology

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

(PMID = 16353151.001).

[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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[Title] Sweet's syndrome with neurologic manifestations in a patient with esophageal adenocarcinoma: case report and review of the literature.

METHODS: This report describes a 62-year-old man with adenocarcinoma of the esophagus who developed Sweet's syndrome and whose postoperative course was complicated by encephalitis.

RESULTS: A diagnosis of Sweet's syndrome with neurologic manifestations was made, and the patient was treated with oral corticosteroids.

CONCLUSION: Neurologic symptoms in Sweet's syndrome are infrequently reported and have not been described previously in a patient with adenocarcinoma of the esophagus.

[MeSH-major] Adenocarcinoma / complications. Encephalitis / etiology. Esophageal Neoplasms / complications. Sweet Syndrome / complications. Sweet Syndrome / etiology

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(PMID = 19785087.001).

[ISSN] 1365-4632

[Journal-full-title] International journal of dermatology

[ISO-abbreviation] Int. J. Dermatol.

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] United States

[Number-of-references] 48

   

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[Title] Etiologic clues from the similarity of histology-specific trends in esophageal and lung cancers.

OBJECTIVE: We tested whether descriptive evidence exists for differing roles of specific tobacco constituents on different histologic subtypes of esophageal cancer.

Esophageal adenocarcinoma incidence rates are increasing while squamous cell esophageal cancer rates are declining in Westernized countries as are the histology-specific lung counterparts.

Smoking is also a risk factor for esophageal cancers.

METHODS: We compared patterns of incidence of squamous cell cancers of the lung with those of squamous cell esophageal cancers, and incidence trends in lung adenocarcinomas with those of esophageal adenocarcinomas during the time period from 1976 to 2000 using data from the population-based Los Angeles Cancer Surveillance Program.

RESULTS: Rates of squamous cell esophageal cancer declined in a similar fashion to those of squamous cell lung cancer, while esophageal adenocarcinoma incidence increased at a rate similar to that of lung adenocarcinoma, in both men and women, and blacks and whites.

Histology-specific socio-economic gradients in lung and esophageal cancers were also strikingly similar.

Increases in esophageal adenocarcinoma were confined to the lower third of the esophagus.

CONCLUSIONS: While increases in obesity over time might explain these trends, they are also consistent with a specific effect of some constituent of tobacco smoke working through reflux disease to cause esophageal adenocarcinoma.

[MeSH-major] Esophageal Neoplasms / epidemiology. Esophageal Neoplasms / etiology. Lung Neoplasms / epidemiology. Lung Neoplasms / etiology. Smoking / adverse effects. Tobacco / chemistry

[MeSH-minor] Adenocarcinoma / epidemiology. Adenocarcinoma / etiology. Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / etiology. Female. Humans. Incidence. Los Angeles / epidemiology. Male. Social Class. Socioeconomic Factors

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(PMID = 16184472.001).

[ISSN] 0957-5243

[Journal-full-title] Cancer causes & control : CCC

[ISO-abbreviation] Cancer Causes Control

[Language] eng

[Grant] United States / NIEHS NIH HHS / ES / 5P30 ES07048; United States / NCI NIH HHS / CA / CA 17054; United States / NCI NIH HHS / PC / N01-PC-35139; United States / ODCDC CDC HHS / CC / U55/CCU921930-02

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

[Publication-country] Netherlands

   

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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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NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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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