BioMedLib Search Engine
[ goto HOMEPAGE ]
Locate the most relevant articles, quickly.
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
adenomatous colonic polyps 2005:2010[pubdate] *count=100
749 results
Searchbox
Export
PDF
RSS
Email
Delete
Email this search result to the following email address:
[X] Close
Expand the query
'
adenomatous colonic polyps
' 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 749
1.
Vandrovcova J, Lagerstedt-Robinsson K, Påhlman L, Lindblom A:
Somatic BRAF-V600E mutations in familial colorectal cancer.
Cancer Epidemiol Biomarkers Prev
; 2006 Nov;15(11):2270-3
[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.
The BRAF gene is mutated in 4% to 12% of unselected colorectal cancers, particularly those with high microsatellite instability and in premalignant lesions, such as serrated
adenomas
and hyperplastic
polyps
.
To evaluate the role of oncogenic BRAF mutations in
non
-hereditary nonpolyposis colorectal cancer/
non
-familial
adenomatous
polyposis familial colorectal cancer, we did a mutation screening of the most common BRAF mutation, the V600E mutation, in 194 colorectal tumors from patients with a positive family history of the disease.
Interestingly, families with extracolonic tumors showed a much higher mutation frequency (17.5%) compared with families with
colonic
cancer only (3.5%; P = 0.009).
Subjects from families where the V600E mutation was identified had less
adenomas
compared with those from families where no BRAF mutation had been found (odds ratio, 8.5; 95% confidence interval, 1.1-64.6).
These findings indicate that
adenomas
might be less important in the cancer development in the group of families with BRAF-V600E mutations and indirectly support a previous hypothesis that tumors might develop through the hyperplastic
polyp
-serrated
adenoma
pathway.
Genetic Alliance.
consumer health - Colorectal Cancer
.
Genetic Alliance.
consumer health - Familial Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Colorectal 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 = 17119056.001).
[ISSN]
1055-9965
[Journal-full-title]
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
[ISO-abbreviation]
Cancer Epidemiol. Biomarkers Prev.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
2.
Dubé C, Rostom A, Lewin G, Tsertsvadze A, Barrowman N, Code C, Sampson M, Moher D, U.S. Preventive Services Task Force:
The use of aspirin for primary prevention of colorectal cancer: a systematic review prepared for the U.S. Preventive Services Task Force.
Ann Intern Med
; 2007 Mar 6;146(5):365-75
[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.
DATA SYNTHESIS: Regular use of aspirin reduced the incidence of
colonic
adenomas
in RCTs (relative risk [RR], 0.82 [95% CI, 0.7 to 0.95]), case-control studies (RR, 0.87 [CI, 0.77 to 0.98]), and cohort studies (RR, 0.72 [CI, 0.61 to 0.85]).
CONCLUSIONS: Aspirin appears to be effective at reducing the incidence of
colonic
adenoma
and colorectal cancer, especially if used in high doses for more than 10 years.
[MeSH-major]
Anti-Inflammatory Agents,
Non
-Steroidal / therapeutic use. Aspirin / therapeutic use. Colorectal Neoplasms / prevention & control. Primary Prevention
[MeSH-minor]
Adenoma
/ prevention & control. Adult. Cardiovascular Diseases / chemically induced.
Colonic Polyps
/ prevention & control. Female. Gastrointestinal Diseases / chemically induced. Humans. Incidence. Male. United States / epidemiology
Genetic Alliance.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
ACETYLSALICYLIC ACID
.
PubMed Health.
DARE review
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
ACP J Club. 2007 Jul-Aug;147(1):15-6
[
17608380.001
]
[CommentIn]
Gastroenterology. 2007 Aug;133(2):717-8
[
17681190.001
]
[CommentIn]
Ann Intern Med. 2007 Nov 6;147(9):674; author reply 674-5
[
17975195.001
]
[SummaryForPatientsIn]
Ann Intern Med. 2007 Mar 6;146(5):I35
[
17339615.001
]
(PMID = 17339622.001).
[ISSN]
1539-3704
[Journal-full-title]
Annals of internal medicine
[ISO-abbreviation]
Ann. Intern. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; R16CO5Y76E / Aspirin
[Number-of-references]
61
3.
Johnson CC, Hayes RB, Schoen RE, Gunter MJ, Huang WY, PLCO Trial Team:
Non-steroidal anti-inflammatory drug use and colorectal polyps in the Prostate, Lung, Colorectal, And Ovarian Cancer Screening Trial.
Am J Gastroenterol
; 2010 Dec;105(12):2646-55
[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]
Non
-steroidal anti-inflammatory drug use and colorectal
polyps
in the Prostate, Lung, Colorectal, And Ovarian Cancer Screening Trial.
OBJECTIVES:
Non
-steroidal anti-inflammatory drugs (NSAIDs) have been documented in animal and human studies to reduce risk for colorectal cancer and
adenomatous polyps
, but risk modification for subgroups of the population and effects on hyperplastic
polyps
have been less studied.
Follow-up of detected
polyps
was accomplished outside the Trial setting and relevant records were sought and abstracted.
Cases (n=4,017) included subjects with a biopsy-proven
polyp
in the left side of the
colon
(descending
colon
, sigmoid, and rectum) detected as a consequence of PLCO screening; controls (n=38,396) were subjects with no left-sided
colon polyp
.
RESULTS: Regular use of aspirin (≥ 4 times/month) in the past year was inversely associated with hyperplastic
polyps
(odds ratios (OR)=0.8, 95% confidence interval (CI)=0.7-0.9),
adenomatous polyps
(OR=0.8, 95% CI=0.8-0.9), and advanced
adenomas
(OR=0.8, 95% CI=0.7-0.9).
As frequency of aspirin use increased, the prevalence of
polyps
decreased significantly for each histological classification (P for trend ≤ 0.0004).
Similar patterns were found for
adenomas
and ibuprofen.
Overall protection was consistent in both the descending
colon
or sigmoid and the rectum, but more evident in males.
CONCLUSIONS: This study of a large general risk population supports previous work that recent use of aspirin and ibuprofen is associated with a decreased risk of colorectal
adenomas
and demonstrates that this protective effect may be stronger in certain population subgroups and is also evident for aspirin and hyperplastic
polyps
.
[MeSH-major]
Anti-Inflammatory Agents,
Non
-Steroidal / therapeutic use. Aspirin / therapeutic use.
Colonic Polyps
/ prevention & control. Ibuprofen / therapeutic use
Genetic Alliance.
consumer health - Colorectal Cancer
.
Genetic Alliance.
consumer health - Lung Cancer
.
Genetic Alliance.
consumer health - Ovarian cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
IBUPROFEN
.
Hazardous Substances Data Bank.
ACETYLSALICYLIC ACID
.
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 Causes Control. 2005 Oct;16(8):965-73
[
16132805.001
]
[Cites]
Curr Ther Res Clin Exp. 2004 Jul;65(4):345-52
[
24672089.001
]
[Cites]
Int J Epidemiol. 2007 Oct;36(5):957-9
[
17921194.001
]
[Cites]
Gastroenterology. 2008 Jan;134(1):341-3
[
18166360.001
]
[Cites]
Ann Intern Med. 2007 Mar 6;146(5):376-89
[
17339623.001
]
[Cites]
N Engl J Med. 2005 Mar 31;352(13):1293-304
[
15753114.001
]
[Cites]
Oncol Rep. 2005 Apr;13(4):559-83
[
15756426.001
]
[Cites]
N Engl J Med. 2003 Mar 6;348(10):891-9
[
12621133.001
]
[Cites]
Annu Rev Med. 2000;51:511-23
[
10774479.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2008 Apr;17(4):827-33
[
18398023.001
]
[Cites]
JAMA. 2003 Dec 10;290(22):2959-67
[
14665657.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 Jul;14(7):1613-8
[
16030091.001
]
[Cites]
BMJ. 2000 Nov 11;321(7270):1183-7
[
11073508.001
]
[Cites]
Science. 2005 Jun 10;308(5728):1572
[
15947169.001
]
[Cites]
Med Sci Monit. 2001 Jul-Aug;7(4):837-41
[
11433218.001
]
[Cites]
N Engl J Med. 1995 Sep 7;333(10):609-14
[
7637720.001
]
[Cites]
N Engl J Med. 2005 Mar 31;352(13):1366-8
[
15755763.001
]
[Cites]
Ann Intern Med. 2004 Feb 3;140(3):157-66
[
14757613.001
]
[Cites]
Ann Intern Med. 1994 Aug 15;121(4):241-6
[
8037405.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1998 Mar;7(3):227-30
[
9521438.001
]
[Cites]
Gastroenterology. 2008 Jan;134(1):21-8
[
18005960.001
]
[Cites]
Gastroenterology. 2008 Jan;134(1):29-38
[
18022173.001
]
[Cites]
N Engl J Med. 2003 Mar 6;348(10):883-90
[
12621132.001
]
[Cites]
Cancer Res. 2001 May 1;61(9):3566-9
[
11325819.001
]
[Cites]
Br J Cancer. 2006 Nov 6;95(9):1277-9
[
17060932.001
]
[Cites]
N Engl J Med. 2006 Aug 31;355(9):873-84
[
16943400.001
]
[Cites]
Lancet Oncol. 2002 Mar;3(3):166-74
[
11902503.001
]
[Cites]
Am J Med. 2006 Jun;119(6):494-502
[
16750963.001
]
[Cites]
Nat Rev Cancer. 2006 Feb;6(2):130-40
[
16491072.001
]
[Cites]
J Clin Gastroenterol. 2002 Feb;34(2):117-25
[
11782603.001
]
[Cites]
Cancer Causes Control. 2006 Dec;17(10):1299-304
[
17111262.001
]
[Cites]
Ann Intern Med. 2007 Mar 6;146(5):361-4
[
17339621.001
]
[Cites]
N Engl J Med. 2000 Jun 29;342(26):1946-52
[
10874062.001
]
[Cites]
Lancet. 2007 May 12;369(9573):1603-13
[
17499602.001
]
[Cites]
Br J Cancer. 1999 Sep;81(1):62-8
[
10487613.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):555-6
[
15767326.001
]
[Cites]
Dis Colon Rectum. 2004 May;47(5):665-73
[
15054679.001
]
[Cites]
Pharmacogenomics J. 2008 Aug;8(4):237-47
[
18195728.001
]
[Cites]
Cancer Causes Control. 2003 Jun;14(5):403-11
[
12946034.001
]
[Cites]
Gastroenterology. 2003 Aug;125(2):328-36
[
12891533.001
]
[Cites]
Gastroenterology. 2008 Apr;134(4):1224-37
[
18395100.001
]
[Cites]
JAMA. 2005 Aug 24;294(8):914-23
[
16118381.001
]
[Cites]
Chest. 2004 Sep;126(3 Suppl):234S-264S
[
15383474.001
]
[Cites]
J Natl Cancer Inst. 2002 Feb 20;94(4):252-66
[
11854387.001
]
[Cites]
Eur J Biochem. 1980 Aug;109(1):1-8
[
6773769.001
]
[Cites]
J Natl Cancer Inst. 1998 Oct 21;90(20):1529-36
[
9790545.001
]
[Cites]
Ann Intern Med. 2007 Mar 6;146(5):365-75
[
17339622.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2008 Aug;17(8):1858-61
[
18708372.001
]
[Cites]
Br J Cancer. 2005 Mar 28;92 (6):1137-43
[
15770215.001
]
[Cites]
Ann Pharmacother. 2003 Nov;37(11):1664-74
[
14565811.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):616-9
[
15767339.001
]
[Cites]
Cochrane Database Syst Rev. 2004;(2):CD004079
[
15106236.001
]
[Cites]
N Engl J Med. 2003 Mar 6;348(10):879-80
[
12621130.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2002 Jul;11(7):622-9
[
12101109.001
]
[Cites]
Lancet. 2002 Sep 21;360(9337):942-4
[
12354487.001
]
[Cites]
Epidemiology. 2000 Jul;11(4):376-81
[
10874542.001
]
[Cites]
Postgrad Med J. 2005 Apr;81(954):223-7
[
15811884.001
]
[Cites]
Am J Epidemiol. 2007 Apr 15;165(8):874-81
[
17244633.001
]
[Cites]
J Natl Cancer Inst. 2005 Jul 6;97(13):989-97
[
15998952.001
]
[Cites]
BMJ. 2005 Jun 11;330(7504):1366
[
15947398.001
]
[Cites]
J Natl Cancer Inst. 2005 Mar 16;97(6):457-60
[
15770010.001
]
[Cites]
N Engl J Med. 1991 Dec 5;325(23):1593-6
[
1669840.001
]
[Cites]
Am J Epidemiol. 2005 Sep 15;162(6):548-58
[
16093288.001
]
[Cites]
Drugs Aging. 2006;23(6):513-23
[
16872234.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2008 Aug;17(8):1852-7
[
18708371.001
]
[Cites]
Clin Gastroenterol Hepatol. 2004 Jan;2(1):1-8
[
15017625.001
]
[Cites]
JAMA. 2005 Jul 6;294(1):47-55
[
15998890.001
]
(PMID = 20808298.001).
[ISSN]
1572-0241
[Journal-full-title]
The American journal of gastroenterology
[ISO-abbreviation]
Am. J. Gastroenterol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / N01 CN25522; United States / Intramural NIH HHS / /
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; R16CO5Y76E / Aspirin; WK2XYI10QM / Ibuprofen
Advertisement
4.
Poshkus T, Samalavichus NE, Dracutene G:
[Flat adenomas of the colon].
Ter Arkh
; 2007;79(2):77-81
[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]
[Flat
adenomas of the colon
].
[MeSH-major]
Adenoma
/ pathology.
Adenomatous Polyps
/ pathology.
Colonic
Neoplasms / pathology
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17460974.001).
[ISSN]
0040-3660
[Journal-full-title]
Terapevticheskiĭ arkhiv
[ISO-abbreviation]
Ter. Arkh.
[Language]
rus
[Publication-type]
Journal Article; Review
[Publication-country]
Russia (Federation)
[Number-of-references]
79
5.
Fujita K, Mondal AM, Horikawa I, Nguyen GH, Kumamoto K, Sohn JJ, Bowman ED, Mathe EA, Schetter AJ, Pine SR, Ji H, Vojtesek B, Bourdon JC, Lane DP, Harris CC:
p53 isoforms Delta133p53 and p53beta are endogenous regulators of replicative cellular senescence.
Nat Cell Biol
; 2009 Sep;11(9):1135-42
[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.
The senescence-associated signature of p53 isoform expression (that is, elevated p53beta and reduced Delta133p53) was observed in vivo in
colon adenomas
with senescent phenotypes.
The increased Delta133p53 and decreased p53beta isoform expression found in
colon
carcinoma may signal an escape from the senescence barrier during the progression from
adenoma
to carcinoma.
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
[Cites]
Oncogene. 2008 Mar 6;27(11):1562-71
[
17873905.001
]
[Cites]
Cell. 2008 Feb 8;132(3):363-74
[
18267069.001
]
[Cites]
Cancer Res. 2008 May 1;68(9):3193-203
[
18451145.001
]
[Cites]
Cell. 2008 Jun 13;133(6):1006-18
[
18555777.001
]
[Cites]
Cell. 2008 Jun 13;133(6):1019-31
[
18555778.001
]
[Cites]
Oncogene. 2008 Sep 4;27(39):5204-13
[
18504438.001
]
[Cites]
Proc Natl Acad Sci U S A. 2008 Sep 9;105(36):13421-6
[
18755897.001
]
[Cites]
Genes Dev. 2009 Feb 1;23(3):278-90
[
19204115.001
]
[Cites]
Mol Cell Biol. 2000 Apr;20(8):2803-8
[
10733583.001
]
[Cites]
Gastroenterology. 2000 Oct;119(4):929-42
[
11040180.001
]
[Cites]
EMBO J. 2003 Mar 3;22(5):1210-22
[
12606585.001
]
[Cites]
Mol Cell. 2004 May 21;14(4):501-13
[
15149599.001
]
[Cites]
Carcinogenesis. 1980 May;1(5):375-80
[
7273277.001
]
[Cites]
Nature. 1990 Aug 30;346(6287):866-8
[
2392154.001
]
[Cites]
Cell. 1992 Sep 18;70(6):937-48
[
1525830.001
]
[Cites]
Exp Gerontol. 1992 Jul-Aug;27(4):375-82
[
1459213.001
]
[Cites]
Hum Mol Genet. 1995 Feb;4(2):313-4
[
7757087.001
]
[Cites]
Cell. 1997 Mar 7;88(5):593-602
[
9054499.001
]
[Cites]
Science. 1997 Aug 8;277(5327):831-4
[
9242615.001
]
[Cites]
Cell. 1998 Feb 6;92(3):401-13
[
9476899.001
]
[Cites]
J Biol Chem. 1998 May 15;273(20):11995-8
[
9575138.001
]
[Cites]
J Clin Invest. 2004 Nov;114(9):1299-307
[
15520862.001
]
[Cites]
J Cell Sci. 2005 Feb 1;118(Pt 3):485-96
[
15657080.001
]
[Cites]
Nature. 2005 Aug 4;436(7051):642
[
16079833.001
]
[Cites]
Genes Dev. 2005 Sep 15;19(18):2122-37
[
16131611.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Mar;15(3):573-7
[
16537718.001
]
[Cites]
Nat Cell Biol. 2006 Aug;8(8):877-84
[
16862142.001
]
[Cites]
Nature. 2006 Nov 30;444(7119):633-7
[
17136093.001
]
[Cites]
Cell Death Differ. 2007 Jan;14(1):3-9
[
17068503.001
]
[Cites]
Proc Natl Acad Sci U S A. 2007 May 15;104(20):8334-9
[
17488820.001
]
[Cites]
Mol Cell. 2007 Jun 8;26(5):731-43
[
17540598.001
]
[Cites]
Mol Cell. 2007 Jun 8;26(5):745-52
[
17540599.001
]
[Cites]
Nature. 2007 Jun 28;447(7148):1130-4
[
17554337.001
]
[Cites]
Cell. 2007 Jul 27;130(2):223-33
[
17662938.001
]
[Cites]
Curr Biol. 2007 Aug 7;17(15):1298-307
[
17656095.001
]
[Cites]
Proc Natl Acad Sci U S A. 2007 Sep 25;104(39):15472-7
[
17875987.001
]
[Cites]
Oncogene. 2007 Nov 15;26(52):7302-12
[
17533371.001
]
[Cites]
Cancer Res. 2007 Dec 15;67(24):11677-86
[
18089797.001
]
[Cites]
JAMA. 2008 Jan 30;299(4):425-36
[
18230780.001
]
[Cites]
Science. 2008 Mar 7;319(5868):1352-5
[
18323444.001
]
(PMID = 19701195.001).
[ISSN]
1476-4679
[Journal-full-title]
Nature cell biology
[ISO-abbreviation]
Nat. Cell Biol.
[Language]
ENG
[Grant]
United States / Intramural NIH HHS / / Z01 BC005480-22; United States / Intramural NIH HHS / / ZIA BC010878-02; United Kingdom / Cancer Research UK / / ; United States / Intramural NIH HHS / / Z01 BC005795-13; United States / Intramural NIH HHS / / Z01 BC005795-14; United States / Intramural NIH HHS / / ZIA BC005795-15; United States / Intramural NIH HHS / / Z01 BC010878-01
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / MIRN34 microRNA, human; 0 / MicroRNAs; 0 / Protein Isoforms; 0 / Tumor Suppressor Protein p53
[Other-IDs]
NLM/ NIHMS161529; NLM/ PMC2802853
6.
Perçinel S, Savaş B, Ensari A, Kuzu I, Kuzu MA, Bektaş M, Cetinkaya H, Kurşun N:
Mucins in the colorectal neoplastic spectrum with reference to conventional and serrated adenomas.
Turk J Gastroenterol
; 2007 Dec;18(4):230-8
[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]
Mucins in the colorectal neoplastic spectrum with reference to conventional and serrated
adenomas
.
BACKGROUND/AIMS: Alterations in expression of mucins and aberrant expression of various types of mucin genes were observed in colorectal
adenomas
and carcinomas, though their significance in neoplastic transformation of colorectal epithelium is yet to be determined.
The aim of this study was to determine expression of MUC1, MUC2, MUC5AC, and MUC6 through conventional
adenoma
-carcinoma sequence and
polyps
involved in the "serrated" pathway of the colorectum using tissue array technique.
METHODS: In this study, a total of 172 cases including 100 colorectal
polyps
[8 hyperplastic
polyps
, 10 sessile serrated
adenomas
, 19 tubular, 37 tubulovillous, and 26 villous
adenomas
], 16
adenomas
with intramucosal carcinoma, 28 conventional colorectal cancers, and 28 normal mucosae were examined.
Sessile serrated
adenomas
exhibited the highest MUC5AC expression while
adenomatous polyps
showed an increase in MUC5AC expression in parallel with neoplastic progression (p<0.001).
Hyperplastic
polyps
seemed to lie between normal mucosa and sessile serrated
adenomas
in terms of mucin expression, suggesting that they are morphologically and histogenetically linked.
CONCLUSIONS: Upregulation of MUC1 and MUC6 through
the adenoma
-carcinoma sequence together with downregulation of MUC2 and MUC5AC at the neoplastic end of the spectrum seem to follow the steps of malignant transformation.
[MeSH-major]
Adenoma
/ metabolism.
Colonic Polyps
/ metabolism. Colorectal Neoplasms / metabolism. Mucins / metabolism
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
MedlinePlus Health Information.
consumer health - Colorectal 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
(PMID = 18080919.001).
[ISSN]
2148-5607
[Journal-full-title]
The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology
[ISO-abbreviation]
Turk J Gastroenterol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Turkey
[Chemical-registry-number]
0 / Mucins
7.
Schrier JC, Ouwehand F, Aronson DC, Booij KA, Benninga MA, Verbeek PC:
[A colo-colic invagination on the basis of MutYH-associated polyposis in a boy aged 14].
Ned Tijdschr Geneeskd
; 2007 Jul 14;151(28):1589-92
[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.
Colo-colic intussusception was diagnosed by means of a
colonic
contrast X-ray.
Hundreds of
polyps
were seen throughout the entire
colon
.
The pathology specimen showed an intramucosal carcinoma and multiple
adenomas
.
[MeSH-major]
Adenomatous
Polyposis Coli / diagnosis.
Colonic
Diseases / diagnosis. DNA Glycosylases / genetics. Intussusception / diagnosis
MedlinePlus Health Information.
consumer health - Colonic Diseases
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Ned Tijdschr Geneeskd. 2008 Jan 5;152(1):56-7; author reply 57
[
18240762.001
]
(PMID = 17715770.001).
[ISSN]
0028-2162
[Journal-full-title]
Nederlands tijdschrift voor geneeskunde
[ISO-abbreviation]
Ned Tijdschr Geneeskd
[Language]
dut
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Netherlands
[Chemical-registry-number]
EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
8.
Woerner SM, Kloor M, Mueller A, Rueschoff J, Friedrichs N, Buettner R, Buzello M, Kienle P, Knaebel HP, Kunstmann E, Pagenstecher C, Schackert HK, Möslein G, Vogelsang H, von Knebel Doeberitz M, Gebert JF, German HNPCC Consortium:
Microsatellite instability of selective target genes in HNPCC-associated colon adenomas.
Oncogene
; 2005 Apr 7;24(15):2525-35
[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]
Microsatellite instability of selective target genes in HNPCC-associated
colon adenomas
.
Instability at coding microsatellites (cMS) in
specific
target genes causes frameshift mutations and functional inactivation of affected proteins, thereby providing a selective growth advantage to MMR deficient cells.
In this study, we examined 30 HNPCC-associated MSI-H colorectal
adenomas of
different grades of dysplasia for frameshift mutations in 26 cMS-bearing genes, which, according to our previous model, represent Selective Target genes of MSI.
About 30% (8/26) of these genes showed a high mutation frequency (> or =50%) in colorectal
adenomas
, similar to the frequencies reported for colorectal carcinomas.
Mutations in one gene (PTHL3) occurred significantly less frequently in MSI
adenomas
compared to published mutation rates in MSI carcinomas (36.0 vs 85.7%, P=0.023).
[MeSH-major]
Adenoma
/ genetics.
Adenoma
/ physiopathology. Cell Transformation, Neoplastic / genetics. Chromosomal Instability.
Colonic
Neoplasms / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Microsatellite Repeats
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 = 15735733.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
9.
Lee SE, Park NH, Park IA, Kang SB, Lee HP:
Tubulo-villous adenoma of the vagina.
Gynecol Oncol
; 2005 Feb;96(2):556-8
[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]
Tubulo-villous
adenoma of
the vagina.
BACKGROUND: Tubulo-villous
adenomas
are common in
the colon
and rectum, but extremely rare in the vagina.
As far as we know, only two cases of tubulo-villous
adenoma
have ever been reported.
We report the third case of enteric-type tubulo-villous
adenoma of
the vagina.
The tumor was excised and pathologically confirmed as a tubulo-villous
adenoma
.
CONCLUSION: Because some tubulo-villous
adenomas
in
the colon
and rectum can progress to the cancer, this case requires long-term follow-up to detect recurrence and malignant transformation.
[MeSH-major]
Adenoma
, Villous / pathology. Vaginal Neoplasms / pathology
MedlinePlus Health Information.
consumer health - Vaginal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15661252.001).
[ISSN]
0090-8258
[Journal-full-title]
Gynecologic oncology
[ISO-abbreviation]
Gynecol. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Number-of-references]
17
10.
Harewood GC, Rathore O, Patchett S, Murray F:
Assessment of adherence to published surveillance guidelines--opportunity to enhance efficiency of endoscopic practice.
Ir Med J
; 2008 Sep;101(8):248-50
[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.
Surveillance procedures were classified as: a) Barrett's oesophagus, b) chronic IBD, c) prior
adenomatous
colorectal
polyps
and, d) prior surgical resection of colorectal cancer.
Of these, 50 of 133 (37.6%) Barrett's patients, 92 of 213 (43.2%) patients with prior
colonic polyps
, 36 of 48 (75.0%) patients with prior
colonic
malignancy and 17 of 47 (36.2%) patients for IBD surveillance were scheduled prematurely.
[MeSH-minor]
Adenomatous
Polyposis Coli / diagnosis. Barrett Esophagus / diagnosis. Colorectal Neoplasms / diagnosis. Databases as Topic. Great Britain. Humans. Inflammatory Bowel Diseases / diagnosis. Ireland
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18990956.001).
[ISSN]
0332-3102
[Journal-full-title]
Irish medical journal
[ISO-abbreviation]
Ir Med J
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article
[Publication-country]
Ireland
11.
Winawer SJ, Zauber AG, Fletcher RH, Stillman JS, O'brien MJ, Levin B, Smith RA, Lieberman DA, Burt RW, Levin TR, Bond JH, Brooks D, Byers T, Hyman N, Kirk L, Thorson A, Simmang C, Johnson D, Rex DK:
Guidelines for colonoscopy surveillance after polypectomy: a consensus update by the US Multi-Society Task Force on Colorectal Cancer and the American Cancer Society.
CA Cancer J Clin
; 2006 May-Jun;56(3):143-59; quiz 184-5
[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.
Adenomatous polyps
are the most common neoplastic findings uncovered in people who undergo colorectal screening or have a diagnostic workup for symptoms.
It was common practice in the 1970s for these patients to have annual follow-up surveillance examinations to detect additional new
adenomas
as well as missed synchronous
adenomas
.
As a result of the National
Polyp
Study report in 1993, which demonstrated clearly in a randomized design that the first postpolypectomy examination could be deferred for 3 years, guidelines published by a gastrointestinal consortium in 1997 recommended that the first follow-up surveillance be 3 years after polypectomy for most patients.
In 2003, these guidelines were updated, colonoscopy was recommended as the only follow-up examination, and stratification at baseline into lower and higher risk for subsequent
adenomas
was suggested.
In the present paper, a careful analytic approach was designed addressing all evidence available in the literature to delineate predictors of advanced pathology, both cancer and advanced
adenomas
, so that patients can be more definitely stratified at their baseline colonoscopy into those at lower or increased risk for a subsequent advanced neoplasia.
People at increased risk have either three or more
adenomas
, or high-grade dysplasia, or villous features, or an
adenoma
> or =1 cm in size.
People at lower risk who have one or two small (< 1 cm) tubular
adenomas
with no high-grade dysplasia can have a follow-up in 5 to 10 years, whereas people with hyperplastic
polyps
only should have a 10-year follow-up as average-risk people.
It has been shown that the first screening colonoscopy and polypectomy produces the greatest effects on reducing the incidence of colorectal cancer in patients with
adenomatous polyps
.
[MeSH-minor]
Adenomatous Polyps
/ epidemiology.
Adenomatous Polyps
/ prevention & control.
Adenomatous Polyps
/ surgery. American Cancer Society.
Colonic Polyps
/ epidemiology.
Colonic Polyps
/ prevention & control.
Colonic Polyps
/ surgery. Humans. Societies, Medical. United States / epidemiology
Genetic Alliance.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Colonoscopy
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16737947.001).
[ISSN]
0007-9235
[Journal-full-title]
CA: a cancer journal for clinicians
[ISO-abbreviation]
CA Cancer J Clin
[Language]
eng
[Publication-type]
Journal Article; Practice Guideline
[Publication-country]
United States
12.
Siddiqui AA, Patel A, Huerta S:
Determinants of compliance with colonoscopy in patients with adenomatous colon polyps in a veteran population.
Aliment Pharmacol Ther
; 2006 Dec;24(11-12):1623-30
[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]
Determinants of compliance with colonoscopy in patients with
adenomatous
colon
polyps
in a veteran population.
AIM: To determine factors affecting compliance of a follow-up colonoscopy in patients with previously diagnosed
adenomatous
colon
polyps
.
METHODS: A retrospective review was performed on patients with
adenomatous polyps
excised between January and December 1998.
RESULTS: One hundred and nineteen patients with
adenomatous
colon
polyps
were identified.
In a univariate analysis, greater number of
polyps
(P = 0.04), NSAID use (P = 0.02), statin use (P = 0.005), first-degree relatives with
colon
cancer (P = 0.05) and compliance with out-patient clinic follow-up (P < 0.001) were significantly associated with patient compliance.
Multivariate analysis revealed statin use (P = 0.05), first-degree relatives with
colon
cancer (P = 0.06) and compliance with out-patient clinic follow-up (P < 0.001) were independent predictors of compliance.
CONCLUSIONS: History of statin use and family history
of colon
cancer are good predictors of compliance.
Strong efforts should be directed at improving patient education about
colon
cancer by the physician and facilitating patient compliance.
[MeSH-major]
Adenomatous Polyps
/ pathology.
Colonic
Neoplasms / pathology.
Colonic Polyps
/ pathology. Colonoscopy. Patient Compliance
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
MedlinePlus Health Information.
consumer health - Colonoscopy
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17206950.001).
[ISSN]
0269-2813
[Journal-full-title]
Alimentary pharmacology & therapeutics
[ISO-abbreviation]
Aliment. Pharmacol. Ther.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
13.
Bafandeh Y, Khoshbaten M, Eftekhar-Sadat AT, Farhang S:
Colorectal neoplasms in symptomatic patients without evidence of bleeding: a prospective study in an Iranian population.
Asian Pac J Cancer Prev
; 2007 Oct-Dec;8(4):485-8
[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.
Data on its prevalence are lacking in Iran, as well as for
adenomatous polyps
.
This study was conducted to estimate prevalence of CRC in patients with long lasting
colonic
symptoms (except for known risk factors for cancer and those with rectal bleeding) who underwent total colonoscopy.
RESULTS: Thirty four subjects (14.9%) were found to have colorectal neoplasia and 112 (49.1%) had a completely normal
colon
.
Adenomatous polyps
were detected in 27 patients, which included 15.6% of men and 7.0% of women.
Mean age of patients with a
polyp
(51.1+/-12.5 years) was not significantly different compared to others (p=0.381) nor mean duration of symptoms (21.1 months, p=0.435).
None of the symptoms were predictors of cancer or
polyps
.
CONCLUSION: The low prevalence of colorectal neoplasms as well as the less advanced pattern
of adenomas
in Iran are compatible with other data from Asia and the Middle East, contrasting with western countries.
[MeSH-major]
Adenoma
/ diagnosis.
Colonic Polyps
/ diagnosis. Colorectal Neoplasms / diagnosis
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18260716.001).
