BioMedLib Search Engine
[ goto HOMEPAGE ]
Save time; Find better answers!
Skip to content
Advanced Search
Search History
MeSH Query
Page Format
Clarify the query
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
lesion pre malignant drug therapy 2000:2010[pubdate] *count=100
86 results
Searchbox
Export
PDF
RSS
Email
Delete
Email this search result to the following email address:
[X] Close
Expand the query
'
drug therapy
' expands to
2 meanings
. Choose the one you intended:
Concept C0013216: drug therapy procedure;
details
Concept C0013217: pharmacologic therapy;
details
'
lesion pre malignant
' 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 86 of about 86
1.
Gately S, Kerbel R:
Therapeutic potential of selective cyclooxygenase-2 inhibitors in the management of tumor angiogenesis.
Prog Exp Tumor Res
; 2003;37:179-92
[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]
Therapeutic
potential of selective cyclooxygenase-2 inhibitors in the management of tumor angiogenesis.
Selective
pharmacologic
inhibition of COX-2 represents a viable
therapeutic
option for the
treatment
of malignancies.
Agents that selectively inhibit COX-2 appear to be safe, and well tolerated suggesting that chronic
treatment
for angiogenesis inhibition is feasible [107-110].
Because these agents inhibit angiogenesis, they should have at least additive benefit in combination with standard
chemotherapy
[111] and radiation
therapy
[24, 112].
In preclinical models, a selective inhibitor of COX-2 was shown to potentiate the beneficial antitumor effects of ionizing radiation with no increase in normal
tissue
cytotoxicity [113-115].
This antiangiogenic
chemotherapy
regimen could be enhanced by the concurrent administration of an angiogenesis inhibitor [116-119].
Given the safety and tolerability of the selective COX-2 inhibitors, and the potent antiangiogenic properties of these agents, the combination of antiangiogenic
chemotherapy with
a COX-2 inhibitor warrants clinical evaluation [118, 121, 122].
In conclusion, the contribution of COX-2 at multiple points in the angiogenic cascade makes it an ideal target for
pharmacologic
inhibition.
As
premalignant lesions
progress towards malignancy, there is a switch to the angiogenic phenotype that is subsequently followed by rapid tumor growth [128, 129].
[MeSH-major]
Cyclooxygenase Inhibitors /
therapeutic
use. Isoenzymes / antagonists & inhibitors. Neoplasms / blood supply. Neoplasms /
drug therapy
. Neovascularization, Pathologic /
drug therapy
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
COS Scholar Universe.
author profiles
.
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 = 12795055.001).
[ISSN]
0079-6263
[Journal-full-title]
Progress in experimental tumor research
[ISO-abbreviation]
Prog Exp Tumor Res
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Endothelial Growth Factors; 0 / Intercellular Signaling Peptides and Proteins; 0 / Isoenzymes; 0 / Lymphokines; 0 / Membrane Proteins; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 57576-52-0 / Thromboxane A2; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
[Number-of-references]
131
2.
Giraudo E, Inoue M, Hanahan D:
An amino-bisphosphonate targets MMP-9-expressing macrophages and angiogenesis to impair cervical carcinogenesis.
J Clin Invest
; 2004 Sep;114(5):623-33
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
A mouse model involving the human papillomavirus
type
-16 oncogenes develops cervical cancers by lesional stages analogous to those in humans.
Preclinical trials sought to target MMP-9 and angiogenesis with a prototypical MMP inhibitor and with a bisphosphonate, zoledronic acid (ZA), revealing both to be antiangiogenic, producing effects comparable to a Mmp9 gene KO in impairing angiogenic switching, progression of
premalignant lesions
, and tumor growth.
ZA
therapy
increased neoplastic epithelial and endothelial cell apoptosis without affecting hyperproliferation, indicating that ZA was not antimitotic.
Given its track record in clinical use with limited toxicity, ZA holds promise as an "unconventional" MMP-9 inhibitor for antiangiogenic
therapy
of cervical cancer and potentially for additional cancers and other diseases where MMP-9 expression by infiltrating macrophages is evident.
[MeSH-major]
Cervical Intraepithelial Neoplasia / blood supply. Diphosphonates / pharmacology. Imidazoles / pharmacology. Macrophages /
drug
effects. Matrix Metalloproteinase Inhibitors. Neovascularization, Pathologic /
drug therapy
. Uterine Cervical Neoplasms / blood supply
[MeSH-minor]
Angiogenesis Inhibitors / pharmacology. Animals. Cell Movement /
drug
effects. Enzyme Activation /
drug
effects. Female. Humans. Macrophage Activation /
drug
effects. Matrix Metalloproteinase 9 / metabolism. Mice. Mice, Transgenic. Vascular Endothelial Growth Factors / metabolism
MedlinePlus Health Information.
consumer health - Cervical Cancer
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
International Agency for Research on Cancer - Screening Group.
diagnostics - Histopathology and cytopathology of the uterine cervix - digital atlas
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Res. 2000 Mar 1;60(5):1267-75
[
10728686.001
]
[Cites]
Cancer Res. 2003 Oct 1;63(19):6537-42
[
14559848.001
]
[Cites]
Cancer Res. 2000 Jun 1;60(11):2949-54
[
10850442.001
]
[Cites]
Cancer. 2000 Jun 15;88(12 Suppl):2961-78
[
10898340.001
]
[Cites]
Nat Cell Biol. 2000 Oct;2(10):737-44
[
11025665.001
]
[Cites]
Cell. 2000 Oct 27;103(3):481-90
[
11081634.001
]
[Cites]
Bone. 2001 May;28(5):465-73
[
11344045.001
]
[Cites]
Int J Biochem Cell Biol. 2001 Oct;33(10):960-70
[
11470230.001
]
[Cites]
J Biol Chem. 2003 Oct 31;278(44):43603-14
[
12933798.001
]
[Cites]
Nat Rev Cancer. 2004 Jan;4(1):71-8
[
14708027.001
]
[Cites]
Cancer Res. 2004 Feb 1;64(3):952-61
[
14871825.001
]
[Cites]
Development. 1992 Feb;114(2):447-56
[
1317291.001
]
[Cites]
Cancer Res. 1994 Feb 1;54(3):800-4
[
7508337.001
]
[Cites]
J Virol. 1994 Jul;68(7):4358-68
[
7515971.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Oct 23;98(22):12485-90
[
11606713.001
]
[Cites]
Science. 2002 Mar 29;295(5564):2387-92
[
11923519.001
]
[Cites]
Br J Cancer. 2002 May 6;86(9):1479-86
[
11986784.001
]
[Cites]
Cell. 2002 May 31;109(5):625-37
[
12062105.001
]
[Cites]
Cancer Cell. 2002 May;1(4):339-53
[
12086849.001
]
[Cites]
J Natl Cancer Inst. 2002 Aug 7;94(15):1134-42
[
12165638.001
]
[Cites]
J Pharmacol Exp Ther. 2002 Sep;302(3):1055-61
[
12183663.001
]
[Cites]
Br J Cancer. 2002 Aug 27;87(5):537-44
[
12189553.001
]
[Cites]
Cancer Cell. 2002 Oct;2(4):289-300
[
12398893.001
]
[Cites]
Oncologist. 2002;7(5):393-400
[
12401901.001
]
[Cites]
Cancer Res. 2002 Nov 15;62(22):6538-44
[
12438248.001
]
[Cites]
Clin Cancer Res. 2003 Jan;9(1):295-306
[
12538482.001
]
[Cites]
Cancer. 2003 Feb 1;97(3 Suppl):840-7
[
12548584.001
]
[Cites]
Anticancer Res. 2002 Nov-Dec;22(6C):3925-31
[
12553014.001
]
[Cites]
Br J Cancer. 2003 Jan 13;88(1):63-73
[
12556961.001
]
[Cites]
J Bone Miner Res. 2003 Feb;18(2):204-12
[
12568397.001
]
[Cites]
Curr Opin Hematol. 2003 Mar;10(2):136-41
[
12579040.001
]
[Cites]
Trends Mol Med. 2003 Mar;9(3):109-17
[
12657432.001
]
[Cites]
J Cancer Res Clin Oncol. 2003 Feb;129(2):123-31
[
12669237.001
]
[Cites]
J Biol Chem. 2003 Apr 25;278(17):15056-64
[
12586837.001
]
[Cites]
Circ Res. 2003 May 2;92(8):827-39
[
12730128.001
]
[Cites]
Nature. 2003 May 15;423(6937):337-42
[
12748652.001
]
[Cites]
Nat Rev Cancer. 2003 Jun;3(6):401-10
[
12778130.001
]
[Cites]
J Urol. 2003 Jul;170(1):246-52
[
12796698.001
]
[Cites]
J Immunol. 2003 Jul 1;171(1):142-51
[
12816992.001
]
[Cites]
Cancer Cell. 2003 Jun;3(6):589-601
[
12842087.001
]
[Cites]
Lancet. 2003 Jun 28;361(9376):2217-25
[
12842378.001
]
[Cites]
Clin Cancer Res. 2003 Jul;9(7):2394-9
[
12855610.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Apr 2;93(7):2930-5
[
8610145.001
]
[Cites]
Am J Pathol. 1996 Dec;149(6):1899-917
[
8952526.001
]
[Cites]
Cancer Res. 1997 Apr 1;57(7):1294-300
[
9102216.001
]
[Cites]
Br J Cancer. 1997;76(11):1410-5
[
9400935.001
]
[Cites]
Cancer Res. 1998 Mar 1;58(5):1048-51
[
9500469.001
]
[Cites]
J Bone Miner Res. 1998 Apr;13(4):581-9
[
9556058.001
]
[Cites]
Cancer Res. 1998 May 1;58(9):1952-9
[
9581838.001
]
[Cites]
Cell. 1998 May 1;93(3):411-22
[
9590175.001
]
[Cites]
Gynecol Oncol. 1999 Mar;72(3):380-6
[
10053110.001
]
[Cites]
Science. 1999 Apr 30;284(5415):808-12
[
10221914.001
]
[Cites]
Genes Dev. 1999 Jun 1;13(11):1382-97
[
10364156.001
]
[Cites]
Ann N Y Acad Sci. 1999 Jun 30;878:372-87
[
10415742.001
]
[Cites]
Ann N Y Acad Sci. 1999 Jun 30;878:453-65
[
10415748.001
]
[Cites]
J Natl Cancer Inst. 1995 Aug 16;87(16):1237-45
[
7563170.001
]
[Cites]
Cold Spring Harb Symp Quant Biol. 2002;67:293-300
[
12858552.001
]
[Cites]
Semin Oncol. 2003 Aug;30(4 Suppl 9):80-94
[
12908139.001
]
[Cites]
Cancer Res. 2003 Aug 15;63(16):4862-71
[
12941807.001
]
[Cites]
Life Sci. 2003 Sep 26;73(19):2413-20
[
12954450.001
]
[Cites]
Cancer Res. 2003 Sep 1;63(17):5224-9
[
14500349.001
]
[Cites]
Biochem Biophys Res Commun. 2003 Oct 24;310(3):816-23
[
14550277.001
]
[Cites]
J Clin Invest. 2000 Apr;105(8):1045-7
[
10772648.001
]
(PMID = 15343380.001).
[ISSN]
0021-9738
[Journal-full-title]
The Journal of clinical investigation
[ISO-abbreviation]
J. Clin. Invest.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Angiogenesis Inhibitors; 0 / Diphosphonates; 0 / Imidazoles; 0 / Matrix Metalloproteinase Inhibitors; 0 / Vascular Endothelial Growth Factors; 6XC1PAD3KF / zoledronic acid; EC 3.4.24.35 / Matrix Metalloproteinase 9
[Other-IDs]
NLM/ PMC514591
3.
Lippman SM, Sudbø J, Hong WK:
Oral cancer prevention and the evolution of molecular-targeted drug development.
J Clin Oncol
; 2005 Jan 10;23(2):346-56
[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.
[Title]
Oral cancer prevention and the evolution of molecular-targeted
drug
development.
Biomarkers of genomic instability, such as aneuploidy and allelic imbalance, can accurately measure the cancer risk of oral
premalignant lesions
, or intraepithelial neoplasia (IEN).
[MeSH-major]
Carcinoma in Situ / prevention & control.
Drug
Delivery Systems. Mouth Neoplasms / prevention & control. Technology, Pharmaceutical
[MeSH-minor]
Aneuploidy. Biomarkers, Tumor. Cyclooxygenase 2. Green Fluorescent Proteins / antagonists & inhibitors. Humans. Isoenzymes / antagonists & inhibitors. Membrane Proteins. Precancerous Conditions /
drug therapy
. Precancerous Conditions / genetics. Prostaglandin-Endoperoxide Synthases. Risk Assessment. Risk Factors
Genetic Alliance.
consumer health - Oral cancer
.
MedlinePlus Health Information.
consumer health - Oral Cancer
.
COS Scholar Universe.
author profiles
.
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
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15637397.001).
[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 / CA 16672; United States / NCI NIH HHS / CN / N01 CN 35159; United States / NCI NIH HHS / CA / P01 CA 106451; United States / NCI NIH HHS / CA / P01 CA 52051; United States / NCI NIH HHS / CA / U01 CA 79437
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
[Number-of-references]
92
Advertisement
4.
Klaassen I, Braakhuis BJ:
Anticancer activity and mechanism of action of retinoids in oral and pharyngeal cancer.
Oral Oncol
; 2002 Sep;38(6):532-42
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Administration of retinoids has been shown to elicit responses in leukoplakia, a
premalignant
lesion
of the oral mucosa that frequently develops into invasive cancer.
Because of the short duration of the response, the intrinsic resistance to retinoids and the toxic side effects, the
treatment with
this class of compounds has not become a standard
therapy
.
This review gives an update on the role of retinoids in oral and oropharyngeal cancer and their precursor
lesions
.
[MeSH-major]
Anticarcinogenic Agents /
therapeutic
use. Mouth Neoplasms / prevention & control. Pharyngeal Neoplasms / prevention & control. Retinoids /
therapeutic
use
[MeSH-minor]
Humans. Leukoplakia, Oral /
drug therapy
. Neoplasms, Second Primary / prevention & control
Genetic Alliance.
consumer health - Oral cancer
.
MedlinePlus Health Information.
consumer health - Oral Cancer
.
MedlinePlus Health Information.
consumer health - Throat Cancer
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 12167430.001).
[ISSN]
1368-8375
[Journal-full-title]
Oral oncology
[ISO-abbreviation]
Oral Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Anticarcinogenic Agents; 0 / Retinoids
[Number-of-references]
107
5.
Sharma RA:
The advancement of cancer chemoprevention by revision of clinical trial strategies.
Panminerva Med
; 2002 Mar;44(1):41-5
[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.
After a quarter of a century of rapid advances in cancer research, the focus of oncological
drug
development has shifted from cytotoxic
chemotherapy
to rationally designed agents that target specific molecules associated with
malignant
cells or their environment.
As a consequence of greater public awareness of health related issues and population screening, the
detection
of early cancer or
premalignant lesions
has demonstrated the potential that exists for targeting the same molecules during carcinogenesis.
This structured approach currently emerging is providing
pharmacological
and mechanistic data on novel agents which will prove essential in the planning of larger-scale commitments.
MedlinePlus Health Information.
consumer health - Clinical Trials
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 11887091.001).
[ISSN]
0031-0808
[Journal-full-title]
Panminerva medica
[ISO-abbreviation]
Panminerva Med
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Italy
[Number-of-references]
38
6.
Amini S, Viera MH, Valins W, Berman B:
Nonsurgical innovations in the treatment of nonmelanoma skin cancer.
J Clin Aesthet Dermatol
; 2010 Jun;3(6):20-34
[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]
Nonsurgical innovations in the
treatment
of nonmelanoma skin cancer.
Basal cell carcinoma and squamous cell carcinoma are the most frequent
types
of cancer in the United States and represent 75 percent and 20 percent, respectively, of all nonmelanoma skin cancers.
Additional preventive measures include identifying high-risk individuals for early
detection
along with using agents, such as retinoids, that are effective in decreasing the risk of
premalignant
cells further developing into carcinomas.
Procedural modalities are currently the standard of
treatment
, but recent evidence has consistently shown that newer (nonsurgical)
therapies
, such as interferon, imiquimod, retinoids, and 5-fluorouracil, can be used effectively either as monotherapies or as adjuvants to those surgical modalities for the
treatment
of superficial nonmelanoma skin cancers and
premalignant lesions
.
These newer
therapies
have achieved significant reductions in morbidity and mortality.
Procedural modalities that have been evolving into important tools for the
treatment
of actinic keratosis and nonmelanoma skin cancers include photodynamic
therapy
and lasers.
Nonsurgical
therapies
currently proving to be effective in clinical trials include ingenol mebutate and cyclooxygenase-2 inhibitors.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Nutr Cancer. 2008;60(3):325-30
[
18444166.001
]
[Cites]
J Drugs Dermatol. 2008 Apr;7(4):405-8
[
18459526.001
]
[Cites]
Expert Opin Biol Ther. 2008 Jun;8(6):829-38
[
18476794.001
]
[Cites]
Br J Dermatol. 2008 Jul;159(1):205-10
[
18476957.001
]
[Cites]
J Drugs Dermatol. 2008 May;7(5):483-5
[
18505144.001
]
[Cites]
J Dermatolog Treat. 2008;19(3):159-63
[
18569272.001
]
[Cites]
J Drugs Dermatol. 2008 Jul;7(7):669-73
[
18664159.001
]
[Cites]
J Dtsch Dermatol Ges. 2009 Feb;7(2):128-33
[
18808378.001
]
[Cites]
Nat Rev Cancer. 2008 Oct;8(10):743-54
[
18813320.001
]
[Cites]
J Am Acad Dermatol. 2009 Jan;60(1):59-62
[
18937999.001
]
[Cites]
Expert Rev Anticancer Ther. 2008 Nov;8(11):1713-7
[
18983231.001
]
[Cites]
Molecules. 2008;13(12):3224-35
[
19104487.001
]
[Cites]
Int J Dermatol. 2008 Dec;47(12):1334-6
[
19126041.001
]
[Cites]
J Am Acad Dermatol. 2004 May;50(5):722-33
[
15097956.001
]
[Cites]
Br J Dermatol. 2007 Dec;157 Suppl 2:56-8
[
18067634.001
]
[Cites]
J Am Acad Dermatol. 2008 May;58(5 Suppl 2):S149-54
[
18410801.001
]
[Cites]
N Engl J Med. 1994 May 5;330(18):1272-5
[
8145782.001
]
[Cites]
Photochem Photobiol. 1993 Aug;58(2):304-12
[
8415922.001
]
[Cites]
Antiviral Res. 1995 Nov;28(3):253-64
[
8629817.001
]
[Cites]
Science. 1996 Jun 14;272(5268):1668-71
[
8658145.001
]
[Cites]
Dermatol Surg. 1997 Oct;23(10):885-9
[
9357496.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1997 Nov;6(11):949-56
[
9367069.001
]
[Cites]
Arch Dermatol. 1997 Oct;133(10):1239-42
[
9382562.001
]
[Cites]
Australas J Dermatol. 1997 Nov;38(4):187-9
[
9431711.001
]
[Cites]
Cancer Res. 1998 Feb 15;58(4):711-6
[
9485025.001
]
[Cites]
Clin Plast Surg. 1998 Jan;25(1):1-19
[
9507793.001
]
[Cites]
J Invest Dermatol. 1998 May;110(5):734-9
[
9579537.001
]
[Cites]
Genes Dev. 1998 Jun 1;12(11):1551-70
[
9620844.001
]
[Cites]
Carcinogenesis. 1998 May;19(5):723-9
[
9635856.001
]
[Cites]
Development. 1998 Sep;125(18):3553-62
[
9716521.001
]
[Cites]
Altern Med Rev. 1998 Dec;3(6):448-57
[
9855569.001
]
[Cites]
Cell Immunol. 1999 Jan 10;191(1):10-9
[
9918682.001
]
[Cites]
J Nutr. 1999 Mar;129(3):775S-778S
[
10082788.001
]
[Cites]
Ther Clin Risk Manag. 2008 Oct;4(5):1085-95
[
19209288.001
]
[Cites]
Arch Dermatol. 2009 Feb;145(2):203-5
[
19221274.001
]
[Cites]
Pharmacoepidemiol Drug Saf. 2009 Apr;18(4):276-83
[
19226541.001
]
[Cites]
Am J Otolaryngol. 2009 Mar-Apr;30(2):121-33
[
19239954.001
]
[Cites]
J Am Acad Dermatol. 2009 Apr;60(4):615-25
[
19293009.001
]
[Cites]
Br J Dermatol. 2009 Jul;161(1):170-3
[
19302071.001
]
[Cites]
Photodiagnosis Photodyn Ther. 2008 Jun;5(2):127-33
[
19356643.001
]
[Cites]
Photodiagnosis Photodyn Ther. 2008 Jun;5(2):134-8
[
19356644.001
]
[Cites]
Photomed Laser Surg. 2009 Apr;27(2):345-9
[
19382838.001
]
[Cites]
Am J Otolaryngol. 2009 May-Jun;30(3):181-92
[
19410124.001
]
[Cites]
Int J Cancer. 2009 Oct 1;125(7):1678-84
[
19462452.001
]
[Cites]
J Am Acad Dermatol. 2009 Jun;60(6):934-43
[
19467365.001
]
[Cites]
J Eur Acad Dermatol Venereol. 2009 Sep;23(9):1061-5
[
19470041.001
]
[Cites]
BMC Cancer. 2009;9:262
[
19643007.001
]
[Cites]
Facial Plast Surg Clin North Am. 2009 Aug;17(3):301-7
[
19698912.001
]
[Cites]
Facial Plast Surg Clin North Am. 2009 Aug;17(3):309-24
[
19698913.001
]
[Cites]
N Engl J Med. 2009 Sep 17;361(12):1173-8
[
19726761.001
]
[Cites]
N Engl J Med. 2009 Sep 17;361(12):1164-72
[
19726763.001
]
[Cites]
N Engl J Med. 2009 Sep 17;361(12):1202-5
[
19726764.001
]
[Cites]
Dermatol Surg. 2009 Nov;35(11):1776-87
[
19737291.001
]
[Cites]
Semin Cutan Med Surg. 2009 Sep;28(3):180-9
[
19782942.001
]
[Cites]
Br J Dermatol. 2010 Jan;162(1):171-5
[
19863513.001
]
[Cites]
J Invest Dermatol. 2009 Dec;129(12):2745-6
[
19901945.001
]
[Cites]
Expert Opin Pharmacother. 2009 Dec;10(18):3015-31
[
19925043.001
]
[Cites]
J Cutan Med Surg. 2005 Oct;9(5):209-14
[
16502198.001
]
[Cites]
Dermatol Online J. 2006;12(3):10
[
16638424.001
]
[Cites]
J Fam Pract. 2006 May;55(5):suppl 1-8
[
16672155.001
]
[Cites]
J Drugs Dermatol. 2006 Apr;5(4):368-9
[
16673807.001
]
[Cites]
Dermatol Surg. 2006 Apr;32(4):562-8
[
16681667.001
]
[Cites]
J Am Acad Dermatol. 2006 Jun;54(6):1025-32
[
16713457.001
]
[Cites]
J Am Acad Dermatol. 2006 Jun;54(6):1033-8
[
16713458.001
]
[Cites]
J Invest Dermatol. 2006 Aug;126(8):1869-78
[
16763547.001
]
[Cites]
J Am Acad Dermatol. 2006 Aug;55(2):324-7
[
16844522.001
]
[Cites]
Arch Dermatol. 2006 Aug;142(8):976-82
[
16924046.001
]
[Cites]
J Dtsch Dermatol Ges. 2006 Sep;4(9):717-20
[
16928239.001
]
[Cites]
Dermatol Ther. 2006 Sep-Oct;19(5):306-14
[
17014486.001
]
[Cites]
J Immunol. 2006 Dec 1;177(11):8123-32
[
17114487.001
]
[Cites]
Nat Prod Rep. 2006 Dec;23(6):919-42
[
17119640.001
]
[Cites]
J Am Acad Dermatol. 2007 Jan;56(1):125-43
[
17190630.001
]
[Cites]
Br J Dermatol. 2007 Feb;156(2):320-8
[
17223873.001
]
[Cites]
Int J Dermatol. 2007 Mar;46(3):318-9
[
17343595.001
]
[Cites]
Dermatol Surg. 2007 Apr;33(4):427-31; discussion 431-2
[
17430376.001
]
[Cites]
Br J Dermatol. 2007 May;156 Suppl 3:53-6
[
17488408.001
]
[Cites]
Br J Dermatol. 2007 Jul;157(1):133-41
[
17501955.001
]
[Cites]
Nat Clin Pract Oncol. 2007 Aug;4(8):462-9
[
17657251.001
]
[Cites]
J Drugs Dermatol. 2007 Aug;6(8):778-81
[
17763606.001
]
[Cites]
Int J Dermatol. 2007 Nov;46(11):1113-7
[
17988327.001
]
[Cites]
J Eur Acad Dermatol Venereol. 2008 Apr;22(4):426-30
[
18031503.001
]
[Cites]
Indian J Dermatol Venereol Leprol. 2007 Nov-Dec;73(6):423-5
[
18032866.001
]
[Cites]
J Cutan Med Surg. 2007 Nov-Dec;11(6):195-201
[
18042331.001
]
[Cites]
Br J Dermatol. 2007 Dec;157 Suppl 2:8-13
[
18067624.001
]
[Cites]
Br J Dermatol. 2007 Dec;157 Suppl 2:25-31
[
18067628.001
]
[Cites]
Br J Dermatol. 2007 Dec;157 Suppl 2:41-6
[
18067631.001
]
[Cites]
Nature. 1994 Nov 3;372(6501):107-11
[
7969403.001
]
[Cites]
J Am Acad Dermatol. 1994 Mar;30(3):447-51
[
8113458.001
]
[Cites]
Recent Results Cancer Res. 1999;151:45-67
[
10337718.001
]
[Cites]
Br J Cancer. 1999 Apr;80(1-2):1-8
[
10389969.001
]
[Cites]
Int J Cancer. 1999 Aug 27;82(5):648-56
[
10417761.001
]
[Cites]
Mol Carcinog. 1999 Aug;25(4):231-40
[
10449029.001
]
[Cites]
Dermatol Surg. 1999 Jun;25(6):513-6
[
10469105.001
]
[Cites]
Carcinogenesis. 1999 Oct;20(10):1939-44
[
10506108.001
]
[Cites]
J Am Acad Dermatol. 1999 Dec;41(6):1002-7
[
10570388.001
]
[Cites]
Br J Dermatol. 1999 Sep;141(3):415-23
[
10583044.001
]
[Cites]
Cell. 2000 Jan 21;100(2):185-8
[
10660040.001
]
[Cites]
Ann Clin Lab Sci. 2000 Jan;30(1):3-21
[
10678579.001
]
[Cites]
J Nutr. 2000 Feb;130(2S Suppl):479S-482S
[
10721933.001
]
[Cites]
Am J Clin Oncol. 2000 Apr;23(2):181-4
[
10776981.001
]
[Cites]
Eur J Cancer. 2000 Jun;36(10):1292-7
[
10882869.001
]
[Cites]
J Dermatolog Treat. 2008;19(5):293-9
[
19160536.001
]
[Cites]
Chem Biol Interact. 2009 May 15;179(2-3):145-53
[
19161993.001
]
[Cites]
Australas J Dermatol. 2009 Feb;50(1):16-22
[
19178487.001
]
[Cites]
J Drugs Dermatol. 2009 Jan;8(1):35-9
[
19180894.001
]
[Cites]
J Dermatolog Treat. 2003 Jun;14(2):99-106
[
12775317.001
]
[Cites]
Oncogene. 2003 May 19;22(20):3152-61
[
12789291.001
]
[Cites]
J Natl Cancer Inst. 2003 Aug 6;95(15):1138-49
[
12902443.001
]
[Cites]
JAMA. 2003 Oct 22;290(16):2149-58
[
14570950.001
]
[Cites]
Clin Exp Dermatol. 2003 Nov;28 Suppl 1:13-5
[
14616805.001
]
[Cites]
J Eur Acad Dermatol Venereol. 2004 Jan;18(1):93-5
[
14678542.001
]
[Cites]
J Drugs Dermatol. 2003 Dec;2(6):629-35
[
14711141.001
]
[Cites]
J Drugs Dermatol. 2003 Dec;2(6):669-73
[
14711149.001
]
[Cites]
Skin Therapy Lett. 2004 Jan;9(1):1-3
[
14716439.001
]
[Cites]
Arch Dermatol. 2004 Jan;140(1):33-40
[
14732657.001
]
[Cites]
Arch Dermatol. 2004 Jan;140(1):41-6
[
14732659.001
]
[Cites]
Lasers Surg Med. 2004;34(2):114-9
[
15004822.001
]
[Cites]
Cancer Detect Prev. 2004;28(2):127-42
[
15068837.001
]
[Cites]
Cancer Res. 2004 Apr 15;64(8):2833-9
[
15087400.001
]
[Cites]
Arch Dermatol. 2004 Apr;140(4):404-6
[
15096367.001
]
[Cites]
J Am Acad Dermatol. 2004 May;50(5):714-21
[
15097955.001
]
[Cites]
J Am Acad Dermatol. 2002 Sep;47(3):390-8
[
12196749.001
]
[Cites]
Arch Dermatol. 2002 Sep;138(9):1165-71
[
12224977.001
]
[Cites]
J Am Acad Dermatol. 2002 Oct;47(4 Suppl):S225-8
[
12271283.001
]
[Cites]
J Am Acad Dermatol. 2002 Oct;47(4):571-7
[
12271303.001
]
[Cites]
Cutis. 2002 Aug;70(2 Suppl):22-9
[
12353677.001
]
[Cites]
Breast Cancer Res Treat. 2002 Nov;76(1):57-64
[
12408376.001
]
[Cites]
Mutat Res. 2002 Nov 30;509(1-2):221-6
[
12427541.001
]
[Cites]
Arch Dermatol. 2002 Nov;138(11):1498-502
[
12437457.001
]
[Cites]
J Cutan Med Surg. 2003 Mar-Apr;7(2):101-5
[
12447619.001
]
[Cites]
Br J Dermatol. 2002 Dec;147(6):1227-36
[
12452875.001
]
[Cites]
Int J Dermatol. 2002 Nov;41(11):810-6
[
12453012.001
]
[Cites]
Arch Dermatol. 2003 Jan;139(1):66-70
[
12533168.001
]
[Cites]
Dermatologica. 1979;158(5):368-72
[
437226.001
]
[Cites]
Hautarzt. 1978 Jun;29(6):313-8
[
659114.001
]
[Cites]
Arch Dermatol. 1978 Jul;114(7):1021-2
[
686718.001
]
[Cites]
Acta Derm Venereol Suppl (Stockh). 1975 Jan 27-29;74:163-6
[
816129.001
]
[Cites]
Med J Aust. 1976 Jun 12;1(24):928
[
979751.001
]
[Cites]
Arch Dermatol. 1992 Nov;128(11):1486-9
[
1444502.001
]
[Cites]
Nature. 1992 Jul 2;358(6381):15-6
[
1614522.001
]
[Cites]
J Am Acad Dermatol. 1992 Jul;27(1):65-9
[
1619079.001
]
[Cites]
J Am Acad Dermatol. 1991 Oct;25(4):665-7
[
1791225.001
]
[Cites]
J Am Acad Dermatol. 1991 May;24(5 Pt 1):731-4
[
1869644.001
]
[Cites]
Nutr Cancer. 1991;15(2):97-106
[
2038569.001
]
[Cites]
J Am Acad Dermatol. 1991 Mar;24(3):448-51
[
2061443.001
]
[Cites]
EMBO J. 1990 Dec;9(13):4443-54
[
2176152.001
]
[Cites]
J Am Acad Dermatol. 1990 Oct;23(4 Pt 1):694-700
[
2229497.001
]
[Cites]
J Dermatol Surg Oncol. 1990 May;16(5):446-9
[
2341658.001
]
[Cites]
Cancer Res. 1988 Feb 15;48(4):759-74
[
3123052.001
]
[Cites]
J Biol Chem. 1988 Aug 5;263(22):11008-14
[
3134356.001
]
[Cites]
Australas J Dermatol. 1988;29(3):127-30
[
3272119.001
]
[Cites]
Arch Dermatol. 1986 Jul;122(7):779-82
[
3524471.001
]
[Cites]
J Am Acad Dermatol. 1986 Sep;15(3):437-43
[
3760271.001
]
[Cites]
Arch Dermatol. 1985 Feb;121(2):207-13
[
3977335.001
]
[Cites]
Cancer Res. 1985 Dec;45(12 Pt 1):6254-9
[
4063976.001
]
[Cites]
Agents Actions. 1970 Aug;1(4):172-5
[
5520364.001
]
[Cites]
Proc Natl Acad Sci U S A. 1980 Oct;77(10):5754-8
[
6777774.001
]
[Cites]
Dermatology. 1995;190(3):214-7
[
7599384.001
]
[Cites]
J Leukoc Biol. 1995 Sep;58(3):365-72
[
7665993.001
]
[Cites]
Arch Dermatol. 2009 Dec;145(12):1431-8
[
20026854.001
]
[Cites]
Exp Dermatol. 2010 Feb;19(2):151-3
[
20156290.001
]
[Cites]
J Am Acad Dermatol. 2003 Feb;48(2):227-32
[
12582393.001
]
[Cites]
Br J Dermatol. 2003 Mar;148(3):539-43
[
12653747.001
]
[Cites]
J Invest Dermatol. 2004 May;122(5):1266-76
[
15140231.001
]
[Cites]
Acta Derm Venereol. 2004;84(3):227-8
[
15202841.001
]
[Cites]
Clin Dermatol. 2004 May-Jun;22(3):183-8
[
15262303.001
]
[Cites]
J Am Acad Dermatol. 2004 Oct;51(4):547-55
[
15389189.001
]
[Cites]
J Drugs Dermatol. 2005 Mar-Apr;4(2):221-2
[
15776781.001
]
[Cites]
Arch Dermatol. 2005 Apr;141(4):467-73
[
15837864.001
]
[Cites]
Dermatol Surg. 2005 Mar;31(3):371-4
[
15841646.001
]
[Cites]
Br J Dermatol. 2005 May;152(5):939-47
[
15888150.001
]
[Cites]
Acta Derm Venereol. 2005;85(5):424-8
[
16159735.001
]
[Cites]
Clin Exp Dermatol. 2005 Nov;30(6):712-3
[
16197397.001
]
[Cites]
Dermatol Clin. 2006 Jan;24(1):63-74
[
16311168.001
]
[Cites]
Dermatol Clin. 2006 Jan;24(1):105-17
[
16311173.001
]
[Cites]
Br J Dermatol. 2006 Jan;154(1):72-8
[
16403097.001
]
[Cites]
Dermatol Surg. 2006 Feb;32(2):261-7
[
16442048.001
]
[Cites]
J Drugs Dermatol. 2006 Feb;5(2):156-9
[
16485883.001
]
[Cites]
J Drugs Dermatol. 2006 Feb;5(2):167-73
[
16485885.001
]
[Cites]
Nutrition. 2000 Nov-Dec;16(11-12):1084-9
[
11118831.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2000 Dec;9(12):1281-6
[
11142412.001
]
[Cites]
Arch Dermatol. 2001 Jan;137(1):14-6
[
11176654.001
]
[Cites]
Lancet. 2001 Mar 24;357(9260):926-9
[
11289350.001
]
[Cites]
J Am Acad Dermatol. 2001 Jun;44(6):1054
[
11369927.001
]
[Cites]
Dermatol Surg. 2001 Jun;27(6):561-4
[
11442593.001
]
[Cites]
J Invest Dermatol. 2001 Nov;117(5):1212-7
[
11710935.001
]
[Cites]
Int J Dermatol. 2001 Nov;40(11):709-13
[
11737438.001
]
[Cites]
Clin Cancer Res. 2002 Jan;8(1):149-55
[
11801552.001
]
[Cites]
Nat Immunol. 2002 Feb;3(2):196-200
[
11812998.001
]
[Cites]
Cell. 2002 Jan 25;108(2):153-64
[
11832206.001
]
[Cites]
Br J Dermatol. 2002 Jan;146(1):94-100
[
11841372.001
]
[Cites]
Dermatol Surg. 2002 Feb;28(2):187
[
11860435.001
]
[Cites]
J Am Acad Dermatol. 2002 Mar;46(3):470-1
[
11862196.001
]
[Cites]
Crit Rev Oncol Hematol. 2002 Mar;41(3):269-85
[
11880204.001
]
[Cites]
J Am Acad Dermatol. 2002 Apr;46(4):545-8
[
11907505.001
]
[Cites]
Clin Cancer Res. 2002 Jul;8(7):2067-72
[
12114405.001
]
[Cites]
Clin Ther. 2002 Jun;24(6):990-1000
[
12117087.001
]
[Cites]
Photochem Photobiol. 2002 Jul;76(1):73-80
[
12126310.001
]
[Cites]
J Am Acad Dermatol. 2002 Aug;47(2):258-62
[
12140473.001
]
(PMID = 20725548.001).
