BioMedLib Search Engine
[ goto HOMEPAGE ]
Save time; Find better answers!
Skip to content
Advanced Search
Search History
MeSH Query
Page Format
Query is expanded
Login
Skip to content
Export Citations
Search Results
RSS
Email
Articles' Details
Start new query
Reset All
Refine your query
(more in Advanced-Search):
Search all of MEDLINE
Focus on the recent 5 years
Focus on the current year
Focus on the last 30 days
More choices ...
Focus on articles with free fulltexts
More choices ...
Do simple 'keyword' search (no query expansion)
[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click
here to
RESET
all values
Click
here to
GO BACK
without resetting any value
Advanced Search
Submit one or more of the following items, and they will be searched along with your query in the search box above.
Any submit button will submit all of the items you have changed.
+
Publication-Date
Published in the last:
30 days
60 days
90 days
6 months
12 months
this year
2 years
3 years
5 years
10 years
Or published in the following date range: From (yyyy/mm/dd - month and day are optional)
to ('to' is optional)
+
Full Text
Retrieve articles with hyperlinks to:
full text (either free or subscription)
free full text
subscription full text
no full text link
+
Sort-Order
Sort the retrieved articles by:
relevance
publication date
+
Language
And with languages:
English
French
German
Italian
Japanese
Russian
Spanish
More languages:
Afrikaans
Albanian
Amharic
Arabic
Armenian
Azerbaijani
Bengali
Bosnian
Bulgarian
Catalan
Chinese
Czech
Danish
Dutch
Esperanto
Estonian
Finnish
Georgian
Scottish Gaelic
Greek, Modern
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Kinyarwanda
Korean
Latin
Latvian
Lithuanian
Macedonian
Malayalam
Maori
Malay
Multiple languages
Norwegian
Persian
Polish
Portuguese
Pushto
Romanian
Sanskrit
Serbian
Croatian
Slovak
Slovenian
Swedish
Thai
Turkish
Ukrainian
Undetermined
Urdu
Vietnamese
Welsh
+
Publication-Type
And with publication types:
Clinical Trial
Editorial
Letter
Meta-Analysis
Practice Guideline
Randomized Controlled Trial
Review
More publication types:
Addresses
Bibliography
Biography
Case Reports
Classical Article
Clinical Conference
Clinical Trial, Phase I
Clinical Trial, Phase II
Clinical Trial, Phase III
Clinical Trial, Phase IV
Comment
Comparative Study
Congresses
Consensus Development Conference
Consensus Development Conference, NIH
Controlled Clinical Trial
Corrected and Republished Article
Dictionary
Directory
Duplicate Publication
English Abstract
Evaluation Studies
Festschrift
Government Publications
Guideline
Historical Article
Interactive Tutorial
Interview
Introductory Journal Article
In Vitro
Journal Article
Lectures
Legal Cases
Legislation
Multicenter Study
News
Newspaper Article
Overall
Patient Education Handout
Periodical Index
Portraits
Published Erratum
Retracted Publication
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
Retraction of Publication
Scientific Integrity Review
Technical Report
Twin Study
Validation Studies
+
Species
And for:
Humans
Animals
+
Gender
And for:
Male
Female
+
Age
And for these age groups:
Newborn: birth to 1 month
Infant: 1 to 23 months
Preschool child: 2 to 5 years
Child: 6 to 12 years
Adolescent: 13 to 18 years
Adult: 19 to 44 years
Middle aged: 45 to 64 years
Aged: 65+ years
80 and over: 80+ years
+
Title
And for this query matching the titles:
+
Transliterated-Title
And for this query matching the title in original language:
+
Abstract
And for this query matching the abstratcs:
+
Major-Mesh
And for this query matching the MeSH-Major terms:
+
Mesh
And for this query matching any MeSH terms:
+
Journal
And for one or more of these journal abbreviated names:
OR
OR
(see
title abbreviations
)
+
Volume
And with journal volume number:
+
Issue
And with journal issue number:
+
Page
And with page number:
+
ISSN
And with ISSN:
+
Publication-Place
And with journal's country of publication:
+
Author
And for...
all these author names:
AND
AND
(see
help
)
one or more of these author names:
OR
OR
but not having any of these unwanted author names:
NOT
NOT
+
Affiliation
And with affiliation to:
+
Has-Abstract
Find MEDLINE records with the abstract status:
has abstract
does not have abstract
include both record types
include both record types but rank higher the records having abstract (the default BML behavior)
+
PMID
Show me only articles for these PMIDs (PubMed IDs):
+
Semantic-Type
And with semantic types:
A. Entity
A1. Physical Object
A1.1. Organism
A1.1.1. Archaeon
A1.1.2. Bacterium
A1.1.3. Eukaryote
A1.1.3.1. Animal
A1.1.3.1.1. Vertebrate
A1.1.3.1.1.1. Amphibian
A1.1.3.1.1.2. Bird
A1.1.3.1.1.3. Fish
A1.1.3.1.1.4. Mammal
A1.1.3.1.1.4.1. Human
A1.1.3.1.1.5. Reptile
A1.1.3.2. Fungus
A1.1.3.3. Plant
A1.1.4. Virus
A1.2. Anatomical Structure
A1.2.1. Embryonic Structure
A1.2.2. Anatomical Abnormality
A1.2.2.1. Congenital Abnormality
A1.2.2.2. Acquired Abnormality
A1.2.3. Fully Formed Anatomical Structure
A1.2.3.1. Body Part, Organ, or Organ Component
A1.2.3.2. Tissue
A1.2.3.3. Cell
A1.2.3.4. Cell Component
A1.2.3.5. Gene or Genome
A1.3. Manufactured Object
A1.3.1. Medical Device
A1.3.1.1. Drug Delivery Device
A1.3.2. Research Device
A1.3.3. Clinical Drug
A1.4. Substance
A1.4.1. Chemical
A1.4.1.1. Chemical Viewed Functionally
A1.4.1.1.1. Pharmacologic Substance
A1.4.1.1.1.1. Antibiotic
A1.4.1.1.2. Biomedical or Dental Material
A1.4.1.1.3. Biologically Active Substance
A1.4.1.1.3.1. Neuroreactive Substance or Biogenic Amine
A1.4.1.1.3.2. Hormone
A1.4.1.1.3.3. Enzyme
A1.4.1.1.3.4. Vitamin
A1.4.1.1.3.5. Immunologic Factor
A1.4.1.1.3.6. Receptor
A1.4.1.1.4. Indicator, Reagent, or Diagnostic Aid
A1.4.1.1.5. Hazardous or Poisonous Substance
A1.4.1.2. Chemical Viewed Structurally
A1.4.1.2.1. Organic Chemical
A1.4.1.2.1.5. Nucleic Acid, Nucleoside, or Nucleotide
A1.4.1.2.1.6. Organophosphorus Compound
A1.4.1.2.1.7. Amino Acid, Peptide, or Protein
A1.4.1.2.1.8. Carbohydrate
A1.4.1.2.1.9. Lipid
A1.4.1.2.1.9.1. Steroid
A1.4.1.2.1.9.2. Eicosanoid
A1.4.1.2.2. Inorganic Chemical
A1.4.1.2.3. Element, Ion, or Isotope
A1.4.2. Body Substance
A1.4.3. Food
A2. Conceptual Entity
A2.1. Idea or Concept
A2.1.1. Temporal Concept
A2.1.2. Qualitative Concept
A2.1.3. Quantitative Concept
A2.1.4. Functional Concept
A2.1.4.1. Body System
A2.1.5. Spatial Concept
A2.1.5.1. Body Space or Junction
A2.1.5.2. Body Location or Region
A2.1.5.3. Molecular Sequence
A2.1.5.3.1. Nucleotide Sequence
A2.1.5.3.2. Amino Acid Sequence
A2.1.5.3.3. Carbohydrate Sequence
A2.1.5.4. Geographic Area
A2.2. Finding
A2.2.1. Laboratory or Test Result
A2.2.2. Sign or Symptom
A2.3. Organism Attribute
A2.3.1. Clinical Attribute
A2.4. Intellectual Product
A2.4.1. Classification
A2.4.2. Regulation or Law
A2.5. Language
A2.6. Occupation or Discipline
A2.6.1. Biomedical Occupation or Discipline
A2.7. Organization
A2.7.1. Health Care Related Organization
A2.7.2. Professional Society
A2.7.3. Self-help or Relief Organization
A2.8. Group Attribute
A2.9. Group
A2.9.1. Professional or Occupational Group
A2.9.2. Population Group
A2.9.3. Family Group
A2.9.4. Age Group
A2.9.5. Patient or Disabled Group
B. Event
B1. Activity
B1.1. Behavior
B1.1.1. Social Behavior
B1.1.2. Individual Behavior
B1.2. Daily or Recreational Activity
B1.3. Occupational Activity
B1.3.1. Health Care Activity
B1.3.1.1. Laboratory Procedure
B1.3.1.2. Diagnostic Procedure
B1.3.1.3. Therapeutic or Preventive Procedure
B1.3.2. Research Activity
B1.3.2.1. Molecular Biology Research Technique
B1.3.3. Governmental or Regulatory Activity
B1.3.4. Educational Activity
B1.4. Machine Activity
B2. Phenomenon or Process
B2.1. Human-caused Phenomenon or Process
B2.1.1. Environmental Effect of Humans
B2.2. Natural Phenomenon or Process
B2.2.1. Biologic Function
B2.2.1.1. Physiologic Function
B2.2.1.1.1. Organism Function
B2.2.1.1.1.1. Mental Process
B2.2.1.1.2. Organ or Tissue Function
B2.2.1.1.3. Cell Function
B2.2.1.1.4. Molecular Function
B2.2.1.1.4.1. Genetic Function
B2.2.1.2. Pathologic Function
B2.2.1.2.1. Disease or Syndrome
B2.2.1.2.1.1. Mental or Behavioral Dysfunction
B2.2.1.2.1.2. Neoplastic Process
B2.2.1.2.2. Cell or Molecular Dysfunction
B2.2.1.2.3. Experimental Model of Disease
B2.3. Injury or Poisoning
Page Format
Any submit button will submit all of the items you have changed.
[theme]
Use this page design theme:
original
twenty ten
[shown]
Results per page:
5
10
20
50
100
200
500
[expand/collapse]
show these sections expanded by default:
Advanced search
MeSH query
Search history
Page format
Query expansion
Articles details
Export citations
Email
[text size]
use this font size for text:
25%
50%
75%
100%
125%
150%
200%
or enter your choice of font size:
[page width]
use this page width (relative to the default initial value):
25%
50%
75%
100%
125%
150%
200%
or enter your choice of page width:
[highlight color]
use this color to highlight query words in the articles:
red
green
blue
black
purple
yellow
orange
navy
olive
maroon
none
[query history]
maximum number of queries shown in the history section:
[annotate]
Annotate these parts of each article:
title
abstract
both
none
Reset all values
Find best MeSH terms for
Search History
1
adenocarcinoma of oesophagus 2005:2010[pubdate] *count=100
1491 results
Searchbox
Export
PDF
RSS
Email
Delete
Email this search result to the following email address:
[X] Close
Expand the query
'
adenocarcinoma of oesophagus
' expanded to all its synonyms;
details
Email the results to the following email address:
Export the checked citations in RIS format (RIS format is used by RefWorks, Endnote, among others).
Items 1 to 100 of about 1491
1.
Chandrasoma P:
The price of doubt is esophageal adenocarcinoma.
Ann Surg
; 2008 Mar;247(3):558-9; author reply 559-60
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The price of doubt is
esophageal
adenocarcinoma
.
[MeSH-major]
Adenocarcinoma
/ prevention & control.
Esophageal
Neoplasms / prevention & control. Gastroesophageal Reflux / surgery
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - GERD
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[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
2.
Abdel-Latif MM, Kelleher D, Reynolds JV:
Potential role of NF-kappaB in esophageal adenocarcinoma: as an emerging molecular target.
J Surg Res
; 2009 May 1;153(1):172-80
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
3.
Liu G, Zhou W, Yeap BY, Su L, Wain JC, Poneros JM, Nishioka NS, Lynch TJ, Christiani DC:
XRCC1 and XPD polymorphisms and esophageal adenocarcinoma risk.
Carcinogenesis
; 2007 Jun;28(6):1254-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 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
Advertisement
4.
Yong TY, Klebe S, Li JY:
Acute critical leg ischemia: an uncommon initial manifestation of esophageal adenocarcinoma.
J Palliat Med
; 2009 Sep;12(9):841-4
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Acute critical leg ischemia: an uncommon initial manifestation of
esophageal
adenocarcinoma
.
This report describes a patient who presented with acute critical right leg ischemia leading to
the diagnosis
of
esophageal
adenocarcinoma
with widespread metastases.
However, he died 3 weeks after presentation due to progressive
cancer
.
[MeSH-major]
Esophageal
Neoplasms / complications. Ischemia / etiology. Leg / blood supply
[MeSH-minor]
Acute Disease.
Adenocarcinoma
/ complications.
Adenocarcinoma
/ pathology. Adult. Disease Progression. Fatal Outcome. Humans. Male. Risk Factors. Time Factors
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19719377.001).
[ISSN]
1557-7740
[Journal-full-title]
Journal of palliative medicine
[ISO-abbreviation]
J Palliat Med
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
5.
DeMeester SR:
Reflux, Barrett's, and adenocarcinoma of the esophagus: can we disrupt the pathway?
J Gastrointest Surg
; 2010 Jun;14(6):941-5
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
Genetic Alliance.
consumer health - Barrett's Esophagus
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - GERD
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Clin Invest. 1996 Nov 1;98(9):2120-8
[
8903332.001
]
[Cites]
Eur J Surg. 1997 Jun;163(6):469-71
[
9231860.001
]
[Cites]
Ann Surg. 2007 Jul;246(1):11-21
[
17592284.001
]
[Cites]
J Thorac Cardiovasc Surg. 1999 Mar;117(3):572-80
[
10047662.001
]
[Cites]
Am J Gastroenterol. 2000 Apr;95(4):921-4
[
10763938.001
]
[Cites]
Arch Surg. 2001 Nov;136(11):1267-73
[
11695971.001
]
[Cites]
Am J Surg. 1992 Nov;164(5):522-6; discussion 526-7
[
1443381.001
]
[Cites]
Physiol Rev. 2007 Oct;87(4):1343-75
[
17928586.001
]
[Cites]
Dig Dis Sci. 2008 Dec;53(12):3076-81
[
18438712.001
]
[Cites]
Am J Gastroenterol. 2006 Jul;101(7):1458-66
[
16863546.001
]
[Cites]
Am J Gastroenterol. 2004 Oct;99(10):1877-83
[
15447744.001
]
[Cites]
Arch Surg. 2007 Jun;142(6):554-9; discussion 559-60
[
17576892.001
]
[Cites]
Surgery. 1997 Nov;122(5):874-81
[
9369886.001
]
[Cites]
Gut. 2002 Sep;51(3):316-22
[
12171950.001
]
[Cites]
Surgery. 2006 Jan;139(1):46-53
[
16364717.001
]
[Cites]
Dev Biol. 2005 Aug 1;284(1):157-70
[
15992795.001
]
[Cites]
Scand J Gastroenterol. 2007 Nov;42(11):1271-4
[
17852872.001
]
[Cites]
Am J Surg Pathol. 2000 Mar;24(3):402-9
[
10716154.001
]
[Cites]
Carcinogenesis. 2009 Jan;30(1):122-30
[
18845559.001
]
[Cites]
Am J Gastroenterol. 2002 Apr;97(4):851-6
[
12003418.001
]
[Cites]
J Gastrointest Surg. 2009 Apr;13(4):602-10
[
19050984.001
]
[Cites]
Ann Surg. 2002 Mar;235(3):338-45
[
11882755.001
]
[Cites]
Am J Gastroenterol. 1993 Mar;88(3):402-8
[
8438848.001
]
[Cites]
Surgery. 2004 Sep;136(3):633-40
[
15349112.001
]
[Cites]
Gastroenterology. 2001 Dec;121(6):1286-93
[
11729107.001
]
[Cites]
Am J Surg Pathol. 2001 Sep;25(9):1188-93
[
11688579.001
]
[Cites]
Ann Surg. 1995 Oct;222(4):525-31; discussion 531-3
[
7574932.001
]
[Cites]
Gastroenterology. 1994 Sep;107(3):747-54
[
8076761.001
]
[Cites]
Gastroenterology. 1999 Aug;117(2):327-35
[
10419913.001
]
[Cites]
Gastroenterology. 1960 Jul;39:104-10
[
13850707.001
]
[Cites]
J Pathol. 2003 Jan;199(1):36-40
[
12474224.001
]
[Cites]
World J Surg. 2003 Sep;27(9):986-93
[
14560363.001
]
[Cites]
Am J Gastroenterol. 1998 Apr;93(4):536-41
[
9576444.001
]
[Cites]
J Pathol. 2004 Aug;203(4):904-8
[
15258992.001
]
[Cites]
Ann Surg. 2003 Mar;237(3):291-8
[
12616111.001
]
[Cites]
Ann Surg. 2000 Mar;231(3):303-21
[
10714623.001
]
[Cites]
N Engl J Med. 1976 Aug 26;295(9):476-80
[
940579.001
]
[Cites]
Ann Surg. 2001 Nov;234(5):619-26
[
11685024.001
]
[Cites]
Ann Surg. 2001 Nov;234(5):627-32
[
11685025.001
]
[Cites]
Arch Surg. 2000 Jun;135(6):651-5; discussion 655-6
[
10843360.001
]
[Cites]
Scand J Gastroenterol. 2000 Dec;35(12):1238-44
[
11199360.001
]
[Cites]
Hum Pathol. 2009 Jan;40(1):65-74
[
18755496.001
]
[Cites]
Gastroenterology. 2005 Nov;129(5):1696-710
[
16285967.001
]
(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
6.
Tutuian R:
Update in the diagnosis of gastroesophageal reflux disease.
J Gastrointestin Liver Dis
; 2006 Sep;15(3):243-7
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
Genetic Alliance.
consumer health - Gastroesophageal Reflux
.
MedlinePlus Health Information.
consumer health - GERD
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
7.
Murray L, Romero Y:
Role of obesity in Barrett's esophagus and cancer.
Surg Oncol Clin N Am
; 2009 Jul;18(3):439-52
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
Genetic Alliance.
consumer health - Barrett's Esophagus
.
Genetic Alliance.
consumer health - Obesity
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - GERD
.
MedlinePlus Health Information.
consumer health - Obesity
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
8.
Ku GY, Ilson DH:
Role of neoadjuvant therapy for esophageal adenocarcinoma.
Surg Oncol Clin N Am
; 2009 Jul;18(3):533-46
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
Hazardous Substances Data Bank.
CIS-DIAMINEDICHLOROPLATINUM
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
9.
Anandasabapathy S, Jhamb J, Davila M, Wei C, Morris J, Bresalier R:
Clinical and endoscopic factors predict higher pathologic grades of Barrett dysplasia.
Cancer
; 2007 Feb 15;109(4):668-74
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Hiatal Hernia
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17211862.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
10.
Howard JM, Pidgeon GP, Reynolds JV:
Leptin and gastro-intestinal malignancies.
Obes Rev
; 2010 Dec;11(12):863-74
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
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.
MedlinePlus Health Information.
consumer health - Obesity
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[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
11.
Sarosi GA Jr:
Introduction: esophagus, dysplasia, and early esophageal adenocarcinoma: managing the transition.
J Gastrointest Surg
; 2010 Jun;14(6):935-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Introduction:
esophagus
, dysplasia, and early
esophageal
adenocarcinoma
: managing the transition.
[MeSH-major]
Adenocarcinoma
/ pathology. Barrett
Esophagus
/ pathology.
Esophageal
Neoplasms / pathology.
Esophagus
/ pathology
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Natl Cancer Inst. 2005 Jan 19;97(2):142-6
[
15657344.001
]
[Cites]
Am J Gastroenterol. 2008 Mar;103(3):788-97
[
18341497.001
]
[Cites]
Cancer Lett. 2009 Mar 18;275(2):170-7
[
18703277.001
]
[Cites]
JAMA. 2002 Apr 17;287(15):1972-81
[
11960540.001
]
[Cites]
Int J Cancer. 2008 Sep 15;123(6):1422-8
[
18546259.001
]
[Cites]
Gastroenterology. 2005 Dec;129(6):1825-31
[
16344051.001
]
(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
12.
Bhat MA, Naikoo ZA, Dass TA, Lone RA, Dar AM:
Role of intraoperative sentinel lymph node mapping in the management of carcinoma of the esophagus.
Saudi J Gastroenterol
; 2010 Jul-Sep;16(3):168-73
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
Hazardous Substances Data Bank.
METHYLENE BLUE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Treat Res. 2005;127:123-39
[
16209080.001
]
[Cites]
Surg Clin North Am. 2000 Dec;80(6):1799-809
[
11140874.001
]
[Cites]
Surg Oncol Clin N Am. 2002 Apr;11(2):293-304
[
12424851.001
]
[Cites]
J Am Coll Surg. 2003 Jan;196(1):68-74
[
12517553.001
]
[Cites]
Br J Surg. 2003 Feb;90(2):178-82
[
12555293.001
]
[Cites]
Am J Surg. 2004 Feb;187(2):270-3
[
14769318.001
]
[Cites]
Ann Surg Oncol. 2004 Mar;11(3 Suppl):245S-9S
[
15023761.001
]
[Cites]
Ann Surg Oncol. 2004 Mar;11(3 Suppl):255S-8S
[
15023763.001
]
[Cites]
J Surg Oncol. 2004 Jul 15;87(1):32-8
[
15221917.001
]
[Cites]
Cancer. 1977 Feb;39(2):456-66
[
837331.001
]
[Cites]
Gut. 1992 Jan;33(1):11-5
[
1740265.001
]
[Cites]
Arch Surg. 1992 Apr;127(4):392-9
[
1558490.001
]
[Cites]
Ann Surg. 1994 Sep;220(3):391-8; discussion 398-401
[
8092905.001
]
[Cites]
World J Surg. 1997 Oct;21(8):822-31
[
9327673.001
]
[Cites]
Br J Surg. 1999 Apr;86(4):482-6
[
10215818.001
]
[Cites]
Ann Surg. 1955 Sep;142(3):486-506
[
13249345.001
]
[Cites]
Br J Surg. 2005 Jan;92(1):60-7
[
15584066.001
]
[Cites]
Zhonghua Wai Ke Za Zhi. 2005 May 1;43(9):569-72
[
15938926.001
]
[Cites]
Cancer Metastasis Rev. 2006 Jun;25(2):269-77
[
16770539.001
]
[Cites]
Best Pract Res Clin Gastroenterol. 2006;20(5):893-906
[
16997168.001
]
[Cites]
Ann Surg Oncol. 2008 Jan;15(1):80-7
[
18004627.001
]
[Cites]
Ann Thorac Surg. 2008 Feb;85(2):S751-6
[
18222210.001
]
[Cites]
Ned Tijdschr Geneeskd. 2008 Jan 5;152(1):38-45
[
18240761.001
]
[Cites]
Eur J Cardiothorac Surg. 2008 Aug;34(2):427-31
[
18502142.001
]
[Cites]
Surg Endosc. 2008 Dec;22(12):2753-60
[
18813994.001
]
[Cites]
Pathol Oncol Res. 1999;5(4):291-6
[
10607924.001
]
[Cites]
Cancer. 2000 Nov 1;89(9):1869-73
[
11064342.001
]
[Cites]
J Gastroenterol Hepatol. 2002 Apr;17(4):374-81
[
11982715.001
]
(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
13.
Gockel I, Sultanov FS, Domeyer M, Trinh TT, Gönner U, Junginger T:
[Surgical therapy for esophageal carcinoma: a prospective 20-year analysis].
Zentralbl Chir
; 2008 Jun;133(3):260-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 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
14.
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
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
15.
Madani K, Zhao R, Lim HJ, Casson SM, Casson AG:
Obesity is not associated with adverse outcome following surgical resection of oesophageal adenocarcinoma.
Eur J Cardiothorac Surg
; 2010 Nov;38(5):604-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
Genetic Alliance.
consumer health - Obesity
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Obesity
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[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
16.
Islami F, Kamangar F:
Helicobacter pylori and esophageal cancer risk: a meta-analysis.