[ISSN]
2476-762X
[Journal-full-title]
Asian Pacific journal of cancer prevention : APJCP
[ISO-abbreviation]
Asian Pac. J. Cancer Prev.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Thailand
14.
Matusiak D, Benya RV:
CYP27A1 and CYP24 expression as a function of malignant transformation in the colon.
J Histochem Cytochem
; 2007 Dec;55(12):1257-64
[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]
CYP27A1 and CYP24 expression as a function of malignant transformation in
the colon
.
However, vitamin D precursors do not present toxicity concerns and may be sufficient for CRC chemoprevention or chemotherapy, providing the appropriate enzymes are present in
colonic
epithelia.
We previously showed that CYP27B1 is present at equally high levels in
the colon
and CRC irrespective of differentiation but was not present in metastases.
In this study we used quantitative immunohistochemistry to show that CYP27A1, converting D3 to 25-hydroxycholecalciferol, is present in increasing concentrations in the nuclei of normal
colonic
epithelia, aberrant crypt foci (ACF), and
adenomatous polyps
.
Similarly, increasing amounts of the deactivating enzyme CYP24 are present in the nuclei of normal
colonic
epithelia, ACFs, and
adenomatous polyps
.
These data indicate that
non
-toxic vitamin D precursors should be sufficient for CRC chemoprevention, but that neither vitamin D nor its precursors may be sufficient for CRC chemotherapy.
[MeSH-minor]
Adenomatous Polyps
/ enzymology.
Adenomatous Polyps
/ ultrastructure.
Colon
/ enzymology.
Colon
/ pathology.
Colon
/ ultrastructure. Humans. Immunohistochemistry. Intestinal Mucosa / enzymology. Intestinal Mucosa / ultrastructure. Lymphatic Metastasis. Vitamin D3 24-Hydroxylase
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17875655.001).
[ISSN]
0022-1554
[Journal-full-title]
The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
[ISO-abbreviation]
J. Histochem. Cytochem.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA-094346
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
EC 1.14.- / Steroid Hydroxylases; EC 1.14.13.126 / Vitamin D3 24-Hydroxylase; EC 1.14.13.15 / CYP27A1 protein, human; EC 1.14.13.15 / Cholestanetriol 26-Monooxygenase
15.
Srivastava A, Redston M, Farraye FA, Yantiss RK, Odze RD:
Hyperplastic/serrated polyposis in inflammatory bowel disease: a case series of a previously undescribed entity.
Am J Surg Pathol
; 2008 Feb;32(2):296-303
[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.
Herein, we describe the clinical, pathologic, immunohistochemical, and molecular features of 3 unique patients with long standing inflammatory bowel disease, all of whom developed numerous discrete hyperplastic/serrated
colonic polyps
similar to those described in the hyperplastic/serrated polyposis syndrome.
The 3 patients (2 with ulcerative colitis and 1 with Crohn ileo-colitis) were evaluated for a variety of clinical, histologic (including the type, location and number of
polyps
in
the colon
), and immunohistochemical features [MLH-1, MSH-2, MGMT (O(6)-methylguanine-DNA methyltransferase), beta-catenin, and p53].
KRAS and BRAF mutation analysis was also performed on a subset of
polyps
from 2 patients.
All patients had moderate-severe pancolitis of more than 10 years duration and had >20
colonic polyps
.
None had
polyps
in the upper gastrointestinal tract.
Pathologically, a combination of conventional hyperplastic
polyps
and sessile serrated
polyps
(
adenomas
) were present in the 3 cases.
In addition, serrated
adenomas
were present in 2 and conventional
adenomas
in 1.
However, 2 cases showed loss of MGMT in several serrated
polyps
, and one also in adjacent colitic mucosa.
KRAS mutations were detected in 5/11 serrated
polyps
.
However, BRAF mutations were not present in any of the
polyps
tested.
[MeSH-major]
Adenomatous Polyps
/ pathology.
Colonic
Neoplasms / pathology.
Colonic Polyps
/ pathology. Inflammatory Bowel Diseases / pathology. Precancerous Conditions / pathology
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
COS Scholar Universe.
author profiles
.
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 = 18223333.001).
[ISSN]
0147-5185
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / Biomarkers, Tumor; 0 / MLH1 protein, human; 0 / MLH2 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
16.
Zhao C, Ivanov I, Dougherty ER, Hartman TJ, Lanza E, Bobe G, Colburn NH, Lupton JR, Davidson LA, Chapkin RS:
Noninvasive detection of candidate molecular biomarkers in subjects with a history of insulin resistance and colorectal adenomas.
Cancer Prev Res (Phila)
; 2009 Jun;2(6):590-7
[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]
Noninvasive detection of candidate molecular biomarkers in subjects with a history of insulin resistance and colorectal
adenomas
.
We have developed novel molecular methods using a stool sample, which contains intact sloughed
colon
cells, to quantify
colonic
gene expression profiles.
For this purpose, the effects of a legume-enriched, low glycemic index, high fermentable fiber diet was evaluated in subjects with four possible combinations of risk factors, including insulin resistance and a history of
adenomatous polyps
.
Linear discriminant analysis was successfully used to identify the best single genes and two- to three-gene combinations for distinguishing subjects with insulin resistance, a history of
polyps
, or exposure to a chemoprotective legume-rich diet.
These results support our premise that gene products (RNA) isolated from stool have diagnostic value in terms of assessing
colon
cancer risk.
MedlinePlus Health Information.
consumer health - Bowel Movement
.
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Dietary Fiber
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cell Death Differ. 2009 Jan;16(1):87-93
[
18806760.001
]
[Cites]
Cell Cycle. 2008 May 1;7(9):1178-83
[
18418037.001
]
[Cites]
Gastroenterology. 2009 Feb;136(2):459-70
[
19026650.001
]
[Cites]
Gastroenterology. 2000 Nov;119(5):1219-27
[
11054379.001
]
[Cites]
Eur J Cancer. 2001 Jan;37(2):224-33
[
11166150.001
]
[Cites]
Mol Cancer Ther. 2002 Nov;1(13):1229-36
[
12479704.001
]
[Cites]
Cancer Res. 2003 Jan 1;63(1):60-6
[
12517778.001
]
[Cites]
Biomarkers. 2003 Jan-Feb;8(1):51-61
[
12519636.001
]
[Cites]
J Virol. 2003 Feb;77(3):2233-42
[
12525658.001
]
[Cites]
Trends Genet. 2003 Jul;19(7):362-5
[
12850439.001
]
[Cites]
Int J Oncol. 2003 Sep;23(3):617-25
[
12888896.001
]
[Cites]
Gastroenterology. 2008 Sep;135(3):907-16, 916.e1-2
[
18655788.001
]
[Cites]
Ann Intern Med. 2008 Oct 7;149(7):441-50, W81
[
18838724.001
]
[Cites]
Cancer Res. 2003 Nov 15;63(22):7708-16
[
14633695.001
]
[Cites]
Gastroenterology. 2004 Aug;127(2):422-7
[
15300574.001
]
[Cites]
Cancer Res. 2004 Sep 15;64(18):6797-804
[
15374999.001
]
[Cites]
Biochim Biophys Acta. 1979 Aug 10;560(2):281-99
[
380653.001
]
[Cites]
Diabetes Care. 1988 Feb;11(2):149-59
[
3383733.001
]
[Cites]
Int J Cancer. 1992 Sep 30;52(3):347-50
[
1383164.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1995 Sep;4(6):643-7
[
8547831.001
]
[Cites]
Carcinogenesis. 1997 Feb;18(2):351-7
[
9054628.001
]
[Cites]
Carcinogenesis. 1998 Feb;19(2):253-7
[
9498273.001
]
[Cites]
Am J Physiol. 1999 May;276(5 Pt 1):G1087-93
[
10329998.001
]
[Cites]
N Engl J Med. 2004 Dec 23;351(26):2704-14
[
15616205.001
]
[Cites]
Nat Rev Cancer. 2005 Mar;5(3):199-209
[
15738983.001
]
[Cites]
Cancer Causes Control. 2005 Apr;16(3):225-33
[
15947874.001
]
[Cites]
J Natl Cancer Inst. 2005 Aug 3;97(15):1124-32
[
16077070.001
]
[Cites]
Mol Cell Biol. 2005 Dec;25(23):10454-64
[
16287858.001
]
[Cites]
Cancer Res. 2006 Apr 1;66(7):3942-53
[
16585224.001
]
[Cites]
Gastroenterology. 2006 Apr;130(4):1030-8
[
16618396.001
]
[Cites]
Ann Surg. 2006 May;243(5):619-25; discussion 625-7
[
16632996.001
]
[Cites]
J Nutr. 2006 Jul;136(7):1896-903
[
16772456.001
]
[Cites]
Bioinformatics. 2006 Oct 1;22(19):2430-6
[
16870934.001
]
[Cites]
Nat Med. 2006 Nov;12(11):1294-300
[
17057710.001
]
[Cites]
Clin Gastroenterol Hepatol. 2007 Jan;5(1):111-7
[
17161655.001
]
[Cites]
Nutr Rev. 2007 Feb;65(2):51-62
[
17345958.001
]
[Cites]
Nat Cell Biol. 2007 Apr;9(4):445-52
[
17351641.001
]
[Cites]
Clin Chem. 2007 Sep;53(9):1646-51
[
17712002.001
]
[Cites]
J Cell Biochem. 2007 Dec 15;102(6):1420-31
[
17471513.001
]
[Cites]
Biochimie. 2008 Feb;90(2):313-23
[
17928127.001
]
[Cites]
Oncogene. 2008 Feb 21;27(9):1315-9
[
17704798.001
]
[Cites]
N Engl J Med. 2008 Mar 13;358(11):1148-59
[
18337604.001
]
[Cites]
Cancer Res. 2008 Apr 15;68(8):2813-9
[
18413749.001
]
[Cites]
Nutr Cancer. 2008;60(3):373-81
[
18444172.001
]
[Cites]
Cancer Prev Res (Phila). 2009 Jan;2(1):60-9
[
19139019.001
]
(PMID = 19470793.001).
[ISSN]
1940-6215
[Journal-full-title]
Cancer prevention research (Philadelphia, Pa.)
[ISO-abbreviation]
Cancer Prev Res (Phila)
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / R01 DK071707-02; United States / NCI NIH HHS / CA / R01 CA129444-01; United States / NIDDK NIH HHS / DK / R01 DK071707-01A2; United States / NIDDK NIH HHS / DK / R01 DK071707-01A2S1; United States / NCI NIH HHS / CA / R01 CA059034-05; United States / NCI NIH HHS / CA / CA059034-12; United States / NCI NIH HHS / CA / CA059034-08; United States / NIEHS NIH HHS / ES / P30ES09106; United States / NCI NIH HHS / CA / R01 CA059034-07; United States / NCI NIH HHS / CA / CA059034-13; United States / NCI NIH HHS / CA / R01 CA059034; United States / NIDDK NIH HHS / DK / DK071707; United States / NCI NIH HHS / CA / R01 CA059034-15; United States / NCI NIH HHS / CA / R01 CA059034-11; United States / NCI NIH HHS / CA / CA059034-06; United States / NCI NIH HHS / CA / R01 CA059034-09; United States / NIDDK NIH HHS / DK / R01 DK071707-03; United States / NCI NIH HHS / CA / CA059034-09; United States / NIDDK NIH HHS / DK / DK071707-03; United States / NCI NIH HHS / CA / R01 CA129444-02; United States / NCI NIH HHS / CA / R01 CA059034-08; United States / NCI NIH HHS / CA / CA59034; United States / NCI NIH HHS / CA / CA059034-05; United States / NCI NIH HHS / CA / R01 CA059034-10; United States / NCI NIH HHS / CA / CA129444-01; United States / NCI NIH HHS / CA / CA059034-10; United States / NCI NIH HHS / CA / R01 CA059034-14; United States / NCI NIH HHS / CA / R01 CA059034-12; United States / NIDDK NIH HHS / DK / DK071707-01A2S1; United States / NIDDK NIH HHS / DK / DK071707-01A2; United States / NCI NIH HHS / CA / CA129444-02; United States / NCI NIH HHS / CA / CA059034-15; United States / NIDDK NIH HHS / DK / DK071707-02; United States / NCI NIH HHS / CA / CA059034-11; United States / NCI NIH HHS / CA / CA129444; United States / NCI NIH HHS / CA / CA059034-14; United States / NIDDK NIH HHS / DK / R01 DK071707; United States / NIEHS NIH HHS / ES / P30 ES009106; United States / NCI NIH HHS / CA / CA059034-07; United States / NCI NIH HHS / CA / R01 CA059034-06; United States / NCI NIH HHS / CA / R01 CA059034-13; United States / NCI NIH HHS / CA / R01 CA129444
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / RNA, Messenger
[Other-IDs]
NLM/ NIHMS120536; NLM/ PMC2745241
17.
Barreda B F, Combe G J, Valdez P LA, Sánchez L J:
[Clinical aspects in polyps of the colon].
Rev Gastroenterol Peru
; 2007 Apr-Jun;27(2):131-47
[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]
[Clinical aspects in
polyps
of the
colon
].
[Transliterated title]
Aspectos clínicos
de
los pólipos colónicos.
INTRODUCTION: The colonics
polyps
according to their number, size, location, age of presentation and mainly, according to their histology, have the potentiality of malignant degeneration, which makes of a continuous study and pursuit susceptible.
OBJECTIVES: To evaluate the relation between the histologic type of the
colon
polyps
, its location, the degree of dysplasia, the size, its possible commitment by carcinoma, the age, sex and the handling that has occurred them, in a series of 684 patients of the National Institute of Enfermedades Neoplásicas (INEN) between the 1 of January from 1974 to the 31 of March of the 2004.
MATERIAL AND METHODS: The revision of clinical histories of 840 patients with the diagnosis
of colon polyp
was made who attended the service of Gastroenterology of the INEN between the 1 of January from 1974 to the 31 of March of 2004 and a card predesigned for each clinical history filled.
1162 resecteds
polyps
evaluated themselves in this period.
The final sample was of 684 patients, in whom it was 1057
polyps
.
Other endoscopic findings were: internal hemorrhoids (172),
colonic
diverticulosis (50), anal fissure (4), and nonspecific ulcerative colitis (2).
RESULTS: 1057
polyps
extirpated, by means of the endoscopy polipectomy were 1016, with colectomy were 32 and with transanal resection without colectomy they 9.
Within the histology of the 1057
polyps
, 331 was briefed (31.3%) that were hyperplasic, 448 (42.4%)
adenomas
, 278 (26.3%) others and 35 (8.2%) adenocarcinomas on
adenomas
.
The location but frequence of the
adenomas
was in the left
colon
(76.6%).
Adenocarcinoma (carcinomas on
adenomas
), was present mainly in
polyps
villous type, with dysplasia severe and greater to 10 mm.
Nevertheless, in smaller
polyps
of 5mm with dysplasia severe, was a
polyp
invaded by cancer, that represents the 0,8% of millimetric
polyps
.
The made handling was mainly endoscopic, with 96% of the resected
polyps
this way, also slogan transanal resection and segmental
colonic
resection.
The colectomy was necessary in 3% of all the made interventions, dysplasia severe or carcinoma was made in
adenomatous polyps
with, and in greater percentage in greater
polyps
of 20 mm (53%).
On the other hand, in
polyps
with level of invasion Haggitt 3 and 4, the colectomy was the election treatment.
CONCLUSIONS: The Evaluation of
colonic polyps
in INEN is predominantly by endoscopy.
The
polyps
are more frequent over the 50 years and have preferred location in the left
colon
.
The carcinoma is more probable with severe dysplasia and greater size of the
adenoma
.
All
polyps
, from the millimetric ones, including the hyperplasic, must be considered marks of neoplasia and extirpated in its totality.
[MeSH-major]
Colonic Polyps
/ pathology.
Colonic Polyps
/ surgery
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17712391.001).
[ISSN]
1022-5129
[Journal-full-title]
Revista de gastroenterología del Perú : órgano oficial de la Sociedad de Gastroenterología del Perú
[ISO-abbreviation]
Rev Gastroenterol Peru
[Language]
spa
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Peru
18.
Landau D, Garrett C, Chodkiewicz C:
A case of primary squamous cell colon cancer.
J Oncol Pharm Pract
; 2007 Mar;13(1):47-8
[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]
A case of primary squamous cell
colon
cancer.
Carcinomas of the
colon
are a common cancer seen in both inpatient and outpatient settings with approximately 145,000 new cases being diagnosed every year in the USA.
Despite the frequency of these cancers being seen, it continues to be a rarity to see a primary squamous cell cancer of the
colon
.
While the exact aetiology of this rare tumour is currently still not completely understood, various aetiologies include chronic irritation leading to squamous differentiation, embryonic migration of ectodermal cells to
the colon
, or
adenomas
undergoing squamous transformation.
[MeSH-major]
Carcinoma, Squamous Cell / pathology.
Colonic
Neoplasms / pathology
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17621567.001).
[ISSN]
1078-1552
[Journal-full-title]
Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners
[ISO-abbreviation]
J Oncol Pharm Pract
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
19.
Pranesh N, Haboubi NY, O'Dwyer ST:
Pigmented mesenteric lymphadenopathy in familial adenomatous polyposis - an unusual cause of intraoperative abandonment of ileo-anal pouch.
Ann R Coll Surg Engl
; 2005 Jul;87(4):W1-4
[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.
[Title]
Pigmented mesenteric lymphadenopathy in familial
adenomatous
polyposis - an unusual cause of intraoperative abandonment of ileo-anal pouch.
Familial
adenomatous
polyposis (FAP) is an autosomal dominant condition with near complete penetrance, characterised by the presence of numerous
adenomatous polyps
of the
colon
and rectum.
Melanosis coli describes the brownish-black discolouration of the
colon
resulting from the accumulation of a granular pigment in the phagosomes of macrophages in the
colonic
lamina propria.
The presence of melanosis pigment in pericolonic lymph nodes has been reported in patients with coincidental melanosis coli, following segmental
colonic
resection.
[MeSH-major]
Adenomatous
Polyposis Coli / surgery. Lymphatic Diseases / complications. Melanosis / complications. Mesentery. Peritoneal Diseases / complications
[MeSH-minor]
Adolescent.
Colonic
Pouches. Female. Humans. Intraoperative Complications / etiology. Proctocolectomy, Restorative. Reoperation
Genetic Alliance.
consumer health - Familial Adenomatous Polyposis (FAP)
.
Genetic Alliance.
consumer health - Familial Polyposis
.
MedlinePlus Health Information.
consumer health - Lymphatic Diseases
.
MedlinePlus Health Information.
consumer health - Peritoneal Disorders
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16884599.001).
[ISSN]
0035-8843
[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
[Other-IDs]
NLM/ PMC1963935
20.
Juhn E, Khachemoune A:
Gardner syndrome: skin manifestations, differential diagnosis and management.
Am J Clin Dermatol
; 2010;11(2):117-22
[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.
Gardner syndrome is a variant of familial
adenomatous
polyposis (FAP) and results in the manifestation of numerous external and internal symptoms including gastrointestinal
polyps
, osteomas, tumors, and epidermoid cysts.
Stemming from a mutation in the
adenomatous
polyposis coli (APC) gene, Gardner syndrome shares genetic correlations with the FAP phenotype; as a result, it becomes all the more crucial for physicians to be able to discern Gardner syndrome from other differential diagnoses such as Turcot syndrome, FAP, and other attenuated forms of familial polyposis.
Fortunately, Gardner syndrome has characteristic
polyps
in
the colon
, osteomas, and also exhibits abnormalities in the retinal epithelium that discern it from others.
Surgery is the most effective method of management for Gardner syndrome; restorative proctocolectomy with ileal pouch anal anastomosis with mucosectomy is the top choice for
colonic
malignancies, and skin manifestations can be treated through a variety of excisions and therapy depending on location, size, and number of malignancies.
Currently, there are no
specific
screening recommendations for Gardner syndrome, but testing following general screening recommendations for extra-
colonic
malignancies, genetic counseling, and endoscopy are encouraged.
[MeSH-minor]
Adenomatous
Polyposis Coli / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis. Colorectal Neoplasms, Hereditary Nonpolyposis / pathology. Colorectal Neoplasms, Hereditary Nonpolyposis / therapy. Diagnosis, Differential. Genetic Counseling / methods. Humans. Mutation
Genetic Alliance.
consumer health - Gardner Syndrome
.
The Weizmann Institute of Science GeneCards and MalaCards databases.
gene/protein/disease-specific - MalaCards for gardner syndrome
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20141232.001).
[ISSN]
1175-0561
[Journal-full-title]
American journal of clinical dermatology
[ISO-abbreviation]
Am J Clin Dermatol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
New Zealand
[Number-of-references]
29
21.
Herbst A, Bommer GT, Kriegl L, Jung A, Behrens A, Csanadi E, Gerhard M, Bolz C, Riesenberg R, Zimmermann W, Dietmaier W, Wolf I, Brabletz T, Göke B, Kolligs FT:
ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition.
Gastroenterology
; 2009 Aug;137(2):639-48, 648.e1-9
[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]
ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at
the adenoma
-carcinoma transition.
RESULTS: ITF-2B is strongly expressed in
colon adenomas
but frequently down-regulated in carcinomas because of LOH at 18q21.
Loss of ITF-2B expression correlates with loss of p21(Cip1) expression in primary
colon
carcinomas.
ITF-2B, which is up-regulated during early colorectal carcinogenesis because of loss of
adenomatous
polyposis coli, is a target for LOH on chromosome 18q, along with deleted in colorectal carcinoma and Smad4.
This finding, along with the fact that ITF-2B is a regulator of the key cell cycle inhibitor p21(Cip1), indicates that ITF-2B is a tumor suppressor that has an important function at
the adenoma
to carcinoma transition.
[MeSH-major]
Adenocarcinoma / genetics.
Adenomatous
Polyposis Coli / genetics. Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 18 / genetics. Colorectal Neoplasms / genetics. DNA-Binding Proteins / genetics. Transcription Factors / genetics
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
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
(PMID = 19394332.001).
[ISSN]
1528-0012
[Journal-full-title]
Gastroenterology
[ISO-abbreviation]
Gastroenterology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / TCF3 protein, human; 0 / TCF4 protein, human; 0 / Transcription Factors
22.
Ye C, Shrubsole MJ, Cai Q, Ness R, Grady WM, Smalley W, Cai H, Washington K, Zheng W:
Promoter methylation status of the MGMT, hMLH1, and CDKN2A/p16 genes in non-neoplastic mucosa of patients with and without colorectal adenomas.
Oncol Rep
; 2006 Aug;16(2):429-35
[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]
Promoter methylation status of the MGMT, hMLH1, and CDKN2A/p16 genes in
non
-neoplastic mucosa of patients with and without colorectal
adenomas
.
CpG island methylation has been observed in aberrant crypt foci (ACF) and
adenomas
in
the colon
, implicating it in the earliest aspects
of colon
cancer formation.
In addition, some investigators have identified an age-related increase in DNA methylation of the ESR1 locus in
the colon
mucosa, suggesting that DNA methylation may be a pre-neoplastic change that increases the risk
of colon adenomas
and
colon
cancer.
We investigated the methylation status in the promoter regions of the CDKN2A/p16, hMLH1, and MGMT genes in human
non
-neoplastic rectal mucosa and evaluated whether these methylation markers may predict the presence of
adenomatous polyps
in
the colon
.
The promoter methylation patterns of these genes were examined in rectal biopsies (mucosa samples) of 97 colorectal
adenoma
cases and 94 healthy controls using methylation-
specific
PCR (MSP) assays.
The methylation status of these genes in rectal mucosa biopsies detected by MSP assays may not distinguish between patients with and without
adenomas
in
the colon
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
COS Scholar Universe.
author profiles
.
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
(PMID = 16820927.001).
[ISSN]
1021-335X
[Journal-full-title]
Oncology reports
[ISO-abbreviation]
Oncol. Rep.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / P50 CA95103; United States / NCI NIH HHS / CA / R01CA97386
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
Greece
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / MLH1 protein, human; 0 / Nuclear Proteins; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
23.
Glazer E, Golla V, Forman R, Zhu H, Levi G, Bodenheimer HC Jr:
Serrated adenoma is a risk factor for subsequent adenomatous polyps.
Dig Dis Sci
; 2008 Aug;53(8):2204-7
[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]
Serrated
adenoma
is a risk factor for subsequent
adenomatous polyps
.
BACKGROUND: Serrated
adenomas
(SA) are histologically defined by the presence of both hyperplastic and
adenomatous
features.
These uncommon
polyps
are thought to play an important role in the development of sporadic colorectal cancers (CRC) with microsatellite instability (MSI).
This study was undertaken to define the relationship between SA and the future development of
adenomatous polyps
.
These were matched to controls by age, sex, indication for colonoscopy,
polyp
type and number and duration of follow-up.
Of these, 80 patients (0.5%) with SA were found, and of these SA, 80% were found in the left
colon
.
On follow-up examination four patients (24%) and no controls had
adenomatous polyps
(P = 0.01).
Serrated
adenomas
appear to be found more commonly in the left
colon
and in older patients.
This study found a significant association between SA and the subsequent development of
adenomatous polyps
.
[MeSH-major]
Adenoma
/ pathology.
Colonic
Neoplasms / pathology.
Colonic Polyps
/ pathology. Precancerous Conditions / pathology
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Am J Surg Pathol. 1990 Jun;14(6):524-37
[
2186644.001
]
[Cites]
Am J Surg Pathol. 1984 Jul;8(7):551-6
[
6742315.001
]
[Cites]
Am J Clin Pathol. 2005 Mar;123(3):349-59
[
15716230.001
]
[Cites]
Clin Cancer Res. 2004 May 1;10 (9):3082-90
[
15131047.001
]
[Cites]
Am J Gastroenterol. 2004 Nov;99(11):2242-55
[
15555008.001
]
[Cites]
Gastroenterology. 2001 Dec;121(6):1300-9
[
11729109.001
]
[Cites]
J Pathol. 2001 Mar;193(3):286-94
[
11241406.001
]
[Cites]
Am J Clin Pathol. 2005 Sep;124(3):380-91
[
16191506.001
]
[Cites]
Gut. 2004 Aug;53(8):1137-44
[
15247181.001
]
[Cites]
J Natl Cancer Inst. 2001 Sep 5;93(17 ):1307-13
[
11535705.001
]
[Cites]
N Engl J Med. 1988 Sep 1;319(9):525-32
[
2841597.001
]
[Cites]
Am J Pathol. 2003 Mar;162(3):815-22
[
12598316.001
]
[Cites]
Science. 1989 Apr 14;244(4901):207-11
[
2565047.001
]
[Cites]
Anticancer Res. 2000 Mar-Apr;20(2B):1141-7
[
10810411.001
]
[Cites]
J Clin Pathol. 1999 Jan;52(1):5-9
[
10343605.001
]
[Cites]
Gastrointest Endosc. 1995 Aug;42(2):114-22
[
7590045.001
]
(PMID = 18320324.001).
[ISSN]
0163-2116
[Journal-full-title]
Digestive diseases and sciences
[ISO-abbreviation]
Dig. Dis. Sci.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
24.
Jones LE Jr, Ying L, Hofseth AB, Jelezcova E, Sobol RW, Ambs S, Harris CC, Espey MG, Hofseth LJ, Wyatt MD:
Differential effects of reactive nitrogen species on DNA base excision repair initiated by the alkyladenine DNA glycosylase.
Carcinogenesis
; 2009 Dec;30(12):2123-9
[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.
To understand the effects of RNS on BER in vivo, we examined intestinal
adenomas
for levels of inducible nitric oxide synthase (iNOS) and AAG.
We found AAG to be nitrated in human
adenomas
, suggesting that this RNS modification is relevant in the human disease.
POLbeta protein was increased in nearly all
adenomas
compared with adjacent
non
-tumor tissues, whereas APE1 expression was only increased in approximately half of the
adenomas
and also was relocalized to the cytoplasm in
adenomas
.
Collectively, the results suggest that BER is dysregulated in
colon adenomas
.
COS Scholar Universe.
author profiles
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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]
Int J Cancer. 2000 Jul 1;87(1):1-4
[
10861445.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Nov 25;94(24):13087-92
[
9371804.001
]
[Cites]
Free Radic Biol Med. 2000 May 15;28(10):1478-86
[
10927172.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Dec 5;97(25):13573-8
[
11106395.001
]
[Cites]
J Biol Chem. 2001 Aug 10;276(32):30085-91
[
11404354.001
]
[Cites]
Cancer Res. 2001 Sep 1;61(17):6388-93
[
11522631.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3481-6
[
11904413.001
]
[Cites]
Carcinogenesis. 2002 Jun;23(6):993-1001
[
12082021.001
]
[Cites]
J Biol Chem. 2002 Jul 26;277(30):26987-93
[
12016206.001
]
[Cites]
J Biol Chem. 2002 Aug 30;277(35):31673-8
[
12077143.001
]
[Cites]
Chem Biol. 2002 Sep;9(9):1033-41
[
12323378.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):12691-6
[
12226478.001
]
[Cites]
Biochemistry. 2003 Apr 1;42(12):3608-16
[
12653565.001
]
[Cites]
Arch Biochem Biophys. 2003 Sep 1;417(1):3-11
[
12921773.001
]
[Cites]
Trends Biochem Sci. 2003 Dec;28(12):646-54
[
14659696.001
]
[Cites]
J Clin Invest. 2003 Dec;112(12):1887-94
[
14679184.001
]
[Cites]
Arch Biochem Biophys. 2004 Mar 1;423(1):12-22
[
14989259.001
]
[Cites]
J Biol Chem. 2004 Mar 12;279(11):9750-7
[
14688248.001
]
[Cites]
J Comput Chem. 2004 Oct;25(13):1605-12
[
15264254.001
]
[Cites]
J Biol Chem. 2004 Sep 10;279(37):38177-83
[
15247209.001
]
[Cites]
J Med Chem. 1991 Nov;34(11):3242-7
[
1956043.001
]
[Cites]
Cancer Res. 1994 Nov 15;54(22):5947-52
[
7954427.001
]
[Cites]
J Biol Chem. 1996 Sep 27;271(39):23690-7
[
8798591.001
]
[Cites]
EMBO J. 1998 Jan 15;17(2):363-7
[
9430628.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):9997-10002
[
9707589.001
]
[Cites]
Cell. 1998 Oct 16;95(2):249-58
[
9790531.001
]
[Cites]
J Natl Cancer Inst. 1999 Jan 6;91(1):86-8
[
9890175.001
]
[Cites]
Mutat Res. 1999 Mar 8;424(1-2):37-49
[
10064848.001
]
[Cites]
J Surg Oncol. 1999 Apr;70(4):222-9
[
10219017.001
]
[Cites]
Chem Res Toxicol. 2005 Jan;18(1):87-94
[
15651853.001
]
[Cites]
Antioxid Redox Signal. 2005 Mar-Apr;7(3-4):367-84
[
15706084.001
]
[Cites]
Cancer Res. 2005 Oct 15;65(20):9132-6
[
16230367.001
]
[Cites]
Mutat Res. 2005 Dec 11;591(1-2):34-44
[
16099477.001
]
[Cites]
J Biol Chem. 2005 Dec 9;280(49):40684-98
[
16176930.001
]
[Cites]
Chem Res Toxicol. 2006 Jan;19(1):50-7
[
16411656.001
]
[Cites]
Mol Carcinog. 2006 Feb;45(2):93-105
[
16329147.001
]
[Cites]
Mol Cancer Res. 2006 Apr;4(4):221-33
[
16603636.001
]
[Cites]
Chem Res Toxicol. 2006 Dec;19(12):1580-94
[
17173371.001
]
[Cites]
DNA Repair (Amst). 2007 Jun 1;6(6):695-711
[
17337257.001
]
[Cites]
Nucleic Acids Res. 2007;35(8):2522-32
[
17403694.001
]
[Cites]
Nat Rev Drug Discov. 2007 Aug;6(8):662-80
[
17667957.001
]
[Cites]
Carcinogenesis. 2007 Aug;28(8):1807-13
[
17347141.001
]
[Cites]
J Biol Chem. 2007 Oct 12;282(41):30078-84
[
17716976.001
]
[Cites]
Science. 2008 May 23;320(5879):1050-4
[
18497292.001
]
[Cites]
Cancer Res. 2008 Jun 1;68(11):4142-9
[
18519673.001
]
[Cites]
Free Radic Biol Med. 2008 Jul 1;45(1):18-31
[
18439435.001
]
[Cites]
J Clin Invest. 2008 Jul;118(7):2516-25
[
18521188.001
]
[Cites]
Nitric Oxide. 2008 Sep;19(2):146-51
[
18474261.001
]
[Cites]
Mol Pharmacol. 2008 Aug;74(2):505-16
[
18477668.001
]
[Cites]
Carcinogenesis. 2008 Sep;29(9):1799-806
[
18567620.001
]
[Cites]
DNA Repair (Amst). 2008 Oct 1;7(10):1731-45
[
18706524.001
]
[Cites]
Arch Biochem Biophys. 2009 Apr 15;484(2):134-45
[
19056332.001
]
[Cites]
Cancer Res. 1997 May 1;57(9):1794-7
[
9135024.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Nov 25;94(24):12869-74
[
9371767.001
]
[Cites]
Ann N Y Acad Sci. 2000;899:209-21
[
10863541.001
]
(PMID = 19864471.001).