[ISSN]
1941-2789
[Journal-full-title]
The Journal of clinical and aesthetic dermatology
[ISO-abbreviation]
J Clin Aesthet Dermatol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2921754
7.
Scardina GA, Ruggieri A, Messina P:
Chronic hyperplastic candidosis: a pilot study of the efficacy of 0.18% isotretinoin.
J Oral Sci
; 2009 Sep;51(3):407-10
[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.
Chronic hyperplastic candidosis (CHC) is considered a
premalignant
lesion
of the oral mucosa, occurring as speckled or homogeneous white
lesions
.
If the
lesions
are untreated, a minor proportion may become dysplastic and progress to carcinoma.
The traditional
treatment
of this
lesion
is based on the use of antifungal agents.
The aim of this study was to examine the efficacy of 0.18% isotretinoin for
treatment
of nystatin-resistant candidiasis.
In all six patients, daily antimycotic topical
therapy
with nystatin for 30 days had failed to resolve the candidal stomatitis.
After one month of isotretinoin
treatment
, five of the six patients were negative for Candida, whereas in untreated control patients the situation was unchanged.
None of the patients had any complaints about the
medication
.
[MeSH-major]
Antifungal Agents /
therapeutic
use. Candidiasis, Oral /
drug therapy
. Isotretinoin /
therapeutic
use
[MeSH-minor]
Administration, Topical. Chronic Disease.
Drug
Resistance, Fungal. Female. Humans. Male. Middle Aged. Nystatin / pharmacology. Pilot Projects
Hazardous Substances Data Bank.
NYSTATIN
.
Hazardous Substances Data Bank.
13-CIS-RETINOIC ACID
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19776507.001).
[ISSN]
1880-4926
[Journal-full-title]
Journal of oral science
[ISO-abbreviation]
J Oral Sci
[Language]
eng
[Publication-type]
Controlled Clinical Trial; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antifungal Agents; 1400-61-9 / Nystatin; EH28UP18IF / Isotretinoin
8.
Unger M:
Endobronchial therapy of neoplasms.
Chest Surg Clin N Am
; 2003 Feb;13(1):129-47
[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]
Endobronchial
therapy
of neoplasms.
The majority of these obstructions are part of pulmonary involvement by primary lung neoplasms or metastatic
lesions
from other organs.
Benign
lesions
, although capable of producing similar symptoms, are more rare.
Successful endobronchial management of airway obstruction not only provides significant improvement in patients' quality of life, it also adds to their survival
time
.
Both results fulfill the stated goals of appropriate and desired palliative
therapy
.
Interventional pulmonology also contributes to research of the process of lung carcinogenesis and the introduction of targeted
therapy
for early minimally invasive cancer and the potential
chemotherapy
of
premalignant lesions
.
[MeSH-major]
Bronchial Neoplasms /
therapy
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 12698642.001).
[ISSN]
1052-3359
[Journal-full-title]
Chest surgery clinics of North America
[ISO-abbreviation]
Chest Surg. Clin. N. Am.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
53
9.
Baroli A, Pedrazzini L, Lomuscio G, Marzoli L:
Anaplastic thyroid carcinoma. Practical aspects of multimodal therapy and data emerging from a 40-year experience at a single Italian institution.
Minerva Endocrinol
; 2010 Mar;35(1):9-16
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Anaplastic thyroid carcinoma. Practical aspects of multimodal
therapy
and data emerging from a 40-year experience at a single Italian institution.
Anaplastic thyroid carcinoma is a rare
malignant
neoplasia with high biological aggressiveness and rapid and lethal clinical course.
In selected patients, an aggressive multimodal
therapy
could decrease illness progression both in the neck e in other sites.
However, it is not clear if these combined
treatments
improve survival.
In our institution, the Department of Nuclear Medicine has a 40-year experience in monitor and
treatment
of a group of 48 patient with ATC confirmation that clinical presentation could overlap
pre
-existent nodular goitre or rapid enlarging mass of recent onset.
A better mean survival was noticed in those patients who respond to the multimodal
therapy
(8 months vs 4.6 months).
Radioiodine (131 I)
therapy
is unnecessary due to the loss of NIS expression of the ATC cells.
Therefore, after quick clinical and instrumental work up, our experience and the literature data suggest that the first line
therapy
is represented from external radiotherapy combined also with cisplatin or doxorubicin, followed by "curative" surgical
procedure
of the primary
lesion
in the neck and subsequent
chemotherapy
.
For those patients who show distant metastasis at onset
chemotherapy
is the first line
therapy
followed by external radiotherapy and when possible subsequent surgical
procedure
.
[MeSH-major]
Carcinoma / diagnosis. Carcinoma /
therapy
. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms /
therapy
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Antineoplastic Combined
Chemotherapy
Protocols /
therapeutic
use.
Chemotherapy
, Adjuvant / methods. Cisplatin / administration & dosage. Doxorubicin / administration & dosage. Female. Follow-Up Studies. Humans. Incidence. Italy / epidemiology. Male. Middle Aged. Prevalence. Prognosis. Radiotherapy, Adjuvant / methods. Research Design / statistics & numerical data. Survival Rate.
Treatment
Outcome
MedlinePlus Health Information.
consumer health - Thyroid Cancer
.
Hazardous Substances Data Bank.
CIS-DIAMINEDICHLOROPLATINUM
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20386523.001).
[ISSN]
0391-1977
[Journal-full-title]
Minerva endocrinologica
[ISO-abbreviation]
Minerva Endocrinol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Italy
[Chemical-registry-number]
80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin
[Number-of-references]
29
10.
Cao DZ, Sun WH, Ou XL, Yu Q, Yu T, Zhang YZ, Wu ZY, Xue QP, Cheng YL:
Effects of folic acid on epithelial apoptosis and expression of Bcl-2 and p53 in premalignant gastric lesions.
World J Gastroenterol
; 2005 Mar 21;11(11):1571-6
[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]
Effects of folic acid on epithelial apoptosis and expression of Bcl-2 and p53 in
premalignant
gastric
lesions
.
AIM: To evaluate the effects of folic acid on epithelial apoptosis and expression of Bcl-2 and p53 in the
tissues
of
premalignant
gastric
lesions
.
METHODS: Thirty-eight patients,
with premalignant
gastric
lesions
including 18 colonic-
type
intestinal metaplasia (IM) and 20 mild or moderate dysplasia, were randomly divided into a
treatment
group (n = 19) receiving folic acid 10 mg thrice daily and a control group (n = 19) receiving sucralfate 1,000 mg thrice daily for 3 mo.
All patients underwent endoscopies and four biopsies were taken prior to
treatment
and repeated after concluding
therapy
.
RESULTS: The mean of folate concentration in gastric mucosa was 9.03+/-3.37 microg/g wet wt in the folic acid
treatment
group, which was significantly higher than 6.83+/-3.02 microg/g wet wt in the control group.
Both the epithelial apoptosis rate and the tumor suppressor p53 expression in gastric mucosa significantly increased after folic acid
treatment
.
In contrast, the expression of Bcl-2 oncogene protein decreased after folic acid
therapy
.
CONCLUSION: These data indicate that folic acid may play an important role in the chemoprevention of gastric carcinogenesis by enhancing gastric epithelial apoptosis in the patients
with premalignant lesions
.
[MeSH-major]
Folic Acid / administration & dosage. Hematinics / administration & dosage. Precancerous Conditions /
drug therapy
. Proto-Oncogene Proteins c-bcl-2 / metabolism. Stomach Neoplasms /
drug therapy
. Tumor Suppressor Protein p53 / metabolism
[MeSH-minor]
Adult. Apoptosis /
drug
effects. Epithelial Cells / metabolism. Epithelial Cells / pathology. Female. G1 Phase /
drug
effects. Gastric Mucosa / metabolism. Gastric Mucosa / pathology. Humans. Male. Middle Aged
MedlinePlus Health Information.
consumer health - Folic Acid
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
Hazardous Substances Data Bank.
FOLIC ACID
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15786529.001).
[ISSN]
1007-9327
[Journal-full-title]
World journal of gastroenterology
[ISO-abbreviation]
World J. Gastroenterol.
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Hematinics; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 935E97BOY8 / Folic Acid
[Other-IDs]
NLM/ PMC4305933
11.
Khuri FR:
Primary and secondary prevention of non-small-cell lung cancer: the SPORE Trials of Lung Cancer Prevention.
Clin Lung Cancer
; 2003 Sep;5 Suppl 1:S36-40
[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.
The aims of chemoprevention in lung cancer are to prevent the appearance of disease (primary prevention) and to stop or reverse the progression of
premalignant lesions
(secondary prevention).
However, the results achieved with tamoxifen in the prevention of breast cancer, and the emergence of new
therapies
specifically targeted to molecules involved in the pathogenesis of lung cancer have set the stage for investigation of these agents for chemoprevention of lung cancer.
The SPORE (Specialized Program of Research Excellence) Trials of Lung Cancer Prevention (STOP) are 2 parallel studies that will investigate the potential effectiveness of gefitinib and tipifarnib in preventing the appearance and progression of
premalignant lesions
in former or current smokers with a history of smoking-related cancer.
The STOP trial objectives are to evaluate the effect of gefitinib and tipifarnib on histologic and biologic parameters in patients with evidence of sputum atypia, to evaluate various parameters as potential predictors of the effectiveness of these agents, and to evaluate the tolerability of these agents over a 6-month course of
treatment
.
Histologic response, defined as prevention of appearance or progression of
premalignant lesions
, is the primary endpoint of these trials.
New targeted molecular
therapies
such as gefitinib and tipifarnib may offer the opportunity to make chemoprevention a viable
treatment
modality in lung cancer as well as in other human solid tumors.
[MeSH-major]
Antineoplastic Agents /
therapeutic
use. Carcinoma, Non-Small-Cell Lung / prevention & control. Chemoprevention. Lung Neoplasms / prevention & control. Quinazolines /
therapeutic
use. Quinolones /
therapeutic
use
[MeSH-minor]
Biomarkers, Tumor. Clinical Trials as Topic. Disease Progression. Epidermal Growth Factor / antagonists & inhibitors. Humans. Precancerous Conditions /
drug therapy
. Protein-Tyrosine Kinases / antagonists & inhibitors
Genetic Alliance.
consumer health - Lung Cancer
.
Genetic Alliance.
consumer health - Non-small cell lung cancer
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
MedlinePlus Health Information.
consumer health - Lung 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 = 14641993.001).
[ISSN]
1525-7304
[Journal-full-title]
Clinical lung cancer
[ISO-abbreviation]
Clin Lung Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Quinazolines; 0 / Quinolones; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Protein-Tyrosine Kinases; MAT637500A / tipifarnib; S65743JHBS / gefitinib
[Number-of-references]
43
12.
Oldenburg J, Alfsen GC, Lien HH, Aass N, Waehre H, Fossa SD:
Postchemotherapy retroperitoneal surgery remains necessary in patients with nonseminomatous testicular cancer and minimal residual tumor masses.
J Clin Oncol
; 2003 Sep 1;21(17):3310-7
[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.
PURPOSE: To determine preoperative parameters that predict the histology of specimens obtained by retroperitoneal lymph node dissection (RPLND) in patients with nonseminomatous germ cell cancer (NSGCT) whose residual mass was </= 20 mm in diameter after modern cisplatin-based induction
chemotherapy
.
PATIENTS AND METHODS: Eighty-seven patients with metastatic NSGCT underwent RPLND after having received cisplatin- or carboplatin-based induction
chemotherapy
.
In all patients, the largest diameter of the residual mass on the transaxial plane was </= 20 mm, as assessed by abdominal computed
tomography
(CT) immediately before RPLND.
RESULTS: Complete fibrosis or necrosis was found in 58 patients (67%), teratoma was found in 23 patients (26%), and vital
malignant
germ cell tumor was found in six patients (7%), including one patient with rhabdomyosarcoma in the RPLND specimen.
In five of the six latter patients, the residual
lesion
was </= 10 mm at
pre
-RPLND CT.
No
pre
- or postchemotherapy clinical or radiologic parameter was identified that significantly predicted the histology of the residual mass.
CONCLUSION: One third of retroperitoneal postchemotherapy
lesions
</= 20 mm contained residual vital tumor
tissue
, despite modern
chemotherapy
regimens.
Therefore, postchemotherapy RPLND remains necessary in patients with minimal-size residual
lesions
to facilitate easy and safe follow-up and initiate additional
therapy
as early as possible, thus avoiding recurrences.
[MeSH-minor]
Adolescent. Adult. Antineoplastic Combined
Chemotherapy
Protocols /
therapeutic
use. Bleomycin / administration & dosage. Carboplatin / administration & dosage. Chi-Square Distribution. Cisplatin / administration & dosage. Combined Modality
Therapy
. Etoposide / administration & dosage. Humans. Ifosfamide / administration & dosage. Lymph Node Excision. Male. Middle Aged. Neoplasm Staging. Peritoneum. Statistics, Nonparametric.
Tomography
, X-Ray Computed.
Treatment
Outcome
Genetic Alliance.
consumer health - Testicular cancer
.
MedlinePlus Health Information.
consumer health - Testicular Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
BLEOMYCIN
.
Hazardous Substances Data Bank.
CIS-DIAMINEDICHLOROPLATINUM
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
Hazardous Substances Data Bank.
IFOSFAMIDE
.
Hazardous Substances Data Bank.
CARBOPLATIN
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
J Clin Oncol. 2005 Jun 1;23(16):3853
[
15923581.001
]
(PMID = 12947067.001).
[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
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
11056-06-7 / Bleomycin; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin; Q20Q21Q62J / Cisplatin; UM20QQM95Y / Ifosfamide
13.
Ong CA, Lao-Sirieix P, Fitzgerald RC:
Biomarkers in Barrett's esophagus and esophageal adenocarcinoma: predictors of progression and prognosis.
World J Gastroenterol
; 2010 Dec 07;16(45):5669-81
[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.
Barrett's esophagus is a well-known
premalignant
lesion
of the lower esophagus that is characterized by intestinal metaplasia of the squamous epithelium.
In addition, when patients develop EA, the current staging modalities are limited in stratifying patients into different prognostic groups in order to guide the optimal
therapy
for an individual patient.
[MeSH-minor]
Cell Cycle Proteins / analysis. Cell Proliferation. Disease Progression. Early
Detection
of Cancer. Epigenesis, Genetic. Genetic Markers. Humans. Loss of Heterozygosity. Ploidies. Predictive Value of Tests. Prognosis
Genetic Alliance.
consumer health - Barrett's Esophagus
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
BMC Clin Pathol. 2005 Aug 12;5:7
[
16095543.001
]
[Cites]
Cancer. 1995 Jan 15;75(2):423-9
[
7812911.001
]
[Cites]
Cancer Invest. 2001;19(5):554-68
[
11458821.001
]
[Cites]
J Natl Cancer Inst. 2001 Jul 18;93(14):1054-61
[
11459866.001
]
[Cites]
J Clin Oncol. 2006 Jan 10;24(2):259-67
[
16344314.001
]
[Cites]
BMJ. 2009;338:b604
[
19336487.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Jul 9;93(14):7081-4
[
8692948.001
]
[Cites]
Oncogene. 2002 Jan 17;21(3):475-8
[
11821959.001
]
[Cites]
Gastroenterology. 2000 Aug;119(2):333-8
[
10930368.001
]
[Cites]
Methods Inf Med. 2001 Mar;40(1):1-5
[
11310153.001
]
[Cites]
Am J Gastroenterol. 2008 Mar;103(3):788-97
[
18341497.001
]
[Cites]
Hum Pathol. 2001 Apr;32(4):368-78
[
11331953.001
]
[Cites]
Dis Esophagus. 2004;17(2):136-40
[
15230726.001
]
[Cites]
Cancer Res. 2006 May 15;66(10):5021-8
[
16707423.001
]
[Cites]
Gut. 2000 Aug;47(2):251-5
[
10896917.001
]
[Cites]
Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):659-65
[
17255290.001
]
[Cites]
Cancer Res. 1997 Mar 15;57(6):1030-4
[
9067264.001
]
[Cites]
Mod Pathol. 2009 Jan;22(1):58-65
[
18820669.001
]
[Cites]
Lancet. 2003 Nov 1;362(9394):1439-44
[
14602436.001
]
[Cites]
Gut. 2006 Oct;55(10):1390-7
[
16682429.001
]
[Cites]
Clin Cancer Res. 2004 Apr 15;10(8):2738-41
[
15102678.001
]
[Cites]
BMJ. 2009;338:b375
[
19237405.001
]
[Cites]
Br J Cancer. 2005 Aug 22;93(4):387-91
[
16106245.001
]
[Cites]
Nucleic Acids Res. 1994 Aug 11;22(15):2990-7
[
8065911.001
]
[Cites]
Cancer Res. 2000 Sep 15;60(18):5021-6
[
11016622.001
]
[Cites]
PLoS Med. 2007 Feb;4(2):e67
[
17326708.001
]
[Cites]
Clin Cancer Res. 2007 Feb 1;13(3):912-9
[
17289885.001
]
[Cites]
Gut. 2009 Nov;58(11):1451-9
[
19651633.001
]
[Cites]
Genome Res. 1999 May;9(5):482-91
[
10330128.001
]
[Cites]
Nucleic Acids Res. 2002 Apr 1;30(7):e28
[
11917034.001
]
[Cites]
Surg Endosc. 2010 May;24(5):1144-50
[
19997751.001
]
[Cites]
BMC Cancer. 2008;8:254
[
18778486.001
]
[Cites]
Gastroenterology. 2003 Dec;125(6):1670-7
[
14724819.001
]
[Cites]
Nature. 2002 Jan 31;415(6871):530-6
[
11823860.001
]
[Cites]
Clin Cancer Res. 2001 May;7(5):1118-26
[
11350874.001
]
[Cites]
J Clin Oncol. 2006 Aug 10;24(23):3789-98
[
16785472.001
]
[Cites]
Nat Rev Genet. 2010 Mar;11(3):191-203
[
20125086.001
]
[Cites]
Ann Surg Oncol. 2008 Dec;15(12):3459-70
[
18825457.001
]
[Cites]
Cancer Res. 2001 Nov 15;61(22):8284-9
[
11719461.001
]
[Cites]
BMJ. 2009;338:b606
[
19502216.001
]
[Cites]
Cell. 2000 Jan 7;100(1):57-70
[
10647931.001
]
[Cites]
J Clin Oncol. 2006 Feb 10;24(5):748-54
[
16401681.001
]
[Cites]
Int J Cancer. 2005 Jun 20;115(3):351-8
[
15688381.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Mar;15(3):509-16
[
16537709.001
]
[Cites]
Gastrointest Endosc. 2005 Oct;62(4):488-98
[
16185958.001
]
[Cites]
Am J Gastroenterol. 2001 Nov;96(11):3071-83
[
11721752.001
]
[Cites]
Int J Cancer. 2007 May 1;120(9):1914-21
[
17236199.001
]
[Cites]
Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9523-7
[
1946366.001
]
[Cites]
Am J Gastroenterol. 2010 Jul;105(7):1523-30
[
20461069.001
]
[Cites]
Gastroenterology. 1996 Feb;110(2):614-21
[
8566611.001
]
[Cites]
Dis Esophagus. 2008;21(2):97-102
[
18269642.001
]
[Cites]
J Clin Oncol. 2007 Feb 20;25(6):698-707
[
17308274.001
]
[Cites]
Clin Cancer Res. 2003 Aug 1;9(8):2912-9
[
12912936.001
]
[Cites]
Lab Invest. 2007 May;87(5):466-72
[
17310216.001
]
[Cites]
Gastroenterology. 2002 Aug;123(2):461-7
[
12145799.001
]
[Cites]
Gastroenterology. 2010 Dec;139(6):1995-2004.e15
[
20621683.001
]
[Cites]
N Engl J Med. 2006 Aug 10;355(6):560-9
[
16899776.001
]
[Cites]
Lancet. 2005 Feb 5-11;365(9458):488-92
[
15705458.001
]
[Cites]
Am J Gastroenterol. 2009 Sep;104(9):2153-60
[
19584833.001
]
[Cites]
BMC Cancer. 2006;6:134
[
16712734.001
]
[Cites]
Aliment Pharmacol Ther. 2006 Mar 1;23(5):587-93
[
16480397.001
]
[Cites]
Int J Cancer. 2006 Jul 15;119(2):264-8
[
16477636.001
]
[Cites]
Mol Pathol. 2003 Dec;56(6):313-7
[
14645692.001
]
[Cites]
Genome Res. 2006 Aug;16(8):1046-55
[
16809668.001
]
[Cites]
Scand J Gastroenterol. 2007 Nov;42(11):1271-4
[
17852872.001
]
[Cites]
Cancer Prev Res (Phila). 2008 Nov;1(6):413-23
[
19138988.001
]
[Cites]
Dis Esophagus. 2003;16(1):17-23
[
12581249.001
]
[Cites]
Clin Cancer Res. 1998 Jul;4(7):1755-63
[
9676852.001
]
[Cites]
Am J Gastroenterol. 2000 Jul;95(7):1669-76
[
10925966.001
]
[Cites]
Am J Gastroenterol. 2006 Jan;101(1):12-7
[
16405528.001
]
[Cites]
Ann Surg Oncol. 2007 Dec;14(12):3602-9
[
17896157.001
]
[Cites]
Cancer Res. 2009 May 15;69(10):4112-5
[
19435894.001
]
[Cites]
Cancer Res. 2001 Apr 15;61(8):3410-8
[
11309301.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2284-9
[
9122186.001
]
[Cites]
Br J Cancer. 2000 Feb;82(4):865-70
[
10732760.001
]
[Cites]
J Natl Cancer Inst. 2000 Nov 15;92(22):1805-11
[
11078757.001
]
[Cites]
Gut. 2008 Aug;57(8):1041-8
[
18305067.001
]
[Cites]
Gut. 2002 Mar;50(3):373-7
[
11839717.001
]
[Cites]
Clin Cancer Res. 2003 Jul;9(7):2560-6
[
12855631.001
]
[Cites]
BMJ. 2009;338:b605
[
19477892.001
]
[Cites]
Mol Carcinog. 2006 Oct;45(10):786-94
[
16921482.001
]
[Cites]
Eur J Cancer. 2008 Mar;44(4):588-99
[
18272361.001
]
[Cites]
Anticancer Res. 2004 Jul-Aug;24(4):2579-83
[
15330218.001
]
[Cites]
Gut. 1998 Aug;43(2):216-22
[
10189847.001
]
[Cites]
Am J Gastroenterol. 2004 Oct;99(10):1887-94
[
15447746.001
]
[Cites]
Mol Cell Proteomics. 2002 Nov;1(11):845-67
[
12488461.001
]
[Cites]
Scand J Gastroenterol. 2007 Jun;42(6):682-8
[
17505989.001
]
[Cites]
Clin Cancer Res. 2010 Jan 1;16(1):330-7
[
20028767.001
]
[Cites]
Gastroenterology. 2005 Dec;129(6):1825-31
[
16344051.001
]
[Cites]
Gut. 2006 Apr;55(4):442
[
16531521.001
]
[Cites]
Am J Gastroenterol. 2001 May;96(5):1355-62
[
11374668.001
]
[Cites]
Anticancer Res. 2000 May-Jun;20(3B):1933-7
[
10928129.001
]
[Cites]
Cancer. 2007 Feb 15;109(4):658-67
[
17211865.001
]
[Cites]
Gut. 2006 Dec;55(12):1810-20
[
17124160.001
]
[Cites]
Hum Pathol. 1988 Feb;19(2):166-78
[
3343032.001
]
[Cites]
Am J Med. 2010 May;123(5):462-7
[
20399324.001
]
[Cites]
Clin Cancer Res. 2008 Dec 15;14(24):8279-87
[
19088045.001
]
[Cites]
Genome Res. 2006 Mar;16(3):383-93
[
16449502.001
]
[Cites]
Clin Cancer Res. 2009 Oct 1;15(19):6192-200
[
19789312.001
]
[Cites]
Oncogene. 2005 Jun 9;24(25):4138-48
[
15824739.001
]
[Cites]
Nat Genet. 2005 Aug;37(8):853-62
[
16007088.001
]
[Cites]
Cancer. 2008 May 15;112(10):2173-80
[
18348304.001
]
[Cites]
Ann Surg Oncol. 2007 Feb;14(2):977-91
[
17122988.001
]
[Cites]
Nat Rev Cancer. 2010 Feb;10(2):87-101
[
20094044.001
]
[Cites]
Am J Gastroenterol. 2000 Aug;95(8):1888-93
[
10950031.001
]
[Cites]
Gastroenterology. 2002 Jun;122(7):1800-7
[
12055587.001
]
[Cites]
J Clin Pathol. 2006 Jun;59(6):631-4
[
16731604.001
]
[Cites]
Am J Gastroenterol. 2009 May;104(5):1093-6
[
19417749.001
]
[Cites]
Drug Discov Today. 2005 Jul 15;10(14):965-76
[
16023055.001
]
[Cites]
Ann Thorac Surg. 2001 Sep;72(3):859-66
[
11565671.001
]
[Cites]
Am J Gastroenterol. 2009 Oct;104(10):2588-94
[
19623166.001
]
[Cites]
N Engl J Med. 1976 Aug 26;295(9):476-80
[
940579.001
]
[Cites]
Hum Pathol. 2000 Jan;31(1):35-9
[
10665910.001
]
[Cites]
Gastroenterology. 2001 Jun;120(7):1607-19
[
11375943.001
]
[Cites]
Cancer Metastasis Rev. 2009 Dec;28(3-4):317-26
[
19997771.001
]
[Cites]
Am J Gastroenterol. 2001 Oct;96(10):2839-48
[
11693316.001
]
[Cites]
Am J Gastroenterol. 2009 Feb;104(2):502-13
[
19174812.001
]
[Cites]
Hum Pathol. 2005 Sep;36(9):955-61
[
16153457.001
]
[Cites]
J Natl Cancer Inst. 2000 Aug 16;92(16):1316-21
[
10944553.001
]
(PMID = 21128316.001).
[ISSN]
2219-2840
[Journal-full-title]
World journal of gastroenterology
[ISO-abbreviation]
World J. Gastroenterol.
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / MC/ U105365007
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Genetic Markers
[Other-IDs]
NLM/ PMC2997982
14.
Vignot S, Spano JP, Lantuejoul S, André F, Le Chevalier T, Soria JC:
Chemoprevention of lung cancer.
Recent Results Cancer Res
; 2005;166:145-65
[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.
Lung cancer remains a major cause of mortality worldwide, despite advances in surgery, radiotherapy and
chemotherapy
.
Most patients present with advanced disease, and early
detection
approaches are still experimental.
Identification of molecular defects involved in
premalignant lesions
and/or invasive cancer could lead to clinical studies with new molecular-targeted agents (mainly tyrosine kinase inhibitors, farnesyl-transferase inhibitors and/or antiangiogenic molecules) and the development of surrogate biomarkers.
Such biomarkers would be essential to detect high-risk patients, select adequate chemoprevention strategies and monitor
drug
efficacy.
[MeSH-major]
Anticarcinogenic Agents /
therapeutic
use. Lung Neoplasms /
drug therapy
Genetic Alliance.
consumer health - Lung Cancer
.
MedlinePlus Health Information.
consumer health - Lung Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15648189.001).
[ISSN]
0080-0015
[Journal-full-title]
Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
[ISO-abbreviation]
Recent Results Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Anticarcinogenic Agents; 0 / Biomarkers, Tumor
[Number-of-references]
88
15.
Strecker TE, Shen Q, Zhang Y, Hill JL, Li Y, Wang C, Kim HT, Gilmer TM, Sexton KR, Hilsenbeck SG, Osborne CK, Brown PH:
Effect of lapatinib on the development of estrogen receptor-negative mammary tumors in mice.
J Natl Cancer Inst
; 2009 Jan 21;101(2):107-13
[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.
Lapatinib, a selective orally available inhibitor of epidermal growth factor receptor (EGFR) and ErbB2 receptor tyrosine kinases, is a promising agent for the
treatment
of breast cancer.