Cancer Prev Res (Phila)
; 2008 Oct;1(5):329-38
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
Genetic Alliance.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Helicobacter Pylori Infections
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Res. 1998 Feb 15;58(4):588-90
[
9485003.001
]
[Cites]
Am J Gastroenterol. 1998 Apr;93(4):542-6
[
9576445.001
]
[Cites]
Gastroenterology. 1998 Jul;115(1):50-7
[
9649458.001
]
[Cites]
Cancer. 1998 Nov 15;83(10):2049-53
[
9827707.001
]
[Cites]
N Engl J Med. 1999 Mar 18;340(11):825-31
[
10080844.001
]
[Cites]
Arch Surg. 1999 Jul;134(7):722-6
[
10401822.001
]
[Cites]
Int J Cancer. 1999 Aug 12;82(4):520-4
[
10404065.001
]
[Cites]
Int J Cancer. 2005 Jan 20;113(3):456-63
[
15455378.001
]
[Cites]
Am J Gastroenterol. 2004 Dec;99(12):2297-301
[
15571572.001
]
[Cites]
J Infect Dis. 2005 Mar 1;191(5):761-7
[
15688293.001
]
[Cites]
Sci Am. 2005 Feb;292(2):38-45
[
15715390.001
]
[Cites]
Am J Gastroenterol. 2005 Mar;100(3):588-93
[
15743356.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 Jul;14(7):1754-61
[
16030113.001
]
[Cites]
J Clin Oncol. 2006 May 10;24(14):2137-50
[
16682732.001
]
[Cites]
EMBO Rep. 2006 Oct;7(10):956-60
[
17016449.001
]
[Cites]
J Natl Cancer Inst. 2006 Oct 18;98(20):1445-52
[
17047193.001
]
[Cites]
Arch Intern Med. 2007 Apr 23;167(8):821-7
[
17452546.001
]
[Cites]
Gastroenterology. 2007 May;132(6):2116-30
[
17498507.001
]
[Cites]
J Infect Dis. 1993 Jul;168(1):219-21
[
8515114.001
]
[Cites]
Am J Epidemiol. 1994 Nov 1;140(9):771-8
[
7977286.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1995 Mar;4(2):85-92
[
7742727.001
]
[Cites]
Biometrics. 1994 Dec;50(4):1088-101
[
7786990.001
]
[Cites]
Dis Esophagus. 1997 Jul;10(3):196-200
[
9280079.001
]
[Cites]
J Natl Cancer Inst. 1997 Sep 3;89(17):1277-84
[
9293918.001
]
[Cites]
Am J Surg Pathol. 1997 Sep;21(9):1023-9
[
9298878.001
]
[Cites]
Am J Gastroenterol. 2007 Jun;102(6):1166-72
[
17378911.001
]
[Cites]
Am J Epidemiol. 2007 Jun 15;165(12):1424-33
[
17420181.001
]
[Cites]
Cancer Causes Control. 2007 Sep;18(7):713-22
[
17562192.001
]
[Cites]
Scand J Gastroenterol. 2007 Aug;42(8):933-40
[
17613922.001
]
[Cites]
Am J Gastroenterol. 2007 Aug;102(8):1603-9
[
17488251.001
]
[Cites]
Clin Gastroenterol Hepatol. 2007 Dec;5(12):1413-7, 1417.e1-2
[
17997357.001
]
[Cites]
Gut. 2008 Feb;57(2):173-80
[
17932103.001
]
[Cites]
Gut. 2008 Mar;57(3):298-305
[
17965056.001
]
[Cites]
Br J Cancer. 2008 Feb 26;98(4):689-92
[
18253117.001
]
[Cites]
Gut. 2008 May;57(5):561-7
[
18194986.001
]
[Cites]
Gut. 2008 Jun;57(6):734-9
[
18025067.001
]
[Cites]
J Infect Dis. 2008 Aug 15;198(4):553-60
[
18598192.001
]
[Cites]
Am J Gastroenterol. 2000 Feb;95(2):387-94
[
10685740.001
]
[Cites]
Aust N Z J Surg. 2000 Jan;70(1):26-33
[
10696939.001
]
[Cites]
Br J Cancer. 2007 Jan 15;96(1):172-6
[
17179990.001
]
[Cites]
BMC Cancer. 2006;6:287
[
17173682.001
]
[Cites]
Cancer. 2007 Feb 15;109(4):668-74
[
17211862.001
]
[Cites]
Eur J Gastroenterol Hepatol. 1999 May;11(5):503-9
[
10755253.001
]
[Cites]
J Infect Dis. 2000 Apr;181(4):1359-63
[
10762567.001
]
[Cites]
Cancer. 2000 Jun 1;88(11):2520-8
[
10861428.001
]
[Cites]
Digestion. 2000;62(4):225-31
[
11070405.001
]
[Cites]
J Clin Invest. 2001 Apr;107(7):767-73
[
11285290.001
]
[Cites]
J Natl Cancer Inst. 2001 Jun 20;93(12):937-41
[
11416115.001
]
[Cites]
BMJ. 2001 Jul 14;323(7304):101-5
[
11451790.001
]
[Cites]
Gut. 2001 Sep;49(3):347-53
[
11511555.001
]
[Cites]
Am J Gastroenterol. 2001 Dec;96(12):3406-10
[
11774957.001
]
[Cites]
Int J Epidemiol. 2001 Dec;30(6):1415-25
[
11821356.001
]
[Cites]
Gut. 2002 Mar;50(3):295-8
[
11839704.001
]
[Cites]
Helicobacter. 2001 Dec;6(4):310-6
[
11843963.001
]
[Cites]
Lancet. 2002 Mar 16;359(9310):931-5
[
11918912.001
]
[Cites]
Am J Gastroenterol. 2002 Jun;97(6):1375-80
[
12094853.001
]
[Cites]
Gut. 2002 Sep;51(3):457-8
[
12171977.001
]
[Cites]
N Engl J Med. 2002 Oct 10;347(15):1175-86
[
12374879.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2002 Oct;11(10 Pt 1):1095-9
[
12376513.001
]
[Cites]
Int J Cancer. 2002 Dec 1;102(4):422-7
[
12402314.001
]
[Cites]
Clin Diagn Lab Immunol. 2002 Nov;9(6):1313-7
[
12414766.001
]
[Cites]
Surg Oncol Clin N Am. 2002 Apr;11(2):235-56
[
12424848.001
]
[Cites]
J Natl Cancer Inst. 2002 Nov 20;94(22):1680-7
[
12441323.001
]
[Cites]
Int J Cancer. 2003 Mar 1;103(6):815-21
[
12516104.001
]
[Cites]
Science. 2003 Mar 7;299(5612):1582-5
[
12624269.001
]
[Cites]
Gastroenterology. 2003 May;124(5):1193-201
[
12730860.001
]
[Cites]
BMJ. 2003 Sep 6;327(7414):557-60
[
12958120.001
]
[Cites]
Eur J Cancer. 2003 Nov;39(17):2487-94
[
14602134.001
]
[Cites]
World J Gastroenterol. 2003 Nov;9(11):2501-4
[
14606084.001
]
[Cites]
Gastroenterology. 2003 Dec;125(6):1636-44
[
14724815.001
]
[Cites]
J Natl Cancer Inst. 2004 Mar 3;96(5):388-96
[
14996860.001
]
[Cites]
Br J Cancer. 2004 Apr 5;90(7):1402-6
[
15054463.001
]
[Cites]
Nat Rev Cancer. 2004 Sep;4(9):688-94
[
15343275.001
]
[Cites]
Lancet. 1984 Jun 16;1(8390):1311-5
[
6145023.001
]
[Cites]
Mod Pathol. 1989 Sep;2(5):473-6
[
2479007.001
]
[Cites]
J Natl Cancer Inst. 1991 Dec 4;83(23):1734-9
[
1770552.001
]
[Cites]
Hum Pathol. 1997 Sep;28(9):1007-9
[
9308723.001
]
[Cites]
BMJ. 1997 Sep 13;315(7109):629-34
[
9310563.001
]
[Cites]
Oncology. 1998 Jan-Feb;55(1):16-9
[
9428370.001
]
[Cites]
BMJ. 1998 Jan 10;316(7125):140-4
[
9462324.001
]
[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
17.
Wang RH, Ou-Yang Q, Chen X, Li GD, Xiang JY:
[Chemoprevention of Barrett's esophagus by celecoxib in rats].
Zhejiang Da Xue Xue Bao Yi Xue Ban
; 2009 Sep;38(5):498-504
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Chemoprevention of Barrett's
esophagus
by celecoxib in rats].
OBJECTIVE: To examine the chemopreventive effect of selective cyclooxygenase-2 (COX-2) inhibitor celecoxib for Barrett's
esophagus
in rats.
METHODS: Fifty 8-week-old male Sprague Dawley rats underwent esophagojejunostomy to induce Barrett's
esophagus
model.
The degree of inflammation, Barrett's
esophagus
,
adenocarcinoma
, COX-2 expression and PGE(2) of animals were assessed.
The incidence of mild, moderate and severe degree
esophageal
inflammation in celecoxib group and control group was 14/19(73.68%), 4/19(21.05%), 1/19(5.26%); 4/17(23.53%), 5/17(29.41%), 8/17(47.06%)(P<0.05), respectively.
The incidence of Barrett's
esophagus
was 7/19(36.84%), 13/17(76.47%) in two group respectively(P<0.05); The incidence of Barrett's
esophagus
with dysplasia was 2/19(10.53%), 8/17(47.06%)(P<0.05), respectively.
No
esophageal
pathological changes were found in sham operation group.
CONCLUSION: Selective COX-2 inhibitors celecoxib can inhibit inflammations, development of Barrett's
esophagus
and
esophagus
adenocarcinoma
.
[MeSH-major]
Barrett
Esophagus
/ prevention & control. Cyclooxygenase 2 Inhibitors / therapeutic use. Pyrazoles / therapeutic use. Sulfonamides / therapeutic use
Hazardous Substances Data Bank.
CELECOXIB
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19830863.001).
[ISSN]
1008-9292
[Journal-full-title]
Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
[ISO-abbreviation]
Zhejiang Da Xue Xue Bao Yi Xue Ban
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / Cyclooxygenase 2 Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib; K7Q1JQR04M / Dinoprostone
18.
Kiss J:
[Surgical management of Barrett's esophagus].
Magy Seb
; 2005 Dec;58(6):368-72
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
Genetic Alliance.
consumer health - Barrett's Esophagus
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
19.
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
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
20.
Souza RF:
Molecular mechanisms of acid exposure in Barrett's esophagus.
Inflammopharmacology
; 2007 Jun;15(3):95-100
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
Genetic Alliance.
consumer health - Barrett's Esophagus
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - GERD
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
21.
Graham TA, McDonald SA:
Genetic diversity during the development of Barrett's oesophagus-associated adenocarcinoma: how, when and why?
Biochem Soc Trans
; 2010 Apr;38(2):374-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 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
22.
Cooper SC, Croft S, Day R, Thomson CS, Trudgill NJ:
The risk of oesophageal cancer is not affected by a diagnosis of breast cancer.
Eur J Cancer Prev
; 2010 May;19(3):182-5
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
Genetic Alliance.
consumer health - Breast Cancer
.
MedlinePlus Health Information.
consumer health - Breast Cancer
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
23.
Bosetti C, Gallus S, Garavello W, La Vecchia C:
Smoking cessation and the risk of oesophageal cancer: An overview of published studies.
Oral Oncol
; 2006 Nov;42(10):957-64
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Quitting Smoking
.
MedlinePlus Health Information.
consumer health - Smoking
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
24.
Konda Vani JA, Chennat J, Waxman I:
New directions in endoscopic therapy of Barrett' s esophagus.
Minerva Gastroenterol Dietol
; 2010 Dec;56(4):421-35
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
New directions in endoscopic therapy of Barrett' s
esophagus
.
The key to prevention and early treatment of
esophageal
adenocarcinoma
is the detection and eradication of neoplasia found in patients with Barrett's
esophagus
(BE).
The goals of endoscopic therapy of Barrett's neoplasia are to preserve
the esophagus
while ablating or removing the entire Barrett's segment.
Endoscopic resection is a tool to accurately provide a histological
diagnosis
of lesions in addition to treat neoplasia.
[MeSH-major]
Adenocarcinoma
/ therapy. Barrett
Esophagus
/ therapy.
Esophageal
Neoplasms / therapy. Esophagoscopy / trends. Precancerous Conditions / therapy
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 21139541.001).
[ISSN]
1121-421X
[Journal-full-title]
Minerva gastroenterologica e dietologica
[ISO-abbreviation]
Minerva Gastroenterol Dietol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Italy
25.
Soma T, Kaganoi J, Kawabe A, Kondo K, Tsunoda S, Imamura M, Shimada Y:
Chenodeoxycholic acid stimulates the progression of human esophageal cancer cells: A possible mechanism of angiogenesis in patients with esophageal cancer.
Int J Cancer
; 2006 Aug 15;119(4):771-82
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Chenodeoxycholic acid stimulates the progression of human
esophageal cancer
cells: A possible mechanism of angiogenesis in patients with
esophageal cancer
.
Bile acids are known to promote the growth of gastrointestinal
cancer
.
In vitro,
esophageal
squamous cell carcinoma (ESCC) cells and
esophageal
adenocarcinoma
cells were studied.
Our results suggest that bile acids, important constituents of duodenal fluid, stimulate the development of human
esophageal cancer
by promoting angiogenesis via the COX-2 pathway.
[MeSH-major]
Chenodeoxycholic Acid / pharmacology.
Esophageal
Neoplasms / blood supply.
Esophageal
Neoplasms / pathology
Genetic Alliance.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2006 Wiley-Liss, Inc.
(PMID = 16557574.001).
[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
[Chemical-registry-number]
0 / Interleukin-6; 0 / Vascular Endothelial Growth Factor A; 0GEI24LG0J / Chenodeoxycholic Acid; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; K7Q1JQR04M / Dinoprostone
26.
van Heijl M, Sprangers MA, de Boer AG, Lagarde SM, Reitsma HB, Busch OR, Tilanus HW, van Lanschot JJ, van Berge Henegouwen MI:
Preoperative and early postoperative quality of life predict survival in potentially curable patients with esophageal cancer.
Ann Surg Oncol
; 2010 Jan;17(1):23-30
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
Genetic Alliance.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Br J Surg. 2000 Dec;87(12):1716-21
[
11122191.001
]
[Cites]
Biometrics. 2001 Mar;57(1):114-9
[
11252585.001
]
[Cites]
Gut. 2001 Aug;49(2):227-30
[
11454799.001
]
[Cites]
Ann Thorac Surg. 2001 Jul;72(1):306-13
[
11465217.001
]
[Cites]
Eur J Cancer. 2002 Jul;38(10):1351-7
[
12091066.001
]
[Cites]
N Engl J Med. 2002 Nov 21;347(21):1662-9
[
12444180.001
]
[Cites]
Br J Surg. 2003 Nov;90(11):1367-72
[
14598416.001
]
[Cites]
Qual Life Res. 2004 Mar;13(2):311-20
[
15085903.001
]
[Cites]
J Clin Oncol. 2004 Jun 15;22(12):2395-403
[
15197201.001
]
[Cites]
Med Care. 1988 Jul;26(7):724-35
[
3393032.001
]
[Cites]
Br J Cancer. 1990 Dec;62(6):1034-8
[
2257209.001
]
[Cites]
J Clin Oncol. 1992 Dec;10(12):1833-8
[
1453197.001
]
[Cites]
Ann Surg. 1999 Sep;230(3):392-400; discussion 400-3
[
10493486.001
]
[Cites]
Ann Oncol. 2005 Jul;16(7):1005-53
[
15939716.001
]
[Cites]
J Clin Oncol. 2005 Oct 1;23(28):6865-72
[
16192578.001
]
[Cites]
J Clin Oncol. 2006 Sep 10;24(26):4347-55
[
16963732.001
]
[Cites]
Qual Life Res. 2006 Oct;15(8):1297-306
[
16830258.001
]
[Cites]
Lancet Oncol. 2007 Mar;8(3):226-34
[
17329193.001
]
[Cites]
Ann Thorac Surg. 2007 Apr;83(4):1257-64
[
17383322.001
]
[Cites]
Br J Surg. 2007 Nov;94(11):1361-8
[
17582230.001
]
[Cites]
Ann Surg. 2007 Dec;246(6):992-1000; discussion 1000-1
[
18043101.001
]
[Cites]
Br J Cancer. 2008 Mar 11;98(5):888-93
[
18268490.001
]
[Cites]
J Clin Oncol. 2008 Mar 10;26(8):1355-63
[
18227528.001
]
[Cites]
Endoscopy. 2008 Jun;40(6):464-71
[
18543134.001
]
[Cites]
Ann Surg Oncol. 2008 Nov;15(11):3289-98
[
18670823.001
]
[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
27.
Chung SM, Kao J, Hyjek E, Chen YT:
p53 in esophageal adenocarcinoma: a critical reassessment of mutation frequency and identification of 72Arg as the dominant allele.
Int J Oncol
; 2007 Dec;31(6):1351-5
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 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
28.
Sharma P, Wani S, Bansal A:
The quest for intestinal metaplasia--is it worth the effort?
Am J Gastroenterol
; 2007 Jun;102(6):1162-5
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
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
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[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
29.
Lisovsky M, Falkowski O, Bhuiya T:
Expression of alpha-methylacyl-coenzyme A racemase in dysplastic Barrett's epithelium.
Hum Pathol
; 2006 Dec;37(12):1601-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
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
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
30.
Michor F, Polyak K:
The origins and implications of intratumor heterogeneity.
Cancer Prev Res (Phila)
; 2010 Nov;3(11):1361-4
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
This phenotypic and genetic heterogeneity plays an important role in neoplasia,
cancer
progression, and therapeutic resistance.
In this issue of the journal (beginning on page 1388), Merlo et al. report their use of molecular data from 239 patients with Barrett's
esophagus
to evaluate the propensity of major diversity indices for predicting progression to
esophageal
adenocarcinoma
.
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
©2010 AACR.
[Cites]
Cell Stem Cell. 2010 Feb 5;6(2):141-52
[
20144787.001
]
[Cites]
J Clin Invest. 2010 Feb;120(2):636-44
[
20101094.001
]
[Cites]
Cancer Prev Res (Phila). 2010 May;3(5):579-87
[
20424132.001
]
[Cites]
Cancer Prev Res (Phila). 2010 Nov;3(11):1388-97
[
20947487.001
]
[Cites]
Science. 2000 Sep 8;289(5485):1754-7
[
10976069.001
]
[Cites]
Nature. 2001 Nov 1;414(6859):105-11
[
11689955.001
]
[Cites]
Genetics. 2003 Apr;163(4):1527-32
[
12702695.001
]
[Cites]
Cancer Res. 2003 Oct 1;63(19):6212-20
[
14559806.001
]
[Cites]
Cancer Res. 2003 Oct 15;63(20):6635-42
[
14583456.001
]
[Cites]
J Theor Biol. 2003 Dec 7;225(3):377-82
[
14604590.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):14966-9
[
14657359.001
]
[Cites]
Bull Math Biol. 2004 Jul;66(4):663-87
[
15210312.001
]
[Cites]
Oncogene. 2004 Sep 20;23(43):7274-82
[
15378087.001
]
[Cites]
Cancer Res. 1978 Sep;38(9):2651-60
[
354778.001
]
[Cites]
Cancer Treat Rep. 1983 Oct;67(10):923-31
[
6627236.001
]
[Cites]
Cancer Res. 1984 Jun;44(6):2259-65
[
6372991.001
]
[Cites]
Nature. 2005 Jun 30;435(7046):1267-70
[
15988530.001
]
[Cites]
Semin Cell Dev Biol. 2005 Aug-Oct;16(4-5):554-63
[
16144692.001
]
[Cites]
Nat Rev Cancer. 2005 Nov;5(11):899-904
[
16327766.001
]
[Cites]
Blood. 2010 Mar 11;115(10):1976-84
[
20053758.001
]
[Cites]
Curr Pharm Des. 2006;12(3):261-71
[
16454743.001
]
[Cites]
Cancer Res. 2006 Feb 15;66(4):1891-5; discussion 1890
[
16488984.001
]
[Cites]
Nat Genet. 2006 Apr;38(4):468-73
[
16565718.001
]
[Cites]
J Theor Biol. 2006 Jun 21;240(4):521-30
[
16343545.001
]
[Cites]
Leuk Lymphoma. 2006 Oct;47(10):2017-27
[
17071472.001
]
[Cites]
Nat Rev Cancer. 2006 Dec;6(12):924-35
[
17109012.001
]
[Cites]
Cell Cycle. 2007 Feb 15;6(4):461-6
[
17329969.001
]
[Cites]
Semin Cancer Biol. 2007 Jun;17(3):204-13
[
16787749.001
]
[Cites]
Oncogene. 2007 Apr 26;26(19):2695-706
[
17057735.001
]
[Cites]
Cell Cycle. 2007 Oct 1;6(19):2332-8
[
17786053.001
]
[Cites]
PLoS Comput Biol. 2007 Dec;3(12):e250
[
18085819.001
]
[CommentOn]
Cancer Prev Res (Phila). 2010 Nov;3(11):1388-97
[
20947487.001
]
(PMID = 20959519.001).
[ISSN]
1940-6215
[Journal-full-title]
Cancer prevention research (Philadelphia, Pa.)
[ISO-abbreviation]
Cancer Prev Res (Phila)
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U54 CA143798; United States / NCI NIH HHS / CA / U54CA143798
[Publication-type]
Comment; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS240068; NLM/ PMC3633425
31.
Lugli A, Spichtin H, Maurer R, Mirlacher M, Kiefer J, Huusko P, Azorsa D, Terracciano L, Sauter G, Kallioniemi OP, Mousses S, Tornillo L:
EphB2 expression across 138 human tumor types in a tissue microarray: high levels of expression in gastrointestinal cancers.
Clin Cancer Res
; 2005 Sep 15;11(18):6450-8
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
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.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
32.
Quaroni L, Casson AG:
Characterization of Barrett esophagus and esophageal adenocarcinoma by Fourier-transform infrared microscopy.
Analyst
; 2009 Jun;134(6):1240-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
33.
Javle M, Ailawadhi S, Yang GY, Nwogu CE, Schiff MD, Nava HR:
Palliation of malignant dysphagia in esophageal cancer: a literature-based review.
J Support Oncol
; 2006 Sep;4(8):365-73, 379
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
Genetic Alliance.
consumer health - Dysphagia
.
Genetic Alliance.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Palliative Care
.
MedlinePlus Health Information.
consumer health - Swallowing Disorders
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[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
34.
Mukherjee K, Chakravarthy AB, Goff LW, El-Rifai W:
Esophageal adenocarcinoma: treatment modalities in the era of targeted therapy.