[ISSN]
1460-2180
[Journal-full-title]
Carcinogenesis
[ISO-abbreviation]
Carcinogenesis
[Language]
ENG
[Grant]
United States / NCRR NIH HHS / RR / P20 RR017698; United States / NCRR NIH HHS / RR / P20 RR17698; United States / NCI NIH HHS / CA / R01 CA100450; United States / Intramural NIH HHS / /
[Publication-type]
Journal Article; 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.
[Publication-country]
England
[Chemical-registry-number]
0 / Reactive Nitrogen Species; EC 2.7.7.- / DNA Polymerase beta; EC 3.2.2.- / 3-methyladenine-DNA glycosylase; EC 3.2.2.- / DNA Glycosylases; EC 4.2.99.18 / APEX1 protein, human; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase
[Other-IDs]
NLM/ PMC2792317
25.
García Sánchez Mdel V, González R, Iglesias Flores E, Gómez Camacho F, Casais Juanena L, Cerezo Ruiz A, Montero Pérez-Barquero M, Muntané J, de Dios Vega JF:
[Diagnostic value of fecal calprotectin in predicting an abnormal colonoscopy].
Med Clin (Barc)
; 2006 Jun 10;127(2):41-6
[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.
[Transliterated title]
Precisión diagnóstica
de
la calprotectina fecal para predecir una colonoscopia patológica.
The colonoscopy is the gold standard method of detecting an organic pathology in
the colon
.
Fecal calprotectin (FCP) is a marker that may detect organic pathologies of the
colon
.
People were divided in: normal colonoscopy: 117 people, and 28
colon adenomas
, 20 colorectal cancer (CRC) and 25 IBD.
217 mg/kg was the best cut-off for discriminating patients with organic
colon
disorders.
The measurement of FCP is a
non
-invasive, inexpensive, reliable and easily measured test.
[MeSH-major]
Colonic
Diseases / diagnosis.
Colonic
Neoplasms / diagnosis. Colonoscopy. Feces / chemistry. Inflammatory Bowel Diseases / diagnosis. Leukocyte L1 Antigen Complex / analysis
MedlinePlus Health Information.
consumer health - Bowel Movement
.
MedlinePlus Health Information.
consumer health - Colonic Diseases
.
MedlinePlus Health Information.
consumer health - Colonoscopy
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16801001.001).
[ISSN]
0025-7753
[Journal-full-title]
Medicina clínica
[ISO-abbreviation]
Med Clin (Barc)
[Language]
spa
[Publication-type]
Clinical Trial; English Abstract; Journal Article
[Publication-country]
Spain
[Chemical-registry-number]
0 / Leukocyte L1 Antigen Complex
26.
Yuan B, Jin X, Zhu R, Zhang X, Liu J, Wan H, Lu H, Shen Y, Wang F:
Cronkhite-Canada syndrome associated with rib fractures: a case report.
BMC Gastroenterol
; 2010;10:121
[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.
Esophagogastroduodenoscopy, video capsule endoscopy and colonoscopy revealed various sizes of generalized gastrointestinal
polyps
.
Histological examination of the biopsy specimens obtained from the stomach and
the colon
showed
adenomatous
polyp
and inflammatory
polyp
respectively.
MedlinePlus Health Information.
consumer health - Chest Injuries and Disorders
.
MedlinePlus Health Information.
consumer health - Osteoporosis
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Gastrointest Endosc. 2001 Sep;54(3):388-91
[
11522989.001
]
[Cites]
Aliment Pharmacol Ther. 2002 Mar;16(3):333-42
[
11876685.001
]
[Cites]
Expert Opin Pharmacother. 2003 Mar;4(3):385-9
[
12614190.001
]
[Cites]
Am J Gastroenterol. 2003 Jun;98(6):1444-6
[
12818298.001
]
[Cites]
Gastrointest Endosc. 2008 Mar;67(3):570-2
[
18294523.001
]
[Cites]
Medicine (Baltimore). 1982 Sep;61(5):293-309
[
7109958.001
]
[Cites]
Gastrointest Endosc. 1997 Dec;46(6):537-41
[
9434222.001
]
[Cites]
N Engl J Med. 1955 Jun 16;252(24):1011-5
[
14383952.001
]
[Cites]
Digestion. 2007;75(2-3):96-7
[
17510553.001
]
[Cites]
Digestion. 2004;69(1):57-62
[
14755154.001
]
(PMID = 20955587.001).
[ISSN]
1471-230X
[Journal-full-title]
BMC gastroenterology
[ISO-abbreviation]
BMC Gastroenterol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC2972238
27.
Arber N, Kuwada S, Leshno M, Sjodahl R, Hultcrantz R, Rex D, Exisulind Study Group:
Sporadic adenomatous polyp regression with exisulind is effective but toxic: a randomised, double blind, placebo controlled, dose-response study.
Gut
; 2006 Mar;55(3):367-73
[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]
Sporadic
adenomatous
polyp
regression with exisulind is effective but toxic: a randomised, double blind, placebo controlled, dose-response study.
The aim of our study was to investigate if exisulind induces regression of sporadic
colonic
adenomas
.
At baseline colonoscopy, left sided
polyps
(3-10 mm) were tattooed, measured, and left in place.
Follow up sigmoidoscopy was performed after six months, and removal of any remaining
polyps
at the 12 month colonoscopy.
The primary efficacy variable was change in
polyp
size from baseline.
The decrease in median
polyp
size was significantly greater (p=0.03) in patients who received exisulind 400 mg (-10 mm2) compared with those who received placebo (-4 mm2).
CONCLUSION: Exisulind caused significant regression of sporadic
adenomatous polyps
but was associated with more toxicity.
This model
of polyp
regression, short in its term and involving a comparatively small patient sample size, may be the best available tool to assess a therapeutic regimen before launching into large preventive clinical studies.
[MeSH-major]
Adenomatous
Polyposis Coli / drug therapy. Antineoplastic Agents / therapeutic use. Sulindac / analogs & derivatives
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
N Engl J Med. 1993 Dec 30;329(27):1977-81
[
8247072.001
]
[Cites]
Am J Gastroenterol. 1993 Oct;88(10):1652-6
[
8213705.001
]
[Cites]
Gastroenterology. 1995 Apr;108(4):1083-7
[
7698575.001
]
[Cites]
Gastroenterology. 1996 Feb;110(2):654-5
[
8566622.001
]
[Cites]
Cancer Res. 1997 Jun 15;57(12):2452-9
[
9192825.001
]
[Cites]
Am J Gastroenterol. 1997 Jul;92(7):1117-20
[
9219781.001
]
[Cites]
Cancer Res. 1997 Jul 15;57(14):2909-15
[
9230200.001
]
[Cites]
J Clin Invest. 1997 Sep 15;100(6):1325-9
[
9294096.001
]
[Cites]
Eur J Surg Suppl. 1998;(582):111-4
[
10029375.001
]
[Cites]
Scand J Gastroenterol. 1999 Jan;34(1):4-11
[
10048725.001
]
[Cites]
N Engl J Med. 1999 Jun 17;340(24):1888-99
[
10369853.001
]
[Cites]
Gut. 1997 Mar;40(3):344-9
[
9135523.001
]
[Cites]
Clin Cancer Res. 2000 Jan;6(1):78-89
[
10656435.001
]
[Cites]
Can J Gastroenterol. 2000 Apr;14(4):299-307
[
10799083.001
]
[Cites]
Cancer Res. 2000 Jul 1;60(13):3338-42
[
10910034.001
]
[Cites]
Gastroenterology. 2000 Sep;119(3):837-53
[
10982778.001
]
[Cites]
Gastroenterology. 2000 Sep;119(3):854-65
[
10982779.001
]
[Cites]
Med Clin North Am. 2000 Sep;84(5):1163-82, viii
[
11026923.001
]
[Cites]
Expert Opin Investig Drugs. 2001 Oct;10(10):1875-82
[
11772293.001
]
[Cites]
J Clin Epidemiol. 2003 Oct;56(10):968-76
[
14568628.001
]
[Cites]
Int J Cancer. 2004 Sep 10;111(4):633-9
[
15239144.001
]
[Cites]
J Surg Oncol. 1983 Sep;24(1):83-7
[
6887943.001
]
[Cites]
Gastroenterology. 1987 Nov;93(5):1009-13
[
3653628.001
]
[Cites]
Am J Surg. 1989 Jan;157(1):175-9
[
2535920.001
]
[Cites]
Bull World Health Organ. 1990;68(6):789-95
[
2073716.001
]
[Cites]
Gastroenterology. 1991 Sep;101(3):635-9
[
1650315.001
]
[Cites]
Ann Intern Med. 1991 Dec 15;115(12):952-4
[
1659272.001
]
[Cites]
N Engl J Med. 1993 May 6;328(18):1313-6
[
8385741.001
]
[Cites]
Ann Intern Med. 1993 Oct 15;119(8):836-43
[
8379605.001
]
[Cites]
Adv Intern Med. 1994;39:123-47
[
8140953.001
]
(PMID = 16150858.001).
[ISSN]
0017-5749
[Journal-full-title]
Gut
[ISO-abbreviation]
Gut
[Language]
eng
[Publication-type]
Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 184SNS8VUH / Sulindac; K619IIG2R9 / sulindac sulfone
[Other-IDs]
NLM/ PMC1856089
28.
Lee SS, Park SH, Choi EK, Kim SY, Kim MJ, Lee KH, Kim YH:
Colorectal polyps on portal phase contrast-enhanced CT colonography: lesion attenuation and distinction from tagged feces.
AJR Am J Roentgenol
; 2007 Jul;189(1):35-40
[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]
Colorectal
polyps
on portal phase contrast-enhanced CT colonography: lesion attenuation and distinction from tagged feces.
OBJECTIVE: The purpose of our study was to determine the attenuation of colorectal
polyps
on portal phase contrast-enhanced CT colonography (CTC) and evaluate whether enhanced
polyps
can be clearly distinguished from tagged feces during CTC review.
Forty-eight colonoscopy-proven
polyps
(6-20 mm) and 41 polypoid tagged feces (6-19 mm) were selected from contrast-enhanced CTC performed without (n = 37 examinations) and with (n = 10 examinations) fecal tagging, respectively.
Attenuation of the
polyps
and tagged feces was measured.
Four independent blinded radiologists reviewed the
polyps
and tagged feces at both wide (width, 1,500 H; level -400 H) and soft-tissue (width, 400 H; level, 20 H) window settings to distinguish them by using subjective visual assessment.
RESULTS:
Polyp
attenuation on the portal phase was not correlated with size (R = -0.003; p = 0.99) and was not different between histologic types (p = 0.884).
Enhanced
polyps
(mean +/- SD, 119.9 +/- 25.3 H; range, 50-173 H) showed significantly lower attenuation than did tagged feces (1,521.4 +/- 683.6 H; range, 495-2,683 H) without any overlap (p < 0.0005).
An 8-mm sessile
adenomatous
polyp
was misinterpreted as tagged feces by one reviewer.
CONCLUSION:
Polyp
attenuation on portal phase contrast-enhanced CTC ranges from 50 to 173 H.
Contrast-enhanced
polyps
are clearly and consistently distinguished from barium-tagged polypoid feces.
[MeSH-major]
Colonic Polyps
/ radiography. Colonography, Computed Tomographic / methods. Contrast Media / administration & dosage. Feces. Radiographic Image Enhancement / methods. Rectal Diseases / radiography
MedlinePlus Health Information.
consumer health - Bowel Movement
.
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
MedlinePlus Health Information.
consumer health - Rectal Disorders
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17579149.001).
[ISSN]
1546-3141
[Journal-full-title]
AJR. American journal of roentgenology
[ISO-abbreviation]
AJR Am J Roentgenol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Contrast Media
29.
Kim MS, Jung HK, Jung HS, Choi JY, Na YJ, Pyun GW, Ryu JH, Moon IH, Jo MS:
[A Case of Cronkhite-Canada syndrome showing resolution with Helicobacter pylori eradication and omeprazole].
Korean J Gastroenterol
; 2006 Jan;47(1):59-64
[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.
We describe a 58-year-old woman who was incidentally found to have gastric and
colonic
polyposis, hypoalbuminemia, cutaneous hyperpigmentation and onychodystrophy (Cronkhite-Canada syndrome).
Histology of
polyps
from the stomach showed features of juvenile or retention type (hamartomatous)
polyps
with Helicobacter pylori (H. pylori) infection.
The large pedunculated
colonic polyps
showed hamartomatous
polyps
with
adenomatous
component and polypectomy was performed.
After the treatment with H. pylori eradication and omeprazole, the gastric polyposis, hypoalbuminemia and anemia regressed, and endoscopic polypectomy of gastric
polyps
were performed.
[MeSH-major]
Anti-Ulcer Agents / therapeutic use. Helicobacter Infections / drug therapy. Helicobacter pylori. Omeprazole / therapeutic use.
Polyps
/ complications. Stomach Neoplasms / complications
[MeSH-minor]
Colonic Polyps
/ complications.
Colonic Polyps
/ microbiology.
Colonic Polyps
/ pathology. Female. Humans. Hyperpigmentation / pathology. Middle Aged. Nails, Malformed / pathology. Proton Pump Inhibitors. Syndrome
MedlinePlus Health Information.
consumer health - Helicobacter Pylori Infections
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
Hazardous Substances Data Bank.
OMEPRAZOLE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16434870.001).
[ISSN]
1598-9992
[Journal-full-title]
The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
[ISO-abbreviation]
Korean J Gastroenterol
[Language]
kor
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Korea (South)
[Chemical-registry-number]
0 / Anti-Ulcer Agents; 0 / Proton Pump Inhibitors; KG60484QX9 / Omeprazole
30.
Scott RH, Mansour S, Pritchard-Jones K, Kumar D, MacSweeney F, Rahman N:
Medulloblastoma, acute myelocytic leukemia and colonic carcinomas in a child with biallelic MSH6 mutations.
Nat Clin Pract Oncol
; 2007 Feb;4(2):130-4
[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]
Medulloblastoma, acute myelocytic leukemia and
colonic
carcinomas in a child with biallelic MSH6 mutations.
Background A 13-year-old girl presented with rectal bleeding and was found to have two
colonic
carcinomas (stage Dukes' C) and multiple
colonic polyps
.
A three-generation family history identified no relatives with
colonic
carcinomas or polyposis.
Investigations Immunohistochemical analysis was performed on a sample of
colonic
adenoma
.
[MeSH-major]
Cerebellar Neoplasms / genetics.
Colonic
Neoplasms / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Medulloblastoma / genetics
Genetic Alliance.
consumer health - Acute Myelocytic Leukemia
.
Genetic Alliance.
consumer health - Medulloblastoma
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
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 = 17259933.001).
[ISSN]
1743-4262
[Journal-full-title]
Nature clinical practice. Oncology
[ISO-abbreviation]
Nat Clin Pract Oncol
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / G-T mismatch-binding protein
31.
Stergiou N, Frenz MB, Menke D, Riphaus A, Wehrmann T:
Reduction of miss rates of colonic adenomas by zoom chromoendoscopy.
Int J Colorectal Dis
; 2006 Sep;21(6):560-5
[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]
Reduction of miss rates of
colonic
adenomas
by zoom chromoendoscopy.
BACKGROUND AND AIMS: The aim of this study was to determine the detection rate of
polyps
using zoom chromoendoscopy (ZE) compared with standard video colonoscopy.
The second colonoscopy (C2) was done with a zoom colonoscope spraying the whole
colon
with indigocarmine (0.4%).
During C1, 56 lesions were detected in 26 of 50 patients (34 hyperplastic and 22
adenomatous
).
During C2, 19 additional
polyps
were documented prior to ZE (15% tandem miss rate), and 20 further lesions were detected with ZE (21% additional
polyp
detection rate compared to C1 and C2 without ZE).
Of the 39 additional lesions removed during C2 after ZE, 29 were hyperplastic and 10 were
adenomatous
.
Most
adenomas
detected during the second investigation were found in patients in whom
adenomatous polyps
had already been removed during the initial colonoscopy (9 of 26 patients vs 1 of 24 patients, p<0.02).
The pit pattern classification allowed a correct differentiation between hyperplastic and
adenomatous polyps
(accuracy 93%, sensitivity 90%, specificity 97%).
CONCLUSION: Using zoom chromoendoscopy, the rate of detecting
colonic polyps
can be increased at the cost of a longer retrieval time.
[MeSH-major]
Adenoma
/ pathology.
Colonic
Neoplasms / pathology. Colonoscopy / methods. Coloring Agents. Diagnostic Errors / prevention & control. Indigo Carmine
MedlinePlus Health Information.
consumer health - Colonoscopy
.
Hazardous Substances Data Bank.
INDIGO
.
Hazardous Substances Data Bank.
Indigotindisulfonate sodium
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Am J Gastroenterol. 2002 Jul;97(7):1696-700
[
12135020.001
]
[Cites]
Endoscopy. 2001 Dec;33(12):1001-6
[
11740641.001
]
[Cites]
Dis Colon Rectum. 1982 Oct;25(7):669-72
[
7128368.001
]
[Cites]
J Clin Pathol. 1994 Oct;47(10):880-5
[
7962600.001
]
[Cites]
Endoscopy. 2001 Apr;33(4):367-73
[
11315901.001
]
[Cites]
N Engl J Med. 1993 Dec 30;329(27):1977-81
[
8247072.001
]
[Cites]
Gastrointest Endosc. 2002 Sep;56(3):333-8
[
12196768.001
]
[Cites]
Endoscopy. 2004 Dec;36(12):1109-14
[
15578305.001
]
[Cites]
Endoscopy. 1998 Jun;30(5):437-43
[
9693889.001
]
[Cites]
Endoscopy. 2001 Apr;33(4):306-10
[
11315890.001
]
[Cites]
N Engl J Med. 1992 Mar 5;326(10):658-62
[
1736104.001
]
[Cites]
J Natl Cancer Inst. 1992 Oct 21;84(20):1572-5
[
1404450.001
]
[Cites]
Gastrointest Endosc. 1996 Jul;44(1):8-14
[
8836710.001
]
[Cites]
N Engl J Med. 1992 Mar 5;326(10):653-7
[
1736103.001
]
[Cites]
Am J Gastroenterol. 2002 Jul;97(7):1587-90
[
12135005.001
]
[Cites]
Gastrointest Endosc. 1999 Mar;49(3 Pt 2):S63-6
[
10049451.001
]
[Cites]
World J Surg. 1997 Sep;21(7):694-701
[
9276699.001
]
[Cites]
Gut. 1996 Sep;39(3):449-56
[
8949653.001
]
[Cites]
Gastrointest Endosc. 2002 May;55(6):687-94
[
11979251.001
]
[Cites]
Dis Colon Rectum. 1987 Apr;30(4):247-50
[
3829872.001
]
[Cites]
Am J Gastroenterol. 2001 Sep;96(9):2628-32
[
11569686.001
]
[Cites]
Gastroenterology. 1997 Jan;112(1):24-8
[
8978338.001
]
[Cites]
Gastroenterology. 1996 Apr;110(4):1253-8
[
8613016.001
]
[Cites]
Endoscopy. 2001 Dec;33(12):1036-41
[
11764766.001
]
(PMID = 16283340.001).
[ISSN]
0179-1958
[Journal-full-title]
International journal of colorectal disease
[ISO-abbreviation]
Int J Colorectal Dis
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Coloring Agents; D3741U8K7L / Indigo Carmine
32.
Bretthauer M, Hoff G:
[Prevention and early diagnosis of colorectal cancer].
Tidsskr Nor Laegeforen
; 2007 Oct 18;127(20):2688-91
[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.
CRC develops from benign
adenomas
in
the colon
over a long time.
RESULTS AND INTERPRETATION: Acetylsalicylic-acid,
non
-steroidal anti-inflammatory drugs and COX-2 inhibitors are shown to reduce
adenoma
growth, but it remains uncertain whether these drugs reduce the incidence of CRC.
[MeSH-minor]
Colon
/ radiography. Colonoscopy. Early Diagnosis. Evidence-Based Medicine. Humans. Mass Screening. Occult Blood. Prognosis. Randomized Controlled Trials as Topic. Sigmoidoscopy
Genetic Alliance.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17952153.001).
[ISSN]
0807-7096
[Journal-full-title]
Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
[ISO-abbreviation]
Tidsskr. Nor. Laegeforen.
[Language]
nor
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Norway
[Number-of-references]
35
33.
Kim DK, Myung SJ, Yang SK, Hong SS, Kim KJ, Byeon JS, Lee GH, Kim JH, Min YI, Lee SM, Jeong JY, Song K, Jung SA:
Analysis of PTEN gene mutations in Korean patients with Cowden syndrome and polyposis syndrome.
Dis Colon Rectum
; 2005 Sep;48(9):1714-22
[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.
We analyzed the DNA of various organs and lesions in Korean patients with Cowden syndrome, their family members, and patients with familial
adenomatous
polyposis for germline or somatic PTEN mutations.
METHODS: The 11 patients included in this study were 5 patients with Cowden syndrome, 4 of their family members, and 2 patients with familial
adenomatous
polyposis.
Deletions and mutations in exons 1 to 9 of the PTEN gene were evaluated by polymerase chain reaction-single strand conformation polymorphism and sequencing analysis in esophageal acanthosis, gastric
polyps
,
colonic polyps
, skin lesions, and peripheral blood mononuclear cells.
RESULTS: All patients with Cowden syndrome showed several to numerous
polyps
in the gastrointestinal tract.
Identical mutations were found in all tissue samples, including
colonic polyps
, from each patient.
No PTEN mutations were found in their family members or in any patient with familial
adenomatous
polyposis.
[MeSH-major]
Adenomatous
Polyposis Coli / genetics. Chromosomes, Human, Pair 10. Germ-Line Mutation. Hamartoma Syndrome, Multiple / genetics. Phosphoric Monoester Hydrolases / genetics. Tumor Suppressor Proteins / genetics
Genetic Alliance.
consumer health - Cowden Syndrome
.
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 = 16007494.001).
[ISSN]
0012-3706
[Journal-full-title]
Diseases of the colon and rectum
[ISO-abbreviation]
Dis. Colon Rectum
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Tumor Suppressor Proteins; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
34.
Glei M, Hovhannisyan G, Pool-Zobel BL:
Use of Comet-FISH in the study of DNA damage and repair: review.
Mutat Res
; 2009 Jan-Feb;681(1):33-43
[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 Comet-FISH technique is a useful tool to detect overall and region-
specific
DNA damage and repair in individual cells.
Whereas the Comet assay allows separating fragmented from
non
-fragmented DNA, FISH helps to detect specifically labelled DNA sequences of interest, including whole chromosomes.
Thus the combination of both techniques has been applied in particular for detection of site-
specific
breaks in DNA regions which are relevant for development of different diseases.
This paper reviews the relevant literature and presents three examples on how Comet-FISH was used for studying the induction of DNA damage by genotoxic compounds related to oxidative stress in
colon
cancer-relevant genes (TP53, APC, KRAS) of a
colon adenoma
cell line.
A third example relates to measuring repair
of specific
gene regions using Comet-FISH, a method that can be developed to biomarker application.
Taken together, available data suggests that Comet-FISH helps to get further insights into sensitivity
of specific
DNA regions and consequently in mechanisms of carcinogenesis.
Although the nature of the measured Comet-FISH endpoint precludes us from stating basically that damage and repair are occurring within
the specific
gene, it is at least possible to evaluate whether the damage and repair are occurring within the vicinity of the gene of interest.
[MeSH-minor]
Cell Line, Tumor.
Colonic
Neoplasms / genetics.
Colonic
Neoplasms / metabolism. Genes, APC / drug effects. Genes, p53 / drug effects. Genes, ras / drug effects. Genetic Markers. Humans. Mutagens / toxicity. Oxidative Stress / genetics. Telomere / drug effects. Telomere / genetics
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18304859.001).
[ISSN]
0027-5107
[Journal-full-title]
Mutation research
[ISO-abbreviation]
Mutat. Res.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Genetic Markers; 0 / Mutagens
[Number-of-references]
88
35.
Bastos P, Cardoso H, Ferreira F, Pimentel-Nunes P, Bartosch C, Souto-Moura C, Ribeiro A, Macedo G:
Adenocarcinoma of the colon associated with hyperplastic polyposis.
Gastroenterol Hepatol
; 2010 Jun-Jul;33(6):470-1
[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]
Adenocarcinoma of the
colon
associated with hyperplastic polyposis.
[MeSH-major]
Adenocarcinoma, Mucinous / pathology.
Adenomatous Polyps
/ pathology.
Colonic
Neoplasms / pathology.
Colonic Polyps
/ pathology. Neoplasms, Multiple Primary / pathology. Neoplastic Syndromes, Hereditary / diagnosis
[MeSH-minor]
Adenoma
, Villous / pathology.
Adenoma
, Villous / surgery.
Adenomatous
Polyposis Coli / diagnosis. Adult. Colectomy. Colonoscopy. CpG Islands. DNA Methylation / genetics. Diagnosis, Differential. Female. Humans. Hyperplasia. Proto-Oncogene Proteins B-raf / genetics
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
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 = 20363055.001).
[ISSN]
0210-5705
[Journal-full-title]
Gastroenterología y hepatología
[ISO-abbreviation]
Gastroenterol Hepatol
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
Spain
[Chemical-registry-number]
EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
36.
Ashktorab H, Belgrave K, Hosseinkhah F, Brim H, Nouraie M, Takkikto M, Hewitt S, Lee EL, Dashwood RH, Smoot D:
Global histone H4 acetylation and HDAC2 expression in colon adenoma and carcinoma.
Dig Dis Sci
; 2009 Oct;54(10):2109-17
[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]
Global histone H4 acetylation and HDAC2 expression in
colon adenoma
and carcinoma.
Chromatin remodeling and activation of transcription are important aspects of gene regulation, but these often go awry in disease progression, including during
colon
cancer development.
We investigated the status of global histone acetylation (by measuring H3, H4 acetylation of lysine residues, which also occur over large regions of chromatin including coding regions and
non
-promoter sequences) and expression of histone deacetylase 2 (HDAC2) in colorectal cancer (CRC) tissue microarrays using immunohistochemical staining.
Specifically, HDAC2 and the acetylation of histones H4K12 and H3K18 were evaluated in 134
colonic
adenomas
, 55 moderate to well differentiated carcinomas, and 4 poorly differentiated carcinomas compared to matched normal tissue.
HDAC2 nuclear expression was detected at high levels in 81.9%, 62.1%, and 53.1% of CRC,
adenomas
, and normal tissue, respectively (P = 0.002).
HDAC2 expression was correlated significantly with progression
of adenoma
to carcinoma (P = 0.002), with a discriminative power of 0.74, when comparing cancer and
non
-cancer cases.
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]
Mol Cell Biol. 2000 Aug;20(15):5540-53
[
10891493.001
]
[Cites]
Lung Cancer. 2008 Jan;59(1):24-31
[
17854949.001
]
[Cites]
J Natl Cancer Inst. 2001 Jun 6;93(11):824-42
[
11390532.001
]
[Cites]
Science. 2001 Aug 10;293(5532):1074-80
[
11498575.001
]
[Cites]
Curr Opin Oncol. 2001 Nov;13(6):477-83
[
11673688.001
]
[Cites]
J Cell Sci. 2002 Feb 15;115(Pt 4):689-98
[
11865025.001
]
[Cites]
Nature. 2002 May 23;417(6887):455-8
[
12024216.001
]
[Cites]
Br J Cancer. 2002 Jun 5;86(11):1817-23
[
12087472.001
]
[Cites]
Oncogene. 2002 Aug 12;21(35):5427-40
[
12154405.001
]
[Cites]
J Exp Clin Cancer Res. 2002 Sep;21(3):377-82
[
12385581.001
]
[Cites]
Chem Biol. 2002 Nov;9(11):1167-73
[
12445767.001
]
[Cites]
Cancer Res. 2002 Dec 15;62(24):7213-8
[
12499261.001
]
[Cites]
Biochem J. 2003 Mar 15;370(Pt 3):737-49
[
12429021.001
]
[Cites]
Clin Cancer Res. 2003 Mar;9(3):1112-7
[
12631615.001
]
[Cites]
Ann N Y Acad Sci. 2003 Mar;983:220-31
[
12724227.001
]
[Cites]
J Biol Chem. 2003 Sep 12;278(37):35775-80
[
12837748.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 May 11;101(19):7398-403
[
15123805.001
]
[Cites]
Mol Cell Biol. 2004 Jun;24(12):5106-18
[
15169878.001
]
[Cites]
J Cell Physiol. 2000 Jul;184(1):1-16
[
10825229.001
]
[Cites]
J Assoc Acad Minor Phys. 1999;10(3):59-67
[
10826011.001
]
[Cites]
Cancer. 1980 Mar 15;45(5 Suppl):1185-92
[
7357511.001
]
[Cites]
Cell. 1997 Aug 22;90(4):595-606
[
9288740.001
]
[Cites]
Cancer. 1997 Nov 1;80(9):1803-4
[
9351551.001
]
[Cites]
Cancer. 1999 Apr 15;85(8):1670-6
[
10223559.001
]
[Cites]
J Pathol. 2005 Jan;205(1):65-73
[
15586362.001
]
[Cites]
Nat Genet. 2005 Apr;37(4):391-400
[
15765097.001
]
[Cites]
Cancer Res. 2005 Apr 1;65(7):2684-9
[
15805266.001
]
[Cites]
Nature. 2005 Jun 30;435(7046):1262-6
[
15988529.001
]
[Cites]
Int J Cancer. 2005 Oct 10;116(6):914-9
[
15856472.001
]
[Cites]
Ann Thorac Surg. 2006 Aug;82(2):396-401; discussion 401
[
16863736.001
]
[Cites]
Methods Enzymol. 2006;410:400-15
[
16938563.001
]
[Cites]
Science. 2006 Oct 13;314(5797):268-74
[
16959974.001
]
[Cites]
Histopathology. 2007 Jan;50(1):113-30
[
17204026.001
]
[Cites]
CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66
[
17237035.001
]
[Cites]
Cell. 2007 Feb 23;128(4):669-81
[
17320505.001
]
[Cites]
Cancer Res. 2007 Mar 15;67(6):2685-92
[
17363589.001
]
[Cites]
Semin Cancer Biol. 2007 Oct;17(5):363-9
[
17555985.001
]
[Cites]
Virchows Arch. 2007 Oct;451(4):763-9
[
17674041.001
]
[Cites]
J Clin Oncol. 2007 Oct 1;25(28):4358-64
[
17906200.001
]
[Cites]
Science. 2007 Nov 16;318(5853):1108-13
[
17932254.001
]
[Cites]
Hum Mol Genet. 2001 Apr;10(7):687-92
[
11257100.001
]
(PMID = 19057998.001).
[ISSN]
1573-2568
[Journal-full-title]
Digestive diseases and sciences
[ISO-abbreviation]
Dig. Dis. Sci.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA122959; United States / NCI NIH HHS / CA / CA122959-02; United States / NCI NIH HHS / CA / R01 CA122959-02; United States / PHS HHS / / A102681; United States / NCI NIH HHS / CA / R01 CA122959
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Histones; EC 3.5.1.98 / Histone Deacetylases
[Other-IDs]
NLM/ NIHMS118762; NLM/ PMC2737733
37.