We examined the effect of lapatinib on the development of mammary tumors in MMTV-erbB2 transgenic mice, which express wild-
type
ErbB2 under the control of the mouse mammary tumor virus promoter and spontaneously develop estrogen receptor (ER)-negative and ErbB2-positive mammary tumors by 14 months of age.
By 328 days after the start of
treatment
, all 17 (100%) of the vehicle-treated mice vs five (31%) of the 16 mice treated with high-dose lapatinib
developed
mammary tumors (P < .001).
Among MMTV-erbB2 mice treated for 5 months (n = 20 mice per group), those treated with lapatinib had fewer
premalignant lesions
and noninvasive cancers in their mammary glands than those treated with vehicle (P = .02).
[MeSH-minor]
Animals. Breast Neoplasms /
drug therapy
. Carcinoma, Intraductal, Noninfiltrating /
drug therapy
. Cyclin D1 /
drug
effects. Cyclin D1 / metabolism. Epidermal Growth Factor /
drug
effects. Epidermal Growth Factor / metabolism. Epiregulin. Female. Gene Expression Regulation, Neoplastic /
drug
effects. Humans. Mice. Mice, Transgenic. RNA, Messenger /
drug
effects. RNA, Messenger / metabolism. Receptors, Estrogen / analysis. Signal Transduction /
drug
effects
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 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
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Mol Endocrinol. 2005 Feb;19(2):362-78
[
15514030.001
]
[Cites]
Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5321-5
[
1351679.001
]
[Cites]
J Clin Oncol. 2005 Apr 10;23(11):2502-12
[
15684311.001
]
[Cites]
J Clin Oncol. 2005 Aug 10;23(23):5305-13
[
15955900.001
]
[Cites]
Oncogene. 2005 Sep 15;24(41):6213-21
[
16091755.001
]
[Cites]
Cancer Res. 2005 Dec 1;65(23):11018-25
[
16322251.001
]
[Cites]
Cancer Res. 2006 Feb 1;66(3):1630-9
[
16452222.001
]
[Cites]
Cancer Res. 2006 Feb 1;66(3):1640-7
[
16452223.001
]
[Cites]
Dev Biol. 2006 Jul 15;295(2):589-603
[
16678816.001
]
[Cites]
Lung Cancer. 2006 Aug;53(2):255
[
16762444.001
]
[Cites]
Nat Rev Mol Cell Biol. 2006 Jul;7(7):505-16
[
16829981.001
]
[Cites]
Cancer Res. 2006 Dec 15;66(24):12009-18
[
17178900.001
]
[Cites]
N Engl J Med. 2006 Dec 28;355(26):2733-43
[
17192538.001
]
[Cites]
Cancer Res. 2007 Feb 1;67(3):1170-5
[
17283152.001
]
[Cites]
Cancer Res. 2007 Feb 15;67(4):1487-93
[
17308086.001
]
[Cites]
Curr Opin Cell Biol. 2007 Apr;19(2):124-34
[
17314037.001
]
[Cites]
BMC Cancer. 2007;7:51
[
17374153.001
]
[Cites]
J Thorac Oncol. 2007 Jan;2(1):22-8
[
17410005.001
]
[Cites]
J Natl Cancer Inst. 2007 Apr 18;99(8):628-38
[
17440164.001
]
[Cites]
J Thorac Oncol. 2007 May;2(5):423-9
[
17473658.001
]
[Cites]
Mol Cancer Ther. 2007 May;6(5):1629-40
[
17513611.001
]
[Cites]
Mol Cell Endocrinol. 2007 Oct 15;277(1-2):13-25
[
17825481.001
]
[Cites]
Clin Cancer Res. 2007 Oct 15;13(20):6224-31
[
17947490.001
]
[Cites]
Oncogene. 2008 Jan 10;27(3):366-77
[
17637753.001
]
[Cites]
DNA Cell Biol. 1999 Oct;18(10):731-41
[
10541432.001
]
[Cites]
Pathol Oncol Res. 1999;5(4):255-71
[
10607920.001
]
[Cites]
Cancer Res. 2001 Dec 15;61(24):8887-95
[
11751413.001
]
[Cites]
FASEB J. 2002 Jun;16(8):881-3
[
11967232.001
]
[Cites]
Oncogene. 2002 Sep 12;21(41):6255-63
[
12214266.001
]
[Cites]
Cancer Res. 2002 Nov 15;62(22):6376-80
[
12438218.001
]
[Cites]
Mol Cancer Ther. 2001 Dec;1(2):85-94
[
12467226.001
]
[Cites]
Clin Cancer Res. 2003 Mar;9(3):923-30
[
12631589.001
]
[Cites]
Exp Cell Res. 2003 Mar 10;284(1):31-53
[
12648464.001
]
[Cites]
Breast Cancer Res Treat. 2003 Aug;80(3):353-61
[
14503808.001
]
[Cites]
J Natl Cancer Inst. 2003 Dec 17;95(24):1825-33
[
14679152.001
]
[Cites]
J Natl Cancer Inst. 2004 May 5;96(9):715; author reply 715-6
[
15126613.001
]
[Cites]
N Engl J Med. 2004 May 20;350(21):2129-39
[
15118073.001
]
[Cites]
Science. 2004 Jun 4;304(5676):1497-500
[
15118125.001
]
[Cites]
FEBS Lett. 2004 Jul 2;569(1-3):332-6
[
15225657.001
]
[Cites]
Science. 1987 Jan 9;235(4785):177-82
[
3798106.001
]
[Cites]
Cell. 1988 Jul 1;54(1):105-15
[
2898299.001
]
[Cites]
Cancer Res. 1990 Jul 15;50(14):4332-7
[
1973070.001
]
[Cites]
Cancer Res. 2005 Feb 1;65(3):840-9
[
15705882.001
]
(PMID = 19141783.001).
[ISSN]
1460-2105
[Journal-full-title]
Journal of the National Cancer Institute
[ISO-abbreviation]
J. Natl. Cancer Inst.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P50 CA58183
[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 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / EREG protein, human; 0 / Epiregulin; 0 / Ereg protein, mouse; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / RNA, Messenger; 0 / Receptors, Estrogen; 0VUA21238F / lapatinib; 136601-57-5 / Cyclin D1; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
[Other-IDs]
NLM/ PMC2639315
16.
Okamoto Y, Liu X, Suzuki N, Okamoto K, Kim HJ, Laxmi YR, Sayama K, Shibutani S:
Equine estrogen-induced mammary tumors in rats.
Toxicol Lett
; 2010 Apr 1;193(3):224-8
[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.
Long-term hormone replacement
therapy
is associated with an increased risk of breast, ovarian and endometrial cancers in women.
Equine estrogens are a principal component of hormone replacement
therapy
; however, their tumorigenic potential toward mammary
tissue
and reproductive organs has not been extensively explored.
Histological examination revealed
premalignant lesions
such as apocrine metaplasia in whole-mount preparations of mammary gland from the equilin-treated rats.
ACI rats given 10mg equilin
developed
palpable mammary tumors at 13 weeks of
treatment
, and 37.5% of the rats
developed
mammary tumors within 15 weeks.
For 2.5mg equilin, palpable tumors were observed in 8.3% of the rats after 8 weeks'
treatment
; the frequency was lower than that (42.9%) observed with 2.5mg E(2).
Evidently, equilin is a mammary carcinogen, and this potential may be associated with development of breast and reproductive cancers in women receiving hormone replacement
therapy
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
2010 Elsevier Ireland Ltd. All rights reserved.
[Cites]
Chem Res Toxicol. 2000 May;13(5):342-50
[
10813650.001
]
[Cites]
Chem Res Toxicol. 2008 May;21(5):1120-4
[
18447394.001
]
[Cites]
JAMA. 2002 Feb 13;287(6):734-41
[
11851540.001
]
[Cites]
Chem Res Toxicol. 2002 Mar;15(3):305-11
[
11896676.001
]
[Cites]
Chem Res Toxicol. 2002 Apr;15(4):512-9
[
11952337.001
]
[Cites]
JAMA. 2002 Jul 17;288(3):334-41
[
12117398.001
]
[Cites]
Carcinogenesis. 2002 Sep;23(9):1467-74
[
12189189.001
]
[Cites]
Endocrinology. 2003 Jun;144(6):2669-75
[
12746331.001
]
[Cites]
J Am Soc Mass Spectrom. 2003 May;14(5):482-91
[
12745217.001
]
[Cites]
Carcinogenesis. 2003 May;24(5):911-7
[
12771036.001
]
[Cites]
Lancet. 2003 Aug 9;362(9382):419-27
[
12927427.001
]
[Cites]
Biochemistry. 2004 Sep 7;43(35):11312-20
[
15366941.001
]
[Cites]
Cancer Res. 1971 Feb;31(2):166-8
[
5545267.001
]
[Cites]
Physiol Behav. 1973 Mar;10(3):543-7
[
4708519.001
]
[Cites]
J Natl Cancer Inst. 1975 Dec;55(6):1437-45
[
1206762.001
]
[Cites]
J Natl Cancer Inst. 1981 Aug;67(2):455-9
[
6943382.001
]
[Cites]
Arzneimittelforschung. 1982;32(7):787-91
[
6289846.001
]
[Cites]
Cancer Res. 1987 Aug 15;47(16):4508-16
[
3607779.001
]
[Cites]
Cancer. 1993 May 15;71(10):3036-43
[
8387875.001
]
[Cites]
Epidemiology. 1994 Jul;5(4):415-21
[
7918811.001
]
[Cites]
Obstet Gynecol. 1995 Feb;85(2):304-13
[
7824251.001
]
[Cites]
N Engl J Med. 1995 Jun 15;332(24):1589-93
[
7753136.001
]
[Cites]
Cancer Res. 1995 Oct 1;55(19):4347-51
[
7671246.001
]
[Cites]
Carcinogenesis. 1995 Oct;16(10):2571-4
[
7586168.001
]
[Cites]
Carcinogenesis. 1997 Aug;18(8):1595-601
[
9276635.001
]
[Cites]
Chem Res Toxicol. 1998 Feb;11(2):94-101
[
9511900.001
]
[Cites]
Chem Res Toxicol. 1998 Sep;11(9):1105-11
[
9760286.001
]
[Cites]
Chem Res Toxicol. 1998 Oct;11(10):1113-27
[
9778307.001
]
[Cites]
Chem Res Toxicol. 1999 Feb;12(2):204-13
[
10027800.001
]
[Cites]
J Endocrinol. 2004 Oct;183(1):91-9
[
15525577.001
]
[Cites]
Biochemistry. 2006 May 16;45(19):6187-94
[
16681391.001
]
[Cites]
J Mol Biol. 2007 Aug 31;371(5):1151-62
[
17603077.001
]
[Cites]
Proc Natl Acad Sci U S A. 2008 Mar 4;105(9):3527-32
[
18299580.001
]
[Cites]
Chem Res Toxicol. 2001 Dec;14(12):1654-9
[
11743748.001
]
(PMID = 20096754.001).
[ISSN]
1879-3169
[Journal-full-title]
Toxicology letters
[ISO-abbreviation]
Toxicol. Lett.
[Language]
ENG
[Grant]
United States / NIEHS NIH HHS / ES / ES012408-05; United States / NIEHS NIH HHS / ES / R01 ES012408; United States / NIEHS NIH HHS / ES / ES012408; United States / NIEHS NIH HHS / ES / R01 ES012408-05
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Estrogens, Conjugated (USP)
[Other-IDs]
NLM/ NIHMS177456; NLM/ PMC2837116
17.
Luchman HA, Benediktsson H, Villemaire ML, Peterson AC, Jirik FR:
The pace of prostatic intraepithelial neoplasia development is determined by the timing of Pten tumor suppressor gene excision.
PLoS One
; 2008;3(12):e3940
[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.
Given that the prostate undergoes rapid androgen-dependent growth at puberty, and that Pten excisions during this
time
might be especially tumorigenic, we hypothesized that delaying prostate-specific Pten deletions until immediately after puberty might alter the pace of tumorigenesis.
Despite evidence of increased Akt/mTOR/S6K axis activity at early
time
points in Pten-deficient epithelial cells, excisions induced in the post-pubertal (6 wk-old) prostate yielded gradual acquisition of a range of
lesions
.
These progressed from
pre
-
malignant
changes (nuclear atypia, focal hyperplasia) and low grade prostatic intraepithelial neoplasia (PIN) at 16-20 wks post-tamoxifen exposure, to overtly
malignant
lesions
by approximately 1 yr of age, characterized by high-grade PIN and microinvasive carcinoma.
In contrast, when Pten excisions were triggered in the
pre
-pubertal (2 week-old) prostate, neoplasia evolved over a more abbreviated
time
-frame, with a spectrum of
premalignant lesions
, as well as overt PIN and microinvasive carcinoma by 10-12 wks post-tamoxifen exposure.
[MeSH-minor]
Androgen-Binding Protein / genetics. Animals. Apoptosis. Arrestins / metabolism. Cell Proliferation. Crosses, Genetic. Disease Progression. Epithelium / enzymology. Epithelium / pathology. Female. Humans. Integrases / metabolism. Male. Mice. Neoplasm Invasiveness. Phosphatidylinositol 3-Kinases / metabolism. Precancerous Conditions /
drug therapy
. Precancerous Conditions / enzymology. Precancerous Conditions / genetics. Precancerous Conditions / pathology. Rats. Ribosomal Protein S6 / metabolism. Tamoxifen / analogs & derivatives. Tamoxifen /
therapeutic
use.
Time
Factors. Up-Regulation
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
TAMOXIFEN
.
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
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Cell. 2003 Sep;4(3):209-21
[
14522255.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7841-6
[
12799464.001
]
[Cites]
PLoS Biol. 2003 Dec;1(3):E59
[
14691534.001
]
[Cites]
Mol Endocrinol. 1994 Feb;8(2):230-9
[
8170479.001
]
[Cites]
J Biol Chem. 1994 Dec 16;269(50):31763-9
[
7989349.001
]
[Cites]
Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3439-43
[
7724580.001
]
[Cites]
Prostate. 1997 Jul 1;32(2):129-39
[
9215401.001
]
[Cites]
J Androl. 1999 Mar-Apr;20(2):251-8
[
10232660.001
]
[Cites]
J Mol Endocrinol. 1999 Jun;22(3):313-25
[
10343290.001
]
[Cites]
Development. 1999 Aug;126(16):3693-701
[
10409514.001
]
[Cites]
J Cell Biochem. 2005 Feb 1;94(2):279-97
[
15565647.001
]
[Cites]
J Clin Pathol. 2005 Jul;58(7):673-84
[
15976331.001
]
[Cites]
Cancer Res. 2005 Jul 1;65(13):5730-9
[
15994948.001
]
[Cites]
Nature. 2005 Aug 4;436(7051):725-30
[
16079851.001
]
[Cites]
Nat Rev Drug Discov. 2006 Aug;5(8):671-88
[
16883305.001
]
[Cites]
Cancer Lett. 2006 Sep 28;241(2):184-96
[
16412571.001
]
[Cites]
Clin Cancer Res. 2006 Sep 15;12(18):5305-11
[
17000663.001
]
[Cites]
Biochem Soc Trans. 2006 Nov;34(Pt 5):647-62
[
17052169.001
]
[Cites]
CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66
[
17237035.001
]
[Cites]
Annu Rev Pathol. 2006;1:243-71
[
18039115.001
]
[Cites]
Cancer Cell. 2007 Dec;12(6):572-85
[
18068633.001
]
[Cites]
Proc Natl Acad Sci U S A. 2008 Feb 19;105(7):2521-6
[
18268330.001
]
[Cites]
Genesis. 2008 Apr;46(4):229-34
[
18395839.001
]
[Cites]
Cell. 2008 May 2;133(3):403-14
[
18455982.001
]
[Cites]
Biochem J. 2000 Mar 15;346 Pt 3:561-76
[
10698680.001
]
[Cites]
Genesis. 2000 Feb;26(2):154-6
[
10686616.001
]
[Cites]
Endocrinology. 2000 Dec;141(12):4698-710
[
11108285.001
]
[Cites]
Mech Dev. 2001 Mar;101(1-2):61-9
[
11231059.001
]
[Cites]
Trends Genet. 2002 May;18(5):S1-5
[
12047956.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Feb 10;101(6):1725-30
[
14747659.001
]
(PMID = 19081794.001).
[ISSN]
1932-6203
[Journal-full-title]
PloS one
[ISO-abbreviation]
PLoS ONE
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgen-Binding Protein; 0 / Arrestins; 0 / Ribosomal Protein S6; 0 / beta-arrestin; 094ZI81Y45 / Tamoxifen; 17197F0KYM / afimoxifene; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
[Other-IDs]
NLM/ PMC2597775
18.
Lakatos PL, Lakatos L:
[Current concepts in the genetics of hereditary and sporadic colorectal cancer and the role of genetics in clinical practice: sporadic and IBD-associated colorectal tumors, significance of genetic tests in diagnosis, prognosis and assessment of chemotherapy outcome].
Orv Hetil
; 2006 Mar 12;147(10):449-55
[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]
[Current concepts in the genetics of hereditary and sporadic colorectal cancer and the role of genetics in clinical practice: sporadic and IBD-associated colorectal tumors, significance of genetic tests in diagnosis, prognosis and assessment of
chemotherapy
outcome].
Reason for this is partly that CRC has a strong hereditary trait and
premalignant lesions
are frequent and easily accessible.
In the second part of the review the authors discuss the genetic background of sporadic and IBD associated colorectal cancers as well as the role of genetics in the diagnosis, prognosis and prediction of
therapy
.
Similarly, genetic investigation may play an increasing role in the prediction of prognosis,
therapy
and complication of
chemotherapy
.
A more distant goal may be the individualization of the
therapy
.
[MeSH-major]
Antineoplastic Combined
Chemotherapy
Protocols /
therapeutic
use. Colorectal Neoplasms / genetics. Irritable Bowel Syndrome / complications
[MeSH-minor]
Adenomatous Polyposis Coli / genetics. Chromosomal Instability. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. DNA Methylation. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Microsatellite Repeats. Mutation. Peutz-Jeghers Syndrome / genetics. Pharmacogenetics. Prognosis.
Treatment
Outcome
Genetic Alliance.
consumer health - Colorectal Cancer
.
Genetic Alliance.
consumer health - Hereditary Cancer
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16573174.001).
[ISSN]
0030-6002
[Journal-full-title]
Orvosi hetilap
[ISO-abbreviation]
Orv Hetil
[Language]
hun
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Hungary
[Number-of-references]
50
19.
Doganavsargil B, Argin M, Kececi B, Sezak M, Sanli UA, Oztop F:
Secondary osteosarcoma arising in fibrous dysplasia, case report.
Arch Orthop Trauma Surg
; 2009 Apr;129(4):439-44
[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.
Malignant
transformation of fibrous dysplasia is very rare.
Early radiological features of sarcomatous transformation are moth-eaten or cystic areas of osteolysis, cortical destruction and gradual formation of a soft
tissue
mass.
The prognosis is unfavorable as most of the cases are in an advanced stage in the
time
of diagnosis.
Plain graphies of left femur showed a well-delineated
lesion
with endosteal scalloping and areas having a ground-glass appearance.
The MRI revealed minimal contrast enhancement but no heterogenous signal intensity, cortical destruction, periost reaction or accompanying soft
tissue
component was noted.
The
lesion
was initially curetted.
But being diagnosed as osteosarcoma histologically, classical osteosarcoma protocol
pre
and postoperative
chemotherapy
was applied.
Resected femur showed areas of fibrous dysplasia admixed with osteosarcoma having fibroblastic, chondroblastic and osteoblastic areas that were focally invading the soft
tissue
.
She did not respond to postoperative
chemotherapy
and lost with pulmonary metastases less than a years'
time
after the operation.
The case is presented to increase awareness on the possibility of
malignant
transformation in an otherwise unsuspected fibrous dysplasia.
Genetic Alliance.
consumer health - Fibrous Dysplasia
.
Genetic Alliance.
consumer health - Osteosarcoma
.
MedlinePlus Health Information.
consumer health - Bone 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 = 18560851.001).
[ISSN]
1434-3916
[Journal-full-title]
Archives of orthopaedic and trauma surgery
[ISO-abbreviation]
Arch Orthop Trauma Surg
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
20.
Ravery V:
Chemotherapy of premalignant lesions: new insights.
BJU Int
; 2007 Jul;100 Suppl 2:18-21
[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]
Chemotherapy
of
premalignant lesions
: new insights.
[MeSH-major]
Antineoplastic Agents, Hormonal /
therapeutic
use. Antioxidants /
therapeutic
use. Precancerous Conditions /
drug therapy
. Prostatic Intraepithelial Neoplasia /
drug therapy
. Prostatic Neoplasms /
drug therapy
MedlinePlus Health Information.
consumer health - Antioxidants
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17594352.001).
[ISSN]
1464-4096
[Journal-full-title]
BJU international
[ISO-abbreviation]
BJU Int.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / Antioxidants; EC 3.4.21.77 / Prostate-Specific Antigen
[Number-of-references]
21
21.
Deviere J:
Barrett's oesophagus: the new endoscopic modalities have a future.
Gut
; 2005 Mar;54 Suppl 1:i33-7
[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.
Barrett's oesophagus is defined as the replacement of squamous oesophageal epithelium by intestinal metaplasia in the
distal
oesophagus.
GORD is essential for the development of Barrett's oesophagus.1 Intestinal metaplasia is a
premalignant
lesion
that may further develop into dysplasia and lead to adenocarcinoma of the oesophagus.
Patients with Barrett's oesophagus have a 2-25% risk of developing mild to severe dysplasia and a 2-5% risk of having adenocarcinoma: 30-150
times
higher than the risk in the general population.
[MeSH-minor]
Adenocarcinoma /
drug therapy
. Adenocarcinoma / pathology. Adenocarcinoma / surgery. Esophageal Neoplasms /
drug therapy
. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Esophagoscopy / methods. Esophagus / pathology. Esophagus / surgery. Humans. Metaplasia / surgery. Mucous Membrane / pathology. Mucous Membrane / surgery. Photochemotherapy / methods. Postoperative Complications / etiology. Precancerous Conditions /
drug therapy
. Precancerous Conditions / pathology. Precancerous Conditions / surgery
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Gastrointest Endosc. 2002 Jun;55(7):807-10
[
12024132.001
]
[Cites]
N Engl J Med. 2002 Mar 14;346(11):836-42
[
11893796.001
]
[Cites]
Gut. 2002 Dec;51(6):776-80
[
12427775.001
]
[Cites]
Endoscopy. 2002 Dec;34(12):950-5
[
12471537.001
]
[Cites]
Gut. 2003 Jan;52(1):14-5
[
12477751.001
]
[Cites]
Endoscopy. 2003 Jun;35(6):496-501
[
12783347.001
]
[Cites]
N Engl J Med. 1989 Jun 1;320(22):1497-8
[
2716804.001
]
[Cites]
Ann Thorac Surg. 1990 Apr;49(4):537-41; discussion 541-2
[
2322047.001
]
[Cites]
Br J Surg. 1992 Oct;79(10):1050-3
[
1422717.001
]
[Cites]
Aliment Pharmacol Ther. 1993 Dec;7(6):623-8
[
8161668.001
]
[Cites]
Br J Surg. 1995 Jun;82(6):806-10
[
7627517.001
]
[Cites]
Aliment Pharmacol Ther. 1995 Aug;9(4):451-4
[
8527623.001
]
[Cites]
Gastrointest Endosc. 1996 Dec;44(6):700-5
[
8979061.001
]
[Cites]
Am J Gastroenterol. 1997 Apr;92(4):556-8
[
9128299.001
]
[Cites]
Gut. 1997 Sep;41(3):281-4
[
9378378.001
]
[Cites]
Gastroenterology. 1998 Mar;114(3):448-55
[
9496934.001
]
[Cites]
Am J Gastroenterol. 1998 May;93(5):763-7
[
9625124.001
]
[Cites]
Aliment Pharmacol Ther. 1998 Sep;12(9):893-7
[
9768533.001
]
[Cites]
Am J Gastroenterol. 1998 Oct;93(10):1810-5
[
9772036.001
]
[Cites]
Gut. 1998 Dec;43(6):747-51
[
9824599.001
]
[Cites]
Scand J Gastroenterol. 1998 Nov;33(11):1130-4
[
9867088.001
]
[Cites]
Gastrointest Endosc. 1999 Jan;49(1):1-7
[
9869715.001
]
[Cites]
Aliment Pharmacol Ther. 1998 Dec;12(12):1231-4
[
9882031.001
]
[Cites]
N Engl J Med. 1999 Mar 18;340(11):825-31
[
10080844.001
]
[Cites]
Gastrointest Endosc. 1999 Apr;49(4 Pt 1):442-6
[
10202056.001
]
[Cites]
Gastrointest Endosc. 1999 Jul;50(1):18-22
[
10385716.001
]
[Cites]
Gastroenterology. 1999 Aug;117(2):327-35
[
10419913.001
]
[Cites]
Aliment Pharmacol Ther. 1999 Sep;13(9):1205-9
[
10468702.001
]
[Cites]
Dig Dis Sci. 2003 Jul;48(7):1273-83
[
12870783.001
]
[Cites]
Dis Esophagus. 2003;16(3):193-8
[
14641308.001
]
[Cites]
Gastroenterology. 1989 May;96(5 Pt 1):1249-56
[
2703113.001
]
[Cites]
Gastroenterology. 2000 Apr;118(4):670-7
[
10734018.001
]
[Cites]
Gastrointest Endosc. 2000 Jun;51(6):659-63
[
10840296.001
]
[Cites]
Am J Gastroenterol. 2000 Jul;95(7):1661-8
[
10925965.001
]
[Cites]
Br J Surg. 2000 Aug;87(8):1106-10
[
10931059.001
]
[Cites]
Gastrointest Endosc. 2000 Sep;52(3):328-32
[
10968845.001
]
[Cites]
Baillieres Best Pract Res Clin Gastroenterol. 2000 Oct;14(5):857-79
[
11003814.001
]
[Cites]
Med Clin North Am. 2000 Sep;84(5):1137-61
[
11026922.001
]
[Cites]
Gut. 2000 Nov;47(5):612-7
[
11034574.001
]
[Cites]
Ann Surg. 2001 Jan;233(1):34-8
[
11141222.001
]
[Cites]
Am J Gastroenterol. 2001 Feb;96(2):331-7
[
11232672.001
]
[Cites]
Gut. 2001 Apr;48(4):580-1
[
11288739.001
]
[Cites]
Gastrointest Endosc. 2001 May;53(6):554-8
[
11323578.001
]
[Cites]
Br J Surg. 2001 Oct;88(10):1357-62
[
11578292.001
]
[Cites]
Endoscopy. 2002 Aug;34(8):604-10
[
12173079.001
]
(PMID = 15711006.001).
[ISSN]
0017-5749
[Journal-full-title]
Gut
[ISO-abbreviation]
Gut
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Number-of-references]
50
[Other-IDs]
NLM/ PMC1867791
22.
Serdar ZA, Eren PA, Canbakan M, Turan K, Tellioglu G, Gülle S, Ozgezer T, Kara M, Berber I, Titiz MI:
Dermatologic findings in renal transplant recipients: Possible effects of immunosuppression regimen and p53 mutations.
Transplant Proc
; 2010 Sep;42(7):2538-41
[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.
OBJECTIVE: To analyze the dermatologic
lesions
and possible effects of immunosuppression
treatment
and p53 gene mutations on dermatologic findings in renal transplant recipients.
Patients were categorized into 3 groups according to
time
since the transplantation
procedure
.
The most frequently observed
drug
-related
lesion
was hypertrichosis, in 46 of 150 patients.
Of 115
lesions
, the most commonly observed were verruca vulgaris (n = 34) from viruses, and pityriasis versicolor (n = 21) from superficial fungal infections.
Compared with the entire cohort, the group
with premalignant lesions
demonstrated more p53 mutations (11% vs 50%; P = .004).
Patients given cyclosporine
therapy
exhibited more
premalignant
or
malignant
cutaneous
lesions
compared with patients who received other agents (P = .03).
CONCLUSION: Patients carrying p53 mutations
developed
a
malignant lesion
in the late posttransplantation period, which suggests the importance of prediction of risk.
[MeSH-minor]
Adult. Dermatomycoses / epidemiology.
Drug Therapy
, Combination. Exons / genetics. Female. Follow-Up Studies. Humans. Male. Middle Aged. Polymorphism, Single-Stranded Conformational. Postoperative Complications / genetics. Precancerous Conditions / genetics. Skin Diseases, Bacterial / epidemiology. Skin Diseases, Viral / epidemiology.
Time
Factors
MedlinePlus Health Information.
consumer health - Kidney Transplantation
.
MedlinePlus Health Information.
consumer health - Skin Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
2010 Elsevier Inc. All rights reserved.
(PMID = 20832539.001).
[ISSN]
1873-2623
[Journal-full-title]
Transplantation proceedings
[ISO-abbreviation]
Transplant. Proc.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Immunosuppressive Agents
23.
Huber S, Wagner M, Zuna I, Medl M, Czembirek H, Delorme S:
Locally advanced breast carcinoma: evaluation of mammography in the prediction of residual disease after induction chemotherapy.
Anticancer Res
; 2000 Jan-Feb;20(1B):553-8
[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]
Locally advanced breast carcinoma: evaluation of mammography in the prediction of residual disease after induction
chemotherapy
.
BACKGROUND: We aimed to assess the mammographic features of locally advanced breast carcinoma treated with neoadjuvant
chemotherapy
and to evaluate morphological criteria that determine the value of mammography in
therapy
monitoring.
MATERIALS AND METHODS: We reviewed the
pre
- and post-
therapeutic
mammograms of 44 patients with stage III-breast carcinoma with regard to tumor characteristics and
malignant
calcifications and compared to histopathological results.
In 34 tumors more than 50% of the
lesion
was defined; these showed a high correlation between the mammographically determined tumor diameter and that determined on histopathological examination (r = 0.77).
CONCLUSIONS: The diagnostic value of mammography in the evaluation of tumor response to induction
chemotherapy
depends primarily on the extent to which the tumor can be delineated from the adjacent breast
tissue
.
[MeSH-major]
Antineoplastic Combined
Chemotherapy
Protocols /
therapeutic
use. Breast Neoplasms / radiography. Mammography
[MeSH-minor]
Calcinosis / etiology. Calcinosis / radiography.
Chemotherapy
, Adjuvant. Combined Modality
Therapy
. Female. Humans. Mastectomy. Neoplasm, Residual. Retrospective Studies.
Treatment
Outcome
MedlinePlus Health Information.
consumer health - Breast Cancer
.
MedlinePlus Health Information.
consumer health - Mammography
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 10769724.001).
[ISSN]
0250-7005
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
GREECE
24.
Nucci V, Torchia D, Cappugi P:
Treatment of anogenital condylomata acuminata with topical photodynamic therapy: report of 14 cases and review.
Int J Infect Dis
; 2010 Sep;14 Suppl 3:e280-2
[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]
Treatment
of anogenital condylomata acuminata with topical photodynamic
therapy
: report of 14 cases and review.
Photodynamic
therapy
(PDT) with 5-aminolevulinic acid (ALA) is an emerging technique for the
treatment
of genital human papillomavirus (HPV)-induced benign and
premalignant lesions
.
We conclude that PDT can be considered a highly effective and safe
treatment
option for anogenital condylomata acuminata.
[MeSH-major]
Condylomata Acuminata /
drug therapy
. Photochemotherapy
[MeSH-minor]
Administration, Topical. Adolescent. Adult. Aminolevulinic Acid / administration & dosage. Aminolevulinic Acid /
therapeutic
use. Anus Diseases /
drug therapy
. Anus Diseases / pathology. Female. Genital Diseases, Female /
drug therapy
. Genital Diseases, Female / pathology. Genital Diseases, Male /
drug therapy
. Genital Diseases, Male / pathology. Humans. Male. Photosensitizing Agents / administration & dosage. Photosensitizing Agents /
therapeutic
use.
Treatment
Outcome. Young Adult
MedlinePlus Health Information.
consumer health - Genital Warts
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright © 2010 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.
(PMID = 20346722.001).
[ISSN]
1878-3511
[Journal-full-title]
International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases
[ISO-abbreviation]
Int. J. Infect. Dis.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Canada
[Chemical-registry-number]
0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
25.
Podhorecka M:
[gamma H2AX in the recognition of DNA double-strand breaks].
Postepy Hig Med Dosw (Online)
; 2009 Feb 27;63:92-8
[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.
Double-strand breaks (DSBs) are highly deleterious DNA
lesions
because they can lead to chromosome aberrations or apoptosis.
The development of immunocytochemical methods of gamma H2AX
detection
provided a convenient tool for research and is considered a gold standard for DSB analysis.
These methods are sensitive and specific in the
detection
of a single DSB.
Assessment of H2AX phosphorylation can be used in clinical practice as a marker of
premalignant lesions
and to predict cell sensitivity to radiotherapy and
chemotherapy
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19252467.001).
[ISSN]
1732-2693
[Journal-full-title]
Postepy higieny i medycyny doswiadczalnej (Online)
[ISO-abbreviation]
Postepy Hig Med Dosw (Online)
[Language]
POL
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Poland
[Chemical-registry-number]
0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / H2AFX protein, human; 0 / Histones; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
[Number-of-references]
68
26.
Papanikolaou A:
Osseous hydatid disease.
Trans R Soc Trop Med Hyg
; 2008 Mar;102(3):233-8
[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.
Pre
-operative diagnosis is based on radiological findings and serological assays, which lack high sensitivity and specificity.
The
treatment
of choice is surgical, following the principles of a locally
malignant lesion
.
Chemotherapy
(albendazole alone or in combination with praziquantel) is used as an adjuvant
treatment
or when surgery is not possible.
The prognosis is often poor, especially in the spine: most patients do not recover neurologically, the mortality and complication rate is high and many cases recur, as it is often impossible to radically excise the pathologic
tissue
.
[MeSH-minor]
Animals. Diagnosis, Differential. Humans. Sheep / parasitology.
Tomography
Scanners, X-Ray Computed
MedlinePlus Health Information.
consumer health - Bone Infections
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17996916.001).
[ISSN]
0035-9203
[Journal-full-title]
Transactions of the Royal Society of Tropical Medicine and Hygiene
[ISO-abbreviation]
Trans. R. Soc. Trop. Med. Hyg.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Number-of-references]
39
27.
Braga L, Semelka RC, Pedro MS, de Barros N:
Post-treatment malignant liver lesions. MR imaging.
Magn Reson Imaging Clin N Am
; 2002 Feb;10(1):53-73
[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]
Post-
treatment
malignant
liver
lesions
. MR imaging.
MR imaging is also an excellent method for evaluation of the liver after surgical resection, systemic or local tumor
therapies
, and liver transplantation.
It permits early recognition of complications and the presence of recurrent tumor, providing an opportunity to repeat
treatment
or use alternative
treatment
.
Surgical resection remains the standard
therapy
for treating liver metastases.
The variety of techniques and the sensitivity for contrast enhancement have made MR imaging an ideal method to follow the response of tumors to various
treatment
approaches.
The appearance of tumor recurrence and the response to
treatment
are relatively consistently shown on MR images; however, the
time
course of change in
lesion
appearance has not been fully elucidated, particularly in the setting of
chemotherapy
.
Evaluating the response to
chemotherapy
is rendered complex because of the longer duration of the
therapy
, the
types
of response that various chemotherapeutic agents engender, the method of action of this
therapy
and the
time
of imaging in relation to
therapy
.
The various local
therapies
share some general principles of action, and many have similar MR imaging findings.
Some local
therapies
are effective only with certain malignancies (e.g., alcohol
therapy
and HCC), whereas other
therapies
are more limited because of the size of the tumor kill zone (e.g., interstitial laser
therapy
).
We are in the early stages of using MR imaging to guide local
therapies
and to monitor response during
treatment
in real
time
.
The role of MR imaging in liver transplantation involves
pre
- and postoperative investigation of both donors (in the case of living-related transplantation) and recipients.
[MeSH-major]
Liver Neoplasms / diagnosis. Liver Neoplasms /
therapy
. Magnetic Resonance Imaging
[MeSH-minor]
Cryotherapy. Embolization,
Therapeutic
. Hepatectomy. Humans. Laser Coagulation. Liver Transplantation. Microwaves /
therapeutic
use
MedlinePlus Health Information.
consumer health - Liver Cancer
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 11998575.001).
[ISSN]
1064-9689
[Journal-full-title]
Magnetic resonance imaging clinics of North America
[ISO-abbreviation]
Magn Reson Imaging Clin N Am
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
101
28.
Hersmus R, de Leeuw BH, Stoop H, Bernard P, van Doorn HC, Brüggenwirth HT, Drop SL, Oosterhuis JW, Harley VR, Looijenga LH:
A novel SRY missense mutation affecting nuclear import in a 46,XY female patient with bilateral gonadoblastoma.
Eur J Hum Genet
; 2009 Dec;17(12):1642-9
[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.
Patients with disorders of sex development (DSD), especially those with gonadal dysgenesis and hypovirilization, are at risk of developing the so-called
type
II germ cell tumors (GCTs).
Both carcinoma in situ and gonadoblastoma (GB) can be the precursor
lesion
, resulting in a seminomatous or non-seminomatous invasive cancer.
The
premalignant
lesion
of the initially removed gonad was positive for OCT3/4, TSPY and stem cell factor in germ cells, and for FOXL2 in the stromal component (ie, granulosa cells), but not for SOX9.
On the basis of these findings, prophylactical gonadectomy of the other gonad was performed, also showing a GB
lesion
positive for both FOXL2 (ovary) and SOX9 (testis).
The identified W70L mutation in the SRY gene resulted in a 50% reduction in the nuclear accumulation of the mutant protein compared with wild
type
.
This case shows the value of the proper diagnosis of human GCTs in identification of patients with DSD, which allows subsequent early diagnosis and prevention of the development of an invasive cancer, likely to be treated by
chemotherapy
at young age.
Genetic Alliance.
consumer health - XY Female
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Br J Cancer. 2001 Jul 20;85(2):213-20
[
11461079.001
]
[Cites]
Dev Biol. 2001 Dec 1;240(1):92-107
[
11784049.001
]
[Cites]
J Neurosci. 2002 Oct 15;22(20):9005-14
[
12388607.001
]
[Cites]
Cancer Res. 2003 May 1;63(9):2244-50
[
12727846.001
]
[Cites]
Genetics. 2003 May;164(1):277-88
[
12750339.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Jun 10;100(12):7045-50
[
12764225.001
]
[Cites]
J Biol Chem. 2003 Sep 5;278(36):33839-47
[
12810722.001
]
[Cites]
Brain Res Mol Brain Res. 2003 Oct 21;118(1-2):82-90
[
14559357.001
]
[Cites]
Development. 2004 Feb;131(4):933-42
[
14736745.001
]
[Cites]
Hum Mol Genet. 2004 Jun 1;13(11):1171-81
[
15056605.001
]
[Cites]
J Pathol. 2004 Jul;203(3):849-57
[
15221945.001
]
[Cites]
Dev Biol. 2004 Oct 15;274(2):271-9
[
15385158.001
]
[Cites]
Cancer. 1970 Jun;25(6):1340-56
[
4193741.001
]
[Cites]
Development. 1987;101 Suppl:151-5
[
3503713.001
]
[Cites]
Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3368-72
[
8159753.001
]
[Cites]
Nucleic Acids Res. 1994 Apr 25;22(8):1500-1
[
8190643.001
]
[Cites]
Nature. 1994 Dec 8;372(6506):525-30
[
7990924.001
]
[Cites]
Nat Genet. 1996 Sep;14(1):62-8
[
8782821.001
]
[Cites]
Hum Mol Genet. 1996 Nov;5(11):1801-7
[
8923009.001
]
[Cites]
Am J Hum Genet. 1999 Apr;64(4):921-7
[
10090875.001
]
[Cites]
EMBO Rep. 2004 Nov;5(11):1078-83
[
15486564.001
]
[Cites]
Nat Rev Cancer. 2005 Mar;5(3):210-22
[
15738984.001
]
[Cites]
J Pathol. 2005 Jun;206(2):242-9
[
15818593.001
]
[Cites]
Hum Reprod. 2005 Jun;20(6):1466-76
[
15734757.001
]
[Cites]
Hum Pathol. 2005 May;36(5):512-21
[
15948118.001
]
[Cites]
Genesis. 2005 Aug;42(4):263-75
[
16035036.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Sep;90(9):5295-303
[
15998778.001
]
[Cites]
Dev Biol. 2005 Nov 1;287(1):111-24
[
16185683.001
]
[Cites]
Cell Tissue Res. 2005 Oct;322(1):159-65
[
15846514.001
]
[Cites]
Biol Reprod. 2006 Jan;74(1):195-201
[
16207837.001
]
[Cites]
Curr Biol. 2006 Feb 21;16(4):415-20
[
16488877.001
]
[Cites]
Arch Dis Child. 2006 Jul;91(7):554-63
[
16624884.001
]
[Cites]
Nat Rev Genet. 2006 Aug;7(8):620-31
[
16832429.001
]
[Cites]
BMC Cancer. 2006;6:154
[
16762081.001
]
[Cites]
Endocr Rev. 2006 Aug;27(5):468-84
[
16735607.001
]
[Cites]
J Pathol. 2007 Jan;211(1):1-9
[
17117392.001
]
[Cites]
Hum Pathol. 2007 Oct;38(10):1470-81
[
17521702.001
]
[Cites]
J Pathol. 2008 May;215(1):31-8
[
18348162.001
]
[Cites]
Nature. 2008 Jun 12;453(7197):930-4
[
18454134.001
]
[Cites]
J Pathol. 2008 Sep;216(1):43-54
[
18566970.001
]
[Cites]
Oncogene. 2000 Nov 30;19(51):5858-62
[
11127816.001
]
[Cites]
Cytogenet Cell Genet. 2000;91(1-4):160-4
[
11173850.001
]
(PMID = 19513096.001).
[ISSN]
1476-5438
[Journal-full-title]
European journal of human genetics : EJHG
[ISO-abbreviation]
Eur. J. Hum. Genet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / SRY protein, human; 0 / Sex-Determining Region Y Protein
[Other-IDs]
NLM/ PMC2987026
29.
Obszynska JA, Atherfold PA, Nanji M, Glancy D, Santander S, Graham TA, Otto WR, West K, Harrison RF, Jankowski JA:
Long-term proton pump induced hypergastrinaemia does induce lineage-specific restitution but not clonal expansion in benign Barrett's oesophagus in vivo.
Gut
; 2010 Feb;59(2):156-63
[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: Barrett's oesophagus is a common
premalignant
lesion
caused partly by acid reflux.
Although the requisite
therapy
, proton pump inhibitors (PPIs), have been implicated in the progression of Barrett's oesophagus in animal models, harmful effects of prolonged PPI
therapy
in Barrett's oesophagus is both inconclusive and controversial.
We therefore aimed to test the role of PPI-induced hypergastrinaemia in vitro and see whether any biological parameters were useful surrogates of long-term
therapy
in man.
METHODS: We undertook detailed serological and
tissue
assessment of gastrin and CCK(2) receptors in 90 patients randomised to different doses of PPI
therapy
during a detailed 2-year follow-up.
CONCLUSION: While the short-term effects of gastrin enhance epithelial restitution in Barrett's oesophagus (but not squamous mucosa) there is no clinical evidence that Barrett's oesophagus length expands over
time
.
This study, which is the largest and longest term randomised controlled trial of gastrin biology in Barrett's oesophagus, is further proof of the clinical safety of PPI
therapy
.
[MeSH-major]
Barrett Esophagus /
drug therapy
. Esophageal Neoplasms /
drug therapy
. Gastrins / biosynthesis. Precancerous Conditions /
drug therapy
. Proton Pump Inhibitors /
therapeutic
use
[MeSH-minor]
Adult. Aged. Cell Movement /
drug
effects. Cell Proliferation /
drug
effects. Dose-Response Relationship,
Drug
. Enzyme-Linked Immunosorbent Assay / methods. Esophagus / metabolism. Female. Gastric Mucosa / metabolism. Gene Expression. Humans. Male. Middle Aged. RNA, Messenger / genetics. Receptor, Cholecystokinin B / biosynthesis. Receptor, Cholecystokinin B / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Cells, Cultured
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
COS Scholar Universe.
author profiles
.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Gut. 2010 Aug;59(8):1157-8; authr reply 1158
[
20639256.001
]
[CommentIn]
Gut. 2010 Feb;59(2):148-9
[
20176635.001
]
(PMID = 19651631.001).
[ISSN]
1468-3288
[Journal-full-title]
Gut
[ISO-abbreviation]
Gut
[Language]
eng
[Grant]
United Kingdom / Cancer Research UK / /
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Gastrins; 0 / Proton Pump Inhibitors; 0 / RNA, Messenger; 0 / Receptor, Cholecystokinin B
30.
Sehr P, Pawlita M, Lewis J:
Evaluation of different glutathione S-transferase-tagged protein captures for screening E6/E6AP interaction inhibitors using AlphaScreen.
J Biomol Screen
; 2007 Jun;12(4):560-7
[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.
Human papillomavirus (HPV) infection is responsible for the development of cervical cancer and its
premalignant lesions
in women.
The virus-encoded oncogene E6 is a promising target for an anti-HPV
drug therapy
.
The results obtained with both
types
of GST-detecting reagents correlated very well and demonstrated the great potential of the newly
developed
glutathione-coated Acceptor beads as a
detection
reagent for GST fusion proteins.
[MeSH-minor]
Amino Acid Sequence. Binding, Competitive.
Drug
Evaluation, Preclinical. Humans. Molecular Sequence Data. Pilot Projects. Protein Binding. Protein Interaction Mapping
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17478484.001).
[ISSN]
1087-0571
[Journal-full-title]
Journal of biomolecular screening
[ISO-abbreviation]
J Biomol Screen
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / E6 protein, Human papillomavirus type 16; 0 / Oncogene Proteins, Viral; 0 / Repressor Proteins; 0 / UBE3A protein, human; EC 2.5.1.18 / Glutathione Transferase; EC 6.3.2.19 / Ubiquitin-Protein Ligases
31.
Mutter GL, Bergeron C, Deligdisch L, Ferenczy A, Glant M, Merino M, Williams AR, Blithe DL:
The spectrum of endometrial pathology induced by progesterone receptor modulators.
Mod Pathol
; 2008 May;21(5):591-8
[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.
Progesterone receptor modulators (PRM) are hormonally active
drugs
effective in the management of endometriosis and uterine leiomyomata.
Overtly
premalignant lesions
(atypical hyperplasia or EIN) were not seen.
In a subset of cases, asymmetry of stromal and epithelial growth resulted in prominent cystically dilated glands with admixed estrogen (mitotic) and progestin (secretory) epithelial effects of a
type
not encountered in contemporary clinical practice.
The variety of endometrial appearances suggested that findings might differ by agent and dose over
time
according to relationships that must be specified for each agent.
[MeSH-major]
Endometrium /
drug
effects. Endometrium / pathology. Hormone Antagonists / adverse effects. Receptors, Progesterone /
drug
effects
[MeSH-minor]
Clinical Trials as Topic. Endometriosis /
drug therapy
. Female. Humans. Leiomyoma /
drug therapy
. Uterine Neoplasms /
drug therapy
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
(PMID = 18246050.001).
[ISSN]
0893-3952
[Journal-full-title]
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
[ISO-abbreviation]
Mod. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Hormone Antagonists; 0 / Receptors, Progesterone
32.
Dong Y, Ip C, Ganther H:
Evidence of a field effect associated with mammary cancer chemoprevention by methylseleninic acid.
Anticancer Res
; 2002 Jan-Feb;22(1A):27-32
[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 first approach examined the modulation of biomarkers in pathologically-defined
premalignant lesions
of the rat mammary gland.
The second approach involved the use of cDNA microarray technology to characterize the profile of gene expression changes in the whole mammary
tissue
.
Treatment with
methylseleninic acid led to quantifiable changes in the expression of selective cell cycle and apoptosis regulatory proteins in the
premalignant lesions
.
These were found to be modulated in a manner that was consistent with a reduction in the development of
premalignant lesions
by methylseleninic acid.
Microarray analysis using RNA isolated from the whole mammary gland provided highly suggestive clues that methylseleninic acid was able to produce a widespread effect on gene expression in adipocytes and stromal cells, which are present in abundance in the mammary
tissue
.
Thus, epithelial cells may not be the only targets for the action of selenium, even though the focus of selenium chemoprevention is to inhibit
premalignant lesions
and cancers arising from the epithelial cells.
[MeSH-minor]
Animals. Biomarkers, Tumor / biosynthesis. Biomarkers, Tumor / genetics. Cell Cycle Proteins / biosynthesis. Cell Cycle Proteins / genetics. Female. Gene Expression /
drug
effects. Gene Expression Profiling. Mammary Glands, Animal /
drug
effects. Mammary Glands, Animal / metabolism. Mammary Glands, Animal / physiology. Oligonucleotide Array Sequence Analysis. Precancerous Conditions /
drug therapy
. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Rats. Rats, Sprague-Dawley
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 = 12017302.001).
[ISSN]
0250-7005
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA 16056; United States / NCI NIH HHS / CA / CA 27706
[Publication-type]
Journal Article; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
Greece
[Chemical-registry-number]
0 / Anticarcinogenic Agents; 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Organoselenium Compounds; 28274-57-9 / methylselenic acid
33.
Marana HR, de Andrade JM, da Silva Mathes AC, Duarte G, da Cunha SP, Bighetti S:
Chemotherapy in the treatment of locally advanced cervical cancer and pregnancy.
Gynecol Oncol
; 2001 Feb;80(2):272-4
[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]
Chemotherapy
in the
treatment
of locally advanced cervical cancer and pregnancy.
BACKGROUND: Carcinoma of the cervix is the most common
malignant
tumor associated with pregnancy.
The initial stages and
premalignant lesions
apparently present the same prognosis in pregnant and nonpregnant women; however, there are limited data regarding outcome for locally advanced cervical cancer in pregnancy.
CASE: A 26-year-old woman, gravida 4, para 3, at 14 weeks and 4 days' gestation, was diagnosed with a FIGO stage IIB squamous cell carcinoma of the cervix, treated by primary
chemotherapy with
cisplatin and bleomycin, until pregnancy resolution at 38 weeks.
CONCLUSION: The present case demonstrates that
chemotherapy
was harmless for the child up to the present
time
.
[MeSH-major]
Carcinoma, Squamous Cell /
drug therapy
. Pregnancy Complications, Neoplastic /
drug therapy
. Uterine Cervical Neoplasms /
drug therapy
Genetic Alliance.
consumer health - Pregnancy
.
Genetic Alliance.
consumer health - Cervical cancer
.
MedlinePlus Health Information.
consumer health - Cervical Cancer
.
MedlinePlus Health Information.
consumer health - Tumors and Pregnancy
.
COS Scholar Universe.
author profiles
.
International Agency for Research on Cancer - Screening Group.
diagnostics - Histopathology and cytopathology of the uterine cervix - digital atlas
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Gynecol Oncol. 2001 Aug;82(2):409-10
[
11531309.001
]
(PMID = 11161872.001).
[ISSN]
0090-8258
[Journal-full-title]
Gynecologic oncology
[ISO-abbreviation]
Gynecol. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
34.
Marks F, Fürstenberger G, Neufang G, Müller-Decker K:
Mouse skin as a model for cancer chemoprevention by nonsteroidal anti-inflammatory drugs.
Recent Results Cancer Res
; 2003;163:46-57; discussion 264-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Mouse skin as a model for cancer chemoprevention by nonsteroidal anti-inflammatory
drugs
.
While
therapeutic
gene repair is a still unrealized dream, tumor promotion provides an attractive target for cancer prevention.
A key event in epithelial tumor development is an aberrant constitutive overexpression of cyclooxygenase-2 (COX-2), being detectable already in
premalignant lesions
and leading to an overproduction of prostaglandins.
The well-established chemopreventive effect of nonsteroidal anti-inflammatory
drugs
seems to be mainly due to COX-2 inhibition.
Targeted transgenic overexpression of COX-2 in mouse epidermis induces a preneoplastic phenotype and renders the
tissue
extremely sensitive to genotoxic carcinogens; i.e., for the induction of skin tumor development, tumor promoter
treatment
can be omitted in those animals.
[MeSH-major]
Anti-Inflammatory Agents, Non-Steroidal /
therapeutic
use. Cyclooxygenase Inhibitors /
therapeutic
use. Disease Models, Animal. Isoenzymes / metabolism. Neoplasms, Experimental / prevention & control. Neoplasms, Experimental /
therapy
. Prostaglandin-Endoperoxide Synthases / metabolism
[MeSH-minor]
Animals. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Gene Expression /
drug
effects. Mice. Mice, Transgenic. Phenotype. Precancerous Conditions / pathology. Prostaglandins / biosynthesis. Skin /
drug
effects. Skin / enzymology. Skin / pathology. Skin Neoplasms / enzymology. Skin Neoplasms / prevention & control. Skin Neoplasms /
therapy
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 12903842.001).
[ISSN]
0080-0015
[Journal-full-title]
Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
[ISO-abbreviation]
Recent Results Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Prostaglandins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
[Number-of-references]
85
35.
Dragnev KH, Rigas JR, Dmitrovsky E:
The retinoids and cancer prevention mechanisms.
Oncologist
; 2000;5(5):361-8
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Carcinogenesis is a multistep process that converts normal cells into
malignant
cells.
Once transformed,
malignant
cells acquire the ability to invade and metastasize, leading to clinically evident disease.
During this continuum from normal to metastatic cells, carcinogenic steps can be arrested or reversed through
pharmacological treatments
, known as cancer chemoprevention.
Chemoprevention strategies represent
therapeutic
interventions at early stages of carcinogenesis, before the onset of invasive cancer.
Effective chemoprevention should reduce or avoid the clinical consequences of overt malignancies by treating early neoplastic
lesions
before development of clinically apparent signs or symptoms.
Preclinical, clinical, and epidemiological data provide considerable support for cancer chemoprevention as an attractive
therapeutic
strategy.
Derivatives of vitamin A, the retinoids, have reported activity in treating specific
premalignant lesions
and reducing incidence of second primary tumors in patients with prior head and neck, lung or liver cancers.
An improved understanding of cancer prevention mechanisms should aid in the discovery of new
therapeutic
targets and chemoprevention agents.
[MeSH-major]
Anticarcinogenic Agents /
therapeutic
use. Neoplasms / prevention & control. Retinoids /
therapeutic
use
[MeSH-minor]
Animals. Cell Cycle /
drug
effects. Clinical Trials as Topic.
Drug
Evaluation, Preclinical. Humans. Receptors, Retinoic Acid
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
(PMID = 11040271.001).
[ISSN]
1083-7159
[Journal-full-title]
The oncologist
[ISO-abbreviation]
Oncologist
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01-CA54494; United States / NCI NIH HHS / CA / R01-CA62275; United States / NCI NIH HHS / CA / R01-CA87546
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
[Publication-country]
UNITED STATES
[Chemical-registry-number]
0 / Anticarcinogenic Agents; 0 / Receptors, Retinoic Acid; 0 / Retinoids
[Number-of-references]
85
36.
Stockfleth E, Meyer T, Benninghoff B, Christophers E:
Successful treatment of actinic keratosis with imiquimod cream 5%: a report of six cases.
Br J Dermatol
; 2001 May;144(5):1050-3
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Successful
treatment
of actinic keratosis with imiquimod cream 5%: a report of six cases.
BACKGROUND: Actinic keratoses (AK) are
premalignant lesions
, which are routinely treated by destructive procedures such as cryotherapy, electrodessication or topical 5-fluorouracil.
OBJECTIVES: The aim of this study is to report six cases of AK treated with a potential new topical
therapy
, imiquimod.
All six men were treated with imiquimod 5% cream three
times
a week for 6-8 weeks.
In the event of a local skin reaction
treatment
was modified to two
times
per week.
RESULTS: All the AK
lesions
were successfully cleared after
treatment with
imiquimod cream 5% for 6-8 weeks.
CONCLUSIONS: This study suggests that imiquimod may be useful as a new
therapy
for the
treatment
of actinic keratoses.
[MeSH-major]
Aminoquinolines /
therapeutic
use. Antineoplastic Agents /
therapeutic
use. Keratosis /
drug therapy
. Precancerous Conditions /
drug therapy
. Skin Neoplasms /
drug therapy
[MeSH-minor]
Administration, Cutaneous. Aged.
Drug
Administration Schedule. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasms, Radiation-Induced /
drug therapy
. Neoplasms, Radiation-Induced / pathology. Recurrence. Scalp Dermatoses /
drug therapy
. Scalp Dermatoses / pathology
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
MedlinePlus Health Information.
consumer health - Skin Cancer
.
Hazardous Substances Data Bank.
Imiquimod
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 11359396.001).
[ISSN]
0007-0963
[Journal-full-title]
The British journal of dermatology
[ISO-abbreviation]
Br. J. Dermatol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
37.
Ibáñez de Cáceres I, Cairns P:
Methylated DNA sequences for early cancer detection, molecular classification and chemotherapy response prediction.
Clin Transl Oncol
; 2007 Jul;9(7):429-37
[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]
Methylated DNA sequences for early cancer
detection
, molecular classification and
chemotherapy
response prediction.
Molecular studies of many
types
of cancer have revealed that clinically evident tumours carry multiple genetic and epigenetic abnormalities, including DNA sequence alterations, chromosome copy number changes and aberrant promoter hypermethylation.
In many cases these abnormalities can be found in
premalignant lesions
and even in histological normal adjacent cells.
Many tumour
types
are difficult to detect early and are frequently resistant to available
chemotherapy
and radiotherapy.
Therefore, the early
detection
, chemoprevention and the design of new
therapeutic
strategies based on the increased understanding of cancer molecular changes are one of the great challenges nowadays.
Thus, hypermethylated DNA sequences from tumours are one of the most promising markers for early
detection
screenings as well as tumour classification and
chemotherapy
response in many
types
of cancer.
[MeSH-major]
DNA Methylation. Neoplasms / diagnosis. Neoplasms /
drug therapy
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Mol Cell Biol. 2001 Nov;21(22):7587-600
[
11604495.001
]
[Cites]
Br J Cancer. 2006 Apr 24;94(8):1087-92
[
16495912.001
]
[Cites]
Cancer Res. 2005 May 15;65(10):4218-27
[
15899813.001
]
[Cites]
Mol Cancer. 2004 May 18;3:16
[
15149548.001
]
[Cites]
Cancer Res. 2006 May 15;66(10):5021-8
[
16707423.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9821-6
[
8790415.001
]
[Cites]
Science. 2006 Jan 20;311(5759):395-8
[
16424344.001
]
[Cites]
BMC Cancer. 2005 Jul 18;5:78
[
16026610.001
]
[Cites]
Cancer Res. 2004 Aug 1;64(15):5511-7
[
15289362.001
]
[Cites]
Clin Cancer Res. 2002 Dec;8(12):3669-75
[
12473575.001
]
[Cites]
Int J Cancer. 2001 Oct 15;94(2):153-6
[
11668491.001
]
[Cites]
Clin Cancer Res. 2005 Dec 1;11(23):8321-5
[
16322291.001
]
[Cites]
N Engl J Med. 2000 Nov 9;343(19):1350-4
[
11070098.001
]
[Cites]
Cancer Res. 2004 Sep 15;64(18):6476-81
[
15374957.001
]
[Cites]
Cancer Res. 2001 Feb 15;61(4):1659-65
[
11245480.001
]
[Cites]
Cancer Res. 2003 Dec 15;63(24):8695-9
[
14695183.001
]
[Cites]
Biotechniques. 2002 Sep;33(3):632, 634, 636-49
[
12238773.001
]
[Cites]
Clin Cancer Res. 2004 Sep 15;10(18 Pt 1):6189-93
[
15448006.001
]
[Cites]
Curr Opin Cell Biol. 1994 Jun;6(3):380-9
[
7917329.001
]
[Cites]
Lancet. 2001 Apr 28;357(9265):1335-6
[
11343741.001
]
[Cites]
Cancer Cell. 2002 Dec;2(6):485-95
[
12498717.001
]
[Cites]
Clin Cancer Res. 2002 Dec;8(12):3796-802
[
12473592.001
]
[Cites]
Nat Genet. 1999 Feb;21(2):163-7
[
9988266.001
]
[Cites]
Genes Dev. 2002 Jan 1;16(1):6-21
[
11782440.001
]
[Cites]
Cancer Res. 2000 Nov 1;60(21):5954-8
[
11085511.001
]
[Cites]
PLoS Med. 2006 Dec;3(12):e486
[
17194187.001
]
[Cites]
Proc Natl Acad Sci U S A. 1990 Jun;87(12):4692-6
[
2352943.001
]
[Cites]
Eur Urol. 2004 Nov;46(5):660-9; discussion 669
[
15474280.001
]
[Cites]
Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1827-31
[
1542678.001
]
[Cites]
Nucleic Acids Res. 2000 Apr 15;28(8):E32
[
10734209.001
]
[Cites]
Cancer Res. 2002 Feb 15;62(4):961-6
[
11861364.001
]
[Cites]
Cancer Cell Int. 2006 Jan 31;6:2
[
16448574.001
]
[Cites]
Cell Mol Life Sci. 2004 Oct;61(19-20):2571-87
[
15526163.001
]
[Cites]
Cancer Res. 2001 Apr 15;61(8):3419-24
[
11309302.001
]
[Cites]
Trends Genet. 2000 Apr;16(4):168-74
[
10729832.001
]
[Cites]
Cancer Res. 2004 Sep 1;64(17):5982-7
[
15342377.001
]
[Cites]
Nat Genet. 1994 Aug;7(4):536-40
[
7951326.001
]
[Cites]
Cancer Res. 1996 Aug 15;56(16):3655-8
[
8706002.001
]
[Cites]
Science. 2003 Apr 18;300(5618):489-92
[
12702876.001
]
[Cites]
Cancer Res. 2007 May 15;67(10):4545-9
[
17510378.001
]
[Cites]
Nature. 2004 May 27;429(6990):457-63
[
15164071.001
]
[Cites]
Adv Cancer Res. 1998;72:141-96
[
9338076.001
]
[Cites]
Cell. 1983 May;33(1):9-10
[
6205762.001
]
[Cites]
J Natl Cancer Inst. 2005 Aug 3;97(15):1124-32
[
16077070.001
]
[Cites]
N Engl J Med. 2003 Nov 20;349(21):2042-54
[
14627790.001
]
[Cites]
Br J Haematol. 2003 Jul;122(1):70-7
[
12823347.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3740-5
[
11891299.001
]
[Cites]
Cancer Res. 2003 Jul 1;63(13):3735-42
[
12839967.001
]
[Cites]
Hum Mol Genet. 2000 Oct;9(16):2395-402
[
11005794.001
]
[Cites]
Clin Cancer Res. 2001 Sep;7(9):2727-30
[
11555585.001
]
[Cites]
Clin Cancer Res. 2004 Mar 15;10(6):1887-93
[
15041703.001
]
[Cites]
Nat Genet. 2002 Jun;31(2):141-9
[
11992124.001
]
[Cites]
J Natl Cancer Inst. 2002 May 15;94(10):755-61
[
12011226.001
]
[Cites]
Clin Cancer Res. 2004 Jun 15;10(12 Pt 1):4010-4
[
15217932.001
]
(PMID = 17652056.001).
[ISSN]
1699-048X
[Journal-full-title]
Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
[ISO-abbreviation]
Clin Transl Oncol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Italy
[Chemical-registry-number]
0 / Biomarkers; 0 / Biomarkers, Tumor; 9007-49-2 / DNA
[Number-of-references]
54
38.
Kwak EL, Jankowski J, Thayer SP, Lauwers GY, Brannigan BW, Harris PL, Okimoto RA, Haserlat SM, Driscoll DR, Ferry D, Muir B, Settleman J, Fuchs CS, Kulke MH, Ryan DP, Clark JW, Sgroi DC, Haber DA, Bell DW:
Epidermal growth factor receptor kinase domain mutations in esophageal and pancreatic adenocarcinomas.
Clin Cancer Res
; 2006 Jul 15;12(14 Pt 1):4283-7
[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.
We also identified the TKI
drug
resistance-associated EGFR T790M mutation in an untreated case of Barrett's esophagus and the corresponding adenocarcinoma.
EGFR mutations in
premalignant lesions
of Barrett's esophagus also point to these as an early event in transformation of the esophageal epithelium.
The role of genotype-directed TKI
therapy
should be tested in prospective clinical trials.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Pancreatic Cancer
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Proc Natl Acad Sci U S A. 2005 Mar 8;102(10):3788-93
[
15731348.001
]
[Cites]
Clin Cancer Res. 2005 Mar 15;11(6):2244-51
[
15788673.001
]
[Cites]
J Clin Oncol. 2005 Apr 10;23(11):2493-501
[
15710947.001
]
[Cites]
J Clin Oncol. 2005 Apr 10;23(11):2513-20
[
15738541.001
]
[Cites]
Clin Cancer Res. 2005 Apr 15;11(8):2879-82
[
15837736.001
]
[Cites]
J Natl Cancer Inst. 2005 May 4;97(9):643-55
[
15870435.001
]
[Cites]
Clin Cancer Res. 2005 May 15;11(10):3750-7
[
15897572.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 May 24;102(21):7665-70
[
15897464.001
]
[Cites]
Ann Oncol. 2005 Jul;16(7):1081-6
[
15851406.001
]
[Cites]
PLoS Med. 2005 Mar;2(3):e73
[
15737014.001
]
[Cites]
N Engl J Med. 2005 Jul 14;353(2):123-32
[
16014882.001
]
[Cites]
Ann Oncol. 2005 Aug;16(8):1334-42
[
15956035.001
]
[Cites]
Clin Cancer Res. 2005 Aug 1;11(15):5539-48
[
16061871.001
]
[Cites]
Cancer Res. 2005 Aug 15;65(16):7096-101
[
16103058.001
]
[Cites]
Cancer Res. 2005 Sep 1;65(17):7568-72
[
16140919.001
]
[Cites]
J Clin Oncol. 2005 Oct 1;23(28):6838-45
[
15998906.001
]
[Cites]
J Clin Oncol. 2005 Oct 1;23(28):6829-37
[
15998907.001
]
[Cites]
Clin Cancer Res. 2005 Oct 1;11(19 Pt 1):6816-22
[
16203769.001
]
[Cites]
Ann Oncol. 2005 Nov;16(11):1848-9
[
16012179.001
]
[Cites]
J Cancer Res Clin Oncol. 2005 Oct;131(10):649-52
[
16032426.001
]
[Cites]
J Clin Oncol. 2005 Nov 1;23(31):8081-92
[
16204011.001
]
[Cites]
Clin Cancer Res. 2005 Nov 15;11(22):8105-8
[
16299242.001
]
[Cites]
Nat Genet. 2005 Dec;37(12):1315-6
[
16258541.001
]
[Cites]
Clin Cancer Res. 2005 Dec 1;11(23):8418-24
[
16322304.001
]
[Cites]
Int J Cancer. 2006 Feb 15;118(4):963-9
[
16152581.001
]
[Cites]
Oncogene. 2006 Feb 23;25(8):1205-15
[
16205628.001
]
[Cites]
Cancer Biol Ther. 2006 Feb;5(2):152-5
[
16357520.001
]
[Cites]
J Clin Oncol. 2006 Oct 20;24(30):4922-7
[
17050876.001
]
[Cites]
J Clin Oncol. 2007 May 20;25(15):1960-6
[
17452677.001
]
[Cites]
Science. 2002 Jul 5;297(5578):63-4
[
12098689.001
]
[Cites]
J Clin Oncol. 2003 May 15;21(10):1980-7
[
12743152.001
]
[Cites]
J Clin Oncol. 2003 Jun 15;21(12):2237-46
[
12748244.001
]
[Cites]
JAMA. 2003 Oct 22;290(16):2149-58
[
14570950.001
]
[Cites]
Clin Cancer Res. 2003 Oct 15;9(13):4819-25
[
14581353.001
]
[Cites]
N Engl J Med. 2004 May 20;350(21):2129-39
[
15118073.001
]
[Cites]
Science. 2004 Jun 4;304(5676):1497-500
[
15118125.001
]
[Cites]
Cancer Cell. 2004 Jul;6(1):11-6
[
15261138.001
]
[Cites]
Science. 2004 Aug 20;305(5687):1163-7
[
15284455.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13306-11
[
15329413.001
]
[Cites]
Cancer Res. 2004 Oct 15;64(20):7241-4
[
15492241.001
]
[Cites]
Int J Cancer. 1993 May 8;54(2):213-9
[
8098013.001
]
[Cites]
Clin Cancer Res. 2004 Dec 15;10(24):8195-203
[
15623594.001
]
[Cites]
N Engl J Med. 2004 Dec 30;351(27):2883
[
15625347.001
]
[Cites]
Cancer Res. 2005 Jan 1;65(1):226-35
[
15665299.001
]
[Cites]
Clin Cancer Res. 2005 Feb 1;11(3):1167-73
[
15709185.001
]
[Cites]
N Engl J Med. 2005 Feb 24;352(8):786-92
[
15728811.001
]
[Cites]
J Natl Cancer Inst. 2005 Mar 2;97(5):339-46
[
15741570.001
]
[Cites]
Clin Cancer Res. 2005 Feb 15;11(4):1368-71
[
15746034.001
]
(PMID = 16857803.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / K08 DK071329; United States / NCI NIH HHS / CA / R01 CA115830; United States / PHS HHS / / P01 95281; United States / NCI NIH HHS / CA / R01 CA11530
[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 / Antineoplastic Agents; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
[Other-IDs]
NLM/ NIHMS519524; NLM/ PMC3807136
39.
Taub AF:
Photodynamic therapy in dermatology: history and horizons.
J Drugs Dermatol
; 2004 Jan-Feb;3(1 Suppl):S8-25
[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]
Photodynamic
therapy
in dermatology: history and horizons.
Photodynamic
therapy
(PDT) uses a photosensitizer, light, and molecular oxygen to selectively kill cells.
When localized in the target
tissue
, the photosensitizer is activated by light to produce oxygen intermediates that destroy target
tissue
cells.
The easy access of skin to light-based
therapy
has led dermatologists to apply PDT to cutaneous disorders.
This has led to new interest in PDT not only for nonmelanoma skin cancer and
premalignant lesions
but also in the
treatment
of acne and as an adjuvant to photorejuvenation procedures.
[MeSH-major]
Photochemotherapy / methods. Photochemotherapy / trends. Skin Diseases /
drug therapy
[MeSH-minor]
Humans. Lasers. Skin Neoplasms /
drug therapy
MedlinePlus Health Information.
consumer health - Skin Conditions
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 14964757.001).
[ISSN]
1545-9616
[Journal-full-title]
Journal of drugs in dermatology : JDD
[ISO-abbreviation]
J Drugs Dermatol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
153
40.
Moll A, Krenauer A, Bierbach U, Till H, Hirsch W, Leuschner I, Schmitz N, Wittekind C, Aigner T:
Mixed hepatoblastoma and teratoma of the liver in a 3-year-old child: a unique combination and clinical challenge.
Diagn Pathol
; 2009;4:37
[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.
Primary liver tumors in children are rare with
malignant
hepatoblastoma being the most common neoplasm.
In this report, we describe the diagnosis and clinical management of a large liver tumor in a 3-year-old child that displayed the features of both, conventional hepatoblastoma and
malignant
teratoma.
Pathological assessment on a
pre
-operative bioptical specimen showed an immature teratoid tumor with no area of hepatoblastic differentiation present.
Histological and immunohistological examination of the resected tumor specimen additionally showed tumor areas of very different differentiation pattern intermixed with each other, namely areas of hepatoblastoma-typical and neuroblastoma-like morphology as well as areas of rhadomyosarcomatous differentiation.After
chemotherapy
the tumor size increased and an extended right hemihepatectomy was performed.
Post-operatively, the general condition of the child improved and adjuvant
chemotherapy
was started two weeks later.
36 months after initial diagnosis the patient is healthy, in good general condition, and without any sign of residual tumor disease.Overall, we describe the diagnosis and clinical management of a large liver tumor in a 3-year-old child that displayed the features of both, conventional hepatoblastoma and
malignant
teratoma and was designated as mixed hepatoblastoma and teratoma.
Though mesenchymal tumor portions can occur within hepatoblastomas, most commonly osteoid or chondroid, our case is different as it presents a large spectrum of mesenchymal and epithelial differentiation pattern in most of the
lesion
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Surg Oncol. 2007 Nov;16(3):195-203
[
17714939.001
]
[Cites]
Diagn Pathol. 2009;4:17
[
19523243.001
]
[Cites]
J Clin Oncol. 2000 Feb;18(4):832-9
[
10673525.001
]
[Cites]
Histopathology. 2003 Sep;43(3):306-8
[
12940789.001
]
[Cites]
Indian J Pathol Microbiol. 2003 Oct;46(4):658-9
[
15025371.001
]
[Cites]
Pediatr Radiol. 2006 Mar;36(3):183-6
[
16404556.001
]
[Cites]
J Clin Oncol. 1991 Dec;9(12):2167-76
[
1720452.001
]
[Cites]
Cancer. 1993 Nov 15;72(10):2910-3
[
8221556.001
]
[Cites]
J Clin Gastroenterol. 1993 Dec;17(4):308-10
[
8308217.001
]
[Cites]
Eur J Surg Oncol. 2005 Dec;31(10):1160-5
[
16157464.001
]
[Cites]
Cancer. 1986 Jun 1;57(11):2168-74
[
2421866.001
]
(PMID = 19909520.001).
[ISSN]
1746-1596
[Journal-full-title]
Diagnostic pathology
[ISO-abbreviation]
Diagn Pathol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC2784753
41.
Ram H, Mohammad S, Husain N, Gupta PN:
Ameloblastic carcinoma.
J Maxillofac Oral Surg
; 2010 Dec;9(4):415-9
[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.
Ameloblastic carcinoma (AC) is a rare aggressive
malignant
epithelial odontogenic tumor of the maxillofacial skeleton with a distinct predilection in the mandible.
It may appear de novo or originate from a
pre
-existing ameloblastoma or odontogenic cyst.
It may present as a cystic
lesion
with benign clinical features or as a large
tissue
mass with ulceration, significant bone resorption and tooth mobility.
Wide local excision is the
treatment
of choice.
Radiotherapy and
chemotherapy
have limited role in the
treatment
of ameloblastic carcinomas.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 22190836.001).
[ISSN]
0974-942X
[Journal-full-title]
Journal of maxillofacial and oral surgery
[ISO-abbreviation]
J Maxillofac Oral Surg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
[Other-IDs]
NLM/ PMC3177477
[Keywords]
NOTNLM ; Ameloblastic carcinoma / Ameloblastoma / Odontogenic tumor
42.
Jiang Y, Liang ZD, Wu TT, Cao L, Zhang H, Xu XC:
Ataxia-telangiectasia mutated expression is associated with tobacco smoke exposure in esophageal cancer tissues and benzo[a]pyrene diol epoxide in cell lines.
Int J Cancer
; 2007 Jan 1;120(1):91-5
[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]
Ataxia-telangiectasia mutated expression is associated with tobacco smoke exposure in esophageal cancer
tissues
and benzo[a]pyrene diol epoxide in cell lines.
To understand how this binding affects the alteration of ATM expression and to identify biomarkers for the
detection
of esophageal cancer, we analyzed ATM mRNA expression in
tissue
specimens from patients with esophageal SCC and
premalignant lesions
using in situ hybridization.
We found that ATM expression was increased in esophageal SCC and its
premalignant lesions
when compared with normal
tissues
and that increased ATM expression was associated with tobacco smoke exposure and tumor de-differentiation.
Moreover, BPDE induced ATM expression in esophageal SCC cell lines in a
time
-dependent manner.
In summary, the BPDE in tobacco smoke may be responsible for increased ATM expression in
premalignant
and
malignant
esophageal
tissues
.
Our findings suggest that the ATM gene should be further evaluated as a biomarker for the early
detection
of esophageal cancer and tobacco use in patients.
[MeSH-major]
7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide / toxicity. Carcinogens / toxicity. Carcinoma, Squamous Cell / genetics. Cell Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Esophageal Neoplasms / genetics. Gene Expression Regulation, Neoplastic /
drug
effects. Protein-Serine-Threonine Kinases / genetics. Smoking. Tumor Suppressor Proteins / genetics
[MeSH-minor]
Ataxia Telangiectasia Mutated Proteins. Biomarkers, Tumor / genetics. Blotting, Western. Case-Control Studies. Humans. In Situ Hybridization. Precancerous Conditions /
drug therapy
. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. RNA, Messenger / metabolism. Tumor Cells, Cultured
Genetic Alliance.
consumer health - Esophageal Cancer
.
Genetic Alliance.
consumer health - Ataxia
.
Genetic Alliance.
consumer health - Ataxia Telangiectasia
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Smoking
.
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 = 17019709.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R21 CA102265
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Carcinogens; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 55097-80-8 / 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
43.
Kershenbaum A, Lavi I, Rennert G, Almog R:
Fecal occult blood test performance indicators in warfarin-treated patients.
Dis Colon Rectum
; 2010 Feb;53(2):224-9
[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: Antithrombotic
drugs
such as warfarin cause a general increase in bleeding tendency and therefore could influence fecal occult blood test results.
Data on lower gastrointestinal evaluation were collected on 425 cases with a positive fecal occult blood test: all positives on warfarin and positive cases of a subsample of those tests in the group without antithrombotic
treatment
.
The
detection
rates of both clinically significant adenomas and findings not indicative of significant neoplasia were increased in the warfarin group (8.9/1000 and 32.5/1000 respectively) compared with the no-antithrombotic group (4.0/1000 and 11.3/1000) (P = .02 and P <.0001 respectively), whereas that of carcinoma was not found to be different (3.7/1000 in the warfarin group vs 3.3/1000, P = .85).
CONCLUSIONS: Fecal occult blood test screening in warfarin users results in a higher, yet reasonable, positivity load and in a higher
detection
of
premalignant lesions
than in the general population.
[MeSH-minor]
Aged. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Incidence. Israel / epidemiology. Male. Mass Screening / methods. Middle Aged. Retrospective Studies. Thrombosis / complications. Thrombosis /
drug therapy
MedlinePlus Health Information.
consumer health - Blood Thinners
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Gastrointestinal Bleeding
.
Hazardous Substances Data Bank.
WARFARIN
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20087099.001).
[ISSN]
1530-0358
[Journal-full-title]
Diseases of the colon and rectum
[ISO-abbreviation]
Dis. Colon Rectum
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Anticoagulants; 5Q7ZVV76EI / Warfarin
44.
Smith W, Saba N:
Retinoids as chemoprevention for head and neck cancer: where do we go from here?
Crit Rev Oncol Hematol
; 2005 Aug;55(2):143-52
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Adhering to the concept of field cancerization and following multi-step carcinogenesis,
premalignant lesions
of the head and neck have long been the focus of intervention with retinoids.
Similarly, these agents have been applied towards preventing second primary malignancies from developing following curative
therapy
for upper aerodigestive cancers.
[MeSH-major]
Chemoprevention / methods. Head and Neck Neoplasms /
drug therapy
. Retinoids /
therapeutic
use
[MeSH-minor]
Humans. Precancerous Conditions /
drug therapy
MedlinePlus Health Information.
consumer health - Head and Neck Cancer
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15886010.001).
[ISSN]
1040-8428
[Journal-full-title]
Critical reviews in oncology/hematology
[ISO-abbreviation]
Crit. Rev. Oncol. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Retinoids
[Number-of-references]
75
45.
González-Peramato P, Regadera J, Juarranz A:
[Photodynamic therapy in urology. Biologic and pathologic mechanisms of action].
Arch Esp Urol
; 2008 Nov;61(9):1135-44
[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]
[Photodynamic
therapy
in urology. Biologic and pathologic mechanisms of action].
[Transliterated title]
La
terapia
fotodinámica en urologia. Mecanismos de acción biológicos y patológicos.
Photodynamic
Therapy
(FDT) is a minimally invasive
therapeutic
modality extraordinarily useful.
In urology, FDT is very useful and may be applied through endoscopes or directly, with excellent results obtained for the diagnosis and
treatment
of bladder tumors, in the
treatment
of prostate cancer and its recurrences, and in the
treatment
of dermatological
premalignant lesions
and carcinomas of the penis.
FDT is founded on the use of photosensitizing products which selectively accumulate in tumor
tissues
.
The irradiation of these
tissues with
a proper wavelength light (generally in the red region of the visible spectrum lambda > or = 600 nm) produces the formation of oxygen reactive species with cytotoxic effects leading to selective death of neoplastic cells, and tumor regression.
The main advantage of FDT is the restriction of cellular damage to the irradiation area, with the associated decrease of secondary effects on healthy
tissues
near the tumor, on the contrary to what happen with other conventional
therapies
for some tumors of the urinary tract.
Moreover, FDT may be used in combination with radiotherapy and
chemotherapy
.
[MeSH-major]
Photochemotherapy. Urologic Neoplasms /
drug therapy
[MeSH-minor]
Humans. Male. Photosensitizing Agents /
therapeutic
use. Prostatic Neoplasms /
drug therapy
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19140598.001).
[ISSN]
0004-0614
[Journal-full-title]
Archivos españoles de urología
[ISO-abbreviation]
Arch. Esp. Urol.
[Language]
spa
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Spain
[Chemical-registry-number]
0 / Photosensitizing Agents
46.
Raben D, Helfrich BA, Chan D, Johnson G, Bunn PA Jr:
ZD1839, a selective epidermal growth factor receptor tyrosine kinase inhibitor, alone and in combination with radiation and chemotherapy as a new therapeutic strategy in non-small cell lung cancer.
Semin Oncol
; 2002 Feb;29(1 Suppl 4):37-46
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
ZD1839, a selective epidermal growth factor receptor tyrosine kinase inhibitor, alone and in combination with radiation and
chemotherapy
as a new
therapeutic
strategy in non-small cell lung cancer.
Preclinical studies have shown additive to synergistic effects when ZD1839 is combined with radiation or
chemotherapy
in colon, head and neck, and non-small cell lung cancers.
Future studies will certainly combine ZD1839
with chemotherapy
or radiation.
ZD1839 also may be effective as a chemoprevention agent because
premalignant lesions
often overexpress epidermal growth factor receptor.
[MeSH-major]
Antineoplastic Agents / pharmacology. Carcinoma, Non-Small-Cell Lung /
drug therapy
. Head and Neck Neoplasms /
drug therapy
. Lung Neoplasms /
drug therapy
. Quinazolines / pharmacology. Receptor, Epidermal Growth Factor / biosynthesis. Receptor, Epidermal Growth Factor / metabolism
[MeSH-minor]
Administration, Oral. Animals. Cell Cycle /
drug
effects. Chemoprevention. Clinical Trials as Topic. Combined Modality
Therapy
. Disease Models, Animal. Humans. Signal Transduction /
drug
effects. Transplantation, Heterologous. Up-Regulation
Genetic Alliance.
consumer health - Lung Cancer
.
Genetic Alliance.
consumer health - Non-small cell lung cancer
.
MedlinePlus Health Information.
consumer health - Head and Neck Cancer
.
MedlinePlus Health Information.
consumer health - Lung Cancer
.
COS Scholar Universe.
author profiles
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 11894012.001).
[ISSN]
0093-7754
[Journal-full-title]
Seminars in oncology
[ISO-abbreviation]
Semin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
[Number-of-references]
36
47.
Rogers CL, Theodore N, Dickman CA, Sonntag VK, Thomas T, Lam S, Speiser BL:
Surgery and permanent 125I seed paraspinal brachytherapy for malignant tumors with spinal cord compression.
Int J Radiat Oncol Biol Phys
; 2002 Oct 1;54(2):505-13
[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]
Surgery and permanent 125I seed paraspinal brachytherapy for
malignant
tumors with spinal cord compression.
PURPOSE: To evaluate the functional outcome, predictors of response, and toxicity from spinal surgery and 125I brachytherapy in patients with
malignant
tumors resulting in spinal cord compression.
Surgical procedures were based on the location of the impinging
lesion
: corpectomy or spondylectomy in 13 cases and laminectomy in 12.
Three had no EBRT: 1 had lymphoma treated
with chemotherapy
, 1 had remote previous EBRT for a childhood tumor, and 1 refused EBRT.
The mean
time
to recurrence for these 4 patients was 20.3 months.
An ambulatory function score was assigned
pre
- and postoperatively: I, normal ambulation; II, abnormal not requiring assistance; III, abnormal requiring assistance; and IV, unable to ambulate.
All patients with score I, 91% of those with score II, 67% of those with score III, and 67% of those with score IV were ambulatory after the
procedure
; 84% had either normal or improved ambulation postoperatively.
CONCLUSION: This is the largest series in the literature exploring surgery and 125I brachytherapy in the
treatment
of
malignant
spinal cord compression.
Our results suggest a benefit to aggressive local
therapy
in selected patients with spinal cord compression.
[MeSH-major]
Brachytherapy / methods. Iodine Radioisotopes /
therapeutic
use. Spinal Cord Compression / radiotherapy. Spinal Neoplasms / radiotherapy. Spinal Neoplasms / secondary
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Analysis of Variance. Female. Follow-Up Studies. Humans. Male. Middle Aged. Radiotherapy, Adjuvant. Recovery of Function. Survival Analysis.
Treatment
Outcome
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 12243829.001).
[ISSN]
0360-3016
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Iodine Radioisotopes
48.
Strauss HG, Wolters M, Methfessel G, Buchmann J, Koelbl H:
Significance of endovaginal ultrasonography in assessing tamoxifen-associated changes of the endometrium. A prospective study.
Acta Obstet Gynecol Scand
; 2000 Aug;79(8):697-701
[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.
However, the role of vaginal ultrasound in screening for endometrial cancer or
premalignant lesions
remains uncertain.
[MeSH-major]
Antineoplastic Agents, Hormonal / adverse effects. Endometrium /
drug
effects. Tamoxifen / adverse effects. Vagina / ultrasonography
[MeSH-minor]
Aged. Aged, 80 and over. Breast Neoplasms /
drug therapy
. False Positive Reactions. Female. Humans. Middle Aged. Prospective Studies
Hazardous Substances Data Bank.
TAMOXIFEN
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 10949237.001).
[ISSN]
0001-6349
[Journal-full-title]
Acta obstetricia et gynecologica Scandinavica
[ISO-abbreviation]
Acta Obstet Gynecol Scand
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
DENMARK
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 094ZI81Y45 / Tamoxifen
49.
Narducci F, Orazi G, Cosson M:
[Ovarian cyst: surgical indications and access].
J Gynecol Obstet Biol Reprod (Paris)
; 2001 Nov;30(1 Suppl):S59-67
[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.
Laparoscopic
treatment
of adnexal masses is indicated when all criteria of a benign
lesion
are present: transvaginal ultrasound demonstrates a mass < 5 cm, with liquid or dermoid content, with less than 3 fine partitions (< 3 mm), a thin wall (< 3 mm), no vegetations, normal Doppler.
Since the benign or
malignant
nature of an ovarian mass cannot be determined macroscopically, precaution must be taken to avoid potential laparoscopic dissemination: use of an extraction pouch, instrument cleaning, cytotoxic agent (chlorexidine or povidone-iodine) for trocar tracts, prevention of gas leakage, 3-plane suture of trocar orifices measuring > 10 mm, short interval between laparoscopic diagnosis of cancer and onset of
chemotherapy
or complete surgery (1 week).
In case of
pre
- or peroperatively suspected malignancy, cytology examination of the peritoneal fluid and careful peroperative exploration of the abdomen and pelvis with peritoneal biopsy as needed are required.
MedlinePlus Health Information.
consumer health - Ovarian Cysts
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 11917377.001).
[ISSN]
0368-2315
[Journal-full-title]
Journal de gynécologie, obstétrique et biologie de la reproduction
[ISO-abbreviation]
J Gynecol Obstet Biol Reprod (Paris)
[Language]
fre
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
France
[Number-of-references]
65
50.
Hampson L, Kitchener HC, Hampson IN:
Specific HIV protease inhibitors inhibit the ability of HPV16 E6 to degrade p53 and selectively kill E6-dependent cervical carcinoma cells in vitro.
Antivir Ther
; 2006;11(6):813-25
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Although HIV protease inhibitor (PI)
drugs
predominantly target HIV proteases 1 and 2, it is also known that part of their efficacy is due to selective inhibition of the proteasome.
Comparison of the ability of the PIs indinavir, ritonavir, amprenavir, lopinavir, atazanavir, nelfinavir and saquinavir to inhibit E6-mediated proteasomal degradation of mutant p53 in E6-transfected C33A cells showed that 15 microM lopinavir, 1 mM indinavir or 125 microM ritonavir
treatment
for 24 h produced a stable increase in the level of nuclear p53 in these cells with minimal cell death.
After 4 h exposure of HPV16+ve SiHa cells to 15 microM lopinavir, a transient increase in wild-
type
p53 expression was observed associated with a 7% reduction in the chymotryptic activity of the 205 proteasome and apoptosis after 24h.
In conclusion, these data show that specific HIV PIs such as lopinavir and possibly indinavir, can induce selective toxicity of HPV-transformed cervical carcinoma cells expressing wild-
type
p53 and may form the basis of a topically applied alternative to surgery for the
treatment
of HPV-related
premalignant lesions
of the cervix.
[MeSH-minor]
Animals. Carcinoma /
drug therapy
. Carcinoma / virology. Cell Line, Tumor /
drug
effects. Female. Humans. Lopinavir. Mice. NIH 3T3 Cells. Proteasome Endopeptidase Complex / metabolism. Transfection. Uterine Cervical Neoplasms /
drug therapy
. Uterine Cervical Neoplasms / virology
Genetic Alliance.
consumer health - HIV
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
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
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17310826.001).
[ISSN]
1359-6535
[Journal-full-title]
Antiviral therapy
[ISO-abbreviation]
Antivir. Ther. (Lond.)
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / E6 protein, Human papillomavirus type 16; 0 / HIV Protease Inhibitors; 0 / Oncogene Proteins, Viral; 0 / Pyrimidinones; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53; 2494G1JF75 / Lopinavir; EC 3.4.25.1 / Proteasome Endopeptidase Complex
51.
Milas L, Mason KA, Crane CH, Liao Z, Masferrer J:
Improvement of radiotherapy or chemoradiotherapy by targeting COX-2 enzyme.
Oncology (Williston Park)
; 2003 May;17(5 Suppl 5):15-24
[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.
Radiation
therapy
has traditionally been the
treatment
of choice for locally or regionally advanced cancer, but its
therapeutic
efficacy is often hindered by limited tolerance of normal
tissues
and by tumor radioresistance.
To improve
therapeutic
outcome, radiotherapy is frequently combined with chemotherapeutic
drugs
that are themselves cytotoxic and may sensitize cells to radiation.
These
therapeutic
improvements, however, have been achieved at the expense of considerable normal
tissue
toxicity.
Preclinical studies have shown that these agents are potent radiosensitizers, providing a strong biologic rationale for using these
drugs
in combination with radiotherapy.
These studies also generated information critical for designing effective
treatment
schedules in clinical settings.
The
therapeutic
efficacy of topoisomerase inhibitor-radiation combinations is currently being tested clinically.
COX-2 is often overexpressed in
premalignant lesions
and cancer, and is involved in carcinogenesis, tumor growth, and metastatic spread.
Preclinical studies provided solid evidence that inhibition of this enzyme with selective COX-2 inhibitors prevents carcinogenesis, slows the growth of established tumors, and enhances tumor response to radiation without appreciably affecting normal
tissue
radioresponse.
Additional
therapeutic
benefit was observed for celecoxib (Celebrex), a selective COX-2 inhibitor, consisting of a strong reduction in irinotecan-induced diarrhea.
Thus, selective targeting of COX-2 may potentially improve radiotherapy,
chemotherapy
, or chemoradiotherapy--a
therapeutic
strategy that is currently being tested in clinical trials.
[MeSH-major]
Antineoplastic Combined
Chemotherapy
Protocols /
therapeutic
use. Camptothecin / analogs & derivatives. Isoenzymes /
drug
effects. Isoenzymes / radiation effects. Prostaglandin-Endoperoxide Synthases /
drug
effects. Prostaglandin-Endoperoxide Synthases / radiation effects. Radiotherapy
[MeSH-minor]
Animals. Clinical Trials as Topic. Combined Modality
Therapy
. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Cyclooxygenase Inhibitors /
therapeutic
use. Humans. Membrane Proteins. Neoplasms /
drug therapy
. Neoplasms / enzymology. Neoplasms / radiotherapy
MedlinePlus Health Information.
consumer health - Radiation Therapy
.
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
(PMID = 12800601.001).
[ISSN]
0890-9091
[Journal-full-title]
Oncology (Williston Park, N.Y.)
[ISO-abbreviation]
Oncology (Williston Park, N.Y.)
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA-06294; United States / NCI NIH HHS / CA / CA-16672
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 7673326042 / irinotecan; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; XT3Z54Z28A / Camptothecin
[Number-of-references]
77
52.
Lysa B, Tartler U, Wolf R, Arenberger P, Benninghoff B, Ruzicka T, Hengge UR, Walz M:
Gene expression in actinic keratoses: pharmacological modulation by imiquimod.
Br J Dermatol
; 2004 Dec;151(6):1150-9
[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]
Gene expression in actinic keratoses:
pharmacological
modulation by imiquimod.
BACKGROUND: Actinic keratoses (AKs) are
premalignant lesions
that can progress into squamous cell carcinoma.
Imiquimod, which belongs to the new class of immune-response modifiers, was recently shown to be effective in the
treatment
of AKs.
OBJECTIVES: To study the expression of individual genes in uninvolved skin and AKs before
therapy
and to elucidate the way in which the expression of these genes is influenced by imiquimod
therapy
.
METHODS: We treated 13 patients with AK with imiquimod and compared gene expression before, during (five patients) and after (eight patients)
therapy
with that in uninvolved skin.
During imiquimod
therapy
, we detected a further upregulation of interferon-alpha, IL-6, IL-10 receptor 1 and TLR7.
[MeSH-major]
Aminoquinolines / pharmacology. Antineoplastic Agents / pharmacology. Gene Expression Regulation /
drug
effects. Interferon Inducers / pharmacology. Keratosis /
drug therapy
[MeSH-minor]
Aged. Apoptosis / genetics. Cell Adhesion Molecules / metabolism. Cytokines / genetics. Cytokines / metabolism. Genes, p53. Humans. Male. Membrane Glycoproteins / metabolism. Middle Aged. Neoplasms, Radiation-Induced /
drug therapy
. Neoplasms, Radiation-Induced / genetics. Neoplasms, Radiation-Induced / metabolism. Precancerous Conditions /
drug therapy
. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Receptors, Cell Surface / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Skin Neoplasms /
drug therapy
. Skin Neoplasms / genetics. Skin Neoplasms / metabolism. Toll-Like Receptor 7. Toll-Like Receptor 8. Toll-Like Receptors
Hazardous Substances Data Bank.
Imiquimod
.
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 = 15606509.001).
[ISSN]
0007-0963
[Journal-full-title]
The British journal of dermatology
[ISO-abbreviation]
Br. J. Dermatol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Aminoquinolines; 0 / Antineoplastic Agents; 0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / Interferon Inducers; 0 / Membrane Glycoproteins; 0 / Receptors, Cell Surface; 0 / TLR7 protein, human; 0 / TLR8 protein, human; 0 / Toll-Like Receptor 7; 0 / Toll-Like Receptor 8; 0 / Toll-Like Receptors; 99011-02-6 / imiquimod
53.
Sato M, Shames DS, Gazdar AF, Minna JD:
A translational view of the molecular pathogenesis of lung cancer.
J Thorac Oncol
; 2007 Apr;2(4):327-43
[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.
In many cases these abnormalities can be found in
premalignant lesions
and in histologically normal lung bronchial epithelial cells.
Lung cancer has a high morbidity because it is difficult to detect early and is frequently resistant to available
chemotherapy
and radiotherapy.
New, rationally designed early
detection
, chemoprevention, and
therapeutic
strategies based on the growing understanding of the molecular changes important to lung cancer are under investigation.
For example, methylated tumor DNA sequences in sputum or blood are being investigated for early
detection
screening, and new
treatments
that specifically target molecules such as vascular endothelial growth factor and the epidermal growth factor receptor are becoming available.
Meanwhile, global gene expression signatures from individual tumors are showing potential as prognostic and
therapeutic
indicators, such that molecular typing of individual tumors for
therapy
selection is not far away.
Genetic Alliance.
consumer health - Lung Cancer
.
MedlinePlus Health Information.
consumer health - Lung Cancer
.
MedlinePlus Health Information.
consumer health - Smoking
.
COS Scholar Universe.
author profiles
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17409807.001).
[ISSN]
1556-1380
[Journal-full-title]
Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
[ISO-abbreviation]
J Thorac Oncol
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CN / N01-CN-43301; United States / NCI NIH HHS / CA / P50CA75907
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Neoplasm; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
[Number-of-references]
187
54.
Brown KS, Kane MA:
Chemoprevention of squamous cell carcinoma of the oral cavity.
Otolaryngol Clin North Am
; 2006 Apr;39(2):349-63
[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.
Because of the poor out-comes associated with the disease, the presence of identifiable
premalignant lesions
, and the failure of local preventive
therapies
, such as surgery, many investigators have hoped to find an effective chemopreventive compound.
[MeSH-minor]
Antineoplastic Agents /
therapeutic
use. Ascorbic Acid /
therapeutic
use.
Drugs
, Chinese Herbal /
therapeutic
use. Flavonoids /
therapeutic
use. Folic Acid /
therapeutic
use. Humans. Precancerous Conditions /
drug therapy
. Retinoids /
therapeutic
use. Selenium /
therapeutic
use. Vitamin A /
therapeutic
use. Vitamin E /
therapeutic
use
Genetic Alliance.
consumer health - Carcinoma, Squamous Cell
.
Genetic Alliance.
consumer health - Oral squamous cell carcinoma
.
MedlinePlus Health Information.
consumer health - Oral Cancer
.
Hazardous Substances Data Bank.
Sodium ascorbate
.
Hazardous Substances Data Bank.
L-Ascorbic Acid
.
Hazardous Substances Data Bank.
FOLIC ACID
.
Hazardous Substances Data Bank.
VITAMIN A
.
Hazardous Substances Data Bank.
SELENIUM, ELEMENTAL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16580916.001).
[ISSN]
0030-6665
[Journal-full-title]
Otolaryngologic clinics of North America
[ISO-abbreviation]
Otolaryngol. Clin. North Am.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Drugs, Chinese Herbal; 0 / Flavonoids; 0 / Retinoids; 11103-57-4 / Vitamin A; 1406-18-4 / Vitamin E; 935E97BOY8 / Folic Acid; H6241UJ22B / Selenium; PQ6CK8PD0R / Ascorbic Acid
[Number-of-references]
82
55.
Liao Z, Milas L, Komaki R, Stevens C, Cox JD:
Combination of a COX-2 inhibitor with radiotherapy or radiochemotherapy in the treatment of thoracic cancer.
Am J Clin Oncol
; 2003 Aug;26(4):S85-91
[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]
Combination of a COX-2 inhibitor with radiotherapy or radiochemotherapy in the
treatment
of thoracic cancer.
The enzyme is often overexpressed in
premalignant lesions
and cancer, including cancers of the lung and esophagus.
[MeSH-major]
Anti-Inflammatory Agents, Non-Steroidal /
therapeutic
use. Antineoplastic Agents /
therapeutic
use. Cyclooxygenase Inhibitors /
therapeutic
use. Esophageal Neoplasms /
drug therapy
. Esophageal Neoplasms / radiotherapy. Isoenzymes / antagonists & inhibitors. Lung Neoplasms /
drug therapy
. Lung Neoplasms / radiotherapy. Radiation-Sensitizing Agents /
therapeutic
use. Sulfonamides /
therapeutic
use
[MeSH-minor]
Carcinoma, Non-Small-Cell Lung /
drug therapy
. Carcinoma, Non-Small-Cell Lung / radiotherapy. Celecoxib. Clinical Trials as Topic. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Humans. Membrane Proteins. Prostaglandin-Endoperoxide Synthases / metabolism. Pyrazoles
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
MedlinePlus Health Information.
consumer health - Esophageal Cancer
.
MedlinePlus Health Information.
consumer health - Lung Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
CELECOXIB
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 12902863.001).
[ISSN]
1537-453X
[Journal-full-title]
American journal of clinical oncology
[ISO-abbreviation]
Am. J. Clin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Pyrazoles; 0 / Radiation-Sensitizing Agents; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; JCX84Q7J1L / Celecoxib
[Number-of-references]
51
56.
Nakamura T, Kusuzaki K, Seto M, Matsumine A, Uchida A:
Case report: recurrence of soft tissue MFH in bone due to minute intravenous tumor emboli detected by MRI.
Oncol Rep
; 2003 Nov-Dec;10(6):1957-60
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Case report: recurrence of soft
tissue
MFH in bone due to minute intravenous tumor emboli detected by MRI.
We recently encountered a case with local recurrence of
malignant
fibrous histiocytoma (MFH) in the bone after wide resection, caused by minute intravenous tumor emboli which were retrospectively detected in MR imaging.
The patient received postoperative brachytherapy, but no
chemotherapy
.
We reviewed the
pre
-operative films obtained by various imaging modalities, as well as the histology of the primary tumor, and found minute intravenous tumor emboli in the MR imaging obtained before surgery.
Such intravenous tumor emboli have recently been implicated in the development of regional bone metastasis near the site of the primary
lesion
in cases of
malignant
soft
tissue
tumors.
It is therefore emphasized that MR images should be carefully reviewed for the presence of such intravenous tumor emboli before surgery in cases of high-grade
malignant
sarcomas.
As at the
time
of writing, our patient remains alive and disease-free, with no evidence of any local recurrence or distant metastasis after wide tumor resection for the recurrent tumor.
[MeSH-major]
Bone Neoplasms / diagnosis. Bone Neoplasms / secondary. Histiocytoma, Benign Fibrous / diagnosis. Histiocytoma, Benign Fibrous / metabolism. Magnetic Resonance Imaging / methods. Recurrence. Soft
Tissue
Neoplasms / diagnosis. Soft
Tissue
Neoplasms / metabolism
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 14534725.001).
[ISSN]
1021-335X
[Journal-full-title]
Oncology reports
[ISO-abbreviation]
Oncol. Rep.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Greece
57.
Armstrong WB, Wan XS, Kennedy AR, Taylor TH, Meyskens FL Jr:
Development of the Bowman-Birk inhibitor for oral cancer chemoprevention and analysis of Neu immunohistochemical staining intensity with Bowman-Birk inhibitor concentrate treatment.
Laryngoscope
; 2003 Oct;113(10):1687-702
[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]
Development of the Bowman-Birk inhibitor for oral cancer chemoprevention and analysis of Neu immunohistochemical staining intensity with Bowman-Birk inhibitor concentrate
treatment
.
The retinoids are archetypal chemopreventive agents for oral
premalignant lesions
.
The purposes of the study were to summarize the preclinical and clinical development of Bowman-Birk Inhibitor and a Bowman-Birk Inhibitor concentrate against oral
premalignant lesions
and to evaluate Neu immunohistochemical staining intensity for
lesions
and simultaneously obtained biopsy specimens of normal-appearing mucosa from the Phase IIa Bowman-Birk Inhibitor concentrate oral leukoplakia chemoprevention trial.
METHODS: Thirty-two sets of biopsy specimens from
lesions
and uninvolved oral mucosa before and after
treatment with
Bowman-Birk Inhibitor concentrate in doses ranging from 200 to 1066 chymotrypsin inhibitory units were examined in blinded fashion for Neu immunohistochemical staining intensity using the 3B-5 monoclonal antibody.
Staining intensity scores among the
lesion
and control biopsy specimens before and after Bowman-Birk Inhibitor concentrate
treatment
were analyzed and compared with previously obtained values for serum Neu, oral mucosal cell Neu, protease activity, and clinical response to
treatment
.
RESULTS: Mean Neu staining score was significantly higher in
lesions
compared with uninvolved mucosa (P <.001).
Pretreatment staining scores for biopsy specimens of
lesions
and control biopsy specimens of normal-appearing
tissues
were correlated (Spearman correlation coefficient [r] = 0.375, P =.045), but no correlation between
lesion
and control biopsy specimen scores was evident after
treatment
.
The change in Neu staining score with Bowman-Birk Inhibitor concentrate
treatment
in control site biopsy specimens demonstrated an inverse relationship of change in
lesion
area with Bowman-Birk Inhibitor concentrate
treatment
(Spearman r = -0.493, P <.007).
The current investigation identified increased Neu staining intensity in hyperplastic
lesions
compared with simultaneously obtained biopsy specimens of normal-appearing mucosa both before and after Bowman-Birk Inhibitor concentrate
treatment
.
This finding supports prior observations that increased Neu expression is present in a subset of oral
premalignant lesions
and head and neck cancers.
The trend of increased Neu staining score in control biopsy
tissues
of subjects exhibiting decreased
lesion
area following Bowman-Birk Inhibitor concentrate
treatment
raises questions about the mechanisms of Bowman-Birk Inhibitor concentrate action.
Further study of modulation of Neu and protease activity by Bowman-Birk Inhibitor concentrate
treatment
may provide insights into the role of proteases and protease inhibitors in oral
premalignant lesions
and the mechanisms underlying Bowman-Birk Inhibitor concentrate effects.
[MeSH-major]
Anticarcinogenic Agents /
therapeutic
use. Head and Neck Neoplasms /
drug therapy
. Plant Proteins /
therapeutic
use. Trypsin Inhibitor, Bowman-Birk Soybean /
therapeutic
use
[MeSH-minor]
Animals. Chemoprevention. Humans. Immunohistochemistry. Leukoplakia, Oral /
drug therapy
. Leukoplakia, Oral / metabolism. Receptor, ErbB-2 / metabolism. Trypsin Inhibitors. alpha-Amylases / antagonists & inhibitors
Genetic Alliance.
consumer health - Oral cancer
.
MedlinePlus Health Information.
consumer health - Head and Neck Cancer
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
eScholarship, California Digital Library, University of California.
Full text from University of California eScholarship
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 14520092.001).
[ISSN]
0023-852X
[Journal-full-title]
The Laryngoscope
[ISO-abbreviation]
Laryngoscope
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA 62203; United States / NCI NIH HHS / CA / U01 CA 46496
[Publication-type]
Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Anticarcinogenic Agents; 0 / Plant Proteins; 0 / Trypsin Inhibitor, Bowman-Birk Soybean; 0 / Trypsin Inhibitors; EC 2.7.10.1 / Receptor, ErbB-2; EC 3.2.1.1 / alpha-Amylases
[Number-of-references]
162
[Keywords]
NASA ; Non-programmatic
58.
Nagy K, Szöke I, Sonkodi I, Nagy E, Mari A, Szolnoky G, Newman HN:
Inhibition of microflora associated with oral malignancy.
Oral Oncol
; 2000 Jan;36(1):32-6
[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.
Changes in the microflora on oral carcinoma surfaces may lead to both local and systemic infections, which may complicate the morbidity of the patient suffering from oral
malignant
neoplasms.
Thus, anticancer
therapy
, irradiation,
chemotherapy
or surgery impairs the defence mechanism of the oral mucosa and is accompanied by proliferation of the mucosal biofilm with overgrowth of yeast and bacteria.
Biofilm samples were obtained from the central surface (1 cm2) of each
lesion
in 10 patients (eight male, two female; mean age: 47.6 years; SD +/- 7.6) before any antibiotherapy or tumour
treatment
.
Samples were transported in
pre
-reduced brain heart infusion broth and cultured within 1 h of removal, using aerobic and anaerobic complete and selective media.
) It was concluded that 7-days (three
times
a day) Meridol rinsing significantly reduced the surface biofilm of oral carcinoma compared to rinsing with placebo.
The findings of the present study indicate that in addition to any other oral focus, the
lesion
itself, when ulcerated, should receive direct antimicrobial
treatment
so as to reduce patient morbidity and enhance quality of life.
[MeSH-major]
Bacterial Infections / prevention & control. Biofilms. Carcinoma, Squamous Cell / microbiology. Mouth Neoplasms / microbiology. Mouthwashes /
therapeutic
use
MedlinePlus Health Information.
consumer health - Bacterial Infections
.
MedlinePlus Health Information.
consumer health - Oral Cancer
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 10889916.001).
[ISSN]
1368-8375
[Journal-full-title]
Oral oncology
[ISO-abbreviation]
Oral Oncol.
[Language]
eng
[Publication-type]
Clinical Trial; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
ENGLAND
[Chemical-registry-number]
0 / Mouthwashes
59.
Yasuda Y, Shimizu M, Shirakami Y, Sakai H, Kubota M, Hata K, Hirose Y, Tsurumi H, Tanaka T, Moriwaki H:
Pitavastatin inhibits azoxymethane-induced colonic preneoplastic lesions in C57BL/KsJ-db/db obese mice.
Cancer Sci
; 2010 Jul;101(7):1701-7
[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]
Pitavastatin inhibits azoxymethane-induced colonic preneoplastic
lesions
in C57BL/KsJ-db/db obese mice.
Statins, which are commonly used for the
treatment
of hyperlipidemia, are known to possess anti-inflammatory effects.
The present study examined the effects of pitavastatin, a recently
developed
lipophilic statin, on the development of azoxymethane (AOM)-initiated colonic
premalignant lesions
in C57BL/KsJ-db/db (db/db) obese mice.
Feeding with either dose of pitavastatin significantly reduced the number of colonic
premalignant lesions
, beta-catenin accumulated crypts, by inhibiting proliferation and the surrounding inflammation.
In addition, the expression levels of TNF-alpha, IL-6, IL-18, and COX-2 mRNAs on the colonic mucosa of AOM-treated mice were decreased by
treatment with
this agent.
These findings suggest that pitavastatin attenuates chronic inflammation and improves the imbalance of adipocytokines, both of which are caused by the presence of excess adipose
tissues
, thereby preventing the development of colonic premalignancies in an obesity-related colon cancer model.
Therefore, some
types
of statins, including pitavastatin, may be a useful chemoprevention modality for colon cancer in obese individuals.
[MeSH-major]
Azoxymethane / toxicity. Colonic Neoplasms / prevention & control. Hydroxymethylglutaryl-CoA Reductase Inhibitors /
therapeutic
use. Precancerous Conditions / prevention & control. Quinolines /
therapeutic
use
[MeSH-minor]
Animals. Carcinogens / toxicity. Cell Division /
drug
effects. Cytokines /
drug
effects. Cytokines / metabolism. Humans. Inflammation / prevention & control. Male. Mice. Mice, Inbred C57BL. Mice, Obese. Obesity / complications. Obesity /
drug therapy
MedlinePlus Health Information.
consumer health - Statins
.
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 = 20398056.001).
[ISSN]
1349-7006
[Journal-full-title]
Cancer science
[ISO-abbreviation]
Cancer Sci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Carcinogens; 0 / Cytokines; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Quinolines; M5681Q5F9P / pitavastatin; MO0N1J0SEN / Azoxymethane
60.
Yang Y, Ge JP, Zhou ZT:
Effects of thalidomide on DMBA-induced oral carcinogenesis in hamster with respect to angiogenesis.
J Oral Pathol Med
; 2009 May;38(5):455-62
[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: Thalidomide has been shown to have anti-angiogenic effects in
pre
-clinical models as well as a significant antitumor effect in hematologic tumors.
However, the effects of thalidomide on oral
pre
-
malignant
lesions
and oral carcinogenesis remain unexplored.
DMBA solution (0.5% in acetone) was applied topically to the left cheek pouch of male Syrian golden hamsters in group A and B, while animals in group C were painted with acetone, three
times
a week for 6 weeks.
Animals in group E received no
treatment
and served as blank control.
At the end of the experiment, animals were killed and
tissue
samples were collected for examinations.
CONCLUSIONS: Thalidomide has inhibitory effect against the
malignant
transformation of oral
pre
-cancerous
lesion
and angiogenesis during oral carcinogenesis.
[MeSH-major]
Angiogenesis Inhibitors /
therapeutic
use. Carcinoma, Squamous Cell / prevention & control. Mouth Mucosa /
drug
effects. Mouth Neoplasms / prevention & control. Neoplasms, Experimental / prevention & control. Thalidomide /
therapeutic
use
[MeSH-minor]
9,10-Dimethyl-1,2-benzanthracene. Animals. Anticarcinogenic Agents /
therapeutic
use. Carcinogens. Cell Transformation, Neoplastic / chemically induced. Cell Transformation, Neoplastic /
drug
effects. Chemoprevention / methods. Cricetinae. Male. Mesocricetus. Neovascularization, Pathologic / prevention & control. Precancerous Conditions / chemically induced. Precancerous Conditions /
drug therapy
. RNA, Messenger / analysis. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism
MedlinePlus Health Information.
consumer health - Oral Cancer
.
Hazardous Substances Data Bank.
THALIDOMIDE
.
Hazardous Substances Data Bank.
7,12-DIMETHYLBENZ(A)ANTHRACENE
.
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 = 19141066.001).
[ISSN]
1600-0714
[Journal-full-title]
Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
[ISO-abbreviation]
J. Oral Pathol. Med.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Angiogenesis Inhibitors; 0 / Anticarcinogenic Agents; 0 / Carcinogens; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 4Z8R6ORS6L / Thalidomide; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene
61.
Stan SD, Singh SV, Brand RE:
Chemoprevention strategies for pancreatic cancer.
Nat Rev Gastroenterol Hepatol
; 2010 Jun;7(6):347-56
[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 low survival rate of patients with pancreatic cancer points towards an increased need for novel
therapeutic
and chemopreventive strategies and also early
detection
of this disease.
Some chemopreventive agents (for example, curcumin or resveratrol) have also been reported to sensitize pancreatic cancer cells to standard chemotherapeutic
drugs
(for example, gemcitabine or erlotinib), which suggests that chemopreventive agents could potentially be used as potentiators of standard
chemotherapy
.
Further development of pancreatic cancer chemopreventive agents may prove to be tremendously valuable for individuals at high risk of developing pancreatic cancer and patients who present
with premalignant lesions
.
[MeSH-minor]
Alkyl and Aryl Transferases /
therapeutic
use. Animals. Antineoplastic Agents / pharmacology. Antineoplastic Combined
Chemotherapy
Protocols /
therapeutic
use. Camellia sinensis. Celecoxib. Cell Transformation, Neoplastic / genetics. Curcumin / administration & dosage. Curcumin /
therapeutic
use. Cyclooxygenase 2 Inhibitors / pharmacology. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Deoxycytidine /
therapeutic
use. Disease Models, Animal. Down-Regulation /
drug
effects.
Drug
Synergism. Humans. Isothiocyanates /
therapeutic
use. Phototherapy. Pyrazoles /
therapeutic
use. Sulfonamides /
therapeutic
use. Tea. Vitamin D / analogs & derivatives. Vitamin E / administration & dosage. beta Carotene /
therapeutic
use
Genetic Alliance.
consumer health - Pancreatic cancer
.
MedlinePlus Health Information.
consumer health - Pancreatic Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
CELECOXIB
.
Hazardous Substances Data Bank.
CURCUMIN
.
Hazardous Substances Data Bank.
BETA-CAROTENE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Int J Cancer. 2006 Jun 1;118(11):2866-70
[
16385571.001
]
[Cites]
Genes Dev. 2006 May 15;20(10):1218-49
[
16702400.001
]
[Cites]
Cancer. 2006 Jun 1;106(11):2503-13
[
16628653.001
]
[Cites]
Crit Rev Oncol Hematol. 2006 Jun;58(3):231-41
[
16725343.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Sep;15(9):1688-95
[
16985031.001
]
[Cites]
Cancer Res. 2006 Oct 15;66(20):10213-9
[
17047087.001
]
[Cites]
Cancer Res. 2006 Nov 1;66(21):10553-9
[
17079479.001
]
[Cites]
Anticancer Res. 2006 Nov-Dec;26(6B):4423-30
[
17201164.001
]
[Cites]
J Pharmacol Exp Ther. 2007 Mar;320(3):1163-70
[
17138864.001
]
[Cites]
Ann N Y Acad Sci. 2006 Dec;1091:151-69
[
17341611.001
]
[Cites]
Cancer Res. 2007 Apr 15;67(8):3853-61
[
17440100.001
]
[Cites]
Gut. 2007 Aug;56(8):1134-52
[
17625148.001
]
[Cites]
Cancer Res. 2007 Aug 1;67(15):7068-71
[
17652141.001
]
[Cites]
Gut. 2007 Oct;56(10):1460-9
[
17872573.001
]
[Cites]
Cancer Invest. 2007 Sep;25(6):411-8
[
17882652.001
]
[Cites]
Am J Gastroenterol. 2007 Nov;102(11):2564-9
[
17958761.001
]
[Cites]
Eur J Cancer Prev. 2007 Dec;16(6):542-8
[
18090127.001
]
[Cites]
Best Pract Res Clin Gastroenterol. 2008;22(1):65-73
[
18206813.001
]
[Cites]
Biochem Pharmacol. 2008 Feb 15;75(4):787-809
[
17900536.001
]
[Cites]
Mol Cancer Ther. 2008 Mar;7(3):464-73
[
18347134.001
]
[Cites]
Am J Clin Oncol. 2008 Apr;31(2):157-62
[
18391600.001
]
[Cites]
J Surg Res. 2008 Jun 15;147(2):194-9
[
18498869.001
]
[Cites]
Mol Cancer Ther. 2008 Jun;7(6):1708-19
[
18566242.001
]
[Cites]
Tohoku J Exp Med. 2008 Jun;215(2):149-57
[
18577844.001
]
[Cites]
Ann Oncol. 2008 Jul;19(7):1224-30
[
18381371.001
]
[Cites]
Pancreas. 2008 Jul;37(1):25-30
[
18580440.001
]
[Cites]
Clin Cancer Res. 2008 Jul 15;14(14):4491-9
[
18628464.001
]
[Cites]
Pharm Res. 2008 Sep;25(9):2117-24
[
18427961.001
]
[Cites]
Mol Cancer. 2008;7:64
[
18652674.001
]
[Cites]
Nutr Cancer. 2008;60 Suppl 1:81-9
[
19003584.001
]
[Cites]
Apoptosis. 2008 Dec;13(12):1465-78
[
19002586.001
]
[Cites]
Biochem Pharmacol. 2008 Dec 1;76(11):1340-51
[
18755156.001
]
[Cites]
J Immunol. 2009 Jan 1;182(1):216-24
[
19109152.001
]
[Cites]
Am J Clin Nutr. 2009 Feb;89(2):584-91
[
19116326.001
]
[Cites]
Cancer Res. 2009 Feb 15;69(4):1439-47
[
19208842.001
]
[Cites]
Int J Cancer. 2009 Apr 15;124(8):1926-34
[
19107929.001
]
[Cites]
Cell Cycle. 2009 Jun 15;8(12):1860-4
[
19440048.001
]
[Cites]
Gut. 2009 Jul;58(7):949-63
[
18829980.001
]
[Cites]
Anticancer Drugs. 2009 Jul;20(6):444-9
[
19384191.001
]
[Cites]
Nat Rev Gastroenterol Hepatol. 2009 Jul;6(7):412-22
[
19506583.001
]
[Cites]
Pharm Res. 2009 Aug;26(8):1874-80
[
19421843.001
]
[Cites]
CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49
[
19474385.001
]
[Cites]
World J Gastroenterol. 2009 Jul 21;15(27):3349-54
[
19610135.001
]
[Cites]
Gastroenterology. 2009 Aug;137(2):482-8
[
19375425.001
]
[Cites]
Int J Oncol. 2009 Sep;35(3):593-9
[
19639179.001
]
[Cites]
Cancer Res. 2009 Aug 15;69(16):6539-45
[
19679549.001
]
[Cites]
Curr Opin Pharmacol. 2009 Aug;9(4):411-8
[
19589727.001
]
[Cites]
Carcinogenesis. 2009 Oct;30(10):1744-53
[
19549704.001
]
[Cites]
Cancer Cell. 2009 Nov 6;16(5):379-89
[
19878870.001
]
[Cites]
Adv Med Sci. 2009;54(2):136-42
[
19758972.001
]
[Cites]
Biochim Biophys Acta. 2010 Jan;1805(1):97-104
[
19853645.001
]
[Cites]
Int J Cancer. 2010 Jul 15;127(2):257-68
[
19908231.001
]
[Cites]
Nutr Cancer. 1999;35(1):80-6
[
10624710.001
]
[Cites]
J Surg Res. 2000 Jan;88(1):23-5
[
10644462.001
]
[Cites]
Anticancer Res. 2000 Jul-Aug;20(4):2625-31
[
10953335.001
]
[Cites]
Cancer Lett. 2000 Nov 28;160(2):141-7
[
11053643.001
]
[Cites]
Phytochemistry. 2001 Jan;56(1):5-51
[
11198818.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2001 Jan;10(1):53-8
[
11205489.001
]
[Cites]
Cancer. 2001 Jan 15;91(2):333-8
[
11180079.001
]
[Cites]
Gastroenterology. 2001 Apr;120(5):1263-70
[
11266389.001
]
[Cites]
Anticancer Res. 2001 Jul-Aug;21(4B):2895-900
[
11712783.001
]
[Cites]
Br J Cancer. 2002 Mar 4;86(5):680-5
[
11875725.001
]
[Cites]
Pancreatology. 2002;2(1):54-60
[
12120008.001
]
[Cites]
Pancreatology. 2001;1(5):416-22
[
12120218.001
]
[Cites]
Pancreas. 2002 Jul;25(1):45-8
[
12131770.001
]
[Cites]
J Natl Cancer Inst. 2002 Aug 7;94(15):1168-71
[
12165642.001
]
[Cites]
Pancreas. 2002 Nov;25(4):e71-6
[
12409844.001
]
[Cites]
Nat Rev Cancer. 2002 Dec;2(12):897-909
[
12459728.001
]
[Cites]
Clin Cancer Res. 2003 Jan;9(1):346-54
[
12538487.001
]
[Cites]
Cancer Detect Prev. 2003;27(2):87-93
[
12670518.001
]
[Cites]
Int J Cancer. 2003 Jul 20;105(6):735-46
[
12767057.001
]
[Cites]
Gastroenterology. 2003 Sep;125(3):891-905
[
12949733.001
]
[Cites]
Clin Cancer Res. 2003 Aug 15;9(9):3312-9
[
12960117.001
]
[Cites]
Dig Dis Sci. 2003 Oct;48(10):1972-8
[
14627343.001
]
[Cites]
J Natl Cancer Inst. 2004 Jan 7;96(1):22-8
[
14709735.001
]
[Cites]
Cancer Res. 2004 Mar 15;64(6):2030-8
[
15026340.001
]
[Cites]
Pancreas. 2004 May;28(4):e90-5
[
15097869.001
]
[Cites]
Clin Cancer Res. 2004 Apr 15;10(8):2846-50
[
15102693.001
]
[Cites]
Mol Cancer. 2003 Jan 7;2:10
[
12575899.001
]
[Cites]
Carcinogenesis. 2004 Sep;25(9):1701-9
[
15117814.001
]
[Cites]
Clin Cancer Res. 2004 Oct 15;10(20):6847-54
[
15501961.001
]
[Cites]
Scand J Gastroenterol. 2004 Sep;39(9):882-5
[
15513387.001
]
[Cites]
J Chronic Dis. 1983;36(3):251-6
[
6826689.001
]
[Cites]
J Natl Cancer Inst. 1986 Jan;76(1):49-60
[
3455742.001
]
[Cites]
Br J Cancer. 1986 Oct;54(4):677-83
[
3778808.001
]
[Cites]
Carcinogenesis. 1990 Mar;11(3):393-5
[
2311181.001
]
[Cites]
Carcinogenesis. 1991 Nov;12(11):2157-61
[
1934304.001
]
[Cites]
J Clin Invest. 1992 Oct;90(4):1352-60
[
1401070.001
]
[Cites]
Jpn J Clin Oncol. 1992 Aug;22(4):286-91
[
1434027.001
]
[Cites]
Int J Cancer. 1993 Feb 20;53(4):601-7
[
8436433.001
]
[Cites]
Indian J Physiol Pharmacol. 1992 Oct;36(4):273-5
[
1291482.001
]
[Cites]
Am J Pathol. 1993 Aug;143(2):545-54
[
8342602.001
]
[Cites]
Int J Cancer. 1994 Jul 1;58(1):46-9
[
8014014.001
]
[Cites]
Cancer Res. 1994 Nov 15;54(22):5775-8
[
7954397.001
]
[Cites]
J Cell Biochem Suppl. 1994;20:282-99
[
7616751.001
]
[Cites]
Cancer Lett. 1995 Sep 4;96(1):15-21
[
7553603.001
]
[Cites]
Carcinogenesis. 1996 Jun;17(6):1381-4
[
8681460.001
]
[Cites]
Int J Cancer. 1997 Jan 27;70(3):255-8
[
9033623.001
]
[Cites]
Lipids. 1997 Feb;32(2):151-6
[
9075204.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1997 Apr;6(4):267-82
[
9107432.001
]
[Cites]
Cancer Res. 1997 Jun 1;57(11):2140-3
[
9187111.001
]
[Cites]
J Clin Oncol. 1997 Jun;15(6):2403-13
[
9196156.001
]
[Cites]
Pancreas. 1997 Aug;15(2):109-12
[
9260194.001
]
[Cites]
Carcinogenesis. 1997 Aug;18(8):1655-8
[
9276644.001
]
[Cites]
Br J Cancer. 1997;76(7):884-9
[
9328147.001
]
[Cites]
Br J Cancer. 1997;76(8):1017-20
[
9376260.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1997 Dec;6(12):1081-6
[
9419407.001
]
[Cites]
Pancreas. 1998 Jan;16(1):13-8
[
9436857.001
]
[Cites]
Clin Cancer Res. 1999 Jan;5(1):119-27
[
9918209.001
]
[Cites]
Cancer Res. 1999 Mar 1;59(5):987-90
[
10070951.001
]
[Cites]
Cancer. 1999 Jul 1;86(1):37-42
[
10391561.001
]
[Cites]
Cancer Res. 1999 Sep 1;59(17):4356-62
[
10485483.001
]
[Cites]
Cancer. 2005 Sep 15;104(6):1322-31
[
16092118.001
]
[Cites]
J Natl Cancer Inst. 2005 Oct 5;97(19):1458-65
[
16204695.001
]
[Cites]
Int J Cancer. 2006 Apr 15;118(8):1930-6
[
16284950.001
]
[Cites]
Biomed Pharmacother. 2005 Oct;59 Suppl 2:S276-80
[
16507392.001
]
(PMID = 20440279.001).
[ISSN]
1759-5053
[Journal-full-title]
Nature reviews. Gastroenterology & hepatology
[ISO-abbreviation]
Nat Rev Gastroenterol Hepatol
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA101753; United States / NCI NIH HHS / CA / R01 CA101753-07; United States / NCI NIH HHS / CA / R01CA101753
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Isothiocyanates; 0 / Pyrazoles; 0 / Sulfonamides; 0 / Tea; 01YAE03M7J / beta Carotene; 0W860991D6 / Deoxycytidine; 1406-16-2 / Vitamin D; 1406-18-4 / Vitamin E; B76N6SBZ8R / gemcitabine; EC 2.5.- / Alkyl and Aryl Transferases; IT942ZTH98 / Curcumin; JCX84Q7J1L / Celecoxib
[Number-of-references]
118
[Other-IDs]
NLM/ NIHMS228764; NLM/ PMC2927967
62.
Zhang X, Chen ZG, Khuri FR, Shin DM:
Induction of cell cycle arrest and apoptosis by a combined treatment with 13-cis-retinoic acid, interferon-alpha2a, and alpha-tocopherol in squamous cell carcinoma of the head and neck.
Head Neck
; 2007 Apr;29(4):351-61
[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]
Induction of cell cycle arrest and apoptosis by a combined
treatment with
13-cis-retinoic acid, interferon-alpha2a, and alpha-tocopherol in squamous cell carcinoma of the head and neck.
BACKGROUND: We have previously conducted phase II trials with a combination of 13-cis-retinoic acid (13-cRA), interferon-alpha2a (IFN-alpha2a), and alpha-tocopherol (alpha-TF) in patients with advanced oral
premalignant lesions
and locally advanced head and neck cancer in the adjuvant settings and achieved promising outcomes.
The present study was conducted in vitro to elucidate the mechanisms of anti-tumor activity of this 3-
drug
combination in squamous cell carcinoma of the head and neck (SCCHN).
METHODS: Five SCCHN cell lines were treated with 13-cRA, IFN-alpha2a, and alpha-TF as single agents or 2- to 3-
drug
combinations for 72 hours.
Inhibition of cell growth and cell cycle progression and induction of apoptosis by the
treatments
were evaluated.
RESULTS: Our results demonstrated that although each single-agent and 2-
drug
combination showed a certain level of cell growth inhibition, the 3-
drug
combination apparently further inhibited cell growth in comparison to any single agents and 2-
drug
combinations in the 5 SCCHN cell lines.
Cell cycle analysis on Tu212 and 886LN cells by flow cytometry exhibited significant accumulation of the cells at S phase in the 3-
drug
combination.
On the other hand, Annexin-V binding assay demonstrated that the 3-
drug
combination induced more profound apoptosis than any of the single agents or 2-
drug
combinations.
In parallel, proteolytic cleavages of pro-caspase-8, -9, -3 and poly (ADP ribose) polymerase as well as caspase-3 activity induced by the 3-
drug
treatment
were observed.
CONCLUSIONS: Our data suggests that 3-
drug
combination biochemopreventive regimen has cooperative inhibitory effect on the growth of SCCHN cells.
Both cell cycle arrest and apoptosis contribute to cell growth inhibition of this 3-
drug
combination
therapy
.
[MeSH-major]
Apoptosis /
drug
effects. Carcinoma, Squamous Cell / pathology. Cell Cycle /
drug
effects. Interferon-alpha / pharmacology. Isotretinoin / pharmacology. Otorhinolaryngologic Neoplasms / pathology. alpha-Tocopherol / pharmacology
[MeSH-minor]
Caspase 3 / analysis. Cell Line, Tumor. Cell Proliferation /
drug
effects. Chemoprevention.
Drug Therapy
, Combination. Humans. Recombinant Proteins
Genetic Alliance.
consumer health - Carcinoma, Squamous Cell
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
13-CIS-RETINOIC ACID
.
Hazardous Substances Data Bank.
VITAMIN E
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
(c) 2006 Wiley Periodicals, Inc.
(PMID = 17163463.001).
[ISSN]
1043-3074
[Journal-full-title]
Head & neck
[ISO-abbreviation]
Head Neck
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA101244; United States / NCI NIH HHS / CA / CA75603
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Interferon-alpha; 0 / Recombinant Proteins; 76543-88-9 / interferon alfa-2a; EC 3.4.22.- / Caspase 3; EH28UP18IF / Isotretinoin; H4N855PNZ1 / alpha-Tocopherol
63.
Papadimitrakopoulou VA, William WN Jr, Dannenberg AJ, Lippman SM, Lee JJ, Ondrey FG, Peterson DE, Feng L, Atwell A, El-Naggar AK, Nathan CO, Helman JI, Du B, Yueh B, Boyle JO:
Pilot randomized phase II study of celecoxib in oral premalignant lesions.
Clin Cancer Res
; 2008 Apr 1;14(7):2095-101
[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]
Pilot randomized phase II study of celecoxib in oral
premalignant lesions
.
In this pilot randomized phase II study, we evaluated the efficacy and safety of the COX-2 inhibitor celecoxib in patients with oral
premalignant lesions
(OPL).
[MeSH-major]
Anti-Inflammatory Agents, Non-Steroidal /
therapeutic
use. Cyclooxygenase 2 Inhibitors /
therapeutic
use. Mouth Neoplasms / prevention & control. Precancerous Conditions /
drug therapy
. Pyrazoles /
therapeutic
use. Sulfonamides /
therapeutic
use
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Celecoxib. Cyclooxygenase 2 / biosynthesis. Female. Humans. Hyperplasia /
drug therapy
. Male. Middle Aged. Pilot Projects. Placebos. Polymerase Chain Reaction. RNA, Messenger / analysis
MedlinePlus Health Information.
consumer health - Oral Cancer
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
Hazardous Substances Data Bank.
CELECOXIB
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18381950.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Placebos; 0 / Pyrazoles; 0 / RNA, Messenger; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib
64.
Lerner SP, Grossman HB, Messing EM, Kibel AS, Stephenson A, Gee JR, O'Donnell MA, Reid RD, Kamat AM, Parnes HL, House MG:
BCAN Think Tank session 3: Prevention of bladder cancer.
Urol Oncol
; 2010 May-Jun;28(3):338-42
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Experts sought to define primary, secondary, and tertiary prevention and discussed clinical trials performed to date testing retinoids, difluoromethylornithine, celecoxib, and other oral agents in a tertiary prevention setting following transurethral resection with or without intravesical
therapy
.
Urologists practice tertiary prevention in the form of intravesical
therapy
, and strategies were discussed to identify biomarkers, including urinary cytokines and pathway single nucleotide polymorphism analysis associated with response to
treatment
.
Optimizing delivery of intravesical
chemotherapy
to the target
tissue with
simple
pharmacologic
manipulations or packaging
drugs
in nanoparticles may improve
treatment
outcome.
Defining a
premalignant
lesion
should be a focus of future research as a strategy for early
detection
and secondary prevention.
Genetic Alliance.
consumer health - Bladder cancer
.
MedlinePlus Health Information.
consumer health - Bladder Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright (c) 2010 Elsevier Inc. All rights reserved.
(PMID = 20439034.001).
[ISSN]
1873-2496
[Journal-full-title]
Urologic oncology
[ISO-abbreviation]
Urol. Oncol.
[Language]
eng
[Publication-type]
Congresses
[Publication-country]
United States
65.
Draudin-Krylenko VA, Petukhov AB, Kuvshinov IuP, Levchuk AA, Bukin IuV:
[Effect of antioxidant use in dietary therapy in patients with chronic athrofic hastritis].
Vopr Pitan
; 2006;75(5):53-5
[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]
[Effect of antioxidant use in dietary
therapy
in patients with chronic athrofic hastritis].
In the 1-year double-blind placebo-controlled intervention trial, it was shown that daily supplementation of patients with gastric
premalignant lesions
(intestinal metaplasia, IM) with a complex, containing Ester-C with antioxidantsand (2100 mg of Ca-ascorbate + 340 mg of bioflavonoids), produced a sharp decrease of abnormally high ornithine decarboxylase activity in IM gastric mucosa that was accom panied by practically total IM regression in 11 of 18 (61%) patients.
[MeSH-major]
Antioxidants / administration & dosage. Ascorbic Acid / administration & dosage. Gastritis, Atrophic / diet
therapy
. Gastritis, Atrophic /
drug therapy
. Helicobacter Infections / diet
therapy
. Helicobacter Infections /
drug therapy
[MeSH-minor]
Adult. Aged. Chronic Disease. Double-Blind Method. Female. Gastric Mucosa / enzymology. Gastric Mucosa / microbiology. Gastric Mucosa / pathology. Humans. Intestines / enzymology. Intestines / pathology. Male. Metaplasia / diet
therapy
. Metaplasia /
drug therapy
. Metaplasia / enzymology. Metaplasia / pathology. Middle Aged. Ornithine Decarboxylase / metabolism
MedlinePlus Health Information.
consumer health - Antioxidants
.
MedlinePlus Health Information.
consumer health - Helicobacter Pylori Infections
.
MedlinePlus Health Information.
consumer health - Vitamin C
.
Hazardous Substances Data Bank.
Sodium ascorbate
.
Hazardous Substances Data Bank.
L-Ascorbic Acid
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17172172.001).
[ISSN]
0042-8833
[Journal-full-title]
Voprosy pitaniia
[ISO-abbreviation]
Vopr Pitan
[Language]
rus
[Publication-type]
Comparative Study; English Abstract; Journal Article; Randomized Controlled Trial
[Publication-country]
Russia (Federation)
[Chemical-registry-number]
0 / Antioxidants; EC 4.1.1.17 / Ornithine Decarboxylase; PQ6CK8PD0R / Ascorbic Acid
66.
Zöller JE, Scheer M:
[Current status and prospects of chemoprevention in oral squamous epithelial carcinomas and precancerous lesions].
Mund Kiefer Gesichtschir
; 2000 May;4 Suppl 1:S160-8
[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]
[Current status and prospects of chemoprevention in oral squamous epithelial carcinomas and precancerous
lesions
].
Second primary tumors in initially cured patients remain the greatest challenge in
therapy
for oral squamous cell carcinomas.
The second group included 24 patients
with premalignant lesions
after R0-resection of primary oral squamous cell carcinoma.
Biopsies were taken from both groups prior to
therapy
and after 12 weeks follow-up.
These results indicate that the chosen combination has substantial activity in oral
premalignant lesions
.
[MeSH-major]
Anticarcinogenic Agents /
therapeutic
use. Carcinoma, Squamous Cell / prevention & control. Mouth Neoplasms / prevention & control. Neoplasms, Second Primary / prevention & control. Precancerous Conditions /
drug therapy
[MeSH-minor]
Cell Transformation, Neoplastic /
drug
effects. Humans. Leukoplakia, Oral /
drug therapy
MedlinePlus Health Information.
consumer health - Oral Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 10938656.001).
[ISSN]
1432-9417
[Journal-full-title]
Mund-, Kiefer- und Gesichtschirurgie : MKG
[ISO-abbreviation]
Mund Kiefer Gesichtschir
[Language]
ger
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Anticarcinogenic Agents
[Number-of-references]
57
67.
Roth JA, Grammer SF:
Gene replacement therapy for non-small cell lung cancer: a review.
Hematol Oncol Clin North Am
; 2004 Feb;18(1):215-29
[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]
Gene replacement
therapy
for non-small cell lung cancer: a review.
Current
therapy
such as radiation and
chemotherapy
controls less than 50% of lung cancers, summoning the development of novel
therapeutic
strategies that can directly target the underlying mechanisms of tumorigenesis.
The clinical trials summarized in this article clearly demonstrate that contrary to initial predictions that gene
therapy
would not be suitable for cancer, gene replacement
therapy
is a viable potential addition to the arsenal for cancer.
Clinical trials have demonstrated that direct intratumor injection can cause tumor regression or prolonged stabilization of local disease, and the low toxicity associated with gene transfer indicates that tumor suppressor gene replacement can be readily combined with existing and future
treatments
.
Initial concerns that the wide diversity of genetic
lesions
in cancer cells would prevent the application of gene
therapy
to cancer appear unfounded; on the contrary, correction of a single genetic
lesion
has resulted in significant tumor regression.
Studies combining transfer of tumor suppressor genes with conventional DNA-damaging
treatments
indicate that correction of a defect in apoptosis induction can restore sensitivity to radiation and
chemotherapy
in some resistant tumors, and indications that sensitivity to killing might be enhanced in already sensitive tumors may eventually lead to reduced toxicity from
chemotherapy
and radiation
therapy
.
The most recent data from the laboratory demonstrating damage to tumor suppressor genes in normal
tissue
and
premalignant lesions
even suggest that these genes may someday be useful in early intervention, diagnosis, and even prevention of cancer.
At the current rate of biotechnology development, it is only a matter of
time
until technical limitations that currently prevent the widespread application of gene
therapy
to cancer are overcome by development of more efficient vectors, discovery of novel genes, and development of combined modality approaches.
[MeSH-major]
Carcinoma, Non-Small-Cell Lung /
therapy
. Genetic
Therapy
. Lung Neoplasms /
therapy
[MeSH-minor]
Clinical Trials as Topic. Combined Modality
Therapy
. Gene Transfer Techniques. Genes, p53 / physiology. Genetic Vectors. Humans
Genetic Alliance.
consumer health - Lung Cancer
.
Genetic Alliance.
consumer health - Non-small cell lung cancer
.
MedlinePlus Health Information.
consumer health - Genes and Gene Therapy
.
MedlinePlus Health Information.
consumer health - Lung Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15005290.001).
[ISSN]
0889-8588
[Journal-full-title]
Hematology/oncology clinics of North America
[ISO-abbreviation]
Hematol. Oncol. Clin. North Am.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / 2P50-CA70970-04; United States / NCI NIH HHS / CA / P01 CA7877-01A1
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
[Publication-country]
United States
[Number-of-references]
74
68.
Howell A, Bundred NJ, Cuzick J, Allred DC, Clarke R:
Response and resistance to the endocrine prevention of breast cancer.
Adv Exp Med Biol
; 2008;617:201-11
[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.
Ovarian suppression is thought to give lifelong protection and recent data indicate that the effectiveness of Tam continues after cessation of
treatment
at 5-8 years.
The question arises whether the information we have concerning the responsiveness of ERalpha+ cells in TDLU,
premalignant lesions
, and invasive cancers give an indication of the targets for endocrine prevention.
The data also suggest that ERalpha+ DCIS is responsive to estrogen and ED supporting
premalignant lesions
is a target as does the data from the NSABP P1 trial indicating a marked preventive effect of Tam in women previously diagnosed with atypical ductal hyperplasia and a preventative effect on CIS.
[MeSH-major]
Breast Neoplasms / prevention & control.
Drug
Resistance, Neoplasm. Hormone Replacement
Therapy
Genetic Alliance.
consumer health - Breast Cancer
.
MedlinePlus Health Information.
consumer health - Breast Cancer
.
MedlinePlus Health Information.
consumer health - Hormone Replacement Therapy
.
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 = 18497044.001).
[ISSN]
0065-2598
[Journal-full-title]
Advances in experimental medicine and biology
[ISO-abbreviation]
Adv. Exp. Med. Biol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
63
69.
Hadjiiski L, Mukherji SK, Gujar SK, Sahiner B, Ibrahim M, Street E, Moyer J, Worden FP, Chan HP:
Treatment response assessment of head and neck cancers on CT using computerized volume analysis.
AJNR Am J Neuroradiol
; 2010 Oct;31(9):1744-51
[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]
Treatment
response assessment of head and neck cancers on CT using computerized volume analysis.
Our aim was to evaluate the potential usefulness of a computerized system for segmenting
lesions
in head and neck CT scans and for estimation of volume change of head and neck
malignant
tumors in response to
treatment
.
MATERIALS AND METHODS: CT scans from a pretreatment examination and a post 1-cycle
chemotherapy
examination of 34 patients with 34 head and neck primary-site cancers were collected.
The computerized system was
developed
in our laboratory.
It performs 3D segmentation on the basis of a level-set model and uses as input an approximate bounding box for the
lesion
of interest.
As a reference standard, 1 radiologist outlined full 3D contours for each of the 34 primary tumors for both the
pre
- and posttreatment scans and a second radiologist verified the contours.
RESULTS: The correlation between the automatic and manual estimates for both the
pre
- to post-
treatment
volume change and the percentage volume change for the 34 primary-site tumors was 0.95, with an average error of -2.4 ± 8.5% by automatic segmentation.
There was no substantial difference and specific trend in the automatic segmentation accuracy for the different
types
of primary head and neck tumors, indicating that the computerized segmentation performs relatively robustly for this application.
CONCLUSIONS: The tumor size change in response to
treatment
can be accurately estimated by the computerized segmentation system relative to radiologists' manual estimations for different
types
of head and neck tumors.
[MeSH-major]
Antineoplastic Agents /
therapeutic
use. Head and Neck Neoplasms /
drug therapy
. Head and Neck Neoplasms / radiography. Imaging, Three-Dimensional / methods. Radiographic Image Interpretation, Computer-Assisted / methods.
Tomography
, X-Ray Computed / methods
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Prognosis. Reproducibility of Results. Sensitivity and Specificity.
Treatment
Outcome
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
MedlinePlus Health Information.
consumer health - CT Scans
.
MedlinePlus Health Information.
consumer health - Head and Neck Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Natl Cancer Inst. 2000 Feb 2;92(3):205-16
[
10655437.001
]
[Cites]
AJR Am J Roentgenol. 2010 Apr;194(4):1083-9
[
20308515.001
]
[Cites]
Lancet. 2000 Mar 18;355(9208):949-55
[
10768432.001
]
[Cites]
J Clin Oncol. 2003 Jan 1;21(1):92-8
[
12506176.001
]
[Cites]
N Engl J Med. 2003 Nov 27;349(22):2091-8
[
14645636.001
]
[Cites]
Br J Cancer. 2004 Jun 14;90(12):2256-60
[
15150551.001
]
[Cites]
Lancet. 1986 Feb 8;1(8476):307-10
[
2868172.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1990 Aug;19(2):485-90
[
2394626.001
]
[Cites]
N Engl J Med. 1991 Jun 13;324(24):1685-90
[
2034244.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1995 Sep 30;33(2):281-7
[
7673015.001
]
[Cites]
J Natl Cancer Inst. 1996 Jul 3;88(13):890-9
[
8656441.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1997 Mar 15;37(5):1011-21
[
9169807.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1997 Oct 1;39(3):711-9
[
9336154.001
]
[Cites]
J Clin Oncol. 1999 Feb;17(2):631-7
[
10080608.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1999 Jul 1;44(4):755-65
[
10386632.001
]
[Cites]
J Clin Oncol. 2005 Jan 1;23(1):88-95
[
15625363.001
]
[Cites]
Cancer. 2005 Jun 15;103(12):2616-22
[
15887218.001
]
[Cites]
Curr Opin Oncol. 2007 May;19(3):188-94
[
17414635.001
]
[Cites]
Med Phys. 2007 Nov;34(11):4399-408
[
18072505.001
]
[Cites]
Psychol Bull. 1979 Mar;86(2):420-8
[
18839484.001
]
[Cites]
J Clin Oncol. 2000 Apr;18(7):1458-64
[
10735893.001
]
(PMID = 20595363.001).
[ISSN]
1936-959X
[Journal-full-title]
AJNR. American journal of neuroradiology
[ISO-abbreviation]
AJNR Am J Neuroradiol
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA093517
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents
[Other-IDs]
NLM/ NIHMS495353; NLM/ PMC3767432
70.
de Jong JS, van Ginkel RJ, Slart RH, Lemstra CL, Paans AM, Mulder NH, Hoekstra HJ:
FDG-PET probe-guided surgery for recurrent retroperitoneal testicular tumor recurrences.
Eur J Surg Oncol
; 2010 Nov;36(11):1092-5
[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.
METHODS: Three patients with resectable 2nd or 3rd recurrent testicular cancer based on elevated tumor markers after previous various
chemotherapy
schedules and resections of residual retroperitoneal tumor masses were included in this study.
RESULTS: All patients showed extended adhesions and scar
tissue
in the retroperitoneal area due to the previous surgeries.
Pre
-operative PET/CT scan showed a good correlation with intra-operative PET probe-guided
detection
of recurrent
lesions
.
There was a high target to background ratio (TGB) of 5:1 during the
procedure
.
In one patient, a 2 cm large
lesion
, which did not show on
pre
-operative FDG-PET scan, was detected with the PET probe.
Histopathologic
tissue
evaluation demonstrated recurrent vital tumor in all PET probe positive
lesions
.
CONCLUSIONS: PET probe-guided surgery seems to be a promising tool to localize FDG-PET positive
lesion
in recurrent testicular cancer in hardly accessible surgical locations.
PET probe-guided surgery might be a useful technique in surgical oncology for recurrent testicular cancer and has the potential to be applied in surgery of other
malignant
diseases.
[MeSH-major]
Dysgerminoma / secondary. Dysgerminoma / surgery. Fluorodeoxyglucose F18. Positron-Emission
Tomography
. Retroperitoneal Neoplasms / secondary. Retroperitoneal Neoplasms / surgery. Testicular Neoplasms / pathology. Testicular Neoplasms / surgery.
Tomography
, X-Ray Computed
[MeSH-minor]
Adult. Gamma Rays. Humans. Male. Predictive Value of Tests. Radiopharmaceuticals.
Time
Factors
MedlinePlus Health Information.
consumer health - CT Scans
.
MedlinePlus Health Information.
consumer health - Testicular Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright © 2010 Elsevier Ltd. All rights reserved.
(PMID = 20828977.001).
[ISSN]
1532-2157
[Journal-full-title]
European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
[ISO-abbreviation]
Eur J Surg Oncol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
71.
Liao Z, Komaki R, Mason KA, Milas L:
Role of cyclooxygenase-2 inhibitors in combination with radiation therapy in lung cancer.
Clin Lung Cancer
; 2003 May;4(6):356-65
[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.
[Title]
Role of cyclooxygenase-2 inhibitors in combination with radiation
therapy
in lung cancer.
The enzyme is often overexpressed in
premalignant lesions
and cancer of the lung.
Clinical trials of the combination of selective COX-2 inhibitors with radiation
therapy
,
chemotherapy
, or both in patients with lung cancer have been initiated and some preliminary results are available.
In this review, we describe the relationship between overexpression of COX-2 and lung cancer, the antitumor effect of selective COX-2 inhibitors, discuss the rationale for using selective COX-2 inhibitors combined with radiation
therapy
and
chemotherapy
, and summarize current clinical protocols and initial findings.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 14599301.001).
[ISSN]
1525-7304
[Journal-full-title]
Clinical lung cancer
[ISO-abbreviation]
Clin Lung Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
72.
Lu X, Arbiser JL, West J, Hoedt-Miller M, Sheridan A, Govindarajan B, Harral JW, Rodman DM, Fouty B:
Tumor necrosis factor-related apoptosis-inducing ligand can induce apoptosis in subsets of premalignant cells.
Am J Pathol
; 2004 Nov;165(5):1613-20
[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]
Tumor necrosis factor-related apoptosis-inducing ligand can induce apoptosis in subsets of
premalignant
cells.
During the transformation from a normal to a
malignant
cell, several mutations are required to bypass the pathways responsible for controlling proliferation.
Premalignant
cells have acquired some, but not all of these mutations and consequently have not yet attained a
malignant
phenotype characterized by tumor formation in vivo.
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis in
malignant
cells while sparing normal ones and is currently being considered as adjuvant
therapy
for various human malignancies.
Whether TRAIL is effective in inducing apoptosis in
premalignant
cells is unclear, however.
We studied the effect of TRAIL on two human
premalignant
cell lines the SV7tert and HA1E cells.
Both cell lines had been immortalized by the addition of simian virus 40 large T antigen and the telomerase subunit hTERT, but had not been transformed into
malignant
cells.
These results suggest that TRAIL can induce apoptosis in
premalignant
cells and suggests a novel
therapy
for the
treatment
of
premalignant lesions
in vivo.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
CYCLOHEXIMIDE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Nat Cell Biol. 2000 Apr;2(4):241-3
[
10783243.001
]
[Cites]
Lung Cancer. 2000 Jul;29(1):11-22
[
10880843.001
]
[Cites]
Curr Opin Cell Biol. 2000 Dec;12(6):705-9
[
11063935.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12776-81
[
11070089.001
]
[Cites]
Am J Pathol. 2000 Dec;157(6):1937-45
[
11106566.001
]
[Cites]
Leukemia. 2001 Jul;15(7):1022-32
[
11455969.001
]
[Cites]
Am J Pathol. 2001 Aug;159(2):483-91
[
11485907.001
]
[Cites]
J Invest Dermatol. 2001 Aug;117(2):360-4
[
11511316.001
]
[Cites]
Oncogene. 2001 Sep 20;20(42):6073-83
[
11593415.001
]
[Cites]
Cancer Res. 2001 Dec 15;61(24):8838-44
[
11751406.001
]
[Cites]
Neoplasia. 2001 Nov-Dec;3(6):535-46
[
11774036.001
]
[Cites]
Cancer Metastasis Rev. 2001;20(1-2):51-6
[
11831647.001
]
[Cites]
Mol Cell Biol. 2002 Apr;22(7):2111-23
[
11884599.001
]
[Cites]
Nat Rev Cancer. 2001 Nov;1(2):142-50
[
11905805.001
]
[Cites]
Oncogene. 2002 Jul 4;21(29):4577-86
[
12085236.001
]
[Cites]
J Mol Diagn. 2003 May;5(2):103-12
[
12707375.001
]
[Cites]
Lung Cancer. 2003 Aug;41 Suppl 1:S29-42
[
12867060.001
]
[Cites]
Lung Cancer. 2003 Aug;41 Suppl 1:S147-54
[
12867073.001
]
[Cites]
Cancer Res. 1995 Nov 1;55(21):5049-53
[
7585550.001
]
[Cites]
Annu Rev Biochem. 1996;65:337-65
[
8811183.001
]
[Cites]
Nature. 1997 Jul 10;388(6638):190-5
[
9217161.001
]
[Cites]
Int J Cancer. 1998 Feb 20;79(1):66-70
[
9495361.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14723-8
[
9843956.001
]
[Cites]
Int J Cancer. 1999 Jun 11;81(6):845-50
[
10362127.001
]
[Cites]
Nature. 1999 Jul 29;400(6743):464-8
[
10440377.001
]
[Cites]
Nat Med. 1999 Oct;5(10):1164-70
[
10502820.001
]
(PMID = 15509531.001).
[ISSN]
0002-9440
[Journal-full-title]
The American journal of pathology
[ISO-abbreviation]
Am. J. Pathol.
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HL / P01 HL014985; United States / NHLBI NIH HHS / HL / HL48038-09; United States / NHLBI NIH HHS / HL / P01 HL14985-29; United States / NHLBI NIH HHS / HL / R01 HL57282-03
[Publication-type]
Journal Article; 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.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Polyomavirus Transforming; 0 / Apoptosis Regulatory Proteins; 0 / DNA-Binding Proteins; 0 / Membrane Glycoproteins; 0 / Protein Synthesis Inhibitors; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 98600C0908 / Cycloheximide; EC 2.7.7.49 / Telomerase; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
[Other-IDs]
NLM/ PMC1618658
73.
Klass CM, Shin DM:
Current status and future perspectives of chemoprevention in head and neck cancer.
Curr Cancer Drug Targets
; 2007 Nov;7(7):623-32
[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 five-year survival rate for patients with SCCHN in the United States and other
developed
countries is still poor, approximately 40%, and even those patients who do not experience recurrence of the original cancer, have a high risk of developing a second primary malignancy.
Ever since the last two decades have seen the rise and fall of the results of clinical trials using carotinoids and retinoids as chemopreventive agents, new
treatment
strategies are needed.
Selective and nonselective COX-1/2 inhibitors and EGFR tyrosine kinase inhibitors have shown promising results in cancer
therapy
and are currently evaluated in chemoprevention trials.
However, associated high costs and side effects make these less attractive to patients
with premalignant lesions
.
Since
premalignant lesions
of the oral cavity are easily accessible for topical
treatments
, it remains to be seen if there is a role for topical
treatments
.
Current clinical trials using these novel agents for prevention of second primary tumors or
treatment
of
premalignant lesions
will further elucidate which agents should be used but also will help to establish the role of chemoprevention in head and neck cancer.
[MeSH-major]
Antineoplastic Agents /
therapeutic
use. Carcinoma, Squamous Cell / prevention & control.
Drugs
, Investigational /
therapeutic
use. Head and Neck Neoplasms / prevention & control
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
MedlinePlus Health Information.
consumer health - Head and Neck Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18045067.001).
[ISSN]
1873-5576
[Journal-full-title]
Current cancer drug targets
[ISO-abbreviation]
Curr Cancer Drug Targets
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA112643; United States / NCI NIH HHS / CA / U01 CA101244
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Drugs, Investigational
[Number-of-references]
181
74.
Kouwenhoven ST, Liefers GJ, van Erkel AR:
The pre-operative stratification of patients with colorectal liver metastases: computed tomography arterial portography (CTAP) has no added value.
Eur J Surg Oncol
; 2010 Jan;36(1):36-42
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The
pre
-operative stratification of patients with colorectal liver metastases: computed
tomography
arterial portography (CTAP) has no added value.
AIMS: The purpose of this study was to determine if Computed
Tomography
Arterial Portography (CTAP) has additional value to Contrast Enhanced helical CT (CE-CT) in selecting patients for hepatic surgery or Isolated Hepatic Perfusion/systemic
chemotherapy
.
All CT's were performed in the normal
pre
-operative work-up of patients with liver metastases in our regular clinical setting and reviewed blinded by a radiologist.
For CE-CT and CTAP the number, size (largest diameter) and location of all suspected
malignant
liver
lesions
were recorded.
The favourable
treatment
option was determined based on the results of CE-CT and CTAP independently.
The
therapeutic decision
based on CE-CT and CTAP was compared with the definite
treatment
.
For all patients with recorded findings during surgery, consisting of intra-operative ultrasound, liver palpation and histology a standard of reference for
lesion
detection
was available.
For these patients
detection
rates and the fraction of false positive
lesions
were calculated.
Fourteen patients were treated
with chemotherapy
, 4 with Isolated Hepatic Perfusion (IHP) and 10 with systemic
therapy
.
Based on the findings on CTAP, surgery should be the
treatment
of choice in 29 patients and 12 patients were classified non-surgical.
CONCLUSION: Despite a significantly higher
detection
rate for hepatic metastases, CTAP has no added value in the
therapeutic
stratification in candidates for resection of hepatic metastases of colorectal cancer.
[MeSH-major]
Colorectal Neoplasms / pathology. Liver Neoplasms / radiography. Liver Neoplasms / secondary. Portography.
Tomography
, Spiral Computed.
Tomography
, X-Ray Computed
[MeSH-minor]
Adult. Aged. Aged, 80 and over.
Chemotherapy
, Cancer, Regional Perfusion. Contrast Media. False Positive Reactions. Female. Hepatectomy. Humans. Male. Middle Aged
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - CT Scans
.
MedlinePlus Health Information.
consumer health - Liver Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright (c) 2009 Elsevier Ltd. All rights reserved.
(PMID = 19556096.001).
[ISSN]
1532-2157
[Journal-full-title]
European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
[ISO-abbreviation]
Eur J Surg Oncol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Contrast Media
75.
Liao Z, Mason KA, Milas L:
Cyclo-oxygenase-2 and its inhibition in cancer: is there a role?
Drugs
; 2007;67(6):821-45
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Despite recent improvements in
chemotherapy
and radiation
therapy
in cancer management with the addition of biological agents, novel
treatment
approaches are needed to further benefit patients.
The enzyme is commonly expressed in both
premalignant lesions
and
malignant
tumours of different
types
.
A growing body of evidence suggests an association of COX-2 with tumour development, aggressive biological tumour behaviour, resistance to standard cancer
treatment
, and adverse patient outcome.
Clinical trials of the combination of selective COX-2 inhibitors with radiotherapy,
chemotherapy
or both in patients with a number of cancers have been initiated, and preliminary results are encouraging.
This review discusses the role of COX-2, its products (prostaglandins) and its inhibitors in tumour growth and
treatment
.
[MeSH-major]
Antineoplastic Agents / pharmacology. Cyclooxygenase 2 / physiology. Cyclooxygenase 2 Inhibitors / pharmacology. Neoplasms /
drug therapy
[MeSH-minor]
Antineoplastic Combined
Chemotherapy
Protocols /
therapeutic
use. Combined Modality
Therapy
.
Drug
Delivery Systems.
Drug
Resistance, Neoplasm. Humans. Prostaglandins / biosynthesis. Prostaglandins / physiology
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
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]
Am J Clin Oncol. 2003 Aug;26(4):S66-9
[
12902859.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Sep;15(9):1598-606
[
16985019.001
]
[Cites]
Eur J Med Chem. 2001 Feb;36(2):109-26
[
11311743.001
]
[Cites]
Cancer Res. 2002 Mar 1;62(5):1567-72
[
11888937.001
]
[Cites]
J Lab Clin Med. 1993 Nov;122(5):518-23
[
8228569.001
]
[Cites]
Clin Cancer Res. 1999 Dec;5(12):4191-8
[
10632360.001
]
[Cites]
Neoplasia. 2001 Sep-Oct;3(5):402-10
[
11687951.001
]
[Cites]
N Engl J Med. 2005 Mar 17;352(11):1092-102
[
15713943.001
]
[Cites]
Cancer Res. 2005 Jun 1;65(11):4496-9
[
15930264.001
]
[Cites]
Med Oncol. 2005;22(4):389-97
[
16260857.001
]
[Cites]
Eur J Cancer. 1998 Jul;34(8):1250-9
[
9849488.001
]
[Cites]
Histopathology. 2005 Mar;46(3):287-95
[
15720414.001
]
[Cites]
Cancer Res. 2001 Dec 15;61(24):8617-23
[
11751373.001
]
[Cites]
Am J Pathol. 2000 Jul;157(1):29-35
[
10880372.001
]
[Cites]
Arch Otolaryngol Head Neck Surg. 2005 Feb;131(2):147-52
[
15723947.001
]
[Cites]
J Immunol. 1995 Apr 1;154(7):3383-90
[
7897221.001
]
[Cites]
Biochem Soc Trans. 2000 Feb;28(2):7-12
[
10816090.001
]
[Cites]
Ann Thorac Surg. 2005 Mar;79(3):990-5; discussion 990-5
[
15734421.001
]
[Cites]
Am J Pathol. 2002 Mar;160(3):893-903
[
11891188.001
]
[Cites]
J Biol Chem. 2002 May 24;277(21):18649-57
[
11901151.001
]
[Cites]
JAMA. 2000 Sep 13;284(10):1247-55
[
10979111.001
]
[Cites]
Lancet Oncol. 2003 Oct;4(10):605-15
[
14554238.001
]
[Cites]
Ann Surg. 2005 Dec;242(6):840-9, discussion 849-50
[
16327494.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2002 Nov 1;54(3):886-94
[
12377342.001
]
[Cites]
Gastroenterology. 2005 May;128(5):1445-61
[
15887126.001
]
[Cites]
Cancer Res. 1995 Sep 1;55(17):3785-9
[
7641194.001
]
[Cites]
Cancer Res. 2002 Mar 15;62(6):1676-81
[
11912139.001
]
[Cites]
J Urol. 2003 Nov;170(5):2036-9
[
14532848.001
]
[Cites]
J Biol Chem. 2000 May 19;275(20):14838-45
[
10809726.001
]
[Cites]
Curr Opin Chem Biol. 2000 Oct;4(5):545-52
[
11006543.001
]
[Cites]
Clin Cancer Res. 2005 Dec 1;11(23):8341-7
[
16322294.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1998 Nov 1;42(4):899-903
[
9845118.001
]
[Cites]
Mol Carcinog. 1999 Aug;25(4):231-40
[
10449029.001
]
[Cites]
Am J Clin Oncol. 2001 Oct;24(5):438-42
[
11586092.001
]
[Cites]
Cancer Res. 2005 Sep 1;65(17):8022-7
[
16140976.001
]
[Cites]
Am J Physiol. 1996 Mar;270(3 Pt 1):G393-400
[
8638704.001
]
[Cites]
Arch Pathol Lab Med. 2005 Sep;129(9):1113-7
[
16119982.001
]
[Cites]
Am J Gastroenterol. 1996 Jan;91(1):44-8
[
8561142.001
]
[Cites]
Anticancer Res. 1998 Mar-Apr;18(2A):775-82
[
9615719.001
]
[Cites]
J Biol Chem. 1990 Oct 5;265(28):16737-40
[
2120205.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2001 Apr 1;49(5):1213-7
[
11286825.001
]
[Cites]
J Clin Invest. 2000 Jun;105(11):1589-94
[
10841517.001
]
[Cites]
Clin Cancer Res. 2006 Jan 1;12(1):214-22
[
16397045.001
]
[Cites]
Int J Mol Med. 2006 Feb;17(2):221-8
[
16391819.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2000 Sep 1;48(2):325-8
[
10974444.001
]
[Cites]
Cancer Res. 1998 Dec 15;58(24):5686-9
[
9865723.001
]
[Cites]
Cell. 1995 Dec 1;83(5):803-12
[
8521497.001
]
[Cites]
Cancer Metastasis Rev. 1994 Dec;13(3-4):303-8
[
7712592.001
]
[Cites]
Gut. 2006 Jan;55(1):115-22
[
16118353.001
]
[Cites]
Gynecol Oncol. 2000 Mar;76(3):320-5
[
10684704.001
]
[Cites]
J Immunol. 1980 Jun;124(6):2682-7
[
6154736.001
]
[Cites]
Crit Rev Neurobiol. 1999;13(1):45-82
[
10223523.001
]
[Cites]
Cancer Lett. 1999 Jun 1;140(1-2):27-35
[
10403538.001
]
[Cites]
Carcinogenesis. 2001 Jan;22(1):5-10
[
11159734.001
]
[Cites]
Cell. 1996 Nov 29;87(5):783-6
[
8945503.001
]
[Cites]
J Huazhong Univ Sci Technolog Med Sci. 2004;24(4):326-8
[
15587390.001
]
[Cites]
Trends Pharmacol Sci. 2003 Feb;24(2):96-102
[
12559775.001
]
[Cites]
Ann Intern Med. 1994 Aug 15;121(4):241-6
[
8037405.001
]
[Cites]
Int J Oncol. 2005 May;26(5):1393-9
[
15809733.001
]
[Cites]
Hepatogastroenterology. 1999 Jan-Feb;46(25):407-12
[
10228831.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2005 Oct 1;63(2):520-8
[
16168844.001
]
[Cites]
Cancer Res. 1995 Aug 15;55(16):3564-8
[
7627965.001
]
[Cites]
Am J Pathol. 2005 Nov;167(5):1293-300
[
16251413.001
]
[Cites]
J Surg Oncol. 2001 Jan;76(1):26-30
[
11223821.001
]
[Cites]
Cancer Res. 1998 Sep 1;58(17):3761-4
[
9731479.001
]
[Cites]
Mol Cancer Ther. 2005 Jan;4(1):51-9
[
15657353.001
]
[Cites]
Int J Pancreatol. 1999 Oct;26(2):69-76
[
10597402.001
]
[Cites]
Cancer Res. 1988 Jun 1;48(11):3002-7
[
3130182.001
]
[Cites]
Cancer. 2002 Aug 15;95(4):801-7
[
12209724.001
]
[Cites]
N Engl J Med. 2006 Aug 31;355(9):885-95
[
16943401.001
]
[Cites]
Clin Cancer Res. 2001 Apr;7(4):861-7
[
11309334.001
]
[Cites]
Genes Dev. 1999 Jun 15;13(12):1561-74
[
10385625.001
]
[Cites]
Cancer Res. 1999 Mar 1;59(5):987-90
[
10070951.001
]
[Cites]
Nature. 1980 Dec 11;288(5791):597-600
[
7003398.001
]
[Cites]
Expert Opin Investig Drugs. 1999 Oct;8(10):1623-1638
[
11139815.001
]
[Cites]
Am J Physiol Gastrointest Liver Physiol. 2000 Nov;279(5):G858-65
[
11052981.001
]
[Cites]
Int J Radiat Biol. 1997 Mar;71(3):259-64
[
9134015.001
]
[Cites]
Eur J Cancer. 2000 Mar;36(5):664-74
[
10738133.001
]
[Cites]
Cell Immunol. 1980 Jun;52(1):29-37
[
6446407.001
]
[Cites]
N Engl J Med. 2006 Aug 31;355(9):873-84
[
16943400.001
]
[Cites]
Am J Pathol. 2000 Sep;157(3):729-35
[
10980112.001
]
[Cites]
J Clin Oncol. 2005 Jan 10;23(2):254-66
[
15637389.001
]
[Cites]
Clin Cancer Res. 2005 Nov 15;11(22):7995-8005
[
16299228.001
]
[Cites]
Cancer Cell. 2003 Dec;4(6):431-6
[
14706335.001
]
[Cites]
Oncologist. 2005 Oct;10 (9):710-7
[
16249351.001
]
[Cites]
J Clin Oncol. 2003 Jul 15;21(14):2645-50
[
12860939.001
]
[Cites]
Radiat Res. 1993 Jul;135(1):88-92
[
8327666.001
]
[Cites]
Clin Cancer Res. 2006 Jan 1;12(1):314-20
[
16397057.001
]
[Cites]
Cancer Res. 2000 Mar 1;60(5):1326-31
[
10728694.001
]
[Cites]
Int J Cancer. 2005 Sep 10;116(4):536-46
[
15825163.001
]
[Cites]
Cancer. 2001 Jan 15;91(2):333-8
[
11180079.001
]
[Cites]
Cancer Lett. 2005 Jan 10;217(1):11-6
[
15596291.001
]
[Cites]
Cancer Res. 1995 Jun 15;55(12):2556-9
[
7780968.001
]
[Cites]
N Engl J Med. 2000 Jun 29;342(26):1946-52
[
10874062.001
]
[Cites]
Clin Cancer Res. 2005 Mar 1;11(5):1999-2007
[
15756026.001
]
[Cites]
Cancer Res. 2005 Jun 15;65(12):5211-20
[
15958566.001
]
[Cites]
Cancer Chemother Pharmacol. 2006 Jan;57(2):185-90
[
16151811.001
]
[Cites]
Cancer Res. 2002 Feb 1;62(3):625-31
[
11830509.001
]
[Cites]
J Clin Oncol. 2005 May 20;23(15):3536-44
[
15908664.001
]
[Cites]
Med J Aust. 2001 Aug 20;175(4):214-7
[
11587283.001
]
[Cites]
Breast Cancer Res Treat. 1995;36(2):227-36
[
8534870.001
]
[Cites]
Annu Rev Cell Dev Biol. 1996;12:335-63
[
8970730.001
]
[Cites]
Epidemiology. 1994 Mar;5(2):138-46
[
8172988.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2005 Jul 1;62(3):725-32
[
15936552.001
]
[Cites]
Clin Cancer Res. 2000 Feb;6(2):701-8
[
10690556.001
]
[Cites]
Clin Cancer Res. 2005 Jun 1;11(11):4191-7
[
15930356.001
]
[Cites]
Br J Cancer. 2002 Jul 15;87(2):231-7
[
12107848.001
]
[Cites]
Anticancer Res. 2001 Mar-Apr;21(2B):1291-4
[
11396201.001
]
[Cites]
Cancer Res. 2005 Jun 15;65(12):5038-44
[
15958546.001
]
[Cites]
Cancer Res. 2005 Feb 1;65(3):982-90
[
15705899.001
]
[Cites]
Cancer Res. 1988 Jun 1;48(11):3008-13
[
3365690.001
]
[Cites]
Breast Cancer Res Treat. 2005 Feb;89(3):215-20
[
15754118.001
]
[Cites]
Blood. 2005 Dec 15;106(13):4330-8
[
16123214.001
]
[Cites]
Cancer Res. 1991 May 15;51(10):2552-8
[
2021936.001
]
[Cites]
J Pathol. 1999 Feb;187(3):295-301
[
10398082.001
]
[Cites]
Ann Oncol. 2005 Jan;16(1):51-5
[
15598938.001
]
[Cites]
Am J Clin Oncol. 2001 Oct;24(5):447-52
[
11586094.001
]
[Cites]
Cancer Res. 2002 Apr 15;62(8):2343-6
[
11956094.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2004 Feb 1;58(2):369-75
[
14751505.001
]
[Cites]
Oncology (Williston Park). 2004 Dec;18(14 Suppl 14):18-21
[
15685829.001
]
[Cites]
J Clin Endocrinol Metab. 2005 May;90(5):2563-70
[
15687328.001
]
[Cites]
Annu Rev Biochem. 1987;56:615-49
[
3113327.001
]
[Cites]
Biochem J. 1989 Apr 15;259(2):315-24
[
2655580.001
]
[Cites]
Cancer Res. 1999 Jul 15;59(14):3374-8
[
10416597.001
]
[Cites]
Int J Radiat Biol. 1992 Apr;61(4):533-7
[
1349335.001
]
[Cites]
Proc Soc Exp Biol Med. 1983 Feb;172(2):214-8
[
6572402.001
]
[Cites]
Am J Gastroenterol. 1999 Feb;94(2):451-5
[
10022645.001
]
[Cites]
Pancreatology. 2005;5(4-5):361-9
[
15980665.001
]
[Cites]
Anticancer Res. 2000 Sep-Oct;20(5A):2867-72
[
11062695.001
]
[Cites]
J Immunol. 2000 Jan 1;164(1):361-70
[
10605031.001
]
[Cites]
J Clin Endocrinol Metab. 2001 May;86(5):2243-9
[
11344234.001
]
[Cites]
J Biol Chem. 2002 Oct 11;277(41):38915-20
[
12138126.001
]
[Cites]
Gastroenterology. 1994 Oct;107(4):1183-8
[
7926468.001
]
[Cites]
Clin Cancer Res. 2005 May 1;11(9):3363-8
[
15867236.001
]
[Cites]
Cancer Res. 1990 Aug 1;50(15):4473-7
[
2369725.001
]
[Cites]
Cancer Res. 2001 Jan 1;61(1):303-8
[
11196178.001
]
[Cites]
Clin Cancer Res. 2005 Oct 15;11(20):7362-8
[
16243808.001
]
[Cites]
Semin Radiat Oncol. 2001 Oct;11(4):281-9
[
11677653.001
]
[Cites]
Clin Cancer Res. 2005 Sep 15;11(18):6634-40
[
16166442.001
]
[Cites]
Radiat Res. 1983 Nov;96(2):393-8
[
6647767.001
]
[Cites]
Clin Cancer Res. 2005 Jul 1;11(13):4754-60
[
16000571.001
]
[Cites]
Clin Cancer Res. 2002 Jul;8(7):2443-7
[
12114451.001
]
[Cites]
J Natl Cancer Inst. 1982 Aug;69(2):475-82
[
6180207.001
]
[Cites]
Am J Pathol. 2002 Mar;160(3):1129-41
[
11891209.001
]
[Cites]
J Neurooncol. 2005 Jan;71(2):141-8
[
15690129.001
]
[Cites]
Gynecol Oncol. 2005 Jan;96(1):159-67
[
15589595.001
]
[Cites]
Cancer Sci. 2005 Feb;96(2):93-9
[
15723653.001
]
[Cites]
Br J Pharmacol. 1979 Jul;66(3):451P
[
526739.001
]
[Cites]
Ann Oncol. 2002 May;13(5):669-78
[
12075734.001
]
[Cites]
Cancer Res. 2000 Apr 15;60(8):2101-3
[
10786667.001
]
[Cites]
Drug Saf. 2002;25(12):829-35
[
12241124.001
]
[Cites]
Clin Cancer Res. 2001 Oct;7(10):2998-3005
[
11595687.001
]
[Cites]
Br J Cancer. 2003 Apr 7;88(7):1143-51
[
12671717.001
]
[Cites]
Cell. 1996 Nov 29;87(5):803-9
[
8945508.001
]
[Cites]
Oncogene. 2001 Jul 12;20(31):4228-34
[
11464289.001
]
[Cites]
Br J Pharmacol. 2000 Jun;130(3):641-9
[
10821793.001
]
[Cites]
Cell. 1995 Nov 3;83(3):493-501
[
8521479.001
]
[Cites]
Int J Mol Med. 2001 Jul;8(1):31-6
[
11408945.001
]
[Cites]
Radiat Res. 1999 Oct;152(4):398-403
[
10477916.001
]
[Cites]
Cancer Res. 1993 Mar 15;53(6):1322-7
[
8443812.001
]
[Cites]
Oncol Rep. 2000 Nov-Dec;7(6):1377-81
[
11032948.001
]
[Cites]
JAMA. 2001 Aug 22-29;286(8):954-9
[
11509060.001
]
[Cites]
Cancer. 2002 Feb 15;94(4):1023-31
[
11920472.001
]
[Cites]
Semin Oncol. 2004 Feb;31(1 Suppl 1):47-53
[
14981580.001
]
[Cites]
Clin Cancer Res. 2005 Sep 1;11(17):6261-9
[
16144930.001
]
[Cites]
Expert Rev Anticancer Ther. 2004 Aug;4(4):543-60
[
15270659.001
]
[Cites]
Gastroenterology. 2001 Dec;121(6):1339-47
[
11729113.001
]
[Cites]
FEBS Lett. 1999 Oct 22;460(1):145-8
[
10571077.001
]
[Cites]
Clin Cancer Res. 2005 May 1;11(9):3342-8
[
15867233.001
]
[Cites]
JAMA. 1999 Oct 6;282(13):1254-7
[
10517428.001
]
[Cites]
Mol Cancer Ther. 2005 Sep;4(9):1358-63
[
16170027.001
]
[Cites]
Cancer Res. 2000 Sep 15;60(18):5040-4
[
11016626.001
]
[Cites]
Cancer Res. 2005 Jul 15;65(14):6275-81
[
16024629.001
]
[Cites]
J Cancer Res Clin Oncol. 2001 Jul;127(7):411-7
[
11469677.001
]
[Cites]
Cancer Res. 1998 Nov 15;58(22):4997-5001
[
9823297.001
]
[Cites]
Cancer Lett. 2005 Jul 28;225(2):283-9
[
15978332.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2003 Dec 1;57(5):1405-12
[
14630280.001
]
[Cites]
Cancer. 2000 Dec 15;89(12):2637-45
[
11135226.001
]
[Cites]
Semin Oncol. 2004 Apr;31(2 Suppl 7):22-9
[
15179621.001
]
[Cites]
Gastroenterology. 2002 Jun;122(7):1800-7
[
12055587.001
]
[Cites]
J Biol Chem. 2001 May 25;276(21):18563-9
[
11278747.001
]
[Cites]
Int J Cancer. 2005 May 1;114(5):696-701
[
15609300.001
]
[Cites]
Cancer Res. 2002 Feb 1;62(3):632-5
[
11830510.001
]
[Cites]
Cancer Res. 1999 Mar 1;59(5):991-4
[
10070952.001
]
[Cites]
Anticancer Res. 2001 May-Jun;21(3C):2141-7
[
11501838.001
]
[Cites]
Cancer Chemother Pharmacol. 2003 Nov;52(5):377-82
[
12879280.001
]
[Cites]
J Natl Cancer Inst. 1999 Sep 1;91(17):1501-4
[
10469752.001
]
[Cites]
Clin Cancer Res. 2001 Feb;7(2):429-34
[
11234900.001
]
[Cites]
Clin Cancer Res. 2001 Jul;7(7):1923-31
[
11448905.001
]
[Cites]
Eur J Cancer. 1996 Dec;32A(14):2438-50
[
9059332.001
]
[Cites]
Cancer. 2005 Jan 15;103(2):329-38
[
15558802.001
]
[Cites]
Clin Cancer Res. 2000 Jun;6(6):2424-30
[
10873095.001
]
[Cites]
Cancer Res. 2000 Nov 1;60(21):6045-51
[
11085526.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Apr 29;94(9):4312-7
[
9113986.001
]
[Cites]
Cancer Res. 1998 Jul 15;58(14):2929-34
[
9679948.001
]
[Cites]
Cancer Res. 2002 Oct 1;62(19):5405-7
[
12359744.001
]
[Cites]
Pharmacol Ther. 1992;53(2):261-73
[
1641409.001
]
[Cites]
Biochem Pharmacol. 2004 Apr 15;67(8):1469-78
[
15041464.001
]
[Cites]
Br J Cancer. 2005 Aug;93 Suppl 1:S10-5
[
16100520.001
]
[Cites]
Cancer. 2002 Mar 1;94(5):1565-73
[
11920515.001
]
[Cites]
Cancer Res. 2002 Oct 15;62(20):5778-84
[
12384538.001
]
[Cites]
Cancer Res. 2000 Mar 1;60(5):1306-11
[
10728691.001
]
[Cites]
Cancer Res. 1998 Mar 15;58(6):1208-16
[
9515807.001
]
[Cites]
Br J Pharmacol. 2001 Nov;134(6):1137-50
[
11704632.001
]
[Cites]
Am J Pathol. 2001 Mar;158(3):849-53
[
11238034.001
]
[Cites]
Cancer Res. 2001 Feb 15;61(4):1733-40
[
11245490.001
]
[Cites]
J Natl Cancer Inst. 1987 Apr;78(4):735-41
[
3470548.001
]
[Cites]
Cancer Res. 1999 Jan 1;59(1):198-204
[
9892207.001
]
[Cites]
Clin Cancer Res. 1999 May;5(5):1001-5
[
10353732.001
]
[Cites]
Nat Med. 2000 Sep;6(9):1024-8
[
10973323.001
]
[Cites]
Clin Cancer Res. 2001 May;7(5):1410-8
[
11350912.001
]
[Cites]
Histol Histopathol. 1998 Apr;13(2):591-7
[
9589912.001
]
[Cites]
Am J Obstet Gynecol. 2005 Apr;192(4):1262-71; discussion 1271-3
[
15846217.001
]
[Cites]
Clin Cancer Res. 2004 Dec 15;10(24):8465-71
[
15623626.001
]
[Cites]
Gastroenterology. 2005 Aug;129(2):565-76
[
16083713.001
]
[Cites]
Virchows Arch. 2004 Dec;445(6):564-71
[
15372235.001
]
[Cites]
Cancer Immunol Immunother. 2005 Oct;54(10):981-7
[
15891886.001
]
[Cites]
Adv Space Res. 1992;12(2-3):265-71
[
11537017.001
]
[Cites]
Clin Cancer Res. 2000 Jun;6(6):2513-20
[
10873107.001
]
(PMID = 17428102.001).
[ISSN]
0012-6667
[Journal-full-title]
Drugs
[ISO-abbreviation]
Drugs
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
New Zealand
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Prostaglandins; EC 1.14.99.1 / Cyclooxygenase 2
[Number-of-references]
233
76.
Brandes AA, Tosoni A, Franceschi E, Reni M, Gatta G, Vecht C:
Glioblastoma in adults.
Crit Rev Oncol Hematol
; 2008 Aug;67(2):139-52
[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.
Glioblastoma (GBM) is the most
malignant
among astrocytic tumours and is associated with a poor prognosis.
Surgery aimed to complete resection should be the first
therapeutic
modality in the management of glioblastoma.
Postoperative concomitant chemo-radiation is the standard
treatment
and consists of 60Gy of external-beam radiotherapy (to be delivered to a target volume including a 2-3cm ring of
tissue
surrounding the perimeter of the contrast enhancing
lesion
on
pre
-operative CT/MRI scans) plus temozolomide (TMZ) administered concomitantly (75mg/m(2) daily) and after radiotherapy (150-200mg/m(2), for 5 days every 4 weeks).
At
time
of recurrence/progression, a nitrosourea-based
chemotherapy
constitutes a reasonable option, as well as a temozolomide re-challenge for patients without progression during prior temozolomide
treatment
.
[MeSH-major]
Glioblastoma /
therapy
[MeSH-minor]
Adult. Combined Modality
Therapy
. Humans. Neoplasm Staging
Genetic Alliance.
consumer health - Glioblastoma
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18394916.001).
[ISSN]
1040-8428
[Journal-full-title]
Critical reviews in oncology/hematology
[ISO-abbreviation]
Crit. Rev. Oncol. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Ireland
[Number-of-references]
98
77.
Hornung R:
Photomedical approaches for the diagnosis and treatment of gynecologic cancers.
Curr Drug Targets Immune Endocr Metabol Disord
; 2001 Aug;1(2):165-77
[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]
Photomedical approaches for the diagnosis and
treatment
of gynecologic cancers.
Malignant
tumors of the female reproductive organs have a high incidence and mortality.
Despite modern technology, diagnostics and
therapeutics
have substantial limitations.
Detection
of autofluorescence, photosensitizer mediated fluorescence, and near-infrared-spectra are new approaches to diagnose gynecologic malignancies and
premalignant lesions
.
Photodynamic
therapy
(PDT) is currently being evaluated for the
treatment
of gynecologic cancers and precancers.
New porphyrin based photosensitizers promise a selective tumor targeting and consequently a selective
treatment
of surgically not removable cancers.
The present article summarizes the role of photomedicine in diagnostics and
treatments
of
malignant
disease of the female genital tract.
[MeSH-major]
Genital Neoplasms, Female / diagnosis. Genital Neoplasms, Female /
therapy
. Photochemotherapy. Photosensitizing Agents /
therapeutic
use
[MeSH-minor]
Animals. Combined Modality
Therapy
. Female. Humans. Spectroscopy, Near-Infrared
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 12476797.001).
[ISSN]
1568-0088
[Journal-full-title]
Current drug targets. Immune, endocrine and metabolic disorders
[ISO-abbreviation]
Curr. Drug Targets Immune Endocr. Metabol. Disord.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Photosensitizing Agents
[Number-of-references]
144
78.
Konturek PC, Rembiasz K, Konturek SJ, Stachura J, Bielanski W, Galuschka K, Karcz D, Hahn EG:
Gene expression of ornithine decarboxylase, cyclooxygenase-2, and gastrin in atrophic gastric mucosa infected with Helicobacter pylori before and after eradication therapy.
Dig Dis Sci
; 2003 Jan;48(1):36-46
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Gene expression of ornithine decarboxylase, cyclooxygenase-2, and gastrin in atrophic gastric mucosa infected with Helicobacter pylori before and after eradication
therapy
.
Recently, the increased expression of ornithine decarboxylase (ODC), gastrin and cyclooxygenase (COX)-2 has been shown to be increased in
premalignant lesions
in gastric mucosa and to play an essential role in the
malignant
transformation.
The aim of the study is to assess the effect of eradication
therapy
on atrophic gastritis and analyze the gene expression for ODC, COX-2 and gastrin in gastric mucosa after succesful eradication in patients with atrophic gastritis.
The patients were then eradicated with triple
therapy
consiting of omeprazol (2 x 20 mg), amoxycillin (2 x 1 g) and clarithromycin (2 x 500 mg) for seven days and vitamin C 1 g/day for three months.
After triple
therapy
the successful eradication assessed by UBT was observed in 95% of patients.
The expression of COX-2 and ODC was significantly up-regulated in the gastric mucosa of patients with atrophic gastritis and significantly reduced after eradication
therapy
.
(1) Hp eradication leads to the decrease in ODC and COX-2 gene expression in the gastric mucosa, and this may be relevant for the prevention of the Hp-associated gastric carcinogenesis; and (2) gastric atrophy ameliorates upon successful Hp eradication
therapy
.
[MeSH-major]
Gastric Mucosa / microbiology. Gastrins / genetics. Gastritis, Atrophic /
drug therapy
. Gastritis, Atrophic / metabolism. Helicobacter Infections /
drug therapy
. Helicobacter Infections / metabolism. Helicobacter pylori. Isoenzymes / genetics. Ornithine Decarboxylase / genetics. Prostaglandin-Endoperoxide Synthases / genetics
[MeSH-minor]
Amoxicillin /
therapeutic
use. Anti-Ulcer Agents /
therapeutic
use. Clarithromycin /
therapeutic
use. Cyclooxygenase 2.
Drug Therapy
, Combination. Female. Gene Expression. Humans. Male. Membrane Proteins. Middle Aged. Omeprazole /
therapeutic
use. Peroxidases / genetics. RNA, Messenger / biosynthesis
MedlinePlus Health Information.
consumer health - Helicobacter Pylori Infections
.
Hazardous Substances Data Bank.
AMOXICILLIN
.
Hazardous Substances Data Bank.
OMEPRAZOLE
.
Hazardous Substances Data Bank.
Clarithromycin
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Physiol Pharmacol. 1996 Mar;47(1):161-75
[
8777296.001
]
[Cites]
Prostaglandins Other Lipid Mediat. 2001 Aug;66(1):39-51
[
11519793.001
]
[Cites]
Am J Physiol Gastrointest Liver Physiol. 2000 Oct;279(4):G791-8
[
11005767.001
]
[Cites]
Curr Gastroenterol Rep. 2001 Dec;3(6):509-15
[
11696289.001
]
[Cites]
Dig Dis Sci. 2002 Sep;47(9):1984-91
[
12353842.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1995 Dec;4(8):865-70
[
8634659.001
]
[Cites]
Int J Oncol. 2001 Dec;19(6):1179-86
[
11713587.001
]
[Cites]
Ann Intern Med. 2001 Mar 6;134(5):380-6
[
11242498.001
]
[Cites]
Am J Gastroenterol. 1994 Jun;89(6):888-93
[
8198100.001
]
[Cites]
Gastroenterology. 2000 Jan;118(1):36-47
[
10611152.001
]
[Cites]
J Exp Clin Cancer Res. 2001 Mar;20(1):117-29
[
11370818.001
]
[Cites]
Am J Surg Pathol. 1996 Oct;20(10):1161-81
[
8827022.001
]
[Cites]
Cancer Res. 1997 Apr 1;57(7):1276-80
[
9102213.001
]
[Cites]
Am J Pathol. 2000 Sep;157(3):729-35
[
10980112.001
]
[Cites]
Nature. 1992 Nov 26;360(6402):355-8
[
1280331.001
]
[Cites]
Gastroenterology. 2000 Jul;119(1):7-14
[
10889149.001
]
[Cites]
Gut. 1996 Dec;39(6):807-10
[
9038661.001
]
[Cites]
Aliment Pharmacol Ther. 2001 Jul;15(7):989-99
[
11421874.001
]
[Cites]
Scand J Gastroenterol. 2001 Sep;36(9):897-903
[
11521977.001
]
[Cites]
Differentiation. 1981;19(1):1-20
[
6173280.001
]
[Cites]
J Clin Gastroenterol. 1993;17 Suppl 1:S40-5
[
7904286.001
]
[Cites]
Lancet. 1992 Mar 21;339(8795):745-6
[
1347613.001
]
[Cites]
Cancer Res. 1992 Dec 15;52(24):6735-40
[
1458460.001
]
[Cites]
Am J Gastroenterol. 1999 Sep;94(9):2398-402
[
10483998.001
]
[Cites]
Helicobacter. 1998 Dec;3(4):236-40
[
9844064.001
]
[Cites]
Aliment Pharmacol Ther. 2000 May;14(5):625-34
[
10792127.001
]
[Cites]
Lancet. 1984 Jun 16;1(8390):1311-5
[
6145023.001
]
[Cites]
N Engl J Med. 2001 Sep 13;345(11):784-9
[
11556297.001
]
[Cites]
Gut. 2001 Jun;48(6):743-7
[
11358884.001
]
[Cites]
J Natl Cancer Inst. 1991 May 1;83(9):640-3
[
2023282.001
]
[Cites]
Dig Dis Sci. 1997 Mar;42(3):576-9
[
9073141.001
]
[Cites]
Gastroenterology. 1998 Jun;114(6):1169-79
[
9609753.001
]
[Cites]
N Engl J Med. 1991 Apr 11;324(15):1043-8
[
2005942.001
]
[Cites]
Anal Biochem. 1987 Apr;162(1):156-9
[
2440339.001
]
[Cites]
J Physiol Pharmacol. 1996 Sep;47(3):545-53
[
8877910.001
]
[Cites]
Gut. 1995 Jul;37(1):13-6
[
7672662.001
]
[Cites]
Gastroenterol Clin North Am. 2000 Sep;29(3):687-703, viii
[
11030081.001
]
(PMID = 12645788.001).
[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
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Ulcer Agents; 0 / Gastrins; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / RNA, Messenger; 804826J2HU / Amoxicillin; EC 1.11.1.- / Peroxidases; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 4.1.1.17 / Ornithine Decarboxylase; H1250JIK0A / Clarithromycin; KG60484QX9 / Omeprazole
79.
Saba NF, Choi M, Muller S, Shin HJ, Tighiouart M, Papadimitrakopoulou VA, El-Naggar AK, Khuri FR, Chen ZG, Shin DM:
Role of cyclooxygenase-2 in tumor progression and survival of head and neck squamous cell carcinoma.
Cancer Prev Res (Phila)
; 2009 Sep;2(9):823-9
[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.
Inhibition of cyclooxygenase-2 (COX-2) pathways may have significant implications for the prevention and
treatment
of head and neck squamous cell carcinoma (HNSCC).
COX-2 is overexpressed in both
premalignant lesions
and invasive HNSCC.
We examined COX-2 expression by immunohistochemistry in normal
tissues
, different stages of
premalignant lesions
, and carcinoma in situ (CIS).
Tissue
specimens were obtained from the following:
premalignant lesions
from 25 subjects enrolled in a biochemoprevention trial, tumor samples collected at diagnosis from 38 HNSCC patients enrolled in an induction
chemotherapy
trial, and normal control
tissues
from 10 noncancer, nonsmoking subjects.
COX-2 was expressed in early and intermediate stages of
premalignant lesions
, increasing first in the basal and parabasal layers, then lower spinous, and upper spinous layers.
COX-2 expression in tumors from patients treated with induction
chemotherapy
was correlated with overall survival after controlling for clinical variables.
These findings elucidate the differential expression pattern of COX-2 in stages of head and neck
premalignant lesions
and invasive carcinoma, supporting the rationale for COX-2 inhibition as an important strategy for cancer chemoprevention.
Genetic Alliance.
consumer health - Carcinoma, Squamous Cell
.
MedlinePlus Health Information.
consumer health - Head and Neck Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
TAXOL
.
Hazardous Substances Data Bank.
IFOSFAMIDE
.
Hazardous Substances Data Bank.
CARBOPLATIN
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Laryngoscope. 1996 Feb;106(2 Pt 1):129-34
[
8583839.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1994 Dec;3(8):697-709
[
7881344.001
]
[Cites]
Gastroenterology. 1996 Oct;111(4):1134-40
[
8831610.001
]
[Cites]
Am J Otolaryngol. 1997 Jan-Feb;18(1):1-8
[
9006670.001
]
[Cites]
Am J Physiol. 1998 Jun;274(6 Pt 1):G1061-7
[
9696706.001
]
[Cites]
Surgery. 1999 Aug;126(2):364-70
[
10455907.001
]
[Cites]
Arch Otolaryngol Head Neck Surg. 1999 Oct;125(10):1083-9
[
10522499.001
]
[Cites]
J Clin Oncol. 2005 Jan 10;23(2):254-66
[
15637389.001
]
[Cites]
Oral Oncol. 2005 Mar;41(3):304-12
[
15743693.001
]
[Cites]
Eur Respir J. 2005 Aug;26(2):198-203
[
16055866.001
]
[Cites]
Oncology. 2005;69 Suppl 1:28-32
[