Dig Dis Sci
; 2010 Dec;55(12):3304-14
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Surg Oncol. 2004 Aug 1;87(2):95-104
[
15282704.001
]
[Cites]
Mod Pathol. 2004 Oct;17(10):1282-8
[
15167938.001
]
[Cites]
Int J Cancer. 2004 Dec 10;112(5):747-53
[
15386389.001
]
[Cites]
Ann Thorac Surg. 2004 Nov;78(5):1790-800
[
15511476.001
]
[Cites]
Surg Gynecol Obstet. 1981 Nov;153(5):690-2
[
6794167.001
]
[Cites]
World J Surg. 1987 Aug;11(4):426-32
[
3630187.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1989 Feb;16(2):325-7
[
2646253.001
]
[Cites]
Br J Surg. 1990 Aug;77(8):845-57
[
2203505.001
]
[Cites]
N Engl J Med. 1992 Jun 11;326(24):1593-8
[
1584260.001
]
[Cites]
World J Surg. 1992 Nov-Dec;16(6):1104-9; discussion 1110
[
1455880.001
]
[Cites]
Int J Cancer. 1993 May 8;54(2):213-9
[
8098013.001
]
[Cites]
N Engl J Med. 1996 Aug 15;335(7):462-7
[
8672151.001
]
[Cites]
Am J Surg. 1997 Sep;174(3):320-4
[
9324146.001
]
[Cites]
Eur J Cardiothorac Surg. 1997 Sep;12(3):361-4; discussion 364-5
[
9332912.001
]
[Cites]
Ann Thorac Surg. 1998 Mar;65(3):787-92
[
9527214.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1998 Jun 1;41(3):579-83
[
9635705.001
]
[Cites]
Nat Genet. 1998 Oct;20(2):189-93
[
9771714.001
]
[Cites]
Am J Physiol Gastrointest Liver Physiol. 2008 Aug;295(2):G211-8
[
18556417.001
]
[Cites]
J Natl Cancer Inst. 2008 Aug 20;100(16):1184-7
[
18695138.001
]
[Cites]
Cancer Lett. 2009 Mar 18;275(2):170-7
[
18703277.001
]
[Cites]
J Hepatol. 2009 Mar;50(3):518-27
[
19155085.001
]
[Cites]
Oncogene. 2009 Feb 12;28(6):866-75
[
19060929.001
]
[Cites]
J Thorac Cardiovasc Surg. 2009 Mar;137(3):587-95; discussion 596
[
19258071.001
]
[Cites]
Gastroenterol Clin North Am. 2009 Mar;38(1):135-52, ix
[
19327572.001
]
[Cites]
Expert Opin Investig Drugs. 2009 Apr;18(4):379-98
[
19335272.001
]
[Cites]
J Am Coll Surg. 2009 Apr;208(4):553-6
[
19476789.001
]
[Cites]
Mol Cancer Ther. 2009 Jun;8(6):1547-56
[
19509244.001
]
[Cites]
Ann Oncol. 2009 Sep;20(9):1522-8
[
19465425.001
]
[Cites]
World J Gastroenterol. 2009 Dec 21;15(47):5983-91
[
20014464.001
]
[Cites]
Breast Cancer Res Treat. 2010 Feb;120(1):47-57
[
19301121.001
]
[Cites]
Clin Colorectal Cancer. 2010 Jan;9(1):8-14
[
20100683.001
]
[Cites]
J Clin Oncol. 2006 Oct 20;24(30):4922-7
[
17050876.001
]
[Cites]
J Clin Oncol. 2006 Nov 20;24(33):5201-6
[
17114652.001
]
[Cites]
Clin Cancer Res. 2006 Dec 1;12(23):6869-75
[
17145803.001
]
[Cites]
Mod Pathol. 2007 Jan;20(1):120-9
[
17143264.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2007 Feb 1;67(2):405-9
[
17097832.001
]
[Cites]
Cancer Sci. 2007 Mar;98(3):357-63
[
17270025.001
]
[Cites]
Cancer. 2007 Feb 15;109(4):658-67
[
17211865.001
]
[Cites]
Ann Oncol. 2007 Mar;18(3):510-7
[
17164226.001
]
[Cites]
Lancet Oncol. 2007 Mar;8(3):226-34
[
17329193.001
]
[Cites]
Oncogene. 2007 Mar 29;26(14):2006-16
[
17001310.001
]
[Cites]
Proc Natl Acad Sci U S A. 2008 Aug 26;105(34):12480-4
[
18711136.001
]
[Cites]
Clin Cancer Res. 2008 Sep 1;14(17):5437-46
[
18765535.001
]
[Cites]
Biochim Biophys Acta. 2008 Sep;1786(1):60-72
[
18662747.001
]
[Cites]
APMIS. 2008 Jul-Aug;116(7-8):629-37
[
18834407.001
]
[Cites]
Am J Clin Oncol. 2008 Aug;31(4):329-34
[
18845990.001
]
[Cites]
Cancer Res. 2008 Nov 1;68(21):8998-9004
[
18974145.001
]
[Cites]
Carcinogenesis. 2008 Dec;29(12):2330-4
[
18780893.001
]
[Cites]
Gut. 2009 Jan;58(1):5-15
[
18664505.001
]
[Cites]
Cancer Lett. 2009 Mar 8;275(1):117-26
[
19027227.001
]
[Cites]
J Gastrointest Surg. 2009 Feb;13(2):212-22
[
18854960.001
]
[Cites]
Cancer. 1998 Nov 15;83(10):2049-53
[
9827707.001
]
[Cites]
N Engl J Med. 1998 Dec 31;339(27):1979-84
[
9869669.001
]
[Cites]
J Thorac Cardiovasc Surg. 1999 Jan;117(1):16-23; discussion 23-5
[
9869753.001
]
[Cites]
N Engl J Med. 1999 Mar 18;340(11):825-31
[
10080844.001
]
[Cites]
JAMA. 1999 May 5;281(17):1623-7
[
10235156.001
]
[Cites]
World J Surg. 1999 Oct;23(10):1010-8
[
10512940.001
]
[Cites]
Cancer Invest. 2004;22(5):670-7
[
15581047.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2005 Jan 1;61(1):203-11
[
15629613.001
]
[Cites]
J Natl Cancer Inst. 2005 Jan 19;97(2):142-6
[
15657344.001
]
[Cites]
J Am Coll Surg. 2005 Mar;200(3):336-44
[
15737843.001
]
[Cites]
Oncogene. 2005 Jul 28;24(32):5005-15
[
16049526.001
]
[Cites]
Cancer Res. 2005 Aug 1;65(15):6583-92
[
16061638.001
]
[Cites]
Lancet Oncol. 2005 Sep;6(9):659-68
[
16129366.001
]
[Cites]
Ann Surg. 2005 Oct;242(4):566-73; discussion 573-5
[
16192817.001
]
[Cites]
Neoplasia. 2005 Sep;7(9):854-61
[
16229808.001
]
[Cites]
Surgery. 2005 Nov;138(5):924-31
[
16291394.001
]
[Cites]
Anticancer Drugs. 2006 Jan;17(1):95-102
[
16317296.001
]
[Cites]
Cancer Causes Control. 2006 Feb;17(1):81-3
[
16411056.001
]
[Cites]
Ann Surg Oncol. 2006 Feb;13(2):214-20
[
16418887.001
]
[Cites]
Int J Cancer. 2006 Apr 1;118(7):1814-22
[
16217753.001
]
[Cites]
Ann Surg. 2006 Mar;243(3):334-40
[
16495697.001
]
[Cites]
Radiother Oncol. 2006 Mar;78(3):236-44
[
16545878.001
]
[Cites]
Arch Surg. 2006 May;141(5):476-81; discussion 481-2
[
16702519.001
]
[Cites]
N Engl J Med. 2006 Jul 6;355(1):11-20
[
16822992.001
]
[Cites]
Mol Cancer Res. 2006 Jul;4(7):449-55
[
16849520.001
]
[Cites]
Cochrane Database Syst Rev. 2006;(3):CD001556
[
16855972.001
]
[Cites]
Clin Cancer Res. 2006 Jul 15;12(14 Pt 1):4283-7
[
16857803.001
]
[Cites]
Nat Clin Pract Oncol. 2006 Aug;3(8):448-57
[
16894390.001
]
[Cites]
Diagn Mol Pathol. 2006 Sep;15(3):125-30
[
16932066.001
]
[Cites]
Neoplasia. 2007 Apr;9(4):341-8
[
17460778.001
]
[Cites]
Clin Cancer Res. 2007 May 15;13(10):3100-4
[
17505013.001
]
[Cites]
Ann Surg. 2007 Jul;246(1):1-8
[
17592282.001
]
[Cites]
Clin Cancer Res. 2007 Oct 1;13(19):5869-75
[
17908981.001
]
[Cites]
J Am Coll Surg. 2007 Dec;205(6):735-40
[
18035255.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2008 Feb 1;70(2):391-5
[
17980508.001
]
[Cites]
Ann Thorac Surg. 2008 Feb;85(2):424-9
[
18222237.001
]
[Cites]
Arthritis Rheum. 2008 Feb;58(2):571-6
[
18240225.001
]
[Cites]
PLoS One. 2008;3(4):e1890
[
18382671.001
]
[Cites]
Cancer. 2008 Apr 15;112(8):1688-98
[
18311783.001
]
[Cites]
Cancer Res. 2008 May 1;68(9):3077-80; discussion 3080
[
18451130.001
]
[Cites]
Cancer Res. 2008 May 1;68(9):3081-6; discussion 3086
[
18451131.001
]
[Cites]
Anesthesiol Clin. 2008 Jun;26(2):293-304, vi
[
18456214.001
]
[Cites]
Scand J Gastroenterol. 2007 Dec;42(12):1460-5
[
17852856.001
]
[Cites]
J Thorac Cardiovasc Surg. 2008 Jun;135(6):1228-36
[
18544359.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2008 Jun;17(6):1380-5
[
18559552.001
]
[Cites]
Oncology. 2007;73(5-6):281-9
[
18477853.001
]
[Cites]
Hepatogastroenterology. 2008 Mar-Apr;55(82-83):475-81
[
18613391.001
]
[Cites]
Clin Cancer Res. 2008 Jul 15;14(14):4564-71
[
18579663.001
]
[Cites]
J Thorac Cardiovasc Surg. 2000 Feb;119(2):277-88
[
10649203.001
]
[Cites]
Hum Pathol. 2000 Jan;31(1):35-9
[
10665910.001
]
[Cites]
Recent Results Cancer Res. 2000;155:29-41
[
10693236.001
]
[Cites]
J Gastroenterol Hepatol. 2000 Jul;15(7):730-6
[
10937677.001
]
[Cites]
Chest Surg Clin N Am. 2000 Aug;10(3):451-69
[
10967750.001
]
[Cites]
Gastroenterology. 2001 Sep;121(3):592-8
[
11522743.001
]
[Cites]
J Cell Biol. 2002 Feb 4;156(3):437-51
[
11827981.001
]
[Cites]
Lancet. 2002 May 18;359(9319):1727-33
[
12049861.001
]
[Cites]
Cancer Res. 2002 Jul 15;62(14):4061-4
[
12124342.001
]
[Cites]
N Engl J Med. 2002 Nov 21;347(21):1662-9
[
12444180.001
]
[Cites]
Arch Surg. 2003 Mar;138(3):303-8
[
12611579.001
]
[Cites]
Am J Surg. 2003 Jun;185(6):538-43
[
12781882.001
]
[Cites]
Clin Cancer Res. 2003 Dec 15;9(17):6461-8
[
14695149.001
]
[Cites]
Cancer Res. 2004 Mar 1;64(5):1561-9
[
14996709.001
]
[Cites]
J Gastrointest Surg. 2004 May-Jun;8(4):448-53
[
15120370.001
]
[Cites]
Gut. 2004 Jul;53(7):925-30
[
15194636.001
]
(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
35.
Raggi M, Langer R, Feith M, Friess H, Schauer M, Theisen J:
Successful evaluation of a new animal model using mice for esophageal adenocarcinoma.
Langenbecks Arch Surg
; 2010 Apr;395(4):347-50
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Surg Res. 2000 Jun 15;91(2):111-7
[
10839958.001
]
[Cites]
Ann Surg. 2004 Jul;240(1):57-67
[
15213619.001
]
[Cites]
J Thorac Cardiovasc Surg. 2001 Oct;122(4):809-14
[
11581618.001
]
[Cites]
Br J Cancer. 1994 Aug;70(2):185-9
[
8054264.001
]
[Cites]
Scand J Gastroenterol. 2003 Jul;38(7):687-92
[
12889552.001
]
[Cites]
Int J Cancer. 1996 Jul 17;67(2):269-74
[
8760598.001
]
[Cites]
Carcinogenesis. 2000 Aug;21(8):1587-91
[
10910963.001
]
[Cites]
Carcinogenesis. 2000 Feb;21(2):257-63
[
10657966.001
]
[Cites]
J Gastrointest Surg. 1998 May-Jun;2(3):260-8
[
9841983.001
]
[Cites]
Carcinogenesis. 1997 Nov;18(11):2265-70
[
9395230.001
]
[Cites]
J Surg Res. 2006 Oct;135(2):337-44
[
16926029.001
]
[Cites]
J Surg Res. 1999 May 1;83(1):48-55
[
10210642.001
]
[Cites]
Anticancer Res. 2002 Jan-Feb;22(1A):39-44
[
12017320.001
]
(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
36.
Aklilu M, Ilson DH:
Targeted agents and esophageal cancer--the next step?
Semin Radiat Oncol
; 2007 Jan;17(1):62-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
Genetic Alliance.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
37.
Wen D, Zhang N, Shan B, Wang S:
Helicobacter pylori infection may be implicated in the topography and geographic variation of upper gastrointestinal cancers in the Taihang Mountain high-risk region in northern China.
Helicobacter
; 2010 Oct;15(5):416-21
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Chronic infection of the bacterial not only causes distal stomach
cancer
, but also confers risk to gastric cardia
adenocarcinoma
.
Because H. pylori infection is inversely associated with
esophageal
adenocarcinoma
, globally the infection rate is significantly correlated with the ratio of squamous carcinoma to
adenocarcinoma of
the esophagus
.
These agree with the topography of upper gastrointestinal
cancer
observed in the Taihang Mountain high-risk region where both gastric cardia and non-cardia
adenocarcinoma
coincide with
esophageal
squamous
cancer
, but with almost no distal
esophageal
adenocarcinoma
.
Because H. pylori infection is a definite carcinogen to gastric
adenocarcinoma
and is more prevalent in the mountain than in plain areas due to undeveloped living conditions, the observation gives the impression as though H. pylori infection is implicated.
AIMS: This article aims to note the role of H. pylori infection in upper gastrointestinal
cancer
in the Taihang Mountain high-risk region in northern China.
MATERIALS AND METHODS: First the unique topography and geographic variation of upper gastrointestinal
cancer
in the region is described to indicate a possible role of H. pylori infection, then we review studies on prevalence of H. pylori infection in the high-risk region and describe difference in socioeconomic development and water hygiene between the plains and the mountains as related to the prevalence of H. pylori infection.
RESULTS: Coincidence of gastric
cancer
in the region and a progressively increasing rate of
the cancer
from the plain towards the mountains indicate H. pylori infection may be implicated in upper gastrointestinal
cancer
.
CONCLUSION: International collaboration is needed to study H. pylori and upper gastrointestinal
cancer
in the region when rapid industrialization is just beginning.
[MeSH-major]
Adenocarcinoma
/ epidemiology.
Adenocarcinoma
/ microbiology. Gastrointestinal Neoplasms / epidemiology. Gastrointestinal Neoplasms / microbiology. Helicobacter Infections / complications. Helicobacter Infections / epidemiology. Helicobacter pylori / isolation & purification
MedlinePlus Health Information.
consumer health - Helicobacter Pylori Infections
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
© 2010 Blackwell Publishing Ltd.
(PMID = 21083747.001).
[ISSN]
1523-5378
[Journal-full-title]
Helicobacter
[ISO-abbreviation]
Helicobacter
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
38.
Labutina IuO:
[Barrett's esophagus: contemporary diagnostic and therapeutic approaches].
Klin Med (Mosk)
; 2006;84(11):25-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
Genetic Alliance.
consumer health - Barrett's Esophagus
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
39.
Wu G, Bybel B, Brunken R, Lin H, Neumann D:
PET detection of solitary distant skeletal muscle metastasis of esophageal adenocarcinoma.
Clin Nucl Med
; 2005 May;30(5):335-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
40.
Freedman ND, Derakhshan MH, Abnet CC, Schatzkin A, Hollenbeck AR, McColl KE:
Male predominance of upper gastrointestinal adenocarcinoma cannot be explained by differences in tobacco smoking in men versus women.
Eur J Cancer
; 2010 Sep;46(13):2473-8
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Smoking
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2010 Elsevier Ltd. All rights reserved.
[Cites]
J Womens Health (Larchmt). 2002 Dec;11(10):899-906
[
12630407.001
]
[Cites]
Eur J Cancer. 2010 Apr;46(6):1093-100
[
20188539.001
]
[Cites]
Int J Cancer. 2003 Nov 20;107(4):629-34
[
14520702.001
]
[Cites]
Mutat Res. 2003 Dec 10;533(1-2):153-71
[
14643418.001
]
[Cites]
J Natl Cancer Inst. 2004 Jun 2;96(11):826-34
[
15173266.001
]
[Cites]
N Engl J Med. 1972 Feb 10;286(6):316-7
[
5007231.001
]
[Cites]
Am J Public Health. 1981 Mar;71(3):308-11
[
7468869.001
]
[Cites]
World J Surg. 1991 Mar-Apr;15(2):228-34
[
2031359.001
]
[Cites]
Cancer. 1993 Aug 15;72(4):1155-8
[
8339208.001
]
[Cites]
Int J Cancer. 1997 Aug 7;72(4):565-73
[
9259392.001
]
[Cites]
J Natl Cancer Inst. 1997 Sep 3;89(17):1277-84
[
9293918.001
]
[Cites]
Am J Public Health. 1998 Oct;88(10):1503-9
[
9772852.001
]
[Cites]
Am J Epidemiol. 2005 Jun 15;161(12):1115-22
[
15937020.001
]
[Cites]
Cancer Causes Control. 2005 Apr;16(3):285-94
[
15947880.001
]
[Cites]
Int J Cancer. 2005 Nov 1;117(2):294-9
[
15900604.001
]
[Cites]
Int J Cancer. 2005 Nov 20;117(4):643-7
[
15929082.001
]
[Cites]
Am J Epidemiol. 2005 Dec 1;162(11):1050-61
[
16221805.001
]
[Cites]
Eur J Cancer. 2010 Apr;46(6):1101-10
[
20219351.001
]
[Cites]
Am J Epidemiol. 2001 Dec 15;154(12):1119-25
[
11744517.001
]
[Cites]
Lancet. 2002 Mar 16;359(9310):931-5
[
11918912.001
]
[Cites]
Br J Cancer. 2006 Jan 16;94(1):136-41
[
16404367.001
]
[Cites]
Gastroenterol Clin Biol. 2005 Dec;29(12):1258-63
[
16518284.001
]
[Cites]
Int J Cancer. 2007 Jan 1;120(1):128-32
[
17036324.001
]
[Cites]
Jpn J Clin Oncol. 2006 Dec;36(12):800-7
[
17210611.001
]
[Cites]
Helicobacter. 2007 Apr;12(2):164-9
[
17309754.001
]
[Cites]
Br J Cancer. 2007 Jun 4;96(11):1767-71
[
17505507.001
]
[Cites]
Am J Epidemiol. 2007 Jun 15;165(12):1424-33
[
17420181.001
]
[Cites]
Br J Cancer. 2007 Sep 3;97(5):700-4
[
17637680.001
]
[Cites]
Gut. 2007 Dec;56(12):1671-7
[
17627962.001
]
[Cites]
Gut. 2008 Feb;57(2):173-80
[
17932103.001
]
[Cites]
Eur J Cancer Prev. 2008 Aug;17(4):345-53
[
18562960.001
]
[Cites]
Lancet Oncol. 2008 Jul;9(7):649-56
[
18556244.001
]
[Cites]
Cancer Causes Control. 2008 Sep;19(7):689-701
[
18293090.001
]
[Cites]
Gut. 2009 Jan;58(1):16-23
[
18838486.001
]
[Cites]
Helicobacter. 2009 Feb;14(1):40-6
[
19191895.001
]
[Cites]
Int J Cancer. 2003 May 20;105(1):101-7
[
12672038.001
]
(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
41.
Lin L, Wang Z, Prescott MS, van Dekken H, Thomas DG, Giordano TJ, Chang AC, Orringer MB, Gruber SB, Moran JV, Glover TW, Beer DG:
Multiple forms of genetic instability within a 2-Mb chromosomal segment of 3q26.3-q27 are associated with development of esophageal adenocarcinoma.
Genes Chromosomes Cancer
; 2006 Apr;45(4):319-31
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
42.
Szachnowicz S, Cecconello I, Ribeiro U, Iriya K, El Ibrahim R, Takeda FR, Corbett CE, Vaz Safatle-Ribeiro A:
Mucin pattern reflects the origin of the adenocarcinoma in Barrett's esophagus: a retrospective clinical and laboratorial study.
World J Surg Oncol
; 2009;7:27
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
Genetic Alliance.
consumer health - Barrett's Esophagus
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Histopathology. 1999 Dec;35(6):517-24
[
10583575.001
]
[Cites]
Clinics (Sao Paulo). 2005 Apr;60(2):103-12
[
15880245.001
]
[Cites]
Gut. 2000 Dec;47(6):753-61
[
11076872.001
]
[Cites]
Hum Pathol. 2002 Jun;33(6):660-8
[
12152167.001
]
[Cites]
Gan. 1968 Jun;59(3):251-8
[
5726267.001
]
[Cites]
Histochem J. 1981 Nov;13(6):931-9
[
7338482.001
]
[Cites]
Hum Pathol. 1983 Jan;14(1):42-61
[
6832749.001
]
[Cites]
Am J Clin Pathol. 1984 Apr;81(4):500-3
[
6702752.001
]
[Cites]
Am J Surg. 1985 Sep;150(3):365-9
[
4037198.001
]
[Cites]
Gut. 1986 Sep;27(9):1062-8
[
3758820.001
]
[Cites]
J Biol Chem. 1989 Apr 15;264(11):6480-7
[
2703501.001
]
[Cites]
Virchows Arch A Pathol Anat Histopathol. 1989;414(4):359-63
[
2496524.001
]
[Cites]
Cancer. 1991 Oct 15;68(8):1731-6
[
1913516.001
]
[Cites]
Crit Rev Biochem Mol Biol. 1992;27(1-2):57-92
[
1727693.001
]
[Cites]
Dig Dis Sci. 1992 Jan;37(1):137-43
[
1728519.001
]
[Cites]
Gastroenterol Clin North Am. 1991 Dec;20(4):817-34
[
1787015.001
]
[Cites]
Am J Gastroenterol. 1992 Jun;87(6):746-50
[
1590313.001
]
[Cites]
Am J Respir Cell Mol Biol. 1992 Dec;7(6):557-64
[
1449803.001
]
[Cites]
Cancer Res. 1993 Feb 1;53(3):641-51
[
7678777.001
]
[Cites]
J Histochem Cytochem. 1993 Oct;41(10):1479-85
[
8245407.001
]
[Cites]
J Biol Chem. 1994 Jan 28;269(4):2440-6
[
8300571.001
]
[Cites]
Gastroenterology. 1994 Apr;106(4):973-81
[
8144002.001
]
[Cites]
Gastroenterology. 1994 Jul;107(1):28-36
[
8020672.001
]
[Cites]
Lancet. 1994 Dec 3;344(8936):1533-6
[
7983953.001
]
[Cites]
Am J Surg Pathol. 1995 Feb;19(2):183-91
[
7832278.001
]
[Cites]
Cancer Res. 1995 Jun 15;55(12):2681-90
[
7780985.001
]
[Cites]
Biochem J. 1995 Jul 1;309 ( Pt 1):221-9
[
7619060.001
]
[Cites]
Gastroenterology. 1995 Nov;109(5):1541-6
[
7557137.001
]
[Cites]
Biochem Soc Trans. 1995 Nov;23(4):795-9
[
8654840.001
]
[Cites]
Biochem Soc Trans. 1995 Nov;23(4):840-5
[
8654850.001
]
[Cites]
Am J Gastroenterol. 1997 Mar;92(3):414-8
[
9068460.001
]
[Cites]
Am J Gastroenterol. 1998 Jul;93(7):1028-32
[
9672324.001
]
[Cites]
Cancer Res. 1999 Mar 1;59(5):1003-7
[
10070955.001
]
[Cites]
Am J Pathol. 1999 Apr;154(4):965-73
[
10233832.001
]
[Cites]
Ann Surg. 2000 Mar;231(3):303-21
[
10714623.001
]
(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
43.
Siewert JR, Lordick F, Ott K, Stein HJ, Weber WA, Becker K, Peschel C, Fink U, Schwaiger M:
Induction chemotherapy in Barrett cancer: influence on surgical risk and outcome.
Ann Surg
; 2007 Oct;246(4):624-8; discussion 628-31
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[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
44.
Reid BJ:
Early events during neoplastic progression in Barrett's esophagus.
Cancer Biomark
; 2010;9(1-6):307-24
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
.