Rennert G, Almog R, Tomsho LP, Low M, Pinchev M, Chaiter Y, Bonner JD, Rennert HS, Greenson JK, Gruber SB:
Colorectal polyps in carriers of the APC I1307K polymorphism.
Dis Colon Rectum
; 2005 Dec;48(12):2317-21
[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]
Colorectal
polyps
in carriers of the APC I1307K polymorphism.
The prevalence of
polyps
and
adenomas
in specimens of colorectal cancer who are carriers and noncarriers of the APC I1307K polymorphism is compared.
METHOD: Prevalence of
adenomatous polyps
in the pathology specimens of the study participants, stratified by their APC I1307K polymorphism status, was studied in 900 consecutive cases of colorectal cancer diagnosed in northern Israel between 1998 and 2002, within the framework of a population-based, case-controlled study (MECC Study).
Prevalence was higher among Ashkenazi Jews (11.2 percent) than among
non
-Ashkenazi Jews (2.7 percent) or Arabs (3.1 percent).
After adjustment for age, APC I1307K carriers were significantly more likely than noncarriers to have
polyps
in their surgical specimen (51.3 percent vs. 32.6 percent, P = 0.002).
Adenomas
with a tubular component (either tubular
adenomas
or tubulovillous
adenomas
), but not villous
adenomas
, were significantly more frequent among carriers (37.2 percent vs. 23.6 percent, P = 0.005).
CONCLUSION: Together with former evidence of I1307K being a risk factor for colorectal cancer, these data suggest that colonoscopic surveillance for colorectal
adenomas
and cancer may be warranted in I1307K carriers, even in the absence of other identifiable risk factors.
[MeSH-major]
Adenoma
/ genetics.
Colonic Polyps
/ genetics. Colorectal Neoplasms / genetics. Genes, APC. Polymorphism, Genetic
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16228836.001).
[ISSN]
0012-3706
[Journal-full-title]
Diseases of the colon and rectum
[ISO-abbreviation]
Dis. Colon Rectum
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
38.
Suzuki R, Kohno H, Sugie S, Tanaka T:
Dose-dependent promoting effect of dextran sodium sulfate on mouse colon carcinogenesis initiated with azoxymethane.
Histol Histopathol
; 2005 04;20(2):483-92
[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]
Dose-dependent promoting effect of dextran sodium sulfate on mouse
colon
carcinogenesis initiated with azoxymethane.
We previously reported a powerful tumor-promoting ability of dextran sodium sulfate (DSS) in a novel mouse model for colitis-related
colon
carcinogenesis initiated with azoxymethane (AOM).
All animals were sacrificed at week 14 and histological alterations in their
colon
and nitrotyrosine immunohistochemistry were examined to evaluate the nitrosative stress.
In the mice which received AOM and 2% DSS, the incidences (multiplicity) of
colonic
tubular
adenoma
and adenocarcinoma were 75% (1.25+/-1.26/mouse) and 100% (2.75+/-2.22/mouse), respectively.
Mice given AOM and 1% DSS had 80% incidence
of adenoma
(1.00+/-0.71/mouse) and 60% incidence of adenocarcinoma (1.40+/-2.07/mouse) in
the colon
.
In a mouse treated with AOM and 0.5% DSS, only one
colonic
adenoma
(20% incidence with 0.20+/-0.45 multiplicity) developed.
Higher frequency of high-grade
colonic
dysplasia was noted in mice given AOM and 2% or 1% DSS when compared with mice treated with AOM and lower doses of DSS.
Also, scoring of inflammation and nitrotyrosine immunoreactivity suggested that severe inflammation and nitrosation stress caused by high-doses (2% and 1%) of DSS contribute its tumor-promoting effects in mouse
colon
carcinogenesis initiated with a low dose of AOM.
[MeSH-major]
Carcinogens / toxicity.
Colonic
Neoplasms / chemically induced. Dextran Sulfate / toxicity. Tyrosine / analogs & derivatives
[MeSH-minor]
Animals. Azoxymethane / administration & dosage. Azoxymethane / toxicity. Cocarcinogenesis. Colitis / chemically induced. Colitis / pathology.
Colonic
Diseases / chemically induced.
Colonic
Diseases / pathology. Dose-Response Relationship, Drug. Intestinal Mucosa / drug effects. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Male. Mice. Mice, Inbred ICR. Ulcer / chemically induced. Ulcer / pathology
Hazardous Substances Data Bank.
L-TYROSINE
.
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15736053.001).
[ISSN]
0213-3911
[Journal-full-title]
Histology and histopathology
[ISO-abbreviation]
Histol. Histopathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Spain
[Chemical-registry-number]
0 / Carcinogens; 3604-79-3 / 3-nitrotyrosine; 42HK56048U / Tyrosine; 9042-14-2 / Dextran Sulfate; MO0N1J0SEN / Azoxymethane
39.
Martínez Torrente F, Orts Castro A, García-Montoto F, Pérez-Cerdá F:
[Patient with right ventricular arrhythmogenic dysplasia, ascites and ulcerative colitis: anesthetic management during major abdominal surgery].
Rev Esp Anestesiol Reanim
; 2005 Dec;52(10):631-3
[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.
[Transliterated title]
Manejo anestésico
de
un paciente con displasia arritmogénica
de
ventrículo derecho, ascitis y colitis ulcerosa para una cirugía abdominal mayor.
A 43-year-old man with ulcerative colitis was scheduled for pancolectomy owing to
adenomatous
transformation of
polyps
.
[MeSH-minor]
Adenomatous Polyps
/ surgery. Adult. Analgesia, Epidural / methods. Atracurium / analogs & derivatives. Catheter Ablation.
Colonic
Neoplasms / surgery.
Colonic Polyps
/ surgery. Defibrillators, Implantable. Equipment Failure. Fentanyl. Humans. Isoflurane. Male. Monitoring, Intraoperative. Pain, Postoperative / drug therapy. Postoperative Care. Postoperative Complications / surgery. Preanesthetic Medication. Respiration, Artificial. Thiopental
Genetic Alliance.
consumer health - Ulcerative Colitis
.
MedlinePlus Health Information.
consumer health - Ulcerative Colitis
.
Hazardous Substances Data Bank.
Isoflurane
.
Hazardous Substances Data Bank.
FENTANYL
.
Hazardous Substances Data Bank.
Thiopental
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16435619.001).
[ISSN]
0034-9356
[Journal-full-title]
Revista española de anestesiología y reanimación
[ISO-abbreviation]
Rev Esp Anestesiol Reanim
[Language]
spa
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Spain
[Chemical-registry-number]
64228-79-1 / Atracurium; 76-75-5 / Thiopental; CYS9AKD70P / Isoflurane; QX62KLI41N / cisatracurium; UF599785JZ / Fentanyl
40.
Hoffman A, Sar F, Goetz M, Tresch A, Mudter J, Biesterfeld S, Galle PR, Neurath MF, Kiesslich R:
High definition colonoscopy combined with i-Scan is superior in the detection of colorectal neoplasias compared with standard video colonoscopy: a prospective randomized controlled trial.
Endoscopy
; 2010 Oct;42(10):827-33
[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 primary endpoint was the detection of patients having
colon
cancer or at least one
adenoma
.
Significantly more neoplastic (
adenomatous
and cancerous) lesions and more flat
adenomas
could be detected using high definition endoscopy with surface enhancement.
[MeSH-major]
Adenoma
/ diagnosis.
Colonic Polyps
/ diagnosis. Colonoscopy / methods. Colorectal Neoplasms / diagnosis. Image Enhancement / instrumentation. Image Enhancement / methods
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
MedlinePlus Health Information.
consumer health - Colonoscopy
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
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]
© Georg Thieme Verlag KG Stuttgart · New York.
[CommentIn]
Endoscopy. 2010 Oct;42(10):866-9
[
20886407.001
]
(PMID = 20803419.001).
[ISSN]
1438-8812
[Journal-full-title]
Endoscopy
[ISO-abbreviation]
Endoscopy
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Randomized Controlled Trial
[Publication-country]
Germany
41.
Jurek D, Fleckl E, Marian B:
Bile acid induced gene expression in LT97 colonic adenoma cells.
Food Chem Toxicol
; 2005 Jan;43(1):87-93
[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]
Bile acid induced gene expression in LT97
colonic
adenoma
cells.
LT97 human
colonic
adenoma
cells reflecting early premalignant genotype and growth characteristics have been posed to tumor promoting bile acids in order to identify marker genes that permit identification of tumor promoters in vitro.
Physiologically relevant concentrations of desoxycholate (DOC) and chenodesoxycholate (CDC) upregulated expression
of c
-fos and COX-2 in a concentration- and time-dependent manner.
Transient induction
of c
-fos was seen with
the non
-promoting taurodesoxycholate (TDOC) as well as DOC, however extended induction at 3 h was only achieved by DOC and CDC reaching 3-6-fold as compared to the control.
Stimulation of COX-2 expression was completely
specific
for the tumor promoting analogs DOC and CDC.
Expression of VEGF was stimulated 4-5-fold in the tumor promoter (DOC and CDC) groups and about 2-fold in
the non
-promoting controls TDOC and GCDC.
At later times the tumor promoter
specific
difference was lost.
Our results show that all three genes are modulated in a tumor promoter dependent way and that their upregulation in LT97
adenoma
cells can be used for in vitro testing
of colon
tumor promoters and chemopreventive compounds.
[MeSH-major]
Adenoma
/ metabolism. Bile Acids and Salts / pharmacology. Biomarkers, Tumor / metabolism.
Colonic
Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / drug effects
Hazardous Substances Data Bank.
DEOXYCHOLIC ACID
.
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 = 15582199.001).
[ISSN]
0278-6915
[Journal-full-title]
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
[ISO-abbreviation]
Food Chem. Toxicol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Bile Acids and Salts; 0 / Biomarkers, Tumor; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins c-fos; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 005990WHZZ / Deoxycholic Acid; 0GEI24LG0J / Chenodeoxycholic Acid; 516-50-7 / Taurodeoxycholic Acid; 63231-63-0 / RNA; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases
42.
Buecher B, Bezieau S, Dufilhol C, Cauchin E, Heymann MF, Mosnier JF:
[Emerging concepts in colorectal serrated polyps].
Gastroenterol Clin Biol
; 2007 Jan;31(1):39-54
[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]
[Emerging concepts in colorectal serrated
polyps
].
Colorectal serrated
polyps
are heterogeneous epithelial lesions characterized by a serrated architecture.
They include the classical hyperplastic
polyps
and the much rarer serrated
adenomas
and mixed
polyps
.
Whereas serrated
adenomas
are composed of an unequivocal
adenomatous
epithelium with architectural serrated, mixed
polyps
include two separate hyperplastic and
adenomatous
components.
During the past few years, another type of serrated
polyp
with only very subtle proliferation abnormalities has been described.
These atypical serrated
polyps
may occur either sporadically or in the context of colorectal polyposis.
Despite their close resemblance to traditional hyperplastic
polyps
, some authors argued that they should be regarded as authentically neoplastic lesions and have proposed to call them "sessile serrated
adenomas
".
This article reviews the histological features, the endoscopic appearance, the natural history and the molecular phenotype of the different categories of serrated
polyps
and introduces the concept of "serrated neoplastic pathway" in the development of colorectal cancer.
[MeSH-major]
Adenoma
/ pathology.
Colonic Polyps
/ pathology. Colorectal Neoplasms / pathology
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
MedlinePlus Health Information.
consumer health - Colorectal 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 = 17273130.001).
[ISSN]
0399-8320
[Journal-full-title]
Gastroentérologie clinique et biologique
[ISO-abbreviation]
Gastroenterol. Clin. Biol.
[Language]
fre
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
France
[Number-of-references]
90
43.
van Kouwen MC, Laverman P, van Krieken JH, Oyen WJ, Nagengast FM, Drenth JP:
Noninvasive monitoring of colonic carcinogenesis: feasibility of [(18)F]FDG-PET in the azoxymethane model.
Nucl Med Biol
; 2006 Feb;33(2):245-8
[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]
Noninvasive monitoring of
colonic
carcinogenesis: feasibility of [(18)F]FDG-PET in the azoxymethane model.
BACKGROUND: Azoxymethane (AOM) is a potent carcinogen that induces colorectal cancer and
adenomas
in rats.
At present, it is unknown at which stage FDG accumulation occurs during
the adenoma
carcinoma sequence.
RESULTS: Macroscopic examination revealed 21 tumors (7 located in the small bowel and 14 in
the colon
) in 19 rats.
On histological examination, we found 10
colonic
adenocarcinomas (the first being observed at Week 22) and 7 adenocarcinoma in the small bowel.
In total, seven
colon adenomas
were found in five rats, six of which expressed high-grade dysplasia.
[(18)F]FDG uptake was lower in
adenomas
than in carcinomas.
[MeSH-major]
Adenocarcinoma / metabolism. Adenocarcinoma / radionuclide imaging.
Colonic
Neoplasms / metabolism.
Colonic
Neoplasms / radionuclide imaging. Disease Models, Animal. Fluorodeoxyglucose F18 / pharmacokinetics
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16546679.001).
[ISSN]
0969-8051
[Journal-full-title]
Nuclear medicine and biology
[ISO-abbreviation]
Nucl. Med. Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; MO0N1J0SEN / Azoxymethane
44.
Goldstein NS:
Serrated pathway and APC (conventional)-type colorectal polyps: molecular-morphologic correlations, genetic pathways, and implications for classification.
Am J Clin Pathol
; 2006 Jan;125(1):146-53
[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]
Serrated pathway and APC (conventional)-type colorectal
polyps
: molecular-morphologic correlations, genetic pathways, and implications for classification.
This review addresses the genetic mutations and cell signaling pathway alterations in colorectal premalignant
polyps
, focusing on the link between molecular changes and morphologic features.
Biallelic APC (
adenomatous
polyposis coli) mutations are directly responsible for
the specific
and characteristic cytologic features of dysplastic cells in conventional tubular
adenomas
.
Sessile serrated
adenomas
(SSAs) are the precursor lesions of the serrated neoplasia pathway.
Intracellular butyrate inhibits histone deacetylase, allowing histone hyperacetylation and, eventually, transcriptional activation
of specific
genes.
Progressive loss of cell cycle control and decreased and altered cytoplasmic differentiation produce the characteristic constellation of morphologic changes of SSAs and traditional serrated
adenomas
.
[MeSH-major]
Adenomatous
Polyposis Coli / pathology.
Colonic Polyps
/ pathology
[MeSH-minor]
Adaptor Proteins, Signal Transducing.
Adenomatous
Polyposis Coli Protein / physiology. Carrier Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Nuclear Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
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 = 16483003.001).
[ISSN]
0002-9173
[Journal-full-title]
American journal of clinical pathology
[ISO-abbreviation]
Am. J. Clin. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / CDKN1A protein, human; 0 / Carrier Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / MLH1 protein, human; 0 / Nuclear Proteins; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
[Number-of-references]
123
45.
Tobi M, Kam M, Ullah N, Qureshi K, Yordanova V, Hatfield J, Fligiel SE, Sochacki P, McGarrity T, Cole C, Lawson M, Jacoby R:
An anti-adenoma antibody, Adnab-9, may reflect the risk for neoplastic progression in familial hamartomatous polyposis syndromes.
Dig Dis Sci
; 2008 Mar;53(3):723-9
[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]
An anti-
adenoma
antibody, Adnab-9, may reflect the risk for neoplastic progression in familial hamartomatous polyposis syndromes.
Patients with the hamartomatous polyposis Peutz-Jeghers and familial juvenile polyposis syndromes are predisposed to colorectal cancer but lack early genetic alterations found in
adenomatous
premalignant lesions.
We studied hamartomatous
polyps
for the expression of an early preneoplastic colorectal neoplasia risk marker also found in familial
adenomatous
polyposis patients.
Retrospective, genetic, and hospital archival tissue immunohistochemistry using Adnab-9, a premalignant marker often found in Paneth-like cells (PCs), was performed on sections of
polyps
from eight patients with Peutz-Jeghers syndrome, eight patients with familial juvenile polyposis, and 36 hyperplastic
polyp
control sections.
Hamartomatous polyposis patients also underwent
specific
genetic analysis.
Eighty-nine percent of Peutz-Jeghers syndrome
polyps
labeled with Adnab-9 compared with 63% for AD5; 88% of familial juvenile polyposis sections also labeled with Adnab-9.
Of the 36 hyperplastic
polyp
sections, only four (11%) labeled with Adnab-9 and one (3%) with AD5.
Adnab-9 labeling of PCs in the epithelial elements of hamartomatous
colonic
lesions of hereditary hamartomatous syndrome patients reflects the predisposition to colorectal cancer, further justifying early intervention strategies.
[MeSH-major]
Adenomatous
Polyposis Coli / pathology. Antibodies, Monoclonal. Biomarkers, Tumor.
Colon
/ pathology.
Colonic Polyps
/ pathology. Peutz-Jeghers Syndrome / pathology
Genetic Alliance.
consumer health - Familial Polyposis
.
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Am J Gastroenterol. 2000 Mar;95(3):596-604
[
10710046.001
]
[Cites]
Dig Dis Sci. 2003 Jan;48(1):223-9
[
12645814.001
]
[Cites]
Am J Gastroenterol. 2003 Mar;98(3):671-8
[
12650805.001
]
[Cites]
Scand J Gastroenterol. 1992 Sep;27(9):737-42
[
1411278.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2003 Oct;12(10):1095-9
[
14578149.001
]
[Cites]
J Histochem Cytochem. 1981 Apr;29(4):577-80
[
6166661.001
]
[Cites]
Dig Dis Sci. 2002 Feb;47(2):317-21
[
11855547.001
]
[Cites]
Scand J Gastroenterol. 1993 Dec;28(12):1025-34
[
8303203.001
]
[Cites]
Ann Surg Oncol. 1998 Dec;5(8):751-6
[
9869523.001
]
[Cites]
N Engl J Med. 1987 Jun 11;316(24):1511-4
[
3587280.001
]
[Cites]
Front Biosci. 1999 Mar 15;4:D329-38
[
10077546.001
]
[Cites]
Dig Dis Sci. 2002 Jun;47(6):1349-55
[
12064812.001
]
[Cites]
Dig Dis Sci. 2005 Apr;50(4):708-13
[
15844706.001
]
[Cites]
Am J Gastroenterol. 1999 Jan;94(1):257-61
[
9934767.001
]
[Cites]
Clin Genet. 2002 Oct;62(4):282-7
[
12372054.001
]
[Cites]
Gastroenterology. 1997 Apr;112(4):1398-403
[
9098028.001
]
[Cites]
Clin Genet. 1999 Aug;56(2):136-41
[
10517250.001
]
[Cites]
Int J Pancreatol. 2001;29(3):141-50
[
12067217.001
]
[Cites]
Gut. 2001 Feb;48(2):176-85
[
11156637.001
]
[Cites]
Hum Pathol. 1999 Apr;30(4):467-73
[
10208470.001
]
[Cites]
Science. 1996 Jan 19;271(5247):350-3
[
8553070.001
]
[Cites]
Clin Gastroenterol Hepatol. 2004 Mar;2(3):246-51
[
15017609.001
]
[Cites]
Gastroenterology. 2004 Oct;127(4):1030-7
[
15480979.001
]
(PMID = 17934846.001).
[ISSN]
0163-2116
[Journal-full-title]
Digestive diseases and sciences
[ISO-abbreviation]
Dig. Dis. Sci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Adnab-9; 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / alpha-Defensins; 0 / alpha-defensin 5, human; EC 2.7.1.- / STK11 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
46.
Lee HL, Son BK, Lee OY, Jeon YC, Han DS, Sohn JH, Yoon BC, Choi HS, Hahm JS, Lee MH, Lee DH, Kee CS:
[Abdominal obesity, insulin resistance, and the risk of colonic adenoma].
Korean J Gastroenterol
; 2007 Mar;49(3):147-51
[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]
[Abdominal obesity, insulin resistance, and the risk of
colonic
adenoma
].
BACKGROUND/AIMS: Abdominal obesity and hyperinsulinemia or insulin resistance are of interest in connection with
colon
carcinogenesis.
We conducted a prospective case controlled study for the evaluation of relationship between abdominal obesity, insulin resistance, and colorectal
adenoma
.
METHODS: Fifty patients with colorectal
adenoma
and fifty healthy subjects were included in this study.
RESULTS: There were no differences in sex, serum insulin, FBS, HOMA-IR, TG, CROL between
adenoma
and control group.
Subjects with high BMI, WHR, percent body fat, and obesity were more likely to have
colonic
adenoma
.
Multiple logistic regression analysis after adjusting confounding factors, had revealed that WHR was the most important independent risk factor for
colon adenoma
.
CONCLUSIONS: Abdominal obesity was most closely related to
colonic
adenoma
.
However, insulin resistance was not related to
colonic
adenoma
.
[MeSH-major]
Abdominal Fat.
Adenoma
/ etiology.
Colonic
Neoplasms / etiology. Insulin Resistance. Obesity / complications
Genetic Alliance.
consumer health - Obesity
.
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
[CommentIn]
Korean J Gastroenterol. 2007 Mar;49(3):192-5
[
18172350.001
]
(PMID = 18172342.001).
[ISSN]
1598-9992
[Journal-full-title]
The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
[ISO-abbreviation]
Korean J Gastroenterol
[Language]
kor
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Korea (South)
47.
Park JG, Kim IJ:
[Hereditary colorectal cancer].
Korean J Gastroenterol
; 2005 Feb;45(2):78-87
[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.
Hereditary CRC is conventionally divided into two major categories: hereditary
non
-polyposis colorectal cancer (HNPCC) and those related to polyposis syndromes including familial
adenomatous
polyposis (FAP), Peutz-Jegher syndrome (PJS), and juvenile polyposis (JP).
Germ-line mutation of the APC gene induces FAP, an autosomal dominant
disorder
, characterized by the development of hundreds to thousands of
colonic
adenomas
.
Recently, a mutation on the MYH gene is increasingly being investigated in patients with multiple
polyps
, and autosomal recessive MYH polyposis is considered to be a new category of polyposis.
Although there is no polyposis,
polyps
seem to be more villous and dysplastic and appear to grow rapidly into CRCs.
PJS and JP are reported to be characterized by hamartomatous
polyps
throughout the GI tract and germ-line mutations in the STK11 gene (PJS) and the DPC4/BMPR1A gene (JP).
[MeSH-major]
Adenomatous
Polyposis Coli / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Intestinal Polyposis / genetics. Peutz-Jeghers Syndrome / genetics
Genetic Alliance.
consumer health - Colorectal Cancer
.
Genetic Alliance.
consumer health - Hereditary 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 = 15725711.001).
[ISSN]
1598-9992
[Journal-full-title]
The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
[ISO-abbreviation]
Korean J Gastroenterol
[Language]
kor
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Korea (South)
[Number-of-references]
40
48.
Knoll N, Weise A, Claussen U, Sendt W, Marian B, Glei M, Pool-Zobel BL:
2-Dodecylcyclobutanone, a radiolytic product of palmitic acid, is genotoxic in primary human colon cells and in cells from preneoplastic lesions.
Mutat Res
; 2006 Feb 22;594(1-2):10-9
[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]
2-Dodecylcyclobutanone, a radiolytic product of palmitic acid, is genotoxic in primary human
colon
cells and in cells from preneoplastic lesions.
Results of previous in vitro studies with primary human
colon
cells and in vivo experiments with rats fed with 2-alkylcyclobutanones indicated that these radiolytic derivatives may be genotoxic and enhance the progression
of colon
tumors.
In particular, we explored the relative sensitivities of human
colon
cells, representing different stages of tumor development and healthy
colon
tissues, respectively.
HT29clone19A cells, LT97
adenoma
cells and primary human epithelial cells were exposed to 2dDCB (150-2097 microM).
Genotoxicity, reflected as strand breaks, was assessed using the alkaline version of the comet assay and chromosomal abnormalities were investigated by 24-
color
fluorescence-in-situ-hybridization.
2dDCB was cytotoxic in a time- and dose-dependent manner in LT97
adenoma
cells and in freshly isolated primary cells but not in the human
colon
tumor cell line.
Associated with this was a marked induction of DNA damage by 2dDCB in LT97
adenoma
cells and in freshly isolated colonocytes, whereas in the HT29clone19A cells no strand breaks were detectable.
A long-term incubation of LT97
adenoma
cells with lower concentrations of 2dDCB revealed cytogenetic effects.
In summary, 2dDCB was clearly genotoxic in healthy human
colon
epithelial cells and in cells representing preneoplastic
colon adenoma
.
These findings provide additional evidence that this compound may be regarded as a possible risk factor for processes in
colon
carcinogenesis related to initiation and progression.
[MeSH-major]
Colon
/ drug effects. Cyclobutanes / toxicity. Mutagens / toxicity. Palmitic Acid / metabolism. Precancerous Conditions / genetics
Hazardous Substances Data Bank.
PALMITIC ACID
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16153665.001).
[ISSN]
0027-5107
[Journal-full-title]
Mutation research
[ISO-abbreviation]
Mutat. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Cyclobutanes; 0 / Mutagens; 2V16EO95H1 / Palmitic Acid; 35493-46-0 / 2-dodecylcyclobutanone
49.
Folker MB, Bernstein IT, Holck S:
[Serrated, hyperplastic and hyperplasia-like colorectal polyps].
Ugeskr Laeger
; 2006 Nov 13;168(46):4005-9
[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]
[Serrated, hyperplastic and hyperplasia-like colorectal
polyps
].
The colorectal hyperplastic
polyp
has generally been considered a finding of no clinical significance.
Recent research has, however, called attention to the existence of some variants of hyperplastic
polyp
which are potentially malignant.
The term "advanced serrated
polyp
" has been coined for such cases, which comprise mixed hyperplastic/
adenomatous
tissue, serrated
adenoma
, and sessile serrated
polyp
, in contrast to the traditional hyperplastic
polyp
.
Since epithelial dysplasia is an integrated component of mixed hyperplastic/
adenomatous
polyp
and of the serrated
adenoma
, such a diagnosis would dictate control colonoscopy comparable to the guidelines for subjects with conventional
adenomas
.
The cytology of the sessile serrated
polyp
is, however, closer to that of the traditional hyperplastic
polyp
, whereas the architecture mimics that of the serrated
adenoma
.
For this reason, a consensus regarding the optimal management of such patients has not been obtained, but if
the polyp
is sizeable and located in the right
colon
, control should be considered.
The small, usually left-sided traditional
polyp
as a rule needs no follow-up, but the context in which such a lesion is found and its morphology may influence the clinical decision.
Future large-scale investigations of serrated colorectal
polyps
, including interobserver studies, will be required to identify histological details of clinical utility which can be adopted in daily routine practice.
[MeSH-major]
Adenoma
/ pathology.
Colonic Polyps
/ pathology. Colorectal Neoplasms / pathology
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17125655.001).
[ISSN]
1603-6824
[Journal-full-title]
Ugeskrift for laeger
[ISO-abbreviation]
Ugeskr. Laeg.
[Language]
dan
[Publication-type]
Comparative Study; English Abstract; Journal Article; Review
[Publication-country]
Denmark
[Number-of-references]
40
50.
Brouland JP, Gélébart P, Kovàcs T, Enouf J, Grossmann J, Papp B:
The loss of sarco/endoplasmic reticulum calcium transport ATPase 3 expression is an early event during the multistep process of colon carcinogenesis.
Am J Pathol
; 2005 Jul;167(1):233-42
[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]
The loss of sarco/endoplasmic reticulum calcium transport ATPase 3 expression is an early event during the multistep process
of colon
carcinogenesis.
To better characterize the role of SERCA3 in
colon
carcinogenesis, its expression has been investigated in
colonic
epithelium, benign lesions,
adenomas
, and adenocarcinomas.
In addition, the regulation of SERCA3 expression was analyzed in the context of the
adenomatous
polyposis coli/beta-catenin/T-cell factor 4 (TCF4) pathway and of specificity protein 1 (Sp1)-like factor-dependent transcription.
We report that SERCA3 expression increased along the crypts as cells differentiated in normal
colonic
mucosa and in hyperplastic
polyps
, was moderately and heterogeneously expressed in
colonic
adenomas
with expression levels inversely correlated with the degree of dysplasia, was barely detectable in well and moderately differentiated adenocarcinomas, and was absent in poorly differentiated tumors.
Inhibition of Sp1-like factor-dependent transcription blocked SERCA3 expression during cell differentiation, and SERCA3 expression was induced by the expression of dominant-negative TCF4 in
colon
cancer cells.
These data link SERCA3 expression to the state of differentiation of
colonic
epithelial cells, and relate SERCA3 expression, already decreased in
adenomas
, to enhanced
adenomatous
polyposis coli/beta-catenin/TCF4-dependent signaling and deficient Sp1-like factor-dependent transcription.
In conclusion, intracellular calcium homeostasis becomes progressively anomalous during
colon
carcinogenesis as reflected by deficient SERCA3 expression.
[MeSH-major]
Biomarkers, Tumor / analysis. Calcium / metabolism. Calcium-Transporting ATPases / biosynthesis.
Colonic
Neoplasms / enzymology. Intestinal Mucosa / metabolism
[MeSH-minor]
Adenomatous
Polyposis Coli Protein / genetics. Blotting, Western. Cell Line, Tumor. Cell Transformation, Neoplastic.
Colonic Polyps
/ enzymology. Cytoskeletal Proteins / genetics. DNA-Binding Proteins. Endoplasmic Reticulum / metabolism. Humans. Immunohistochemistry. Sarcoplasmic Reticulum Calcium-Transporting ATPases. TCF Transcription Factors. Trans-Activators / genetics. Transcription Factor 7-Like 2 Protein. Transcription Factors. Transfection. Transgenes. beta Catenin
Hazardous Substances Data Bank.
CALCIUM, ELEMENTAL
.
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]
Blood. 1999 Jun 15;93(12):4395-405
[
10361138.001
]
[Cites]
J Immunol. 1999 Jul 1;163(1):82-92
[
10384103.001
]
[Cites]
Annu Rev Nutr. 1999;19:545-86
[
10448536.001
]
[Cites]
Cancer Res. 1999 Sep 1;59(17):4266-70
[
10485470.001
]
[Cites]
Cancer Res. 1994 Nov 1;54(21):5523-6
[
7923189.001
]
[Cites]
Gene. 1999 Nov 29;240(2):261-7
[
10580145.001
]
[Cites]
J Biol Chem. 1992 Jul 15;267(20):14483-9
[
1385815.001
]
[Cites]
Am J Physiol. 1992 Sep;263(3 Pt 1):G371-9
[
1415549.001
]
[Cites]
Cell Calcium. 1993 Jul;14(7):531-8
[
8402836.001
]
[Cites]
J Clin Invest. 1993 Dec;92(6):2916-21
[
7504695.001
]
[Cites]
Am J Med Sci. 1994 Mar;307(3):167-72
[
8160706.001
]
[Cites]
J Mol Recognit. 1994 Sep;7(3):189-97
[
7880543.001
]
[Cites]
Gastroenterology. 1995 Nov;109(5):1468-74
[
7557127.001
]
[Cites]
Southeast Asian J Trop Med Public Health. 1995;26 Suppl 1:190-6
[
8629105.001
]
[Cites]
Biosci Rep. 1995 Oct;15(5):299-306
[
8825032.001
]
[Cites]
J Biol Chem. 1996 Nov 8;271(45):28220-8
[
8910439.001
]
[Cites]
Biochem Biophys Res Commun. 1997 Mar 6;232(1):80-3
[
9125156.001
]
[Cites]
J Biol Chem. 1997 Apr 18;272(16):10746-50
[
9099725.001
]
[Cites]
J Biol Chem. 1997 Aug 29;272(35):22199-206
[
9268365.001
]
[Cites]
Virchows Arch. 1997 Aug;431(2):111-7
[
9293892.001
]
[Cites]
Cytokines Mol Ther. 1996 Jun;2(2):111-4
[
9384695.001
]
[Cites]
Biochem Biophys Res Commun. 1997 Dec 8;241(1):142-50
[
9405248.001
]
[Cites]
J Biol Chem. 2000 Jan 14;275(2):1371-6
[
10625687.001
]
[Cites]
Ann N Y Acad Sci. 1999;886:195-9
[
10667218.001
]
[Cites]
Science. 2000 Apr 14;288(5464):331-3
[
10764645.001
]
[Cites]
Nucleic Acids Res. 2000 Aug 1;28(15):2969-76
[
10908361.001
]
[Cites]
FEBS Lett. 2000 Jul 7;476(3):203-7
[
10913614.001
]
[Cites]
Biol Pharm Bull. 2000 Aug;23(8):926-9
[
10963297.001
]
[Cites]
Leuk Res. 2000 Oct;24(10):795-804
[
10996197.001
]
[Cites]
Am J Physiol Gastrointest Liver Physiol. 2000 Oct;279(4):G806-14
[
11005769.001
]
[Cites]
Lancet. 2000 Oct 14;356(9238):1300-6
[
11073017.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12625-30
[
11035797.001
]
[Cites]
Hepatogastroenterology. 2000 Sep-Oct;47(35):1291-7
[
11100335.001
]
[Cites]
Cancer Res. 2001 Jan 15;61(2):570-6
[
11212251.001
]
[Cites]
Mol Cell Biol. 2001 Apr;21(7):2413-22
[
11259590.001
]
[Cites]
Biol Chem. 2001 Feb;382(2):329-42
[
11308031.001
]
[Cites]
J Cell Physiol. 2001 Aug;188(2):143-60
[
11424081.001
]
[Cites]
J Biol Chem. 2001 Jul 13;276(28):25742-52
[
11337508.001
]
[Cites]
Am J Surg Pathol. 2002 Feb;26(2):249-56
[
11812948.001
]
[Cites]
FEBS Lett. 2002 Mar 13;514(2-3):122-8
[
11943137.001
]
[Cites]
J Biol Chem. 2002 May 10;277(19):16673-81
[
11872750.001
]
[Cites]
J Biol Chem. 2002 Jul 19;277(29):26310-20
[
11986315.001
]
[Cites]
Biochem Pharmacol. 2002 Jul 15;64(2):307-15
[
12123752.001
]
[Cites]
J Biol Chem. 2002 Sep 27;277(39):36471-8
[
12119294.001
]
[Cites]
FEBS Lett. 2002 Oct 23;530(1-3):147-52
[
12387883.001
]
[Cites]
Diabetes. 2002 Nov;51(11):3245-53
[
12401716.001
]
[Cites]
Cell. 2002 Oct 18;111(2):241-50
[
12408868.001
]
[Cites]
J Biol Chem. 2002 Nov 22;277(47):45579-91
[
12207029.001
]
[Cites]
Cancer Res. 2003 Jan 1;63(1):67-71
[
12517779.001
]
[Cites]
Cell Calcium. 2002 Nov-Dec;32(5-6):269-78
[
12543089.001
]
[Cites]
Cell Calcium. 2002 Nov-Dec;32(5-6):279-305
[
12543090.001
]
[Cites]
Cell Calcium. 2002 Nov-Dec;32(5-6):405-11
[
12543099.001
]
[Cites]
J Mol Biol. 2003 Feb 21;326(3):665-77
[
12581631.001
]
[Cites]
Eur J Surg Oncol. 2003 Mar;29(2):107-17
[
12633551.001
]
[Cites]
Blood. 2003 Apr 15;101(8):3220-8
[
12515718.001
]
[Cites]
J Cell Sci. 2003 May 15;116(Pt 10):1861-2
[
12692187.001
]
[Cites]
Biochem Biophys Res Commun. 2003 May 9;304(3):445-54
[
12729578.001
]
[Cites]
J Biol Chem. 2003 May 16;278(20):17785-91
[
12624107.001
]
[Cites]
J Mol Endocrinol. 2003 Jun;30(3):399-409
[
12790808.001
]
[Cites]
Oncogene. 2003 Sep 4;22(38):6023-31
[
12955081.001
]
[Cites]
J Biol Chem. 2003 Sep 12;278(37):35775-80
[
12837748.001
]
[Cites]
J Biol Chem. 2003 Nov 28;278(48):47877-89
[
12975374.001
]
[Cites]
Oncogene. 2003 Nov 24;22(53):8608-18
[
14634622.001
]
[Cites]
Nat Cell Biol. 2003 Dec;5(12):1041-3
[
14647298.001
]
[Cites]
Biochem Biophys Res Commun. 2004 Apr 23;317(1):235-43
[
15047174.001
]
[Cites]
Curr Mol Med. 2004 May;4(3):313-22
[
15101688.001
]
[Cites]
Annu Rev Biochem. 2004;73:437-65
[
15189149.001
]
[Cites]
Biochem Biophys Res Commun. 2004 Oct 1;322(4):1223-36
[
15336970.001
]
[Cites]
Arch Pathol. 1970 Apr;89(4):349-54
[
5435674.001
]
[Cites]
Gastroenterology. 1974 Mar;66(3):347-56
[
4813500.001
]
[Cites]
Am J Surg Pathol. 1984 Sep;8(9):687-98
[
6476197.001
]
[Cites]
Am J Med Sci. 1987 Nov;294(5):388-94
[
2962490.001
]
[Cites]
Nihon Ketsueki Gakkai Zasshi. 1988 Jul;51(4):746-51
[
3144112.001
]
[Cites]
Nucleic Acids Res. 1989 Jul 25;17(14):5447-59
[
2548163.001
]
[Cites]
Blood. 1990 Dec 15;76(12):2483-92
[
1702327.001
]
[Cites]
J Biol Chem. 1998 May 29;273(22):13982-94
[
9593748.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):9855-60
[
9707565.001
]
[Cites]
Biochim Biophys Acta. 1999 Jan 18;1444(1):85-91
[
9931450.001
]
[Cites]
Nutr Rev. 1999 Apr;57(4):124-6
[
10228349.001
]
[Cites]
Biochem Cell Biol. 1998;76(5):779-85
[
10353711.001
]
(PMID = 15972967.001).
[ISSN]
0002-9440
[Journal-full-title]
The American journal of pathology
[ISO-abbreviation]
Am. J. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Adenomatous Polyposis Coli Protein; 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Trans-Activators; 0 / Transcription Factor 7-Like 2 Protein; 0 / Transcription Factors; 0 / beta Catenin; EC 3.6.3.8 / ATP2A3 protein, human; EC 3.6.3.8 / Calcium-Transporting ATPases; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; SY7Q814VUP / Calcium
[Other-IDs]
NLM/ PMC1603437
51.
Hawk ET, Levin B:
Colorectal cancer prevention.
J Clin Oncol
; 2005 Jan 10;23(2):378-91
[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.
Four classes of chemopreventive compounds have demonstrated efficacy in reducing recurrent colorectal
adenomas
and/or cancer in randomized, controlled trials.
Considerable effort is being expended to define chemopreventive activity, optimal dose, administration schedule, and toxicity for the coxibs in
adenoma
recurrence prevention trials.
[MeSH-minor]
Adenomatous Polyps
/ complications.
Adenomatous Polyps
/ diagnosis. Anti-Inflammatory Agents,
Non
-Steroidal / therapeutic use. Aspirin / therapeutic use. Clinical Trials as Topic.
Colonic Polyps
/ diagnosis. Cyclooxygenase Inhibitors / therapeutic use. Female. Forecasting. Humans. Male. Patient Selection. Precancerous Conditions / diagnosis. Precancerous Conditions / therapy. Risk
Genetic Alliance.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
Hazardous Substances Data Bank.
ACETYLSALICYLIC ACID
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15637400.001).
[ISSN]
0732-183X
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA131378; United States / NCI NIH HHS / CA / R01 CA148817; United States / NCI NIH HHS / CA / R01 CA155638
[Publication-type]
Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase Inhibitors; R16CO5Y76E / Aspirin
[Number-of-references]
167
52.
Murff HJ, Shrubsole MJ, Smalley WE, Wu H, Shyr Y, Ness RM, Zheng W:
The interaction of age and hormone replacement therapy on colon adenoma risk.
Cancer Detect Prev
; 2007;31(2):161-5
[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]
The interaction of age and hormone replacement therapy on
colon adenoma
risk.
BACKGROUND: Several studies have identified a possible interaction between age and hormone replacement therapy on
colon
neoplasm risk.
RESULTS: There was a significant interaction between age and hormone replacement therapy use (P=0.03) with current estrogen users who were over 56 years of age having a reduced odds
of colon adenoma
(OR, 0.40; 95% CI, 0.16-0.98) when compared to never users.
Both older women who had used hormone replacement therapy for 3 or less years (OR, 0.07; 95% CI, 0.006-0.81) and those reporting greater than 10 years of use (OR, 0.27; 95% CI, 0.09-0.80) had a reduced adjusted odds for
adenomas
when compared to
non
-users.
CONCLUSIONS: Duration of use is not likely to explain the stronger association of hormone replacement therapy use with
colon
neoplasm in older women.
MedlinePlus Health Information.
consumer health - Hormone Replacement Therapy
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Epidemiol Biomarkers Prev. 2000 Apr;9(4):443-7
[
10794491.001
]
[Cites]
Obstet Gynecol. 1999 May;93(5 Pt 2):880-8
[
10912438.001
]
[Cites]
Cancer Res. 2001 Jan 1;61(1):126-30
[
11196149.001
]
[Cites]
J Natl Cancer Inst. 2001 Dec 5;93(23):1799-805
[
11734596.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2002 Jul;11(7):622-9
[
12101109.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2004 Apr;13(4):546-52
[
15066918.001
]
[Cites]
Lancet. 1970 Sep 12;2(7672):535-7
[
4195202.001
]
[Cites]
Cancer Causes Control. 1994 Jul;5(4):359-66
[
8080948.001
]
[Cites]
Nat Genet. 1994 Aug;7(4):536-40
[
7951326.001
]
[Cites]
J Natl Cancer Inst. 1995 Jul 19;87(14):1067-71
[
7616598.001
]
[Cites]
Cancer Causes Control. 1997 Mar;8(2):130-8
[
9134236.001
]
[Cites]
Cancer Causes Control. 1997 Mar;8(2):146-58
[
9134238.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1998 Apr;7(4):329-33
[
9568789.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1998 Aug;7(8):653-9
[
9718216.001
]
[Cites]
N Engl J Med. 1999 Jan 14;340(2):101-7
[
9887161.001
]
[Cites]
Dis Colon Rectum. 1999 Feb;42(2):212-7
[
10211498.001
]
[Cites]
Am J Med. 1999 May;106(5):574-82
[
10335731.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 May;14(5):1219-23
[
15894675.001
]
[Cites]
Cancer Causes Control. 2005 Oct;16(8):965-73
[
16132805.001
]
(PMID = 17433566.001).
[ISSN]
0361-090X
[Journal-full-title]
Cancer detection and prevention
[ISO-abbreviation]
Cancer Detect. Prev.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / K07 CA114029; United States / NCI NIH HHS / CA / R01 CA097386-01; United States / NCI NIH HHS / CA / K07 CA114029-01A2; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / P50 CA095103-01; United States / NCI NIH HHS / CA / CA95103; United States / NCI NIH HHS / CA / CA097386-01; United States / NCI NIH HHS / CA / R01 CA97386
[Publication-type]
Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Other-IDs]
NLM/ NIHMS24075; NLM/ PMC1949417
53.
Knöbel Y, Glei M, Weise A, Osswald K, Schäferhenrich A, Richter KK, Claussen U, Pool-Zobel BL:
Uranyl nitrilotriacetate, a stabilized salt of uranium, is genotoxic in nontransformed human colon cells and in the human colon adenoma cell line LT97.
Toxicol Sci
; 2006 Oct;93(2):286-97
[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]
Uranyl nitrilotriacetate, a stabilized salt of uranium, is genotoxic in nontransformed human
colon
cells and in the human
colon adenoma
cell line LT97.
To assess possible hazards, we investigated the genotoxic effects of uranyl nitrilotriacetate (U-NTA) in human
colon
tumor cells (HT29 clone 19A),
adenoma
cells (LT97), and nontransformed primary
colon
cells.
Colon
cells were incubated with U-NTA.
Cell survival, cytotoxicity, cellular glutathione (GSH) levels, genotoxicity, and DNA repair capacity (comet assay), as well as gene- and chromosome-
specific
damage combination of comet assay and fluorescence in situ hybridization [FISH], 24-
color
FISH) were determined.
U-NTA was also genotoxic in LT97 cells and primary
colon
cells, where it additionally increased migration of TP53 into the comet tail.
[MeSH-major]
Colon
/ drug effects. Uranium / toxicity
[MeSH-minor]
Adenoma
/ genetics.
Adenoma
/ pathology. Cell Line, Tumor. Cell Survival / drug effects. Chromosome Aberrations.
Colonic
Neoplasms / genetics.
Colonic
Neoplasms / pathology. DNA Damage. Glutathione / analysis. Humans. In Situ Hybridization, Fluorescence. Reactive Oxygen Species. Tumor Suppressor Protein p53 / analysis
Hazardous Substances Data Bank.
URANIUM, ELEMENTAL
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16840563.001).
[ISSN]
1096-6080
[Journal-full-title]
Toxicological sciences : an official journal of the Society of Toxicology
[ISO-abbreviation]
Toxicol. Sci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Reactive Oxygen Species; 0 / Tumor Suppressor Protein p53; 4OC371KSTK / Uranium; GAN16C9B8O / Glutathione
54.
Varey AH, Rennel ES, Qiu Y, Bevan HS, Perrin RM, Raffy S, Dixon AR, Paraskeva C, Zaccheo O, Hassan AB, Harper SJ, Bates DO:
VEGF 165 b, an antiangiogenic VEGF-A isoform, binds and inhibits bevacizumab treatment in experimental colorectal carcinoma: balance of pro- and antiangiogenic VEGF-A isoforms has implications for therapy.
Br J Cancer
; 2008 Apr 22;98(8):1366-79
[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.
Using isoform-
specific
enzyme-linked immunosorbent assay and quantitative polymerase chain reaction, we found that over 90% of the VEGF in normal
colonic
tissue was VEGF(xxx)b, but there was a variable upregulation of VEGF(xxx) and downregulation of VEGF(xxx)b in paired human CRC samples.
Furthermore, cultured
colonic
adenoma
cells expressed predominantly VEGF(xxx)b, whereas
colonic
carcinoma cells expressed predominantly VEGF(xxx).
However,
adenoma
cells exposed to hypoxia switched their expression from predominantly VEGF(xxx)b to predominantly VEGF(xxx).
VEGF(165)b overexpression in LS174t
colon
cancer cells inhibited
colon
carcinoma growth in mouse xenograft models.
However, although bevacizumab effectively inhibited the rapid growth
of colon
carcinomas expressing VEGF(165), it did not affect the slower growth of tumours from
colonic
carcinoma cells expressing VEGF(165)b.
Both bevacizumab and anti-VEGF(165)b-
specific
antibodies were cytotoxic to
colonic
epithelial cells, but less so to
colonic
carcinoma cells.
Together with the identification of an autocrine cytoprotective role for VEGF(165)b in
colonic
epithelial cells, these results indicate that bevacizumab treatment of human CRC may depend upon this balance of VEGF isoforms.
[MeSH-minor]
Animals. Antibodies, Monoclonal, Humanized. Bevacizumab. Cell Line, Tumor. Cell Proliferation.
Colon
/ metabolism. Humans. Mice. Protein Isoforms. RNA Splicing. RNA, Messenger / analysis
MedlinePlus Health Information.
consumer health - Colorectal 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]
Oncologist. 2000;5 Suppl 1:11-5
[
10804085.001
]
[Cites]
Biomed Pharmacother. 2008 Mar;62(3):158-63
[
17851027.001
]
[Cites]
Hepatogastroenterology. 2002 Jan-Feb;49(43):116-23
[
11941933.001
]
[Cites]
Cancer Res. 2002 Jul 15;62(14):4123-31
[
12124351.001
]
[Cites]
Microsc Res Tech. 2003 Feb 1;60(2):199-207
[
12539174.001
]
[Cites]
J Clin Invest. 2003 Mar;111(5):649-58
[
12618519.001
]
[Cites]
Br J Cancer. 2003 Jun 16;88(12):1979-86
[
12799646.001
]
[Cites]
N Engl J Med. 2003 Jul 31;349(5):427-34
[
12890841.001
]
[Cites]
Eur J Gastroenterol Hepatol. 2004 Apr;16(4):397-402
[
15028972.001
]
[Cites]
N Engl J Med. 2004 Jun 3;350(23):2335-42
[
15175435.001
]
[Cites]
Adv Cancer Res. 1985;43:175-203
[
2581424.001
]
[Cites]
Anal Biochem. 1987 Apr;162(1):156-9
[
2440339.001
]
[Cites]
Int J Cancer. 1988 Jun 15;41(6):908-12
[
3372063.001
]
[Cites]
Cancer Res. 1990 Aug 1;50(15):4724-30
[
2369746.001
]
[Cites]
Growth Factors. 1992;7(1):53-64
[
1380254.001
]
[Cites]
Nature. 1993 Apr 29;362(6423):841-4
[
7683111.001
]
[Cites]
Proc Natl Acad Sci U S A. 1993 Nov 15;90(22):10705-9
[
8248162.001
]
[Cites]
Nat Med. 1995 Jan;1(1):27-31
[
7584949.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14765-70
[
8962129.001
]
[Cites]
Cancer Res. 1997 Oct 15;57(20):4593-9
[
9377574.001
]
[Cites]
Structure. 1997 Oct 15;5(10):1325-38
[
9351807.001
]
[Cites]
Nature. 1997 Nov 27;390(6658):404-7
[
9389480.001
]
[Cites]
Eur Surg Res. 1998;30(4):273-8
[
9704754.001
]
[Cites]
Int J Cancer. 1998 Sep 11;77(6):933-6
[
9714067.001
]
[Cites]
Hepatogastroenterology. 1999 Mar-Apr;46(26):920-3
[
10370639.001
]
[Cites]
Cancer Res. 2004 Nov 1;64(21):7822-35
[
15520188.001
]
[Cites]
World J Gastroenterol. 2005 Mar 14;11(10):1535-9
[
15770733.001
]
[Cites]
J Natl Cancer Inst. 2005 Jul 6;97(13):981-9
[
15998951.001
]
[Cites]
Diabetologia. 2005 Nov;48(11):2422-7
[
16193288.001
]
[Cites]
J Clin Oncol. 2006 Jan 10;24(2):217-27
[
16365183.001
]
[Cites]
J Physiol. 2006 Apr 1;572(Pt 1):243-57
[
16423853.001
]
[Cites]
Arch Surg. 2006 Apr;141(4):367-74; discussion 374
[
16618894.001
]
[Cites]
Clin Cancer Res. 2006 May 15;12(10):3124-9
[
16707611.001
]
[Cites]
Mol Vis. 2006;12:626-32
[
16735996.001
]
[Cites]
Cell Mol Life Sci. 2006 Sep;63(17):2067-77
[
16909199.001
]
[Cites]
Br J Cancer. 2007 Jul 16;97(2):223-30
[
17595666.001
]
[Cites]
Cancer Res. 2000 Oct 1;60(19):5565-70
[
11034104.001
]
(PMID = 18349829.001).
[ISSN]
1532-1827
[Journal-full-title]
British journal of cancer
[ISO-abbreviation]
Br. J. Cancer
[Language]
eng
[Grant]
United Kingdom / British Heart Foundation / / FS/06/038; United Kingdom / British Heart Foundation / / BS/06/005/20340; United Kingdom / British Heart Foundation / / FS/04/22; United Kingdom / Cancer Research UK / / A8451; United Kingdom / Cancer Research UK / / ; United Kingdom / British Heart Foundation / / BS/2001003/12790; United Kingdom / British Heart Foundation / / BB2000003
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 2S9ZZM9Q9V / Bevacizumab
[Other-IDs]
NLM/ PMC2361696; NLM/ UKMS2582
55.
Knöbel Y, Weise A, Glei M, Sendt W, Claussen U, Pool-Zobel BL:
Ferric iron is genotoxic in non-transformed and preneoplastic human colon cells.
Food Chem Toxicol
; 2007 May;45(5):804-11
[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]
Ferric iron is genotoxic in
non
-transformed and preneoplastic human
colon
cells.
We previously demonstrated genotoxic effects by ferric iron using the human
colon
cancer cell line HT29.
Here we investigated ferric iron in primary
non
-transformed
colon
cells and in a preneoplastic
colon adenoma
cell line (LT97), which both are suitable models to study effects of carcinogens during early stages of cell transformation.
Comet FISH (fluorescence in situ hybridization) was used to assess
specific
effects on TP53.
Fe-NTA (0-1000 microM, 30 min, 37 degrees C) significantly induced single strand breaks in primary
colon
cells (500 microM Fe-NTA: Tail intensity [TI] 22.6%+/-5.0% versus RPMI control: TI 10.6%+/-3.9%, p<0.01) and in LT97 cells (1000 microM Fe-NTA: TI 26.8%+/-7.3% versus RPMI control: TI 11.1%+/-3.7%, p<0.01).
With the Comet FISH protocol lower concentrations of Fe-NTA significantly increased DNA damage already at 100 and 250 microM Fe-NTA in primary
colon
and LT97
adenoma
cells, respectively.
In conclusion, Fe-NTA acts genotoxic in
non
-transformed and in preneoplastic human
colon
cells, in which it also enhances migration of TP53 at relatively low concentrations.
Translated to the in vivo situation these results suggest that iron overload putatively contributes to a genotoxic risk during early stages of colorectal carcinogenesis on account of its genotoxic potential in
non
-tumorigenic human
colon
cells.
[MeSH-major]
Colon
/ drug effects. DNA Damage / drug effects. Ferric Compounds / toxicity. Nitrates / toxicity
[MeSH-minor]
Adenoma
/ genetics.
Adenoma
/ pathology. Cell Line, Tumor. Chromosome Aberrations.
Colonic
Neoplasms / genetics.
Colonic
Neoplasms / pathology. Comet Assay. Dose-Response Relationship, Drug. Humans. In Situ Hybridization, Fluorescence. Reactive Oxygen Species / metabolism. Tumor Suppressor Protein p53 / analysis
Hazardous Substances Data Bank.
FERRIC NITRATE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17157427.001).
[ISSN]
0278-6915
[Journal-full-title]
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
[ISO-abbreviation]
Food Chem. Toxicol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Ferric Compounds; 0 / Nitrates; 0 / Reactive Oxygen Species; 0 / Tumor Suppressor Protein p53; N8H8402XOB / ferric nitrate
56.
Paskett ED, Reeves KW, Pineau B, Albert PS, Caan B, Hasson M, Iber F, Kikendall JW, Lance P, Shike M, Slattery ML, Weissfeld J, Kahle L, Schatzkin A, Lanza E, Polyp Prevention Trial Study Group:
The association between cigarette smoking and colorectal polyp recurrence (United States).
Cancer Causes Control
; 2005 Nov;16(9):1021-33
[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 association between cigarette smoking and colorectal
polyp
recurrence (United States).
OBJECTIVE: Although evidence exists linking smoking to precancerous colorectal
adenomatous polyps
, few studies have examined the association between cigarette smoking and recurrence of colorectal
polyps
.
This association was investigated prospectively with data from
the Polyp
Prevention Trial.
The study was completed by 1872 men and women with presence
of adenomas
at baseline colonoscopy.
Multiple logistic regression analysis was used to examine the association between cigarette smoking and
polyp
recurrence (
adenomatous
and hyperplastic) up to four years from baseline.
RESULTS:
Adenoma
recurrence was not related to cigarette smoking.
Current smokers had increased odds of hyperplastic
polyps
at follow-up compared to never smokers (OR 2.88, 95% CI 2.06-4.01).
Current smoking was associated with subsequent distal (OR 3.44, 95% CI 2.38-4.95) and rectal (OR 3.53, 95% CI 2.15-5.78) hyperplastic
polyps
, but not subsequent proximal hyperplastic
polyps
.
Cigarette smoking was associated with subsequent multiple and small size (4 mm) hyperplastic
polyps
.
Significant linear trends were observed between development of subsequent hyperplastic
polyps
and all smoking variables.
CONCLUSIONS: Although no association with recurrent
adenomas
was observed, cigarette smoking was significantly associated with hyperplastic
polyp
development, except for those in the proximal
colon
.
This prospective study confirms that cigarette smoking has a significant effect on the development of hyperplastic colorectal
polyps
.
[MeSH-major]
Colonic Polyps
/ pathology. Precancerous Conditions. Smoking / epidemiology
[MeSH-minor]
Adenoma
/ epidemiology.
Adenoma
/ pathology. Aged. Colonoscopy. Epidemiologic Studies. Female. Humans. Hyperplasia / epidemiology. Hyperplasia / pathology. Male. Middle Aged. Recurrence. Risk Assessment. Risk Factors. Surveys and Questionnaires. Time Factors. United States
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
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 = 16184467.001).
[ISSN]
0957-5243
[Journal-full-title]
Cancer causes & control : CCC
[ISO-abbreviation]
Cancer Causes Control
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
57.
Roberts ML, Drosopoulos KG, Vasileiou I, Stricker M, Taoufik E, Maercker C, Guialis A, Alexis MN, Pintzas A:
Microarray analysis of the differential transformation mediated by Kirsten and Harvey Ras oncogenes in a human colorectal adenocarcinoma cell line.
Int J Cancer
; 2006 Feb 1;118(3):616-27
[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.
Colorectal cancer arises after a series of mutational events in
the colon
epithelia and is often used as a model of the multistep progression of tumorigenesis.
In order to examine the distinctive function that Ki-Ras plays in cancer development in
the colon
, we introduced constitutively active mutant Ki- and Ha-Ras genes into an intermediate-stage
colon adenoma
cell line (Caco-2).
We found that mutant active Ha-RasV12 was more efficient at transforming these
colon
epithelial cells as assessed by anchorage-independent growth, tumor formation in SCID mice and the development of mesenchymal morphology compared to transformation by Ki-RasV12.
Specifically, we found that Ki-RasV12 regulated genes involved in cytokine signaling, cell adhesion and
colon
development, whereas Ha-RasV12 mainly regulated genes involved in controlling cell morphology, correlating to an epithelial-mesenchymal transition only observed in these cells.
Our results demonstrate how 2 Ras isoforms regulate disparate biologic processes, revealing a number of genes whose deregulated expression may influence
colon
carcinogenesis (supplementary material for this article can be found on the International Journal of Cancer website at http://www.interscience.wiley.com/jpages/0020-7136/suppmat/index.html).
MedlinePlus Health Information.
consumer health - Colorectal 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
[Copyright]
Copyright 2005 Wiley-Liss, Inc.
(PMID = 16152623.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Neoplasm; 0 / Protein Isoforms
58.
Tajika M, Nakamura T, Nakahara O, Kawai H, Komori K, Hirai T, Kato T, Bhatia V, Baba H, Yamao K:
Prevalence of adenomas and carcinomas in the ileal pouch after proctocolectomy in patients with familial adenomatous polyposis.
J Gastrointest Surg
; 2009 Jul;13(7):1266-73
[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]
Prevalence
of adenomas
and carcinomas in the ileal pouch after proctocolectomy in patients with familial
adenomatous
polyposis.
PURPOSE: Restorative proctocolectomy has become the most common surgical option for patients with familial
adenomatous
polyposis (FAP).
However,
adenomas
may develop in the ileal pouch mucosa over time, and even carcinoma in the pouch has been reported.
Our aim was to evaluate the prevalence, nature, and etiology of ileal pouch and nonpouch
adenomas
and carcinoma in patients with FAP.
All patients were followed with a standardized protocol including chromoendoscopy and biopsies of visible
polyps
in the ileal pouch and nonpouch mucosa.
RESULTS: Sixteen of 24 pouch patients (Kock and IPAA) developed
adenomas
in the ileal pouch mucosa, and all patients with IRA developed
adenomas
in the rectal mucosa.
The prevalence of ileal
adenomas
was significantly higher in pouch patients than in IRA patients (P = 0.002).
Only one patient with Kock showed
adenoma
in the prepouch area.
Two cases of adenocarcinomas and one case of advanced
adenoma
were found in the ileal pouch mucosa.
CONCLUSION: Our results show a high frequency
of adenomas
in the ileal pouch mucosa, with evolution into carcinoma in some patients.
[MeSH-major]
Adenoma
/ epidemiology.
Adenomatous
Polyposis Coli / surgery. Carcinoma / epidemiology.
Colonic
Neoplasms / surgery.
Colonic
Pouches / pathology. Neoplasm Recurrence, Local / pathology
Genetic Alliance.
consumer health - Familial Adenomatous Polyposis (FAP)
.
Genetic Alliance.
consumer health - Familial Polyposis
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Int J Colorectal Dis. 2008 Apr;23(4):437-41
[
18193239.001
]
[Cites]
Indian J Cancer. 1997 Mar;34(1):16-9
[
9491657.001
]
[Cites]
Int J Colorectal Dis. 1994 May;9(2):68-72
[
8064192.001
]
[Cites]
Endoscopy. 2008 Feb;40(2):120-5
[
18067065.001
]
[Cites]
Int J Colorectal Dis. 2008 Mar;23(3):329-30
[
18030481.001
]
[Cites]
Dis Colon Rectum. 2005 Apr;48(4):816-23
[
15747076.001
]
[Cites]
Gastroenterology. 1992 Apr;102(4 Pt 1):1278-88
[
1312975.001
]
[Cites]
Br J Surg. 1996 Apr;83(4):506
[
8665242.001
]
[Cites]
Endoscopy. 2005 May;37(5):499-501
[
15844037.001
]
[Cites]
Br J Surg. 1992 Nov;79(11):1204-6
[
1334761.001
]
[Cites]
Gastroenterology. 1994 Aug;107(2):435-43
[
8039620.001
]
[Cites]
Dis Colon Rectum. 1985 Nov;28(11):875-7
[
4053904.001
]
[Cites]
Lancet. 1996 Aug 17;348(9025):433-5
[
8709782.001
]
[Cites]
Gastroenterology. 2000 Dec;119(6):1454-60
[
11113066.001
]
[Cites]
Dis Colon Rectum. 1989 Jul;32(7):618-20
[
2544383.001
]
[Cites]
Gastroenterology. 1989 Mar;96(3):817-24
[
2914643.001
]
[Cites]
Br J Surg. 1992 Dec;79(12):1372-5
[
1336702.001
]
[Cites]
World J Surg. 1991 Jan-Feb;15(1):47-9
[
1847273.001
]
[Cites]
Gastroenterology. 1992 Oct;103(4):1144-53
[
1397871.001
]
[Cites]
Colorectal Dis. 2003 Nov;5(6):592-4
[
14617250.001
]
[Cites]
J Clin Pathol. 1987 Jun;40(6):601-7
[
3611389.001
]
[Cites]
Dis Colon Rectum. 1996 May;39(5):584-6
[
8620814.001
]
[Cites]
Dis Colon Rectum. 2005 Sep;48(9):1708-13
[
15937627.001
]
[Cites]
Gastroenterology. 1978 Jun;74(6):1325-30
[
348556.001
]
[Cites]
Ann Surg. 2000 Apr;231(4):538-43
[
10749615.001
]
[Cites]
Br J Surg. 1992 Nov;79(11):1209-12
[
1467907.001
]
[Cites]
Dis Colon Rectum. 2001 Mar;44(3):347-53
[
11289279.001
]
[Cites]
Ann Surg. 2001 Mar;233(3):360-4
[
11224623.001
]
[Cites]
Dis Colon Rectum. 1998 May;41(5):552-6; discussion 556-7
[
9593235.001
]
[Cites]
Dis Colon Rectum. 1988 May;31(5):405-7
[
2835218.001
]
[Cites]
Med Princ Pract. 2006;15(1):83-6
[
16340235.001
]
[Cites]
Am J Gastroenterol. 1993 Jul;88(7):1122-4
[
8391212.001
]
[Cites]
Dis Colon Rectum. 1999 Aug;42(8):1028-33; discussion 1033-4
[
10458126.001
]
[Cites]
Gut. 1991 Jan;32(1):61-5
[
1846839.001
]
(PMID = 19333660.001).
[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
59.
Shin JE, Jung SA, Kim SE, Joo YH, Shim KN, Kim TH, Yoo K, Moon IH:
[Expression of MMP-2, HIF-1alpha and VEGF in colon adenoma and colon cancer].
Korean J Gastroenterol
; 2007 Jul;50(1):9-18
[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 of MMP-2, HIF-1alpha and VEGF in
colon adenoma
and
colon
cancer].
BACKGROUND/AIMS: This study was aimed to investigate the expression of matrix metalloproteinase-2 (MMP-2), hypoxia-inducible factor (HIF)-1alpha, and vascular endothelial growth factor (VEGF) in
colonic
adenoma
-carcinoma sequence.