Genetic Alliance.
consumer health - Barrett's Esophagus
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Gastroenterol. 2006 Dec;41(12):1186-96
[
17287898.001
]
[Cites]
PLoS Med. 2007 Feb;4(2):e67
[
17326708.001
]
[Cites]
Am J Gastroenterol. 2007 Mar;102(3):483-93; quiz 694
[
17338734.001
]
[Cites]
Int J Cancer. 2007 May 1;120(9):1914-21
[
17236199.001
]
[Cites]
Genes Chromosomes Cancer. 2007 Jun;46(6):532-42
[
17330261.001
]
[Cites]
Am J Physiol Gastrointest Liver Physiol. 2007 Jul;293(1):G264-70
[
17431220.001
]
[Cites]
J Mol Med (Berl). 2007 Jul;85(7):733-43
[
17415542.001
]
[Cites]
Gastrointest Endosc. 2007 Sep;66(3):460-8
[
17643436.001
]
[Cites]
N Engl J Med. 1992 Mar 12;326(11):737-40
[
1445507.001
]
[Cites]
Gastroenterol Clin North Am. 1991 Dec;20(4):791-816
[
1787014.001
]
[Cites]
Hum Pathol. 1992 May;23(5):479-82
[
1568744.001
]
[Cites]
Cancer Res. 1992 May 15;52(10):2946-50
[
1581911.001
]
[Cites]
Gastroenterol Clin Biol. 1991;15(10):703-10
[
1816011.001
]
[Cites]
Gut. 1992 May;33(5):587-91
[
1351861.001
]
[Cites]
Gut. 1992 Jun;33(6):733-7
[
1624150.001
]
[Cites]
Gastroenterology. 1992 Dec;103(6):1769-76
[
1360434.001
]
[Cites]
Cancer Res. 1993 Mar 15;53(6):1322-7
[
8443812.001
]
[Cites]
Endoscopy. 1993 Nov;25(9):648-51
[
8119224.001
]
[Cites]
Cancer Res. 1994 May 1;54(9):2292-5
[
8162566.001
]
[Cites]
Gastroenterology. 1994 Jun;106(6):1589-95
[
8194706.001
]
[Cites]
Stat Med. 1994 May 15;13(9):955-68
[
8047747.001
]
[Cites]
Gut. 1994 Oct;35(10):1348-51
[
7959183.001
]
[Cites]
Cancer. 1995 Jan 15;75(2):423-9
[
7812911.001
]
[Cites]
Proc Natl Acad Sci U S A. 1995 Jan 3;92(1):151-5
[
7816807.001
]
[Cites]
Br J Surg. 1994 Dec;81(12):1766-8
[
7827934.001
]
[Cites]
Cold Spring Harb Symp Quant Biol. 1994;59:577-83
[
7587115.001
]
[Cites]
Gastroenterology. 2003 Jan;124(1):47-56
[
12512029.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):776-81
[
12552134.001
]
[Cites]
Hum Pathol. 2001 Apr;32(4):368-78
[
11331953.001
]
[Cites]
Gastroenterology. 2001 Jun;120(7):1607-19
[
11375943.001
]
[Cites]
Gastroenterology. 2001 Jun;120(7):1630-9
[
11375945.001
]
[Cites]
Ann Thorac Surg. 2001 Aug;72(2):334-9; discussion 339-41
[
11515862.001
]
[Cites]
Gastroenterology. 2001 Sep;121(3):592-8
[
11522743.001
]
[Cites]
Am J Gastroenterol. 2001 Sep;96(9):2575-83
[
11569678.001
]
[Cites]
Am J Gastroenterol. 2001 Oct;96(10):2839-48
[
11693316.001
]
[Cites]
Cancer Res. 2001 Nov 15;61(22):8284-9
[
11719461.001
]
[Cites]
Am J Gastroenterol. 2001 Nov;96(11):3071-83
[
11721752.001
]
[Cites]
Gastrointest Endosc. 2001 Dec;54(6):682-8
[
11726842.001
]
[Cites]
Neoplasia. 2002 Mar-Apr;4(2):121-8
[
11896567.001
]
[Cites]
Gastroenterology. 2002 Apr;122(4):1101-12
[
11910360.001
]
[Cites]
N Engl J Med. 2002 Apr 11;346(15):1128-37
[
11948273.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jul 9;99(14):9433-8
[
12093899.001
]
[Cites]
Surg Oncol Clin N Am. 2002 Apr;11(2):235-56
[
12424848.001
]
[Cites]
Eur J Gastroenterol Hepatol. 2002 Nov;14(11):1179-86
[
12439111.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Dec 10;99(25):16226-31
[
12446840.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):16910-5
[
12486240.001
]
[Cites]
J Gastroenterol Hepatol. 2003 Jun;18(6):683-9
[
12753151.001
]
[Cites]
Clin Cancer Res. 2003 Jul;9(7):2560-6
[
12855631.001
]
[Cites]
Gut. 2003 Aug;52(8):1081-4
[
12865262.001
]
[Cites]
Cancer Res. 2003 Jul 15;63(14):4211-7
[
12874028.001
]
[Cites]
Clin Cancer Res. 2003 Aug 1;9(8):2912-9
[
12912936.001
]
[Cites]
Nat Rev Cancer. 2003 Sep;3(9):695-701
[
12951588.001
]
[Cites]
Hum Pathol. 1988 Feb;19(2):166-78
[
3343032.001
]
[Cites]
Am J Pathol. 1988 Apr;131(1):53-61
[
3354644.001
]
[Cites]
Gastroenterology. 1989 Feb;96(2 Pt 1):355-67
[
2910757.001
]
[Cites]
Lab Invest. 1989 Jan;60(1):65-71
[
2911184.001
]
[Cites]
Lab Invest. 1989 Mar;60(3):418-32
[
2927081.001
]
[Cites]
Stat Med. 1989 Apr;8(4):431-40
[
2727467.001
]
[Cites]
Gastroenterology. 1989 Oct;97(4):815-20
[
2777038.001
]
[Cites]
J Natl Cancer Inst. 2004 Jun 2;96(11):885-7; author reply 887
[
15173278.001
]
[Cites]
J Pathol. 2004 Jul;203(3):780-8
[
15221937.001
]
[Cites]
Gastroenterology. 2004 Jul;127(1):310-30
[
15236196.001
]
[Cites]
Oncogene. 2007 Sep 20;26(43):6332-40
[
17452981.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2007 Dec;16(12):2649-55
[
18086770.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2008 Jan;17(1):111-7
[
18199717.001
]
[Cites]
Aliment Pharmacol Ther. 2008 Feb 15;27(4):316-20
[
18062791.001
]
[Cites]
Int J Cancer. 2008 Mar 15;122(6):1303-10
[
18000824.001
]
[Cites]
Am J Gastroenterol. 2008 Mar;103(3):788-97
[
18341497.001
]
[Cites]
PLoS One. 2008;3(4):e1890
[
18382671.001
]
[Cites]
Cancer Res. 2008 Jun 1;68(11):4163-72
[
18519675.001
]
[Cites]
Dig Liver Dis. 2008 Jul;40(7):510-22
[
18400571.001
]
[Cites]
Gut. 2008 Aug;57(8):1041-8
[
18305067.001
]
[Cites]
Am J Epidemiol. 2008 Aug 1;168(3):237-49
[
18550563.001
]
[Cites]
Hum Pathol. 2008 Aug;39(8):1128-35
[
18602665.001
]
[Cites]
Genome Res. 2008 Sep;18(9):1518-29
[
18577705.001
]
[Cites]
Science. 2008 Sep 5;321(5894):1280-1
[
18772403.001
]
[Cites]
Gut. 2008 Oct;57(10):1354-9
[
18424568.001
]
[Cites]
Int J Cancer. 2008 Nov 15;123(10):2331-6
[
18729198.001
]
[Cites]
Science. 2008 Sep 26;321(5897):1807-12
[
18772396.001
]
[Cites]
Science. 2008 Sep 26;321(5897):1801-6
[
18772397.001
]
[Cites]
Dis Esophagus. 2008;21(6):529-38
[
18840137.001
]
[Cites]
Mol Cancer. 2008;7:75
[
18831746.001
]
[Cites]
Gastroenterology. 2008 Oct;135(4):1392-1413, 1413.e1-5
[
18801365.001
]
[Cites]
Clin Cancer Res. 2008 Nov 1;14(21):6988-95
[
18980994.001
]
[Cites]
PLoS One. 2008;3(11):e3809
[
19043591.001
]
[Cites]
Cancer Prev Res (Phila). 2008 Nov;1(6):413-23
[
19138988.001
]
[Cites]
Nat Genet. 2009 Feb;41(2):178-86
[
19151715.001
]
[Cites]
Cell Cycle. 2009 Mar 15;8(6):809-17
[
19229128.001
]
[Cites]
Cancer Biomark. 2009;5(3):143-58
[
19407369.001
]
[Cites]
Clin Cancer Res. 2009 May 15;15(10):3305-14
[
19417022.001
]
[Cites]
Gastrointest Endosc. 1999 Dec;50(6):814-8
[
10570342.001
]
[Cites]
J Natl Cancer Inst. 1999 Dec 15;91(24):2087-95
[
10601379.001
]
[Cites]
Cell. 2000 Jan 7;100(1):57-70
[
10647931.001
]
[Cites]
Hum Pathol. 2000 Jan;31(1):35-9
[
10665910.001
]
[Cites]
Am J Pathol. 2000 Feb;156(2):555-66
[
10666385.001
]
[Cites]
Cancer Causes Control. 2000 Mar;11(3):231-8
[
10782657.001
]
[Cites]
Clin Cancer Res. 2000 May;6(5):1702-10
[
10815888.001
]
[Cites]
Am J Gastroenterol. 2000 Jul;95(7):1669-76
[
10925966.001
]
[Cites]
J Natl Cancer Inst. 2000 Aug 16;92(16):1316-21
[
10944553.001
]
[Cites]
Am J Gastroenterol. 2000 Aug;95(8):1888-93
[
10950031.001
]
[Cites]
Genome Res. 2000 Aug;10(8):1126-37
[
10958631.001
]
[Cites]
Cancer Res. 2000 Sep 15;60(18):5021-6
[
11016622.001
]
[Cites]
BMJ. 2000 Nov 18;321(7271):1252-5
[
11082084.001
]
[Cites]
Cancer Res. 2001 Apr 1;61(7):3164-70
[
11306503.001
]
[Cites]
Genes Chromosomes Cancer. 2003 Dec;38(4):302-6
[
14566848.001
]
[Cites]
Mod Pathol. 2004 May;17(5):588-96
[
15017433.001
]
[Cites]
Cancer Res. 2004 May 15;64(10):3414-27
[
15150093.001
]
[Cites]
Clin Gastroenterol Hepatol. 2006 May;4(5):566-72
[
16630761.001
]
[Cites]
Gut. 2006 Jun;55(6):764-74
[
16368780.001
]
[Cites]
Oncogene. 2006 May 18;25(21):3084-92
[
16407829.001
]
[Cites]
Am J Gastroenterol. 2006 Aug;101(8):1900-20; quiz 1943
[
16928254.001
]
[Cites]
Gut. 2006 Oct;55(10):1390-7
[
16682429.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Oct;15(10):1935-40
[
17035402.001
]
[Cites]
Science. 2006 Oct 13;314(5797):268-74
[
16959974.001
]
[Cites]
Clin Cancer Res. 2006 Nov 15;12(22):6637-42
[
17121882.001
]
[Cites]
Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):659-65
[
17255290.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Mar;15(3):509-16
[
16537709.001
]
[Cites]
Nat Genet. 2006 Apr;38(4):468-73
[
16565718.001
]
[Cites]
Cancer Genet Cytogenet. 1989 Oct 15;42(2):281-6
[
2790761.001
]
[Cites]
Science. 1990 Jan 5;247(4938):49-56
[
2294591.001
]
[Cites]
Cancer Res. 1991 Jun 15;51(12):3075-9
[
2039987.001
]
[Cites]
Surg Oncol. 1995 Jun;4(3):163-71
[
7582189.001
]
[Cites]
Cancer Res. 1996 Jan 15;56(2):259-63
[
8542577.001
]
[Cites]
Oncogene. 1996 May 2;12(9):1873-8
[
8649847.001
]
[Cites]
Cancer Res. 2001 Apr 15;61(8):3225-9
[
11309270.001
]
[Cites]
Cancer Res. 2001 Apr 15;61(8):3410-8
[
11309301.001
]
[Cites]
Gut. 2003 May;52(5):623-8
[
12692043.001
]
[Cites]
Cancer. 1995 Oct 1;76(7):1116-9
[
8630885.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Jul 9;93(14):7081-4
[
8692948.001
]
[Cites]
Cancer Res. 1996 Oct 1;56(19):4499-502
[
8813147.001
]
[Cites]
Am J Clin Pathol. 1996 Sep;106(3):298-304
[
8816585.001
]
[Cites]
Gut. 1996 Jul;39(1):5-8
[
8881798.001
]
[Cites]
Oncogene. 1996 Nov 7;13(9):1867-73
[
8934532.001
]
[Cites]
Am J Gastroenterol. 1997 Apr;92(4):586-91
[
9128304.001
]
[Cites]
Surg Oncol Clin N Am. 1997 Jul;6(3):515-31
[
9210354.001
]
[Cites]
J Clin Invest. 1997 Oct 15;100(8):2133-7
[
9329980.001
]
[Cites]
Oncogene. 1997 Oct 2;15(14):1653-9
[
9349498.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1998 Feb;7(2):97-102
[
9488582.001
]
[Cites]
Cancer. 1998 Aug 15;83(4):641-51
[
9708926.001
]
[Cites]
Br J Cancer. 1998 Oct;78(7):950-7
[
9764589.001
]
[Cites]
Cancer Genet Cytogenet. 1998 Oct 1;106(1):11-7
[
9772903.001
]
[Cites]
Gastroenterology. 1998 Dec;115(6):1381-6
[
9834265.001
]
[Cites]
JAMA. 1998 Nov 25;280(20):1747-51
[
9842949.001
]
[Cites]
Cytometry. 1998 Dec 15;34(6):257-63
[
9879642.001
]
[Cites]
N Engl J Med. 1999 Mar 18;340(11):825-31
[
10080844.001
]
[Cites]
Nat Genet. 1999 May;22(1):106-9
[
10319873.001
]
[Cites]
Am J Pathol. 1999 Apr;154(4):965-73
[
10233832.001
]
[Cites]
Gastrointest Endosc. 1999 Jul;50(1):23-6
[
10385717.001
]
[Cites]
Clin Cancer Res. 1999 Jul;5(7):1862-7
[
10430093.001
]
[Cites]
Cancer Res. 1999 Oct 1;59(19):4784-7
[
10519384.001
]
[Cites]
Surgery. 1957 Jun;41(6):881-94
[
13442856.001
]
[Cites]
Semin Cancer Biol. 2005 Feb;15(1):51-60
[
15613288.001
]
[Cites]
Cancer Lett. 2005 Jan 20;217(2):221-30
[
15617840.001
]
[Cites]
J Natl Cancer Inst. 2005 Jan 19;97(2):142-6
[
15657344.001
]
[Cites]
Neoplasia. 2004 Nov-Dec;6(6):751-60
[
15720801.001
]
[Cites]
Am J Gastroenterol. 2005 Apr;100(4):775-83
[
15784018.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 Apr;14(4):830-4
[
15824152.001
]
[Cites]
Cancer Res. 2005 Apr 15;65(8):3146-54
[
15833844.001
]
[Cites]
Oncogene. 2005 Jun 9;24(25):4138-48
[
15824739.001
]
[Cites]
Int J Cancer. 2005 Sep 10;116(4):584-91
[
15825175.001
]
[Cites]
Gastrointest Endosc. 2005 Oct;62(4):488-98
[
16185958.001
]
[Cites]
Gastroenterology. 2005 Oct;129(4):1274-81
[
16230080.001
]
[Cites]
Neoplasia. 2005 Sep;7(9):854-61
[
16229808.001
]
[Cites]
Lancet Oncol. 2005 Dec;6(12):945-52
[
16321762.001
]
[Cites]
J Pathol. 2006 Jan;208(1):100-7
[
16278815.001
]
[Cites]
Gastroenterology. 2005 Dec;129(6):1825-31
[
16344051.001
]
[Cites]
Nat Rev Genet. 2006 Jan;7(1):21-33
[
16369569.001
]
[Cites]
Am J Gastroenterol. 2005 Dec;100(12):2616-21
[
16393209.001
]
[Cites]
J Natl Cancer Inst. 2003 Sep 17;95(18):1404-13
[
13130116.001
]
[Cites]
Am J Gastroenterol. 2003 Sep;98(9):1931-9
[
14499768.001
]
[Cites]
Clin Cancer Res. 2007 Nov 1;13(21):6293-300
[
17975140.001
]
[Cites]
Aliment Pharmacol Ther. 2007 Dec;26(11-12):1465-77
[
17900269.001
]
[Cites]
Am J Physiol Gastrointest Liver Physiol. 2007 Dec;293(6):G1106-13
[
17932229.001
]
[Cites]
Cancer Res. 2004 Oct 15;64(20):7629-33
[
15492292.001
]
[Cites]
Science. 1976 Oct 1;194(4260):23-8
[
959840.001
]
[Cites]
Gastroenterology. 1978 Oct;75(4):683-7
[
710836.001
]
[Cites]
Arch Surg. 1983 May;118(5):543-9
[
6838359.001
]
[Cites]
Gastroenterology. 1987 Jul;93(1):1-11
[
3582897.001
]
[Cites]
Am J Gastroenterol. 1987 Oct;82(10):1012-5
[
3661507.001
]
[Cites]
Gastroenterology. 1988 Jan;94(1):81-90
[
3335302.001
]
(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
45.
MacInnis RJ, English DR, Hopper JL, Giles GG:
Body size and composition and the risk of gastric and oesophageal adenocarcinoma.
Int J Cancer
; 2006 May 15;118(10):2628-31
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
COS Scholar Universe.
author profiles
.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[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
46.
Howard JM, Beddy P, Ennis D, Keogan M, Pidgeon GP, Reynolds JV:
Associations between leptin and adiponectin receptor upregulation, visceral obesity and tumour stage in oesophageal and junctional adenocarcinoma.
Br J Surg
; 2010 Jul;97(7):1020-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Associations between leptin and adiponectin receptor upregulation, visceral obesity and tumour stage in
oesophageal
and junctional
adenocarcinoma
.
BACKGROUND: Obesity is associated with
oesophageal
adenocarcinoma
, but mechanisms linking fat and carcinogenesis remain poorly understood.
METHODS: Seventy-five patients with
oesophageal
adenocarcinoma
underwent anthropometric and radiological assessment of obesity.
The human
oesophageal
adenocarcinoma
cell line OE33 was used as the calibrator sample.
CONCLUSION: Obesity is associated with upregulated ObR and AdipR2 expression in
oesophageal
adenocarcinoma
.
[MeSH-major]
Adenocarcinoma
.
Esophageal
Neoplasms. Esophagogastric Junction. Obesity, Abdominal / complications. Receptors, Adiponectin / metabolism. Receptors, Leptin / metabolism
Genetic Alliance.
consumer health - Obesity
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright (c) 2010 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.
(PMID = 20632267.001).
[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 / ADIPOR1 protein, human; 0 / ADIPOR2 protein, human; 0 / Adipokines; 0 / Receptors, Adiponectin; 0 / Receptors, Leptin
47.
Sobol UA, Sherman KL, Smith J, Nagda SN, Micetich K, Nickoloff BJ, Shoup MC:
Sweet's syndrome with neurologic manifestations in a patient with esophageal adenocarcinoma: case report and review of the literature.
Int J Dermatol
; 2009 Oct;48(10):1062-5
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Encephalitis
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
48.
Cockburn MG, Wu AH, Bernstein L:
Etiologic clues from the similarity of histology-specific trends in esophageal and lung cancers.
Cancer Causes Control
; 2005 Nov;16(9):1065-74
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Lung Cancer
.
MedlinePlus Health Information.
consumer health - Smoking
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
49.
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
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
50.
Brun R, Naroditsky I, Waterman M, Ben-Izhak O, Groisman G, Ilan N, Vlodavsky I:
Heparanase expression by Barrett's epithelium and during esophageal carcinoma progression.
Mod Pathol
; 2009 Dec;22(12):1548-54
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Heparanase expression by Barrett's epithelium and during
esophageal
carcinoma progression.
More recently, heparanase upregulation was documented in an increasing number of human carcinomas and hematological malignancies, correlating with increased tumor metastasis, vascular density, and shorter post-operative survival of
cancer
patients.
Here, we used immunohistochemical analysis to investigate heparanase expression in normal
esophagus
, Barrett's
esophagus
without dysplasia, Barrett's
esophagus
with low-grade dysplasia, Barrett's
esophagus
with high-grade dysplasia, and
adenocarcinoma of
the esophagus
.
We report that heparanase expression is already induced in Barrett's epithelium without dysplasia, and is further increased during progression through distinct pathological stages, namely, low-grade dysplasia, high-grade dysplasia, and
adenocarcinoma
.
These findings suggest that heparanase function is not limited to the process of tumor metastasis, but rather is engaged at the early stages of
esophagus
carcinoma initiation and progression.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19749739.001).
[ISSN]
1530-0285
[Journal-full-title]
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
[ISO-abbreviation]
Mod. Pathol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA106456; United States / NCI NIH HHS / CA / R01-CA106456
[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 / Biomarkers, Tumor; 0 / Ki-67 Antigen; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
51.
Zagorowicz E, Jankowski J:
Molecular changes in the progression of Barrett's oesophagus.
Postgrad Med J
; 2007 Aug;83(982):529-35
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Molecular changes in the progression of Barrett's
oesophagus
.
Barrett's
oesophagus
is a frequent complication of gastro-
oesophageal
reflux disease predicting
oesophageal
adenocarcinoma
.
The majority of Barrett's patients will not develop
cancer
, so that specific methods of identification of those at risk are required.
The ASPECT trial in the UK aims to establish whether chemoprevention with aspirin and a proton pump inhibitor will reduce
adenocarcinoma
development and mortality in patients with Barrett's
oesophagus
.
[MeSH-major]
Barrett
Esophagus
/ etiology.
Esophageal
Neoplasms / etiology
[MeSH-minor]
Aneuploidy. Apoptosis. Biomarkers, Tumor / metabolism. Cadherins / metabolism. Cell Cycle. Cell Proliferation. Cyclooxygenase 2 / metabolism.
Diagnosis
, Differential. Humans. Telomerase. Tumor Necrosis Factor-alpha / metabolism
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cell. 2000 Jan 7;100(1):57-70
[
10647931.001
]
[Cites]
J Gastrointest Surg. 2000 Mar-Apr;4(2):135-42
[
10675236.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2000 Feb;9(2):127-37
[
10698472.001
]
[Cites]
Gastroenterology. 2000 Mar;118(3):487-96
[
10702199.001
]
[Cites]
Am J Gastroenterol. 2000 Jul;95(7):1669-76
[
10925966.001
]
[Cites]
Gastroenterology. 2000 Aug;119(2):333-8
[
10930368.001
]
[Cites]
J Natl Cancer Inst. 2000 Aug 16;92(16):1316-21
[
10944553.001
]
[Cites]
Am J Gastroenterol. 2000 Aug;95(8):1888-93
[
10950031.001
]
[Cites]
Cancer Res. 2000 Sep 15;60(18):5021-6
[
11016622.001
]
[Cites]
Gastroenterology. 2000 Oct;119(4):961-71
[
11040183.001
]
[Cites]
J Natl Cancer Inst. 2000 Nov 15;92(22):1805-11
[
11078757.001
]
[Cites]
Am J Gastroenterol. 2001 Mar;96(3):624-6
[
11280524.001
]
[Cites]
Cancer Res. 2001 Apr 15;61(8):3410-8
[
11309301.001
]
[Cites]
Am J Gastroenterol. 2001 Apr;96(4):990-6
[
11316217.001
]
[Cites]
Am J Gastroenterol. 2001 May;96(5):1355-62
[
11374668.001
]
[Cites]
Gastroenterology. 2001 Jun;120(7):1607-19
[
11375943.001
]
[Cites]
Gastroenterology. 2001 Jun;120(7):1630-9
[
11375945.001
]
[Cites]
J Natl Cancer Inst. 2001 Jul 18;93(14):1054-61
[
11459866.001
]
[Cites]
Cancer Res. 2001 Nov 15;61(22):8284-9
[
11719461.001
]
[Cites]
Eur J Cancer. 1997 Apr;33(5):787-91
[
9282118.001
]
[Cites]
Am J Pathol. 1998 Jan;152(1):135-44
[
9422531.001
]
[Cites]
Nature. 1998 Mar 26;392(6674):402-5
[
9537325.001
]
[Cites]
Cancer Res. 1998 Jul 15;58(14):2929-34
[
9679948.001
]
[Cites]
Cancer. 1998 Aug 15;83(4):652-9
[
9708927.001
]
[Cites]
Cytometry. 1998 Dec 15;34(6):257-63
[
9879642.001
]
[Cites]
Gastrointest Endosc. 1999 Feb;49(2):170-6
[
9925694.001
]
[Cites]
Hum Mol Genet. 1999 Apr;8(4):607-10
[
10072428.001
]
[Cites]
Gut. 1998 Aug;43(2):216-22
[
10189847.001
]
[Cites]
Dig Dis Sci. 1999 Apr;44(4):659-67
[
10219819.001
]
[Cites]
Nat Genet. 1999 May;22(1):106-9
[
10319873.001
]
[Cites]
Am J Pathol. 1999 Apr;154(4):965-73
[
10233832.001
]
[Cites]
Br J Cancer. 1999 Jul;80(10):1652-7
[
10408414.001
]
[Cites]
Gut. 2005 Mar;54 Suppl 1:i1-5
[
15711002.001
]
[Cites]
Clin Cancer Res. 2005 Mar 15;11(6):2205-14
[
15788668.001
]
[Cites]
Clin Cancer Res. 2005 Apr 1;11(7):2478-85
[
15814623.001
]
[Cites]
Gut. 2005 May;54(5):710-7
[
15831922.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 May 24;102(21):7565-70
[
15894614.001
]
[Cites]
Int J Cancer. 2005 Sep 10;116(4):584-91
[
15825175.001
]
[Cites]
Dis Esophagus. 2005;18(3):170-6
[
16045579.001
]
[Cites]
J Natl Cancer Inst. 2005 Aug 17;97(16):1180-4
[
16106022.001
]
[Cites]
Gastroenterology. 2005 Dec;129(6):1825-31
[
16344051.001
]
[Cites]
Gut. 2006 Jan;55(1):16-25
[
16118348.001
]
[Cites]
Am J Gastroenterol. 2001 Oct;96(10):2839-48
[
11693316.001
]
[Cites]
Clin Cancer Res. 2003 Aug 1;9(8):2912-9
[
12912936.001
]
[Cites]
Gastrointest Endosc Clin N Am. 2003 Apr;13(2):369-97
[
12916666.001
]
[Cites]
Am J Surg Pathol. 2003 Nov;27(11):1442-7
[
14576477.001
]
[Cites]
Neoplasia. 2004 Jan-Feb;6(1):85-92
[
15068673.001
]
[Cites]
Med J Aust. 2004 Apr 19;180(8):387-91
[
15089728.001
]
[Cites]
J Natl Cancer Inst. 2004 Jun 2;96(11):885-7; author reply 887
[
15173278.001
]
[Cites]
Am J Gastroenterol. 2004 Sep;99(9):1657-66
[
15330898.001
]
[Cites]
Am J Gastroenterol. 2004 Oct;99(10):1877-83
[
15447744.001
]
[Cites]
J Clin Pathol. 2004 Oct;57(10):1063-8
[
15452161.001
]
[Cites]
World J Gastroenterol. 2004 Nov 1;10(21):3194-6
[
15457573.001
]
[Cites]
Cancer Res. 2004 Oct 15;64(20):7629-33
[
15492292.001
]
[Cites]
Gastroenterology. 1978 Oct;75(4):683-7
[
710836.001
]
[Cites]
Gut. 1980 Jan;21(1):26-31
[
7364315.001
]
[Cites]
Hum Pathol. 1983 Nov;14(11):931-68
[
6629368.001
]
[Cites]
Gastroenterology. 1987 Jul;93(1):1-11
[
3582897.001
]
[Cites]
Hum Pathol. 1988 Feb;19(2):166-78
[
3343032.001
]
[Cites]
Gastroenterology. 1992 Apr;102(4 Pt 1):1212-9
[
1551528.001
]
[Cites]
Gastroenterology. 1992 Dec;103(6):1769-76
[
1360434.001
]
[Cites]
Am J Gastroenterol. 1995 Oct;90(10):1808-13
[
7572899.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Jul 9;93(14):7081-4
[
8692948.001
]
[Cites]
Gastroenterol Clin Biol. 1996;20(5):430-7
[
8761140.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1996 Jun;5(6):457-9
[
8781742.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1996 Jul;5(7):559-65
[
8827361.001
]
[Cites]
Nucleic Acids Res. 1997 Jul 1;25(13):2595-7
[
9185569.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Jun 24;94(13):6770-5
[
9192640.001
]
[Cites]
Am J Gastroenterol. 2001 Nov;96(11):3071-83
[
11721752.001
]
[Cites]
Gastroenterology. 2002 Feb;122(2):588-90
[
11845805.001
]
[Cites]
J Natl Cancer Inst. 2002 Feb 20;94(4):252-66
[
11854387.001
]
[Cites]
J Gastroenterol. 2002;37(2):94-100
[
11871772.001
]
[Cites]
Gastroenterology. 2002 Apr;122(4):1113-21
[
11910361.001
]
[Cites]
Gastroenterology. 2002 Jun;122(7):1800-7
[
12055587.001
]
[Cites]
Am J Physiol Gastrointest Liver Physiol. 2002 Aug;283(2):G327-34
[
12121879.001
]
[Cites]
Gut. 2002 Sep;51(3):323-8
[
12171951.001
]
[Cites]
Oncogene. 2002 Sep 5;21(39):6071-81
[
12203119.001
]
[Cites]
Gastroenterology. 2003 Jan;124(1):47-56
[
12512029.001
]
[Cites]
Histopathology. 2003 May;42(5):457-65
[
12713622.001
]
[Cites]
Clin Cancer Res. 2003 Jul;9(7):2560-6
[
12855631.001
]
[Cites]
Cancer Res. 1997 Jul 1;57(13):2619-22
[
9205067.001
]
(PMID = 17675546.001).
[ISSN]
1469-0756
[Journal-full-title]
Postgraduate medical journal
[ISO-abbreviation]
Postgrad Med J
[Language]
eng
[Grant]
United Kingdom / Cancer Research UK / / 4584
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Tumor Necrosis Factor-alpha; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.7.49 / Telomerase
[Number-of-references]
84
[Other-IDs]
NLM/ PMC2600113
52.
Abnet CC, Freedman ND, Hollenbeck AR, Fraumeni JF Jr, Leitzmann M, Schatzkin A:
A prospective study of BMI and risk of oesophageal and gastric adenocarcinoma.
Eur J Cancer
; 2008 Feb;44(3):465-71
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
A prospective study of BMI and risk of
oesophageal
and gastric
adenocarcinoma
.
The incidence of
oesophageal
adenocarcinoma
(EADC) is rapidly increasing in Western countries and obesity is thought to be a major risk factor.
We examined the association between BMI and EADC, gastric cardia
adenocarcinoma
and gastric non-cardia
adenocarcinoma
in a cohort of approximately 500,000 people in the United States (US).
We found that compared to people with a BMI of 18.5-25kg/m2, a BMI > or = 35 was associated with significantly increased risk of EADC, HR (95% CI)=2.27 (1.44-3.59) and gastric cardia
adenocarcinoma
2.46 (1.60-3.80), but not gastric non-cardia
adenocarcinoma
0.84 (0.50-1.42).
[MeSH-major]
Adenocarcinoma
/ etiology. Attitude to Health. Body Mass Index. Cardia.
Esophageal
Neoplasms / etiology. Stomach Neoplasms / etiology
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Causes Control. 2005 Apr;16(3):285-94
[
15947880.001
]
[Cites]
Int J Cancer. 2006 May 15;118(10):2628-31
[
16353151.001
]
[Cites]
Ann Surg. 2006 Apr;243(4):479-85
[
16552198.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 May;15(5):872-8
[
16702363.001
]
[Cites]
Eur J Cancer. 2006 May;42(8):1151-8
[
16630714.001
]
[Cites]
N Engl J Med. 2006 Jun 1;354(22):2340-8
[
16738270.001
]
[Cites]
Cancer Causes Control. 2006 Sep;17(7):901-9
[
16841257.001
]
[Cites]
Br J Cancer. 2000 Jul;83(1):127-32
[
10883680.001
]
[Cites]
Cancer. 2001 Aug 1;92(3):549-55
[
11505399.001
]
[Cites]
Cancer Causes Control. 2001 Oct;12(8):721-32
[
11562112.001
]
[Cites]
Am J Epidemiol. 2001 Dec 15;154(12):1119-25
[
11744517.001
]
[Cites]
N Engl J Med. 2003 Dec 4;349(23):2241-52
[
14657432.001
]
[Cites]
J Gastroenterol Hepatol. 2004 Jan;19(1):24-30
[
14675239.001
]
[Cites]
J Natl Cancer Inst. 2004 Sep 15;96(18):1383-7
[
15367571.001
]
[Cites]
Cancer Causes Control. 2004 Oct;15(8):837-43
[
15456997.001
]
[Cites]
J Natl Cancer Inst. 1985 Feb;74(2):319-23
[
3856045.001
]
[Cites]
JAMA. 1991 Mar 13;265(10):1287-9
[
1995976.001
]
[Cites]
J Natl Cancer Inst. 1995 Jan 18;87(2):104-9
[
7707381.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1997 Jul;6(7):481-5
[
9232333.001
]
[Cites]
J Natl Cancer Inst. 1998 Jan 21;90(2):150-5
[
9450576.001
]
[Cites]
Br J Surg. 1998 Nov;85(11):1457-9
[
9823902.001
]
[Cites]
Ann Intern Med. 1999 Jun 1;130(11):883-90
[
10375336.001
]
[Cites]
Int J Cancer. 2005 Jan 20;113(3):456-63
[
15455378.001
]
[Cites]
J Natl Cancer Inst. 2005 Jan 19;97(2):142-6
[
15657344.001
]
(PMID = 18221867.001).
[ISSN]
0959-8049
[Journal-full-title]
European journal of cancer (Oxford, England : 1990)
[ISO-abbreviation]
Eur. J. Cancer
[Language]
eng
[Grant]
United States / Intramural NIH HHS / / Z99 CA999999
[Publication-type]
Journal Article; Multicenter Study; Research Support, N.I.H., Intramural
[Publication-country]
England
[Other-IDs]
NLM/ NIHMS42480; NLM/ PMC2350215
53.
Vigen C, Bernstein L, Wu AH:
Occupational physical activity and risk of adenocarcinomas of the esophagus and stomach.
Int J Cancer
; 2006 Feb 15;118(4):1004-9
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Occupational physical activity and risk of adenocarcinomas of
the esophagus
and stomach.
Physical activity may have a role in many cancers, but little is known about its effect on
esophageal
and gastric
adenocarcinoma
risk.
We investigated occupational physical activity and
esophageal
and gastric
adenocarcinoma
risk in a population-based, case-control study including 212
esophageal
, 264 gastric cardia and 389 distal gastric
cancer
cases, and 1,330 controls in Los Angeles County.
Esophageal
adenocarcinoma
risk tended to decrease with increasing Total Activity Index (OR = 0.67, 95% CI = 0.38,1.19 for highest versus lowest quartile), but neither gastric cardia nor distal gastric
cancer
was associated with the Total Activity Index.
This inverse association held for
esophageal
adenocarcinoma
(OR = 0.61, 95% CI = 0.38,0.99 for highest vs. lowest quartile) and modest associations were observed for gastric cardia (OR = 0.76, 95% CI = 0.49,1.18) and distal gastric
cancer
(OR = 0.77, 95% CI = 0.52,1.14) when based on Average Annual Activity Index before age 65 years.
We found a modest protective effect of Total Activity Index on
esophageal
adenocarcinoma
.
[MeSH-major]
Adenocarcinoma
/ epidemiology.
Esophageal
Neoplasms / epidemiology. Exercise. Occupations. Stomach Neoplasms / epidemiology
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Exercise and Physical Fitness
.
MedlinePlus Health Information.
consumer health - Exercise for Seniors
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16152595.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA59363; United States / NIEHS NIH HHS / ES / P30 ES07048
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
54.
Gottrand F, Sfeir R, Coopman S, Deschildre A, Michaud L:
[Outcome of children with repaired oesophageal atresia].
Arch Pediatr
; 2008 Dec;15(12):1837-42
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Outcome of children with repaired
oesophageal
atresia].
[Transliterated title]
Atrésie
de l'oesophage
: devenir
des
enfants opérés.
Although initial prognosis of
oesophageal
atresia is nowadays excellent with more than 95% of survival, the long-term complications are frequent.
A gastro-
oesophageal
reflux is found in 26 to 75% of the cases, responsible for peptic oesophagitis, anastomotic stenosis and Barrett's
oesophagus
, risk factor
of adenocarcinoma
of the
oesophagus
.
Even if the current prognosis of
oesophageal
atresia is good altogether, the frequency of the complications (digestive, respiratory, nutritional, orthopaedic) far from the initial intervention, and the necessity of a surveillance of the secondary
oesophageal
damages, justifies a systematic and multidisciplinary follow-up until adulthood.
[MeSH-major]
Esophageal
Atresia / surgery. Postoperative Complications
[MeSH-minor]
Adolescent. Adult. Age Factors. Catheterization. Child. Child, Preschool. Deglutition Disorders / etiology.
Esophageal
Stenosis /
diagnosis
.
Esophageal
Stenosis / therapy. Esophagoscopy. Follow-Up Studies. Gastroesophageal Reflux / etiology. Humans. Infant. Prognosis. Quality of Life. Time Factors. Tracheoesophageal Fistula / etiology. Treatment Outcome
MedlinePlus Health Information.
consumer health - After Surgery
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Arch Pediatr. 2010 Mar;17(3):300-1
[
20034771.001
]
(PMID = 18996685.001).
[ISSN]
0929-693X
[Journal-full-title]
Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
[ISO-abbreviation]
Arch Pediatr
[Language]
fre
[Publication-type]
Comparative Study; English Abstract; Journal Article
[Publication-country]
France
55.
Ogunwobi O, Mutungi G, Beales IL:
Leptin stimulates proliferation and inhibits apoptosis in Barrett's esophageal adenocarcinoma cells by cyclooxygenase-2-dependent, prostaglandin-E2-mediated transactivation of the epidermal growth factor receptor and c-Jun NH2-terminal kinase activation.
Endocrinology
; 2006 Sep;147(9):4505-16
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Leptin stimulates proliferation and inhibits apoptosis in Barrett's
esophageal
adenocarcinoma
cells by cyclooxygenase-2-dependent, prostaglandin-E2-mediated transactivation of the epidermal growth factor receptor and c-Jun NH2-terminal kinase activation.
Obesity is an important risk factor for
esophageal
adenocarcinoma
(EAC), and elevated serum leptin is characteristic of obesity.
We hypothesized that leptin may have biological effects in promoting
esophageal
adenocarcinoma
and examined the effects of leptin on the OE33 Barrett's-derived EAC line.
These effects may contribute to the greatly increased risk of
esophageal
adenocarcinoma
in obesity.
[MeSH-major]
Adenocarcinoma
/ pathology. Barrett
Esophagus
/ pathology.
Esophageal
Neoplasms / pathology. JNK Mitogen-Activated Protein Kinases / metabolism. Leptin / pharmacology. Receptor, Epidermal Growth Factor / genetics
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16740977.001).
[ISSN]
0013-7227
[Journal-full-title]
Endocrinology
[ISO-abbreviation]
Endocrinology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Leptin; 0 / PTGER4 protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / Receptors, Leptin; 0 / Receptors, Prostaglandin E; 0 / Receptors, Prostaglandin E, EP4 Subtype; 0 / Recombinant Proteins; 0 / leptin receptor, human; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; K7Q1JQR04M / Dinoprostone
56.
O'Doherty MG, Abnet CC, Murray LJ, Woodside JV, Anderson LA, Brockman JD, Cantwell MM:
Iron intake and markers of iron status and risk of Barrett's esophagus and esophageal adenocarcinoma.
Cancer Causes Control
; 2010 Dec;21(12):2269-79
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Iron intake and markers of iron status and risk of Barrett's
esophagus
and
esophageal
adenocarcinoma
.
OBJECTIVE: To investigate the association between iron intake and iron status with Barrett's
esophagus
(BE) and
esophageal
adenocarcinoma
(EAC).
[MeSH-major]
Adenocarcinoma
/ etiology. Barrett
Esophagus
/ etiology. Eating.
Esophageal
Neoplasms / etiology. Iron, Dietary
Genetic Alliance.
consumer health - Barrett's Esophagus
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Br J Cancer. 2007 Jul 2;97(1):118-22
[
17551493.001
]
[Cites]
Public Health Nutr. 2001 Oct;4(5A):1081-8
[
11820921.001
]
[Cites]
Acta Haematol. 2002;107(3):145-9
[
11978935.001
]
[Cites]
Gastroenterol Clin North Am. 2002 Jun;31(2):421-40, viii
[
12134611.001
]
[Cites]
Nutr Cancer. 2002;42(1):33-40
[
12235648.001
]
[Cites]
Int J Cancer. 2002 Nov 20;102(3):207-11
[
12397637.001
]
[Cites]
Surg Oncol Clin N Am. 2002 Apr;11(2):235-56
[
12424848.001
]
[Cites]
Am J Clin Nutr. 2002 Dec;76(6):1375-84
[
12450906.001
]
[Cites]
Circulation. 2003 Jan 28;107(3):499-511
[
12551878.001
]
[Cites]
Anticancer Res. 2002 Nov-Dec;22(6B):3797-9
[
12552996.001
]
[Cites]
Am J Gastroenterol. 2003 Jul;98(7):1627-33
[
12873590.001
]
[Cites]
Am J Clin Nutr. 2003 Sep;78(3):436-40
[
12936926.001
]
[Cites]
Gastroenterology. 2003 Dec;125(6):1733-41
[
14724826.001
]
[Cites]
J Natl Cancer Inst. 2004 Mar 3;96(5):403-7
[
14996862.001
]
[Cites]
Gastroenterology. 1983 Dec;85(6):1354-8
[
6313466.001
]
[Cites]
Am J Epidemiol. 1986 Jul;124(1):17-27
[
3521261.001
]
[Cites]
Am J Clin Nutr. 1990 Feb;51(2):301-8
[
2407101.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1993 Sep-Oct;2(5):493-7
[
8220096.001
]
[Cites]
Int J Cancer. 1995 Jan 17;60(2):160-2
[
7829208.001
]
[Cites]
J Natl Cancer Inst. 1995 Jan 18;87(2):104-9
[
7707381.001
]
[Cites]
J Biol Chem. 1996 Aug 30;271(35):21177-86
[
8702888.001
]
[Cites]
Epidemiology. 1996 Jul;7(4):384-90
[
8793364.001
]
[Cites]
Int J Cancer. 1996 Nov 4;68(3):300-4
[
8903470.001
]
[Cites]
Eur J Clin Nutr. 1997 Jan;51 Suppl 1:S4-8
[
9023471.001
]
[Cites]
Nutr Cancer. 1997;27(3):298-309
[
9101561.001
]
[Cites]
Cancer Lett. 1997 Mar 19;114(1-2):215-6
[
9103295.001
]
[Cites]
Am J Clin Nutr. 1998 Apr;67(4):593-4
[
9537604.001
]
[Cites]
Am J Clin Nutr. 1998 Apr;67(4):722-33
[
9537620.001
]
[Cites]
Carcinogenesis. 1998 Aug;19(8):1445-9
[
9744541.001
]
[Cites]
Br J Cancer. 1999 Jul;80 Suppl 1:95-103
[
10466767.001
]
[Cites]
Carcinogenesis. 1999 Sep;20(9):1801-8
[
10469627.001
]
[Cites]
Br J Cancer. 2008 Jan 15;98(1):194-8
[
18059399.001
]
[Cites]
Am J Epidemiol. 2008 Apr 1;167(7):839-46
[
18218607.001
]
[Cites]
Am J Clin Nutr. 2008 May;87(5):1298-305
[
18469253.001
]
[Cites]
Int J Cancer. 2008 Aug 15;123(4):852-60
[
18537156.001
]
[Cites]
Anticancer Res. 2008 May-Jun;28(3B):1955-63
[
18630488.001
]
[Cites]
Am J Gastroenterol. 2008 Jul;103(7):1614-23; quiz 1624
[
18494834.001
]
[Cites]
Dis Model Mech. 2008 Jul-Aug;1(1):26-31
[
19048049.001
]
[Cites]
Am J Gastroenterol. 2008 Dec;103(12):2997-3004
[
18853987.001
]
[Cites]
Cancer Prev Res (Phila). 2008 Oct;1(5):329-38
[
19138977.001
]
[Cites]
Cancer Causes Control. 2009 Apr;20(3):279-88
[
18839322.001
]
[Cites]
Helicobacter. 2008 Oct;13(5):323-40
[
19250507.001
]
[Cites]
Am J Gastroenterol. 2009 Mar;104 Suppl 2:S5-9
[
19262546.001
]
[Cites]
Int J Cancer. 2009 Jun 1;124(11):2671-6
[
19230023.001
]
[Cites]
PLoS Med. 2007 Dec;4(12):e325
[
18076279.001
]
[Cites]
Am J Gastroenterol. 2007 Oct;102(10):2323-30; quiz 2331
[
17581269.001
]
[Cites]
Semin Oncol. 1999 Oct;26(5 Suppl 15):2-8
[
10566604.001
]
[Cites]
Carcinogenesis. 2000 Feb;21(2):257-63
[
10657966.001
]
[Cites]
Am J Clin Nutr. 2000 Mar;71(3):746-51
[
10702168.001
]
[Cites]
Gastroenterology. 2000 Aug;119(2):333-8
[
10930368.001
]
[Cites]
Am J Clin Nutr. 2001 Jan;73(1):93-8
[
11124756.001
]
[Cites]
Lancet. 2000 Dec 16;356(9247):2079-85
[
11145505.001
]
[Cites]
Carcinogenesis. 2001 Jan;22(1):199-202
[
11159760.001
]
[Cites]
Hepatology. 2001 Mar;33(3):647-51
[
11230745.001
]
[Cites]
Eur J Cancer Prev. 2001 Aug;10(4):365-9
[
11535879.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2001 Oct;10(10):1055-62
[
11588131.001
]
[Cites]
Onkologie. 2001 Dec;24(6):546-51
[
11799309.001
]
[Cites]
Int J Cancer. 2008 Mar 1;122(5):1118-29
[
17990321.001
]
[Cites]
J Nutr. 2005 Aug;135(8):1974-80
[
16046725.001
]
[Cites]
Int J Cancer. 2005 Nov 20;117(4):643-7
[
15929082.001
]
[Cites]
J Natl Cancer Inst. 2006 Mar 1;98(5):345-54
[
16507831.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Apr;15(4):717-25
[
16614114.001
]
[Cites]
Cancer Res. 2006 May 1;66(9):4975-82
[
16651456.001
]
[Cites]
World J Gastroenterol. 2007 Mar 14;13(10):1585-94
[
17461453.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2007 Jun;16(6):1306-8
[
17548704.001
]
(PMID = 20936528.001).
[ISSN]
1573-7225
[Journal-full-title]
Cancer causes & control : CCC
[ISO-abbreviation]
Cancer Causes Control
[Language]
eng
[Grant]
United States / Intramural NIH HHS / / Z99 CA999999; United States / Intramural NIH HHS / / ZIA CP000185-07
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Biomarkers; 0 / Iron, Dietary
[Other-IDs]
NLM/ NIHMS402473; NLM/ PMC3438890
57.
Chau I, Norman AR, Cunningham D, Oates J, Hawkins R, Iveson T, Nicolson M, Harper P, Seymour M, Hickish T:
The impact of primary tumour origins in patients with advanced oesophageal, oesophago-gastric junction and gastric adenocarcinoma--individual patient data from 1775 patients in four randomised controlled trials.
Ann Oncol
; 2009 May;20(5):885-91
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The impact of primary tumour origins in patients with advanced
oesophageal
, oesophago-gastric junction and gastric
adenocarcinoma
--individual patient data from 1775 patients in four randomised controlled trials.
BACKGROUND: It is unclear if differential chemotherapy effects exist on overall survival (OS), response rate (RR) and toxicity depending on primary tumour origin [
oesophageal
versus oesophago-gastric junction (OGJ) versus gastric
adenocarcinoma
].
This analysis used individual patient data and restricted to patients with
adenocarcinoma
who received one or more dose of chemotherapy.
RESULTS: Of the 2110 patients randomised, 1775 (84%) patients had
adenocarcinoma
with
oesophageal
(n = 485), OGJ (n = 457) and gastric (n = 833) origins.
The median OS was 9.5 months in
oesophageal
, 9.3 months in OGJ and 8.7 months in gastric
cancer
(P = 0.68).
RR was 44.1% in
oesophageal
, 41.1% in OGJ and 35.6% in gastric cancers (P = 0.11 and 0.27, respectively, compared with gastric
cancer
on multivariate analysis).
Toxicity composite end point occurred in 46%, 47% and 45% in
oesophageal
, OGJ and gastric cancers, respectively (P = 0.85 and 0.62 compared with gastric).
CONCLUSIONS: In our large multicentre RCT dataset, no significant differences were demonstrated on multivariate analyses in OS, RR and toxic effects among patients with advanced
oesophageal
, OGJ and gastric
adenocarcinoma
.
Future RCTs should not exclude
oesophageal
adenocarcinoma
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
Hazardous Substances Data Bank.
CAPECITABINE
.
Hazardous Substances Data Bank.
CIS-DIAMINEDICHLOROPLATINUM
.
Hazardous Substances Data Bank.
FLUOROURACIL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19164454.001).
[ISSN]
1569-8041
[Journal-full-title]
Annals of oncology : official journal of the European Society for Medical Oncology
[ISO-abbreviation]
Ann. Oncol.
[Language]
ENG
[Publication-type]
Comparative Study; Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
58.
Starling N, Okines A, Cunningham D, Allum W, Wotherspoon A, Benson M, Thompson J, Thomas J, Brown G, Riddell A, Stavridi F, Ashley S, Oates J, Chau I:
A phase II trial of preoperative chemotherapy with epirubicin, cisplatin and capecitabine for patients with localised gastro-oesophageal junctional adenocarcinoma.
Br J Cancer
; 2009 Jun 2;100(11):1725-30
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
A phase II trial of preoperative chemotherapy with epirubicin, cisplatin and capecitabine for patients with localised gastro-
oesophageal
junctional
adenocarcinoma
.
Preoperative cisplatin/fluorouracil is used for the treatment of localised
oesophageal
carcinoma.
Patients with stage II or III
oesophageal
/gastro-
oesophageal
junctional
adenocarcinoma
from one institution received 4 cycles of ECX (epirubicin 50 mg m(-2) day 1, cisplatin 60 mg m(-2) day 1, capecitabine 625 mg m(-2) b.i.d. daily) followed by surgery.
Although associated with a low pCR rate, survival with ECX was comparable with published studies suggesting that pCR may not correlate with satisfactory outcome from preoperative chemotherapy for localised
oesophageal
adenocarcinoma
.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / therapeutic use. Deoxycytidine / analogs & derivatives. Epirubicin / therapeutic use.
Esophageal
Neoplasms / drug therapy. Fluorouracil / analogs & derivatives. Stomach Neoplasms / drug therapy
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
Hazardous Substances Data Bank.
CAPECITABINE
.
Hazardous Substances Data Bank.
CIS-DIAMINEDICHLOROPLATINUM
.
Hazardous Substances Data Bank.
FLUOROURACIL
.
Hazardous Substances Data Bank.