METHODS: Thirty-two tissue samples
of colon adenoma
, 11 of early
colon
cancer and 36 of advanced
colon
cancer were collected by colonoscopic biopsy.
Normal
colonic
tissues were also collected from the same subjects.
RESULTS: The expression level of MMP-2 mRNA showed a progressive increase in the advance of the colorectal
adenoma
-carcinoma sequence (p<0.05).
In
colon
cancer tissues, the expression level of MMP-2 mRNA showed an increasing trend according to differentiation, lymphatic invasion and Dukes' stage (p<0.05).
The mRNA expression levels of HIF-1alpha and VEGF were greater in tissues of early and advanced
colon
cancer compared with
colon adenoma
(p<0.05; p<0.001).
CONCLUSIONS: MMP-2, HIF-1alpha, and VEGF may be useful in detecting early carcinogenesis and progression
of colon
cancer.
[MeSH-major]
Adenoma
/ metabolism.
Colonic
Neoplasms / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Matrix Metalloproteinase 2 / metabolism. Vascular Endothelial Growth Factor A / metabolism
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18172354.001).
[ISSN]
1598-9992
[Journal-full-title]
The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
[ISO-abbreviation]
Korean J Gastroenterol
[Language]
kor
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Korea (South)
[Chemical-registry-number]
0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; EC 3.4.24.24 / Matrix Metalloproteinase 2
60.
Herszényi L, Lakatos G, Tulassay Z:
[Quality colonoscopy: assumptions and expectations].
Orv Hetil
; 2010 Aug 15;151(33):1331-9
[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.
Colonoscopy has become accepted as the most effective method of screening of the
colon
for neoplasia.
[MeSH-minor]
Adenomatous
Polyposis Coli / diagnosis.
Adenomatous
Polyposis Coli / surgery. Analgesics / administration & dosage.
Colonic Polyps
/ diagnosis.
Colonic Polyps
/ surgery. Computer Simulation. Gastroenterology / education. Gastrointestinal Hemorrhage / etiology. Humans. Medical Records / standards. Preoperative Care / methods
MedlinePlus Health Information.
consumer health - Colonoscopy
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
International Agency for Research on Cancer - Screening Group.
diagnostics - Planning and Implementing Cervical Cancer Prevention and Control Programs: A Manual for Managers
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20693144.001).
[ISSN]
0030-6002
[Journal-full-title]
Orvosi hetilap
[ISO-abbreviation]
Orv Hetil
[Language]
hun
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Hungary
[Chemical-registry-number]
0 / Analgesics
61.
Subramaniam MM, Chan JY, Soong R, Ito K, Yeoh KG, Wong R, Guenther T, Will O, Chen CL, Kumarasinghe MP, Ito Y, Salto-Tellez M:
RUNX3 inactivation in colorectal polyps arising through different pathways of colonic carcinogenesis.
Am J Gastroenterol
; 2009 Feb;104(2):426-36
[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]
RUNX3 inactivation in colorectal
polyps
arising through different pathways of
colonic
carcinogenesis.
OBJECTIVES: We hypothesized that RUNX3 inactivation by promoter hypermethylation in colorectal
polyps
is an early molecular event in colorectal carcinogenesis.
METHODS: RUNX3 protein expression was analyzed immunohistochemically in 50 sporadic colorectal
polyps
comprising 19 hyperplastic
polyps
(HPs), 14 traditional serrated
adenomas
(TSAs), and 17 sporadic traditional
adenomas
(sTAs) as well as in 19 familial
adenomatous
polyposis (FAP) samples from 10 patients showing aberrant crypt foci (ACF) (n=91), small
adenomas
(SmAds) (n=40), and large
adenomas
(LAds) (n=13).
In addition, we assessed the frequency of promoter hypermethylation of RUNX3 by methylation-
specific
PCR (MSP) in all the 50 sporadic
polyps
as well as 38 microdissected FAP
polyps
comprising ACF, SmAds, and LAds obtained from 7 FAP samples.
A total of 12 normal
colon
samples were also included for RUNX3 MSP analysis.
RESULTS: Compared to normal
colon
(2 of 12, 16%) and sTAs (3 of 17, 18%), HPs (15 of 19, 79%) and TSAs (8 of 14, 57%) displayed significant inactivation of RUNX3 (P<0.05).
Promoter hypermethylation of RUNX3 was significantly higher in colorectal
polyps
(64 of 87, 74%) compared to normal
colon
(2 of 12, 16%) (P=0.001).
Serrated
polyps
such as HPs (17 of 19, 89%) and TSAs (12 of 14, 86%) were significantly more methylated than sTAs (7 of 17, 44%) (P=0.004).
RUNX3 hypermethylation was observed in 28 of the total 38 (74%) FAP
polyps
.
Overall, RUNX3 promoter methylation correlated with inactivation of RUNX3 expression in sporadic (27 of 36, 75%) (P=0.022) and FAP (21 of 28, 75%) (P=0.021)
polyps
.
CONCLUSIONS: Our data suggest that RUNX3 inactivation due to promoter hypermethylation in colorectal
polyps
represents an early event in colorectal cancer (CRC) progression.
In addition, epigenetic RUNX3 inactivation is a frequent event in the serrated
colonic polyps
as well as in the ACF of FAP
polyps
.
[MeSH-major]
Adenomatous
Polyposis Coli / genetics.
Colonic
Neoplasms / genetics.
Colonic
Neoplasms / pathology.
Colonic Polyps
/ genetics.
Colonic Polyps
/ pathology. Core Binding Factor Alpha 3 Subunit / genetics
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19174785.001).
[ISSN]
1572-0241
[Journal-full-title]
The American journal of gastroenterology
[ISO-abbreviation]
Am. J. Gastroenterol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Core Binding Factor Alpha 3 Subunit; 0 / Runx3 protein, human
62.
Aust DE, Baretton GB, Members of the Working Group GI-Pathology of the German Society of Pathology:
Serrated polyps of the colon and rectum (hyperplastic polyps, sessile serrated adenomas, traditional serrated adenomas, and mixed polyps)-proposal for diagnostic criteria.
Virchows Arch
; 2010 Sep;457(3):291-7
[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]
Serrated
polyps
of the
colon
and rectum (hyperplastic
polyps
, sessile serrated
adenomas
, traditional serrated
adenomas
, and mixed
polyps
)-proposal for diagnostic criteria.
Until recently, two major types of colorectal epithelial
polyps
were distinguished:
the adenoma
and the hyperplastic
polyp
.
While
adenomas
-because of their cytological atypia-were recognized as the precursor lesions for colorectal carcinoma, hyperplastic
polyps
were perceived as harmless lesions without any potential for malignant progression mainly because hyperplastic
polyps
are missing cytological atypia.
Meanwhile, it is recognized that the lesions, formerly classified as hyperplastic, represent a heterogeneous group of
polyps
with characteristic serrated morphology some of which exhibit a significant risk of neoplastic progression.
These serrated lesions show characteristic epigenetic alterations not commonly seen in colorectal
adenomas
and progress to colorectal carcinoma via the so-called serrated pathway (CpG-island-methylation-phenotype pathway).
This group of
polyps
is comprised not only of hyperplastic
polyps
, but also of sessile serrated
adenomas
, traditional serrated
adenomas
and mixed
polyps
, showing serrated and "classical"
adenomatous
features.
In a consensus conference of the Working Group of Gastroenterological Pathology of the German Society of Pathology, standardization of nomenclature and diagnostic criteria as well as recommendations for clinical management of these serrated
polyps
were formulated and are presented herein.
[MeSH-major]
Colonic Polyps
/ diagnosis. Precancerous Conditions / diagnosis
[MeSH-minor]
Adenoma
/ genetics.
Adenoma
/ pathology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Humans. Rectum / pathology
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Histopathology. 2006 Aug;49(2):121-31
[
16879389.001
]
[Cites]
JAMA. 1962 Feb 3;179:316-21
[
14476361.001
]
[Cites]
Am J Surg Pathol. 1990 Jun;14(6):524-37
[
2186644.001
]
[Cites]
Am J Surg Pathol. 2003 Jan;27(1):65-81
[
12502929.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8681-6
[
10411935.001
]
[Cites]
Am J Clin Pathol. 2005 Mar;123(3):349-59
[
15716230.001
]
[Cites]
J Pathol. 1996 May;179(1):20-5
[
8691339.001
]
[Cites]
Gastroenterology. 2002 Sep;123(3):862-76
[
12198712.001
]
[Cites]
Z Gastroenterol. 2008 Aug;46(8):799-840
[
18759205.001
]
[Cites]
Mod Pathol. 2005 Feb;18(2):170-8
[
15389252.001
]
[Cites]
Colorectal Dis. 2002 May;4(3):213-215
[
12780620.001
]
[Cites]
Cancer Res. 2003 Aug 15;63(16):4878-81
[
12941809.001
]
[Cites]
Histopathology. 2007 Jan;50(1):113-30
[
17204026.001
]
[Cites]
Annu Rev Pathol. 2009;4:343-64
[
19400693.001
]
[Cites]
Am J Surg Pathol. 2002 Feb;26(2):249-56
[
11812948.001
]
[Cites]
J Clin Pathol. 1999 Jun;52(6):455-60
[
10562815.001
]
[Cites]
J Pathol. 2008 Feb;214(3):320-7
[
18098337.001
]
[Cites]
Am J Gastroenterol. 2009 Mar;104(3):695-702
[
19223889.001
]
[Cites]
Gut. 1997 May;40(5):660-3
[
9203947.001
]
[Cites]
Gut. 2004 Aug;53(8):1137-44
[
15247181.001
]
[Cites]
Dig Dis Sci. 2009 Apr;54(4):906-9
[
18688718.001
]
[Cites]
Gastrointest Endosc. 2008 Oct;68(4 Suppl):S3-47
[
18805238.001
]
[Cites]
Mod Pathol. 2008 Jun;21(6):660-9
[
18360351.001
]
[Cites]
Am J Surg Pathol. 2007 Aug;31(8):1238-45
[
17667549.001
]
[Cites]
Am J Surg Pathol. 2008 Jan;32(1):21-9
[
18162766.001
]
[Cites]
Am J Gastroenterol. 1994 Jan;89(1):123-5
[
8273780.001
]
[Cites]
Dis Colon Rectum. 2000 Sep;43(9):1309-13
[
11005503.001
]
[Cites]
World J Gastroenterol. 2008 Jun 14;14 (22):3461-3
[
18567071.001
]
[Cites]
BMC Cancer. 2008 Sep 09;8:255
[
18782444.001
]
[Cites]
Gut. 1998 May;42(5):680-4
[
9659164.001
]
[Cites]
Mod Pathol. 2010 Feb;23(2):169-76
[
19855374.001
]
[Cites]
J Clin Pathol. 1999 Jan;52(1):5-9
[
10343605.001
]
[Cites]
Gastroenterology. 1996 Mar;110(3):748-55
[
8608884.001
]
[Cites]
Am J Clin Pathol. 2006 Jan;125(1):132-45
[
16483002.001
]
(PMID = 20617338.001).
[ISSN]
1432-2307
[Journal-full-title]
Virchows Archiv : an international journal of pathology
[ISO-abbreviation]
Virchows Arch.
[Language]
eng
[Publication-type]
Consensus Development Conference; Journal Article; Review
[Publication-country]
Germany
[Number-of-references]
36
63.
Li SR, Wang HH, Hu JC, Li N, Liu YL, Wu ZT, Zheng Y, Wang HH, Wu K, Ye H:
[Comparison of three FOBT protocols for colorectal cancer screening in Chinese--a multicenter study].
Zhonghua Yi Xue Za Zhi
; 2005 Mar 16;85(10):697-700
[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.
RESULTS: 323 eligible patients including 49 colorectal cancers, 60
colon adenomas
, 60 chronic colitis, 15 hemorrhoids and 139 normal
colon
were observed.
41.6% approximately 48.3%
of adenomas
was found by the 3 protocols, and 87.5%
of adenomas
over 2 cm in diameter were detected by any one of FOBT.
The majority
of adenomas
in that advanced lesion existed might be detected by FOBT.
[MeSH-minor]
Adenoma
/ prevention & control. Colonoscopy. Cost-Benefit Analysis. Female. Humans. Male
Genetic Alliance.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
International Agency for Research on Cancer - Screening Group.
diagnostics - Planning and Implementing Cervical Cancer Prevention and Control Programs: A Manual for Managers
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15932737.001).
[ISSN]
0376-2491
[Journal-full-title]
Zhonghua yi xue za zhi
[ISO-abbreviation]
Zhonghua Yi Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Multicenter Study
[Publication-country]
China
64.
Mukhopadhyay S, Marhaba A, Sidhu JS:
Small advanced neuroendocrine carcinoma of rectum discovered in an adenomatous polyp.
Endoscopy
; 2005 Dec;37(12):1256-7
[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]
Small advanced neuroendocrine carcinoma of rectum discovered in an
adenomatous
polyp
.
[MeSH-major]
Carcinoma, Neuroendocrine / secondary.
Colonic Polyps
/ pathology. Liver Neoplasms / secondary. Rectal Neoplasms / pathology
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
MedlinePlus Health Information.
consumer health - Liver Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16329031.001).
[ISSN]
0013-726X
[Journal-full-title]
Endoscopy
[ISO-abbreviation]
Endoscopy
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
65.
Alferez DG, Ryan AJ, Goodlad RA, Wright NA, Wilkinson RW:
Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model.
Int J Oncol
; 2010 Oct;37(4):767-72
[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]
Effects of vandetanib on
adenoma
formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model.
The Apc(MIN/+) mouse is a well-characterised model of intestinal tumourigenesis in which animals develop macroscopically detectable
adenomas
.
However, most of the
adenomas
are formed in the small intestine and resolution of events in
the colon
, the most relevant site for human disease, is limited.
Inducing colitis with dextran sodium sulphate (DSS) can selectively enhance the development of lesions in
the colon
.
We demonstrated that a DSS pre-treatment is well tolerated and effective at inducing
colon adenomas
in an Apc(MIN/+) mouse model.
We then investigated the effect of inhibiting vascular endothelial growth factor (VEGFR)- and epidermal growth factor receptor (EGFR)-dependent signalling pathways on the development
of adenomas
induced in DSS-pretreated (DSS/Apc(MIN/+)) or
non
-DSS-pretreated (Apc(MIN/+)) mice using vandetanib (ZD6474), a potent and selective inhibitor of VEGFR and EGFR tyrosine kinase activity.
Eight-week old Apc(MIN/+) mice were given either drinking water or 1.8% DSS and then vandetanib (ZD6474) (50 mg/kg/day) or vehicle by oral gavage for 28 days and sacrificed 24 h after the last dose and assessed for
adenoma
formation in the intestines.
DSS pre-treatment was well tolerated and significantly enhanced formation
of adenomas
in
the colon
of control Apc(MIN/+) mice.
Vandetanib treatment significantly reduced
adenoma
formation in the small intestine by 68% (P=0.001) and
the colon
by 77% (from 13.8 to 3.1, P=0.01) of DSS-pretreated Apc(MIN/+) mice.
In the Apc(MIN/+) group, vandetanib also reduced the mean number
of adenomas
in the small intestine by 76% (P<0.001) and in
the colon
by 60% (from 3.9 to 1.5, P=0.1).
DSS-pre-treatment increased the resolution of the model, allowing us to confirm statistically significant effects of vandetanib on the development and growth
of colon adenomas
in the Apc(MIN/+) mouse.
[MeSH-major]
Adenoma
/ prevention & control. Antineoplastic Agents / pharmacology. Colitis / chemically induced.
Colonic
Neoplasms / prevention & control. Dextran Sulfate. Genes, APC. Piperidines / pharmacology. Protein Kinase Inhibitors / pharmacology. Quinazolines / pharmacology
COS Scholar Universe.
author profiles
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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 = 20811697.001).
[ISSN]
1791-2423
[Journal-full-title]
International journal of oncology
[ISO-abbreviation]
Int. J. Oncol.
[Language]
eng
[Grant]
United Kingdom / Cancer Research UK / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / CTNNB1 protein, mouse; 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Piperidines; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / beta Catenin; 9042-14-2 / Dextran Sulfate; EC 2.7.10.1 / EGFR protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
66.
Yamaguchi T, Yamamoto S, Fujita S, Akasu T, Moriya Y:
Long-term outcome of metachronous rectal cancer following ileorectal anastomosis for familial adenomatous polyposis.
J Gastrointest Surg
; 2010 Mar;14(3):500-5
[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]
Long-term outcome of metachronous rectal cancer following ileorectal anastomosis for familial
adenomatous
polyposis.
BACKGROUND: Total colectomy with ileorectal anastomosis (IRA) for familial
adenomatous
polyposis (FAP) carries a potential risk of metachronous cancer in the residual rectum.
The incidence of dense-type rectal
polyps
(4/17, 24%) was significantly higher in patients who developed metachronous rectal cancer following IRA compared to that in patients who did not (1/39, 3%).
Moreover, 60% of patients with dense-type
colon
polyps
developed metachronous rectal cancer compared to 24% in patients without and 80% of those with dense type rectal
polyps
developed metachronous rectal cancer compared to 25% without.
CONCLUSIONS: Effective IRA requires selection of patients without invasive rectal cancer and without dense rectal
polyps
in whom long-term postoperative follow-up of the residual rectum is possible.
[MeSH-major]
Adenomatous
Polyposis Coli / surgery. Anastomosis, Surgical / adverse effects. Ileum / surgery. Neoplasms, Second Primary / etiology. Rectal Neoplasms / etiology. Rectum / surgery
[MeSH-minor]
Adolescent. Adult. Aged. Cohort Studies. Colectomy / adverse effects. Colectomy / methods.
Colonic
Pouches. Comorbidity. Female. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Risk Assessment. Statistics, Nonparametric. Survival Analysis. Treatment Outcome. Young Adult
Genetic Alliance.
consumer health - Familial Adenomatous Polyposis (FAP)
.
Genetic Alliance.
consumer health - Familial Polyposis
.
Genetic Alliance.
consumer health - Rectal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Crit Rev Oncol Hematol. 2007 Feb;61(2):153-61
[
17064931.001
]
[Cites]
Ann Surg. 1993 Feb;217(2):101-8
[
8382467.001
]
[Cites]
Br J Surg. 2006 Apr;93(4):407-17
[
16511903.001
]
[Cites]
Dis Colon Rectum. 1990 Aug;33(8):639-42
[
2165452.001
]
[Cites]
Dis Colon Rectum. 1984 Nov;27(11):726-9
[
6499606.001
]
[Cites]
Br J Surg. 2003 Feb;90(2):227-31
[
12555301.001
]
[Cites]
Arch Surg. 1980 Apr;115(4):460-7
[
7362454.001
]
[Cites]
Dis Colon Rectum. 2000 Dec;43(12):1719-25
[
11156457.001
]
[Cites]
Br J Surg. 1992 Nov;79(11):1204-6
[
1334761.001
]
[Cites]
Gastroenterology. 2000 Dec;119(6):1454-60
[
11113066.001
]
[Cites]
Int J Colorectal Dis. 1997;12(1):9-13
[
9112143.001
]
[Cites]
Br J Surg. 1992 Dec;79(12):1372-5
[
1336702.001
]
[Cites]
World J Surg. 1997 Jul-Aug;21(6):653-8; discussion 659
[
9230666.001
]
[Cites]
Surgery. 1987 Jan;101(1):20-6
[
3026060.001
]
[Cites]
Am J Surg. 1986 Sep;152(3):276-8
[
3752376.001
]
[Cites]
J Surg Oncol. 2007 Jan 1;95(1):28-33
[
17192888.001
]
[Cites]
Colorectal Dis. 2003 Jan;5(1):38-44
[
12780925.001
]
[Cites]
Gut. 2001 Aug;49(2):231-5
[
11454800.001
]
[Cites]
Dis Colon Rectum. 1993 Nov;36(11):1059-62
[
8223060.001
]
[Cites]
Clin Gastroenterol Hepatol. 2007 Mar;5(3):374-8
[
17368237.001
]
[Cites]
Dis Colon Rectum. 2001 Jul;44(7):984-92
[
11496079.001
]
[Cites]
Br J Surg. 2000 May;87(5):590-6
[
10792315.001
]
[Cites]
Gut. 2008 May;57(5):704-13
[
18194984.001
]
[Cites]
Dis Colon Rectum. 1999 Aug;42(8):1028-33; discussion 1033-4
[
10458126.001
]
(PMID = 19937474.001).
[ISSN]
1873-4626
[Journal-full-title]
Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
[ISO-abbreviation]
J. Gastrointest. Surg.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
67.
Kenney BC, Jain D:
Identification of lymphatics within the colonic lamina propria in inflammation and neoplasia using the monoclonal antibody D2-40.
Yale J Biol Med
; 2008 Sep;81(3):103-13
[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]
Identification of lymphatics within the
colonic
lamina propria in inflammation and neoplasia using the monoclonal antibody D2-40.
CONTEXT: Lymphatic vessels are believed to be absent in
the colon
above the level of the mucularis mucosae.
OBJECTIVE: We sought to assess the presence of lymphatics within the
colonic
lamina propria in neoplastic and inflammatory conditions using the lymphatic endothelium-
specific
immunohistochemical marker D2-40.
DESIGN: Representative sections of normal
colon
, inflamed
colon
, hyperplastic
polyps
, inflammatory
polyps
,
adenomatous polyps
,
adenomatous polyps
containing intramucosal carcinoma, and invasive
colonic
adenocarcinomas were subjected to immunohistochemical staining with D2-40.
RESULTS: Lymphatics were not identified within the lamina propria of normal
colon
.
Additionally, there was a
non
-significant trend toward higher lymphatic vessel density in cases with increasing inflammation.
CONCLUSIONS: Lymphatic vessels are present within the lamina propria
of colon
in pathologic states, including cases of intramucosal carcinoma.
[MeSH-major]
Antibodies, Monoclonal / analysis. Biomarkers, Tumor / analysis. Colitis / pathology.
Colonic
Neoplasms / chemistry.
Colonic
Neoplasms / pathology. Lymphatic Vessels / pathology. Mucous Membrane / pathology
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Gastroenterology. 1973 Jan;64(1):51-66
[
4683855.001
]
[Cites]
Gastroenterology. 1966 Dec;51(6):994-1003
[
5958610.001
]
[Cites]
Aust N Z J Surg. 1981 Oct;51(5):429-33
[
6947780.001
]
[Cites]
Br J Surg. 1985 Sep;72(9):698-702
[
4041728.001
]
[Cites]
Lancet. 1986 Oct 18;2(8512):904-7
[
2876336.001
]
[Cites]
N Engl J Med. 1991 Jan 3;324(1):1-8
[
1701519.001
]
[Cites]
J Natl Cancer Inst. 1992 Dec 16;84(24):1875-87
[
1281237.001
]
[Cites]
Cancer. 1994 Nov 1;74(9):2430-5
[
7922996.001
]
[Cites]
J Submicrosc Cytol Pathol. 1998 Oct;30(4):545-53
[
9851063.001
]
[Cites]
Am J Pathol. 1999 Feb;154(2):385-94
[
10027397.001
]
[Cites]
Br J Cancer. 1958 Sep;12(3):309-20
[
13596482.001
]
[Cites]
Breast Cancer Res Treat. 2005 May;91(2):125-32
[
15868440.001
]
[Cites]
J Pathol. 2005 Jun;206(2):170-7
[
15846845.001
]
[Cites]
Hepatogastroenterology. 2005 Jul-Aug;52(64):1057-61
[
16001629.001
]
[Cites]
Mod Pathol. 2006 Oct;19(10):1317-23
[
16799477.001
]
[Cites]
Eur Surg Res. 2006;38(5):438-44
[
16912482.001
]
[Cites]
Dis Colon Rectum. 2007 Jan;50(1):13-21
[
17115337.001
]
[Cites]
Dis Colon Rectum. 2007 Mar;50(3):308-14
[
17164964.001
]
[Cites]
Clin Cancer Res. 2003 Jan;9(1):250-6
[
12538477.001
]
[Cites]
Cancer Res. 2003 Apr 15;63(8):1920-6
[
12702584.001
]
[Cites]
Am J Pathol. 2003 Jun;162(6):1951-60
[
12759251.001
]
[Cites]
Lymphology. 2003 Jun;36(2):52-61
[
12926829.001
]
[Cites]
Oncol Rep. 2004 Jan;11(1):47-50
[
14654901.001
]
[Cites]
World J Gastroenterol. 2004 Nov 15;10(22):3261-3
[
15484296.001
]
[Cites]
Cancer. 1981 Mar 15;47(6):1424-9
[
7226068.001
]
(PMID = 18827885.001).
[ISSN]
1551-4056
[Journal-full-title]
The Yale journal of biology and medicine
[ISO-abbreviation]
Yale J Biol Med
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / monoclonal antibody D2-40
[Other-IDs]
NLM/ PMC2553648
68.
Konda A, Duffy MC:
Surveillance of patients at increased risk of colon cancer: inflammatory bowel disease and other conditions.
Gastroenterol Clin North Am
; 2008 Mar;37(1):191-213, viii
[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]
Surveillance of patients at increased risk
of colon
cancer: inflammatory bowel disease and other conditions.
Colonoscopic screening with removal of
adenomatous polyps
in individuals at average risk is known to decrease the incidence and associated mortality from
colon
cancer.
Certain conditions, notably inflammatory bowel disease involving
the colon
, a family history of
polyps
or cancer, a personal history
of colon
cancer or
polyps
, and other conditions such as acromegaly, ureterosigmoidostomy, and Streptococcus bovis bacteremia are associated with an increased risk of
colonic
neoplasia.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18313546.001).
[ISSN]
0889-8553
[Journal-full-title]
Gastroenterology clinics of North America
[ISO-abbreviation]
Gastroenterol. Clin. North Am.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
157
69.
Habermann N, Lund EK, Pool-Zobel BL, Glei M:
Modulation of gene expression in eicosapentaenoic acid and docosahexaenoic acid treated human colon adenoma cells.
Genes Nutr
; 2009 Mar;4(1):73-6
[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]
Modulation of gene expression in eicosapentaenoic acid and docosahexaenoic acid treated human
colon adenoma
cells.
The aim of the study was to compare the modulation of gene expression in LT97
colon adenoma
cells in response to EPA and DHA treatment.
In our approach, we used preneoplastic
adenoma
cells which are a relevant model for target cells of chemoprevention.
If verified with real time PCR, these results identify genes and targets for chemoprevention
of colon
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]
Eur J Nutr. 2008 Aug;47(5):226-34
[
18636219.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2008 May;17(5):1136-43
[
18483335.001
]
[Cites]
Int J Cancer. 2008 Jun 15;122(12):2647-55
[
18351577.001
]
[Cites]
J Nutr. 2008 Feb;138(2):250-6
[
18203887.001
]
[Cites]
Am J Epidemiol. 2007 Nov 15;166(10):1116-25
[
17823383.001
]
[Cites]
Int J Oncol. 2001 Dec;19(6):1255-62
[
11713597.001
]
[Cites]
J Natl Cancer Inst. 2005 Jun 15;97(12):906-16
[
15956652.001
]
[Cites]
Carcinogenesis. 1999 Apr;20(4):645-50
[
10223194.001
]
[Cites]
Cancer. 2003 Sep 15;98(6):1262-72
[
12973851.001
]
[Cites]
Eur J Cancer. 2002 Sep;38(14):1937-45
[
12204677.001
]
[Cites]
Mutat Res. 2006 Feb 22;594(1-2):10-9
[
16153665.001
]
(PMID = 19234733.001).
[ISSN]
1555-8932
[Journal-full-title]
Genes & nutrition
[ISO-abbreviation]
Genes Nutr
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Other-IDs]
NLM/ PMC2654050
70.
Emmons KM, McBride CM, Puleo E, Pollak KI, Clipp E, Kuntz K, Marcus BH, Napolitano M, Onken J, Farraye F, Fletcher R:
Project PREVENT: a randomized trial to reduce multiple behavioral risk factors for colon cancer.
Cancer Epidemiol Biomarkers Prev
; 2005 Jun;14(6):1453-9
[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]
Project PREVENT: a randomized trial to reduce multiple behavioral risk factors for
colon
cancer.
BACKGROUND: This report examines the outcome data for Project PREVENT, a two-site randomized control trial designed to reduce behavioral risk factors for colorectal cancer among individuals who have been diagnosed with
adenomatous
colon
polyps
.
METHODS: The study sample included 1,247 patients with recent diagnosis of
adenomatous
colorectal
polyps
.
[MeSH-major]
Colonic
Neoplasms / prevention & control. Diet. Health Behavior
[MeSH-minor]
Adenomatous
Polyposis Coli / complications. Adult. Aged. Alcohol Drinking. Exercise. Female. Humans. Male. Middle Aged. Risk Factors. Smoking. Telephone
MedlinePlus Health Information.
consumer health - Healthy Aging
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15941955.001).
[ISSN]
1055-9965
[Journal-full-title]
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
[ISO-abbreviation]
Cancer Epidemiol. Biomarkers Prev.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / 5 R01 CA74000-04
[Publication-type]
Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
71.
Phelps RA, Broadbent TJ, Stafforini DM, Jones DA:
New perspectives on APC control of cell fate and proliferation in colorectal cancer.
Cell Cycle
; 2009 Aug 15;8(16):2549-56
[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.
Aberrant Wnt/beta-catenin signaling following loss of the tumor suppressor
adenomatous
polyposis coli (APC) is thought to initiate
colon adenoma
formation.
However, examination of tumors from familial
adenomatous
polyposis coli (FAP) patients has failed to confirm the presence of nuclear beta-catenin in early lesions following APC loss despite robust staining in later lesions.
This observation presents the possibility that
colon adenomas
arise through a beta-catenin-independent function of APC.
Though there are currently contrasting models to explain
colon
tumorigenesis, our goal is to begin to reconcile data from multiple different model systems and provide a functional view into the initiation and progression
of colon
cancer.
[MeSH-major]
Adenomatous
Polyposis Coli / pathology. Cell Differentiation / physiology. Colorectal Neoplasms / pathology
Genetic Alliance.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19597346.001).
[ISSN]
1551-4005
[Journal-full-title]
Cell cycle (Georgetown, Tex.)
[ISO-abbreviation]
Cell Cycle
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
94
72.
Young J, Jass JR:
The case for a genetic predisposition to serrated neoplasia in the colorectum: hypothesis and review of the literature.
Cancer Epidemiol Biomarkers Prev
; 2006 Oct;15(10):1778-84
[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.
In recent years, an alternative pathway of colorectal cancer development has been described in which serrated
polyps
replace the traditional
adenoma
as the precursor lesion.
Importantly, serrated
polyps
and a subset of colorectal cancer show largely nonoverlapping mutation profiles to those found in
adenomas
and the majority of colorectal cancer.
The two most well-characterized syndromes, familial
adenomatous
polyposis and hereditary nonpolyposis colorectal cancer (Lynch syndrome), both develop via
the adenoma
-carcinoma pathway and together account for approximately one third of familial colorectal cancer.
Further, CIMP is observed in the normal
colonic
mucosa of individuals with hyperplastic polyposis consistent with a field defect in epigenetic regulation.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
COS Scholar Universe.
author profiles
.
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 = 17035382.001).
[ISSN]
1055-9965
[Journal-full-title]
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
[ISO-abbreviation]
Cancer Epidemiol. Biomarkers Prev.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U01 CA097735; United States / PHS HHS / / U-01-74778
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
United States
[Chemical-registry-number]
EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
[Number-of-references]
93
73.
Boissan M, De Wever O, Lizarraga F, Wendum D, Poincloux R, Chignard N, Desbois-Mouthon C, Dufour S, Nawrocki-Raby B, Birembaut P, Bracke M, Chavrier P, Gespach C, Lacombe ML:
Implication of metastasis suppressor NM23-H1 in maintaining adherens junctions and limiting the invasive potential of human cancer cells.
Cancer Res
; 2010 Oct 1;70(19):7710-22
[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.
We silenced NM23-H1 expression in human hepatoma and
colon
carcinoma cells and methodologically investigated effects on cell-cell adhesion, migration, invasion, and signaling linked to cancer progression.
Analysis of NM23-H1 expression in clinical specimens revealed high expression in premalignant lesions (liver cirrhosis and
colon adenoma
) and the central body of primary liver or
colon
tumors, but downregulation at the invasive front of tumors.
[MeSH-minor]
Actins / metabolism. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cell Line, Tumor. Cell Movement / genetics.
Colonic
Neoplasms / genetics.
Colonic
Neoplasms / metabolism.
Colonic
Neoplasms / pathology. Cytoskeleton / metabolism. Cytoskeleton / pathology. Gene Silencing. Humans. Liver Neoplasms / genetics. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Matrix Metalloproteinase 14 / metabolism. Neoplasm Invasiveness. Wnt Proteins / metabolism
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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
.
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
[Copyright]
© 2010 AACR.
(PMID = 20841469.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Actins; 0 / NM23 Nucleoside Diphosphate Kinases; 0 / Wnt Proteins; EC 2.7.4.6 / NME1 protein, human; EC 3.4.24.80 / Matrix Metalloproteinase 14
74.
Dworakowska D, Gueorguiev M, Kelly P, Monson JP, Besser GM, Chew SL, Akker SA, Drake WM, Fairclough PD, Grossman AB, Jenkins PJ:
Repeated colonoscopic screening of patients with acromegaly: 15-year experience identifies those at risk of new colonic neoplasia and allows for effective screening guidelines.
Eur J Endocrinol
; 2010 Jul;163(1):21-8
[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]
Repeated colonoscopic screening of patients with acromegaly: 15-year experience identifies those at risk of new
colonic
neoplasia and allows for effective screening guidelines.
OBJECTIVE: It is suggested that patients with acromegaly have an increased risk of colorectal cancer and pre-malignant
adenomatous polyps
.
RESULTS: The presence of hyperplastic or
adenomatous polyps
was assessed in all patients, while one cancer was detected at the second surveillance.
At the third surveillance, mean (+/-s.d.) serum IGF1 levels (ng/ml) in patients with hyperplastic
polyps
were significantly higher than those with normal colons (P<0.05).
The presence of an
adenoma
rather than a normal
colon
at the first colonoscopy was associated with a significantly increased risk
of adenoma
at the second (odds ratio (OR) 4.4, 95% confidence interval (CI) 1.9-10.4) and at the third (OR 8.8, 95% CI 2.9-26.5) screens.
Conversely, a normal
colon
at the first surveillance gave a high chance of normal findings at the second (78%) or third surveillance (78%), and a normal
colon
at the second colonoscopy was associated with normality at the third colonoscopy (81%).
CONCLUSIONS: Repeated colonoscopic screening of patients with acromegaly demonstrated a high prevalence of new
adenomatous
and hyperplastic
colonic polyps
, dependent on both the occurrence of previous
polyps
and elevated IGF1 levels.
Genetic Alliance.
consumer health - Acromegaly
.
MedlinePlus Health Information.
consumer health - Colonoscopy
.
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).
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20435617.001).
[ISSN]
1479-683X
[Journal-full-title]
European journal of endocrinology
[ISO-abbreviation]
Eur. J. Endocrinol.
[Language]
ENG
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
75.
Loffeld SM, Loffeld RJ:
Colorectal cancer and adenomas are rare in individuals of Turkish descent living in the Zaanstreek region in the Netherlands.
J Cancer Res Clin Oncol
; 2010 Sep;136(9):1439-43
[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]
Colorectal cancer and
adenomas
are rare in individuals of Turkish descent living in the Zaanstreek region in the Netherlands.
Screening and detection of its precursor lesion,
the adenoma
could prevent development of colorectal cancer.
AIM: To evaluate the prevalence of colorectal cancer and
adenoma
in patients living in the Zaanstreek region, the Netherlands, and correlate these findings with ethnicity.
MATERIALS AND METHODS: All patients undergoing endoscopy of the
colon
and rectum during a period of 16 consecutive years in whom colorectal cancer and/or a
polyp
were diagnosed, were included in this study.
A total of 2,744 patients had one or more
polyp
(s) during endoscopy.
CONCLUSION: Colorectal cancer and
colonic
adenoma
are rare in patients of Turkish descent living in the Zaanstreek region, the Netherlands.
[MeSH-major]
Adenoma
/ epidemiology. Colorectal Neoplasms / epidemiology
Genetic Alliance.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer. 2000 May 15;88(10):2398-424
[
10820364.001
]
[Cites]
Cancer. 2009 May 1;115(9):1967-76
[
19235249.001
]
[Cites]
J Natl Cancer Inst. 2003 Sep 3;95(17):1276-99
[
12953083.001
]
[Cites]
Int J Cancer. 2004 Jan 10;108(2):287-92
[
14639617.001
]
[Cites]
Dis Esophagus. 2004;17(1):87-90
[
15209748.001
]
[Cites]
Eur J Epidemiol. 1992 Nov;8(6):845-50
[
1294390.001
]
[Cites]
Arch Fam Med. 1995 Oct;4(10):849-56
[
7551132.001
]
[Cites]
Colorectal Dis. 2005 Nov;7(6):559-62
[
16232235.001
]
[Cites]
Int J Cancer. 2006 Dec 1;119(11):2665-72
[
16929492.001
]
[Cites]
Am J Clin Nutr. 2007 Dec;86(6):1754-64
[
18065596.001
]
[Cites]
Int J Cancer. 2008 May 1;122(9):2106-14
[
18183593.001
]
[Cites]
Turk J Gastroenterol. 2008 Mar;19(1):22-7
[
18386236.001
]
[Cites]
J Natl Med Assoc. 2008 Dec;100(12):1441-4
[
19110912.001
]
[Cites]
Cancer. 2009 Jan 15;115(2):259-70
[
19109815.001
]
[Cites]
Cancer. 2009 Jan 15;115(2):419-27
[
19109819.001
]
[Cites]
J Nutr. 2009 Feb;139(2):340-4
[
19091801.001
]
[Cites]
Genet Mol Res. 2009;8(1):64-75
[
19283674.001
]
[Cites]
Am J Epidemiol. 2002 Jun 15;155(12):1104-13
[
12048224.001
]
(PMID = 20140623.001).
[ISSN]
1432-1335
[Journal-full-title]
Journal of cancer research and clinical oncology
[ISO-abbreviation]
J. Cancer Res. Clin. Oncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Other-IDs]
NLM/ PMC2908754
76.
Al-Thihli K, Palma L, Marcus V, Cesari M, Kushner YB, Barkun A, Foulkes WD:
A case of Cowden's syndrome presenting with gastric carcinomas and gastrointestinal polyposis.
Nat Clin Pract Gastroenterol Hepatol
; 2009 Mar;6(3):184-9
[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.
BACKGROUND: A 73-year-old white man was referred to a cancer genetics clinic for evaluation of a approximately 20-year history of mixed upper and lower gastrointestinal polyposis, including hyperplastic, inflammatory and
adenomatous polyps
,
colonic
ganglioneuromas, and associated diffuse, esophageal glycogenic acanthosis.
Multiple hyperplastic
polyps
and small, sessile
polyps
were also observed in the gastrectomy specimen.
[MeSH-major]
Carcinoma / etiology. Gastrointestinal Diseases / etiology. Hamartoma Syndrome, Multiple / complications.
Polyps
/ etiology. Stomach Neoplasms / etiology
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
CYANOCOBALAMIN
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19190598.001).
[ISSN]
1743-4386
[Journal-full-title]
Nature clinical practice. Gastroenterology & hepatology
[ISO-abbreviation]
Nat Clin Pract Gastroenterol Hepatol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
P6YC3EG204 / Vitamin B 12
77.
Cirocchi R, Coccetta M, De Sol A, Morelli U, Spizzirri A, Cattorini L, Farinella E, Giustozzi G, Sciannameo F:
[Minimally invasive treatment of synchronous colorectal tumours].
Chir Ital
; 2008 Mar-Apr;60(2):237-41
[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.
[Transliterated title]
Trattamento mini-invasivo delle neoplasie sincrone
del colon
-retto.
In patients with colorectal cancers synchronous neoplastic lesions are an increasingly frequent finding at preoperative staging; 3% of the cases are other cancers while 33-35% of the synchronous lesions are villous
adenomas
.
The treatment of most colorectal
adenomas
can be performed by endoscopic poplypectomy.
Surgical timing involved performing a sequential exeresis characterised by a cancer resection, followed by resection of the voluminous
adenoma
: TEM for rectal cancer followed by a laparoscopic right hemicolectomy with an extracorporeal anastomosis for a voluminous villous
adenoma
(1 patient) and laparoscopic right hemicolectomy with an extracorporeal anastomosis for cancer followed by TEM for a voluminous villous
adenoma
(2 patients).
One patient with left
colon
cancer associated with a voluminous villous rectal
adenoma
first underwent TEM for the rectal
adenoma
and then a left laparoscopic hemicolectomy with an extracorporeal anastomosis in order to ease the transit of the circular mechanical stapler.
Another patient with rectal and right
colon adenomas
first underwent TEM for a voluminous rectal sessile
adenoma
and later a right hemicolectomy.
[MeSH-major]
Adenoma
/ surgery. Colectomy / methods. Colorectal Neoplasms / surgery. Laparoscopy. Microsurgery
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18689172.001).
[ISSN]
0009-4773
[Journal-full-title]
Chirurgia italiana
[ISO-abbreviation]
Chir Ital
[Language]
ita
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Italy
78.
Tony J, Harish K, Ramachandran TM, Sunilkumar K, Thomas V:
Profile of colonic polyps in a southern Indian population.
Indian J Gastroenterol
; 2007 May-Jun;26(3):127-9
[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]
Profile of
colonic polyps
in a southern Indian population.
BACKGROUND: In Western countries,
colonic polyps
are usually
adenomatous
in nature, are evenly distributed along the entire
colon
in asymptomatic per-sons and show a left-sided predominance in symptomatic patients.
Clinical features, colonoscopic description and histologic findings of all patients with
polyps
were noted.
Association of the degree of dysplasia with the size, site and type of
polyps
and the person's age was assessed.
RESULTS:
Polyps
were seen in 124 (5.1%) of 2412 complete colonoscopies.
Mean age of patients with
polyps
was 58.1 (SD 19.9) years; ninety were men.
A majority of
polyps
(92%) were located in the left
colon
.
They were
adenomatous
in 99 (79.8%), juvenile in 12 (9.8%), hyperplastic in 11 (8.8 %), inflammatory in 1 (0.8%) and Peutz-Jegher's
polyp
in 1 (0.8%).
Dysplasia was severe in large (>2 cm)
polyps
compared to small (< 1 cm) ones (p< 0.001).
Age of patient and location
of polyp
had no association with degree of dysplasia.
CONCLUSIONS: In southern Indian adults, most
colonic polyps
are
adenomatous
and are in the left
colon
.
Large
polyps
are associated with severe dysplasia.
[MeSH-major]
Colonic Polyps
/ epidemiology
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17704579.001).
[ISSN]
0254-8860
[Journal-full-title]
Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology
[ISO-abbreviation]
Indian J Gastroenterol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
79.
Lee H, Kim JH, Yang SY, Kong J, Oh M, Jeong DH, Chung JI, Bae KB, Shin JY, Hong KH, Choi I:
Peripheral blood gene expression of B7 and CD28 family members associated with tumor progression and microscopic lymphovascular invasion in colon cancer patients.
J Cancer Res Clin Oncol
; 2010 Sep;136(9):1445-52
[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]
Peripheral blood gene expression of B7 and CD28 family members associated with tumor progression and microscopic lymphovascular invasion in
colon
cancer patients.
PURPOSE: To associate the global gene expression of B7/CD28 family transcripts with pathologic features
of colon
cancer, we determined the B7/CD28 family transcripts in peripheral blood mononuclear cells (PBMCs) from normal subjects and patients with
adenomatous polyps
and
colon
cancer, and correlated the results with pathologic features
of colon
cancer.
METHODS: PBMCs from age-matched normal subjects and patients with
adenomatous polyps
and
colon
cancer were analyzed for peripheral blood transcripts (PBTs) of B7/CD28 family using real-time PCR.
Differences in expression levels of B7/CD28 PBTs across all cancer stages and between
colon
cancer patients with or without microscopic lymphovascular invasion (LVI) were analyzed.
RESULTS: The results showed a significant upregulation of PBTs of co-inhibitory molecules such as B7-H3 and PD-1 and a significant PBT downregulation of co-stimulatory molecules including CD28 and ICOS in
colon
cancer patients.
In addition, the ratios of PBT expression of CD28 family to B7 family such as CTLA-4 to B7-H2 and PD-1 to B7-H2 were significantly higher in
colon
cancer patients with microscopic LVI than in those without LVI (P = 0.001 and P = 0.016, respectively).
CONCLUSIONS: Our results suggest that B7/CD28 family PBTs may serve as valuable markers reflecting the pathological features
of colon
cancer.
[MeSH-major]
Antigens, CD28 / genetics. Antigens, CD80 / genetics.
Colonic
Neoplasms / genetics.
Colonic
Neoplasms / pathology. Gene Expression Regulation, Neoplastic. Leukocytes, Mononuclear / pathology
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Res. 2006 Apr 1;66(7):3381-5
[
16585157.001
]
[Cites]
Gynecol Oncol. 2007 Aug;106(2):334-41
[
17498784.001
]
[Cites]
Cancer Res. 2007 Aug 15;67(16):7893-900
[
17686830.001
]
[Cites]
Clin Cancer Res. 2005 Apr 15;11(8):2947-53
[
15837746.001
]
[Cites]
Cancer Lett. 2008 Sep 8;268(1):98-109
[
18486325.001
]
[Cites]
Nat Med. 2003 May;9(5):562-7
[
12704383.001
]
[Cites]
Clin Cancer Res. 2008 Aug 15;14(16):5150-7
[
18694993.001
]
[Cites]
Clin Cancer Res. 2008 Aug 1;14(15):4800-8
[
18676751.001
]
[Cites]
Nature. 2006 Feb 9;439(7077):682-7
[
16382236.001
]
[Cites]
J Immunol. 2003 Nov 1;171(9):4650-4
[
14568939.001
]
[Cites]
J Exp Med. 2006 Apr 17;203(4):871-81
[
16606666.001
]
[Cites]
Eur J Immunol. 2005 Feb;35(2):428-38
[
15682454.001
]
[Cites]
Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19458-63
[
18042703.001
]
[Cites]
Trends Mol Med. 2006 Jun;12(6):244-6
[
16650803.001
]
[Cites]
Clin Cancer Res. 2004 Aug 1;10(15):5094-100
[
15297412.001
]
[Cites]
Annu Rev Immunol. 2005;23:515-48
[
15771580.001
]
[Cites]
Cancer Res. 2005 Feb 1;65(3):1089-96
[
15705911.001
]
[Cites]
World J Gastroenterol. 2006 Jan 21;12(3):457-9
[
16489649.001
]
[Cites]
Nat Med. 2002 Aug;8(8):793-800
[
12091876.001
]
[Cites]
J Leukoc Biol. 2008 Mar;83(3):755-64
[
18086898.001
]
[Cites]
J Immunol. 2004 Aug 15;173(4):2500-6
[
15294965.001
]
(PMID = 20140740.001).
[ISSN]
1432-1335
[Journal-full-title]
Journal of cancer research and clinical oncology
[ISO-abbreviation]
J. Cancer Res. Clin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antigens, CD28; 0 / Antigens, CD80
80.
Coppola D, Parikh V, Boulware D, Blanck G:
Substantially reduced expression of PIAS1 is associated with colon cancer development.
J Cancer Res Clin Oncol
; 2009 Sep;135(9):1287-91
[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]
Substantially reduced expression of PIAS1 is associated with
colon
cancer development.
This project was designed to assess PIAS1 expression in
colon
cancer.
METHODS: To determine whether PIAS1, one of the PIAS family members, or IFN-gamma signaling pathway components could be used to stratify
colon
tumors, we stained tissue microarrays for PIAS1, interferon regulatory factor-1 (IRF-1) and STAT1alpha.
RESULTS: PIAS1 staining of the
colon
cancer tissue microarrays indicated a strong correlation of normal
colon
cells, and
adenomas
, with high expression of both PIAS1 and IRF-1.
CONCLUSION: The PIAS1 results in particular may represent a basis for new approaches for efficiently distinguishing
adenomas
from
colon
cancer.
[MeSH-major]
Colonic
Neoplasms / metabolism.
Colonic
Neoplasms / pathology. Disease Progression. Down-Regulation. Protein Inhibitors of Activated STAT / biosynthesis. Protein Inhibitors of Activated STAT / deficiency. Small Ubiquitin-Related Modifier Proteins / biosynthesis. Small Ubiquitin-Related Modifier Proteins / deficiency
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
antibodies-online.
View related products from antibodies-online.com
(subscription/membership/fee required).
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Biochem Soc Trans. 2007 Dec;35(Pt 6):1405-8
[
18031232.001
]
[Cites]
J Biol Chem. 2005 Oct 28;280(43):36228-36
[
16085646.001
]
[Cites]
Carcinogenesis. 2005 Sep;26(9):1527-35
[
15878912.001
]
[Cites]
Biochem Biophys Res Commun. 1996 Dec 4;229(1):21-6
[
8954078.001
]
[Cites]
Oncogene. 1999 Oct 21;18(43):5889-903
[
10557076.001
]
[Cites]
Stat Appl Genet Mol Biol. 2007;6:Article3
[
17402918.001
]
[Cites]
J Biol Chem. 2004 Jul 16;279(29):30358-68
[
15123634.001
]
[Cites]
J Immunol. 2001 Jan 15;166(2):1041-8
[
11145683.001
]
[Cites]
Lupus. 2001;10 (10 ):691-9
[
11721695.001
]
[Cites]
Ann Surg Oncol. 1999 Sep;6(6):604-8
[
10493631.001
]
[Cites]
J Biol Chem. 2004 May 7;279(19):19712-20
[
14993214.001
]
[Cites]
Gut. 2001 Aug;49(2):251-62
[
11454803.001
]
[Cites]
J Biol Chem. 2007 Mar 30;282(13):9797-804
[
17251186.001
]
[Cites]
J Biol Chem. 2007 Jul 13;282(28):20059-63
[
17502367.001
]
(PMID = 19288270.001).
[ISSN]
1432-1335
[Journal-full-title]
Journal of cancer research and clinical oncology
[ISO-abbreviation]
J. Cancer Res. Clin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Interferon Regulatory Factor-1; 0 / PIAS1 protein, human; 0 / Protein Inhibitors of Activated STAT; 0 / Small Ubiquitin-Related Modifier Proteins
81.
Li FE, Ye HJ, Li J, Wang JP, Liu YG, Yu GY, Yin WH:
[Clinical, enteroscopic, and pathological characteristics of 796 cases of colorectal polyps].
Zhong Nan Da Xue Xue Bao Yi Xue Ban
; 2005 Aug;30(4):463-6
[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]
[Clinical, enteroscopic, and pathological characteristics of 796 cases of colorectal
polyps
].
OBJECTIVE: To study the age, clinical, enteroscopic and pathological characteristics of colorectal
polyps
and factors affected
polyp
-carcinoma.
METHODS: We analyzed the clinical, enteroscopic and pathological characteristics of 7276 cases of colorectal
polyps
.
RESULTS: The incidence of colorectal
polyps
was 10.94%, including 521 men and 275 women.
The rate of colorectal
polyp
was 82.29% in 30-69 year olds.
The
adenomatous
, inflammatory, hyperplastic and juvenile
polyps
were 43.84%, 42.09%, 11.06% and 1.51%, respectively.
The canceration rates in villous, mixed and tubular
adenomas
were 29.73%, 11.11%, and 4.86%.
Conclusion The ages between 30-69 tend to suffer from colorectal
polyps
.
Colorectal
polyps
are more likely to locate in left
colon
.
The common pathological types were
adenomatous
and inflammatory
polyps
.
There is a high canceration of
polyps
in the left
colon
, villous
adenomas
and > or = 2.0 cm
polyps
.
The broader the pedicles and the larger the diameters of
polyps
are, the higher the canceration rate.
All of the
colon
polyps
should be excised and undergo the pathological examination.
[MeSH-major]
Colonic Polyps
/ pathology. Colonoscopy. Colorectal Neoplasms / pathology. Intestinal
Polyps
/ pathology
[MeSH-minor]
Adenoma
/ pathology. Adolescent. Adult. Aged. Aged, 80 and over. Cell Transformation, Neoplastic / pathology. Child. Child, Preschool. Female. Humans. Male
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
MedlinePlus Health Information.
consumer health - Colonoscopy
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16190400.001).
[ISSN]
1672-7347
[Journal-full-title]
Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
[ISO-abbreviation]
Zhong Nan Da Xue Xue Bao Yi Xue Ban
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
82.
Nilbert M, Kristoffersson U, Ericsson M, Johannsson O, Rambech E, Mangell P:
Broad phenotypic spectrum in familial adenomatous polyposis; from early onset and severe phenotypes to late onset of attenuated polyposis with the first manifestation at age 72.
BMC Med Genet
; 2008;9:101
[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]
Broad phenotypic spectrum in familial
adenomatous
polyposis; from early onset and severe phenotypes to late onset of attenuated polyposis with the first manifestation at age 72.
BACKGROUND: Familial
adenomatous
polyposis (FAP) is typically characterized by multiple
colonic polyps
and frequent extracolonic features.
Whereas the number of
colonic polyps
has been linked to the APC gene mutation, possible genotype-phenotype correlations largely remain to be defined for the extracolonic manifestations.
Two sisters with an insertion in codon 528 (c.1582_1583insGC) both showed severe phenotypes with classical polyposis, upper gastrointestinal
polyps
and thyroid cancer.
A woman with a 3'APC mutation (c.5030_5031insAA) developed
colon
cancer at age 72 as the first manifestation of attenuated FAP.
We report novel APC mutations and present two FAP cases that suggest familial aggregation of thyroid cancer and demonstrate the need to consider attenuated FAP also among elderly patients with
colon
cancer.
[MeSH-major]
Adenomatous
Polyposis Coli / genetics. Genes, APC. Mutation. Phenotype
Genetic Alliance.
consumer health - Familial Adenomatous Polyposis (FAP)
.
Genetic Alliance.
consumer health - Familial Polyposis
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Scand J Gastroenterol. 1999 Dec;34(12):1230-5
[
10636071.001
]
[Cites]
Am J Hum Genet. 1998 Jun;62(6):1290-301
[
9585611.001
]
[Cites]
Jpn J Clin Oncol. 2000 Feb;30(2):82-8
[
10768871.001
]
[Cites]
J Clin Oncol. 2000 May;18(9):1967-79
[
10784639.001
]
[Cites]
Scand J Gastroenterol. 2000 Nov;35(11):1200-3
[
11145293.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Mar 5;99(5):2954-8
[
11867715.001
]
[Cites]
Fam Cancer. 2001;1(2):83-6
[
14574002.001
]
[Cites]
Fam Cancer. 2003;2(1):43-55
[
14574166.001
]
[Cites]
Fam Cancer. 2003;2(2):95-9
[
14574158.001
]
[Cites]
Endocr J. 2004 Jun;51(3):317-23
[
15256777.001
]
[Cites]
Gastroenterology. 2004 Aug;127(2):444-51
[
15300576.001
]
[Cites]
Int J Colorectal Dis. 1988 Mar;3(1):29-31
[
2834476.001
]
[Cites]
Science. 1991 Aug 9;253(5020):661-5
[
1651562.001
]
[Cites]
Hum Mutat. 1998;11(6):450-5
[
9603437.001
]
[Cites]
Gut. 2004 Dec;53(12):1832-6
[
15542524.001
]
[Cites]
Genet Test. 2004 Fall;8(3):248-56
[
15727247.001
]
[Cites]
Crit Rev Oncol Hematol. 2007 Feb;61(2):153-61
[
17064931.001
]
[Cites]
Int J Colorectal Dis. 2008 Mar;23(3):331-2
[
17665205.001
]
[Cites]
BMC Med. 2008;6:10
[
18433509.001
]
[Cites]
Cell. 1993 Dec 3;75(5):951-7
[
8252630.001
]
[Cites]
Hum Mutat. 1994;3(2):121-5
[
8199592.001
]
[Cites]
Nucleic Acids Res. 1996 Jan 1;24(1):121-4
[
8594558.001
]
[Cites]
Int J Colorectal Dis. 1996;11(2):88-91
[
8739833.001
]
[Cites]
Hum Genet. 1996 Dec;98(6):727-34
[
8931709.001
]
[Cites]
Br J Cancer. 2000 Jan;82(2):348-53
[
10646887.001
]
(PMID = 19036155.001).
[ISSN]
1471-2350
[Journal-full-title]
BMC medical genetics
[ISO-abbreviation]
BMC Med. Genet.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Other-IDs]
NLM/ PMC2610029
83.
Chimenos-Küstner E, Pascual M, Blanco I, Finestres F:
Hereditary familial polyposis and Gardner's syndrome: contribution of the odonto-stomatology examination in its diagnosis and a case description.
Med Oral Patol Oral Cir Bucal
; 2005 Nov-Dec;10(5):402-9
[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.
Familial
Adenomatous
Polyposis (FAP) and its phenotype variant, Gardner's syndrome, constitute a rare autosomal dominant inherited
disorder
.
They are characterised by the development, generally during the second and third decades of life, of multiple
adenomatous polyps
in
the colon
and rectum.
These
polyps
have a high risk of subsequently becoming malignant, which normally occurs in the third and fourth decades of life.
As well as colorectal
polyps
, these individuals can present with extra-
colonic
symptoms, among which are particularly: gastro-duodenal
polyps
, dermoid and epidermoid cysts, desmoid tumours, congenital hypertrophy of the retinal pigment epithelium, disorders of the maxillary and skeletal bones and dental anomalies.
[MeSH-major]
Adenomatous
Polyposis Coli / diagnosis. Jaw Neoplasms / etiology. Osteoma / etiology
[MeSH-minor]
Adenomatous
Polyposis Coli Protein / genetics. Adult. Cementoma / diagnosis. Cementoma / etiology. Codon, Nonsense. Diagnosis, Differential. Early Diagnosis. Epidermal Cyst / diagnosis. Epidermal Cyst / etiology. Female. Fibroma / diagnosis. Fibroma / etiology. Gardner Syndrome / complications. Gardner Syndrome / diagnosis. Gardner Syndrome / genetics. Genes, APC. Humans. Hypertrophy. Pedigree. Pigment Epithelium of Eye / abnormalities. Prognosis
Genetic Alliance.
consumer health - Familial Polyposis
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16264375.001).
[ISSN]
1698-6946
[Journal-full-title]
Medicina oral, patología oral y cirugía bucal
[ISO-abbreviation]
Med Oral Patol Oral Cir Bucal
[Language]
eng; spa
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Spain
[Chemical-registry-number]
0 / Adenomatous Polyposis Coli Protein; 0 / Codon, Nonsense
84.
Ferrández A, Navarro M, Díez M, Sopena F, Roncalés P, Polo-Tomas M, Sáinz R, Lanas A:
Risk factors for advanced lesions undetected at prior colonoscopy: not always poor preparation.
Endoscopy
; 2010 Dec;42(12):1071-6
[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.
BACKGROUND AND STUDY AIM: Colonoscopy is regarded as the gold standard for diagnosis of
colonic
lesions.
However,
adenoma
miss rates in tandem colonoscopy studies vary from 2 % to 26 %.
Undetected lesions were defined as advanced
adenoma
or colorectal cancer (CRC) not reported in a colonoscopy performed in the previous 2 or 3 years, respectively.
Patients with hereditary nonpolyposis CRC (HNPCC) and familial
adenomatous
polyposis (FAP) were excluded.
RESULTS: Between 2002 and 2005, 795 patients were diagnosed with at least one advanced
adenoma
and 386 with CRC.
Among these, 107/795 patients (13.5 %) had advanced
adenoma
that had been undetected in a previous colonoscopy (39 % [53/135 lesions] in the right
colon
); 92/107 (86 %) had an undetected advanced
adenoma
≥ 10 mm.
Previously undetected CRCs were found in 27/386 patients (6.7 %), located in the left
colon
in 21/27 (78 %); in 7 the area had not been reached in the previous colonoscopy.
Risk factors for undetected advanced
adenoma
were advanced age, male gender, the presence of another advanced
adenoma
at first colonoscopy, and history of advanced neoplasia.
Previously undetected advanced lesions are more frequently found in the left
colon
and rectum.
Risk factors for
non
-detection of advanced
adenoma
are similar to those for advanced neoplasia recurrence.
Lowering
non
-detection rates is crucial for correct follow-up recommendations.
[MeSH-major]
Adenoma
/ diagnosis.
Colonic Polyps
/ diagnosis. Colonoscopy. Colorectal Neoplasms / diagnosis
[MeSH-minor]
Adenomatous
Polyposis Coli / complications. Age Factors. Aged.
Colonic
Neoplasms / diagnosis.
Colonic
Neoplasms / epidemiology.
Colonic
Neoplasms / pathology. Colorectal Neoplasms, Hereditary Nonpolyposis / complications. False Negative Reactions. Female. Humans. Logistic Models. Male. Middle Aged. Rectal Neoplasms / diagnosis. Rectal Neoplasms / epidemiology. Rectal Neoplasms / pathology. Retrospective Studies. Risk Factors. Sex Factors
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
MedlinePlus Health Information.
consumer health - Colonoscopy
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
© Georg Thieme Verlag KG Stuttgart · New York.
(PMID = 20960390.001).
[ISSN]
1438-8812
[Journal-full-title]
Endoscopy
[ISO-abbreviation]
Endoscopy
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
85.
Fernández-Suárez A, Cordero Fernández C, García Lozano R, Pizarro A, Garzón M, Núñez Roldán A:
Clinical and ethical implications of genetic counselling in familial adenomatous polyposis.
Rev Esp Enferm Dig
; 2005 Sep;97(9):654-65
[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]
Clinical and ethical implications of genetic counselling in familial
adenomatous
polyposis.
The association
of specific
genetic disturbances with the development of hereditary cancer helps us to understand the risk of suffering from it, the possibility of an earlier diagnosis, and the treatment and prevention of this disease.
Familial
adenomatous
polyposis (FAP) is a pre-neoplastic syndrome characterized by the presence of hundreds of
adenomatous polyps
in
the colon
, which develop into a carcinoma.
FAP can be diagnosed using sequencing techniques to detect mutations in the germinal line of the APC (
adenomatous
polyposis coli) gene.
[MeSH-major]
Adenomatous
Polyposis Coli / prevention & control. Genetic Counseling
Genetic Alliance.
consumer health - Familial Adenomatous Polyposis (FAP)
.
Genetic Alliance.
consumer health - Familial Polyposis
.
MedlinePlus Health Information.
consumer health - Genetic Counseling
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16266238.001).
[ISSN]
1130-0108
[Journal-full-title]
Revista española de enfermedades digestivas : organo oficial de la Sociedad Española de Patología Digestiva
[ISO-abbreviation]
Rev Esp Enferm Dig
[Language]
eng; spa
[Publication-type]
Journal Article
[Publication-country]
Spain
86.
Galamb O, Gyorffy B, Sipos F, Spisák S, Németh AM, Miheller P, Dinya E, Molnár B, Tulassay Z:
[Identification of colorectal cancer, adenoma, and inflammatory bowel disease specific gene expression patterns using whole genomic oligonucleotide microarray system].
Orv Hetil
; 2007 Nov 4;148(44):2067-79
[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]
[Identification of colorectal cancer,
adenoma
, and inflammatory bowel disease
specific
gene expression patterns using whole genomic oligonucleotide microarray system].
[Transliterated title]
Vastagbél-
adenoma
, vastagbélrák és IBD-specifikus génexpressziós mintázatok meghatározása teljes genomszintu oligonukleotid microarray-rendszerrel.
BACKGROUND: Discrimination and classification of colorectal diseases (
adenoma
, colorectal cancer, inflammatory bowel disease) using biopsy samples and expression microarrays, has not been solved yet, nevertheless, it can contribute to the understanding of the
colonic
diseases.
METHODS: Total ribonucleic acid was extracted, amplified and biotinylated from frozen
colonic
biopsies of 15 patients with colorectal cancer, 15 with
adenoma
, 14 with inflammatory bowel disease and 8 normal controls.
RESULTS: Top validated genes included CD44 antigen, met proto-oncogene, chemokine ligand-12, ADAM-like decysin-1 and ATP-binding casette-A8 genes in
adenoma
; collagen IValpha1, lipocalin-2, calumenin, aquaporin-8 genes in colorectal cancer; and lipocalin-2, ubiquitin D and interferon induced transmembrane protein 2 genes in inflammatory bowel disease.
The expression of 94% of the 52 genes measured by Taqman real-time polymerase chain reaction correlated with the results obtained using Affymetrix microarrays at a significance
of p
< 0.05.
[MeSH-major]
Adenoma
/ diagnosis. Colorectal Neoplasms / diagnosis. Gene Expression Profiling. Inflammatory Bowel Diseases / diagnosis. Oligonucleotide Array Sequence Analysis
Genetic Alliance.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Colorectal 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
.
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 = 17959550.001).
[ISSN]
0030-6002
[Journal-full-title]
Orvosi hetilap
[ISO-abbreviation]
Orv Hetil
[Language]
hun
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Hungary
[Chemical-registry-number]
63231-63-0 / RNA
87.
Oset P, Jasińska A, Szcześniak P, Orszulak-Michalak D, Talar-Wojnarowska R, Małecka-Panas E:
[Analysis of serum gastrin levels in patients with adenomatous polyps of the colon].
Pol Merkur Lekarski
; 2009 May;26(155):458-61
[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]
[Analysis of serum gastrin levels in patients with
adenomatous polyps
of the
colon
].
Adenomatous polyps
are known risk factor
of colon
cancer.
Gastrin is a peptide hormone involved in the growth of both normal and malignant intestinal tissue, which probably may promote progression through
the adenoma
-carcinoma sequence.
AIM OF OUR STUDY: To assess the association between serum gastrin levels and size, type and localization of
colonic
adenomas
.
MATERIAL AND METHODS: The study included 60 patients with
adenomatous polyps
of the
colon
and 30 healthy volunteers.
RESULTS: We observed higher serum gastrin levels in patients with
colonic
adenomas
compared to control group (59.65 pg/ml vs. 46.89 pg/ml; p < 0.05).
There was no association between gastrin levels and size, number, localisation and histologic type of
polyps
(p > 0.05).
CONCLUSION: Despite of elevated serum levels in patients with
colonic
adenomas
we did not observe the association between gastrin levels and size, grade of dysplasia and histologic type of
polyps
.
The exact role of hipergastrinemia in process
of colon
carcinogenesis remains to be determined.
[MeSH-major]
Adenomatous Polyps
/ blood. Gastrins / blood
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19606697.001).
[ISSN]
1426-9686
[Journal-full-title]
Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
[ISO-abbreviation]
Pol. Merkur. Lekarski
[Language]
pol
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Poland
[Chemical-registry-number]
0 / Gastrins
88.
Fujiya M, Moriichi K, Saitoh Y, Watari J, Kohgo Y:
Endoscopic piecemeal resection is a practical option to cure colorectal tumors.
Dig Endosc
; 2009 Jul;21 Suppl 1:S28-30
[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.
Endoscopic mucosal resection (EMR) and endoscopic piecemeal resection (EPMR) are therapeutic options widely accepted for the treatment
of colon adenoma
, intramucosal cancer and minimally invasive submucosal cancer.
[MeSH-major]
Adenoma
/ surgery. Colonoscopy / methods. Colorectal Neoplasms / surgery. Intestinal Mucosa / surgery
MedlinePlus Health Information.
consumer health - Colonoscopy
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19691729.001).
[ISSN]
1443-1661
[Journal-full-title]
Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society
[ISO-abbreviation]
Dig Endosc
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Australia
89.
Anupindi S, Perumpillichira J, Jaramillo D, Zalis ME, Israel EJ:
Low-dose CT colonography in children: initial experience, technical feasibility, and utility.
Pediatr Radiol
; 2005 May;35(5):518-24
[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.
BACKGROUND: CT colonography (CTC) is utilized as a diagnostic tool in the detection
of colon
polyps
and early colorectal cancer in adults.
Large studies in the literature, although focused on adult populations, have shown CTC to be a safe, accurate,
non
-invasive technique.
MATERIALS AND METHODS: From November 2001 to April 2004 we evaluated eight patients (3-17 years) with
non
-contrast CTC.
Sensitivity for
polyps
5-10 mm was 100%, and sensitivity for
polyps
10 mm and larger was 66.7%.
[MeSH-minor]
Adenomatous
Polyposis Coli / diagnostic imaging. Adolescent. Barium Sulfate. Child. Child, Preschool.
Colonic Polyps
/ diagnostic imaging. Colonoscopy. Contrast Media. Enema. Feasibility Studies. Female. Gastrointestinal Hemorrhage / diagnostic imaging. Humans. Image Processing, Computer-Assisted. Imaging, Three-Dimensional. Male. Radiation Dosage. Rectum. Safety. Sensitivity and Specificity
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
Barium sulfate
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[ErratumIn]
Pediatr Radiol. 2005 Jul;35(7):733
[Cites]
Radiology. 2002 Aug;224(2):383-92
[
12147833.001
]
[Cites]
Med J Aust. 2000 May 1;172(9):416-7
[
10870532.001
]
[Cites]
Radiology. 2002 Feb;222(2):337-45
[
11818597.001
]
[Cites]
Radiology. 2003 Dec;229(3):775-81
[
14657315.001
]
[Cites]
N Engl J Med. 2003 Dec 4;349(23 ):2191-200
[
14657426.001
]
[Cites]
Semin Ultrasound CT MR. 2001 Oct;22(5):432-42
[
11665922.001
]
[Cites]
AJR Am J Roentgenol. 1999 Sep;173(3):561-4
[
10470879.001
]
[Cites]
Radiology. 2001 Jan;218(1):274-7
[
11152814.001
]
[Cites]
Br J Radiol. 1996 Jan;69(817):33-41
[
8785619.001
]
[Cites]
Radiology. 2000 May;215(2):353-7
[
10796907.001
]
[Cites]
Med Phys. 2000 May;27(5):828-37
[
10841384.001
]
[Cites]
Radiology. 2003 Mar;226(3):911-7
[
12601218.001
]
[Cites]
Am J Gastroenterol. 2001 Oct;96(10):3009-12
[
11693340.001
]
[Cites]
Radiology. 2004 Mar;230(3):629-36
[
14739311.001
]
[Cites]
AJR Am J Roentgenol. 1997 Dec;169(6):1487-8
[
9393150.001
]
[Cites]
Radiology. 2001 Jun;219(3):685-92
[
11376255.001
]
[Cites]
Radiology. 2002 Jun;223(3):615-9
[
12034925.001
]
[Cites]
AJR Am J Roentgenol. 1997 May;168(5):1181-4
[
9129408.001
]
[Cites]
Radiology. 2002 Jul;224(1):25-33
[
12091658.001
]
[Cites]
Radiology. 2001 May;219(2):461-5
[
11323473.001
]
(PMID = 15789249.001).
[ISSN]
0301-0449
[Journal-full-title]
Pediatric radiology
[ISO-abbreviation]
Pediatr Radiol
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Contrast Media; 25BB7EKE2E / Barium Sulfate
90.
Ye YN, Wu WK, Shin VY, Bruce IC, Wong BC, Cho CH:
Dual inhibition of 5-LOX and COX-2 suppresses colon cancer formation promoted by cigarette smoke.
Carcinogenesis
; 2005 Apr;26(4):827-34
[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]
Dual inhibition of 5-LOX and COX-2 suppresses
colon
cancer formation promoted by cigarette smoke.
Previous studies indicate that the arachidonic acid-metabolizing enzymes COX-2 and 5-LOX are overexpressed during the process of
colonic
adenoma
formation promoted by cigarette smoke.
The aims of the present study were to investigate whether there exists a relationship between COX-2 and 5-LOX, and whether dual inhibition of COX-2 and 5-LOX has an anticarcinogenic effect in the
colonic
tumorigenesis promoted by cigarette smoke.
Results showed that pretreating
colon
cancer cells with cigarette smoke extract (CSE) promoted
colon
cancer growth in the nude mouse xenograft model.
In an in vitro study, we found that the action of CSE on
colon
cancer cells was mediated by 5-LOX DNA demethylation.
In summary, these results indicate that inhibition of COX-2 may lead to a shunt of arachidonic acid metabolism towards the leukotriene pathway during
colonic
tumorigenesis promoted by CSE.
[MeSH-major]
Adenocarcinoma / prevention & control.
Colonic
Neoplasms / prevention & control. Cyclooxygenase Inhibitors / therapeutic use. Lipoxygenase Inhibitors / therapeutic use. Prostaglandin-Endoperoxide Synthases / drug effects
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15637091.001).
[ISSN]
0143-3334
[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 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Lipoxygenase Inhibitors; 0 / RNA, Messenger; 0 / Smoke; 1HGW4DR56D / Leukotriene B4; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; K7Q1JQR04M / Dinoprostone
91.
Qasim A, Muldoon C, McKiernan S:
Colonic adenoma patients have higher incidence of hyperplastic polyps on surveillance colonoscopy.
Eur J Gastroenterol Hepatol
; 2009 Aug;21(8):877-81
[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]
Colonic
adenoma
patients have higher incidence of hyperplastic
polyps
on surveillance colonoscopy.
OBJECTIVES: To determine the incidence of hyperplastic
polyps
in patients undergoing surveillance colonoscopy and to compare with the prevalence in individuals undergoing index colonoscopy.
PATIENTS AND METHODS: This prospective observational study included patients with index colonoscopy findings
of adenomas
,
adenoma
with concomitant hyperplastic
polyps
and advanced neoplasia who subsequently underwent surveillance colonoscopy.
On index colonoscopy,
adenomas
,
adenoma
with concomitant hyperplastic
polyps
and advanced neoplasia were present in 61, 35 and 12 patients, respectively.
Findings on surveillance examination included hyperplastic
polyps
in 35 and 57% of patients with past
adenomas
and
adenoma
with concomitant hyperplastic
polyps
, respectively.
Hyperplastic
polyps
,
adenomas
and advanced neoplasia were found in 155 (4%), 388 (10%) and 60 (1.5%) of patients, respectively.
Hyperplastic
polyps
and
adenoma
were significantly higher in study group as compared with control group (P >0.5).
CONCLUSION: Incidence of hyperplastic
polyps
is significantly higher on surveillance colonoscopy as compared with the prevalence on index colonoscopy.
This may signify a continuous spectrum of biological evolution between hyperplastic
polyps
and
adenomas
.
[MeSH-major]
Adenoma
/ pathology.
Colonic Polyps
/ pathology. Colonoscopy / methods. Colorectal Neoplasms / pathology
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
MedlinePlus Health Information.
consumer health - Colonoscopy
.
MedlinePlus Health Information.
consumer health - Colorectal 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 = 19598329.001).
[ISSN]
1473-5687
[Journal-full-title]
European journal of gastroenterology & hepatology
[ISO-abbreviation]
Eur J Gastroenterol Hepatol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
92.
du Toit J, Hamilton W, Barraclough K:
Risk in primary care of colorectal cancer from new onset rectal bleeding: 10 year prospective study.
BMJ
; 2006 Jul 8;333(7558):69-70
[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.
OBJECTIVE: To measure the risk of colorectal cancer and
adenoma
with new onset rectal bleeding reported to primary care.
MAIN OUTCOME MEASURES: Percentage of participants in whom colorectal cancer or
colonic
adenoma
was identified after investigation of the bowel.
Of these, 15 (5.7%, 95% confidence interval 3.2% to 9.2%) had colorectal cancer, and 13 (4.9%, 2.6% to 8.4%) had
colonic
adenoma
.
CONCLUSIONS: One in 10 patients aged 45 or more with new onset rectal bleeding had
colonic
neoplasia, so investigation of the bowel should be offered to all such patients, whether or not they have other symptoms.
[MeSH-major]
Adenoma
/ etiology. Colorectal Neoplasms / etiology. Gastrointestinal Hemorrhage / etiology. Rectal Diseases / etiology
Genetic Alliance.
consumer health - Colorectal Cancer
.
Genetic Alliance.
consumer health - Rectal Cancer
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Gastrointestinal Bleeding
.
MedlinePlus Health Information.
consumer health - Rectal Disorders
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Br J Gen Pract. 2005 Dec;55(521):949-55
[
16378565.001
]
[Cites]
Br J Cancer. 2005 Aug 22;93(4):399-405
[
16106247.001
]
[Cites]
BMJ. 2000 Oct 21;321(7267):998-9
[
11039968.001
]
[Cites]
Fam Pract. 1995 Sep;12(3):279-86
[
8536830.001
]
[CommentIn]
BMJ. 2006 Jul 8;333(7558):54-5
[
16825205.001
]
[CommentIn]
BMJ. 2006 Jul 22;333(7560):201
[
16858063.001
]
[CommentIn]
BMJ. 2006 Jul 22;333(7560):201-2
[
16858062.001
]
(PMID = 16790459.001).
[ISSN]
1756-1833
[Journal-full-title]
BMJ (Clinical research ed.)
[ISO-abbreviation]
BMJ
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Other-IDs]
NLM/ PMC1489264
93.
Durno CA:
Colonic polyps in children and adolescents.
Can J Gastroenterol
; 2007 Apr;21(4):233-9
[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]
Colonic polyps
in children and adolescents.
Colonic polyps
most commonly present with rectal bleeding in children.
The isolated juvenile
polyp
is the most frequent kind
of polyp
identified in children.
'Juvenile' refers to the histological type
of polyp
and not the age of onset of the
polyp
.
Adolescents and adults with multiple juvenile
polyps
are at a significant risk of intestinal cancer.
Attenuated familial adenamatous polyposis (AFAP) can occur either by a mutation at the extreme ends of the
adenomatous
polyposis coli gene or by biallelic mutations in the mutY homologue (MYH) gene.
Colonic polyps
, including isolated juvenile
polyps
, juvenile polyposis syndrome, FAP, AFAP and MYH-associated polyposis, are discussed in the present review.
[MeSH-major]
Colonic Polyps
[MeSH-minor]
Adenomatous
Polyposis Coli / genetics.
Adenomatous
Polyposis Coli / pathology. Adolescent. Child. DNA Glycosylases / genetics. Genes, APC. Genetic Counseling. Genetic Predisposition to Disease. Genetic Testing. Humans. Mutation
MedlinePlus Health Information.
consumer health - Colonic Polyps
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
N Engl J Med. 2000 Jun 29;342(26):1946-52
[
10874062.001
]
[Cites]
Gut. 2005 Aug;54(8):1146-50
[
15845562.001
]
[Cites]
Gastroenterology. 2001 Nov;121(5):1127-35
[
11677205.001
]
[Cites]
Dis Colon Rectum. 2002 Jan;45(1):127-34; discussion 134-6
[
11786778.001
]
[Cites]
Nat Genet. 2002 Feb;30(2):227-32
[
11818965.001
]
[Cites]
Gut. 2002 May;50(5):636-41
[
11950808.001
]
[Cites]
Dis Colon Rectum. 2002 Jul;45(7):887-9
[
12130875.001
]
[Cites]
J Gastrointest Surg. 2002 Nov-Dec;6(6):831-7; discussion 837
[
12504221.001
]
[Cites]
N Engl J Med. 2003 Feb 27;348(9):791-9
[
12606733.001
]
[Cites]
Lancet. 2003 Jul 5;362(9377):39-41
[
12853198.001
]
[Cites]
Eur J Cancer. 2003 Oct;39(15):2200-4
[
14522379.001
]
[Cites]
Cancer Res. 2003 Nov 15;63(22):7595-9
[
14633673.001
]
[Cites]
Gut. 2004 Mar;53(3):381-6
[
14960520.001
]
[Cites]
Can J Gastroenterol. 2004 Feb;18(2):93-9
[
14997217.001
]
[Cites]
Lancet. 2004 Mar 13;363(9412):852-9
[
15031030.001
]
[Cites]
Clin Gastroenterol Hepatol. 2004 May;2(5):366-75
[
15118973.001
]
[Cites]
Gastroenterology. 2004 Jul;127(1):9-16
[
15236166.001
]
[Cites]
J Med Genet. 2004 Jul;41(7):484-91
[
15235019.001
]
[Cites]
Gastroenterology. 2004 Aug;127(2):444-51
[
15300576.001
]
[Cites]
Dis Colon Rectum. 1972 Jan-Feb;15(1):23-9
[
5058411.001
]
[Cites]
Arch Dis Child. 1983 Dec;58(12):959-62
[
6318669.001
]
[Cites]
Int J Psychiatry Med. 1986-1987;16(3):211-30
[
3026981.001
]
[Cites]
J Natl Cancer Inst. 1988 Dec 21;80(20):1626-8
[
2848134.001
]
[Cites]
Histopathology. 1988 Dec;13(6):619-30
[
2853131.001
]
[Cites]
Lancet. 1989 Sep 30;2(8666):783-5
[
2571019.001
]
[Cites]
Arch Dis Child. 1991 Aug;66(8):971-5
[
1656892.001
]
[Cites]
Dis Colon Rectum. 1992 Apr;35(4):373-4
[
1316263.001
]
[Cites]
Am J Med Genet. 1992 Aug 1;43(6):1023-5
[
1329510.001
]
[Cites]
J Med Genet. 2005 Sep;42(9):e54
[
16140997.001
]
[Cites]
J Pediatr Gastroenterol Nutr. 2006 Jul;43(1):5-15
[
16819371.001
]
[Cites]
Gastroenterology. 1993 Sep;105(3):698-700
[
8395444.001
]
[Cites]
N Engl J Med. 1993 Dec 30;329(27):1982-7
[
8247073.001
]
[Cites]
Arch Dis Child. 1994 Aug;71(2):103-5
[
7944526.001
]
[Cites]
J Natl Cancer Inst Monogr. 1995;(17):67-71
[
8573458.001
]
[Cites]
J Bacteriol. 1996 Jul;178(13):3885-92
[
8682794.001
]
[Cites]
Hum Mutat. 1997;9(1):7-16
[
8990002.001
]
[Cites]
N Engl J Med. 1997 Mar 20;336(12):823-7
[
9062090.001
]
[Cites]
Ann Surg. 1998 Jan;227(1):57-62
[
9445111.001
]
[Cites]
Ann Surg Oncol. 1998 Dec;5(8):751-6
[
9869523.001
]
[Cites]
Endoscopy. 1999 Aug;31(6):412-6
[
10494676.001
]
[Cites]
Clin Genet. 2005 Jan;67(1):104-6
[
15617557.001
]
[Cites]
Am J Gastroenterol. 2005 Feb;100(2):476-90
[
15667510.001
]
[Cites]
Gastroenterology. 2005 May;128(6):1696-716
[
15887160.001
]
[Cites]
J Pediatr. 2001 May;138(5):621-8
[
11343034.001
]
(PMID = 17431512.001).
[ISSN]
0835-7900
[Journal-full-title]
Canadian journal of gastroenterology = Journal canadien de gastroenterologie
[ISO-abbreviation]
Can. J. Gastroenterol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Canada
[Chemical-registry-number]
EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
[Number-of-references]
47
[Other-IDs]
NLM/ PMC2657698
94.
Tan KL, Wilson S, O'Neill C, Gordon D, Napier S:
Something not quite right: Gardner syndrome diagnosed by multiple cutaneous lesions and genetic testing.
Surgeon
; 2005 Dec;3(6):412-5
[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.
Gardner syndrome is a variant of familial
adenomatous
polyposis characterized by intestinal
adenomatous polyps
, which can progress to adenocarcinoma, and a variety of extraintestinal manifestations, including skin cysts, osteomas, soft tissue fibrous tumours and a characteristic ocular lesion.
Gardner syndrome was considered only after excision of subcutaneous fibrous tumours from the mastoid region and paraspinal area and was confirmed by genetic testing in spite of the patient's refusal to undergo
colonic
endoscopic examination.
Subsequent resection revealed approximately 70
adenomatous colonic polyps
in
the colon
and rectum but no invasive tumour, highlighting the benefits of genetic testing in treatment planning.
Genetic Alliance.
consumer health - Gardner Syndrome
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16353862.001).
[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]
Case Reports; Journal Article
[Publication-country]
Scotland
95.
García-Faroldi G, Sánchez-Jiménez F, Fajardo I:
The polyamine and histamine metabolic interplay in cancer and chronic inflammation.
Curr Opin Clin Nutr Metab Care
; 2009 Jan;12(1):59-65
[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.
RECENT FINDINGS: The most recent and relevant findings that might reflect a link between the polyamines/histamine metabolic interplay and the development of cancer and chronic inflammation-related diseases include: the observation that histamine catabolism is downregulated in the
colonic
mucosa of patients with
colonic
adenoma
; the finding that some polyamine and histamine-related metabolites are different between a breast cancer cell line and a reference mammary epithelial cell line; and the demonstration of the critical role that mast cells (a cell type in which the polyamine/histamine metabolic interplay has been confirmed) play in the development of pancreatic tumors.
There is still, however, a lack
of specific
studies elucidating the exact contribution of the polyamine/histamine metabolic interplay in these clinical settings.
Hazardous Substances Data Bank.
HISTAMINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19057189.001).
[ISSN]
1473-6519
[Journal-full-title]
Current opinion in clinical nutrition and metabolic care
[ISO-abbreviation]
Curr Opin Clin Nutr Metab Care
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Polyamines; 7LP2MPO46S / S-Adenosylmethionine; 820484N8I3 / Histamine
[Number-of-references]
64
96.
Tabuchi M, Kitayama J, Nagawa H:
Hypertriglyceridemia is positively correlated with the development of colorectal tubular adenoma in Japanese men.
World J Gastroenterol
; 2006 Feb 28;12(8):1261-4
[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.
[Title]
Hypertriglyceridemia is positively correlated with the development of colorectal tubular
adenoma
in Japanese men.
AIM: To determine the real association between serum lipid levels and
colonic
polyp
formation.
METHODS: We performed a large scale retrospective study to analyze the correlation between the incidence of colorectal
adenoma
or carcinoma and the fasting serum levels of total cholesterol (TC) and triglycerides (TG) in patients who underwent total colonoscopy for screening for
colon
cancer.
RESULTS: Both levels were significantly elevated in patients with
adenomas
as compared with patients without any neoplastic lesion (TC 207.6+/-29.5 vs 199.5+/-34.3, n=4883, P<0.001; TG 135.0+/-82.2 vs 108.7+/-71.5, n=4874, P<0.001).
The difference was significant in patients with tubular
adenoma
but not in those with villous or serrated
adenoma
.
The level of TG in patients with invasive carcinoma did not show a significant elevation from that in patients with
adenoma
.
These findings suggest that hypertriglyceridemia is an independent risk factor for
colonic
adenoma
in men.
[MeSH-major]
Adenoma
/ blood.
Adenoma
/ etiology. Colorectal Neoplasms / blood. Colorectal Neoplasms / etiology. Hypertriglyceridemia / complications
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Triglycerides
.
Hazardous Substances Data Bank.
CHOLESTEROL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Nutr Cancer. 2000;37(1):19-26
[
10965515.001
]
[Cites]
Int J Epidemiol. 1998 Oct;27(5):794-8
[
9839735.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):412-8
[
12750235.001
]
[Cites]
Cancer Res. 2003 Sep 15;63(18):6090-5
[
14522940.001
]
[Cites]
Cancer Sci. 2003 Nov;94(11):960-4
[
14611672.001
]
[Cites]
Cancer. 1977 Jun;39(6):2533-9
[
872053.001
]
[Cites]
Cancer Res. 1981 Sep;41(9 Pt 2):3700-5
[
6266660.001
]
[Cites]
J Chronic Dis. 1982;35(5):313-20
[
7068807.001
]
[Cites]
JAMA. 1986 Jan 17;255(3):365-7
[
3941515.001
]
[Cites]
N Engl J Med. 1986 Dec 25;315(26):1634-8
[
3785334.001
]
[Cites]
Br J Cancer. 1987 Oct;56(4):451-4
[
3689662.001
]
[Cites]
Am J Clin Nutr. 1988 Feb;47(2):312-7
[
3341261.001
]
[Cites]
Hematol Oncol Clin North Am. 1989 Mar;3(1):35-63
[
2537285.001
]
[Cites]
Cancer. 1992 Feb 15;69(4):883-8
[
1735079.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1994 Dec;3(8):687-95
[
7881343.001
]
[Cites]
Cancer Causes Control. 1995 Mar;6(2):164-79
[
7749056.001
]
[Cites]
Eur J Cancer. 1995 Jul-Aug;31A(7-8):1033-8
[
7576987.001
]
[Cites]
Scand J Gastroenterol. 1997 Feb;32(2):162-8
[
9051877.001
]
[Cites]
Carcinogenesis. 1998 Sep;19(9):1679-84
[
9771941.001
]
[Cites]
Climacteric. 2002 Mar;5(1):3-14
[
11974557.001
]
(PMID = 16534881.001).
[ISSN]
1007-9327
[Journal-full-title]
World journal of gastroenterology
[ISO-abbreviation]
World J. Gastroenterol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Triglycerides; 97C5T2UQ7J / Cholesterol
[Other-IDs]
NLM/ PMC4124439
97.
Phelps RA, Chidester S, Dehghanizadeh S, Phelps J, Sandoval IT, Rai K, Broadbent T, Sarkar S, Burt RW, Jones DA:
A two-step model for colon adenoma initiation and progression caused by APC loss.
Cell
; 2009 May 15;137(4):623-34
[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 two-step model for
colon adenoma
initiation and progression caused by APC loss.
Aberrant Wnt/beta-catenin signaling following loss of the tumor suppressor
adenomatous
polyposis coli (APC) is thought to initiate
colon adenoma
formation.
These findings suggest that, following APC loss, CtBP1 contributes to
adenoma
initiation as a first step, whereas KRAS activation and beta-catenin nuclear localization promote
adenoma
progression to carcinomas as a second step.
Consistent with this model, human FAP
adenomas
showed robust upregulation of CtBP1 in the absence of detectable nuclear beta-catenin, whereas nuclear beta-catenin was detected in carcinomas.
COS Scholar Universe.
author profiles
.
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
ZFIN.
ZFIN
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Bioessays. 1999 Dec;21(12):1021-30
[
10580987.001
]
[Cites]
J Clin Oncol. 2004 Nov 15;22(22):4456-62
[
15483017.001
]
[Cites]
EMBO J. 2000 May 15;19(10):2270-9
[
10811618.001
]
[Cites]
J Biol Chem. 2004 Dec 3;279(49):51581-9
[
15358764.001
]
[Cites]
Oncogene. 2004 Dec 16;23(58):9369-80
[
15516977.001
]
[Cites]
J Biol Chem. 2005 Jul 15;280(28):26565-72
[
15899904.001
]
[Cites]
J Biol Chem. 2005 Aug 26;280(34):30490-5
[
15967793.001
]
[Cites]
Gene. 2005 Nov 21;361:1-12
[
16185824.001
]
[Cites]
Science. 2005 Dec 2;310(5753):1504-10
[
16293724.001
]
[Cites]
Genes Dev. 2006 Mar 1;20(5):586-600
[
16510874.001
]
[Cites]
EMBO Rep. 2006 Apr;7(4):444-9
[
16439994.001
]
[Cites]
J Biol Chem. 2006 Apr 14;281(15):9971-6
[
16476742.001
]
[Cites]
EMBO J. 2006 Jun 21;25(12):2735-45
[
16710294.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Sep 5;103(36):13409-14
[
16938888.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Sep 19;103(38):14122-7
[
16959882.001
]
[Cites]
Cell. 2006 Nov 3;127(3):469-80
[
17081971.001
]
[Cites]
J Biol Chem. 2006 Dec 8;281(49):37828-35
[
17028196.001
]
[Cites]
Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4036-41
[
17360473.001
]
[Cites]
Cancer Res. 2007 Mar 15;67(6):2469-79
[
17363564.001
]
[Cites]
Am J Med Genet A. 2007 Jul 1;143A(13):1472-80
[
17551924.001
]
[Cites]
J Biol Chem. 2007 Oct 5;282(40):29394-400
[
17673467.001
]
[Cites]
Cancer Res. 2007 Oct 15;67(20):9721-30
[
17942902.001
]
[Cites]
Science. 2008 Jan 18;319(5861):333-6
[
18202290.001
]
[Cites]
Cell. 2008 Apr 18;133(2):340-53
[
18423204.001
]
[Cites]
Nat Genet. 2008 May;40(5):600-8
[
18372904.001
]
[Cites]
Gastroenterology. 2006 Oct;131(4):1096-109
[
17030180.001
]
[Cites]
Cell. 2000 Oct 13;103(2):311-20
[
11057903.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Feb 5;99(3):1521-6
[
11818567.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jun 25;99(13):8683-8
[
12072559.001
]
[Cites]
Curr Biol. 2002 Jul 23;12(14):R499-R501
[
12176352.001
]
[Cites]
Am J Clin Pathol. 2003 Sep;120(3):418-23
[
14502807.001
]
[Cites]
Nature. 2003 Oct 9;425(6958):633-7
[
14534590.001
]
[Cites]
Genes Dev. 2004 Jun 15;18(12):1385-90
[
15198980.001
]
[Cites]
Curr Opin Cell Biol. 2004 Oct;16(5):528-35
[
15363803.001
]
[Cites]
J Biol Chem. 2004 Oct 8;279(41):43261-72
[
15294912.001
]
[Cites]
Nature. 1987 May 28-Jun 3;327(6120):293-7
[
3587348.001
]
[Cites]
Nature. 1987 May 28-Jun 3;327(6120):298-303
[
2438556.001
]
[Cites]
Cell. 1990 Jun 1;61(5):759-67
[
2188735.001
]
[Cites]
Cell. 1996 Oct 18;87(2):159-70
[
8861899.001
]
[Cites]
Science. 1997 Mar 21;275(5307):1787-90
[
9065402.001
]
[Cites]
Cancer Res. 1997 Oct 15;57(20):4624-30
[
9377578.001
]
[Cites]
Cancer Res. 1998 Mar 1;58(5):1021-6
[
9500465.001
]
[Cites]
Cancer Res. 1998 Mar 15;58(6):1130-4
[
9515795.001
]
[Cites]
Science. 1998 Sep 4;281(5382):1509-12
[
9727977.001
]
[Cites]
Curr Opin Genet Dev. 1999 Feb;9(1):15-21
[
10072352.001
]
[Cites]
Cancer Res. 1999 Apr 1;59(7):1442-4
[
10197610.001
]
[Cites]
Nature. 1999 Apr 1;398(6726):422-6
[
10201372.001
]
[Cites]
Cancer Res. 1999 Aug 15;59(16):3875-9
[
10463573.001
]
[Cites]
Dev Cell. 2004 Nov;7(5):677-85
[
15525529.001
]
[Cites]
Oncogene. 1999 Dec 2;18(51):7219-25
[
10602475.001
]
(PMID = 19450512.001).
[ISSN]
1097-4172
[Journal-full-title]
Cell
[ISO-abbreviation]
Cell
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA073992; United States / NCI NIH HHS / CA / CA116468-03; United States / NCI NIH HHS / CA / CA073992-06A10003; United States / NCI NIH HHS / CA / R01 CA116468-03; United States / NCI NIH HHS / CA / CA96934; United States / NCI NIH HHS / CA / P01 CA073992-06A10003; United States / NCI NIH HHS / CA / R01 CA116468; United States / NCI NIH HHS / CA / P01 CA073992; United States / NCI NIH HHS / CA / CA116468-04; United States / NCI NIH HHS / CA / CA042014; United States / NCI NIH HHS / CA / P30 CA042014; United States / NCI NIH HHS / CA / R01 CA116468-04
[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 / Adenomatous Polyposis Coli Protein; 0 / DNA-Binding Proteins; 0 / Peptide Fragments; 0 / Rac1 GTP-binding protein (17-32); 0 / beta Catenin; EC 1.1.- / Alcohol Oxidoreductases; EC 1.1.1.- / C-terminal binding protein; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf; EC 3.6.5.2 / rac1 GTP-Binding Protein; EC 3.6.5.2 / ras Proteins
[Other-IDs]
NLM/ NIHMS102940; NLM/ PMC2706149
98.
Peeters M:
Cardiovascular risk status can influence the colorectal cancer screening strategy.
Digestion
; 2010;81(1):18-9
[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.
[MeSH-minor]
Adenomatous Polyps
/ complications.
Adenomatous Polyps
/ epidemiology.
Colonic Polyps
/ complications.
Colonic Polyps
/ epidemiology. Humans. Prevalence. Risk Assessment
Genetic Alliance.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.