EPIRUBICIN
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer. 2000 Apr 15;88(8):1788-95
[
10760753.001
]
[Cites]
N Engl J Med. 2008 Jan 3;358(1):36-46
[
18172173.001
]
[Cites]
Br J Surg. 2001 Mar;88(3):338-56
[
11260097.001
]
[Cites]
J Clin Oncol. 2001 Jun 15;19(12):3058-65
[
11408502.001
]
[Cites]
Br J Cancer. 2002 Apr 22;86(8):1223-9
[
11953876.001
]
[Cites]
J Clin Oncol. 2002 Apr 15;20(8):1996-2004
[
11956258.001
]
[Cites]
Gastrointest Endosc. 2002 May;55(6):655-61
[
11979246.001
]
[Cites]
Lancet. 2002 May 18;359(9319):1727-33
[
12049861.001
]
[Cites]
Br J Surg. 2004 Feb;91(2):199-204
[
14760668.001
]
[Cites]
JAMA. 1991 Mar 13;265(10):1287-9
[
1995976.001
]
[Cites]
N Engl J Med. 1996 Aug 15;335(7):462-7
[
8672151.001
]
[Cites]
J Clin Oncol. 1997 Jan;15(1):261-7
[
8996151.001
]
[Cites]
AJR Am J Roentgenol. 1997 Aug;169(2):485-91
[
9242759.001
]
[Cites]
N Engl J Med. 1998 Dec 31;339(27):1979-84
[
9869669.001
]
[Cites]
J Natl Cancer Inst. 1999 Mar 17;91(6):497-8
[
10088616.001
]
[Cites]
CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108
[
15761078.001
]
[Cites]
Br J Cancer. 2005 Jun 6;92(11):1976-83
[
15928658.001
]
[Cites]
J Clin Oncol. 2005 Jul 1;23(19):4330-7
[
15781882.001
]
[Cites]
J Clin Oncol. 2005 Jul 10;23(20):4483-9
[
16002838.001
]
[Cites]
Radiology. 2005 Sep;236(3):841-51
[
16118165.001
]
[Cites]
Lancet Oncol. 2005 Sep;6(9):659-68
[
16129366.001
]
[Cites]
Cancer. 2005 Dec 1;104(11):2365-72
[
16245310.001
]
[Cites]
J Surg Oncol. 2005 Dec 1;92(3):151-9
[
16299786.001
]
[Cites]
Cancer. 2006 May 15;106(10):2119-27
[
16607651.001
]
[Cites]
N Engl J Med. 2006 Jul 6;355(1):11-20
[
16822992.001
]
[Cites]
Cochrane Database Syst Rev. 2006;(3):CD001556
[
16855972.001
]
[Cites]
J Clin Oncol. 2006 Oct 10;24(29):4692-8
[
16966684.001
]
[Cites]
Lancet Oncol. 2007 Mar;8(3):226-34
[
17329193.001
]
[Cites]
Am J Surg. 2007 May;193(5):614-7; discussion 617
[
17434367.001
]
[Cites]
J Clin Oncol. 2007 Aug 20;25(24):3719-25
[
17704421.001
]
[Cites]
Lancet Oncol. 2007 Sep;8(9):797-805
[
17693134.001
]
[Cites]
Ann Oncol. 2007 Oct;18(10):1673-9
[
17660494.001
]
[Cites]
Contemp Clin Trials. 2008 Jan;29(1):32-41
[
17544337.001
]
[Cites]
BMC Med. 2004 Sep 24;2:35
[
15447788.001
]
[Cites]
J Clin Oncol. 2008 Mar 1;26(7):1086-92
[
18309943.001
]
[Cites]
J Clin Oncol. 2001 Jan 15;19(2):305-13
[
11208820.001
]
(PMID = 19436301.001).
[ISSN]
1532-1827
[Journal-full-title]
British journal of cancer
[ISO-abbreviation]
Br. J. Cancer
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0W860991D6 / Deoxycytidine; 3Z8479ZZ5X / Epirubicin; 6804DJ8Z9U / Capecitabine; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
[Other-IDs]
NLM/ PMC2695693
59.
Yoshida T, Shimizu Y, Kato M:
Image of the month. Use of magnifying endoscopy to identify early esophageal adenocarcinoma in ectopic gastric mucosa of the cervical esophagus.
Clin Gastroenterol Hepatol
; 2010 Sep;8(9):e91-3
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Image of the month. Use of magnifying endoscopy to identify early
esophageal
adenocarcinoma
in ectopic gastric mucosa of the cervical
esophagus
.
[MeSH-major]
Adenocarcinoma
/
diagnosis
. Choristoma / pathology. Endoscopy / methods.
Esophageal
Neoplasms /
diagnosis
. Gastric Mucosa / pathology
MedlinePlus Health Information.
consumer health - Endoscopy
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20347051.001).
[ISSN]
1542-7714
[Journal-full-title]
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
[ISO-abbreviation]
Clin. Gastroenterol. Hepatol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
60.
Czito BG, Kelsey CR, Hurwitz HI, Willett CG, Morse MA, Blobe GC, Fernando NH, D'Amico TA, Harpole DH, Honeycutt W, Yu D, Bendell JC:
A Phase I study of capecitabine, carboplatin, and paclitaxel with external beam radiation therapy for esophageal carcinoma.
Int J Radiat Oncol Biol Phys
; 2007 Mar 15;67(4):1002-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
A Phase I study of capecitabine, carboplatin, and paclitaxel with external beam radiation therapy for
esophageal
carcinoma.
PURPOSE: Concurrent chemotherapy and radiation therapy (RT) are used to treat patients with
esophageal cancer
.
METHODS AND MATERIALS: Patients with squamous cell carcinoma or
adenocarcinoma of
the esophagus
initially received capecitabine, carboplatin, and paclitaxel with RT (1.8 Gy daily to 50.4 Gy).
[MeSH-major]
Adenocarcinoma
/ drug therapy.
Adenocarcinoma
/ radiotherapy. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / radiotherapy.
Esophageal
Neoplasms / drug therapy.
Esophageal
Neoplasms / radiotherapy
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
CAPECITABINE
.
Hazardous Substances Data Bank.
TAXOL
.
Hazardous Substances Data Bank.
CARBOPLATIN
.
Hazardous Substances Data Bank.
FLUOROURACIL
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17197129.001).
[ISSN]
0360-3016
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Publication-type]
Clinical Trial, Phase I; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel; U3P01618RT / Fluorouracil
61.
Castillo E, Lawler LP:
Diagnostic radiology and nuclear medicine.
J Surg Oncol
; 2005 Dec 1;92(3):191-202
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
The diagnosis
and accurate staging of
esophageal
adenocarcinoma
remains one of the greatest challenges for non-invasive imaging techniques.
[MeSH-major]
Adenocarcinoma
/
diagnosis
.
Esophageal
Neoplasms /
diagnosis
. Fluorodeoxyglucose F18. Positron-Emission Tomography. Radiopharmaceuticals
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
(c) 2005 Wiley-Liss, Inc.
(PMID = 16299788.001).
[ISSN]
0022-4790
[Journal-full-title]
Journal of surgical oncology
[ISO-abbreviation]
J Surg Oncol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
[Number-of-references]
85
62.
Demeester SR:
Epidemiology and biology of esophageal cancer.
Gastrointest Cancer Res
; 2009 Mar;3(2 Suppl):S2-5
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Epidemiology and biology of
esophageal cancer
.
In the United States and other Western countries, there has been a remarkable change in the epidemiology of
esophageal cancer
over the past 50 years.
Adenocarcinoma of
the esophagus
and gastroesophageal junction has replaced squamous cell as the most common type of
esophageal cancer
in the United States, and the incidence of
esophageal
adenocarcinoma
is increasing faster than that of any other malignancy.
The increasing incidence of
esophageal
adenocarcinoma
and a greater understanding of its underlying biology provide opportunities to devise treatment strategies that maximize survival and minimize morbidity.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Surg Res. 2004 Mar;117(1):58-63
[
15013715.001
]
[Cites]
Gut. 2003 Apr;52(4):486-9
[
12631655.001
]
[Cites]
Am J Gastroenterol. 2004 Apr;99(4):582-8
[
15089886.001
]
[Cites]
Arch Surg. 2004 Jun;139(6):627-31; discussion 631-3
[
15197089.001
]
[Cites]
Ann Thorac Surg. 2004 Nov;78(5):1777-82
[
15511474.001
]
[Cites]
J Natl Cancer Inst. 2005 Jan 19;97(2):142-6
[
15657344.001
]
[Cites]
Ann Surg. 2005 Oct;242(4):566-73; discussion 573-5
[
16192817.001
]
[Cites]
Ann Surg Oncol. 2006 Jan;13(1):12-30
[
16378161.001
]
[Cites]
Gut. 2006 Nov;55(11):1538-44
[
16785284.001
]
[Cites]
J Am Coll Surg. 2006 Aug;203(2):152-61
[
16864027.001
]
[Cites]
J Thorac Cardiovasc Surg. 2007 Mar;133(3):738-45
[
17320575.001
]
[Cites]
Gut. 2007 Nov;56(11):1503-11
[
17337464.001
]
[Cites]
Eur J Cancer. 2007 Jun;43(9):1445-51
[
17512189.001
]
[Cites]
J Gastrointest Surg. 2007 Nov;11(11):1384-93; discussion 1393-4
[
17764019.001
]
[Cites]
Ann Surg. 2007 Oct;246(4):665-71; discussion 671-4
[
17893503.001
]
[Cites]
Gut. 2008 Mar;57(3):298-305
[
17965056.001
]
[Cites]
Ann Surg. 2007 Dec;246(6):992-1000; discussion 1000-1
[
18043101.001
]
[Cites]
Cancer. 2008 Mar 15;112(6):1239-46
[
18224663.001
]
[Cites]
J Clin Oncol. 2008 Mar 1;26(7):1086-92
[
18309943.001
]
[Cites]
Gut. 2008 Sep;57(9):1200-6
[
18460553.001
]
[Cites]
J Thorac Cardiovasc Surg. 2008 Jun;135(6):1228-36
[
18544359.001
]
[Cites]
Ann Surg. 2008 Aug;248(2):221-6
[
18650631.001
]
[Cites]
J Natl Cancer Inst. 2008 Aug 20;100(16):1184-7
[
18695138.001
]
[Cites]
J Exp Med. 1901 Jan 15;5(4):319-32
[
19866948.001
]
[Cites]
N Engl J Med. 1996 Aug 15;335(7):462-7
[
8672151.001
]
[Cites]
J Thorac Cardiovasc Surg. 1997 Dec;114(6):948-55; discussion 955-6
[
9434690.001
]
[Cites]
Br J Surg. 1998 Nov;85(11):1457-9
[
9823902.001
]
[Cites]
J Thorac Cardiovasc Surg. 1999 Jan;117(1):16-23; discussion 23-5
[
9869753.001
]
[Cites]
N Engl J Med. 1999 Mar 18;340(11):825-31
[
10080844.001
]
[Cites]
J Thorac Cardiovasc Surg. 1999 May;117(5):960-8
[
10220691.001
]
[Cites]
Ann Surg. 1999 Sep;230(3):433-8; discussion 438-40
[
10493489.001
]
[Cites]
Int J Cancer. 2000 Feb 1;85(3):340-6
[
10652424.001
]
[Cites]
Ann Intern Med. 2000 Aug 1;133(3):165-75
[
10906830.001
]
[Cites]
Int J Epidemiol. 2000 Aug;29(4):645-54
[
10922340.001
]
[Cites]
J Am Coll Surg. 2000 Aug;191(2):143-8
[
10945357.001
]
[Cites]
J Clin Oncol. 2000 Sep 15;18(18):3202-10
[
10986052.001
]
[Cites]
J Clin Oncol. 2001 Jan 15;19(2):305-13
[
11208820.001
]
[Cites]
Cancer. 2001 Mar 15;91(6):1098-104
[
11267954.001
]
[Cites]
Gastroenterology. 2001 Jun;120(7):1607-19
[
11375943.001
]
[Cites]
Cancer. 2001 Aug 1;92(3):549-55
[
11505399.001
]
[Cites]
Ann Surg. 2001 Nov;234(5):581-7
[
11685019.001
]
[Cites]
J Thorac Cardiovasc Surg. 2001 Dec;122(6):1077-90
[
11726882.001
]
[Cites]
J Am Coll Surg. 2002 Jan;194(1):28-36
[
11803954.001
]
[Cites]
Gut. 2002 Mar;50(3):368-72
[
11839716.001
]
[Cites]
Surg Endosc. 2003 Jan;17(1):43-8
[
12364989.001
]
[Cites]
Cancer. 2002 Nov 15;95(10):2096-102
[
12412162.001
]
[Cites]
Gut. 2004 May;53(5):634-40
[
15082579.001
]
(PMID = 19461918.001).
[ISSN]
1934-7820
[Journal-full-title]
Gastrointestinal cancer research : GCR
[ISO-abbreviation]
Gastrointest Cancer Res
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2684731
63.
Steffen A, Schulze MB, Pischon T, Dietrich T, Molina E, Chirlaque MD, Barricarte A, Amiano P, Quirós JR, Tumino R, Mattiello A, Palli D, Vineis P, Agnoli C, Misirli G, Boffetta P, Kaaks R, Rohrmann S, Bueno-de-Mesquita HB, Peeters PH, May AM, Spencer EA, Allen NE, Bingham S, Tjønneland A, Halkjaer J, Overvad K, Stegger J, Manjer J, Lindkvist B, Hallmanns G, Stenling R, Lund E, Riboli E, Gonzalez CA, Boeing H:
Anthropometry and esophageal cancer risk in the European prospective investigation into cancer and nutrition.
Cancer Epidemiol Biomarkers Prev
; 2009 Jul;18(7):2079-89
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Anthropometry and
esophageal cancer
risk in the European prospective investigation into
cancer
and nutrition.
BACKGROUND: Increasing evidence suggests that general obesity [measured by body mass index (BMI)] is positively associated with risk of
esophageal
adenocarcinoma
(EAC).
In contrast, previous studies have shown inverse relations with
esophageal
squamous cell carcinoma (ESCC).
However, it is still unclear whether body fat distribution, particularly abdominal obesity, is associated with each type of
esophageal cancer
.
METHODS: We applied multivariable adjusted Cox proportional hazards regression to investigate the association between anthropometric measures and risk of EAC and ESCC among 346,554 men and women participating in the European Prospective Investigation into
Cancer
and Nutrition.
[MeSH-major]
Adenocarcinoma
/ epidemiology. Carcinoma, Squamous Cell / epidemiology.
Esophageal
Neoplasms / epidemiology. Obesity / epidemiology
Genetic Alliance.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Obesity
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19567501.001).
[ISSN]
1538-7755
[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 Kingdom / British Heart Foundation / / ; United Kingdom / Cancer Research UK / / ; United Kingdom / Department of Health / / ; United Kingdom / Medical Research Council / / ; United Kingdom / Wellcome Trust / /
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
64.
Dughera L, Navino M, Cassolino P, Pellicano R:
The diagnosis of gastroesophageal reflux disease.
Minerva Gastroenterol Dietol
; 2007 Jun;53(2):143-52
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The diagnosis
of gastroesophageal reflux disease.
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, endoscopy is the main clinical tool for visualizing
esophageal
lesions, but the majority of GERD patients do not have endoscopic visible lesions and other methods are required.
Ambulatory
esophageal
pH monitoring is the gold standard in diagnosing GERD, since it measures distal
esophageal
acid exposure and demonstrates the relationship between symptoms and acid reflux.
[MeSH-major]
Gastroesophageal Reflux /
diagnosis
[MeSH-minor]
Algorithms.
Esophageal
pH Monitoring. Esophagoscopy. Humans. Proton Pump Inhibitors
Genetic Alliance.
consumer health - Gastroesophageal Reflux
.
MedlinePlus Health Information.
consumer health - GERD
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17557042.001).
[ISSN]
1121-421X
[Journal-full-title]
Minerva gastroenterologica e dietologica
[ISO-abbreviation]
Minerva Gastroenterol Dietol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Italy
[Chemical-registry-number]
0 / Proton Pump Inhibitors
[Number-of-references]
25
65.
Siewert JR, Feith M, Stein HJ:
Biologic and clinical variations of adenocarcinoma at the esophago-gastric junction: relevance of a topographic-anatomic subclassification.
J Surg Oncol
; 2005 Jun 1;90(3):139-46; discussion 146
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Biologic and clinical variations
of adenocarcinoma
at the esophago-gastric junction: relevance of a topographic-anatomic subclassification.
A topographic-anatomic subclassification of adenocarcinomas of the esophago-gastric junction (AEG) in distal
esophageal
adenocarcinoma
(AEG Type I), true carcinoma of the cardia (AEG Type II), and subcardial gastric
cancer
(AEG Type III) was introduced in 1987 and is now increasingly accepted and used worldwide.
[MeSH-major]
Adenocarcinoma
/ classification. Cardia.
Esophageal
Neoplasms / classification. Esophagogastric Junction. Stomach Neoplasms / classification
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2005 Wiley-Liss, Inc
(PMID = 15895452.001).
[ISSN]
0022-4790
[Journal-full-title]
Journal of surgical oncology
[ISO-abbreviation]
J Surg Oncol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
35
66.
Duggan SP, Behan FM, Kirca M, Smith S, Reynolds JV, Long A, Kelleher D:
An integrative genomic approach in oesophageal cells identifies TRB3 as a bile acid responsive gene, downregulated in Barrett's oesophagus, which regulates NF-kappaB activation and cytokine levels.
Carcinogenesis
; 2010 May;31(5):936-45
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
An integrative genomic approach in
oesophageal
cells identifies TRB3 as a bile acid responsive gene, downregulated in Barrett's
oesophagus
, which regulates NF-kappaB activation and cytokine levels.
Reflux of gastroduodenal contents and consequent inflammatory responses are associated with the development of Barrett's
oesophagus
(BO) and the promotion of
oesophageal
adenocarcinoma
(OAC).
Deregulation of inflammatory processes is a hallmark of
oesophageal cancer
.
In this study, we aimed to investigate (i) the transcriptional responses to deoxycholic acid (DCA) in cell lines representative of either end of
the oesophageal cancer
sequence, (ii) the expression of DCA-regulated genes in data charting
oesophageal
carcinogenesis and (iii) the impact of these genes on
oesophageal
inflammatory signalling.
This study identifies mechanisms through which bile acids such as DCA, in conjunction with the loss of key signalling molecules, could regulate
oesophageal
metaplasticity.
[MeSH-major]
Barrett
Esophagus
/ etiology. Cell Cycle Proteins / genetics. Deoxycholic Acid / pharmacology.
Esophagus
/ pathology. Interleukin-8 / analysis. NF-kappa B / metabolism. Protein-Serine-Threonine Kinases / genetics. Repressor Proteins / genetics. Response Elements / physiology
COS Scholar Universe.
author profiles
.
Cellosaurus - a cell line knowledge resource.
culture/stock collections - Cellosaurus - a cell line knowledge resource
.
Cellosaurus - a cell line knowledge resource.
culture/stock collections - Cellosaurus - a cell line knowledge resource
.
Hazardous Substances Data Bank.
DEOXYCHOLIC ACID
.
SciCrunch.
ArrayExpress: Data: Microarray
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20139130.001).
[ISSN]
1460-2180
[Journal-full-title]
Carcinogenesis
[ISO-abbreviation]
Carcinogenesis
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Cell Cycle Proteins; 0 / Interleukin-8; 0 / NF-kappa B; 0 / Repressor Proteins; 0 / TRIB3 protein, human; 005990WHZZ / Deoxycholic Acid; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
67.
Li Y, Sun DL, Duan YN, Zhang XJ, Wang N, Zhou RM, Chen ZF, Wang SJ:
Association of functional polymorphisms in MMPs genes with gastric cardia adenocarcinoma and esophageal squamous cell carcinoma in high incidence region of North China.
Mol Biol Rep
; 2010 Jan;37(1):197-205
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Association of functional polymorphisms in MMPs genes with gastric cardia
adenocarcinoma
and
esophageal
squamous cell carcinoma in high incidence region of North China.
The aim of the present study was to investigate the association of single nucleotide polymorphisms (SNPs) in matrix metalloproteinase (MMPs) with the risk of gastric cardia
adenocarcinoma
(GCA) and
esophageal
squamous cell carcinoma (ESCC).
[MeSH-major]
Esophageal
Neoplasms / epidemiology.
Esophageal
Neoplasms / genetics. Genetic Predisposition to Disease. Matrix Metalloproteinases / genetics. Polymorphism, Single Nucleotide / genetics. Stomach Neoplasms / epidemiology. Stomach Neoplasms / genetics
[MeSH-minor]
Adenocarcinoma
/ enzymology.
Adenocarcinoma
/ epidemiology.
Adenocarcinoma
/ genetics. Adult. Aged. Aged, 80 and over. Carcinoma, Squamous Cell / enzymology. Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / genetics. Case-Control Studies. China / epidemiology. Female. Gene Frequency / genetics. Haplotypes / genetics. Humans. Incidence. Male. Middle Aged
Genetic Alliance.
consumer health - Carcinoma, Squamous Cell
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Int J Epidemiol. 2000 Aug;29(4):645-54
[
10922340.001
]
[Cites]
Carcinogenesis. 2005 Jun;26(6):1117-21
[
15731163.001
]
[Cites]
J Biol Chem. 2001 Mar 9;276(10):7549-58
[
11114309.001
]
[Cites]
Matrix Biol. 2002 Oct;21(6):487-98
[
12392760.001
]
[Cites]
Circ Res. 2000 May 12;86(9):998-1003
[
10807873.001
]
[Cites]
Br Heart J. 1995 Mar;73(3):209-15
[
7727178.001
]
[Cites]
Cancer Res. 2001 Nov 1;61(21):7825-9
[
11691799.001
]
[Cites]
Lung Cancer. 2007 May;56(2):273-80
[
17208328.001
]
[Cites]
Cancer Res. 2004 Oct 15;64(20):7622-8
[
15492291.001
]
[Cites]
Nucleic Acids Res. 1988 Feb 11;16(3):1215
[
3344216.001
]
[Cites]
Cancer Res. 1998 Dec 1;58(23):5321-5
[
9850057.001
]
[Cites]
Carcinogenesis. 2004 Dec;25(12):2519-24
[
15319302.001
]
[Cites]
Clin Cancer Res. 2007 May 1;13(9):2614-20
[
17473191.001
]
[Cites]
Arterioscler Thromb Vasc Biol. 2001 Nov;21(11):1834-9
[
11701474.001
]
[Cites]
Clin Cancer Res. 2002 Dec;8(12):3820-3
[
12473595.001
]
[Cites]
Nat Rev Cancer. 2002 Mar;2(3):161-74
[
11990853.001
]
[Cites]
Carcinogenesis. 2006 May;27(5):1024-9
[
16311244.001
]
[Cites]
Breast Cancer Res Treat. 2004 Dec;88(3):197-204
[
15609121.001
]
[Cites]
Br J Surg. 1998 Nov;85(11):1457-9
[
9823902.001
]
[Cites]
Gynecol Obstet Invest. 2008;65(1):68-72
[
17851253.001
]
[Cites]
World J Gastroenterol. 2005 Apr 28;11(16):2385-9
[
15832405.001
]
[Cites]
J Oral Pathol Med. 2004 Aug;33(7):405-9
[
15250832.001
]
[Cites]
FEBS Lett. 1996 Feb 12;380(1-2):17-20
[
8603731.001
]
[Cites]
Carcinogenesis. 2005 Oct;26(10):1748-53
[
15930031.001
]
[Cites]
Cancer Res. 2003 Jul 15;63(14):3987-90
[
12873995.001
]
[Cites]
Semin Cancer Biol. 2000 Dec;10(6):415-33
[
11170864.001
]
[Cites]
Biochem Genet. 2008 Apr;46(3-4):137-44
[
18210196.001
]
(PMID = 19562509.001).
[ISSN]
1573-4978
[Journal-full-title]
Molecular biology reports
[ISO-abbreviation]
Mol. Biol. Rep.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
EC 3.4.24.- / Matrix Metalloproteinases
68.
Hao Y, Triadafilopoulos G, Sahbaie P, Young HS, Omary MB, Lowe AW:
Gene expression profiling reveals stromal genes expressed in common between Barrett's esophagus and adenocarcinoma.
Gastroenterology
; 2006 Sep;131(3):925-33
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Gene expression profiling reveals stromal genes expressed in common between Barrett's
esophagus
and
adenocarcinoma
.
BACKGROUND & AIMS: Barrett's
esophagus
is a precursor of
esophageal
adenocarcinoma
.
DNA microarrays that enable a genome-wide assessment of gene expression enhance the identification of specific genes as well as gene expression patterns that are expressed by Barrett's
esophagus
and
adenocarcinoma
compared with normal tissues.
Barrett's
esophagus
length has also been identified as a risk factor for progression to
adenocarcinoma
, but whether there are intrinsic biological differences between short-segment and long-segment Barrett's
esophagus
can be explored with microarrays.
METHODS: Gene expression profiles for endoscopically obtained biopsy specimens of Barrett's
esophagus
or
esophageal
adenocarcinoma
and associated normal
esophagus
and duodenum were identified for 17 patients using DNA microarrays.
Barrett's
esophagus
and
esophageal
adenocarcinoma
express a unique set of stromal genes that is distinct from normal tissues but similar to other cancers.
Adenocarcinoma
also showed lower and higher expression for many genes compared with Barrett's
esophagus
.
No difference in gene expression was found between short-segment and long-segment Barrett's
esophagus
.
Stromal gene expression in Barrett's
esophagus
and
adenocarcinoma
is similar, indicating that these changes precede malignant transformation.
Genetic Alliance.
consumer health - Barrett's Esophagus
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Nature. 2000 Feb 3;403(6769):503-11
[
10676951.001
]
[Cites]
Cancer Res. 2005 Aug 15;65(16):7127-36
[
16103062.001
]
[Cites]
Genomics. 2000 May 1;65(3):299-302
[
10857754.001
]
[Cites]
Nature. 2000 Aug 17;406(6797):747-52
[
10963602.001
]
[Cites]
Nucleic Acids Res. 2001 Jan 1;29(1):152-5
[
11125075.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21
[
11309499.001
]
[Cites]
Am J Pathol. 2002 Jan;160(1):91-9
[
11786403.001
]
[Cites]
Oncogene. 2002 Jan 17;21(3):475-8
[
11821959.001
]
[Cites]
Nucleic Acids Res. 2002 May 1;30(9):e36
[
11972351.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 May 14;99(10):6567-72
[
12011421.001
]
[Cites]
Nucleic Acids Res. 2001 May 1;29(9):e45
[
11328886.001
]
[Cites]
Nature. 2002 Dec 19-26;420(6917):860-7
[
12490959.001
]
[Cites]
Nucleic Acids Res. 2003 Jan 1;31(1):219-23
[
12519986.001
]
[Cites]
Br J Cancer. 2003 Feb 24;88(4):579-85
[
12592373.001
]
[Cites]
Ai Zheng. 2003 Feb;22(2):123-7
[
12600283.001
]
[Cites]
Exp Cell Res. 2003 Nov 1;290(2):402-13
[
14567997.001
]
[Cites]
Ann Thorac Surg. 2004 Mar;77(3):1008-15
[
14992916.001
]
[Cites]
J Cancer Res Clin Oncol. 1993;119(8):441-9
[
8509434.001
]
[Cites]
Br J Cancer. 1997;75(2):258-63
[
9010035.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Jul 21;95(15):8703-8
[
9671742.001
]
[Cites]
Biochem Biophys Res Commun. 1998 Oct 9;251(1):111-6
[
9790916.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8
[
9843981.001
]
[Cites]
Gastroenterology. 1999 Feb;116(2):277-85
[
9922307.001
]
[Cites]
Br J Cancer. 1999 Feb;79(3-4):595-603
[
10027336.001
]
[Cites]
Am J Surg Pathol. 2005 Mar;29(3):390-9
[
15725809.001
]
[Cites]
Int J Cancer. 2005 May 10;114(6):942-9
[
15645429.001
]
[Cites]
PLoS Biol. 2005 Jun;3(6):e187
[
15869330.001
]
[Cites]
Cancer Cell. 2005 Jun;7(6):499-500
[
15950897.001
]
[Cites]
J Neurochem. 2005 Jul;94(2):520-30
[
15998302.001
]
[Cites]
Nat Genet. 2000 Mar;24(3):227-35
[
10700174.001
]
(PMID = 16952561.001).
[ISSN]
0016-5085
[Journal-full-title]
Gastroenterology
[ISO-abbreviation]
Gastroenterology
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / P30 DK056339; United States / NIDDK NIH HHS / DK / R01 DK063624; United States / NIDDK NIH HHS / DK / P30 DK56339; United States / NIDDK NIH HHS / DK / R01 DK 063624
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Cell Adhesion Molecules; 0 / Chondroitin Sulfate Proteoglycans; 0 / Cspg2 protein, mouse; 0 / DNA, Neoplasm; 0 / Lectins, C-Type; 0 / POSTN protein, human; 0 / VCAN protein, human; 126968-45-4 / Versicans; 9007-34-5 / Collagen
[Other-IDs]
NLM/ NIHMS12359; NLM/ PMC2575112
69.
Steven MJ, Fyfe AH, Raine PA, Watt I:
Esophageal adenocarcinoma: a long-term complication of congenital diaphragmatic hernia?
J Pediatr Surg
; 2007 Jul;42(7):E1-3
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Esophageal
adenocarcinoma
: a long-term complication of congenital diaphragmatic hernia?
A 22-year-old man presented with a lower
esophageal
adenocarcinoma
having been treated for a left-sided congenital diaphragmatic hernia (CDH) as a neonate.
We review the known long-term sequelae of CDH, possible theories for the occurrence
of adenocarcinoma
, and its implications for follow-up of patients with CDH.
[MeSH-major]
Adenocarcinoma
/ etiology.
Esophageal
Neoplasms / etiology. Hernia, Diaphragmatic / complications
[MeSH-minor]
Adult. Biopsy.
Diagnosis
, Differential. Esophagoscopy. Humans. Male. Palliative Care. Tomography, X-Ray Computed
Genetic Alliance.
consumer health - Congenital Diaphragmatic Hernia
.
Genetic Alliance.
consumer health - Diaphragmatic Hernia, Congenital
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17618865.001).
[ISSN]
1531-5037
[Journal-full-title]
Journal of pediatric surgery
[ISO-abbreviation]
J. Pediatr. Surg.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
70.
Pavlov K, Maley CC:
New models of neoplastic progression in Barrett's oesophagus.
Biochem Soc Trans
; 2010 Apr;38(2):331-6
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
New models of neoplastic progression in Barrett's
oesophagus
.
Research in Barrett's
oesophagus
, and neoplastic progression to OAC (
oesophageal
adenocarcinoma
), is hobbled by the lack of good pre-clinical models that capture the evolutionary dynamics of Barrett's cell populations.
Tissue culture models include squamous cell lines, Barrett's
oesophagus
cell lines and OAC cell lines, although it was recognized recently that BIC-1, SEG-1 and TE-7 are not true OAC cell lines.
Some of the unrealistic aspects of the micro-environment in two-dimensional tissue culture may be overcome with the development of three-dimensional organotypic cultures of Barrett's
oesophagus
.
Alternatively, rat surgical models have gained popularity and should be tested for the common genetic features of Barrett's
oesophagus
neoplastic progression in humans including loss of CDKN2A (cyclin-dependent kinase inhibitor 2A) and TP53 (tumour protein 53), generation of aneuploidy and realistic levels of genetic diversity.
This last feature will be important for studying the effects of
cancer
-prevention interventions.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Surg Res. 2000 Feb;88(2):120-4
[
10644476.001
]
[Cites]
Cancer Biol Ther. 2008 Nov;7(11):1753-5
[
18787394.001
]
[Cites]
Cancer Res. 2000 Oct 15;60(20):5767-72
[
11059772.001
]
[Cites]
Artif Life. 2000 Fall;6(4):325-45
[
11348585.001
]
[Cites]
Cell Prolif. 2001 Aug;34(4):253-66
[
11529883.001
]
[Cites]
Dis Esophagus. 2002;15(4):271-7
[
12472470.001
]
[Cites]
Carcinogenesis. 2003 Jul;24(7):1183-90
[
12807723.001
]
[Cites]
Lab Invest. 2004 Jun;84(6):753-65
[
15094711.001
]
[Cites]
Curr Opin Hematol. 2004 Mar;11(2):81-7
[
15257023.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2004 Aug;13(8):1375-84
[
15298961.001
]
[Cites]
Aliment Pharmacol Ther. 2004 Oct;20 Suppl 5:71-80; discussion 95-6
[
15456468.001
]
[Cites]
Clin Cancer Res. 2004 Oct 1;10(19):6703-9
[
15475461.001
]
[Cites]
Cancer Res. 2004 Oct 15;64(20):7629-33
[
15492292.001
]
[Cites]
Arq Gastroenterol. 1983 Apr-Jun;20(2):53-9
[
6661093.001
]
[Cites]
Biophys J. 1987 Aug;52(2):279-94
[
3663832.001
]
[Cites]
Br J Surg. 1988 Feb;75(2):113-5
[
3349294.001
]
[Cites]
J Theor Biol. 1993 Feb 21;160(4):471-91
[
8501919.001
]
[Cites]
Hum Pathol. 1994 Oct;25(10):982-93
[
7927321.001
]
[Cites]
Cancer Lett. 1997 Mar 19;114(1-2):329-31
[
9103323.001
]
[Cites]
J Theor Biol. 1997 May 7;186(1):41-54
[
9176636.001
]
[Cites]
Gastroenterology. 1998 Feb;114(2):295-304
[
9453489.001
]
[Cites]
Cell. 1998 Jun 26;93(7):1159-70
[
9657149.001
]
[Cites]
Carcinogenesis. 1998 Aug;19(8):1445-9
[
9744541.001
]
[Cites]
Br J Cancer. 1999 Feb;79(3-4):595-603
[
10027336.001
]
[Cites]
Carcinogenesis. 1999 Sep;20(9):1801-8
[
10469627.001
]
[Cites]
Carcinogenesis. 2005 Jan;26(1):249-57
[
15498793.001
]
[Cites]
Semin Cancer Biol. 2005 Oct;15(5):329-41
[
15970443.001
]
[Cites]
Cell Prolif. 2006 Jun;39(3):157-81
[
16671995.001
]
[Cites]
Nat Rev Cancer. 2006 Dec;6(12):924-35
[
17109012.001
]
[Cites]
J Theor Biol. 2007 Feb 7;244(3):367-74
[
17049944.001
]
[Cites]
Am J Gastroenterol. 2007 Jan;102(1):21-3
[
17266685.001
]
[Cites]
PLoS Med. 2007 Feb;4(2):e67
[
17326708.001
]
[Cites]
Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4008-13
[
17360468.001
]
[Cites]
World J Gastroenterol. 2007 Mar 7;13(9):1399-407
[
17457972.001
]
[Cites]
Dis Esophagus. 2007;20(3):256-64
[
17509124.001
]
[Cites]
Am J Physiol Gastrointest Liver Physiol. 2007 Jul;293(1):G264-70
[
17431220.001
]
[Cites]
Dis Esophagus. 2007;20(5):372-8
[
17760649.001
]
[Cites]
Cancer Res. 2007 Sep 1;67(17):7996-8001
[
17804709.001
]
[Cites]
Genes Dev. 2007 Nov 1;21(21):2788-803
[
17974918.001
]
[Cites]
Aliment Pharmacol Ther. 2007 Dec;26(11-12):1465-77
[
17900269.001
]
[Cites]
PLoS Comput Biol. 2007 Nov;3(11):e225
[
17997597.001
]
[Cites]
Am J Physiol Gastrointest Liver Physiol. 2007 Dec;293(6):G1106-13
[
17932229.001
]
[Cites]
PLoS Comput Biol. 2007 Dec;3(12):e250
[
18085819.001
]
[Cites]
Cancer Res. 2008 May 1;68(9):3304-13
[
18451157.001
]
[Cites]
Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):15034-9
[
18815380.001
]
[Cites]
Proc Natl Acad Sci U S A. 2008 Oct 21;105(42):16284-9
[
18936480.001
]
[Cites]
PLoS One. 2008;3(10):e3534
[
18953412.001
]
[Cites]
Carcinogenesis. 2009 Jan;30(1):122-30
[
18845559.001
]
[Cites]
Nature. 2009 May 14;459(7244):262-5
[
19329995.001
]
[Cites]
Endoscopy. 2009 Sep;41(9):773-6
[
19746317.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2000 Mar;9(3):249-56
[
10750662.001
]
(PMID = 20298178.001).
[ISSN]
1470-8752
[Journal-full-title]
Biochemical Society transactions
[ISO-abbreviation]
Biochem. Soc. Trans.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P30 CA010815; United States / NCI NIH HHS / CA / R03 CA137811-01; United States / NCI NIH HHS / CA / CA091955-089005; United States / NCI NIH HHS / CA / P01 CA091955; United States / NCI NIH HHS / CA / P01 CA091955-089005; United States / NCI NIH HHS / CA / CA140657-01; United States / NCI NIH HHS / CA / R01 CA140657-01; United States / NCI NIH HHS / CA / CA137811-01; United States / NCI NIH HHS / CA / R03 CA137811; United States / NCI NIH HHS / CA / R03 CA137811-02; United States / NCI NIH HHS / CA / P01 CA91955; United States / NCI NIH HHS / CA / R01 CA140657; United States / NCI NIH HHS / CA / R01 CA119224
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Number-of-references]
53
[Other-IDs]
NLM/ NIHMS199218; NLM/ PMC2866622
71.
Beales IL, Ogunwobi OO:
Leptin synergistically enhances the anti-apoptotic and growth-promoting effects of acid in OE33 oesophageal adenocarcinoma cells in culture.
Mol Cell Endocrinol
; 2007 Aug 15;274(1-2):60-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Leptin synergistically enhances the anti-apoptotic and growth-promoting effects of acid in OE33
oesophageal
adenocarcinoma
cells in culture.
Obesity and gastro-
oesophageal
reflux are the main predisposing factors for
oesophageal
adenocarcinoma
.
We have examined the effects of transient acid exposure and leptin on OE33
oesophageal
adenocarcinoma
cells.
The combination of increased circulating leptin levels in obesity and transient reflux of gastric acid may promote
oesophageal
carcinogenesis by increasing proliferation and inhibiting apoptosis.
[MeSH-major]
Acids / metabolism.
Adenocarcinoma
/ metabolism.
Esophageal
Neoplasms / metabolism. Leptin / metabolism
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17618045.001).
[ISSN]
0303-7207
[Journal-full-title]
Molecular and cellular endocrinology
[ISO-abbreviation]
Mol. Cell. Endocrinol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Acids; 0 / Leptin; 0 / Receptors, Cell Surface; 0 / Receptors, Leptin; 0 / leptin receptor, human; 62229-50-9 / Epidermal Growth Factor; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
72.
Falk J, Carstens H, Lundell L, Albertsson M:
Incidence of carcinoma of the oesophagus and gastric cardia. Changes over time and geographical differences.
Acta Oncol
; 2007;46(8):1070-4
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Incidence of carcinoma of the
oesophagus
and gastric cardia. Changes over time and geographical differences.
BACKGROUND: The incidence
of adenocarcinoma
of the
oesophagus
is rising in many western countries including Sweden.
METHODS: We have studied the latest data concerning this as well as trends in the incidence of squamous cell carcinoma and
adenocarcinoma of
gastric cardia.
Data was extracted from the Swedish
cancer
registry and analyzed regarding gender, age, region, histology and location of tumour.
RESULTS: The results show an increasing incidence
of adenocarcinoma
in both
oesophagus
and gastric cardia.
Adenocarcinoma
is now the most common histological type of
cancer
in
the oesophageal
/cardia region in Sweden.
Results also suggest a possible drift in location
of adenocarcinoma
from gastric cardia towards
oesophagus
.
[MeSH-major]
Adenocarcinoma
/ epidemiology. Carcinoma, Squamous Cell / epidemiology. Cardia.
Esophageal
Neoplasms / epidemiology. Stomach Neoplasms / epidemiology
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17851842.001).
[ISSN]
0284-186X
[Journal-full-title]
Acta oncologica (Stockholm, Sweden)
[ISO-abbreviation]
Acta Oncol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Norway
73.
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
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Quality indicators of surgery for
adenocarcinoma of
the esophagus
and gastroesophageal junction.
Surgical treatment
of adenocarcinoma
of
the esophagus
and gastroesophageal junction is complex and challenging.
As a result there is disagreement on the selection of patients for surgery, type of surgical approach in particular in relation to the extent of lymph node dissection as well as the extent of
esophageal
and/or gastric resection.
[MeSH-major]
Adenocarcinoma
/ surgery.
Esophageal
Neoplasms / surgery. Esophagogastric Junction. Stomach Neoplasms / surgery
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(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
74.
Anand O, Wani S, Sharma P:
When and how to grade Barrett's columnar metaplasia: the Prague system.
Best Pract Res Clin Gastroenterol
; 2008;22(4):661-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Barrett's
oesophagus
(BO), a well-known precursor for
oesophageal
adenocarcinoma
has been generating a great deal of controversy.
The initial step in diagnosing BO requires an accurate endoscopic recognition of the columnar lined
oesophagus
.
A reliable
diagnosis
of BO depends on its effective endoscopic recognition based on the key anatomic landmarks, followed by histological sampling of the columnar-lined epithelium.
Precise localisation of the gastrooesophageal junction is pivotal in the endoscopic
diagnosis
of BO.
Multiple
ad
-hoc grading systems and terminologies of BO have been proposed based on the Z-line appearance, presence or absence of intestinal metaplasia, and the length of Barrett's segment.
[MeSH-major]
Barrett
Esophagus
/ classification. Endoscopy, Gastrointestinal / methods.
Esophagus
/ pathology. Intestinal Mucosa / pathology
[MeSH-minor]
Diagnosis
, Differential. Humans. Metaplasia / pathology. Severity of Illness Index
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18656823.001).
[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]
32
75.
Morgan JL, Khan HN, Lambertz MM:
Oesophageal stenting in a district general hospital.
Surgeon
; 2009 Aug;7(4):203-5
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Oesophageal
stenting in a district general hospital.
BACKGROUND:
Oesophageal
carcinoma is the ninth most common malignancy in the UK with five year survival rate of only 8%.
METHOD: This is a retrospective study of patients presenting to a district general hospital with inoperable
oesophageal
obstruction resulting in stent insertion from December 2000 to September 2006.
Case notes were reviewed for demographics,
diagnosis
, treatment, complication and outcome.
RESULTS: Fifty-seven patients were stented endoscopically by a single surgeon during the study period for incurable
oesophageal
obstruction.
Most common causes were advanced
adenocarcinoma
(34; 60%) and squamous cell carcinoma (16; 28%).
Other rarer causes were benign stricture of the
oesophagus
, lung carcinoma, non-Hodgkin's lymphoma and salivary gland tumour.
Of the 50 patients with
oesophageal
carcinoma, strictures were in the lower third (in 68%), middle third (in 30%) and proximal third (in 2%).
Twenty-four (42%) patients developed a complication, including overgrowth (14; 25%), migration (8; 14%), tracheo-
oesophageal
fistula (2; 4%) and perforation (1; 2%).
CONCLUSION: Endoscopic stenting for advanced
oesophageal
obstruction is a well-tolerated procedure, which is acceptable to patients.
[MeSH-major]
Carcinoma / surgery.
Esophageal
Neoplasms / surgery. Hospitals, District. Hospitals, General. Palliative Care. Stents
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Palliative Care
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19736885.001).
[ISSN]
1479-666X
[Journal-full-title]
The surgeon : journal of the Royal Colleges of Surgeons of Edinburgh and Ireland
[ISO-abbreviation]
Surgeon
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Scotland
76.
Kaijser M, Akre O, Cnattingius S, Ekbom A:
Preterm birth, low birth weight, and risk for esophageal adenocarcinoma.
Gastroenterology
; 2005 Mar;128(3):607-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Preterm birth, low birth weight, and risk for
esophageal
adenocarcinoma
.
BACKGROUND & AIMS: Gastroesophageal reflux is common among preterm infants and those who are small for gestational age, and it is a strong risk factor for
adenocarcinoma of
the esophagus
.
METHODS: In a cohort of 3364 individuals born preterm and/or small for gestational age between 1925 and 1949, we assessed the long-term risk for
esophageal cancer
.
RESULTS: The standardized incidence rate ratio for
esophageal
adenocarcinoma
was increased more than 7-fold in the cohort (standardized incidence rate ratio, 7.27; 95% confidence interval, 1.98-18.62), and a birth weight <2000 g was associated with a more than 11-fold increase in risk (standardized incidence rate ratio, 11.5; 95% confidence interval, 1.39-41.5).
[MeSH-major]
Adenocarcinoma
/ etiology.
Esophageal
Neoplasms / etiology. Infant, Low Birth Weight. Premature Birth / complications
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15765396.001).
[ISSN]
0016-5085
[Journal-full-title]
Gastroenterology
[ISO-abbreviation]
Gastroenterology
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
77.
Colleypriest BJ, Palmer RM, Ward SG, Tosh D:
Cdx genes, inflammation and the pathogenesis of Barrett's metaplasia.
Trends Mol Med
; 2009 Jul;15(7):313-22
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Perhaps one of the best-known examples of metaplasia is Barrett's metaplasia (BM), a pathological condition in which the distal
oesophageal
epithelium switches from stratified squamous to intestinal-type columnar epithelium.
BM predisposes to
oesophageal
adenocarcinoma
and is the consequence of long-term acid bile reflux.
The incidence of BM and
oesophageal
adenocarcinoma
has risen dramatically in recent years.
A key event in the pathogenesis of BM is the induction of
oesophageal
CDX2 expression.
Importantly, recent data reveal the molecular mechanisms that link inflammation in the development of Barrett's metaplasia, CDX2 and the progression to
cancer
.
[MeSH-major]
Barrett
Esophagus
/ immunology. Barrett
Esophagus
/ pathology. Homeodomain Proteins / genetics
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19564133.001).
[ISSN]
1471-499X
[Journal-full-title]
Trends in molecular medicine
[ISO-abbreviation]
Trends Mol Med
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0300415; United Kingdom / Cancer Research UK / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / CDX1 protein, human; 0 / CDX2 Transcription Factor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins
[Number-of-references]
101
78.
Figueroa JD, Terry MB, Gammon MD, Vaughan TL, Risch HA, Zhang FF, Kleiner DE, Bennett WP, Howe CL, Dubrow R, Mayne ST, Fraumeni JF Jr, Chow WH:
Cigarette smoking, body mass index, gastro-esophageal reflux disease, and non-steroidal anti-inflammatory drug use and risk of subtypes of esophageal and gastric cancers by P53 overexpression.
Cancer Causes Control
; 2009 Apr;20(3):361-8
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Cigarette smoking, body mass index, gastro-
esophageal
reflux disease, and non-steroidal anti-inflammatory drug use and risk of subtypes of
esophageal
and gastric cancers by P53 overexpression.
A number of risk factors for
esophageal
and gastric cancers have emerged, yet little is known whether risk factors map to molecular tumor markers such as overexpression of the tumor suppressor TP53.
Using a US multicenter, population-based case-control study (170 cases of
esophageal
adenocarcinomas, 147 gastric cardia adenocarcinomas, 220 non-cardia gastric adenocarcinomas, and 112
esophageal
squamous cell carcinomas), we examined whether the risk associated with cigarette smoking, body mass index (BMI), gastroesophageal reflux disease (GERD), and non-steroidal anti-inflammatory drug (NSAID) use varied by P53 overexpression.
The proportion of cases overexpressing P53 by tumor subtype was 72% for
esophageal
adenocarcinoma
, 69% for gastric cardia
adenocarcinoma
, 52% for non-cardia gastric
adenocarcinoma
, and 67% for
esophageal
squamous cell carcinoma.
For non-cardia gastric
cancer
however, an association with cigarette smoking was suggested for tumors that do not overexpress P53, whereas larger BMI was related to adenocarcinomas that overexpress P53 versus no overexpression.
Overall, this study did not find a clear relationship between P53 protein overexpression and the known risk factors for subtypes of
esophageal
and gastric cancers.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Smoking
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Histochem Cytochem. 1981 Apr;29(4):577-80
[
6166661.001
]
[Cites]
Vojnosanit Pregl. 2005 Dec;62(12):879-85
[
16375215.001
]
[Cites]
Nature. 1991 Jun 6;351(6326):453-6
[
2046748.001
]
[Cites]
Cancer Res. 1994 Jun 1;54(11):2914-8
[
8187077.001
]
[Cites]
Carcinogenesis. 1995 May;16(5):993-1002
[
7767998.001
]
[Cites]
Pathol Res Pract. 1994 Dec;190(12):1141-8
[
7540752.001
]
[Cites]
Int J Cancer. 1996 Jun 21;69(3):225-35
[
8682592.001
]
[Cites]
Cancer. 1997 Feb 1;79(3):425-32
[
9028350.001
]
[Cites]
Cancer Causes Control. 2000 Mar;11(3):231-8
[
10782657.001
]
[Cites]
Mod Pathol. 2001 May;14(5):397-403
[
11353048.001
]
[Cites]
Nat Rev Cancer. 2001 Dec;1(3):233-40
[
11902578.001
]
[Cites]
Oncology. 2002;62(2):175-9
[
11914604.001
]
[Cites]
Hum Mutat. 2002 Jun;19(6):607-14
[
12007217.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2002 Aug;11(8):745-52
[
12163328.001
]
[Cites]
Gastroenterology. 2003 Jan;124(1):47-56
[
12512029.001
]
[Cites]
Br J Cancer. 2003 Nov 3;89(9):1729-35
[
14583777.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2004 Jan;13(1):34-9
[
14744730.001
]
[Cites]
Cancer Res. 2004 Mar 1;64(5):1561-9
[
14996709.001
]
[Cites]
Semin Oncol. 2004 Aug;31(4):450-64
[
15297938.001
]
[Cites]
J Natl Cancer Inst. 1997 Sep 3;89(17):1277-84
[
9293918.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1997 Oct;6(10):779-82
[
9332759.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1997 Dec;6(12):1065-9
[
9419404.001
]
[Cites]
J Natl Cancer Inst. 1998 Jan 21;90(2):150-5
[
9450576.001
]
[Cites]
Br J Cancer. 1998;77(2):277-86
[
9460999.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1998 Feb;7(2):97-102
[
9488582.001
]
[Cites]
Carcinogenesis. 1999 Apr;20(4):591-7
[
10223186.001
]
[Cites]
J Pathol. 1999 Jan;187(1):8-18
[
10341702.001
]
[Cites]
Ann Intern Med. 1999 Jun 1;130(11):883-90
[
10375336.001
]
[Cites]
Ann Surg. 2005 Jan;241(1):63-8
[
15621992.001
]
[Cites]
Clin Gastroenterol Hepatol. 2005 Mar;3(3):225-30
[
15765441.001
]
[Cites]
Cancer Causes Control. 2005 Apr;16(3):285-94
[
15947880.001
]
[Cites]
Ann Intern Med. 2005 Aug 2;143(3):199-211
[
16061918.001
]
[Cites]
J Histochem Cytochem. 1991 Jun;39(6):741-8
[
1709656.001
]
(PMID = 18989634.001).
[ISSN]
1573-7225
[Journal-full-title]
Cancer causes & control : CCC
[ISO-abbreviation]
Cancer Causes Control
[Language]
ENG
[Grant]
None / None / / U01 CA057923-03; United States / NCI NIH HHS / CA / U01 CA057949; United States / NCI NIH HHS / CA / U01 CA057983; None / None / / U01 CA057983-03; United States / Intramural NIH HHS / / Z01 CP010136-12; United States / NCI NIH HHS / CA / U01 CA057923; United States / NCI NIH HHS / CA / U01 CA 57923; United States / NCI NIH HHS / CA / U01 CA057949-03; United States / NCI NIH HHS / CA / U01 CA057923-03; United States / NCI NIH HHS / CA / U01 CA057983-03; United States / NCI NIH HHS / CA / U01 CA 57983; United States / NCI NIH HHS / CA / U01 CA 57049; None / None / / U01 CA057949-03
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Tumor Suppressor Protein p53
[Other-IDs]
NLM/ NIHMS100106; NLM/ PMC2726999
79.
Cook MB, Greenwood DC, Hardie LJ, Wild CP, Forman D:
A systematic review and meta-analysis of the risk of increasing adiposity on Barrett's esophagus.
Am J Gastroenterol
; 2008 Feb;103(2):292-300
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
A systematic review and meta-analysis of the risk of increasing adiposity on Barrett's
esophagus
.
OBJECTIVES:
Esophageal
adenocarcinoma
and its precursor lesion, Barrett's
esophagus
, are increasing in incidence in western populations.
Gastroesophageal reflux disease (GERD) and high body mass index (BMI) are known risk factors, but it is unclear whether BMI mediates its risk on Barrett's
esophagus
independently.
This systematic review and meta-analysis investigated whether increasing BMI is associated with Barrett's
esophagus
as compared to general population and GERD controls.
Studies to be included were required to present "current" BMI data for consecutively recruited Barrett's
esophagus
patients and appropriate comparison arms with a minimum number of 30 subjects in each.
Nine studies comparing the BMI of the Barrett's
esophagus
and GERD groups produced a pooled odds ratio (OR) of 0.99 per kg/m2 (95% confidence interval [CI] 0.97-1.01, I2= 52%), while the pooled estimate of three studies comparing Barrett's
esophagus
with general population controls was 1.02 per kg/m2 (95% CI 1.01-1.04, I2= 0%).
CONCLUSIONS: Increasing adiposity is only an indirect risk factor of Barrett's
esophagus
through the precursor lesion of GERD.
Hence, BMI status has no predictive value with respect to GERD patients and their risk of progression to Barrett's
esophagus
.
[MeSH-major]
Adipose Tissue. Barrett
Esophagus
/ epidemiology. Barrett
Esophagus
/ etiology. Body Mass Index. Gastroesophageal Reflux / complications
Genetic Alliance.
consumer health - Barrett's Esophagus
.
MedlinePlus Health Information.
consumer health - GERD
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Am J Gastroenterol. 2008 Feb;103(2):301-3
[
18289199.001
]
[CommentIn]
Am J Gastroenterol. 2008 May;103(5):1316-7
[
18477363.001
]
(PMID = 17986313.001).
[ISSN]
0002-9270
[Journal-full-title]
The American journal of gastroenterology
[ISO-abbreviation]
Am. J. Gastroenterol.
[Language]
eng
[Publication-type]
Journal Article; Meta-Analysis; Review
[Publication-country]
United States
[Number-of-references]
55
80.
Bani-Hani KE, Bani-Hani BK:
Columnar lined (Barrett's) esophagus: future perspectives.
J Gastroenterol Hepatol
; 2008 Feb;23(2):178-91
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Columnar lined (Barrett's)
esophagus
: future perspectives.
Columnar lined
esophagus
(CLE) or Barrett's
esophagus
is the precursor for
esophageal
adenocarcinoma
.
The rapid increase in incidence of CLE and
adenocarcinoma
raises serious concerns that the current management of gastroesophageal reflux disease (GERD) needs reassessment.
The benefit of surveillance strategies remains unproven and the ideal endoscopic frequency, protocols and markers of
cancer
risk are unknown.
Dysplasia may not provide the gold standard marker of
cancer
risk because of some inherited problems.
To overcome the limitations of histological markers, many other markers of
cancer
risk needs to be developed and validated.
The key question as to whether
cancer
risk is actually reduced by the new ablation modalities remains unanswered.
[MeSH-major]
Barrett
Esophagus
[MeSH-minor]
Adenocarcinoma
/ epidemiology.
Adenocarcinoma
/ etiology.
Adenocarcinoma
/ prevention & control. Biomarkers.
Diagnosis
, Differential.
Esophageal
Neoplasms / epidemiology.
Esophageal
Neoplasms / etiology.
Esophageal
Neoplasms / prevention & control. Gastroenterology / trends. Gastroesophageal Reflux / complications. Gastroesophageal Reflux /
diagnosis
. Humans. Incidence. Intestines / pathology. Metaplasia. Precancerous Conditions / complications. Precancerous Conditions /
diagnosis
. Precancerous Conditions / epidemiology. Precancerous Conditions / therapy. Risk Factors
Genetic Alliance.
consumer health - Barrett's Esophagus
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17854426.001).
[ISSN]
1440-1746
[Journal-full-title]
Journal of gastroenterology and hepatology
[ISO-abbreviation]
J. Gastroenterol. Hepatol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Australia
[Chemical-registry-number]
0 / Biomarkers
[Number-of-references]
122
81.
Wilkins T, Gillies RA:
Office-based unsedated ultrathin esophagoscopy in a primary care setting.
Ann Fam Med
; 2005 Mar-Apr;3(2):126-30
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
PURPOSE: Gastroesophageal reflux disease is common and with time may be complicated by Barrett's
esophagus
and
esophageal
adenocarcinoma
.
Upper gastrointestinal endoscopy, including esophagoscopy, is the procedure of choice to diagnose Barrett's
esophagus
and other
esophageal
disease.
Barrett's
esophagus
was diagnosed in 5.7% (n = 3) of the patients.
UUE may be an efficient method of examining the distal
esophagus
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Gastrointest Endosc. 2000 Jun;51(6):786-9
[
10840336.001
]
[Cites]
J Thorac Cardiovasc Surg. 1993 Mar;105(3):383-7; discussion 387-8
[
8445916.001
]
[Cites]
Curr Probl Cancer. 2000 Nov-Dec;24(6):297-373
[
11198836.001
]
[Cites]
Otolaryngol Head Neck Surg. 2001 Sep;125(3):170-5
[
11555750.001
]
[Cites]
Otolaryngol Head Neck Surg. 2001 Dec;125(6):588-9
[
11743456.001
]
[Cites]
Gastrointest Endosc. 2002 Apr;55(4):484-7
[
11923758.001
]
[Cites]
Gastrointest Endosc. 2002 May;55(6):620-3
[
11979240.001
]
[Cites]
Gastroenterology. 2002 Aug;123(2):461-7
[
12145799.001
]
[Cites]
Gastrointest Endosc. 2002 Aug;56(2):180-9
[
12145594.001
]
[Cites]
Am J Gastroenterol. 2002 Aug;97(8):1888-95
[
12190150.001
]
[Cites]
Gastrointest Endosc. 2002 Oct;56(4):472-8
[
12297760.001
]
[Cites]
Am J Med. 2002 Oct 15;113(6):499-505
[
12427500.001
]
[Cites]
Laryngoscope. 2002 Dec;112(12):2242-3
[
12461347.001
]
[Cites]
Gastrointest Endosc. 2003 Mar;57(3):300-4
[
12612506.001
]
[Cites]
Gastrointest Endosc. 2003 Mar;57(3):305-10
[
12612507.001
]
[Cites]
Gastrointest Endosc. 2003 Mar;57(3):311-8
[
12612508.001
]
[Cites]
Am J Gastroenterol. 2003 Sep;98(9):1931-9
[
14499768.001
]
[Cites]
Am J Gastroenterol. 2003 Nov;98(11):2342-4
[
14638331.001
]
[Cites]
Am J Gastroenterol. 2003 Nov;98(11):2383-9
[
14638337.001
]
[Cites]
Gastrointest Endosc. 2004 Mar;59(3):349-54
[
14997130.001
]
[Cites]
Gastroenterology. 2004 Jul;127(1):310-30
[
15236196.001
]
[Cites]
J Fam Pract. 1982 Apr;14(4):757, 762-3 passim
[
7069393.001
]
[Cites]
Gastrointest Endosc. 1982 Nov;28(4):233-6
[
7173573.001
]
[Cites]
N Engl J Med. 1986 Aug 7;315(6):362-71
[
2874485.001
]
[Cites]
Gastroenterology. 1990 Oct;99(4):918-22
[
2394347.001
]
[Cites]
N Engl J Med. 1994 Sep 8;331(10):656-60
[
8052276.001
]
[Cites]
Gastroenterology. 1995 Mar;108(3):697-704
[
7875472.001
]
[Cites]
Endoscopy. 1996 Mar;28(3):277-82
[
8781790.001
]
[Cites]
Endoscopy. 2000 Dec;32(12):971-3
[
11147947.001
]
(PMID = 15798038.001).
[ISSN]
1544-1717
[Journal-full-title]
Annals of family medicine
[ISO-abbreviation]
Ann Fam Med
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ PMC1466858
82.
Milano F, Guarriera M, Rygiel AM, Krishnadath KK:
Trastuzumab mediated T-cell response against HER-2/neu overexpressing esophageal adenocarcinoma depends on intact antigen processing machinery.
PLoS One
; 2010 Aug 26;5(8):e12424
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Trastuzumab mediated T-cell response against HER-2/neu overexpressing
esophageal
adenocarcinoma
depends on intact antigen processing machinery.
BACKGROUND:
Esophageal
adenocarcinoma
(EAC) is a highly aggressive disease with poor prognosis, which frequently exhibits HER-2 gene amplification.
This enhances the ability of HER-2 specific cytotoxic T lymphocytes (CTLs) to recognize and kill
cancer
cells.
[MeSH-major]
ATP-Binding Cassette Transporters / immunology.
Adenocarcinoma
/ immunology. Antibodies, Monoclonal / pharmacology. Antigen Presentation / drug effects.
Esophageal
Neoplasms / immunology. Gene Expression / drug effects. Receptor, ErbB-2 / genetics. T-Lymphocytes / immunology
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
Hazardous Substances Data Bank.
Trastuzumab
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Chest Surg Clin N Am. 2000 Aug;10(3):441-50
[
10967749.001
]
[Cites]
J Natl Cancer Inst. 2010 Feb 24;102(4):271-4
[
20075370.001
]
[Cites]
N Engl J Med. 2001 Mar 15;344(11):783-92
[
11248153.001
]
[Cites]
Int J Oncol. 2001 Dec;19(6):1211-20
[
11713591.001
]
[Cites]
Cancer Res. 2001 Dec 15;61(24):8647-50
[
11751378.001
]
[Cites]
Cancer Immunol Immunother. 2002 Jan;50(11):615-24
[
11807625.001
]
[Cites]
Lancet Oncol. 2002 Mar;3(3):137-44
[
11902499.001
]
[Cites]
Cancer Res. 2002 Apr 15;62(8):2244-7
[
11956077.001
]
[Cites]
Am J Clin Pathol. 2002 Jul;118(1):60-6
[
12109857.001
]
[Cites]
Cancer Res. 2002 Oct 15;62(20):5813-7
[
12384543.001
]
[Cites]
Clin Cancer Res. 2002 Nov;8(11):3394-400
[
12429626.001
]
[Cites]
Clin Cancer Res. 2002 Nov;8(11):3407-18
[
12429628.001
]
[Cites]
Clin Cancer Res. 2003 Aug 15;9(9):3448-53
[
12960136.001
]
[Cites]
World J Surg. 2003 Sep;27(9):999-1008; discussion 1006-8
[
12917764.001
]
[Cites]
J Neurooncol. 2004 Jan;66(1-2):1-8
[
15015764.001
]
[Cites]
J Clin Oncol. 2004 Mar 15;22(6):1063-70
[
15020607.001
]
[Cites]
Ann Thorac Surg. 2004 Apr;77(4):1193-8; discussion 1198-9
[
15063233.001
]
[Cites]
Clin Cancer Res. 2004 Apr 1;10(7):2538-44
[
15073134.001
]
[Cites]
Int J Oncol. 2004 Aug;25(2):487-91
[
15254748.001
]
[Cites]
Ann Thorac Surg. 2004 Nov;78(5):1790-800
[
15511476.001
]
[Cites]
Hum Pathol. 1993 Oct;24(10):1127-34
[
8104858.001
]
[Cites]
Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3353-7
[
7724565.001
]
[Cites]
N Engl J Med. 1997 Jul 17;337(3):161-7
[
9219702.001
]
[Cites]
Semin Oncol. 1999 Aug;26(4 Suppl 12):51-9
[
10482194.001
]
[Cites]
Clin Cancer Res. 2005 Apr 1;11(7):2552-60
[
15814633.001
]
[Cites]
Clin Cancer Res. 2005 Jul 1;11(13):4898-904
[
16000588.001
]
[Cites]
Cancer Immunol Immunother. 2006 Jan;55(1):85-95
[
15948002.001
]
[Cites]
J Immunother. 2006 Jan-Feb;29(1):53-60
[
16365600.001
]
[Cites]
J Immunol. 2006 Mar 15;176(6):3402-9
[
16517708.001
]
[Cites]
Cancer Res. 2006 May 15;66(10):5452-60
[
16707474.001
]
[Cites]
Clin Cancer Res. 2006 Aug 15;12(16):4925-32
[
16914581.001
]
[Cites]
Mod Pathol. 2007 Jan;20(1):120-9
[
17143264.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2007 Feb 1;67(2):405-9
[
17097832.001
]
[Cites]
J Immunol Methods. 2007 Apr 10;321(1-2):94-106
[
17336322.001
]
[Cites]
Cancer. 2007 May 15;109(10):1980-8
[
17385213.001
]
[Cites]
Cancer Immunol Immunother. 2007 Dec;56(12):1967-77
[
17564704.001
]
[Cites]
Cancer Immunol Immunother. 2008 Feb;57(2):197-206
[
17622526.001
]
[Cites]
Cancer Immunol Immunother. 2008 Nov;57(11):1719-26
[
18408926.001
]
[Cites]
Anal Cell Pathol. 2000;20(1):25-32
[
11007435.001
]
(PMID = 20865050.001).
[ISSN]
1932-6203
[Journal-full-title]
PloS one
[ISO-abbreviation]
PLoS ONE
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 3; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 145892-13-3 / TAP2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2; P188ANX8CK / Trastuzumab
[Other-IDs]
NLM/ PMC2928738
83.
Vega KJ, Jamal MM, Wiggins CL:
Changing pattern of esophageal cancer incidence in New Mexico: a 30-year evaluation.
Dig Dis Sci
; 2010 Jun;55(6):1622-6
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Changing pattern of
esophageal cancer
incidence in New Mexico: a 30-year evaluation.
BACKGROUND AND AIM: The incidence of
esophageal
adenocarcinoma
has increased over the last 30 years, especially in non-Hispanic whites (nHw).
It is important to understand the effect of ethnicity on
cancer
occurrence over a prolonged interval.
METHODS: We searched the New Mexico Tumor Registry for all cases of
esophageal cancer
from 1 January 1973 to 31 December 2002.
Inclusion criteria were histologic
diagnosis
of adenocarcinoma
or squamous cell carcinoma, ethnicity and gender.
Esophageal
adenocarcinoma
incidence rates/100,000 population increased significantly over 30 years; 1973-1977, 0.4 cases; 1978-1982, 0.4 cases; 1983-1987, 0.6 cases; 1988-1992, 1.2 cases, 1993-1997, 1.6 cases and 1998-2002, 2.2 cases; P < 0.001.
In nHw and HA,
adenocarcinoma
incidence rates increased significantly during the study period.
CONCLUSIONS:
Esophageal
adenocarcinoma
incidence among nHw and HA increased from 1973 to 2002 in New Mexico.
Ethnicity may influence the histology or indicate an increased risk for certain types of
esophageal cancer
.
[MeSH-major]
Adenocarcinoma
/ ethnology. Carcinoma, Squamous Cell / ethnology.
Esophageal
Neoplasms / ethnology. Ethnic Groups / statistics & numerical data
Genetic Alliance.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Assoc Acad Minor Phys. 1999;10(2):44-7
[
10826008.001
]
[Cites]
CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96
[
18287387.001
]
[Cites]
Am J Gastroenterol. 2004 Apr;99(4):582-8
[
15089886.001
]
[Cites]
N Engl J Med. 1985 Oct 3;313(14):857-9
[
4033716.001
]
[Cites]
Gastroenterology. 1987 Jan;92(1):118-24
[
3781178.001
]
[Cites]
Cancer. 1988 Feb 1;61(3):612-7
[
3338027.001
]
[Cites]
Am J Gastroenterol. 1989 Dec;84(12):1494-6
[
2596449.001
]
[Cites]
Br J Cancer. 1990 Sep;62(3):440-3
[
2206952.001
]
[Cites]
JAMA. 1991 Mar 13;265(10):1287-9
[
1995976.001
]
[Cites]
Arch Intern Med. 1991 Nov;151(11):2212-6
[
1953225.001
]
[Cites]
Gastroenterology. 1993 Feb;104(2):510-3
[
8425693.001
]
[Cites]
Endoscopy. 1995 Jan;27(1):19-26
[
7601030.001
]
[Cites]
J Clin Gastroenterol. 1995 Oct;21(3):254-5
[
8648065.001
]
[Cites]
Ann Clin Lab Sci. 1996 Nov-Dec;26(6):480-6
[
8908317.001
]
[Cites]
J Clin Gastroenterol. 1998 Jan;26(1):11-3
[
9492855.001
]
[Cites]
Dig Dis Sci. 1998 May;43(5):1038-41
[
9590419.001
]
[Cites]
J Natl Med Assoc. 2005 Nov;97(11):1471-8
[
16334494.001
]
[Cites]
Cancer Causes Control. 2007 Aug;18(6):585-93
[
17406989.001
]
[Cites]
Clin Gastroenterol Hepatol. 2008 Jan;6(1):30-4
[
18063419.001
]
[Cites]
Am J Gastroenterol. 2000 Sep;95(9):2352-6
[
11007241.001
]
(PMID = 19688596.001).
[ISSN]
1573-2568
[Journal-full-title]
Digestive diseases and sciences
[ISO-abbreviation]
Dig. Dis. Sci.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2882567
84.
Bradbury PA, Zhai R, Hopkins J, Kulke MH, Heist RS, Singh S, Zhou W, Ma C, Xu W, Asomaning K, Ter-Minassian M, Wang Z, Su L, Christiani DC, Liu G:
Matrix metalloproteinase 1, 3 and 12 polymorphisms and esophageal adenocarcinoma risk and prognosis.
Carcinogenesis
; 2009 May;30(5):793-8
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Matrix metalloproteinase 1, 3 and 12 polymorphisms and
esophageal
adenocarcinoma
risk and prognosis.
We studied the association between four MMP polymorphisms within three MMP genes and
esophageal
adenocarcinoma
(EA) risk and prognosis.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Int J Cancer. 2002 Dec 10;102(5):526-9
[
12432557.001
]
[Cites]
Cancer Res. 2002 May 15;62(10):2819-23
[
12019159.001
]
[Cites]
J Natl Cancer Inst. 2003 Sep 17;95(18):1404-13
[
13130116.001
]
[Cites]
Br J Cancer. 2003 Dec 1;89(11):2116-21
[
14647147.001
]
[Cites]
Anticancer Res. 2004 May-Jun;24(3b):2021-6
[
15274394.001
]
[Cites]
J Biol Chem. 1996 May 31;271(22):13055-60
[
8662692.001
]
[Cites]
Am J Gastroenterol. 1997 Feb;92(2):193-4
[
9040189.001
]
[Cites]
J Pathol. 1998 Jul;185(3):256-61
[
9771478.001
]
[Cites]
Cancer Res. 1998 Dec 1;58(23):5321-5
[
9850057.001
]
[Cites]
Ann N Y Acad Sci. 1998 Oct 23;857:180-93
[
9917841.001
]
[Cites]
N Engl J Med. 1999 Mar 18;340(11):825-31
[
10080844.001
]
[Cites]
Carcinogenesis. 2005 Feb;26(2):481-6
[
15528217.001
]
[Cites]
Breast Cancer Res. 2005;7(4):R506-12
[
15987457.001
]
[Cites]
Carcinogenesis. 2006 May;27(5):1024-9
[
16311244.001
]
[Cites]
World J Gastroenterol. 2007 Feb 7;13(5):676-82
[
17278189.001
]
[Cites]
Carcinogenesis. 2007 Jun;28(6):1254-8
[
17264068.001
]
[Cites]
BMC Cancer. 2007;7:187
[
17919326.001
]
[Cites]
Clin Cancer Res. 2008 May 15;14(10):3216-22
[
18483390.001
]
[Cites]
Cancer Causes Control. 2008 Dec;19(10):1077-83
[
18478337.001
]
[Cites]
Cell. 2000 Jan 7;100(1):57-70
[
10647931.001
]
[Cites]
Circ Res. 2000 May 12;86(9):998-1003
[
10807873.001
]
[Cites]
Aliment Pharmacol Ther. 2001 Aug;15(8):1087-100
[
11472311.001
]
[Cites]
Br J Cancer. 2001 Aug 3;85(3):383-92
[
11487270.001
]
[Cites]
Cancer. 2001 Aug 1;92(3):549-55
[
11505399.001
]
[Cites]
Cancer Res. 2001 Nov 1;61(21):7825-9
[
11691799.001
]
[Cites]
Nat Rev Cancer. 2002 Mar;2(3):161-74
[
11990853.001
]
[Cites]
Am J Respir Crit Care Med. 2003 Apr 15;167(8):1083-9
[
12522030.001
]
(PMID = 19321798.001).
[ISSN]
1460-2180
[Journal-full-title]
Carcinogenesis
[ISO-abbreviation]
Carcinogenesis
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA074386
[Publication-type]
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 3.4.24.65 / Matrix Metalloproteinase 12; EC 3.4.24.7 / Matrix Metalloproteinase 1
[Other-IDs]
NLM/ PMC2675656
85.
Shirin H, Leja M, Niv Y:
Helicobacter pylori and non-malignant diseases.
Helicobacter
; 2008 Oct;13 Suppl 1:23-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
The main problems remain unsolved: peptic ulcer disease negative for H. pylori, synergism of H. pylori infection and aspirin and other nonsteroidal anti-inflammatory drugs or cyclooxygenase 2 specific inhibitors, the role of H. pylori eradication in uninvestigated and nonulcer dyspepsia, and the possible protective effect of H. pylori infection against gastroesophageal reflux disease and its complications such as Barrett's
esophagus
and
adenocarcinoma
.
MedlinePlus Health Information.
consumer health - Helicobacter Pylori Infections
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18783518.001).
[ISSN]
1523-5378
[Journal-full-title]
Helicobacter
[ISO-abbreviation]
Helicobacter
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal
86.
Barritt AS 4th, Shaheen NJ:
Should patients with Barrett's oesophagus be kept under surveillance? The case against.
Best Pract Res Clin Gastroenterol
; 2008;22(4):741-50
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Should patients with Barrett's
oesophagus
be kept under surveillance? The case against.
Barrett's
oesophagus
, or columnar metaplasia of the
oesophagus
, is a known risk factor for
adenocarcinoma of
the
oesophagus
.
Barrett's
oesophagus
is thought to be the result of longstanding gastro-
oesophageal
reflux disease, a very common
diagnosis
in the United States and other western countries.
Because Barrett's
oesophagus
is a transition state between a common complaint and a devastating illness, endoscopic screening and surveillance strategies are commonly employed.
However, neither screening nor surveillance strategies have been proven to reduce mortality from
oesophageal
adenocarcinoma
.
We address the multifaceted case against surveillance for
oesophageal
adenocarcinoma
.
The overall incidence of
oesophageal
adenocarcinoma
is very low, especially compared to other cancers where surveillance is used.
The pace of progression from Barrett's to
adenocarcinoma
is not known.
There are drawbacks to endoscopic surveillance for dysplasia and
adenocarcinoma
in patients with established Barrett's
oesophagus
that include sampling error, inconsistent pathologic interpretation of biopsies, and cost.
Taken individually or together, these limitations make a strong case against surveillance endoscopy in Barrett's
oesophagus
.
[MeSH-major]
Barrett
Esophagus
/
diagnosis
. Endoscopy, Gastrointestinal / contraindications. Mass Screening / methods. Population Surveillance / methods
[MeSH-minor]
Esophageal
Neoplasms /
diagnosis
.
Esophageal
Neoplasms / prevention & control. Humans. Prognosis. Risk Factors
[Email]
Email this result item
Email the results to the following email address: