BioMedLib Search Engine
[ goto HOMEPAGE ]
Search the biomedical literature, for the most relevant articles.
Skip to content
Advanced Search
Search History
MeSH Query
Page Format
Query is expanded
Login
Skip to content
Export Citations
Search Results
RSS
Email
Articles' Details
Start new query
Reset All
Refine your query
(more in Advanced-Search):
Search all of MEDLINE
Focus on the recent 5 years
Focus on the current year
Focus on the last 30 days
More choices ...
Focus on articles with free fulltexts
More choices ...
Do simple 'keyword' search (no query expansion)
[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click
here to
RESET
all values
Click
here to
GO BACK
without resetting any value
Advanced Search
Submit one or more of the following items, and they will be searched along with your query in the search box above.
Any submit button will submit all of the items you have changed.
+
Publication-Date
Published in the last:
30 days
60 days
90 days
6 months
12 months
this year
2 years
3 years
5 years
10 years
Or published in the following date range: From (yyyy/mm/dd - month and day are optional)
to ('to' is optional)
+
Full Text
Retrieve articles with hyperlinks to:
full text (either free or subscription)
free full text
subscription full text
no full text link
+
Sort-Order
Sort the retrieved articles by:
relevance
publication date
+
Language
And with languages:
English
French
German
Italian
Japanese
Russian
Spanish
More languages:
Afrikaans
Albanian
Amharic
Arabic
Armenian
Azerbaijani
Bengali
Bosnian
Bulgarian
Catalan
Chinese
Czech
Danish
Dutch
Esperanto
Estonian
Finnish
Georgian
Scottish Gaelic
Greek, Modern
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Kinyarwanda
Korean
Latin
Latvian
Lithuanian
Macedonian
Malayalam
Maori
Malay
Multiple languages
Norwegian
Persian
Polish
Portuguese
Pushto
Romanian
Sanskrit
Serbian
Croatian
Slovak
Slovenian
Swedish
Thai
Turkish
Ukrainian
Undetermined
Urdu
Vietnamese
Welsh
+
Publication-Type
And with publication types:
Clinical Trial
Editorial
Letter
Meta-Analysis
Practice Guideline
Randomized Controlled Trial
Review
More publication types:
Addresses
Bibliography
Biography
Case Reports
Classical Article
Clinical Conference
Clinical Trial, Phase I
Clinical Trial, Phase II
Clinical Trial, Phase III
Clinical Trial, Phase IV
Comment
Comparative Study
Congresses
Consensus Development Conference
Consensus Development Conference, NIH
Controlled Clinical Trial
Corrected and Republished Article
Dictionary
Directory
Duplicate Publication
English Abstract
Evaluation Studies
Festschrift
Government Publications
Guideline
Historical Article
Interactive Tutorial
Interview
Introductory Journal Article
In Vitro
Journal Article
Lectures
Legal Cases
Legislation
Multicenter Study
News
Newspaper Article
Overall
Patient Education Handout
Periodical Index
Portraits
Published Erratum
Retracted Publication
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
Retraction of Publication
Scientific Integrity Review
Technical Report
Twin Study
Validation Studies
+
Species
And for:
Humans
Animals
+
Gender
And for:
Male
Female
+
Age
And for these age groups:
Newborn: birth to 1 month
Infant: 1 to 23 months
Preschool child: 2 to 5 years
Child: 6 to 12 years
Adolescent: 13 to 18 years
Adult: 19 to 44 years
Middle aged: 45 to 64 years
Aged: 65+ years
80 and over: 80+ years
+
Title
And for this query matching the titles:
+
Transliterated-Title
And for this query matching the title in original language:
+
Abstract
And for this query matching the abstratcs:
+
Major-Mesh
And for this query matching the MeSH-Major terms:
+
Mesh
And for this query matching any MeSH terms:
+
Journal
And for one or more of these journal abbreviated names:
OR
OR
(see
title abbreviations
)
+
Volume
And with journal volume number:
+
Issue
And with journal issue number:
+
Page
And with page number:
+
ISSN
And with ISSN:
+
Publication-Place
And with journal's country of publication:
+
Author
And for...
all these author names:
AND
AND
(see
help
)
one or more of these author names:
OR
OR
but not having any of these unwanted author names:
NOT
NOT
+
Affiliation
And with affiliation to:
+
Has-Abstract
Find MEDLINE records with the abstract status:
has abstract
does not have abstract
include both record types
include both record types but rank higher the records having abstract (the default BML behavior)
+
PMID
Show me only articles for these PMIDs (PubMed IDs):
+
Semantic-Type
And with semantic types:
A. Entity
A1. Physical Object
A1.1. Organism
A1.1.1. Archaeon
A1.1.2. Bacterium
A1.1.3. Eukaryote
A1.1.3.1. Animal
A1.1.3.1.1. Vertebrate
A1.1.3.1.1.1. Amphibian
A1.1.3.1.1.2. Bird
A1.1.3.1.1.3. Fish
A1.1.3.1.1.4. Mammal
A1.1.3.1.1.4.1. Human
A1.1.3.1.1.5. Reptile
A1.1.3.2. Fungus
A1.1.3.3. Plant
A1.1.4. Virus
A1.2. Anatomical Structure
A1.2.1. Embryonic Structure
A1.2.2. Anatomical Abnormality
A1.2.2.1. Congenital Abnormality
A1.2.2.2. Acquired Abnormality
A1.2.3. Fully Formed Anatomical Structure
A1.2.3.1. Body Part, Organ, or Organ Component
A1.2.3.2. Tissue
A1.2.3.3. Cell
A1.2.3.4. Cell Component
A1.2.3.5. Gene or Genome
A1.3. Manufactured Object
A1.3.1. Medical Device
A1.3.1.1. Drug Delivery Device
A1.3.2. Research Device
A1.3.3. Clinical Drug
A1.4. Substance
A1.4.1. Chemical
A1.4.1.1. Chemical Viewed Functionally
A1.4.1.1.1. Pharmacologic Substance
A1.4.1.1.1.1. Antibiotic
A1.4.1.1.2. Biomedical or Dental Material
A1.4.1.1.3. Biologically Active Substance
A1.4.1.1.3.1. Neuroreactive Substance or Biogenic Amine
A1.4.1.1.3.2. Hormone
A1.4.1.1.3.3. Enzyme
A1.4.1.1.3.4. Vitamin
A1.4.1.1.3.5. Immunologic Factor
A1.4.1.1.3.6. Receptor
A1.4.1.1.4. Indicator, Reagent, or Diagnostic Aid
A1.4.1.1.5. Hazardous or Poisonous Substance
A1.4.1.2. Chemical Viewed Structurally
A1.4.1.2.1. Organic Chemical
A1.4.1.2.1.5. Nucleic Acid, Nucleoside, or Nucleotide
A1.4.1.2.1.6. Organophosphorus Compound
A1.4.1.2.1.7. Amino Acid, Peptide, or Protein
A1.4.1.2.1.8. Carbohydrate
A1.4.1.2.1.9. Lipid
A1.4.1.2.1.9.1. Steroid
A1.4.1.2.1.9.2. Eicosanoid
A1.4.1.2.2. Inorganic Chemical
A1.4.1.2.3. Element, Ion, or Isotope
A1.4.2. Body Substance
A1.4.3. Food
A2. Conceptual Entity
A2.1. Idea or Concept
A2.1.1. Temporal Concept
A2.1.2. Qualitative Concept
A2.1.3. Quantitative Concept
A2.1.4. Functional Concept
A2.1.4.1. Body System
A2.1.5. Spatial Concept
A2.1.5.1. Body Space or Junction
A2.1.5.2. Body Location or Region
A2.1.5.3. Molecular Sequence
A2.1.5.3.1. Nucleotide Sequence
A2.1.5.3.2. Amino Acid Sequence
A2.1.5.3.3. Carbohydrate Sequence
A2.1.5.4. Geographic Area
A2.2. Finding
A2.2.1. Laboratory or Test Result
A2.2.2. Sign or Symptom
A2.3. Organism Attribute
A2.3.1. Clinical Attribute
A2.4. Intellectual Product
A2.4.1. Classification
A2.4.2. Regulation or Law
A2.5. Language
A2.6. Occupation or Discipline
A2.6.1. Biomedical Occupation or Discipline
A2.7. Organization
A2.7.1. Health Care Related Organization
A2.7.2. Professional Society
A2.7.3. Self-help or Relief Organization
A2.8. Group Attribute
A2.9. Group
A2.9.1. Professional or Occupational Group
A2.9.2. Population Group
A2.9.3. Family Group
A2.9.4. Age Group
A2.9.5. Patient or Disabled Group
B. Event
B1. Activity
B1.1. Behavior
B1.1.1. Social Behavior
B1.1.2. Individual Behavior
B1.2. Daily or Recreational Activity
B1.3. Occupational Activity
B1.3.1. Health Care Activity
B1.3.1.1. Laboratory Procedure
B1.3.1.2. Diagnostic Procedure
B1.3.1.3. Therapeutic or Preventive Procedure
B1.3.2. Research Activity
B1.3.2.1. Molecular Biology Research Technique
B1.3.3. Governmental or Regulatory Activity
B1.3.4. Educational Activity
B1.4. Machine Activity
B2. Phenomenon or Process
B2.1. Human-caused Phenomenon or Process
B2.1.1. Environmental Effect of Humans
B2.2. Natural Phenomenon or Process
B2.2.1. Biologic Function
B2.2.1.1. Physiologic Function
B2.2.1.1.1. Organism Function
B2.2.1.1.1.1. Mental Process
B2.2.1.1.2. Organ or Tissue Function
B2.2.1.1.3. Cell Function
B2.2.1.1.4. Molecular Function
B2.2.1.1.4.1. Genetic Function
B2.2.1.2. Pathologic Function
B2.2.1.2.1. Disease or Syndrome
B2.2.1.2.1.1. Mental or Behavioral Dysfunction
B2.2.1.2.1.2. Neoplastic Process
B2.2.1.2.2. Cell or Molecular Dysfunction
B2.2.1.2.3. Experimental Model of Disease
B2.3. Injury or Poisoning
Page Format
Any submit button will submit all of the items you have changed.
[theme]
Use this page design theme:
original
twenty ten
[shown]
Results per page:
5
10
20
50
100
200
500
[expand/collapse]
show these sections expanded by default:
Advanced search
MeSH query
Search history
Page format
Query expansion
Articles details
Export citations
Email
[text size]
use this font size for text:
25%
50%
75%
100%
125%
150%
200%
or enter your choice of font size:
[page width]
use this page width (relative to the default initial value):
25%
50%
75%
100%
125%
150%
200%
or enter your choice of page width:
[highlight color]
use this color to highlight query words in the articles:
red
green
blue
black
purple
yellow
orange
navy
olive
maroon
none
[query history]
maximum number of queries shown in the history section:
[annotate]
Annotate these parts of each article:
title
abstract
both
none
Reset all values
Find best MeSH terms for
Search History
1
2 malig neop prostate 2005:2010[pubdate] *count=100
432 results
Searchbox
Export
PDF
RSS
Email
Delete
Email this search result to the following email address:
[X] Close
Expand the query
'
2 malig neop prostate
' expanded to all its synonyms;
details
Email the results to the following email address:
Export the checked citations in RIS format (RIS format is used by RefWorks, Endnote, among others).
Items 1 to 100 of about 432
1.
Kikuchi E, Nakashima J, Ishibashi M, Ohigashi T, Oya M, Nakagawa K, Miyajima A, Murai M:
Usefulness of alpha1-antichymotrypsin-PSA complex for predicting bone metastases of prostate cancer.
Urology
; 2006 Aug;68(2):371-5
[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]
Usefulness of alpha1-antichymotrypsin-PSA complex for predicting bone
metastases of
prostate
cancer
.
OBJECTIVES: To determine the usefulness of alpha1-antichymotrypsin-
prostate
-specific antigen (PSA) complex (PSA-ACT)-based parameters in predicting bone
metastasis in
patients with
prostate
cancer
.
METHODS: PSA-ACT, total PSA, free PSA, their volume-adjusted values, and alkaline phosphatase were evaluated in 220 consecutive patients with newly diagnosed
prostate
cancer
.
RESULTS: Bone
metastases
were detected by bone scan in 27 (12.3%) of the 220 patients.
The serum levels of PSA-ACT, total PSA, free PSA, PSA density, PSA adjusted for transition zone volume, PSA-ACT density, PSA-ACT adjusted for transition zone volume, alkaline phosphatase, PSA-ACT/PSA ratio, and Gleason score in patients with bone
metastases
were each significantly greater than in those without bone
metastases
.
At a sensitivity of 93% (2 patients with bone
metastasis
missed), unnecessary bone scans would have been avoided in 107 and 102 patients using a PSA-ACT cutoff value of 10 ng/mL and total PSA cutoff value of 11.5 ng/mL, respectively.
Multivariate logistic regression analysis demonstrated that PSA-ACT and Gleason score were significant independent predictors of bone
metastasis
.
CONCLUSIONS: PSA-ACT is as useful as total PSA for identifying patients with a low probability of having bone
metastasis
.
PSA-ACT could replace PSA for predicting negative bone scans
in a
clinical setting in which PSA-ACT is used for monitoring and screening patients for
prostate
cancer
.
[MeSH-major]
Bone Neoplasms /
secondary
.
Prostate
-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology. alpha 1-Antichymotrypsin / blood
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer Screening
.
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 = 16904455.001).
[ISSN]
1527-9995
[Journal-full-title]
Urology
[ISO-abbreviation]
Urology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Multiprotein Complexes; 0 / alpha 1-Antichymotrypsin; EC 3.4.21.77 / Prostate-Specific Antigen
2.
Matsunaga S, Iguchi K, Usui S, Hirano K:
Incadronate induces cell detachment and apoptosis in prostatic PC-3 cells.
Anticancer Res
; 2007 Mar-Apr;27(2):927-32
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
BACKGROUND: Bisphosphonates are widely used for the treatment and prevention of osteoporosis and are also effective in the treatment of bone
metastasis of
prostate
cancer
.
Several mechanisms underlying the antitumor effect of bisphosphonates have been proposed, including direct effects on
tumor
cells, such as induction of apoptosis and inhibition of invasion.
[MeSH-minor]
Aspartic Acid / analogs & derivatives. Aspartic Acid / pharmacology. Caspase Inhibitors. Cell Adhesion / drug effects. Cell Line,
Tumor
. Etoposide / pharmacology. Focal Adhesion Protein-Tyrosine Kinases / metabolism. Humans. Male. Mevalonic Acid / pharmacology. Phosphorylation / drug effects. Protease Inhibitors / pharmacology
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
MEVALONIC ACID
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
Hazardous Substances Data Bank.
(L)-ASPARTIC 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 = 17465222.001).
[ISSN]
0250-7005
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Caspase Inhibitors; 0 / Diphosphonates; 0 / Protease Inhibitors; 0 / benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene; 138330-18-4 / cimadronate; 30KYC7MIAI / Aspartic Acid; 6PLQ3CP4P3 / Etoposide; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; S5UOB36OCZ / Mevalonic Acid
3.
Yates CC, Shepard CR, Stolz DB, Wells A:
Co-culturing human prostate carcinoma cells with hepatocytes leads to increased expression of E-cadherin.
Br J Cancer
; 2007 Apr 23;96(8):1246-52
[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]
Co-culturing human
prostate
carcinoma cells with hepatocytes leads to increased expression of E-cadherin.
Metastasis
is a multi-step process wherein
tumour
cells detach from the primary mass, migrate through barrier matrices, gain access to conduits to disseminate, and subsequently survive and proliferate in an ectopic site.
During the initial invasion stage,
prostate
carcinoma cells undergo epithelial-mesenchymal-like transition with gain of autocrine signalling and loss of E-cadherin, hallmarks that appear to enable invasion and dissemination.
However, some
metastases
express E-cadherin, and we found close connections between
prostate
carcinoma cells and hepatocytes
in a
liver microtissue bioreactor.
We hypothesise that phenotypic plasticity occurs late in
prostate
cancer
progression at the site of ectopic seeding.
Immunofluorescence staining for E-cadherin in co-cultures of hepatocytes and DU-145
prostate
cancer
cells revealed E-cadherin upregulation at peripheral sites of contact by day 2 of co-culture; E-cadherin expression also increased in PC-3 cells in co-culture.
Inhibition of autocrine EGFR signalling increased E-cadherin expression and cell-cell heterotypic adhesion; further, expression
of a
downregulation-resistant EGFR variant prevented E-cadherin upregulation.
These findings were supported by finding E-cadherin and catenins but not activated EGFR in human
prostate
metastases to
the liver.
We conclude that the term epithelial-mesenchymal transition only summarises the transient downregulation of E-cadherin for invasion with re-expression of E-cadherin being a physiological consequence
of metastatic
seeding.
[MeSH-minor]
Animals. Cell Adhesion. Cell Communication. Cell Line,
Tumor
. Coculture Techniques. Humans. Male. Rats. Rats, Sprague-Dawley. Receptor, Epidermal Growth Factor / analysis. Receptor, Epidermal Growth Factor / physiology. Signal Transduction
MedlinePlus Health Information.
consumer health - Prostate 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
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Cell Biol. 2003 Jun 23;161(6):1191-203
[
12810698.001
]
[Cites]
BJU Int. 2002 Mar;89(4):400-3
[
11872032.001
]
[Cites]
Nat Rev Cancer. 2003 Dec;3(12):921-30
[
14737122.001
]
[Cites]
Anticancer Drugs. 2004 Feb;15(2):161-7
[
15075673.001
]
[Cites]
Methods Cell Biol. 1976;13:29-83
[
177845.001
]
[Cites]
Proc Natl Acad Sci U S A. 1981 Aug;78(8):4975-9
[
6946443.001
]
[Cites]
J Cell Biol. 1991 Aug;114(3):533-43
[
1860884.001
]
[Cites]
Cancer Res. 1995 Nov 15;55(22):5195-9
[
7585573.001
]
[Cites]
Cancer Res. 1996 Sep 15;56(18):4096-102
[
8797572.001
]
[Cites]
J Pathol. 1999 Jan;187(2):155-7
[
10365089.001
]
[Cites]
Mol Cancer. 2004 Oct 11;3:28
[
15476557.001
]
[Cites]
Cancer Res. 2004 Dec 15;64(24):9209-16
[
15604294.001
]
[Cites]
Hum Pathol. 2004 Dec;35(12):1469-76
[
15619205.001
]
[Cites]
Br J Cancer. 2005 Jan 31;92(2):366-75
[
15655536.001
]
[Cites]
Ann R Coll Surg Engl. 2005 Jan;87(1):15-20
[
15720901.001
]
[Cites]
Cancer Biol Ther. 2005 Apr;4(4):365-70
[
15846061.001
]
[Cites]
Endocr Relat Cancer. 2006 Mar;13(1):197-210
[
16601288.001
]
[Cites]
Cancer Res. 2006 Dec 1;66(23):11271-8
[
17145872.001
]
[Cites]
Adv Cancer Res. 2007;97:225-46
[
17419948.001
]
[Cites]
Nat Rev Cancer. 2002 Jun;2(6):442-54
[
12189386.001
]
[Cites]
Surgery. 2002 Aug;132(2):141-8
[
12219004.001
]
[Cites]
Lab Invest. 2003 Mar;83(3):435-48
[
12649344.001
]
[Cites]
Adv Cancer Res. 2000;78:31-101
[
10547668.001
]
[Cites]
J Urol. 2000 Mar;163(3):985-92
[
10688036.001
]
[Cites]
Hum Pathol. 2001 Jul;32(7):690-7
[
11486167.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10356-61
[
11526241.001
]
[Cites]
Cancer. 2001 Dec 1;92(11):2786-95
[
11753952.001
]
[Cites]
Breast Cancer Res. 2003;5(6):R217-22
[
14580257.001
]
(PMID = 17406365.001).
[ISSN]
0007-0920
[Journal-full-title]
British journal of cancer
[ISO-abbreviation]
Br. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / Cadherins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
[Other-IDs]
NLM/ PMC2360137
Advertisement
4.
Shrivastava V, Christensen R, Poggi MM:
Prostate cancer metastatic to the external auditory canals.
Clin Genitourin Cancer
; 2007 Jun;5(5):341-3
[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]
Prostate
cancer metastatic
to the external auditory canals.
A 58-year-old white man with
prostate
-specific antigen (PSA) level of 6 ng/mL, a Gleason score of 6 (3+3), and T2a adenocarcinoma of the
prostate
underwent prostatectomy.
The PSA continued to increase, and the patient developed bone-only
metastatic
disease.
Six months later, he presented with bilateral hearing loss and was found to have pathologic and radiographic evidence
of metastatic
prostate
cancer to
the external auditory canals.
[MeSH-major]
Adenocarcinoma /
secondary
. Ear Canal / pathology. Ear Neoplasms /
secondary
. Prostatic Neoplasms / pathology
[MeSH-minor]
Fatal Outcome. Humans. Male. Middle Aged.
Prostate
-Specific Antigen / blood. Prostatectomy
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Prostate 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 = 17645833.001).
[ISSN]
1558-7673
[Journal-full-title]
Clinical genitourinary cancer
[ISO-abbreviation]
Clin Genitourin Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
5.
Shih HA, Harisinghani M, Zietman AL, Wolfgang JA, Saksena M, Weissleder R:
Mapping of nodal disease in locally advanced prostate cancer: rethinking the clinical target volume for pelvic nodal irradiation based on vascular rather than bony anatomy.
Int J Radiat Oncol Biol Phys
; 2005 Nov 15;63(4):1262-9
[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]
Mapping of nodal disease in locally advanced
prostate
cancer
: rethinking the clinical target volume for pelvic nodal irradiation based on vascular rather than bony anatomy.
We employed a novel magnetic resonance lymphangiographic technique to highlight the likely sites of occult nodal
metastasis
from
prostate
cancer
.
METHODS AND MATERIALS: Eighteen
prostate
cancer
patients with pathologically confirmed node-positive disease had a total of 69 pathologic nodes identifiable by lymphotropic nanoparticle-enhanced MRI and semiquantitative nodal analysis.
The position of each of these
malignant
nodes was mapped
to a
common template based on its relation to skeletal or vascular anatomy.
In contrast, the nodal
metastases
mapped much more tightly relative to the large pelvic vessels.
A proposed pelvic clinical target volume to encompass the region at greatest risk of containing occult nodal
metastases
would include a 2.0-cm radial expansion volume around the distal common iliac and proximal external and internal iliac vessels that would encompass 94.5% of the pelvic nodes at risk as defined by our node-positive
prostate
cancer
patient cohort.
CONCLUSIONS: Nodal
metastases
from
prostate
cancer
are largely localized along the major pelvic vasculature.
[MeSH-major]
Lymphatic Irradiation / methods. Lymphatic
Metastasis
/ pathology. Magnetic Resonance Imaging / methods. Prostatic Neoplasms / pathology
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Int J Radiat Oncol Biol Phys. 2006 Dec 1;66(5):1592; author reply 1593
[
17126215.001
]
(PMID = 16253781.001).
[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
6.
Kabeer MA, Lloyd-Davies E, Maskell G, Hohle R, Mathew J:
Metastatic prostate cancer masquerading clinically and radiologically as a primary caecal carcinoma.
World J Surg Oncol
; 2007;5:2
[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]
Metastatic
prostate
cancer
masquerading clinically and radiologically as a primary caecal carcinoma.
BACKGROUND: Prostatic carcinoma is the second most common cause
of cancer
-related deaths in males in the West.
Approximately 20% of patients present with
metastatic
disease.
We describe the case
of a
patient with
metastatic
prostate
cancer to
the bowel presenting clinically and radiologically as a primary caecal
cancer
.
The patient was being treated (Zoladex) for prostatic
cancer
diagnosed 6 years previously and was known to have bony
metastases
.
Histology showed a poorly differentiated adenocarcinoma which was PSA positive, confirming
metastatic
prostatic adenocarcinoma to the caecum.
CONCLUSION:
Metastasis of
prostatic carcinoma to the bowel is a very rare occurrence and presents a challenging
diagnosis
.
The diagnosis
is supported by immunohistochemistry for PSA.
The treatment for
metastatic
prostate
cancer
is mainly palliative.
[MeSH-major]
Adenocarcinoma /
secondary
. Cecal Neoplasms /
secondary
. Cecal Neoplasms / therapy. Prostatic Neoplasms / pathology
[MeSH-minor]
Aged. Biopsy, Needle. Chemotherapy, Adjuvant. Colectomy / methods.
Diagnosis
, Differential. Follow-Up Studies. Gastrointestinal Hemorrhage /
diagnosis
. Gastrointestinal Hemorrhage / etiology. Humans. Immunohistochemistry. Male.
Neoplasm
Staging. Prostatectomy / methods. Rectum. Risk Assessment. Tomography, X-Ray Computed. Treatment Outcome
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Neurooncol. 2001 Jan;51(2):167-73
[
11386414.001
]
[Cites]
Urology. 2001 Jul;58(1):106
[
11445497.001
]
[Cites]
Arch Pathol Lab Med. 2001 Aug;125(8):1101-3
[
11473469.001
]
[Cites]
Tumori. 2002 Jan-Feb;88(1):61-4
[
12004853.001
]
[Cites]
Cancer. 2002 Sep 1;95(5):1028-36
[
12209687.001
]
[Cites]
Ann R Coll Surg Engl. 2003 Nov;85(6):382-5
[
14629877.001
]
[Cites]
J Neurooncol. 2004 Feb;66(3):361-3
[
15015669.001
]
[Cites]
Urology. 2004 Apr;63(4):778-9
[
15072903.001
]
[Cites]
J R Soc Promot Health. 2004 Sep;124(5):219-21
[
15493781.001
]
[Cites]
Am J Roentgenol Radium Ther Nucl Med. 1975 Dec;125(4):910-7
[
1239960.001
]
[Cites]
Br J Neurosurg. 2000 Oct;14(5):473-4
[
11198774.001
]
[Cites]
J Laryngol Otol. 1984 Aug;98(8):839-42
[
6470579.001
]
[Cites]
Arch Otorhinolaryngol. 1985;241(3):219-24
[
3896212.001
]
[Cites]
Cancer. 1986 Aug 15;58(4):985-93
[
3719562.001
]
[Cites]
Neurosurgery. 1986 Nov;19(5):820-3
[
3785633.001
]
[Cites]
J Surg Oncol. 1990 Mar;43(3):189-92
[
2314106.001
]
[Cites]
Mo Med. 1991 Sep;88(9):642-4
[
1745221.001
]
[Cites]
J Am Osteopath Assoc. 1991 Sep;91(9):895-7
[
1757281.001
]
[Cites]
J Clin Gastroenterol. 1993 Mar;16(2):143-5
[
8463618.001
]
[Cites]
Surg Today. 1993;23(7):632-4
[
8369615.001
]
[Cites]
Head Neck. 1993 Sep-Oct;15(5):455-8
[
8407319.001
]
[Cites]
Urology. 1995 Sep;46(3):406-7
[
7544935.001
]
[Cites]
J Gastroenterol. 1997 Apr;32(2):236-40
[
9085174.001
]
[Cites]
J Ultrasound Med. 1997 Nov;16(11):751-3
[
9360239.001
]
[Cites]
Tumori. 2004 Nov-Dec;90(6):535-46
[
15762353.001
]
[Cites]
Arch Ital Urol Androl. 2005 Jun;77(2):109-10
[
16146273.001
]
[Cites]
Urology. 2005 Oct;66(4):881
[
16230172.001
]
[Cites]
J Clin Gastroenterol. 2001 May-Jun;32(5):439-40
[
11319319.001
]
[Cites]
J Dermatol. 2006 Jan;33(1):46-51
[
16469085.001
]
[Cites]
Mil Med. 2000 Dec;165(12):973-4
[
11149072.001
]
[Cites]
Cancer. 1981 Sep 1;48(5):1262-4
[
7272958.001
]
(PMID = 17207288.001).
[ISSN]
1477-7819
[Journal-full-title]
World journal of surgical oncology
[ISO-abbreviation]
World J Surg Oncol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC1779271
[General-notes]
NLM/ Original DateCompleted: 20070802
7.
Pontes J Jr, Srougi M, Borra PM, Dall' Oglio MF, Ribeiro-Filho LA, Leite KR:
E-cadherin and beta-catenin loss of expression related to bone metastasis in prostate cancer.
Appl Immunohistochem Mol Morphol
; 2010 Mar;18(2):179-84
[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]
E-cadherin and beta-catenin loss of expression related to bone
metastasis in
prostate
cancer
.
A disturbance in epithelial cell adhesion, which leads
to a
more invasive and
metastatic
phenotype, is a hallmark
of tumor
progression.
Several immunohistochemical studies have reported a strong correlation between loss of their expression to higher stage and grade in
prostate
carcinoma, but their influence
in metastatic
process is not yet known.
The aim of this study is to verify the role of adhesion molecules in the progression of
prostate
cancer
(PC), assessing the expression of E-cadherin and beta-catenin in bone
metastasis
.
MATERIALS AND METHODS: Twenty-eight bone
metastases of
prostate
carcinoma were submitted to immunohistochemistry analysis for E-cadherin and beta-catenin expression.
In 6 patients, we were able to assess the expression of the adhesion molecules in the primary tumors and their respective
metastases
.
The definition of normal expression for both antibodies was strong and diffuse expression in more than 70%
of tumor
cells.
RESULTS: In bone
metastases
, there was loss of expression of E-cadherin and beta-catenin in 86% and 82%, respectively.
Considering the 6 patients with paired primary and bone
metastasis
, we found loss of expression for both E-cadherin and beta-catenin in most of the cases.
CONCLUSIONS: Comparing primary PC and its
metastasis
, we showed persistent loss of E-cadherin and beta-catenin expression.
This phenomenon may be related
to metastatic
potential in PC, because we have shown underexpression for E-cadherin and beta-catenin in 86% and 82% of bone
metastases
.
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate 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 = 18685493.001).
[ISSN]
1533-4058
[Journal-full-title]
Applied immunohistochemistry & molecular morphology : AIMM
[ISO-abbreviation]
Appl. Immunohistochem. Mol. Morphol.
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Cadherins; 0 / beta Catenin
8.
Roma AA, Magi-Galluzzi C, Kral MA, Jin TT, Klein EA, Zhou M:
Peritumoral lymphatic invasion is associated with regional lymph node metastases in prostate adenocarcinoma.
Mod Pathol
; 2006 Mar;19(3):392-8
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Peritumoral lymphatic invasion is associated with regional lymph node
metastases in
prostate
adenocarcinoma.
Lymphangiogenesis, detected by antibodies specific for lymphatic endothelial cells, has been associated with regional lymph node
metastases
and poor prognosis in carcinomas of head and neck, breast and uterine cervix, but remains largely uninvestigated in
prostate
adenocarcinoma.
We evaluated the lymphatic vessel density and lymphatic vessel invasion by
prostate
cancer
cells in the intratumoral, peritumoral and normal
prostate
tissue compartments
in cancer
-bearing
prostate
glands and correlated them with lymph node
metastases
, Gleason score and other pathological parameters.
In all, 26 patients had lymph node dissection, and 14 of them had lymph node
metastasis
.
Lymphatic vessel density in the intratumoral, peritumoral and normal
prostate
compartments was 0.91+/-0.80, 1.54+/-0.68 and 1.58+/-0.96/mm2, respectively.
The intratumoral lymphatic vessel density was significantly lower than that of the peritumoral and normal
prostate
compartments, and the latter two were not significantly different.
The lymphatic vessel density of the three compartments was not significantly different between cases with and without lymph node
metastasis
.
Lymphatic vessel invasion was present in significantly higher percentage of cases with lymph node
metastasis
(9/14, 62.3%), as compared to those without lymph node
metastasis
(1/12, 8.3%, P<0.01).
The peritumoral lymphatic vessel invasion had a better correlation with the presence of lymph node
metastases
than intratumoral lymphatic vessel invasion.
There is no evidence of lymphangiogenesis in
prostate
adenocarcinoma.
Peritumoral lymphatic vessel invasion correlates with regional lymph node
metastases
, suggesting that the peritumoral lymphatic vessels are functionally important and identification of lymphatic vessel invasion in this compartment implies a high probability of regional lymph node
metastases
.
[MeSH-minor]
Aged. Endothelial Cells / chemistry. Endothelial Cells / pathology. Humans. Immunohistochemistry. Lymphatic
Metastasis
. Male. Middle Aged.
Neoplasm
Invasiveness.
Prostate
/ blood supply.
Prostate
/ pathology. Sialoglycoproteins / analysis
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16400321.001).
[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
[Publication-country]
United States
[Chemical-registry-number]
0 / Sialoglycoproteins
9.
Reyes I, Tiwari R, Geliebter J, Reyes N:
DNA microarray analysis reveals metastasis-associated genes in rat prostate cancer cell lines.
Biomedica
; 2007 Jun;27(2):190-203
[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]
DNA microarray analysis reveals
metastasis
-associated genes in rat
prostate
cancer
cell lines.
INTRODUCTION: The molecular and cellular mechanisms involved in
prostate
cancer
progression towards a hormone-independent and highly invasive,
metastatic
phenotype, are not well understood.
Cell lines with different
metastatic
potential, when analyzed by microarray techniques, offer valuable tools for identifying genes associated with
the metastatic
phenotype.
OBJECTIVES: Gene expression profiles were compared for two rat
prostate
cancer
cell lines with differing
metastatic
abilities in order to better characterized molecular underpinnings of the
prostate
cancer metastatic
process.
MATERIALS AND METHODS: Affymetrix arrays were used to analyze gene expression of two rat
prostate
cancer
cell lines, MAT-LyLu and G.
Many of these genes were not previously associated to
prostate
cancer metastasis
.
CONCLUSIONS: Many genes with altered expression associated with
a metastatic
prostate
cancer
phenotype were identified.
Further validation of these genes in human
prostate
samples will determine their usefulness as biomarkers for early
diagnosis of
recurrence or
metastasis of
prostate
cancer
, as well as potential therapeutic targets for this disease.
[MeSH-major]
Neoplasm Metastasis
/ genetics. Oligonucleotide Array Sequence Analysis. Prostatic Neoplasms
[MeSH-minor]
Animals. Biomarkers / metabolism. Cell Line,
Tumor
. Gene Expression Profiling. Humans. Male. Molecular Sequence Data. Phenotype. Rats
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17713630.001).
[ISSN]
0120-4157
[Journal-full-title]
Biomédica : revista del Instituto Nacional de Salud
[ISO-abbreviation]
Biomedica
[Language]
eng
[Databank-accession-numbers]
GEO/ GSE7703
[Grant]
United States / NCI NIH HHS / CA / 1R21 CA 088982
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
Colombia
[Chemical-registry-number]
0 / Biomarkers
10.
Damodaran D, Kathiresan N, Satheesan B:
Oral cavity metastasis: An unusual presentation of carcinoma prostate.
Indian J Urol
; 2008 Jan;24(1):112-3
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Oral cavity
metastasis
: An unusual presentation of carcinoma
prostate
.
The oral cavity is a very rare site for
metastases
and has been described in various cancers, particularly lung, breast, kidney and colon carcinoma.
Here a very rare case
of a
buccal
metastasis
from
prostate
carcinoma that was originally evaluated as a primary oral cavity malignancy is presented.
Histopathological examination
of a
biopsy of the lesion revealed papillary adenocarcinoma Grade II, nuclear Grade II, which initiated the evaluation of
prostate
.
On evaluation
diagnosis of
carcinoma
prostate
was made which was confirmed by immunohistochemistry for PSA.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Int J Cancer. 2005 Sep 20;116(5):740-54
[
15849747.001
]
[Cites]
Pathol Int. 1999 Jun;49(6):500-5
[
10469392.001
]
[Cites]
J Periodontol. 1999 Apr;70(4):441-4
[
10328657.001
]
[Cites]
Br J Oral Maxillofac Surg. 2003 Feb;41(1):3-6
[
12576032.001
]
[Cites]
BJU Int. 1999 Dec;84(9):1028-31
[
10571628.001
]
(PMID = 19468372.001).
[ISSN]
0970-1591
[Journal-full-title]
Indian journal of urology : IJU : journal of the Urological Society of India
[ISO-abbreviation]
Indian J Urol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
[Other-IDs]
NLM/ PMC2684236
[Keywords]
NOTNLM ; Oral cavity metastasis / prostate cancer / prostate specific antigen immunohistochemistry
11.
Shirakawa H, Kozakai N, Sugiura H, Hara S:
[Urinary bladder metastasis of prostate cancer : a case report].
Hinyokika Kiyo
; 2010 Feb;56(2):123-5
[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]
[Urinary bladder
metastasis of
prostate
cancer
: a case report].
The transrectal ultrasonography guided biopsy of the
prostate
revealed
prostate
cancer
.
Computed tomography, magnetic resonance imaging (MRI) and bone scintigraphy showed multiple
metastases to
his bones and lymph nodes.
The MRI incidentally revealed a solitary
tumor
at the right lateral wall of the urinary bladder.
Transurethral resection of the bladder
tumor
was performed, and histopathological examination showed the bladder
tumor
composed of not urothelial carcinoma but
metastatic
adenocarcinoma from
prostate
cancer
.
[MeSH-major]
Adenocarcinoma / pathology. Adenocarcinoma /
secondary
. Prostatic Neoplasms / pathology. Urinary Bladder Neoplasms /
secondary
Genetic Alliance.
consumer health - Bladder cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bladder Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20186001.001).
[ISSN]
0018-1994
[Journal-full-title]
Hinyokika kiyo. Acta urologica Japonica
[ISO-abbreviation]
Hinyokika Kiyo
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
12.
Pinzone JJ, Hall BM, Thudi NK, Vonau M, Qiang YW, Rosol TJ, Shaughnessy JD Jr:
The role of Dickkopf-1 in bone development, homeostasis, and disease.
Blood
; 2009 Jan 15;113(3):517-25
[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.
DKK1 has been implicated in causing erosive arthritis, the osteolytic phenotypes of multiple myeloma and
metastatic
breast
cancer
, and osteoblastic
metastases of
prostate
cancer
.
MedlinePlus Health Information.
consumer health - Bone Diseases
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Biol Chem. 2008 Jul 18;283(29):20505-22
[
18487199.001
]
[Cites]
Mol Cell Biol. 2008 Aug;28(15):4875-82
[
18505822.001
]
[Cites]
Int J Cancer. 2008 Oct 1;123(7):1526-35
[
18623132.001
]
[Cites]
Prostate. 2008 Sep 15;68(13):1396-404
[
18561248.001
]
[Cites]
Calcif Tissue Int. 2008 Jun;82(6):445-53
[
18521528.001
]
[Cites]
Blood. 2009 Jul 9;114(2):371-9
[
19417213.001
]
[Cites]
J Cell Biochem. 2004 Dec 15;93(6):1210-30
[
15486964.001
]
[Cites]
Development. 2005 Jan;132(1):49-60
[
15576404.001
]
[Cites]
Oncogene. 2005 Feb 3;24(6):1098-103
[
15592505.001
]
[Cites]
Annu Rev Immunol. 2005;23:1-21
[
15771564.001
]
[Cites]
Dev Cell. 2005 May;8(5):739-50
[
15866164.001
]
[Cites]
Dev Cell. 2005 May;8(5):751-64
[
15866165.001
]
[Cites]
J Biol Chem. 2005 Jun 3;280(22):21162-8
[
15802266.001
]
[Cites]
Mol Cell Biol. 2005 Jun;25(12):4946-55
[
15923613.001
]
[Cites]
J Biol Chem. 2005 Jul 22;280(29):26770-5
[
15908424.001
]
[Cites]
Cancer Res. 2005 Sep 1;65(17):7554-60
[
16140917.001
]
[Cites]
Blood. 2005 Oct 1;106(7):2472-83
[
15933061.001
]
[Cites]
Br J Haematol. 2005 Oct;131(1):71-3
[
16173965.001
]
[Cites]
J Biol Chem. 2005 Sep 30;280(39):33132-40
[
16043491.001
]
[Cites]
J Cell Biochem. 2006 Mar 1;97(4):661-72
[
16447163.001
]
[Cites]
Nat Immunol. 2006 Apr;7(4):333-7
[
16550195.001
]
[Cites]
J Cell Sci. 2006 Apr 1;119(Pt 7):1283-96
[
16522681.001
]
[Cites]
N Engl J Med. 2006 Mar 30;354(13):1362-9
[
16571879.001
]
[Cites]
Gene. 2006 May 10;372:62-70
[
16574347.001
]
[Cites]
Stem Cells. 2006 Apr;24(4):986-91
[
16293576.001
]
[Cites]
J Bone Miner Res. 2006 Jun;21(6):934-45
[
16753024.001
]
[Cites]
J Cell Sci. 2006 Jun 15;119(Pt 12):2613-20
[
16763196.001
]
[Cites]
Oncogene. 2006 Aug 17;25(36):5027-36
[
16568085.001
]
[Cites]
Cell. 2006 Nov 3;127(3):469-80
[
17081971.001
]
[Cites]
J Biol Chem. 2006 Dec 15;281(50):38276-84
[
17052975.001
]
[Cites]
J Biol Chem. 2007 Jan 5;282(1):526-33
[
17085452.001
]
[Cites]
Am J Pathol. 2007 Jan;170(1):160-75
[
17200191.001
]
[Cites]
Bone. 2007 Feb;40(2):485-92
[
17055793.001
]
[Cites]
Mol Endocrinol. 2007 Feb;21(2):486-98
[
17068196.001
]
[Cites]
Nat Med. 2007 Feb;13(2):156-63
[
17237793.001
]
[Cites]
Ann N Y Acad Sci. 2006 Dec;1092:385-96
[
17308163.001
]
[Cites]
Blood. 2007 Mar 1;109(5):2106-11
[
17068150.001
]
[Cites]
Br J Cancer. 2007 Feb 26;96(4):646-53
[
17245340.001
]
[Cites]
BMC Musculoskelet Disord. 2007;8:12
[
17295923.001
]
[Cites]
Stem Cells. 2007 Mar;25(3):544-52
[
17095705.001
]
[Cites]
Cancer Res. 2007 Mar 15;67(6):2517-25
[
17363569.001
]
[Cites]
FASEB J. 2007 May;21(7):1410-21
[
17283219.001
]
[Cites]
Blood. 2007 May 15;109(10):4470-7
[
17255354.001
]
[Cites]
Front Biosci. 2007;12:3068-92
[
17485283.001
]
[Cites]
Endocrinology. 2007 Jun;148(6):2635-43
[
17395698.001
]
[Cites]
Endocrinology. 2007 Jun;148(6):2630-4
[
17395705.001
]
[Cites]
J Cell Physiol. 2007 Sep;212(3):817-26
[
17458904.001
]
[Cites]
Nat Rev Cancer. 2007 Aug;7(8):585-98
[
17646864.001
]
[Cites]
J Cell Biochem. 2007 Aug 1;101(5):1109-24
[
17546602.001
]
[Cites]
PLoS Med. 2007 Jul 31;4(7):e249
[
17676991.001
]
[Cites]
Bone. 2007 Sep;41(3):331-9
[
17613296.001
]
[Cites]
Blood. 2007 Sep 1;110(5):1587-94
[
17515399.001
]
[Cites]
Leukemia. 2007 Sep;21(9):2035-42
[
17581613.001
]
[Cites]
Br J Cancer. 2007 Oct 8;97(7):964-70
[
17876334.001
]
[Cites]
Br J Haematol. 2007 Nov;139(3):434-8
[
17910634.001
]
[Cites]
J Clin Invest. 2007 Nov;117(11):3248-57
[
17948129.001
]
[Cites]
Nat Cell Biol. 2007 Nov;9(11):1273-85
[
17952062.001
]
[Cites]
Br J Cancer. 2007 Dec 3;97(11):1552-9
[
17987039.001
]
[Cites]
Leuk Lymphoma. 2007 Dec;48(12):2323-9
[
18067006.001
]
[Cites]
Blood. 2008 Mar 1;111(5):2833-42
[
18094333.001
]
[Cites]
Bone. 2008 Apr;42(4):669-80
[
18294945.001
]
[Cites]
Endocrinology. 2008 Apr;149(4):1793-801
[
18174290.001
]
[Cites]
Cell Stem Cell. 2008 Mar 6;2(3):274-83
[
18371452.001
]
[Cites]
Eur J Haematol. 2008 Jun;80(6):490-4
[
18331598.001
]
[Cites]
Mol Biol Cell. 2008 Jun;19(6):2588-96
[
18400942.001
]
[Cites]
Prostate. 2008 Jul 1;68(10):1116-25
[
18461562.001
]
[Cites]
Blood. 2008 Jul 1;112(1):196-207
[
18305214.001
]
[Cites]
Int J Cancer. 2008 Sep 1;123(5):1034-42
[
18546262.001
]
[Cites]
Blood. 2008 Jul 15;112(2):374-82
[
18344425.001
]
[Cites]
Dev Cell. 2008 Jul;15(1):37-48
[
18606139.001
]
[Cites]
Science. 2000 Aug 11;289(5481):950-3
[
10937998.001
]
[Cites]
Am J Hum Genet. 2001 Mar;68(3):577-89
[
11179006.001
]
[Cites]
Nature. 2001 May 17;411(6835):321-5
[
11357136.001
]
[Cites]
Dev Cell. 2001 Sep;1(3):423-34
[
11702953.001
]
[Cites]
Cell. 2001 Nov 16;107(4):513-23
[
11719191.001
]
[Cites]
Am J Hum Genet. 2002 Jan;70(1):11-9
[
11741193.001
]
[Cites]
N Engl J Med. 2002 Feb 21;346(8):564-9
[
11856795.001
]
[Cites]
EMBO J. 2002 Mar 1;21(5):966-75
[
11867524.001
]
[Cites]
J Cell Biol. 2002 Apr 15;157(2):303-14
[
11956231.001
]
[Cites]
N Engl J Med. 2002 May 16;346(20):1513-21
[
12015390.001
]
[Cites]
Nature. 2002 Jun 6;417(6889):664-7
[
12050670.001
]
[Cites]
Dev Biol. 2002 Nov 1;251(1):142-56
[
12413904.001
]
[Cites]
J Clin Invest. 2003 Jun;111(11):1771-82
[
12782679.001
]
[Cites]
J Bone Miner Res. 2003 Jun;18(6):960-74
[
12817748.001
]
[Cites]
N Engl J Med. 2003 Jun 26;348(26):2609-17
[
12826635.001
]
[Cites]
Immunol Rev. 2003 Aug;194:140-63
[
12846813.001
]
[Cites]
J Biol Chem. 2003 Jul 25;278(30):28067-78
[
12740383.001
]
[Cites]
Development. 2003 Sep;130(18):4295-305
[
12900447.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):10954-9
[
12941866.001
]
[Cites]
N Engl J Med. 2003 Dec 25;349(26):2483-94
[
14695408.001
]
[Cites]
Cytokine Growth Factor Rev. 2004 Feb;15(1):49-60
[
14746813.001
]
[Cites]
Development. 2004 Jun;131(11):2543-52
[
15115753.001
]
[Cites]
Dev Biol. 2004 Aug 1;272(1):39-52
[
15242789.001
]
[Cites]
Stem Cells. 2004;22(5):849-60
[
15342948.001
]
[Cites]
J Biol Chem. 1996 Oct 18;271(42):26131-7
[
8824257.001
]
[Cites]
Biochem Biophys Res Commun. 1997 Jul 18;236(2):502-4
[
9240469.001
]
[Cites]
Nature. 1998 Jan 22;391(6665):357-62
[
9450748.001
]
[Cites]
Nature. 1999 Apr 1;398(6726):431-6
[
10201374.001
]
[Cites]
J Bone Miner Res. 2004 Dec;19(12):2033-40
[
15537447.001
]
(PMID = 18687985.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / K08 CA101875; United States / NCI NIH HHS / CA / P01 CA055819; United States / NCI NIH HHS / CA / CA101875; United States / NCI NIH HHS / CA / CA55819
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / DKK1 protein, human; 0 / Intercellular Signaling Peptides and Proteins
[Number-of-references]
100
[Other-IDs]
NLM/ PMC2628360
13.
Saad F:
The role of bisphosphonates in the management of prostate cancer.
Curr Oncol Rep
; 2006 May;8(3):221-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The role of bisphosphonates in the management of
prostate
cancer
.
Current therapies have extended the survival of patients with
prostate
cancer
.
Low bone mineral density (BMD) is prevalent in patients with early-stage
prostate
cancer
, and androgen-deprivation therapy by either pharmaceutical agent (including hormonal) or surgical castration causes significant decreases in BMD.
Fractures can result
in a
loss of independence and have been associated with shorter survival in patients with
prostate
cancer
.
Zoledronic acid is the only bisphosphonate that has demonstrated objective and long-term benefits in reducing skeletal morbidity in patients with bone
metastases
due to
prostate
cancer
, and it has produced long-term reductions in pain levels compared with placebo in this setting.
Therefore, bisphosphonates, particularly zoledronic acid, may provide important benefits for preserving bone health during the course of
prostate
cancer
progression.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Density
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Acta Oncol. 2005;44(3):282-92
[
16076701.001
]
[Cites]
Curr Opin Oncol. 2002 Nov;14(6):609-15
[
12409650.001
]
[Cites]
J Natl Cancer Inst. 2003 Sep 3;95(17 ):1300-11
[
12953084.001
]
[Cites]
J Clin Invest. 1996 Jun 15;97(12):2692-6
[
8675678.001
]
[Cites]
J Urol. 2002 Jun;167(6):2361-7; discussion 2367
[
11992038.001
]
[Cites]
Drugs Aging. 2003;20(3):175-83
[
12578398.001
]
[Cites]
CA Cancer J Clin. 2005 Jan-Feb;55(1):10-30
[
15661684.001
]
[Cites]
J Urol. 2000 Jan;163(1):181-6
[
10604342.001
]
[Cites]
Cancer. 2004 Mar 1;100(5):892-9
[
14983482.001
]
[Cites]
Clin Cancer Res. 2003 Jan;9(1):295-306
[
12538482.001
]
[Cites]
J Urol. 1997 Feb;157(2):439-44
[
8996327.001
]
[Cites]
Cancer. 1998 Oct 15;83(8):1561-6
[
9781950.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Dec;90(12):6410-7
[
16189261.001
]
[Cites]
Am J Clin Oncol. 2002 Dec;25(6 Suppl 1):S10-8
[
12562046.001
]
[Cites]
Cancer. 2000 Jun 15;88(12 Suppl):2989-94
[
10898342.001
]
[Cites]
Br J Cancer. 2003 Jan 27;88(2):195-201
[
12610502.001
]
[Cites]
Eur J Surg. 1994 Oct;160(10):535-42
[
7849154.001
]
[Cites]
Cochrane Database Syst Rev. 2002;(2):CD002068
[
12076438.001
]
[Cites]
Cancer Chemother Pharmacol. 2006 Jan;57(1):46-51
[
16001175.001
]
[Cites]
N Engl J Med. 2001 Sep 27;345(13):948-55
[
11575286.001
]
[Cites]
J Natl Cancer Inst. 2002 Oct 2;94(19):1458-68
[
12359855.001
]
[Cites]
J Urol. 2003 Jun;169(6):2008-12
[
12771706.001
]
[Cites]
Cancer Invest. 2002;20 Suppl 2:45-54
[
12442349.001
]
[Cites]
Semin Oncol. 2002 Dec;29(6 Suppl 21):19-27
[
12584691.001
]
[Cites]
Ann Oncol. 2005 Apr;16(4):579-84
[
15734776.001
]
[Cites]
J Natl Cancer Inst. 2005 Jan 5;97(1):59-69
[
15632381.001
]
[Cites]
J Clin Oncol. 2003 Dec 1;21(23):4277-84
[
14581438.001
]
[Cites]
Semin Nucl Med. 2001 Jan;31(1):62-8
[
11200206.001
]
[Cites]
J Chemother. 2005 Oct;17(5):555-9
[
16323446.001
]
[Cites]
Urology. 2002 Sep;60(3 Suppl 1):79-85; discussion 86
[
12231056.001
]
[Cites]
J Natl Cancer Inst. 2004 Jun 2;96(11):879-82
[
15173273.001
]
[Cites]
J Urol. 2002 Sep;168(3):1005-7
[
12187209.001
]
[Cites]
J Urol. 2000 Oct;164(4):1248-53
[
10992374.001
]
[Cites]
J Urol. 1989 Jan;141(1):85-7
[
2462069.001
]
[Cites]
N Engl J Med. 2005 Jan 13;352(2):154-64
[
15647578.001
]
[Cites]
CMAJ. 1998 Sep 22;159(6):685-91
[
9780970.001
]
[Cites]
Anticancer Res. 1997 Nov-Dec;17(6D):4717-21
[
9494595.001
]
[Cites]
Cancer Metastasis Rev. 2001;20(3-4):333-49
[
12085970.001
]
[Cites]
Cancer Treat Rev. 2001 Jun;27(3):165-76
[
11417967.001
]
[Cites]
Urology. 2005 Nov;66(5):1054-9
[
16286123.001
]
[Cites]
J Neurooncol. 1995;23(2):135-47
[
7543940.001
]
[Cites]
Pain. 1997 Jan;69(1-2):1-18
[
9060007.001
]
[Cites]
Br J Cancer. 1997;76(7):939-42
[
9328156.001
]
[Cites]
BJU Int. 2000 Sep;86(4):449-52
[
10971270.001
]
[Cites]
Cancer. 2001 Jun 15;91(12):2238-45
[
11413511.001
]
[Cites]
Int Urol Nephrol. 1992;24(2):159-66
[
1385586.001
]
[Cites]
J Clin Oncol. 2003 Sep 1;21(17):3335-42
[
12947070.001
]
(PMID = 16618387.001).
[ISSN]
1523-3790
[Journal-full-title]
Current oncology reports
[ISO-abbreviation]
Curr Oncol Rep
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgen Antagonists; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
[Number-of-references]
50
14.
Cai T, Salvadori A, Nesi G, Detti B, Tinacci G, Zini E, Bartoletti R:
Penile metastasis from a T1b prostate carcinoma.
Onkologie
; 2007 May;30(5):249-52
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Penile
metastasis
from a T1b
prostate
carcinoma.
BACKGROUND: Penile
metastasis
from incidental
prostate
carcinoma has not been described to date.
CASE REPORT: The case
of a
72-year-old man affected by penile
metastasis
from incidental
prostate
carcinoma is described.
In March 1998, the patient underwent
prostate
surgery for lower urinary tract symptoms related to benign prostatic obstruction.
Histological examination revealed an incidental adenocarcinoma of the
prostate
.
The pre-operative
prostate
-specific antigen (PSA) value was 3.6 ng/ml.
A
prostate
biopsy in the peripheral
prostate
lobes was negative.
The
prostate
biopsy was repeated and was still negative.
Surgical biopsy showed
a metastasis
from
prostate
adenocarcinoma and he underwent partial penectomy.
CONCLUSION: We underline the uncertainty of the biological behaviour and optimal management of incidentally identified
prostate
carcinoma.
[MeSH-major]
Adenocarcinoma /
secondary
. Penile Neoplasms /
secondary
. Prostatic Neoplasms / pathology
[MeSH-minor]
Aged. Biomarkers,
Tumor
/ blood. Biopsy. Disease Progression. Humans. Incidental Findings. Male.
Neoplasm
Staging. Palliative Care. Penis / pathology.
Prostate
/ pathology.
Prostate
-Specific Antigen / blood. Prostatectomy
MedlinePlus Health Information.
consumer health - Prostate 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 = 17460419.001).
[ISSN]
0378-584X
[Journal-full-title]
Onkologie
[ISO-abbreviation]
Onkologie
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
15.
Challagundla S, Gokden M, Viswamitra S, Kohli M:
Orbital metastasis from prostate cancer: an atypical case of neuroendocrine dedifferentiation during progression from hormone-sensitive to refractory stage.
Clin Prostate Cancer
; 2005 Sep;4(2):134-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Orbital
metastasis
from
prostate
cancer
: an atypical case of neuroendocrine dedifferentiation during progression from hormone-sensitive to refractory stage.
We report a case of orbital
metastasis
from a neuroendocrine dedifferentiated
prostate
cancer
during progression from hormone-sensitive to hormone refractory stage.
A patient receiving androgen deprivation for hormone-sensitive
prostate
cancer
presented with sudden-onset right-sided ptosis and an increasing serum
prostate
-specific antigen level.
Comparison of the
metastatic
histology with the original pathology confirmed a histologic change to poorly differentiated
prostate
adenocarcinoma with neuroendocrine features.
Because
prostate
cancer metastasis
involves hematogenous and lymphatic routes, we also evaluated expression of the vascular endothelial growth factor (VEGF) and receptors (VEGFR-1, VEGFR-2, and VEGFR-3) in the
metastatic
deposit by immunohistochemistry.
Strong expression of VEGFR-2 and VEGFR-3 restricted to the
malignant
epithelium was noted.
We recommend a second biopsy of atypical
prostate
metastasis
associated with sudden change to aggressive clinical behavior in order to evaluate for dedifferentiation features before planning appropriate treatment interventions especially in patients who are candidates for systemic chemotherapy.
[MeSH-major]
Carcinoma, Neuroendocrine /
secondary
. Orbital Neoplasms /
secondary
. Prostatic Neoplasms / pathology
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16197616.001).
[ISSN]
1540-0352
[Journal-full-title]
Clinical prostate cancer
[ISO-abbreviation]
Clin Prostate Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Synaptophysin; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
16.
Ripamonti C, Fagnoni E, Campa T, Seregni E, Maccauro M, Bombardieri E:
Incident pain and analgesic consumption decrease after samarium infusion: a pilot study.
Support Care Cancer
; 2007 Mar;15(3):339-42
[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.
OBJECTIVE: The aim of this pilot study was to observe the variations of pain intensity on movement and at rest and the variation of analgesic drug consumption in patients with
prostate
cancer
and painful bone
metastases
treated with a single dose of 1.0 mCi/kg of samarium-153 (153-Sm) lexidronam.
SETTING: The Nuclear Medicine Unit and Pain Therapy and Palliative Care Unit, National
Cancer
Institute of Milan, Italy.
PATIENTS: Thirteen outpatients with hormone refractory
prostate
cancer
and painful multiple bone
metastases
.
INTERVENTIONS: Infusion
of a
single dose of 1.0 mCi/kg of 153-Sm lexidronam, pain therapy, and the assessment of pain intensity at rest and on movement.
MAIN OUTCOME MEASURES: Variation of pain intensity on movement and at rest by means
of a
verbal scale and the reduction of analgesic drug consumption 4 weeks after infusion of 153-Sm lexidronam.
CONCLUSIONS: In patients with bone
metastases
, pain on movement is a frequent and often difficult clinical problem to treat and the most frequent cause of breakthrough pain.
In patients with painful multiple bone
metastases
due to
prostate
cancer
, the infusion
of a
single dose of 1.0 mCi/kg of 153-Sm lexidronam may be considered an effective and safe treatment for pain either at rest or during movement.
[MeSH-minor]
Aged. Analgesics, Opioid / therapeutic use. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Bone Marrow / drug effects. Bone Neoplasms /
secondary
. Dose-Response Relationship, Drug. Humans. Infusions, Intravenous. Male. Middle Aged. Morphine / therapeutic use. Movement. Pain Measurement. Pilot Projects. Prospective Studies. Prostatic Neoplasms / pathology. Rest. Severity of Illness Index. Treatment Outcome
MedlinePlus Health Information.
consumer health - Pain
.
MedlinePlus Health Information.
consumer health - Pain Relievers
.
Hazardous Substances Data Bank.
MORPHINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Cancer Res Clin Oncol. 2005 Jan;131(1):60-6
[
15449184.001
]
[Cites]
J Pain Symptom Manage. 1995 Jul;10(5):348-55
[
7673767.001
]
[Cites]
J Clin Oncol. 2002 Sep 1;20(17):3719-36
[
12202673.001
]
[Cites]
Eur J Cancer. 1997 Sep;33(10 ):1583-91
[
9389919.001
]
[Cites]
Pain. 1999 Sep;82(3):263-74
[
10488677.001
]
[Cites]
Cancer. 2000 Jun 15;88(12 Suppl):2934-9
[
10898337.001
]
[Cites]
Pain. 1992 Aug;50(2):151-5
[
1408310.001
]
[Cites]
Pain. 1990 Jun;41(3):273-81
[
1697056.001
]
[Cites]
Urology. 2004 May;63(5):940-5
[
15134985.001
]
[Cites]
J Nucl Med. 1992 Aug;33(8):1451-8
[
1378887.001
]
[Cites]
Pain. 1991 Nov;47(2):129-34; discussion 127-8
[
1762805.001
]
[Cites]
Cancer. 2002 Feb 1;94(3):832-9
[
11857319.001
]
[Cites]
J Pain Symptom Manage. 2000 Aug;20(2):87-92
[
10989246.001
]
[Cites]
Lancet Oncol. 2005 Jun;6(6):392-400
[
15925817.001
]
[Cites]
Br J Cancer. 1987 Jan;55(1):61-6
[
3814476.001
]
[Cites]
Pain. 1999 May;81(1-2):129-34
[
10353500.001
]
[Cites]
Cochrane Database Syst Rev. 2003;(4):CD003347
[
14583970.001
]
[Cites]
Pain. 1994 Oct;59(1):141-5
[
7531837.001
]
[Cites]
Pain. 1989 May;37(2):203-9
[
2748193.001
]
[Cites]
J Clin Oncol. 1998 Apr;16(4):1574-81
[
9552068.001
]
[Cites]
J Clin Oncol. 2003 Nov 1;21(21):4042-57
[
12963702.001
]
(PMID = 16967302.001).
[ISSN]
0941-4355
[Journal-full-title]
Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer
[ISO-abbreviation]
Support Care Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Analgesics, Non-Narcotic; 0 / Analgesics, Opioid; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Organometallic Compounds; 0 / Organophosphorus Compounds; 745X144DZY / samarium Sm-153 lexidronam; 76I7G6D29C / Morphine
17.
Salvati M, Frati A, Russo N, Brogna C, Piccirilli M, D'Andrea G, Occhiogrosso G, Pichierri A, Caroli E:
Brain metastasis from prostate cancer. Report of 13 cases and critical analysis of the literature.
J Exp Clin Cancer Res
; 2005 Jun;24(2):203-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Brain
metastasis
from
prostate
cancer
. Report of 13 cases and critical analysis of the literature.
Brain
metastasis
from
prostate
carcinoma occurs very rarely.
We describe 13 patients with single brain
metastasis
from prostatic
cancer
.
Eight patients died for systemic disease after a mean time of 9.2 months with
a diagnosis of metastasis
.
Even if brain
metastasis
from
prostate
cancer
is often a terminal event with death occurring within few months from
diagnosis
, we suggest the same protocol (surgery and/or radiosurgery plus postoperative WBRT) usually adopted to treat brain
metastasis
from other primitive tumours.
A non specific neurological symptomatology and a possible normal dosage of serum specific antigen may contribute
to a
delay
in diagnosis
.
However, considering the rarity of brain
metastasis
from
prostate
carcinoma, standard brain MRI follow-up in men with prostatic
cancer
does not seem to be necessary yet.
[MeSH-major]
Brain Neoplasms /
secondary
. Prostatic Neoplasms / pathology
[MeSH-minor]
Aged. Humans. Male. Middle Aged.
Neoplasm Metastasis
. Time Factors. Treatment Outcome
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Brain Cancer
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16110752.001).
[ISSN]
0392-9078
[Journal-full-title]
Journal of experimental & clinical cancer research : CR
[ISO-abbreviation]
J. Exp. Clin. Cancer Res.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Italy
18.
Kobashi-Katoh R, Tanioka M, Takahashi K, Miyachi Y:
Skin metastasis of prostate adenocarcinoma to glans penis showing no correlation with serum prostate-specific antigen level.
J Dermatol
; 2009 Feb;36(2):106-8
[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]
Skin
metastasis of
prostate
adenocarcinoma to glans penis showing no correlation with serum
prostate
-specific antigen level.
[MeSH-major]
Adenocarcinoma /
secondary
. Biomarkers,
Tumor
/ blood. Penile Neoplasms /
secondary
.
Prostate
-Specific Antigen / blood. Prostatic Neoplasms / pathology. Skin Neoplasms /
secondary
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer Screening
.
MedlinePlus Health Information.
consumer health - Skin Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19284456.001).
[ISSN]
1346-8138
[Journal-full-title]
The Journal of dermatology
[ISO-abbreviation]
J. Dermatol.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
Japan
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
19.
Saeki N, Gu J, Yoshida T, Wu X:
Prostate stem cell antigen: a Jekyll and Hyde molecule?
Clin Cancer Res
; 2010 Jul 15;16(14):3533-8
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Prostate
stem cell antigen: a Jekyll and Hyde molecule?
Prostate
stem cell antigen (PSCA) is a glycosylphosphatidylinositol (GPI)-anchored cell surface protein.
Although PSCA is thought to be involved in intracellular signaling, much remains unknown about its physiological function and regulatory mechanism in normal and
cancer
cells.
It is up-regulated in several major cancers including
prostate
, bladder, and pancreatic cancers.
The expression of PSCA is positively correlated with advanced clinical stage and
metastasis in
prostate
cancers and is also associated with
malignant
progression of premalignant
prostate
lesions.
Therefore, PSCA has been proposed as a biomarker
of diagnosis
and prognosis, as well as a target of therapy for these cancers.
In addition, PSCA has also shown clinical potential in immunotherapy as a
prostate
-specific antigen, which, when presented by dendritic cells, may elicit strong
tumor
-specific immunity.
In contrast, PSCA is down-regulated in esophageal and gastric
cancer
and may have
a tumor
-suppressing function in the gastric epithelium.
Recent exciting findings that genetic variations of PSCA conferred increased risks of gastric
cancer
and bladder
cancer
have opened up a new avenue of research about the pathological function of PSCA.
PSCA seems to be a Jekyll and Hyde molecule that plays differential roles,
tumor
promoting or suppressing, depending on the cellular context.
MedlinePlus Health Information.
consumer health - Bladder Cancer
.
MedlinePlus Health Information.
consumer health - Pancreatic Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2010 AACR.
[Cites]
Protein Sci. 2004 Aug;13(8):2045-58
[
15273305.001
]
[Cites]
J Gene Med. 2007 Aug;9(8):715-26
[
17595048.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1735-40
[
9465086.001
]
[Cites]
Int J Gynecol Pathol. 2005 Jan;24(1):67-72
[
15626919.001
]
[Cites]
Clin Cancer Res. 2005 Apr 1;11(7):2591-6
[
15814638.001
]
[Cites]
Pancreas. 2005 Aug;31(2):119-25
[
16024997.001
]
[Cites]
Cancer Res. 2005 Oct 15;65(20):9495-500
[
16230414.001
]
[Cites]
Prostate. 2005 Dec 1;65(4):299-305
[
16015594.001
]
[Cites]
BJU Int. 2006 Jun;97(6):1202-7
[
16686711.001
]
[Cites]
BJU Int. 2006 Sep;98(3):668-73
[
16925770.001
]
[Cites]
Cancer Immunol Immunother. 2006 Dec;55(12):1524-33
[
16612599.001
]
[Cites]
Int J Cancer. 2006 Nov 15;119(10):2428-34
[
16977630.001
]
[Cites]
Prostate. 2007 May 1;67(6):653-60
[
17342746.001
]
[Cites]
Int J Cancer. 2008 Feb 15;122(4):864-70
[
17957793.001
]
[Cites]
Prostate. 2008 Feb 1;68(2):139-51
[
18044730.001
]
[Cites]
Prostate. 2008 Feb 1;68(2):190-9
[
18076024.001
]
[Cites]
Histopathology. 2008 Jan;52(2):167-74
[
18184265.001
]
[Cites]
Cancer Res. 2008 Feb 1;68(3):861-9
[
18245488.001
]
[Cites]
Lancet. 2008 May 17;371(9625):1710-21
[
18486743.001
]
[Cites]
Nat Genet. 2008 Jun;40(6):730-40
[
18488030.001
]
[Cites]
Mol Cancer Res. 2008 Jul;6(7):1154-68
[
18644980.001
]
[Cites]
Clin Cancer Res. 2008 Nov 15;14(22):7488-96
[
19010866.001
]
[Cites]
Nat Rev Cancer. 2008 Dec;8(12):976-90
[
19029958.001
]
[Cites]
Protein Eng Des Sel. 2009 Mar;22(3):209-16
[
18957406.001
]
[Cites]
ACS Nano. 2009 Mar 24;3(3):502-10
[
19243145.001
]
[Cites]
Clin Chem. 2009 Apr;55(4):765-73
[
19233911.001
]
[Cites]
Mol Ther. 2009 Jun;17(6):1101-8
[
19337234.001
]
[Cites]
Prostate. 2009 Jul 1;69(10):1101-8
[
19343734.001
]
[Cites]
Prostate. 2009 Sep 1;69(12):1292-302
[
19462463.001
]
[Cites]
Nat Genet. 2009 Sep;41(9):991-5
[
19648920.001
]
[Cites]
Nat Rev Cancer. 2009 Dec;9(12):874-85
[
19935676.001
]
[Cites]
J Neurosci. 2009 Nov 25;29(47):14847-54
[
19940180.001
]
[Cites]
J Surg Oncol. 2010 Feb 1;101(2):145-8
[
20039280.001
]
[Cites]
Cancer Treat Rev. 2010 Apr;36(2):131-41
[
19954892.001
]
[Cites]
Carcinogenesis. 2010 Apr;31(4):621-4
[
20083643.001
]
[Cites]
Int J Cancer. 2010 Nov 1;127(9):2183-9
[
20131315.001
]
[Cites]
Mol Imaging. 2007 Mar-Apr;6(2):131-9
[
17445507.001
]
[Cites]
J Immunother. 2007 May-Jun;30(4):396-405
[
17457214.001
]
[Cites]
Leukemia. 2007 May;21(5):868-76
[
17361230.001
]
[Cites]
Genes Chromosomes Cancer. 2000 Jan;27(1):95-103
[
10564591.001
]
[Cites]
Oncogene. 2000 Mar 2;19(10):1288-96
[
10713670.001
]
[Cites]
Biochem Biophys Res Commun. 2000 Sep 7;275(3):783-8
[
10973799.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Feb 27;98(5):2658-63
[
11226295.001
]
[Cites]
Cancer Lett. 2001 Jul 10;168(1):37-43
[
11368875.001
]
[Cites]
Cancer Res. 2001 Jun 1;61(11):4320-4
[
11389052.001
]
[Cites]
Cancer Res. 2001 Jun 15;61(12):4660-5
[
11406532.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):401-6
[
11752398.001
]
[Cites]
Cell Mol Life Sci. 2001 Dec;58(14):1969-87
[
11814051.001
]
[Cites]
Clin Cancer Res. 2002 Jun;8(6):1794-9
[
12060619.001
]
[Cites]
Mol Endocrinol. 2002 Oct;16(10):2323-37
[
12351697.001
]
[Cites]
Mol Cancer Res. 2002 Dec;1(2):113-21
[
12496358.001
]
[Cites]
Int J Cancer. 2003 Mar 1;103(6):768-74
[
12516096.001
]
[Cites]
J Urol. 2003 Jun;169(6):2094-100
[
12771726.001
]
[Cites]
Anticancer Res. 2003 May-Jun;23(3B):2711-6
[
12894563.001
]
[Cites]
Appl Immunohistochem Mol Morphol. 2003 Sep;11(3):238-43
[
12966350.001
]
[Cites]
Nat Rev Cancer. 2003 Oct;3(10):756-67
[
14570040.001
]
[Cites]
J Urol. 2004 Mar;171(3):1117-21
[
14767283.001
]
[Cites]
Prostate. 2007 Jul 1;67(10):1121-31
[
17492652.001
]
[Cites]
Oncol Rep. 2007 Jul;18(1):161-6
[
17549363.001
]
[Cites]
Prostate. 2007 Aug 1;67(11):1143-51
[
17503471.001
]
[Cites]
Arch Immunol Ther Exp (Warsz). 2004 Jul-Aug;52(4):255-66
[
15467490.001
]
(PMID = 20501618.001).
[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 / NCI NIH HHS / CA / P50 CA091846; United States / NCI NIH HHS / CA / R01 CA074880; United States / NCI NIH HHS / CA / U01 CA127615; United States / NCI NIH HHS / CA / CA127615-02; United States / NCI NIH HHS / CA / R01CA74880; United States / NCI NIH HHS / CA / R01 CA131335; United States / NCI NIH HHS / CA / P50CA91846; United States / NCI NIH HHS / CA / R01 CA131335-02; United States / NCI NIH HHS / CA / R01 CA074880-10; United States / NCI NIH HHS / CA / CA091846-090007; United States / NCI NIH HHS / CA / U01 CA127615-02; United States / NCI NIH HHS / CA / R01CA131335; United States / NCI NIH HHS / CA / P50 CA091846-090007; United States / NCI NIH HHS / CA / U01CA127615; United States / NCI NIH HHS / CA / CA074880-10; United States / NCI NIH HHS / CA / R01 CA111922; United States / NCI NIH HHS / CA / CA131335-02
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Neoplasm Proteins; 0 / PSCA protein, human
[Other-IDs]
NLM/ NIHMS204237; NLM/ PMC2905486
20.
Messiou C, Cook G, deSouza NM:
Imaging metastatic bone disease from carcinoma of the prostate.
Br J Cancer
; 2009 Oct 20;101(8):1225-32
[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]
Imaging
metastatic
bone disease from carcinoma of the
prostate
.
Imaging bone
metastases
from
prostate
cancer
presents several challenges.
Bone scintigraphy is the mainstay of lesion detection, but is often not suitable for assessment of treatment response, particularly because
of a
'flare' phenomenon after therapy.
This article reviews the available imaging modalities for evaluating prostatic bony
metastases
, and links them to the underlying pathological changes within bone lesions.
[MeSH-major]
Bone Neoplasms /
diagnosis
. Bone Neoplasms /
secondary
. Prostatic Neoplasms / pathology
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Eur J Nucl Med Mol Imaging. 2008 Oct;35(10):1766-74
[
18465129.001
]
[Cites]
Nucl Med Biol. 2008 Aug;35(6):689-95
[
18678354.001
]
[Cites]
Eur J Cancer. 2009 Jan;45(2):228-47
[
19097774.001
]
[Cites]
Radiology. 2008 Dec;249(3):1017-25
[
18849502.001
]
[Cites]
Cancer. 2002 Sep 1;95(5):1028-36
[
12209687.001
]
[Cites]
Cancer. 2003 Feb 1;97(3 Suppl):739-47
[
12548571.001
]
[Cites]
Cancer. 2003 Feb 1;97(3 Suppl):758-71
[
12548573.001
]
[Cites]
Br J Cancer. 2003 Jan 27;88(2):195-201
[
12610502.001
]
[Cites]
Acta Radiol. 2004 Feb;45(1):71-4
[
15164782.001
]
[Cites]
Radiology. 2004 Aug;232(2):599-605
[
15286325.001
]
[Cites]
Lancet Oncol. 2004 Oct;5(10):607-16
[
15465464.001
]
[Cites]
Radiology. 1983 Feb;146(2):513-8
[
6294738.001
]
[Cites]
Cancer. 1983 Aug 15;52(4):610-4
[
6861098.001
]
[Cites]
AJR Am J Roentgenol. 1984 Apr;142(4):773-6
[
6230903.001
]
[Cites]
Radiographics. 1991 Mar;11(2):219-32
[
2028061.001
]
[Cites]
Mayo Clin Proc. 1994 Jan;69(1):69-79
[
7505870.001
]
[Cites]
Radiology. 1996 Jun;199(3):751-6
[
8638000.001
]
[Cites]
Cancer. 1996 Oct 1;78(7):1388-94
[
8839543.001
]
[Cites]
Invest Radiol. 1997 Jun;32(6):344-50
[
9179709.001
]
[Cites]
J Nucl Med. 1998 Jun;39(6):990-5
[
9627331.001
]
[Cites]
Clin Cancer Res. 1998 Jul;4(7):1765-72
[
9676853.001
]
[Cites]
J Clin Oncol. 1999 Mar;17(3):948-57
[
10071289.001
]
[Cites]
Semin Nucl Med. 2005 Apr;35(2):135-42
[
15765376.001
]
[Cites]
Endocrinology. 2005 Apr;146(4):1727-36
[
15637291.001
]
[Cites]
Clin Cancer Res. 2005 May 1;11(9):3210-6
[
15867215.001
]
[Cites]
Prostate. 2005 Oct 1;65(2):178-87
[
15948151.001
]
[Cites]
Semin Nucl Med. 2006 Jan;36(1):73-92
[
16356797.001
]
[Cites]
J Nucl Med. 2006 Feb;47(2):287-97
[
16455635.001
]
[Cites]
Cancer Imaging. 2006;6:135-43
[
17015238.001
]
[Cites]
Radiology. 2007 Apr;243(1):204-11
[
17392254.001
]
[Cites]
Acta Radiol. 2000 Mar;41(2):178-82
[
10741794.001
]
[Cites]
Hum Pathol. 2000 May;31(5):578-83
[
10836297.001
]
[Cites]
Cancer. 2000 Jun 15;88(12 Suppl):2989-94
[
10898342.001
]
[Cites]
Eur J Nucl Med. 2000 Sep;27(9):1415-9
[
11007527.001
]
[Cites]
AJR Am J Roentgenol. 2001 Jun;176(6):1525-30
[
11373226.001
]
[Cites]
J Nucl Med. 2002 Feb;43(2):181-6
[
11850482.001
]
[Cites]
Urology. 2002 Jun;59(6):913-8
[
12031380.001
]
[Cites]
J Clin Oncol. 2007 Aug 1;25(22):3281-7
[
17664475.001
]
[Cites]
J Nucl Med. 2008 Dec;49(12):2031-41
[
18997047.001
]
(PMID = 19789531.001).
[ISSN]
1532-1827
[Journal-full-title]
British journal of cancer
[ISO-abbreviation]
Br. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0Z5B2CJX4D / Fluorodeoxyglucose F18
[Number-of-references]
39
[Other-IDs]
NLM/ PMC2768452
21.
Lattouf JB, Saad F:
Preservation of bone health in prostate cancer.
Curr Opin Support Palliat Care
; 2007 Oct;1(3):192-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Preservation of bone health in
prostate
cancer
.
PURPOSE OF REVIEW: Bone is the most common site
of metastasis
in
prostate
cancer
.
The burden of disease from bone
metastasis
has repercussions in terms of cost to society, decreased quality of life, and decreased survival.
Given the magnitude of bone-related morbidity in advanced
prostate
cancer
, physicians need to be aware of preventive and therapeutic measures, and to be proactive in implementing them.
RECENT FINDINGS: Patients with
prostate
cancer
are often osteopenic at baseline.
Bisphosphonates reduce androgen-deprivation therapy-related bone loss in
prostate
cancer
patients.
Zoledronic acid is the only bisphosphonate proven to decrease skeletal-related events
in a
randomized controlled trial in patients with
metastatic
prostate
cancer
.
SUMMARY: Bone mineral density loss and skeletal complications are directly related to androgen-deprivation therapy and
metastases in
prostate
cancer
patients.
[MeSH-major]
Androgen Antagonists / adverse effects. Bone Density / drug effects. Bone Density Conservation Agents / therapeutic use. Bone Neoplasms / drug therapy. Bone Neoplasms /
secondary
. Palliative Care / methods. Prostatic Neoplasms / pathology
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Bone Density
.
MedlinePlus Health Information.
consumer health - Palliative Care
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18685362.001).
[ISSN]
1751-4266
[Journal-full-title]
Current opinion in supportive and palliative care
[ISO-abbreviation]
Curr Opin Support Palliat Care
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Bone Density Conservation Agents; 0 / Diphosphonates
[Number-of-references]
61
22.
Suzuki H, Kamiya N, Yano M, Endo T, Takano M, Kawamura K, Imamoto T, Ichikawa T:
[Bone and Men's Health. Bisphosphonate therapy for prostate cancer].
Clin Calcium
; 2010 Feb;20(2):258-66
[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]
[Bone and Men's Health. Bisphosphonate therapy for
prostate
cancer
].
Recently,
prostate
cancer
is one of the common
cancer in
Japanese men, with a high incidence of bone
metastasis
.
Bone
metastasis
is incurable and contributes significantly to disease-specific morbidity and mortality.
And more, there are many opportunity to perform androgen deprivation therapy in
prostate
cancer
patients, but worsen osteoporosis and raise a risk of bone fracture.
The bisphosphonates are targeted to osteoclasts and are considered to be standard management in the care of bone
metastasis
patients in combination with chemotherapy and hormone therapy.
In this review, we summarized the current understanding and therapy of bone
metastasis in
prostate
cancer in
mainly respect to Zoredronic acid use.
[MeSH-major]
Bone Density Conservation Agents / therapeutic use. Bone Neoplasms / drug therapy. Bone Neoplasms /
secondary
. Diphosphonates / therapeutic use. Imidazoles / therapeutic use. Prostatic Neoplasms / drug therapy
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20118519.001).
[ISSN]
0917-5857
[Journal-full-title]
Clinical calcium
[ISO-abbreviation]
Clin Calcium
[Language]
jpn
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Japan
[Chemical-registry-number]
0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
[Number-of-references]
22
23.
Dimitroff CJ, Descheny L, Trujillo N, Kim R, Nguyen V, Huang W, Pienta KJ, Kutok JL, Rubin MA:
Identification of leukocyte E-selectin ligands, P-selectin glycoprotein ligand-1 and E-selectin ligand-1, on human metastatic prostate tumor cells.
Cancer Res
; 2005 Jul 1;65(13):5750-60
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Identification of leukocyte E-selectin ligands, P-selectin glycoprotein ligand-1 and E-selectin ligand-1, on human
metastatic
prostate
tumor
cells.
Prostate
tumor
cells, which characteristically metastasize to bone, initiate binding interactions with bone marrow endothelium under blood flow conditions through binding interactions with E-selectin.
We hypothesized that E-selectin ligands on
prostate
tumor
cells are directly associated with bone-
metastatic
potential.
In this report, we elucidate the identity of E-selectin ligands on human
metastatic
prostate
tumor
cells and examine their association with
prostate
tumor
progression and
metastasis in
vivo.
To our surprise, we found that the E-selectin-binding form of P-selectin glycoprotein ligand-1 (PSGL-1) is expressed on the human bone-
metastatic
prostate
tumor
MDA PCa 2b cell line.
Interestingly, we also found that human
prostate
tumor
cells derived from bone, lymph node, and brain
metastases
expressed another leukocyte E-selectin ligand, E-selectin ligand-1 (ESL-1).
Immunohistochemical analysis of PSGL-1 and ESL-1 in normal
prostate
tissue and in localized and
metastatic
prostate
tumors revealed that ESL-1 was principally localized to intracellular cell membrane and expressed on all normal and
malignant
prostate
tissue, whereas PSGL-1 was notably detected on the surfaces of bone-
metastatic
prostate
tumor
cells.
These findings implicate a functional role of PSGL-1 in the bone tropism of
prostate
tumor
cells and establish a new perspective into the molecular mechanism of human
prostate
tumor metastasis
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Res. 2004 Dec 15;64(24):9209-16
[
15604294.001
]
[Cites]
Int J Cancer. 2004 Aug 10;111(1):152-9
[
15185357.001
]
[Cites]
J Cell Biol. 2001 Jun 11;153(6):1277-86
[
11402070.001
]
[Cites]
Am J Pathol. 2001 Sep;159(3):837-43
[
11549576.001
]
[Cites]
Cancer Res. 2002 Mar 15;62(6):1832-7
[
11912162.001
]
[Cites]
JAMA. 2002 Apr 3;287(13):1662-70
[
11926890.001
]
[Cites]
J Immunol. 2002 Jun 1;168(11):5645-51
[
12023362.001
]
[Cites]
Nat Rev Cancer. 2002 Aug;2(8):563-72
[
12154349.001
]
[Cites]
Nat Rev Cancer. 2002 Aug;2(8):584-93
[
12154351.001
]
[Cites]
J Clin Invest. 2002 Aug;110(4):559-69
[
12189250.001
]
[Cites]
Blood. 2003 Jan 15;101(2):602-10
[
12393521.001
]
[Cites]
Clin Cancer Res. 2000 Mar;6(3):1038-45
[
10741732.001
]
[Cites]
Hum Pathol. 2000 May;31(5):578-83
[
10836297.001
]
[Cites]
Eur J Clin Invest. 2000 Jul;30(7):618-29
[
10886302.001
]
[Cites]
N Engl J Med. 2000 Oct 5;343(14):1020-34
[
11018170.001
]
[Cites]
Neoplasia. 2004 Jul-Aug;6(4):302-9
[
15256052.001
]
[Cites]
FASEB J. 2004 Aug;18(11):1240-2
[
15180966.001
]
[Cites]
Cancer Res. 2004 Aug 1;64(15):5261-9
[
15289332.001
]
[Cites]
Cancer Res. 2004 Aug 15;64(16):5702-11
[
15313910.001
]
[Cites]
Cancer Res. 1984 Aug;44(8):3522-9
[
6744277.001
]
[Cites]
J Biol Chem. 1989 Jan 5;264(1):646-53
[
2909545.001
]
[Cites]
Cell. 1991 Sep 6;66(5):921-33
[
1716182.001
]
[Cites]
J Cell Biol. 1993 Apr;121(2):449-59
[
7682218.001
]
[Cites]
Exp Cell Res. 1995 Aug;219(2):562-70
[
7543854.001
]
[Cites]
Am J Pathol. 1996 Jan;148(1):165-75
[
8546203.001
]
[Cites]
Blood. 1996 Oct 15;88(8):3010-21
[
8874199.001
]
[Cites]
J Biol Chem. 1996 Dec 20;271(51):33002-8
[
8955145.001
]
[Cites]
DNA Cell Biol. 1996 Dec;15(12):1121-8
[
8985126.001
]
[Cites]
J Cell Sci. 1997 Mar;110 ( Pt 6):687-94
[
9099943.001
]
[Cites]
Nature. 1997 Oct 30;389(6654):978-81
[
9353122.001
]
[Cites]
J Natl Cancer Inst. 1998 Jan 21;90(2):118-23
[
9450571.001
]
[Cites]
Clin Cancer Res. 1996 Sep;2(9):1627-36
[
9816342.001
]
[Cites]
Cancer Res. 1999 Jan 1;59(1):241-8
[
9892213.001
]
[Cites]
Clin Cancer Res. 1997 Dec;3(12 Pt 1):2493-500
[
9815652.001
]
[Cites]
Science. 1999 Feb 5;283(5403):845-8
[
9933168.001
]
[Cites]
J Clin Pathol. 1998 Nov;51(11):798-802
[
10193318.001
]
[Cites]
Cancer Metastasis Rev. 1998-1999;17(4):331-6
[
10453276.001
]
[Cites]
Blood. 2004 Nov 15;104(10):3091-6
[
15280192.001
]
[Cites]
Cancer. 2003 Feb 1;97(3 Suppl):739-47
[
12548571.001
]
[Cites]
J Bone Miner Res. 2003 Feb;18(2):190-4
[
12568395.001
]
[Cites]
Urology. 2003 Feb;61(2):277-81
[
12597930.001
]
[Cites]
Int J Oncol. 2003 May;22(5):1045-9
[
12684670.001
]
[Cites]
J Cell Biochem. 2003 Jun 1;89(3):462-73
[
12761880.001
]
[Cites]
Blood. 2003 Sep 15;102(6):2060-7
[
12763924.001
]
[Cites]
J Clin Invest. 2003 Oct;112(7):1008-18
[
14523038.001
]
[Cites]
J Cell Biochem. 2004 Mar 1;91(4):706-17
[
14991762.001
]
[Cites]
Cancer Res. 2004 Mar 15;64(6):2083-9
[
15026347.001
]
[Cites]
Prostate. 2004 May 1;59(2):157-66
[
15042616.001
]
[Cites]
Blood. 2004 Apr 15;103(8):2981-9
[
15070674.001
]
[Cites]
Blood. 2001 May 15;97(10):3283-91
[
11342460.001
]
(PMID = 15994950.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / 1R21 CA102913-02; United States / NCI NIH HHS / CA / CA69568; United States / NIAMS NIH HHS / AR / P30 AR042689; United States / NCI NIH HHS / CA / R21 CA104828; United States / NCI NIH HHS / CA / 1R21 CA104828-01; United States / NCI NIH HHS / CA / P50 CA069568; United States / NCI NIH HHS / CA / CA06516-37; United States / NCI NIH HHS / CA / P30 CA006516; United States / NIAMS NIH HHS / AR / 5P30 AR042689; United States / NCI NIH HHS / CA / R21 CA102913
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / E-Selectin; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / P-selectin ligand protein; 0 / Receptors, Fibroblast Growth Factor; 0 / Sialoglycoproteins; 0 / cysteine-rich fibroblast growth factor receptor
[Other-IDs]
NLM/ NIHMS2052; NLM/ PMC1472661
24.
Podgorski I, Linebaugh BE, Sloane BF:
Cathepsin K in the bone microenvironment: link between obesity and prostate cancer?
Biochem Soc Trans
; 2007 Aug;35(Pt 4):701-3
[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]
Cathepsin K in the bone microenvironment: link between obesity and
prostate
cancer
?
The skeleton is the most common site
of metastasis
in patients with advanced
prostate
cancer
.
Despite many advances in targeting skeletal
metastases
, the mechanisms behind the attraction of
prostate
cancer
cells to the bone are not known.
Osteoclast cathepsin K, due to its ability to effectively degrade bone matrix collagen I, has been implicated in colonization and growth of
prostate
tumours in the bone.
Identification of new cathepsin K substrates in the bone microenvironment and the recent findings demonstrating its involvement in obesity and inflammation suggest additional roles for this enzyme in skeletal
metastases of
prostate
cancer
.
[MeSH-minor]
Bone Neoplasms / pathology. Bone Neoplasms /
secondary
. Cathepsin K. Cell Movement / physiology. Humans. Male
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Obesity
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Obesity
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17635127.001).
[ISSN]
0300-5127
[Journal-full-title]
Biochemical Society transactions
[ISO-abbreviation]
Biochem. Soc. Trans.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
EC 3.4.- / Cathepsins; EC 3.4.22.38 / CTSK protein, human; EC 3.4.22.38 / Cathepsin K
[Number-of-references]
17
25.
Russell MR, Jamieson WL, Dolloff NG, Fatatis A:
The alpha-receptor for platelet-derived growth factor as a target for antibody-mediated inhibition of skeletal metastases from prostate cancer cells.
Oncogene
; 2009 Jan 22;28(3):412-21
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The alpha-receptor for platelet-derived growth factor as a target for antibody-mediated inhibition of skeletal
metastases
from
prostate
cancer
cells.
Bone resorption by osteoclasts is thought to promote the proliferation of
prostate
cancer
cells disseminated to the skeleton (Mundy, 2002).
Using a mouse model of experimental
metastasis
, we found that although late-stage
metastatic
tumors were indeed surrounded by osteoclasts, these cells were spatially unrelated to the small foci
of cancer
cells in early-stage
metastases
.
This is the first evidence that survival and growth of disseminated
prostate
cancer
cells immediately after their extravasation may not depend on osteoclast involvement.
Interestingly,
prostate
cancer
cells expressing the alpha-receptor for platelet-derived growth factor (PDGFRalpha) progress during early-stages of skeletal dissemination, whereas cells expressing lower levels or lacking this receptor fail to survive after extravasation in the bone marrow.
However, non-
metastatic
cells acquire bone-
metastatic
potential upon ectopic overexpression of PDGFRalpha.
Finally, functional blockade of human PDGFRalpha on
prostate
cancer
cells utilizing a novel humanized monoclonal antibody -- soon to undergo phase-II clinical trials -- significantly impairs the establishment of early skeletal
metastases
.
In conclusion, our results strongly implicate PDGFRalpha in
prostate
cancer
bone tropism through its promotion of survival and progression of early-
metastatic
foci, providing ground for therapeutic strategies aimed at preventing or containing the initial progression of skeletal
metastases in
patients affected by
prostate
adenocarcinoma.
[MeSH-major]
Antibodies, Monoclonal / therapeutic use. Bone Neoplasms / prevention & control. Bone Neoplasms /
secondary
. Prostatic Neoplasms / pathology. Receptor, Platelet-Derived Growth Factor alpha / antagonists & inhibitors
[MeSH-minor]
Adolescent. Adult. Animals. Blotting, Western. Bone Marrow / metabolism. Bone Marrow / pathology. Bone and Bones / metabolism. Bone and Bones / pathology. Flow Cytometry. Humans. Immunoenzyme Techniques. Male. Mice. Mice, SCID. Middle Aged. Phosphorylation.
Tumor
Cells, Cultured. Young Adult
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate 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
(PMID = 18850002.001).
[ISSN]
1476-5594
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Grant]
United States / NIGMS NIH HHS / GM / GM067892
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Monoclonal; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
26.
Hövels AM, Heesakkers RA, Adang EM, Jager GJ, Strum S, Hoogeveen YL, Severens JL, Barentsz JO:
The diagnostic accuracy of CT and MRI in the staging of pelvic lymph nodes in patients with prostate cancer: a meta-analysis.
Clin Radiol
; 2008 Apr;63(4):387-95
[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 diagnostic accuracy of CT and MRI in the staging of pelvic lymph nodes in patients with
prostate
cancer
: a meta-analysis.
AIM: To compare the diagnostic accuracy of computed tomography (CT) and magnetic resonance imaging (MRI) in the
diagnosis of
lymph node
metastases in
prostate
cancer
.
METHODS: After a comprehensive literature search, studies were included that allowed construction of contingency tables for detection of lymph node
metastases
using CT or MRI.
CONCLUSION: CT and MRI demonstrate an equally poor performance in the detection of lymph node
metastases
from
prostate
cancer
.
Reliance on either CT or MRI will misrepresent the patient's true status regarding nodal
metastases
, and thus misdirect the therapeutic strategies offered to the patient.
[MeSH-major]
Magnetic Resonance Imaging / standards. Pelvic Neoplasms /
diagnosis
. Prostatic Neoplasms / pathology. Tomography, X-Ray Computed / standards
[MeSH-minor]
Humans. Lymph Nodes. Lymphatic
Metastasis
. Male.
Neoplasm
Staging. ROC Curve. Sensitivity and Specificity
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - CT Scans
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
PubMed Health.
DARE review
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18325358.001).
[ISSN]
0009-9260
[Journal-full-title]
Clinical radiology
[ISO-abbreviation]
Clin Radiol
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article; Meta-Analysis; Review
[Publication-country]
England
[Number-of-references]
41
27.
Divoli A, Bloch G, Chittenden S, Malaroda A, O'Sullivan JM, Dearnaley DP, Flux GD:
Tumor dosimetry on SPECT (186)Re-HEDP scans: variations in the results from the reconstruction methods used.
Cancer Biother Radiopharm
; 2007 Feb;22(1):121-4
[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]
Tumor
dosimetry on SPECT (186)Re-HEDP scans: variations in the results from the reconstruction methods used.
The aim of this work was to estimate
tumor
-absorbed doses delivered from the administration of fixed activities of (186)Re-HEDP for the treatment of bone
metastases
from
prostate
cancer
.
We concluded that the administration of fixed activity resulted
in a
range of absorbed doses, and we showed that, despite using the same approach, the choice of the reconstruction algorithm can result in differences higher than 50% in the estimated
tumor
-absorbed doses.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
1-HYDROXY-1,1-DIPHOSPHONOETHANE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17627420.001).
[ISSN]
1084-9785
[Journal-full-title]
Cancer biotherapy & radiopharmaceuticals
[ISO-abbreviation]
Cancer Biother. Radiopharm.
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0501019; United States / NCI NIH HHS / CA / 1 R21 CA86784-01A1
[Publication-type]
Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Radioisotopes; 7440-15-5 / Rhenium; M2F465ROXU / Etidronic Acid
28.
Zafeirakis A:
Collagenous and non-collagenous biochemical markers of bone metastases from prostate cancer.
Hippokratia
; 2010 Jul;14(3):164-9
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Collagenous and non-collagenous biochemical markers of bone
metastases
from
prostate
cancer
.
The importance of the bone microenvironment to the pathophysiology and morbidity associated with
prostate
cancer
bone
metastasis
is becoming increasingly apparent.
This review will discuss the diagnostic and predictive implications of various collagenous and non-collagenous bone markers, along with the novel markers of osteoclastogenesis and other matrix enzymes such as metalloproteinases and growth factors responsible for the complex biochemical mechanisms that upregulate bone resorption/formation during the development
of metastasis
.
Further prospective studies are needed to determine whether any of these markers measured longitudinally in
prostate
cancer
patients without bone scan evidence of skeletal disease will ultimately predict those patients who will develop bone
metastases
from their malignancy.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20981164.001).
[ISSN]
1790-8019
[Journal-full-title]
Hippokratia
[ISO-abbreviation]
Hippokratia
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Other-IDs]
NLM/ PMC2943353
[Keywords]
NOTNLM ; Prostate cancer / RANKL / bone metastases / bone turnover markers / osteoprotegerin / review / type I collagen
29.
Polascik TJ:
Bisphosphonates in oncology: evidence for the prevention of skeletal events in patients with bone metastases.
Drug Des Devel Ther
; 2009 Sep 21;3:27-40
[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]
Bisphosphonates in oncology: evidence for the prevention of skeletal events in patients with bone
metastases
.
Bone
metastases
frequently occur in patients with advanced solid tumors, particularly breast and
prostate
cancers, and nearly all patients with multiple myeloma have some degree of skeletal involvement.
The results
of a
large, randomized phase 3 study comparing zoledronic acid and pamidronate in breast
cancer
or multiple myeloma patients with osteolytic lesions showed that the incidence of SREs, time to first SRE, and risk of developing a SRE were similar between treatment groups.
However, in patients with solid tumors (excluding breast or
prostate
cancer
)
metastatic to
the bone, only zoledronic acid has demonstrated clinical efficacy.
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]
Cancer Treat Rev. 2008 Nov;34(7):629-39
[
18579314.001
]
[Cites]
Cancer. 2000 Mar 1;88(5):1082-90
[
10699899.001
]
[Cites]
Ann Oncol. 2008 Mar;19(3):420-32
[
17906299.001
]
[Cites]
N Engl J Med. 2007 Nov 1;357(18):1799-809
[
17878149.001
]
[Cites]
J Clin Oncol. 2007 Jun 10;25(17):2464-72
[
17515569.001
]
[Cites]
N Engl J Med. 2007 May 3;356(18):1809-22
[
17476007.001
]
[Cites]
Pediatrics. 2007 Mar;119 Suppl 2:S150-62
[
17332236.001
]
[Cites]
Cancer Biol Ther. 2006 Sep;5(9):1074-7
[
16969118.001
]
[Cites]
Cochrane Database Syst Rev. 2006;(4):CD006250
[
17054286.001
]
[Cites]
Clin Cancer Res. 2006 Oct 15;12(20 Pt 2):6243s-6249s
[
17062708.001
]
[Cites]
Clin Cancer Res. 2006 Oct 15;12(20 Pt 2):6222s-6230s
[
17062705.001
]
[Cites]
Clin Cancer Res. 2006 Oct 15;12(20 Pt 2):6213s-6216s
[
17062703.001
]
[Cites]
Oncologist. 2006 Jul-Aug;11(7):841-8
[
16880243.001
]
[Cites]
Lancet. 2006 Jun 17;367(9527):2010-8
[
16782492.001
]
[Cites]
Clin Ther. 2006 Feb;28(2):151-73
[
16678639.001
]
[Cites]
Oncologist. 2006 Mar;11(3):227-33
[
16549806.001
]
[Cites]
Cochrane Database Syst Rev. 2005;(3):CD003474
[
16034900.001
]
[Cites]
J Clin Oncol. 2005 May 20;23(15):3314-21
[
15738536.001
]
[Cites]
Oncology. 2004;67(5-6):390-6
[
15713995.001
]
[Cites]
J Natl Cancer Inst. 2005 Jan 5;97(1):59-69
[
15632381.001
]
[Cites]
J Intern Med. 1999 Jul;246(1):67-74
[
10447227.001
]
[Cites]
J Clin Oncol. 1999 Mar;17(3):846-54
[
10071275.001
]
[Cites]
Eur J Cancer. 1998 Dec;34(13):2021-6
[
10070304.001
]
[Cites]
J Exp Clin Cancer Res. 1998 Jun;17(2):213-7
[
9700583.001
]
[Cites]
J Clin Oncol. 1998 Jun;16(6):2038-44
[
9626201.001
]
[Cites]
Br J Haematol. 1998 Feb;100(2):317-25
[
9488619.001
]
[Cites]
J Clin Oncol. 1998 Feb;16(2):593-602
[
9469347.001
]
[Cites]
Cancer. 1997 Oct 15;80(8 Suppl):1546-56
[
9362421.001
]
[Cites]
N Engl J Med. 1996 Dec 12;335(24):1785-91
[
8965890.001
]
[Cites]
N Engl J Med. 1996 Feb 22;334(8):488-93
[
8559201.001
]
[Cites]
J Clin Oncol. 1993 Jan;11(1):59-65
[
8418243.001
]
[Cites]
Oncologist. 2004;9 Suppl 4:14-27
[
15459426.001
]
[Cites]
Cancer. 2004 Jun 15;100(12):2613-21
[
15197804.001
]
[Cites]
J Natl Cancer Inst. 2004 Jun 2;96(11):879-82
[
15173273.001
]
[Cites]
Br J Cancer. 2004 Mar 22;90(6):1133-7
[
15026791.001
]
[Cites]
Cancer. 2004 Jan 1;100(1):36-43
[
14692022.001
]
[Cites]
J Clin Oncol. 2003 Dec 1;21(23):4277-84
[
14581438.001
]
[Cites]
J Clin Oncol. 2003 Nov 1;21(21):4042-57
[
12963702.001
]
[Cites]
Cancer. 2003 Oct 15;98(8):1735-44
[
14534891.001
]
[Cites]
J Natl Cancer Inst. 2003 Sep 3;95(17):1300-11
[
12953084.001
]
[Cites]
Ann Oncol. 2003 Sep;14(9):1399-405
[
12954579.001
]
[Cites]
J Clin Oncol. 2003 Aug 15;21(16):3150-7
[
12915606.001
]
[Cites]
J Clin Oncol. 2003 Apr 1;21(7):1404-11
[
12663734.001
]
[Cites]
J Natl Cancer Inst. 2002 Oct 2;94(19):1458-68
[
12359855.001
]
[Cites]
J Clin Oncol. 2002 May 1;20(9):2353-9
[
11981007.001
]
[Cites]
Cancer J. 2001 Sep-Oct;7(5):377-87
[
11693896.001
]
[Cites]
Br J Haematol. 2001 Jun;113(4):1035-43
[
11442499.001
]
[Cites]
J Clin Oncol. 2001 Jan 15;19(2):558-67
[
11208851.001
]
[Cites]
Support Cancer Ther. 2007 Jan 1;4(2):92-100
[
18632473.001
]
(PMID = 19920919.001).
[ISSN]
1177-8881
[Journal-full-title]
Drug design, development and therapy
[ISO-abbreviation]
Drug Des Devel Ther
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
New Zealand
[Other-IDs]
NLM/ PMC2769231
[Keywords]
NOTNLM ; bisphosphonates / bone metastases / cancer / prevention / skeletal-related events
30.
Gálvez R, Ribera V, González-Escalada JR, Souto A, Cánovas ML, Castro A, Herrero B, de Los Angeles Maqueda M, Castilforte M, Marco-Martínez JJ, Pérez C, Vicente-Fatela L, Md CN, Orduña MJ, Padrol A, Reig E, Carballido J, Cózar JM:
Analgesic efficacy of zoledronic acid and its effect on functional status of prostate cancer patients with metastasis.
Patient Prefer Adherence
; 2008;2:215-24
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Analgesic efficacy of zoledronic acid and its effect on functional status of
prostate
cancer
patients with
metastasis
.
OBJECTIVES: A multi-centered observational study evaluated the efficacy of zoledronic acid for improving pain and mobility, and preventing skeletal-related events (SRE) (fracture, spinal compression, pain-relieving radiotherapy), in patients with
prostate
cancer
and bone
metastasis
.
MATERIALS AND METHODS: Males (n = 218) with
prostate
cancer
and bone
metastasis
undergoing oncologic therapy received zoledronic acid (4 mg iv/month) for 6 months.
Of the 212 patients (97.2%) evaluable for safety, 16% suffered adverse events and 66% expressed satisfaction with the treatment DISCUSSION: Zoledronic acid is effective for reducing pain, improving mobility, and increasing the quality of life in patients with
prostate
cancer
with bone
metastasis
.
Its easy administration and good tolerability make zoledronic acid one of the principal therapeutic tools in the management of patients with pain associated with bone
metastasis
from
prostate
cancer
.
Andalusian Health Repository.
Full Text from
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Br J Cancer. 2000 Feb;82(4):858-64
[
10732759.001
]
[Cites]
Cancer. 2000 Jan 1;88(1):6-14
[
10618600.001
]
[Cites]
Cancer Res. 2000 Jun 1;60(11):2949-54
[
10850442.001
]
[Cites]
Cancer. 2000 Jun 15;88(12 Suppl):3015-21
[
10898346.001
]
[Cites]
Cancer. 2000 Jun 15;88(12 Suppl):3047-53
[
10898350.001
]
[Cites]
Breast Cancer. 2000;7(4):361-9
[
11114866.001
]
[Cites]
Cancer Treat Rev. 2001 Jun;27(3):165-76
[
11417967.001
]
[Cites]
N Engl J Med. 2001 Sep 27;345(13):948-55
[
11575286.001
]
[Cites]
J Urol. 2001 Dec;166(6):2023-31
[
11696699.001
]
[Cites]
J Natl Cancer Inst. 2002 Oct 2;94(19):1458-68
[
12359855.001
]
[Cites]
Cancer. 2003 Feb 1;97(3 Suppl):758-71
[
12548573.001
]
[Cites]
J Natl Cancer Inst. 2004 Jun 2;96(11):879-82
[
15173273.001
]
[Cites]
Lancet Oncol. 2004 Oct;5(10):607-16
[
15465464.001
]
[Cites]
Oncologist. 2005 Jan;10(1):52-62
[
15632252.001
]
[Cites]
Oncology (Williston Park). 1992 Oct;6(10):37-43; discussion 43, 47-50
[
1390013.001
]
[Cites]
Oncology (Williston Park). 1991 Aug;5(8):55-60; discussion 60-2, 65
[
1834153.001
]
[Cites]
Br J Urol. 1991 Jul;68(1):74-80
[
1873694.001
]
[Cites]
Cancer. 1993 Dec 1;72(11 Suppl):3443-52
[
8242577.001
]
[Cites]
Cancer. 1993 Feb 1;71(3 Suppl):1131-7
[
8428335.001
]
[Cites]
Drug Saf. 1996 Mar;14(3):158-70
[
8934578.001
]
[Cites]
Hosp J. 1996;11(2):1-10
[
8949010.001
]
[Cites]
J Urol. 1997 Feb;157(2):439-44
[
8996327.001
]
[Cites]
Cancer. 1997 Feb 1;79(3):545-50
[
9028366.001
]
[Cites]
Semin Urol Oncol. 1997 Feb;15(1):28-32
[
9050137.001
]
[Cites]
Cancer. 1997 Oct 15;80(8 Suppl):1652-60
[
9362432.001
]
[Cites]
Drug Saf. 1999 Nov;21(5):389-406
[
10554053.001
]
[Cites]
Leukemia. 2000 May;14(5):841-4
[
10803515.001
]
(PMID = 19920966.001).
[ISSN]
1177-889X
[Journal-full-title]
Patient preference and adherence
[ISO-abbreviation]
Patient Prefer Adherence
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
New Zealand
[Other-IDs]
NLM/ PMC2770417
[Keywords]
NOTNLM ; bone metastasis / pain / prostate cancer / zoledronic acid
31.
Cone LA, Koochek K, Henager HA, Fausel R, Gade-Andavolu R, Potts BE, Jennings LM:
Leptomeningeal carcinomatosis in a patient with metastatic prostate cancer: case report and literature review.
Surg Neurol
; 2006 Apr;65(4):372-5, discussion 375-6
[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]
Leptomeningeal carcinomatosis
in a
patient with
metastatic
prostate
cancer
: case report and literature review.
BACKGROUND: Leptomeningeal
metastasis
is discovered at autopsy in approximately 5% of patients with systemic
cancer
.
Until recently with the introduction of magnetic resonance imaging (MRI), premorbid
diagnosis
was extremely difficult.
Leptomeningeal
metastasis in metastatic
prostate
cancer
has been reported in only 14 patients previously.
CASE DESCRIPTION: We recently studied such a patient and were able to establish a correct
diagnosis
based solely on the MRI and the presence of an elevated cerebrospinal fluid (CSF)
prostate
-specific antigen (PSA).
Only 3 previous patients with leptomeningeal
prostate
metastasis
have undergone CSF PSA evaluations.
[MeSH-major]
Arachnoid / pathology. Carcinoma /
secondary
. Meningeal Neoplasms /
secondary
. Pia Mater / pathology. Prostatic Neoplasms / pathology
[MeSH-minor]
Aged. Anti-Inflammatory Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms /
secondary
. Consciousness Disorders / etiology. Diagnostic Errors / prevention & control. Early
Diagnosis
. Fatal Outcome. Headache / etiology. Humans. Lymph Nodes / pathology. Magnetic Resonance Imaging. Male.
Neoplasm Metastasis
/ drug therapy.
Neoplasm Metastasis
/ pathology.
Neoplasm Metastasis
/ physiopathology.
Prostate
-Specific Antigen / blood.
Prostate
-Specific Antigen / cerebrospinal fluid. Tomography, X-Ray Computed. Treatment Failure
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Prostate 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 = 16531199.001).
[ISSN]
0090-3019
[Journal-full-title]
Surgical neurology
[ISO-abbreviation]
Surg Neurol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents; EC 3.4.21.77 / Prostate-Specific Antigen
32.
Lecouvet FE, Simon M, Tombal B, Jamart J, Vande Berg BC, Simoni P:
Whole-body MRI (WB-MRI) versus axial skeleton MRI (AS-MRI) to detect and measure bone metastases in prostate cancer (PCa).
Eur Radiol
; 2010 Dec;20(12):2973-82
[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]
Whole-body MRI (WB-MRI) versus axial skeleton MRI (AS-MRI) to detect and measure bone
metastases in
prostate
cancer
(PCa).
OBJECTIVE: To compare whole-body MRI (WB-MRI) and axial skeleton MRI (AS-MRI) in detecting and measuring bone
metastases in
patients with
prostate
cancer
(PCa).
METHODS: WB-MRI and AS-MRI examinations were performed in 60 patients with PCa at high risk
of metastases
.
Two radiologists separately categorised the AS-MRI and WB-MRI as negative or positive for
metastases
, and measured focal
metastases
using the "Response evaluation criteria in solid tumours" (RECIST) criteria transposed to bone.
Inter- and intraobserver agreements in establishing the presence/absence
of metastases
were calculated.
RESULTS: Strong to perfect inter- and intraobserver agreements were found between AS-MRI and WB-MRI in defining the presence/absence of bone
metastases
.
There were no patients with isolated "peripheral"
metastases
at WB-MRI, missed at AS-MRI.
CONCLUSIONS: In our series of PCa patients, AS-MRI and WB-MRI were equivalent in determining the presence/absence of bone
metastases
and provided similar evaluation of the
metastatic
burden.
[MeSH-major]
Bone Neoplasms /
diagnosis
. Bone Neoplasms /
secondary
. Bone and Bones / pathology. Magnetic Resonance Imaging / methods. Prostatic Neoplasms /
diagnosis
. Whole Body Imaging / methods
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Med Imaging Radiat Oncol. 2009 Jun;53(3):241-7
[
19624290.001
]
[Cites]
Clin Oncol (R Coll Radiol). 2009 Feb;21(1):39-42
[
18993040.001
]
[Cites]
J Natl Cancer Inst. 2000 Feb 2;92 (3):205-16
[
10655437.001
]
[Cites]
Eur Radiol. 2002 Aug;12 (8):2091-9
[
12136329.001
]
[Cites]
Br J Cancer. 2010 Jan 19;102(2):249-54
[
19935788.001
]
[Cites]
Br J Cancer. 2009 Oct 20;101(8):1225-32
[
19789531.001
]
[Cites]
Clin Radiol. 1999 Jul;54(7):448-51
[
10437696.001
]
[Cites]
Skeletal Radiol. 1998 Oct;27(10):529-45
[
9840389.001
]
[Cites]
Radiology. 2009 Aug;252(2):477-85
[
19703885.001
]
[Cites]
Drug Des Devel Ther. 2009 Sep 21;3:27-40
[
19920919.001
]
[Cites]
Scand J Urol Nephrol. 2001 Dec;35(6):453-8
[
11848423.001
]
[Cites]
Urology. 1999 Jul;54(1):118-23
[
10414737.001
]
[Cites]
J Clin Oncol. 2007 Aug 1;25(22):3281-7
[
17664475.001
]
[Cites]
BJU Int. 2010 Feb;105(4):456-9
[
19930174.001
]
[Cites]
Br J Urol. 1990 Oct;66(4):411-4
[
2224435.001
]
[Cites]
Urology. 2008 Dec;72(6 Suppl):S25-35
[
19095125.001
]
[Cites]
AJR Am J Roentgenol. 2001 Jun;176(6):1525-30
[
11373226.001
]
[Cites]
Prostate. 1994 Sep;25(3):141-6
[
8065995.001
]
[Cites]
Eur Radiol. 2000;10(2):224-9
[
10663751.001
]
[Cites]
Eur J Radiol. 2002 Sep;43(3):256-61
[
12204408.001
]
[Cites]
Eur J Cancer. 2010 Mar;46(4):765-81
[
20116997.001
]
[Cites]
J Urol. 1993 Jun;149(6):1482-4
[
8501793.001
]
[Cites]
Urology. 2005 Jun;65(6 Suppl):2-7
[
15939076.001
]
[Cites]
Hum Pathol. 2000 May;31(5):578-83
[
10836297.001
]
[Cites]
Eur J Nucl Med. 1993 Nov;20(11):1063-9
[
8287874.001
]
[Cites]
Eur Radiol. 2010 Jun;20(6):1366-73
[
19997846.001
]
[Cites]
J Biopharm Stat. 2007;17(4):571-82
[
17613642.001
]
[Cites]
Biometrics. 1977 Mar;33(1):159-74
[
843571.001
]
[Cites]
Semin Musculoskelet Radiol. 2009 Jun;13(2):120-33
[
19455475.001
]
[Cites]
Clin Radiol. 1998 Jul;53(7):493-501
[
9714388.001
]
[Cites]
Nat Clin Pract Urol. 2008 Aug;5(8):434-44
[
18682719.001
]
[Cites]
Radiology. 1990 Oct;177(1):83-8
[
2399343.001
]
[Cites]
Prostate. 2005 Oct 1;65(2):178-87
[
15948151.001
]
[Cites]
Br J Urol. 1995 Jan;75(1):54-8
[
7850297.001
]
[Cites]
Acta Radiol. 2001 Mar;42(2):198-206
[
11259949.001
]
[Cites]
Rofo. 2008 Aug;180(8):746-52
[
18512192.001
]
[Cites]
Eur Radiol. 2009 Jun;19(6):1366-78
[
19190917.001
]
[Cites]
Acta Radiol. 1995 Jan;36(1):9-14
[
7833177.001
]
[Cites]
J Nucl Med. 1993 Dec;34(12 ):2191-8
[
8254410.001
]
[Cites]
Eur J Radiol. 2009 Jun;70(3):393-400
[
19457631.001
]
(PMID = 20661742.001).
[ISSN]
1432-1084
[Journal-full-title]
European radiology
[ISO-abbreviation]
Eur Radiol
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
Germany
33.
English BC, Baum CE, Adelberg DE, Sissung TM, Kluetz PG, Dahut WL, Price DK, Figg WD:
A SNP in CYP2C8 is not associated with the development of bisphosphonate-related osteonecrosis of the jaw in men with castrate-resistant prostate cancer.
Ther Clin Risk Manag
; 2010;6:579-83
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
A SNP in CYP2C8 is not associated with the development of bisphosphonate-related osteonecrosis of the jaw in men with castrate-resistant
prostate
cancer
.
A single nucleotide polymorphism (SNP) in CYP2C8 (rs1934951), was previously identified
in a
genome-wide association study as a risk factor for the development of osteonecrosis of the jaw (ONJ) in patients receiving bisphosphonates (BPs) for multiple myeloma.
To determine if the same SNP is also associated with the development of ONJ in men receiving BPs for bone
metastases
from
prostate
cancer
, we genotyped 100 men with castrate-resistant
prostate
cancer
treated with bisphosphonates for bone
metastases
, 17 of whom developed ONJ.
This intronic SNP in CYP2C8 (rs1934951) does not seem to be a risk factor for the development of bisphosphonate-related ONJ in men with
prostate
cancer
.
It is important to note that this is only the second study to investigate the genetics associated with BP-related ONJ and the first to do so in men with
prostate
cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 21151627.001).
[ISSN]
1178-203X
[Journal-full-title]
Therapeutics and clinical risk management
[ISO-abbreviation]
Ther Clin Risk Manag
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
New Zealand
[Other-IDs]
NLM/ PMC2999510
[Keywords]
NOTNLM ; CYP2C8 / ONJ / bisphosphonates / polymorphism
34.
Rinnab L, Kufer R, Hautmann RE, Gottfried HW:
Use of transrectal ultrasound-guided biopsy in the diagnosis of pelvic malignancies.
J Clin Ultrasound
; 2006 Nov-Dec;34(9):440-5
[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]
Use of transrectal ultrasound-guided biopsy in the
diagnosis of
pelvic malignancies.
METHODS: Eleven patients with clinical suspecion of advanced
malignant
pelvic
tumor
were referred to our institution with a history of unsuccessful CT-guided biopsy, although a target lesion was demonstrated on pelvic CT or MRI.
In all patients, the harvested material was of excellent quality and was adequate for definitive pathological
diagnosis
.
Pathological results included 6 nodal
metastases
from transitional cell carcinoma, 1 case of lymph node
metastasis
from
prostate
cancer
, 1 paravesical recurrence of cervical
cancer
, 1
metastasis
from cecal
cancer
, and 2 cases of paravesical
metastasis of
a gastric
cancer
.
CONCLUSION: TRUS-guided biopsy is a useful technique for
the diagnosis
of pelvic malignancies.
It is faster and less expensive than CT-guided biopsy, and in most cases sufficient material can be harvested for a definitive pathological
diagnosis
.
MedlinePlus Health Information.
consumer health - Biopsy
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2006 Wiley Periodicals, Inc.
(PMID = 17109402.001).
[ISSN]
0091-2751
[Journal-full-title]
Journal of clinical ultrasound : JCU
[ISO-abbreviation]
J Clin Ultrasound
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
35.
Beheshti M, Vali R, Waldenberger P, Fitz F, Nader M, Hammer J, Loidl W, Pirich C, Fogelman I, Langsteger W:
The use of F-18 choline PET in the assessment of bone metastases in prostate cancer: correlation with morphological changes on CT.
Mol Imaging Biol
; 2009 Nov-Dec;11(6):446-54
[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 use of F-18 choline PET in the assessment of bone
metastases in
prostate
cancer
: correlation with morphological changes on CT.
AIM: F-18 fluor choline-positron emission tomography/computed tomography (FCH-PET/CT) has emerged as a new diagnostic tool for the imaging of
prostate
cancer
.
In this study, we have evaluated the potential role of FCH-PET/CT for the assessment of bone
metastases in
patients with
prostate
cancer
.
METHODS: Seventy men with biopsy-proven
prostate
cancer
underwent FCH-PET/CT for preoperative staging or follow-up evaluation.
PET imaging consisted
of a
dynamic PET/CT acquisition of the pelvic region during 8 min (1-min frames) starting 1 min after i.v. injection of 4.07 MBq/kg/bw FCH which was followed immediately by a semi whole body acquisition.
Two hundred ten lesions (210/262) were interpreted as bone
metastases
.
The mean standardized uptake values (SUV) in all
malignant
lesions was 8.1 +/- 3.9.
Forty-nine lesions (24%) had no detectable morphological changes on CT-probably due to bone marrow
metastases
.
Fifty-six sclerotic lesions (having a Hounsfield unit (HU) level of more than 825) were interpreted as highly suspicious for
metastatic
bone disease on CT and/or other imaging modalities such as the bone scan but showed no FCH uptake.
The sensitivity, specificity, and accuracy of FCH-PET/CT in detecting bone
metastases
from
prostate
cancer
was 79%, 97%, and 84%, respectively.
CONCLUSION: FCH-PET/CT showed promising results for the early detection of bone
metastases in
prostate
cancer
patients.
[MeSH-major]
Bone Neoplasms / diagnostic imaging. Bone Neoplasms /
secondary
. Fluorine Radioisotopes. Prostatic Neoplasms / diagnostic imaging. Tomography, X-Ray Computed / methods
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - CT Scans
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
CHOLINE CHLORIDE
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[ErratumIn]
Mol Imaging Biol. 2010 Jun;12(3):360
[Cites]
Eur Urol. 1999;36(1):31-5
[
10364652.001
]
[Cites]
Radiology. 2005 May;235(2):623-8
[
15858102.001
]
[Cites]
CA Cancer J Clin. 2004 Jan-Feb;54(1):8-29
[
14974761.001
]
[Cites]
Eur Urol. 1999 Dec;36(6):582-7
[
10559612.001
]
[Cites]
Eur J Nucl Med Mol Imaging. 2006 Dec;33(12 ):1387-98
[
16865395.001
]
[Cites]
J Nucl Med. 2001 Dec;42(12 ):1800-4
[
11752076.001
]
[Cites]
J Nucl Med. 2007 Oct;48(10 ):1626-32
[
17873129.001
]
[Cites]
BJU Int. 2001 Aug;88(3):226-30
[
11488734.001
]
[Cites]
J Nucl Med. 1995 Sep;36(9):1625-32
[
7658223.001
]
[Cites]
Clin Orthop Relat Res. 1986 Sep;(210):18-30
[
3757360.001
]
[Cites]
Semin Nucl Med. 2007 Nov;37(6):462-9
[
17920353.001
]
[Cites]
Semin Nucl Med. 2005 Apr;35(2):135-42
[
15765376.001
]
[Cites]
Semin Oncol. 2003 Oct;30(5):616-34
[
14571410.001
]
[Cites]
Clin Cancer Res. 2006 Oct 15;12(20 Pt 2):6285s-6290s
[
17062715.001
]
[Cites]
BJU Int. 2004 Aug;94(3):299-302
[
15291855.001
]
[Cites]
Urology. 2001 Jan;57(1):108-11
[
11164153.001
]
[Cites]
Radiology. 1996 Jun;199(3):751-6
[
8638000.001
]
[Cites]
J Nucl Med. 2006 Feb;47(2):287-97
[
16455635.001
]
[Cites]
Semin Nucl Med. 2006 Jan;36(1):73-92
[
16356797.001
]
[Cites]
BJU Int. 2003 May;91(7):613-7
[
12699470.001
]
[Cites]
J Urol. 2003 Feb;169(2):517-23
[
12544300.001
]
[Cites]
J Clin Oncol. 1999 Mar;17 (3):948-57
[
10071289.001
]
[Cites]
J Urol. 2004 Jun;171(6 Pt 1):2122-7
[
15126770.001
]
[Cites]
J Urol. 1996 Mar;155(3):994-8
[
8583625.001
]
[Cites]
J Nucl Med. 1999 Oct;40(10 ):1623-9
[
10520701.001
]
[Cites]
Eur J Nucl Med. 2001 Jul;28(7):919-22
[
11504091.001
]
[Cites]
Clin Cancer Res. 2005 May 1;11(9):3210-6
[
15867215.001
]
[Cites]
J Urol. 2002 Oct;168(4 Pt 1):1423-6
[
12352409.001
]
[Cites]
Prostate. 2006 Nov 1;66(15):1573-84
[
16927388.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2000 Dec 1;48(5):1443-6
[
11121646.001
]
[Cites]
J Nucl Med. 1998 Jun;39(6):990-5
[
9627331.001
]
[Cites]
J Nucl Med. 2006 Aug;47(8):1249-54
[
16883001.001
]
[Cites]
J Clin Oncol. 1999 Aug;17 (8):2381-9
[
10561300.001
]
[Cites]
J Nucl Med. 2006 Feb;47(2):262-9
[
16455632.001
]
[Cites]
J Clin Oncol. 1998 Oct;16(10 ):3375-9
[
9779715.001
]
[Cites]
J Nucl Med. 2004 Feb;45(2):272-8
[
14960647.001
]
[Cites]
Eur J Nucl Med. 1998 Sep;25(9):1219-23
[
9724368.001
]
[Cites]
Nucl Med Biol. 1996 Aug;23 (6):693-7
[
8940712.001
]
[Cites]
Urology. 2002 Jun;59(6):913-8
[
12031380.001
]
[Cites]
Semin Nucl Med. 2004 Oct;34(4):274-92
[
15493005.001
]
(PMID = 19326171.001).
[ISSN]
1860-2002
[Journal-full-title]
Molecular imaging and biology : MIB : the official publication of the Academy of Molecular Imaging
[ISO-abbreviation]
Mol Imaging Biol
[Language]
eng
[Publication-type]
Duplicate Publication; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Fluorine Radioisotopes; 0 / Hormones; N91BDP6H0X / Choline
36.
Zhang X, Ling MT, Wang Q, Lau CK, Leung SC, Lee TK, Cheung AL, Wong YC, Wang X:
Identification of a novel inhibitor of differentiation-1 (ID-1) binding partner, caveolin-1, and its role in epithelial-mesenchymal transition and resistance to apoptosis in prostate cancer cells.
J Biol Chem
; 2007 Nov 16;282(46):33284-94
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Identification
of a
novel inhibitor of differentiation-1 (ID-1) binding partner, caveolin-1, and its role in epithelial-mesenchymal transition and resistance to apoptosis in
prostate
cancer
cells.
Recently, ID-1 (inhibitor of differentiation/DNA binding) is suggested as an oncogene and is reported to promote cell proliferation, invasion, and survival in several types of human
cancer
cells through multiple signaling pathways.
In this study, using a yeast two-hybrid screening technique, we identified a novel Id-1-interacting protein, caveolin-1 (Cav-1), a cell membrane protein, and a positive regulator of cell survival and
metastasis in
prostate
cancer
.
In addition, we also demonstrated that the physical interaction between Id-1 and Cav-1 played a key role in the epithelial-mesenchymal transition and increased cell migration rate as well as resistance to taxol-induced apoptosis in
prostate
cancer
cells.
Our study demonstrates a novel Id-1 binding partner and suggests a molecular mechanism that mediates the function of Id-1 in promoting
prostate
cancer
progression through activation of the Akt pathway leading
to cancer
cell invasion and resistance to anticancer drug-induced apoptosis.
[MeSH-minor]
Cell Movement. Drug Resistance,
Neoplasm
. Humans. Male. Molecular Sequence Data.
Neoplasm
Invasiveness. Paclitaxel / pharmacology. Protein Binding. Two-Hybrid System Techniques
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
Hazardous Substances Data Bank.
TAXOL
.
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 = 17855368.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
eng
[Databank-accession-numbers]
GENBANK/ NM001753
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Caveolin 1; 0 / ID1 protein, human; 0 / Inhibitor of Differentiation Protein 1; P88XT4IS4D / Paclitaxel
37.
Kawashima H, Tanaka T, Kuratsukuri K, Uchida J, Sugimura K, Tamada S, Nishisaka N, Kumata K, Iwai Y, Ikemoto S, Ezaki K, Nakatani T:
Palliative treatment of bone metastases in hormone-refractory prostate cancer: effects of pamidronate on the carboxyterminal telopeptide of type-I collagen level in patients with increasing prostate-specific antigen levels.
Urol Int
; 2007;78(4):345-50
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Palliative treatment of bone
metastases in
hormone-refractory
prostate
cancer
: effects of pamidronate on the carboxyterminal telopeptide of type-I collagen level in patients with increasing
prostate
-specific antigen levels.
PURPOSE: Bisphosphonates have been reported to be effective in reducing bone pain and skeletal-related events associated with bone
metastases in
hormone-refractory
prostate
cancer
(HRPC).
However, whether bone resorption is reduced primarily by these particular drugs is difficult to evaluate because patients with HRPC are usually treated with
secondary
or tertiary hormonal manipulations including second-line antiandrogens, high-dose diethylstilbestrol, or low-dose dexamethasone therapies, some of which may also be effective.
Thus, we assessed changes in the level of the carboxyterminal telopeptide of type-I collagen (ICTP), a bone resorption marker, before and after pamidronate administration in HRPC patients with increasing
prostate
-specific antigen (PSA) levels.
PATIENTS AND METHODS: Twenty-one HRPC patients with bone
metastases
and increasing PSA levels were intravenously treated with pamidronate at a dose of 30 mg either every 2 or every 4 weeks.
CONCLUSION: In 67% of the HRPC patients with increasing PSA levels, pamidronate reduced the accelerated turnover of bone metabolism caused by
metastases of
prostate
cancer
.
[MeSH-major]
Bone Density Conservation Agents / therapeutic use. Bone Neoplasms / drug therapy. Collagen Type I / drug effects. Diphosphonates / therapeutic use.
Prostate
-Specific Antigen / blood. Prostatic Neoplasms / drug therapy
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer Screening
.
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 = 17495494.001).
[ISSN]
0042-1138
[Journal-full-title]
Urologia internationalis
[ISO-abbreviation]
Urol. Int.
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Biomarkers; 0 / Bone Density Conservation Agents; 0 / Collagen Type I; 0 / Diphosphonates; EC 3.4.21.77 / Prostate-Specific Antigen; OYY3447OMC / pamidronate
38.
Sabbota AL, Kim HR, Zhe X, Fridman R, Bonfil RD, Cher ML:
Shedding of RANKL by tumor-associated MT1-MMP activates Src-dependent prostate cancer cell migration.
Cancer Res
; 2010 Jul 1;70(13):5558-66
[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]
Shedding of RANKL by
tumor
-associated MT1-MMP activates Src-dependent
prostate
cancer
cell migration.
We previously found high expression of MT1-MMP in skeletal
metastasis of
prostate
cancer
patients,
in a
pattern similar to RANKL expression.
We also showed that overexpression of MT1-MMP in
prostate
cancer
cells increases
tumor
growth and osteolysis in an intratibial mouse model of bone
metastasis
, and that soluble factor(s) shed by
tumor
-derived MT1-MMP enhance osteoclast differentiation
in a
RANKL-dependent manner.
Recent evidence indicates that the cognate receptor for RANKL, RANK, is expressed in
prostate
cancer
cells, suggesting the presence of an autocrine pathway.
In this study, we show that MT1-MMP-expressing LNCaP
prostate
cancer
cells display enhanced migration.
Moreover, conditioned medium from LNCaP cells expressing both RANKL and MT1-MMP stimulates the migration of MT1-MMP-deficient C42b
prostate
cancer
cells.
These findings indicate that
tumor
-derived MT1-MMP enhances
tumor
cell migration through initiation of an autocrine loop requiring ectodomain shedding of membrane-bound RANKL in
prostate
cancer
cells, and that Src is a key downstream mediator of RANKL-induced migration of
prostate
cancer
cells.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2010 AACR.
[Cites]
Clin Cancer Res. 1999 Dec;5(12):4105-10
[
10632347.001
]
[Cites]
Scand J Clin Lab Invest. 2009;69(1):151-5
[
19058084.001
]
[Cites]
Urology. 2001 Apr;57(4):611-6
[
11306358.001
]
[Cites]
J Biol Chem. 2001 May 4;276(18):14665-74
[
11278735.001
]
[Cites]
J Clin Invest. 2001 May;107(10):1235-44
[
11375413.001
]
[Cites]
J Clin Pathol. 2002 Nov;55(11):877-8
[
12401833.001
]
[Cites]
Cancer Metastasis Rev. 2003 Jun-Sep;22(2-3):177-203
[
12784996.001
]
[Cites]
Cell. 2003 Jul 11;114(1):33-45
[
12859896.001
]
[Cites]
Nature. 2003 Aug 21;424(6951):889-90
[
12931168.001
]
[Cites]
Cancer Res. 2004 Feb 1;64(3):1058-66
[
14871838.001
]
[Cites]
Invest Urol. 1979 Jul;17(1):16-23
[
447482.001
]
[Cites]
Cell. 1991 Feb 22;64(4):693-702
[
1997203.001
]
[Cites]
J Clin Invest. 1992 Oct;90(4):1622-7
[
1383278.001
]
[Cites]
Cancer Res. 1994 May 15;54(10):2577-81
[
8168083.001
]
[Cites]
Int J Cancer. 1994 May 1;57(3):406-12
[
8169003.001
]
[Cites]
J Biol Chem. 1997 Jan 24;272(4):2446-51
[
8999957.001
]
[Cites]
J Biol Chem. 1998 Oct 23;273(43):28355-9
[
9774460.001
]
[Cites]
Nature. 1999 Jan 28;397(6717):315-23
[
9950424.001
]
[Cites]
J Biol Chem. 1999 May 7;274(19):13613-8
[
10224132.001
]
[Cites]
Prostate. 1999 Jun 1;39(4):246-61
[
10344214.001
]
[Cites]
Cell. 1999 Oct 1;99(1):81-92
[
10520996.001
]
[Cites]
J Cell Biol. 2004 Nov 22;167(4):769-81
[
15557125.001
]
[Cites]
Curr Opin Genet Dev. 2005 Feb;15(1):87-96
[
15661538.001
]
[Cites]
Cancer Lett. 2005 Jun 1;223(1):121-8
[
15890244.001
]
[Cites]
Cancer Cell. 2005 May;7(5):485-96
[
15894268.001
]
[Cites]
J Biol Chem. 2005 Oct 7;280(40):33992-4002
[
16046398.001
]
[Cites]
J Cell Physiol. 2006 Jan;206(1):1-8
[
15920734.001
]
[Cites]
J Biol Chem. 2005 Dec 16;280(50):41700-6
[
16234249.001
]
[Cites]
Trends Mol Med. 2006 Jan;12(1):17-25
[
16356770.001
]
[Cites]
Chem Biol Drug Des. 2006 Jan;67(1):46-57
[
16492148.001
]
[Cites]
Nature. 2006 Mar 30;440(7084):692-6
[
16572175.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Jul 18;103(29):10889-94
[
16832052.001
]
[Cites]
Cancer. 2006 Jul 15;107(2):289-98
[
16752412.001
]
[Cites]
J Biol Chem. 2006 Dec 1;281(48):36846-55
[
17018528.001
]
[Cites]
Cancer Res. 2009 Feb 15;69(4):1517-26
[
19208838.001
]
[Cites]
J Urol. 2009 Aug;182(2):509-15; discussion 515-6
[
19524963.001
]
[Cites]
Cancer Res. 2009 Aug 15;69(16):6747-55
[
19679556.001
]
[Cites]
Clin Cancer Res. 2009 Dec 1;15(23):7421-8
[
19920114.001
]
[Cites]
Cancer Treat Rev. 2010 Apr;36(2):177-84
[
20015594.001
]
[Cites]
Bone. 2007 Apr;40(4):981-90
[
17196895.001
]
[Cites]
Am J Pathol. 2007 Jun;170(6):2100-11
[
17525276.001
]
[Cites]
Prostate. 2008 Jan 1;68(1):92-104
[
18008334.001
]
[Cites]
Histol Histopathol. 2008 Jun;23(6):709-15
[
18366009.001
]
[Cites]
Cell Res. 2008 Aug;18(8):858-70
[
18645583.001
]
[Cites]
Oncogene. 2008 Oct 23;27(49):6365-75
[
18679417.001
]
[Cites]
Int J Cancer. 2009 Jan 1;124(1):1-6
[
18942061.001
]
[Cites]
Mol Cell. 1999 Dec;4(6):1041-9
[
10635328.001
]
(PMID = 20551048.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA137280-02; United States / NCI NIH HHS / CA / CA137280; United States / NCI NIH HHS / CA / T32-CA009531; United States / NIDDK NIH HHS / DK / DK067687-05; United States / NCI NIH HHS / CA / R01 CA061986; United States / NIDDK NIH HHS / DK / R01 DK067687-05; United States / NCI NIH HHS / CA / R01 CA061986-15; United States / NIDDK NIH HHS / DK / R01 DK067687; United States / NCI NIH HHS / CA / T32 CA009531; United States / NIDDK NIH HHS / DK / DK67687; United States / NCI NIH HHS / CA / R01 CA137280; United States / NCI NIH HHS / CA / CA061986-15; United States / NCI NIH HHS / CA / CA61986
[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 / RANK Ligand; 0 / TNFSF11 protein, human; EC 2.7.10.2 / src-Family Kinases; EC 3.4.24.80 / MMP14 protein, human; EC 3.4.24.80 / Matrix Metalloproteinase 14
[Other-IDs]
NLM/ NIHMS206695; NLM/ PMC2896434
39.
Stanko C, Grandinetti L, Baldassano M, Mahmoodi M, Kantor GR:
Epidermotropic metastatic prostate carcinoma presenting as an umbilical nodule-Sister Mary Joseph nodule.
Am J Dermatopathol
; 2007 Jun;29(3):290-2
[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]
Epidermotropic
metastatic
prostate
carcinoma presenting as an umbilical nodule-Sister Mary Joseph nodule.
Carcinoma of the
prostate
accounts for fewer than 1% of all skin
metastases
.
Cutaneous
metastases
from
prostate
carcinoma most often involve the penis, the anterior aspect of the thighs, the suprapubic area, and the perineum, but they also have been reported in the scalp, the chest, the back, and even the face.
We report an unusual case
of metastatic
prostate
adenocarcinoma that presented as an umbilical nodule (Sister Mary Joseph nodule) and demonstrated significant epidermotropism histologically.
A review of the literature has found only one documented case of prostatic carcinoma metastasizing to the umbilicus, and one other documented case of epidermotropic
metastatic
prostate
carcinoma.
[MeSH-major]
Adenocarcinoma /
secondary
. Prostatic Neoplasms / pathology. Skin Neoplasms /
secondary
. Umbilicus / pathology
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
MedlinePlus Health Information.
consumer health - Skin Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17519629.001).
[ISSN]
0193-1091
[Journal-full-title]
The American Journal of dermatopathology
[ISO-abbreviation]
Am J Dermatopathol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
40.
Subhawong AP, Subhawong TK, Li QK:
Fine needle aspiration of metastatic prostate carcinoma simulating a primary adrenal cortical neoplasm: a case report and review of the literature.
Diagn Cytopathol
; 2010 Feb;38(2):147-53
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Fine needle aspiration
of metastatic
prostate
carcinoma simulating a primary adrenal cortical
neoplasm
: a case report and review of the literature.
Adrenal
metastases
usually occur in
prostate
cancer
patients with widespread bone and visceral disease.
Autopsy studies have shown that adrenal
metastases
may be found in up to 23% of these patients.
However, the finding of an isolated adrenal
metastasis
without the involvement of other organs
in a
patient with
prostate
cancer
is exceedingly rare.
We report a patient with a history of
prostate
cancer
, status post radiation, and hormonal therapy 4 years before, who presented with a new, single adrenal mass on abdominal imaging studies.
The ultrasound-guided FNA cytology of the adrenal mass revealed cytomorphological features that were suggestive
of a
primary adrenal cortical
neoplasm
, but overlapped with those
of a
prostate
metastasis
.
To our knowledge, FNA findings
of metastatic
prostate
cancer
simulating an adrenal cortical
neoplasm
have not been previously reported in the English literature.
The purpose of our study is to discuss the differential
diagnosis of
these entities.
The accurate
diagnosis
is important because of different prognosis and treatment implications for the various diseases.
[MeSH-major]
Adenocarcinoma /
secondary
. Adrenal Cortex Neoplasms /
secondary
. Biopsy, Fine-Needle. Prostatic Neoplasms / pathology
[MeSH-minor]
Aged. Antineoplastic Agents, Hormonal.
Diagnosis
, Differential. Humans. Immunohistochemistry. Male.
Prostate
-Specific Antigen / blood. Radiotherapy. Tomography, X-Ray Computed. Ultrasonography, Interventional
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19693937.001).
[ISSN]
1097-0339
[Journal-full-title]
Diagnostic cytopathology
[ISO-abbreviation]
Diagn. Cytopathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; EC 3.4.21.77 / Prostate-Specific Antigen
[Number-of-references]
29
41.
Nilsson S, Strang P, Ginman C, Zimmermann R, Edgren M, Nordström B, Ryberg M, Kälkner KM, Westlin JE:
Palliation of bone pain in prostate cancer using chemotherapy and strontium-89. A randomized phase II study.
J Pain Symptom Manage
; 2005 Apr;29(4):352-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Palliation of bone pain in
prostate
cancer
using chemotherapy and strontium-89. A randomized phase II study.
Strontium-89 is an established alternative for the alleviation of bone pain in
prostate
cancer
.
The aim of this randomized phase II study was to assess and compare the analgesic efficacy of strontium-89 and chemotherapy (FEM=5-FU, epirubicin, and mitomycin C) in 35 patients with disseminated, hormone-refractory
prostate
cancer
suffering from persisting bone pain despite analgesic treatment.
The effect of FEM on pain is surprising as chemotherapy has generally only limited effect on
tumor
growth in bone
metastases
due to
prostate
cancer
.
A possible explanation is that FEM has an inhibitory activity on the inflammatory component
of metastases
.
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Pain
.
MedlinePlus Health Information.
consumer health - Palliative Care
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
MITOMYCIN C
.
Hazardous Substances Data Bank.
FLUOROURACIL
.
Hazardous Substances Data Bank.
EPIRUBICIN
.
Hazardous Substances Data Bank.
STRONTIUM, ELEMENTAL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15857738.001).
[ISSN]
0885-3924
[Journal-full-title]
Journal of pain and symptom management
[ISO-abbreviation]
J Pain Symptom Manage
[Language]
eng
[Publication-type]
Clinical Trial; Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial
[Publication-country]
United States
[Chemical-registry-number]
0 / Radiopharmaceuticals; 3Z8479ZZ5X / Epirubicin; 50SG953SK6 / Mitomycin; EKE8PS9J6Z / strontium chloride; U3P01618RT / Fluorouracil; YZS2RPE8LE / Strontium; FEM protocol
42.
Kamiya N, Suzuki H, Kawamura K, Imamoto T, Ichikawa T:
[Bony lesion with prostate cancer].
Clin Calcium
; 2008 Apr;18(4):431-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Bony lesion with
prostate
cancer
].
Bone
metastases of
prostate
cancer
usually have an underlying osteoclastic component.
Bone
metastasis
is incurable and contributes significantly to disease-specific morbidity and mortality.
Several key factors have been found to be important
in tumor
-induced promotion of osteoclast activity.
Receptor activator of nuclear factor-kappa B ligand (RANKL) is produced by bone
metastasis of
prostate
cancer
, enabling these
metastasis to
induce osteolysis through osteoclast activation.
Matrix metalloproteinases (MMPs) are secreted by
prostate
cancer
cells and promote osteolysis primarily through degradation of bone matrix.
In this way, many factors derived from
prostate
cancer metastases
can promote osteolysis, and these factors may serve as therapeutic targets.
The new agents are targeted to osteoclasts (i.e.: zoledronic acid, anti-RANKL monoclonal antibody, cathepsin K inhibitor, and anti-PTHrP monoclonal antibody), are considered to be standard management in the care of bone
metastasis
patients in combination with chemotherapy and hormone therapy.
In this review, we summarized the current understanding and therapy of bone
metastasis in
prostate
cancer
.
[MeSH-major]
Bone Neoplasms /
secondary
. Prostatic Neoplasms / pathology
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate 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 = 18379023.001).
[ISSN]
0917-5857
[Journal-full-title]
Clinical calcium
[ISO-abbreviation]
Clin Calcium
[Language]
jpn
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Azepines; 0 / Diphosphonates; 0 / Enzyme Inhibitors; 0 / Imidazoles; 0 / Parathyroid Hormone-Related Protein; 0 / RANK Ligand; 0 / Sulfones; 0 / TNFSF11 protein, human; 6XC1PAD3KF / zoledronic acid; BL51M8CB8R / relacatib; EC 3.4.- / Cathepsins; EC 3.4.22.38 / CTSK protein, human; EC 3.4.22.38 / Cathepsin K; EC 3.4.24.- / Matrix Metalloproteinases
[Number-of-references]
20
43.
Wei JC, Wu MF, Zhang YT, Zhao LP, Lu YP, Ma D:
[Effects of vimentin on invasion and metastasis of prostate cancer cell lines PC-3M-1E8 and PC-3M-2B4].
Ai Zheng
; 2008 Jan;27(1):30-4
[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]
[Effects of vimentin on invasion and
metastasis of
prostate
cancer
cell lines PC-3M-1E8 and PC-3M-2B4].
This study was to detect the expression of vimentin in
prostate
cancer
cell lines PC-3M-1E8 and PC-3M-2B4, and evaluate the effects of vimentin on invasion and
metastasis of
prostate
cancer
cells.
METHODS: Two-dimensional gel electrophoresis (2-
DE
) followed by matrix-assisted laser desorption/time of flight mass spectrometry (MALDI TOF-MS) were used to detect the expression of vimentin in
prostate
cancer
cell lines PC-3M-1E8 and PC-3M-2B4.
Genetic intervention of vimentin gene and in vitro invasion assay were used to investigate the effects of vimentin on the invasion and
metastasis of
prostate
cancer
cells.
RESULTS: The protein level of vimentin was higher in PC-3M-1E8 cells with high
metastatic
potential than in PC-3M-2B4 cells with low
metastatic
potential.
CONCLUSION: Vimentin is a promising marker for predicting the invasion and
metastasis of
prostate
cancer
cells.
[MeSH-minor]
Cell Line,
Tumor
. DNA, Antisense. Electrophoresis, Gel, Two-Dimensional. Genetic Vectors. Humans. Male.
Neoplasm
Invasiveness.
Neoplasm Metastasis
. Phosphorylation. Plasmids. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Transfection
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18184460.001).
[Journal-full-title]
Ai zheng = Aizheng = Chinese journal of cancer
[ISO-abbreviation]
Ai Zheng
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / DNA, Antisense; 0 / Vimentin; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src)
44.
Chacon G, Alexandraki I, Palacio C:
Collet-sicard syndrome: an uncommon manifestation of metastatic prostate cancer.
South Med J
; 2006 Aug;99(8):898-9
[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]
Collet-sicard syndrome: an uncommon manifestation
of metastatic
prostate
cancer
.
Metastatic
spread of
prostate
adenocarcinoma to the temporal bone is very rare.
A case
of metastatic
prostate
adenocarcinoma involving the temporal bone causing Collet-Sicard syndrome is presented.
This case highlights an uncommon manifestation of
prostate
adenocarcinoma causing symptoms referable to the occipital condyle of the temporal bone.
Few cases have been reported in the literature of Collet-Sicard syndrome due
to metastatic
prostate
cancer
.
[MeSH-major]
Adenocarcinoma /
secondary
. Prostatic Neoplasms / pathology. Skull Neoplasms /
secondary
. Temporal Bone
[MeSH-minor]
Deglutition Disorders /
diagnosis
. Deglutition Disorders / etiology.
Diagnosis
, Differential. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Syndrome. Tomography, X-Ray Computed
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16929891.001).
[ISSN]
0038-4348
[Journal-full-title]
Southern medical journal
[ISO-abbreviation]
South. Med. J.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
45.
Pusulari BB, Akbar RA, Butt M, ul Haq SM:
Hypocalcemia with bony metastases in prostate cancer.
J Ayub Med Coll Abbottabad
; 2008 Jan-Mar;20(1):138-9
[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]
Hypocalcemia with bony
metastases in
prostate
cancer
.
He was found to have had a hepatomegaly & a large nodular
prostate
on rectal examination.
Investigations revealed a normal full blood count and renal profile, raised alkaline phosphatase and
Prostate
Specific Antigen (PSA), and low serum Calcium.
A bone scan was performed which revealed widespread bony
metastases in
the axial and appendicular skeleton resulting
in a
'superscan', consistent with prostatic
metastases
.
We recommend that calcium levels be checked in all patients with
prostate
cancer
and
metastatic
bone disease as this may have a bearing on their symptoms and the use of bisphosphonate therapy.
[MeSH-major]
Bone Neoplasms /
diagnosis
. Bone Neoplasms /
secondary
. Calcium / blood. Hypocalcemia / etiology. Prostatic Neoplasms / pathology
[MeSH-minor]
Aged. Alkaline Phosphatase / blood. Fatigue / etiology. Humans. Low Back Pain / etiology. Male.
Prostate
-Specific Antigen / blood. Risk Factors
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
CALCIUM, ELEMENTAL
.
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 = 19024209.001).
[ISSN]
1025-9589
[Journal-full-title]
Journal of Ayub Medical College, Abbottabad : JAMC
[ISO-abbreviation]
J Ayub Med Coll Abbottabad
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Pakistan
[Chemical-registry-number]
EC 3.1.3.1 / Alkaline Phosphatase; EC 3.4.21.77 / Prostate-Specific Antigen; SY7Q814VUP / Calcium
46.
Shah SH:
Reversible, isolated, unilateral hypoglossal nerve palsy due to metastatic prostate cancer.
Palliat Med
; 2006 Sep;20(6):639-40
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Reversible, isolated, unilateral hypoglossal nerve palsy due
to metastatic
prostate
cancer
.
[MeSH-major]
Hypoglossal Nerve Diseases / etiology. Prostatic Neoplasms. Skull Base Neoplasms /
secondary
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17060260.001).
[ISSN]
0269-2163
[Journal-full-title]
Palliative medicine
[ISO-abbreviation]
Palliat Med
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
47.
DePuy V, Anstrom KJ, Castel LD, Schulman KA, Weinfurt KP, Saad F:
Effects of skeletal morbidities on longitudinal patient-reported outcomes and survival in patients with metastatic prostate cancer.
Support Care Cancer
; 2007 Jul;15(7):869-76
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Effects of skeletal morbidities on longitudinal patient-reported outcomes and survival in patients with
metastatic
prostate
cancer
.
GOALS OF WORK: Patients with
prostate
cancer
metastasized to bone frequently experience skeletal morbidities as a result of their disease.
MATERIALS AND METHODS: Data are from a clinical trial for the treatment of SREs associated with advanced
prostate
cancer metastatic
to bone.
Outcome measures included the Functional Assessment
of Cancer
Therapy-General (FACT-G) and the Brief Pain Inventory.
[MeSH-major]
Bone Neoplasms /
secondary
. Musculoskeletal System / pathology. Prostatic Neoplasms / pathology. Quality of Life. Treatment Outcome
[MeSH-minor]
Aged. Diphosphonates / therapeutic use. Humans. Imidazoles. Male.
Neoplasm Metastasis
. Prognosis. Risk Factors. Survival
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Stat Med. 1992 Jun 30;11(9):1151-70
[
1509217.001
]
[Cites]
Urology. 1997 Dec;50(6):920-8
[
9426724.001
]
[Cites]
Med Care. 2004 Feb;42(2):164-75
[
14734954.001
]
[Cites]
Pain. 1999 Nov;83(2):157-62
[
10534586.001
]
[Cites]
J Clin Oncol. 1997 Mar;15(3):974-86
[
9060536.001
]
[Cites]
Control Clin Trials. 1999 Oct;20(5):408-22
[
10503801.001
]
[Cites]
Ann Acad Med Singapore. 1994 Mar;23(2):129-38
[
8080219.001
]
[Cites]
Am J Clin Oncol. 2001 Dec;24(6):591-6
[
11801761.001
]
[Cites]
Drugs Aging. 1999 Apr;14(4):241-6
[
10319239.001
]
[Cites]
Am J Clin Oncol. 2002 Dec;25(6 Suppl 1):S10-8
[
12562046.001
]
[Cites]
J Natl Cancer Inst. 2002 Oct 2;94(19):1458-68
[
12359855.001
]
[Cites]
J Clin Oncol. 1993 Mar;11(3):570-9
[
8445433.001
]
[Cites]
Ann Oncol. 2005 Apr;16(4):579-84
[
15734776.001
]
[Cites]
Ann Intern Med. 1997 Oct 15;127(8 Pt 2):757-63
[
9382394.001
]
[Cites]
Qual Life Res. 1999 May;8(3):181-95
[
10472150.001
]
[Cites]
J Urol. 2000 Oct;164(4):1248-53
[
10992374.001
]
[Cites]
Eval Health Prof. 2005 Jun;28(2):172-91
[
15851772.001
]
[Cites]
Cancer. 1995 Mar 1;75(5):1151-61
[
7850714.001
]
[Cites]
J Pain Symptom Manage. 1999 Sep;18(3):180-7
[
10517039.001
]
[Cites]
J Clin Oncol. 1983 Nov;1(11):710-9
[
6668489.001
]
[Cites]
J Pain Symptom Manage. 1998 Sep;16(3):171-8
[
9769619.001
]
[Cites]
Qual Life Res. 2002 May;11(3):207-21
[
12074259.001
]
[Cites]
N Engl J Med. 1996 Dec 12;335(24):1785-91
[
8965890.001
]
[Cites]
Pain. 2001 Nov;94(2):149-58
[
11690728.001
]
[Cites]
Drugs Aging. 2001;18(12):899-911
[
11888345.001
]
(PMID = 17262196.001).
[ISSN]
0941-4355
[Journal-full-title]
Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer
[ISO-abbreviation]
Support Care Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
48.
Abouassaly R, Paciorek A, Ryan CJ, Carroll PR, Klein EA:
Predictors of clinical metastasis in prostate cancer patients receiving androgen deprivation therapy: results from CaPSURE.
Cancer
; 2009 Oct 1;115(19):4470-6
[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]
Predictors of clinical
metastasis in
prostate
cancer
patients receiving androgen deprivation therapy: results from CaPSURE.
BACKGROUND: Virtually all patients with
prostate
cancer
who receive androgen deprivation therapy (ADT) will ultimately develop evidence of resistance to treatment.
The prognosis for patients who develop
metastatic
castrate-resistant disease is reported to be poor, with overall survival historically estimated to be 24 to 36 months.
The goal of the current study was to identify predictors of clinical disease progression in patients with
prostate
cancer
who were receiving ADT.
METHODS: Of the 13,740 men with biopsy-proven
prostate
cancer
who were enrolled in the
Cancer of
the
Prostate
Strategic Urological Research Endeavor (CaPSURE) database from 1995 to 2007, 4003 men treated with ADT after
diagnosis
without evidence
of metastases
at treatment initiation were identified.
The primary endpoint was the development of bone
metastasis
.
Clinical and pathologic characteristics were compared between patients who developed
metastasis
and those who did not using chi-square tests
in a
Cox proportional hazards regression model.
One hundred ninety-one men (4.8%) progressed
to metastatic
disease at a median of 18 months from the initiation of ADT (range, 1-139 months).
On multivariate analyses, risk category (hazards ratio [HR], 2.58; P < .0001), percent of biopsies positive >33% (HR, 3.36; P = .003), age </=65 years at
diagnosis
(HR, 2.11; P = .001, and
prostate
-specific antigen velocity on ADT (HR, 1.04; P < .001) were found to be significantly associated with the development
of metastatic
disease after ADT.
This, along with the other prognostic variables established in the current study, may help identify candidates for clinical trials evaluating
secondary
treatments for patients with castrate-resistant disease.
[MeSH-minor]
Adult. Age Factors. Aged. Aged, 80 and over. Databases as Topic. Humans. Male. Middle Aged.
Neoplasm Metastasis
. Prognosis. Risk Assessment
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
2009 American Cancer Society.
(PMID = 19637339.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal
49.
Yu HB, Han XB, Liang YQ, Liu JG, Wang H:
[Expression of osteopontin and survivin in prostate cancer and the clinical significance].
Nan Fang Yi Ke Da Xue Xue Bao
; 2010 May;30(5):1141-3
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Expression of osteopontin and survivin in
prostate
cancer
and the clinical significance].
OBJECTIVE: To determine the expression of osteopontin (OPN) and survivin in
prostate
cancer
tissue, and study their correlation and roles
in tumor
invasion and
metastasis
.
METHODS: The expressions of OPN and survivin in
prostate
cancer
tissue,
prostate
hyperplasia tissue and normal
prostate
tissue were determined by RT-PCR and immunohistochemistry.
RESULTS: The positive expression rates of OPN mRNA and protein in
prostate
cancer
tissue [76.1% (35/46) and 69.6% (32/46)] were significantly correlated to survivin expression [67.4% (31/46) and 67.4% (31/46)] (P<0.05).
The expressions of OPN and survivin were related to the
tumor
grade and clinical stages (P<0.05).
OPN and survivin were not found in
prostate
hyperplasia and normal
prostate
tissues.
CONCLUSION: OPN and survivin may play important roles in the progression of
prostate
cancer
and can be potential markers for invasion and
metastasis of
prostate
cancer
.
OPN and survivin might play synergetic roles in
prostate
carcinogenesis.
[MeSH-minor]
Adult. Aged. Humans. Male. Middle Aged.
Neoplasm
Invasiveness.
Neoplasm Metastasis
. RNA, Messenger / genetics. RNA, Messenger / metabolism
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20501415.001).
[ISSN]
1673-4254
[Journal-full-title]
Nan fang yi ke da xue xue bao = Journal of Southern Medical University
[ISO-abbreviation]
Nan Fang Yi Ke Da Xue Xue Bao
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / RNA, Messenger; 106441-73-0 / Osteopontin
50.
Mentor-Marcel R, Lamartiniere CA, Eltoum IA, Greenberg NM, Elgavish A:
Dietary genistein improves survival and reduces expression of osteopontin in the prostate of transgenic mice with prostatic adenocarcinoma (TRAMP).
J Nutr
; 2005 May;135(5):989-95
[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]
Dietary genistein improves survival and reduces expression of osteopontin in the
prostate
of transgenic mice with prostatic adenocarcinoma (TRAMP).
Studies in vitro suggest that osteopontin (OPN), an extracellular matrix protein secreted by macrophages infiltrating
prostate
tumors, and by
tumor
cells, may have a role in the transition from clinically insignificant tumors
to metastatic
prostate
cancer
(PC).
Our earlier studies in TRAnsgenic Mouse
Prostate
adenocarcinoma (TRAMP) mice showed that genistein, an isoflavone found in soybeans, lowered the incidence of advanced PC.
The steady-state level of OPN mRNA was evaluated by RT-PCR
in a
longitudinal study in 74 TRAMP and 32 nontransgenic litter mates (NTM).
Administration of 250 and 500 mg genistein/kg AIN-76A improved survival (P = 0.008 and P = 0.005, respectively) and reduced mean weight of prostates with poorly differentiated
cancer
(PD) (P < 0.001), as well as the mean weight of periaortic lymph nodes (LN), although the latter was not significant.
OPN mRNA levels in the dorsolateral
prostate
and
metastasis to
LN were significantly correlated (r = 0.643; P = 0.00006).
Genistein had a dose-dependent, significant inhibitory effect on OPN transcript levels in prostates displaying advanced
prostate
cancer
(PD; score 6; P = 0.05).
Studies are consistent with the possibility that dietary genistein may delay the progression from benign
to malignant
tumors by inhibiting OPN expression.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
GENISTEIN
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15867270.001).
[ISSN]
0022-3166
[Journal-full-title]
The Journal of nutrition
[ISO-abbreviation]
J. Nutr.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA 84926
[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.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / RNA, Messenger; 0 / Sialoglycoproteins; 0 / Soybean Proteins; 0 / Spp1 protein, mouse; 106441-73-0 / Osteopontin; DH2M523P0H / Genistein
51.
Shiozawa Y, Havens AM, Jung Y, Ziegler AM, Pedersen EA, Wang J, Wang J, Lu G, Roodman GD, Loberg RD, Pienta KJ, Taichman RS:
Annexin II/annexin II receptor axis regulates adhesion, migration, homing, and growth of prostate cancer.
J Cell Biochem
; 2008 Oct 1;105(2):370-80
[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]
Annexin II/annexin II receptor axis regulates adhesion, migration, homing, and growth of
prostate
cancer
.
One of the most life-threatening complications of
prostate
cancer
is skeletal
metastasis
.
In order to develop treatment for
metastasis
, it is important to understand its molecular mechanisms.
Our work in this field has drawn parallels between hematopoietic stem cell and
prostate
cancer
homing to the marrow.
In this study, we demonstrate that annexin II and its receptor play a crucial role in establishing
metastasis of
prostate
cancer
.
Prostate
cancer
cell lines migrate toward annexin II and the adhesion of
prostate
cancer to
osteoblasts and endothelial cells was inhibited by annexin II.
By blocking annexin II or its receptor in animal models, short-term and long-term localization of
prostate
cancers are limited.
Annexin II may also facilitate the growth of
prostate
cancer in
vitro and in vivo by the MAPK pathway.
These data strongly suggest that annexin II and its receptor axis plays a central role in
prostate
cancer metastasis
, and that
prostate
cancer
utilize the hematopoietic stem cell homing mechanisms to gain access to the niche.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
SciCrunch.
HGNC: Data: Gene Annotation
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
(c) 2008 Wiley-Liss, Inc.
[Cites]
Oncogene. 2003 Mar 13;22(10):1475-85
[
12629510.001
]
[Cites]
J Cell Biochem. 2003 Jun 1;89(3):462-73
[
12761880.001
]
[Cites]
Nature. 2003 Oct 23;425(6960):836-41
[
14574412.001
]
[Cites]
Nature. 2003 Oct 23;425(6960):841-6
[
14574413.001
]
[Cites]
J Urol. 2004 Feb;171(2 Pt 1):916-20
[
14713853.001
]
[Cites]
Cancer Treat Res. 2004;118:291-309
[
15043197.001
]
[Cites]
Gut. 2004 Jul;53(7):993-1000
[
15194650.001
]
[Cites]
Mol Cancer. 2003 Oct 8;2:34
[
14613585.001
]
[Cites]
Cell. 2004 Jul 23;118(2):149-61
[
15260986.001
]
[Cites]
EMBO J. 1984 Jan;3(1):227-33
[
6323166.001
]
[Cites]
Biochemistry. 2000 Mar 7;39(9):2140-8
[
10694379.001
]
[Cites]
Biochim Biophys Acta. 2000 Mar 7;1477(1-2):215-30
[
10708859.001
]
[Cites]
J Cell Biochem. 2000 Oct 20;80(2):259-65
[
11074597.001
]
[Cites]
Blood. 2001 Feb 1;97(3):777-84
[
11157497.001
]
[Cites]
J Clin Invest. 2001 May;107(10):1235-44
[
11375413.001
]
[Cites]
Cancer Res. 2001 Sep 1;61(17):6331-4
[
11522620.001
]
[Cites]
Cancer. 2001 Sep 15;92(6):1419-26
[
11745218.001
]
[Cites]
Ann N Y Acad Sci. 2001 Dec;947:143-55; discussion 155-6
[
11795262.001
]
[Cites]
Cancer Res. 2002 Mar 15;62(6):1832-7
[
11912162.001
]
[Cites]
J Cell Biol. 2002 Jun 10;157(6):1061-9
[
12045186.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Jan 21;100(2):521-6
[
12522268.001
]
[Cites]
J Biol Chem. 2003 Feb 7;278(6):4205-15
[
12431980.001
]
[Cites]
Exp Cell Res. 1986 Jan;162(1):183-90
[
2933269.001
]
[Cites]
Br J Cancer. 1992 Apr;65(4):498-502
[
1314068.001
]
[Cites]
Cancer Res. 1992 Dec 15;52(24):6871-6
[
1333884.001
]
[Cites]
J Cell Sci. 1992 Nov;103 ( Pt 3):733-42
[
1478969.001
]
[Cites]
Carcinogenesis. 1993 Dec;14(12):2575-9
[
8269629.001
]
[Cites]
Biochim Biophys Acta. 1994 Apr 5;1197(1):63-93
[
8155692.001
]
[Cites]
J Exp Med. 1994 May 1;179(5):1677-82
[
7513014.001
]
[Cites]
J Cell Biol. 1994 Jul;126(2):539-48
[
7518469.001
]
[Cites]
J Biol Chem. 1994 Nov 18;269(46):28696-701
[
7961821.001
]
[Cites]
Oncol Res. 1994;6(12):561-7
[
7787249.001
]
[Cites]
J Natl Cancer Inst. 1998 Jan 21;90(2):118-23
[
9450571.001
]
[Cites]
Int J Cancer. 1998 Sep 11;77(6):887-94
[
9714059.001
]
[Cites]
N Engl J Med. 1999 Apr 1;340(13):994-1004
[
10099141.001
]
[Cites]
J Clin Invest. 1999 Jun;103(11):1605-13
[
10359570.001
]
[Cites]
J Bone Miner Res. 2005 Feb;20(2):318-29
[
15647826.001
]
[Cites]
Blood. 2005 Apr 1;105(7):2631-9
[
15585658.001
]
[Cites]
J Biol Chem. 2005 May 27;280(21):20833-41
[
15788416.001
]
[Cites]
Cell. 2005 Jul 1;121(7):1109-21
[
15989959.001
]
[Cites]
Cell Signal. 2005 Dec;17(12):1578-92
[
16005185.001
]
[Cites]
Endocrinology. 2005 Nov;146(11):4584-96
[
16081645.001
]
[Cites]
J Biol Chem. 2005 Oct 28;280(43):36442-51
[
16055444.001
]
[Cites]
Neoplasia. 2006 Jan;8(1):69-78
[
16533428.001
]
[Cites]
BMC Cancer. 2006;6:195
[
16859559.001
]
[Cites]
J Biol Chem. 2006 Oct 13;281(41):30542-50
[
16895901.001
]
[Cites]
Clin Cancer Res. 2006 Oct 15;12(20 Pt 2):6243s-6249s
[
17062708.001
]
[Cites]
Prostate. 2007 Jan 1;67(1):61-73
[
17034033.001
]
[Cites]
Blood. 2007 Jul 1;110(1):82-90
[
17360942.001
]
[Cites]
Cancer Res. 2007 Oct 1;67(19):9417-24
[
17909051.001
]
[Cites]
J Biol Chem. 2008 Feb 15;283(7):4283-94
[
18057003.001
]
[Cites]
Neoplasia. 2008 Apr;10(4):371-80
[
18392141.001
]
(PMID = 18636554.001).
[ISSN]
1097-4644
[Journal-full-title]
Journal of cellular biochemistry
[ISO-abbreviation]
J. Cell. Biochem.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U19 CA113317; United States / NIAMS NIH HHS / AR / P30 AR046024; United States / NCI NIH HHS / CA / P50 CA69568; United States / NCI NIH HHS / CA / P50 CA069568; United States / NCI NIH HHS / CA / U54 CA163124; United States / NCI NIH HHS / CA / P01 CA093900; United States / NCI NIH HHS / CA / CA93900
[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.
[Publication-country]
United States
[Chemical-registry-number]
0 / Annexin A2; 0 / Receptors, Peptide; 0 / annexin II receptor, human
[Other-IDs]
NLM/ NIHMS447506; NLM/ PMC3614912
52.
Hegele A, Wahl HG, Varga Z, Sevinc S, Koliva L, Schrader AJ, Hofmann R, Olbert P:
Biochemical markers of bone turnover in patients with localized and metastasized prostate cancer.
BJU Int
; 2007 Feb;99(2):330-4
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Biochemical markers of bone turnover in patients with localized and metastasized
prostate
cancer
.
OBJECTIVE: To evaluate and compare the value of several markers of bone turnover in different stages of
prostate
cancer
, as bone
metastases
are a common feature in this disease, and for assessing bone
metastases
both bone formation and bone resorption markers are diagnostic.
129 undergoing radical retropubic prostatectomy (RRP) and 25 with bone
metastases
due to
prostate
cancer
, and 65 with benign urological disorders who served as controls.
The controls had the lowest marker levels while patients with bone
metastases
due to
prostate
cancer
had the highest levels, with significance for ALP, osteocalcin and TRACP5b.
Patients with lymph node-positive
cancer
had significantly high serum levels of TRACP5b and ALP but not for osteocalcin and S-CTX.
CONCLUSIONS: Bone turnover markers represent a new diagnostic tool in
prostate
cancer
; the present data show that both bone resorption and bone formation are crucial for detecting bone
metastases in
prostate
cancer
.
The value of bone turnover markers in high-risk patients should be evaluated
in a
longitudinal study.
[MeSH-major]
Biomarkers,
Tumor
/ blood. Bone Neoplasms /
secondary
. Bone Resorption /
diagnosis
. Prostatic Neoplasms / blood
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Humans. Male. Middle Aged.
Neoplasm
Recurrence, Local. Prospective Studies.
Prostate
-Specific Antigen / blood
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17092281.001).
[ISSN]
1464-4096
[Journal-full-title]
BJU international
[ISO-abbreviation]
BJU Int.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
53.
Lee SH, Hatakeyama S, Yu SY, Bao X, Ohyama C, Khoo KH, Fukuda MN, Fukuda M:
Core3 O-glycan synthase suppresses tumor formation and metastasis of prostate carcinoma PC3 and LNCaP cells through down-regulation of alpha2beta1 integrin complex.
J Biol Chem
; 2009 Jun 19;284(25):17157-69
[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]
Core3 O-glycan synthase suppresses
tumor
formation and
metastasis of
prostate
carcinoma PC3 and LNCaP cells through down-regulation of alpha2beta1 integrin complex.
Although there are numerous reports of carbohydrates enriched
in cancer
cells, very few studies have addressed the functions of carbohydrates present in normal cells that decrease
in cancer
cells.
It has been reported that core3 O-glycans are synthesized in normal gastrointestinal cells but are down-regulated
in cancer
cells.
To determine the roles of core3 O-glycans, we transfected PC3 and LNCaP
prostate
cancer
cells with beta3-N-acetylglucosaminyltransferase-6 (core3 synthase) required to synthesize core3 O-glycans.
Upon inoculation into the
prostate
of nude mice, PC3 cells expressing core3 O-glycans produced much smaller tumors without
metastasis to
the surrounding lymph nodes in contrast to robust
tumor
formation and
metastasis
seen in mock-transfected PC3 cells.
Similarly LNCaP cells expressing core3 O-glycans barely produced subcutaneous tumors in contrast to robust
tumor
formation by mock-transfected LNCaP cells.
These findings indicate that addition of core3 O-glycans to beta1 and alpha2 integrin subunits in
prostate
cancer
cells suppresses
tumor
formation and
tumor metastasis
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Biol Chem. 1993 Aug 15;268(23):17597-601
[
7688727.001
]
[Cites]
Eur J Biochem. 1994 Jun 1;222(2):415-24
[
8020479.001
]
[Cites]
Glycobiology. 1995 May;5(3):351-7
[
7655172.001
]
[Cites]
Cancer Res. 1996 May 15;56(10):2237-44
[
8625291.001
]
[Cites]
Cell. 1997 Jul 25;90(2):315-23
[
9244305.001
]
[Cites]
J Biol Chem. 1999 Jan 29;274(5):3215-21
[
9915862.001
]
[Cites]
J Biol Chem. 1999 Feb 19;274(8):4504-12
[
9988682.001
]
[Cites]
Science. 1999 Aug 13;285(5430):1028-32
[
10446041.001
]
[Cites]
J Cell Physiol. 1999 Oct;181(1):33-44
[
10457351.001
]
[Cites]
J Biol Chem. 2005 Mar 4;280(9):8332-42
[
15615721.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Mar 22;102(12):4572-7
[
15755813.001
]
[Cites]
J Exp Med. 2005 Dec 19;202(12):1679-89
[
16352740.001
]
[Cites]
Oncogene. 2006 Jun 1;25(23):3267-76
[
16418723.001
]
[Cites]
Glycoconj J. 2006 Jul;23(5-6):355-69
[
16897178.001
]
[Cites]
J Biol Chem. 2006 Oct 27;281(43):32122-30
[
16940045.001
]
[Cites]
Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19506-11
[
18048329.001
]
[Cites]
Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3095-100
[
19218444.001
]
[Cites]
Int J Cancer. 2003 Dec 20;107(6):949-57
[
14601054.001
]
[Cites]
J Biol Chem. 2004 May 7;279(19):19747-54
[
14998999.001
]
[Cites]
J Cell Sci. 2004 Oct 1;117(Pt 21):5059-69
[
15383613.001
]
[Cites]
J Biol Chem. 1975 Nov 10;250(21):8518-23
[
811657.001
]
[Cites]
Arch Biochem Biophys. 1976 Nov;177(1):330-3
[
999292.001
]
[Cites]
Proc Natl Acad Sci U S A. 1984 Jun;81(11):3389-93
[
6203119.001
]
[Cites]
J Biol Chem. 1984 Sep 10;259(17):10834-40
[
6088518.001
]
[Cites]
Cancer Res. 1984 Nov;44(11):5279-85
[
6386148.001
]
[Cites]
J Biol Chem. 1986 Aug 15;261(23):10772-7
[
3015940.001
]
[Cites]
Cancer Res. 1986 Oct;46(10):5270-5
[
2428477.001
]
[Cites]
Science. 1987 May 1;236(4801):582-5
[
2953071.001
]
[Cites]
J Biol Chem. 2000 Apr 14;275(15):11106-13
[
10753916.001
]
[Cites]
Cell. 2000 Mar 31;101(1):47-56
[
10778855.001
]
[Cites]
Neuron. 2000 Jul;27(1):33-44
[
10939329.001
]
[Cites]
Endocrinology. 2000 Sep;141(9):3172-82
[
10965888.001
]
[Cites]
J Biol Chem. 2006 Nov 3;281(44):33258-67
[
16959765.001
]
[Cites]
Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):3799-804
[
17360433.001
]
[Cites]
Nat Immunol. 2007 Apr;8(4):409-18
[
17334369.001
]
[Cites]
J Exp Med. 2007 Jun 11;204(6):1417-29
[
17517967.001
]
[Cites]
Cancer Res. 2001 Mar 1;61(5):2226-31
[
11280791.001
]
[Cites]
J Biol Chem. 2001 Apr 6;276(14):11007-15
[
11118434.001
]
[Cites]
J Biol Chem. 2002 Apr 12;277(15):12802-9
[
11821425.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10231-3
[
12149519.001
]
[Cites]
Cell. 2002 Sep 20;110(6):673-87
[
12297042.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):16613-8
[
12464682.001
]
[Cites]
J Biol Chem. 2003 Mar 14;278(11):9953-61
[
12529363.001
]
[Cites]
J Biol Chem. 1987 Dec 5;262(34):16403-11
[
2824491.001
]
[Cites]
J Biol Chem. 1988 Oct 15;263(29):15146-50
[
2971663.001
]
[Cites]
Proc Natl Acad Sci U S A. 1992 Oct 1;89(19):9326-330
[
1329093.001
]
[Cites]
Cancer Res. 1993 Aug 1;53(15):3632-7
[
8101764.001
]
(PMID = 19395705.001).
[ISSN]
1083-351X
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA48737; United States / NCI NIH HHS / CA / P01 CA071932; United States / NCI NIH HHS / CA / P01CA71932; United States / NCI NIH HHS / CA / R01 CA048737; United States / NCI NIH HHS / CA / R01 CA033000; United States / NCI NIH HHS / CA / CA33000; United States / NCI NIH HHS / CA / R37 CA033000
[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 / DNA Primers; 0 / Integrin alpha2beta1; 0 / Polysaccharides; 0 / Recombinant Proteins; EC 2.4.1.- / N-Acetylglucosaminyltransferases
[Other-IDs]
NLM/ PMC2719354
54.
Tepper CG, Gregg JP, Shi XB, Vinall RL, Baron CA, Ryan PE, Desprez PY, Kung HJ, deVere White RW:
Profiling of gene expression changes caused by p53 gain-of-function mutant alleles in prostate cancer cells.
Prostate
; 2005 Dec 1;65(4):375-89
[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]
Profiling of gene expression changes caused by p53 gain-of-function mutant alleles in
prostate
cancer
cells.
BACKGROUND:
Tumor
suppressor p53 mutations are associated with the transition of
prostate
cancer to metastatic
, hormone-refractory disease and stable expression of p53 gain-of-function (p53GOF) alleles support growth of LNCaP in androgen-depleted medium.
In this study, we performed gene expression profiling of four LNCaP-p53GOF sublines to test the hypothesis that different p53GOF mutants mediated androgen independence via modulation
of a
common set of genes.
[MeSH-minor]
Cell Line,
Tumor
. Gene Expression Profiling. Humans. Inhibitor of Differentiation Protein 1 / biosynthesis. Inhibitor of Differentiation Protein 1 / genetics. Male. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic. RNA Interference. RNA,
Neoplasm
/ chemistry. RNA,
Neoplasm
/ genetics. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright (c) 2005 Wiley-Liss, Inc.
(PMID = 16037992.001).
[ISSN]
0270-4137
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA93373-01; United States / NCI NIH HHS / CA / R01-CA77662
[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 / Inhibitor of Differentiation Protein 1; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering
55.
Clarke NW, Hart CA, Brown MD:
Molecular mechanisms of metastasis in prostate cancer.
Asian J Androl
; 2009 Jan;11(1):57-67
[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.
[Title]
Molecular mechanisms
of metastasis
in
prostate
cancer
.
Prostate
cancer
(PCa) preferentially metastasizes to the bone marrow stroma of the axial skeleton.
The exact mechanism of PCa
metastasis
is currently unknown, although considerable progress has been made in determining the key players in this process.
In this review, we present the current understanding of the molecular processes driving PCa
metastasis to
the bone.
[MeSH-major]
Bone Neoplasms /
secondary
. Prostatic Neoplasms / pathology
[MeSH-minor]
Cell Adhesion / physiology. Cell Movement / physiology. Chemokines / physiology. Humans. Lipids / physiology. Male.
Neoplasm Metastasis
/ physiopathology
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate 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]
Microsc Res Tech. 1998 Nov 1;43(3):265-75
[
9840805.001
]
[Cites]
Mol Pathol. 1998 Aug;51(4):191-200
[
9893744.001
]
[Cites]
Science. 1999 Feb 5;283(5403):845-8
[
9933168.001
]
[Cites]
Br J Cancer. 1999 Apr;79(11-12):1879-83
[
10206308.001
]
[Cites]
Hum Pathol. 1999 Apr;30(4):458-66
[
10208469.001
]
[Cites]
Urology. 1999 May;53(5):1063-9
[
10223507.001
]
[Cites]
Endocr Rev. 1999 Jun;20(3):345-57
[
10368775.001
]
[Cites]
Eur J Immunol. 1999 Jun;29(6):1823-31
[
10382744.001
]
[Cites]
Endocrinology. 1999 Oct;140(10):4451-8
[
10499498.001
]
[Cites]
Nat Rev Cancer. 2005 Jan;5(1):21-8
[
15630412.001
]
[Cites]
Br J Cancer. 2005 Feb 14;92(3):503-12
[
15668715.001
]
[Cites]
Br J Cancer. 2006 Mar 27;94(6):842-53
[
16523199.001
]
[Cites]
Cancer Res. 1992 May 15;52(10):2916-22
[
1581909.001
]
[Cites]
Cancer Res. 1992 Sep 15;52(18):5104-9
[
1516067.001
]
[Cites]
Cancer Res. 1992 Oct 15;52(20):5770-4
[
1394201.001
]
[Cites]
Cancer Metastasis Rev. 1992 Nov;11(3-4):353-75
[
1423822.001
]
[Cites]
Eur Urol. 1993;24(2):286-90
[
8375452.001
]
[Cites]
Cancer Res. 1993 Oct 1;53(19):4493-8
[
7691397.001
]
[Cites]
J Biol Chem. 1993 Oct 25;268(30):22883-94
[
8226797.001
]
[Cites]
J Clin Invest. 1993 Dec;92(6):3017-22
[
8254056.001
]
[Cites]
Biochim Biophys Acta. 1994 May 27;1198(1):11-26
[
8199193.001
]
[Cites]
J Cell Biol. 1994 Jun;125(6):1341-52
[
8207062.001
]
[Cites]
Cancer Res. 1994 Jul 15;54(14):3929-33
[
7518346.001
]
[Cites]
J Endocrinol. 1994 Sep;142(3):407-15
[
7525824.001
]
[Cites]
J Cell Biochem Suppl. 1994;19:232-7
[
7823596.001
]
[Cites]
Clin Orthop Relat Res. 1995 Mar;(312):19-33
[
7634602.001
]
[Cites]
Clin Exp Metastasis. 1995 Nov;13(6):481-91
[
7586806.001
]
[Cites]
Nat Med. 1995 Sep;1(9):944-9
[
7585222.001
]
[Cites]
Lancet. 1995 Dec 9;346(8989):1528-30
[
7491049.001
]
[Cites]
Cancer Metastasis Rev. 1995 Sep;14(3):219-28
[
8548870.001
]
[Cites]
Am J Pathol. 1996 May;148(5):1375-80
[
8623909.001
]
[Cites]
Cancer Res. 1996 Feb 15;56(4):663-8
[
8630991.001
]
[Cites]
J Urol. 1996 Aug;156(2 Pt 1):526-31
[
8683730.001
]
[Cites]
Urology. 1996 Aug;48(2):317-25
[
8753751.001
]
[Cites]
BJU Int. 1999 Dec;84(9):1032-4
[
10571629.001
]
[Cites]
BJU Int. 2000 Jan;85(1):65-9
[
10619948.001
]
[Cites]
Br J Cancer. 2000 Aug;83(3):360-5
[
10917552.001
]
[Cites]
Science. 2000 Sep 1;289(5484):1504-8
[
10968780.001
]
[Cites]
Clin Cancer Res. 2000 Sep;6(9):3530-5
[
10999740.001
]
[Cites]
J Clin Invest. 2000 Dec;106(11):1331-9
[
11104786.001
]
[Cites]
Nature. 2001 Mar 1;410(6824):50-6
[
11242036.001
]
[Cites]
J Natl Cancer Inst. 2001 Jul 18;93(14):1062-74
[
11459867.001
]
[Cites]
Urology. 2001 Nov;58(5):815-20
[
11711374.001
]
[Cites]
Lancet Oncol. 2001 Jan;2(1):18-26
[
11905614.001
]
[Cites]
Cancer Res. 2002 Mar 15;62(6):1832-7
[
11912162.001
]
[Cites]
Br J Cancer. 2002 Apr 8;86(7):1136-42
[
11953862.001
]
[Cites]
Cancer Res. 2002 May 1;62(9):2708-14
[
11980672.001
]
[Cites]
Urology. 2002 Aug;60(2):270-5
[
12137825.001
]
[Cites]
Nat Rev Cancer. 2002 Aug;2(8):563-72
[
12154349.001
]
[Cites]
Nat Rev Cancer. 2002 Sep;2(9):657-72
[
12209155.001
]
[Cites]
Differentiation. 2002 Oct;70(8):385-96
[
12366376.001
]
[Cites]
Cancer Lett. 2003 Jan 28;189(2):117-28
[
12490304.001
]
[Cites]
Cancer. 2003 Feb 1;97(3 Suppl):779-84
[
12548575.001
]
[Cites]
Blood. 2003 Apr 15;101(8):3126-35
[
12515720.001
]
[Cites]
BJU Int. 2003 May;91(7):716-20
[
12699491.001
]
[Cites]
J Cell Biochem. 2003 Jun 1;89(3):462-73
[
12761880.001
]
[Cites]
FEBS Lett. 2003 Aug 28;550(1-3):79-83
[
12935890.001
]
[Cites]
Nature. 2003 Sep 18;425(6955):307-11
[
13679920.001
]
[Cites]
Oncogene. 2003 Nov 6;22(50):8093-101
[
14603250.001
]
[Cites]
J Urol. 2003 Dec;170(6 Pt 2):S65-7; discussion S67-8
[
14610413.001
]
[Cites]
Prostate Cancer Prostatic Dis. 2002;5(1):59-62
[
15195132.001
]
[Cites]
Int J Cancer. 2004 Sep 20;111(5):783-91
[
15252851.001
]
[Cites]
Eur Urol. 2004 Sep;46(3):389-401; discussion 401-2
[
15306113.001
]
[Cites]
J Urol. 1968 Jan;99(1):87-96
[
4170154.001
]
[Cites]
Nature. 1976 Oct 7;263(5577):507-8
[
972697.001
]
[Cites]
Cancer. 1983 Mar 1;51(5):918-24
[
6681595.001
]
[Cites]
Cancer Res. 1986 Jan;46(1):1-7
[
2998604.001
]
[Cites]
Br J Urol. 1985 Dec;57(6):721-3
[
4084733.001
]
[Cites]
Science. 1991 Mar 22;251(5000):1451-5
[
2006419.001
]
[Cites]
J Cell Biol. 1991 Apr;113(1):173-85
[
2007622.001
]
[Cites]
Cell. 1991 Jul 12;66(1):107-19
[
2070412.001
]
[Cites]
Br J Urol. 1991 Jul;68(1):74-80
[
1873694.001
]
[Cites]
Br J Urol. 1992 Jan;69(1):64-70
[
1737255.001
]
[Cites]
FASEB J. 1992 Apr;6(7):2456-66
[
1563597.001
]
[Cites]
J Exp Med. 1997 Jan 6;185(1):111-20
[
8996247.001
]
[Cites]
Eur J Cancer. 1997 Feb;33(2):263-71
[
9135498.001
]
[Cites]
Clin Exp Metastasis. 1997 May;15(3):218-27
[
9174123.001
]
[Cites]
Int J Cancer. 1997 Aug 22;74(4):374-7
[
9291424.001
]
[Cites]
Ophthal Plast Reconstr Surg. 1997 Dec;13(4):227-38
[
9430298.001
]
[Cites]
J Natl Cancer Inst. 1998 Jan 21;90(2):118-23
[
9450571.001
]
[Cites]
Prostate. 1998 Feb 15;34(3):203-13
[
9492849.001
]
[Cites]
Endocr Rev. 1998 Feb;19(1):18-54
[
9494779.001
]
[Cites]
Clin Exp Metastasis. 1998 Jan;16(1):21-9
[
9502074.001
]
[Cites]
Nature. 1998 Mar 12;392(6672):190-3
[
9515965.001
]
[Cites]
Prostate. 1998 May 15;35(3):185-92
[
9582087.001
]
[Cites]
Cancer Res. 1998 Jun 15;58(12):2520-3
[
9635571.001
]
[Cites]
J Exp Med. 1998 Aug 3;188(3):539-48
[
9687531.001
]
[Cites]
Urology. 1998 Aug;52(2):261-6; discussion 266-7
[
9697792.001
]
(PMID = 19050684.001).
[ISSN]
1008-682X
[Journal-full-title]
Asian journal of andrology
[ISO-abbreviation]
Asian J. Androl.
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0500966
[Publication-type]
Journal Article; Review
[Publication-country]
China
[Chemical-registry-number]
0 / Chemokines; 0 / Lipids
[Number-of-references]
93
[Other-IDs]
NLM/ PMC3735202
56.
Zhang XM, Shen Y, Xianyu ZQ:
[Serum proteomic study of prostate cancer with bone metastasis].
Zhonghua Nan Ke Xue
; 2010 Aug;16(8):721-5
[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]
[Serum proteomic study of
prostate
cancer
with bone
metastasis
].
OBJECTIVE: To screen serum biomarker candidates in
prostate
cancer
with bone
metastasis
by two-dimensional gel electrophoresis (2-DGE) and mass spectrometry.
METHODS: Serum samples were obtained from 5
prostate
cancer
patients with bone
metastasis
, and another 5 without it.
The differentially expressed protein spots in the serum of those with bone
metastases
were identified by peptide-fingerprinting with matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS).
RESULTS: Compared with the serum samples from those without bone
metastasis
, 10 protein spot-features were found to be significantly increased and 5 significantly decreased, and the 3 identified proteins, Zn-alpha2-glycoprotein (ZAG), haptoglobin and apolipoprotein C-III, were all increased in the bone-
metastasis
group.
The identified proteins involved in the formation and progression of
prostate
cancer
bone
metastasis
might be applied as biomarkers for bone
metastasis
from
prostate
cancer
.
[MeSH-major]
Bone Neoplasms / blood. Bone Neoplasms /
secondary
. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology. Proteome / analysis
[MeSH-minor]
Aged. Aged, 80 and over. Case-Control Studies. Electrophoresis, Gel, Two-Dimensional. Humans. Male. Middle Aged.
Neoplasm Metastasis
. Proteomics
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 21090348.001).
[ISSN]
1009-3591
[Journal-full-title]
Zhonghua nan ke xue = National journal of andrology
[ISO-abbreviation]
Zhonghua Nan Ke Xue
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / Proteome
57.
Hong JH, Ahn KS, Bae E, Jeon SS, Choi HY:
The effects of curcumin on the invasiveness of prostate cancer in vitro and in vivo.
Prostate Cancer Prostatic Dis
; 2006;9(2):147-52
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The effects of curcumin on the invasiveness of
prostate
cancer in
vitro and in vivo.
Curcumin has become a focus of interest with regard to its antitumor effects in
prostate
cancer
; however, the effects of this agent on invasion and
metastasis
remain less well understood.
Matrix metalloproteinases (MMPs) are important prerequisite for
tumor
invasion and
metastasis
.
In this study, we evaluated the effects of curcumin on
prostate
cancer
cells (DU-145) invasion in both in vitro and in vivo.
Curcumin treatment resulted not only
in a
significant reduction in the expression of MMP-2 and MMP-9, but also effected the inhibition of invasive ability in vitro.
Curcumin was shown to induce a marked reduction
of tumor
volume, MMP-2, and MMP-9 activity in the
tumor
-bearing site.
The metastatic
nodules in vivo were significantly fewer in the curcumin-treated group than untreated group.
Curcumin appears to constitute a potential agent for the prevention
of cancer
progression, or at least of the initial phase
of metastasis
, in
prostate
cancer
.
[MeSH-major]
Antineoplastic Agents / pharmacology. Curcumin / pharmacology.
Neoplasm
Invasiveness / pathology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
[MeSH-minor]
Animals. Biomarkers,
Tumor
/ analysis. Caspase 3. Caspases / analysis. Caspases / metabolism. Cell Proliferation / drug effects. Disease Models, Animal. Enzyme-Linked Immunosorbent Assay. In Vitro Techniques. Male. Matrix Metalloproteinase 2 / analysis. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 9 / analysis. Matrix Metalloproteinase 9 / metabolism. Mice. Neoplasms, Experimental. Probability. Sensitivity and Specificity. Statistics, Nonparametric. Transplantation, Heterologous.
Tumor
Cells, Cultured / cytology.
Tumor
Cells, Cultured / drug effects
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
CURCUMIN
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16389264.001).
[ISSN]
1365-7852
[Journal-full-title]
Prostate cancer and prostatic diseases
[ISO-abbreviation]
Prostate Cancer Prostatic Dis.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; IT942ZTH98 / Curcumin
58.
Turvey SE, Swart E, Denis MC, Mahmood U, Benoist C, Weissleder R, Mathis D:
Noninvasive imaging of pancreatic inflammation and its reversal in type 1 diabetes.
J Clin Invest
; 2005 Sep;115(9):2454-61
[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.
Importantly, an essentially identical MNP-MRI strategy has previously been used with great success to image lymph node
metastases in
prostate
cancer
patients.
Genetic Alliance.
consumer health - Diabetes
.
MedlinePlus Health Information.
consumer health - Diabetes Type 1
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Annu Rev Immunol. 2001;19:131-61
[
11244033.001
]
[Cites]
J Endocrinol Invest. 1999 Feb;22(2):151-8
[
10195385.001
]
[Cites]
Lancet. 2001 Jul 21;358(9277):221-9
[
11476858.001
]
[Cites]
Diabetes. 2001 Oct;50(10):2231-6
[
11574403.001
]
[Cites]
Nat Immunol. 2001 Dec;2(12):1117-25
[
11713466.001
]
[Cites]
N Engl J Med. 2002 May 30;346(22):1685-91
[
12037147.001
]
[Cites]
N Engl J Med. 2002 May 30;346(22):1692-8
[
12037148.001
]
[Cites]
Radiology. 2003 Jan;226(1):214-20
[
12511693.001
]
[Cites]
Nat Rev Immunol. 2003 Feb;3(2):123-32
[
12563296.001
]
[Cites]
Nat Med. 2003 Jun;9(6):713-25
[
12778170.001
]
[Cites]
N Engl J Med. 2003 Jun 19;348(25):2491-9
[
12815134.001
]
[Cites]
Autoimmun Rev. 2002 May;1(3):139-45
[
12849007.001
]
[Cites]
Nat Med. 2003 Sep;9(9):1202-8
[
12937416.001
]
[Cites]
Tissue Antigens. 2003 Nov;62(5):359-77
[
14617043.001
]
[Cites]
Diabetes. 2004 Jan;53(1):250-64
[
14693724.001
]
[Cites]
Nat Med. 2000 Mar;6(3):351-5
[
10700241.001
]
[Cites]
Curr Diab Rep. 2004 Apr;4(2):87-94
[
15035967.001
]
[Cites]
Endocrinol Metab Clin North Am. 2004 Mar;33(1):113-33, ix-x
[
15053898.001
]
[Cites]
Diabetes. 2004 Jun;53(6):1459-66
[
15161749.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12634-9
[
15304647.001
]
[Cites]
Virchows Arch A Pathol Anat Histopathol. 1985;407(4):359-67
[
2413613.001
]
[Cites]
Virchows Arch A Pathol Anat Histopathol. 1986;410(1):17-21
[
3097948.001
]
[Cites]
Am J Pathol. 1987 Aug;128(2):210-5
[
3618725.001
]
[Cites]
N Engl J Med. 1988 Mar 17;318(11):663-70
[
3125434.001
]
[Cites]
Diabetes. 1988 Oct;37(10):1444-8
[
2458291.001
]
[Cites]
Proc Natl Acad Sci U S A. 1989 Oct;86(20):8000-4
[
2510155.001
]
[Cites]
Science. 1990 Jul 20;249(4966):293-5
[
2115690.001
]
[Cites]
Transplantation. 1990 Oct;50(4):537-44
[
2219269.001
]
[Cites]
Diabetologia. 1992 Dec;35(12):1118-24
[
1478363.001
]
[Cites]
Immunopharmacology. 1993 May-Jun;25(3):229-38
[
8354639.001
]
[Cites]
Cell. 1993 Sep 24;74(6):1089-100
[
8402882.001
]
[Cites]
Proc Natl Acad Sci U S A. 1994 Jan 4;91(1):123-7
[
8278351.001
]
[Cites]
Histol Histopathol. 1993 Oct;8(4):751-9
[
8305825.001
]
[Cites]
Endocr Rev. 1994 Aug;15(4):516-42
[
7988484.001
]
[Cites]
Cell. 1996 May 3;85(3):291-7
[
8616883.001
]
[Cites]
J Immunol. 1997 Mar 15;158(6):2947-54
[
9058834.001
]
[Cites]
Horm Metab Res. 1997 Oct;29(10):510-5
[
9405979.001
]
[Cites]
Autoimmunity. 1998;27(2):65-77
[
9583738.001
]
[Cites]
Endocrinology. 1998 Aug;139(8):3534-41
[
9681505.001
]
[Cites]
Eur J Immunol. 1999 Jan;29(1):245-55
[
9933106.001
]
[Cites]
Diabetes. 2001 Jun;50(6):1269-73
[
11375326.001
]
(PMID = 16110329.001).
[ISSN]
0021-9738
[Journal-full-title]
The Journal of clinical investigation
[ISO-abbreviation]
J. Clin. Invest.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R24 CA092782; United States / NCI NIH HHS / CA / R24 CA92782
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD3; 0 / Immunoglobulin G; 8N3DW7272P / Cyclophosphamide
[Other-IDs]
NLM/ PMC1187933
59.
Khan R, Maheshwari V, Harris SH, Alam K:
Prostatic adenocarcinoma metastasizing to the parietal bones.
Indian J Pathol Microbiol
; 2007 Oct;50(4):759-61
[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.
Prostate
cancer metastasis
to the axial skeleton occurs at high frequency in patients with advanced disease causing significant morbidity and mortality.
Apart from bone, brain is also a common site
of metastasis
but the involvement of the parietal bones is extremely unusual.
Parietal bone
metastasis
from prostatic adenocarcinoma was the initial presentation seen in our patient.
The report is intended to alert the reader of this rare site
of metastasis
from the
prostate
.
[MeSH-major]
Adenocarcinoma /
secondary
. Parietal Bone / pathology. Prostatic Neoplasms / pathology. Skull Neoplasms /
secondary
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18306543.001).
[ISSN]
0377-4929
[Journal-full-title]
Indian journal of pathology & microbiology
[ISO-abbreviation]
Indian J Pathol Microbiol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
India
60.
Tomlins SA, Mehra R, Rhodes DR, Cao X, Wang L, Dhanasekaran SM, Kalyana-Sundaram S, Wei JT, Rubin MA, Pienta KJ, Shah RB, Chinnaiyan AM:
Integrative molecular concept modeling of prostate cancer progression.
Nat Genet
; 2007 Jan;39(1):41-51
[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]
Integrative molecular concept modeling of
prostate
cancer
progression.
Despite efforts to profile
prostate
cancer
, the genetic alterations and biological processes that correlate with the observed histological progression are unclear.
Using laser-capture microdissection to isolate 101 cell populations, we have profiled
prostate
cancer
progression from benign epithelium
to metastatic
disease.
Of note, relative to low-grade
prostate
cancer
(Gleason pattern 3), high-grade
cancer
(Gleason pattern 4) shows an attenuated androgen signaling signature, similar
to metastatic
prostate
cancer
, which may reflect dedifferentiation and explain the clinical association of grade with prognosis.
Taken together, these data show that analyzing gene expression signatures in the context
of a
compendium of molecular concepts is useful in understanding
cancer
biology.
[MeSH-minor]
Androgens / metabolism. Disease Progression. Humans. Male.
Neoplasm Metastasis
. Prostatic Hyperplasia / genetics. Prostatic Hyperplasia / pathology. Prostatic Intraepithelial
Neoplasia
/ genetics. Prostatic Intraepithelial
Neoplasia
/ pathology. Signal Transduction. Systems Integration
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate 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
(PMID = 17173048.001).
[ISSN]
1061-4036
[Journal-full-title]
Nature genetics
[ISO-abbreviation]
Nat. Genet.
[Language]
eng
[Databank-accession-numbers]
GEO/ GSE6099
[Grant]
United States / NCI NIH HHS / CA / 5P30 CA46592; United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / R01 CA102872; United States / NIDA NIH HHS / DA / U54 DA021519-01A1; United States / NCI NIH HHS / CA / UO1 CA111275-01
[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.
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgens
61.
Saleem M, Adhami VM, Ahmad N, Gupta S, Mukhtar H:
Prognostic significance of metastasis-associated protein S100A4 (Mts1) in prostate cancer progression and chemoprevention regimens in an autochthonous mouse model.
Clin Cancer Res
; 2005 Jan 1;11(1):147-53
[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]
Prognostic significance
of metastasis
-associated protein S100A4 (Mts1) in
prostate
cancer
progression and chemoprevention regimens in an autochthonous mouse model.
PURPOSE: We recently showed that
metastasis
-promoting Mts1 gene (S100A4) and protein is overexpressed during progression of
prostate
cancer in
humans.
The purpose of this study was to assess the expression of S100A4 during autochthonous
prostate
cancer
progression in transgenic adenocarcinoma of the mouse
prostate
(TRAMP) model.
Because oral consumption of green tea polyphenols (GTP) has been shown to inhibit
metastasis
and
prostate
cancer in
TRAMP, we further assessed the significance of S100A4 during chemoprevention regimen.
RESULTS: With the progression of age and
prostate
cancer
growth in TRAMP mice, an increase in the expression of S100A4 at mRNA and protein level in dorsolateral
prostate
, but not in nontransgenic mice, occurred.
GTP feeding to TRAMP mice resulted in marked inhibition of
prostate
cancer
progression, which was associated with reduction of S100A4 and restoration of E-cadherin.
CONCLUSIONS: S100A4 represents a promising marker for
prostate
cancer
progression and could be employed as a biomarker in chemoprevention regimens.
[MeSH-minor]
Administration, Oral. Age Factors. Animals. Biomarkers / metabolism. Blotting, Western. Cadherins / metabolism. Cell Line,
Tumor
. DNA, Complementary / metabolism. Densitometry. Disease Progression. Flavonoids / chemistry. Guanosine Triphosphate / metabolism. Immunohistochemistry. Male. Mice. Mice, Inbred C57BL. Phenols / chemistry. Polymerase Chain Reaction. Polyphenols. RNA / metabolism. RNA, Messenger / metabolism. Tea. Time Factors. Transgenes
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
Green tea
.
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
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[ErratumIn]
Clin Cancer Res. 2005 Feb 1;11(3):1353
(PMID = 15671539.001).
[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 / P50DK 65303; United States / NCI NIH HHS / CA / R01 CA 101039; United States / NCI NIH HHS / CA / R01 CA 78809
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers; 0 / Cadherins; 0 / DNA, Complementary; 0 / Flavonoids; 0 / Phenols; 0 / Polyphenols; 0 / RNA, Messenger; 0 / S100 Proteins; 0 / S100a4 protein, mouse; 0 / Tea; 63231-63-0 / RNA; 86-01-1 / Guanosine Triphosphate
62.
Axanova L, Morré DJ, Morré DM:
Growth of LNCaP cells in monoculture and coculture with osteoblasts and response to tNOX inhibitors.
Cancer Lett
; 2005 Jul 8;225(1):35-40
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
An in vitro coculture model of
prostate
cancer
cells (LNCaP) with human osteoblasts (hFOB) was utilized to define the efficacy of the tNOX inhibitors EGCg, capsaicin, Capsibiol-T and phenoxodiol against bone
metastasis of
prostate
cancer
alone and in combination with Taxol and cisplatin.
[MeSH-minor]
Antineoplastic Agents / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Bone Neoplasms / prevention & control. Bone Neoplasms /
secondary
. Cell Survival. Cisplatin / pharmacology. Humans. Isoflavones / pharmacology. Male. Paclitaxel / pharmacology.
Tumor
Cells, Cultured
MedlinePlus Health Information.
consumer health - Antioxidants
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
CIS-DIAMINEDICHLOROPLATINUM
.
Hazardous Substances Data Bank.
TAXOL
.
Hazardous Substances Data Bank.
CAPSAICIN
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15922855.001).
[ISSN]
0304-3835
[Journal-full-title]
Cancer letters
[ISO-abbreviation]
Cancer Lett.
[Language]
eng
[Grant]
United States / NCCIH NIH HHS / AT / P50 AT0047
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Antioxidants; 0 / Capsibiol-T; 0 / Isoflavones; 0 / Plant Extracts; 8R1V1STN48 / Catechin; 995FT1W541 / phenoxodiol; BQM438CTEL / epigallocatechin gallate; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin; S07O44R1ZM / Capsaicin
63.
Kitagawa Y, Konaka H, Mizokami A, Namiki M:
[Clinical implications of bisphosphonate for bone metastases of prostate cancer].
Nihon Rinsho
; 2007 Nov 28;65 Suppl 9:356-9
[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]
[Clinical implications of bisphosphonate for bone
metastases of
prostate
cancer
].
[MeSH-major]
Bone Density Conservation Agents / therapeutic use. Bone Neoplasms /
secondary
. Diphosphonates / therapeutic use. Prostatic Neoplasms / pathology
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18161131.001).
[ISSN]
0047-1852
[Journal-full-title]
Nihon rinsho. Japanese journal of clinical medicine
[ISO-abbreviation]
Nippon Rinsho
[Language]
jpn
[Publication-type]
Journal Article; Review
[Publication-country]
Japan
[Chemical-registry-number]
0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / RANK Ligand
[Number-of-references]
12
64.
Briganti A, Blute ML, Eastham JH, Graefen M, Heidenreich A, Karnes JR, Montorsi F, Studer UE:
Pelvic lymph node dissection in prostate cancer.
Eur Urol
; 2009 Jun;55(6):1251-65
[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]
Pelvic lymph node dissection in
prostate
cancer
.
CONTEXT: Pelvic lymph node dissection (PLND) is considered the most reliable procedure for the detection of lymph node
metastases in
prostate
cancer
(PCa); however, the therapeutic benefit of PLND in PCa management is currently under debate.
Keywords included
prostate
cancer
, pelvic lymph node dissection, radical prostatectomy, imaging, and complications.
Extended PLND (ePLND; ie, removal of obturator, external iliac, hypogastric with or without presacral and common iliac nodes) significantly improves the detection of lymph node
metastases
compared with limited PLND (lPLND; ie, removal of obturator with or without external iliac nodes), which is associated with poor staging accuracy.
Because not all patients with PCa are at the same risk of harbouring nodal
metastases
, several nomograms and tables have been developed and validated to identify candidates for PLND.
According to these prediction models, a staging PLND might be omitted in low-risk PCa patients because of the low rate of lymph node
metastases
found, even after extended dissections (<8%).
Indeed, patients with low-volume nodal
metastases
experience excellent survival rates, regardless of adjuvant treatment.
Patients with low-volume nodal
metastases
have a good long-term prognosis; to what extent this prognosis is the result
of a
positive impact of PLND on PCa outcomes is still to be determined.
[MeSH-major]
Lymph Node Excision / methods. Lymph Nodes / pathology. Lymph Nodes / surgery.
Neoplasm
Staging / methods. Prostatectomy / methods. Prostatic Neoplasms / pathology
[MeSH-minor]
Biopsy, Needle. Humans. Immunohistochemistry. Lymphatic
Metastasis
. Male.
Neoplasm
Invasiveness / pathology. Pelvis. Predictive Value of Tests. Prognosis. Risk Assessment. Survival Analysis
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Eur Urol. 2009 Jun;55(6):1266-8
[
19349110.001
]
[CommentIn]
Eur Urol. 2009 Dec;56(6):e53
[
19773114.001
]
(PMID = 19297079.001).
[ISSN]
1873-7560
[Journal-full-title]
European urology
[ISO-abbreviation]
Eur. Urol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Switzerland
[Number-of-references]
88
65.
Venkitaraman R, Cook GJ, Dearnaley DP, Parker CC, Huddart RA, Khoo V, Eeles R, Horwich A, Sohaib SA:
Does magnetic resonance imaging of the spine have a role in the staging of prostate cancer?
Clin Oncol (R Coll Radiol)
; 2009 Feb;21(1):39-42
[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]
Does magnetic resonance imaging of the spine have a role in the staging of
prostate
cancer
?
AIMS: Magnetic resonance imaging (MRI) is an effective method for evaluating the spine in patients with a high risk
of metastatic
disease.
The aim of this study was to compare MRI spine with radionuclide bone scan in detecting spinal
metastases
for staging
prostate
cancer
patients.
MATERIALS AND METHODS: A cohort of 99 patients with locally advanced
prostate
cancer
at high risk of skeletal
metastasis
(
prostate
-specific antigen>10 ng/ml, composite Gleason score>or=8) or equivocal findings on bone scan were included in the retrospective study, and their MRI spine and bone scans were analysed.
RESULTS: Ten patients were detected to have definite spinal
metastasis
by bone scan, whereas 12 patients had definite skeletal
metastasis
by MRI spine.
Compared with the 'gold standard', derived from clinical and radiological follow-up, the sensitivities for radionuclide bone scan and that for MRI spine for detecting skeletal
metastasis
were 71.4 and 85.7%, respectively (P=0.023), whereas the specificities were 96.5 and 97.7%, respectively (P=0.95).
Of the 34 individual
metastatic
lesions in the spine, 15 were concordantly positive on both scans, whereas five lesions were positive only by bone scan and 11 positive only by MRI.
The addition of MRI spine in the staging for
prostate
cancer
resulted
in a
change of stage and management plan in seven (7%) patients.
CONCLUSION: MRI spine has comparable specificity and slightly better sensitivity than bone scan to detect spinal
metastasis
from
prostate
cancer
.
[MeSH-major]
Magnetic Resonance Imaging. Prostatic Neoplasms / pathology. Spinal Neoplasms /
diagnosis
. Spinal Neoplasms /
secondary
. Spine / pathology
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18993040.001).
[ISSN]
0936-6555
[Journal-full-title]
Clinical oncology (Royal College of Radiologists (Great Britain))
[ISO-abbreviation]
Clin Oncol (R Coll Radiol)
[Language]
eng
[Grant]
United Kingdom / Cancer Research UK / / 10588; United Kingdom / Medical Research Council / / G0501019
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
England
66.
Yonou H, Ochiai A, Ashimine S, Maeda H, Horiguchi Y, Yoshioka K, Ogawa Y, Hatano T, Tachibana M:
The bisphosphonate YM529 inhibits osteoblastic bone tumor proliferation of prostate cancer.
Prostate
; 2007 Jun 15;67(9):999-1009
[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 bisphosphonate YM529 inhibits osteoblastic bone
tumor
proliferation of
prostate
cancer
.
BACKGROUND: In men,
prostate
cancer
frequently metastasizes to the bones, where it forms osteoblastic lesions with an osteolytic element that cause pain.
However, the role of osteoclastogenesis in bone
metastasis of
human
prostate
cancer
is unknown.
Bisphosphonates are already known to be beneficical for treating osteolytic bone
metastases
, so we employed a model of osteoblastic bone
tumor of
human
prostate
cancer to
investigate whether a new bisphosphonate (YM529: minodronate) could inhibit both the formation of bone tumors and the progression of established osteoblastic tumors.
METHODS: Human
prostate
cancer
cells (LNCaP) were injected into adult human bone implants in nonobese diabetic/severe combined immunodeficient mice, after which osteoblastic bone tumors developed.
YM529 (1 microg/day) was administered subcutaneously every day for 2 weeks, starting either immediately or 2 weeks after implantation of the
tumor
cells, and the mice were sacrificed at 4 weeks after implantation.
The bone tumors were examined histologically and the number of tartrate-resistant acid phosphatase-stained osteoclasts in each
tumor
focus was counted.
CONCLUSIONS: YM529 reduced
the tumor
burden in bone by inhibiting both the formation of new lesions and the progression of existing tumors, suggesting that osteoclasts are involved in the formation of bone tumors by
prostate
cancer
.
Treatment with this bisphosphonate may potentially be beneficial for patients with bone
metastases of
prostate
cancer
.
[MeSH-major]
Bone Neoplasms / prevention & control. Bone Neoplasms /
secondary
. Diphosphonates / pharmacology. Imidazoles / pharmacology. Osteoblasts / pathology. Prostatic Neoplasms / pathology
[MeSH-minor]
Animals. Humans. Male. Mice. Mice, Nude.
Neoplasm
Transplantation / pathology. Transplantation, Heterologous
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17440967.001).
[ISSN]
0270-4137
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Diphosphonates; 0 / Imidazoles; 127657-42-5 / YM 529
67.
Compérat E, Azzouzi AR, Chartier-Kastler E, Ménégaux F, Capron F, Richard F, Charlotte F:
Late recurrence of a prostatic adenocarcinoma as a solitary splenic metastasis.
Urol Int
; 2007;78(1):86-8
[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]
Late recurrence
of a
prostatic adenocarcinoma as a solitary splenic
metastasis
.
Splenic
metastases of
solid tumors are exceptional.
We report the first case of an isolated splenic
metastasis
from
prostate
carcinoma, 5 years after radical prostatectomy.
The splenic
tumor
was revealed by a pain and progressive increase in the serum
prostate
-specific antigen (PSA) level.
This case suggests that splenic
metastasis
might be the result of the growth of an early blood-borne micrometastasis within the spleen after a period of clinical latency.
[MeSH-major]
Adenocarcinoma /
secondary
.
Neoplasm
Recurrence, Local /
diagnosis
. Prostatic Neoplasms / pathology. Splenic Neoplasms /
secondary
[MeSH-minor]
Aged. Antineoplastic Agents / therapeutic use.
Diagnosis
, Differential. Follow-Up Studies. Humans. Male. Prostatectomy. Radiation-Sensitizing Agents. Splenectomy. Taxoids / therapeutic use. Tomography, X-Ray Computed
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
DOCETAXEL
.
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 = 17192740.001).
[ISSN]
0042-1138
[Journal-full-title]
Urologia internationalis
[ISO-abbreviation]
Urol. Int.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Radiation-Sensitizing Agents; 0 / Taxoids; 15H5577CQD / docetaxel
68.
Klepzig M, Jonas D, Oremek GM:
Procollagen type 1 amino-terminal propeptide: a marker for bone metastases in prostate carcinoma.
Anticancer Res
; 2009 Feb;29(2):671-3
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Procollagen type 1 amino-terminal propeptide: a marker for bone
metastases in
prostate
carcinoma.
BACKGROUND: The objective of this study was to assess the utility of the bone formation marker procollagen type 1 amino-terminal propeptide (P1NP) in indicating bone
metastases in
patients with
prostate
carcinoma.
Alkaline phosphatase (AP) and
prostate
-specific antigen (PSA) were measured as a comparison.
The patients were divided into three groups, 32 patients with benign
prostate
hyperplasia (BPH), 38 patients with
prostate
carcinoma and 30 patients with
prostate
carcinoma with bone
metastases
.
RESULTS: PINP concentrations were elevated in about 87% of the patients with confirmed bone
metastases
, the P1NP levels were significantly (p < or = 0.001) higher (median: 194.7 ng/ml) than in the patients without bone involvement (median: 38.0 ng/ml) and the BPH patients (median: 42.2 ng/ml), who both presented P1NP levels within the normal range.
CONCLUSION: P1NP is a reliable predictor of the presence or absence of bone
metastases in
prostate
carcinoma.
[MeSH-major]
Biomarkers,
Tumor
/ blood. Bone Neoplasms / blood. Bone Neoplasms /
secondary
. Peptide Fragments / blood. Procollagen / blood. Prostatic Neoplasms / blood
[MeSH-minor]
Aged. Humans. Male.
Prostate
-Specific Antigen / blood. Prostatic Hyperplasia / blood
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
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
(PMID = 19331219.001).
[ISSN]
0250-7005
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Peptide Fragments; 0 / Procollagen; 0 / procollagen type I carboxy terminal peptide; EC 3.4.21.77 / Prostate-Specific Antigen
69.
Pinto F, Brescia A, Sacco E, Volpe A, Gardi M, Gulino G, Bassi P:
Disseminated intravascular coagulation secondary to metastatic prostate cancer: case report and review of the literature.
Arch Ital Urol Androl
; 2009 Dec;81(4):212-4
[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]
Disseminated intravascular coagulation
secondary to metastatic
prostate
cancer
: case report and review of the literature.
Disseminated intravascular coagulation (DIC) is the most frequent coagulation
disorder
associated with
metastatic
prostate
cancer
.
We report a case
of a
60-year-old white man who was admitted in our department with ecchymoses and haematuria
secondary to
a DIC associated with
metastatic
prostate
cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
LEUPROLIDE
.
Hazardous Substances Data Bank.
BICALUTAMIDE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20608143.001).
[ISSN]
1124-3562
[Journal-full-title]
Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica
[ISO-abbreviation]
Arch Ital Urol Androl
[Language]
ENG
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Italy
[Chemical-registry-number]
0 / Anilides; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide; EFY6W0M8TG / Leuprolide
[Number-of-references]
27
70.
Selimoglu H, Duran C, Saraydaroglu O, Guclu M, Kiyici S, Ersoy C, Eren MA, Tuncel E, Imamoglu S:
Prostate cancer metastasis to thyroid gland.
Tumori
; 2007 May-Jun;93(3):292-5
[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]
Prostate
cancer metastasis
to thyroid
gland
.
Metastases to
the thyroid
gland
are rarely encountered in clinical practice.
Prostate
cancer
is one of the most frequent malignancies in men.
It generally has a favorable course, and autopsy series have shown occult
prostate
cancer in
many subjects, especially in aged males.
However,
prostate
cancer
sometimes exhibits an aggressive behavior and cases with a poor prognosis have been reported.
Occasional reports
of metastasis
from
prostate
cancer to
the thyroid
gland
have been documented.
We describe the case
of a
73-year-old patient presenting with thyroid
metastasis
from long-standing
prostate
cancer
.
[MeSH-major]
Adenocarcinoma /
secondary
. Prostatic Neoplasms / pathology. Thyroid Neoplasms /
secondary
[MeSH-minor]
Aged. Biomarkers,
Tumor
/ analysis. Biopsy, Fine-Needle. Humans. Male.
Neoplasm
Proteins / analysis.
Prostate
-Specific Antigen / analysis
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Thyroid Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
MedlinePlus Health Information.
consumer health - Thyroid Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17679467.001).
[ISSN]
0300-8916
[Journal-full-title]
Tumori
[ISO-abbreviation]
Tumori
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; EC 3.4.21.77 / Prostate-Specific Antigen
71.
Nohara T, Kawashima A, Takahashi T, Kitamura M, Akai H, Oka T, Mano M:
[Prostate cancer metastasized to thyroid cartilage: a case report].
Nihon Hinyokika Gakkai Zasshi
; 2005 Nov;96(7):697-700
[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]
[
Prostate
cancer
metastasized to thyroid cartilage: a case report].
A 75-year-old male was diagnosed as
prostate
cancer
(serum PSA: 4,772 ng/ml, Gleason score: 4 + 4 = 8) with multiple bone
metastases
.
And he noticed a painless mass of the frontal neck a month before
the diagnosis
.
Computed tomography of the neck showed
a tumor
in the thyroid cartilage.
Biopsy of the neck
tumor
revealed
metastasis of
prostate
cancer
by positive PSA staining.
Metastasis of malignant tumor
to cartilaginous tissue is extremely rare because there are usually no vessels in it.
Only 4 cases of the
metastasis of
prostate
cancer to
the thyroid cartilage have been reported.
It was thought that tiny bone marrows were formed in the ossified cartilage and it caused hematogenous
metastasis
.
[MeSH-major]
Adenocarcinoma /
secondary
. Bone Neoplasms /
secondary
. Neoplastic Cells, Circulating / pathology. Prostatic Neoplasms / pathology. Thyroid Cartilage / pathology
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Thyroid Cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate 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 = 16363656.001).
[ISSN]
0021-5287
[Journal-full-title]
Nihon Hinyōkika Gakkai zasshi. The japanese journal of urology
[ISO-abbreviation]
Nippon Hinyokika Gakkai Zasshi
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
72.
Venkitaraman R, Cook GJ, Dearnaley DP, Parker CC, Khoo V, Eeles R, Huddart RA, Horwich A, Sohaib SA:
Whole-body magnetic resonance imaging in the detection of skeletal metastases in patients with prostate cancer.
J Med Imaging Radiat Oncol
; 2009 Jun;53(3):241-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Whole-body magnetic resonance imaging in the detection of skeletal
metastases in
patients with
prostate
cancer
.
Whole-body MRI is an effective method for evaluating the entire skeletal system in patients with
metastatic
disease.
This study aimed to compare whole-body MRI and radionuclide bone scintigraph in the detection of skeletal
metastases in
patients with
prostate
cancer
.
Patients with
prostate
cancer
at high risk of skeletal
metastasis
with (i)
prostate
-specific antigen of > or =50 ng/mL;.
(ii) composite Gleason score of > or =8 with
prostate
-specific antigen of >20 ng/mL; or (iii) node-positive disease were enrolled in this prospective study before systemic treatment was initiated.
Seven patients had bone
metastases
on bone scans, while seven patients had skeletal
metastases
by whole-body MRI, with concordant findings only in four patients.
Bone scans detected more rib
metastases
, while MRI identified more
metastatic
lesions in the spine.
Whole-body MRI and radionuclide bone scintigraphy have similar specificity and sensitivity and may be used as complementary investigations to detect skeletal
metastases
from
prostate
cancer
.
[MeSH-major]
Algorithms. Bone Neoplasms /
diagnosis
. Bone Neoplasms /
secondary
. Image Interpretation, Computer-Assisted / methods. Magnetic Resonance Imaging / methods. Prostatic Neoplasms /
diagnosis
. Whole Body Imaging / methods
[MeSH-minor]
Aged. Aged, 80 and over. Humans. Image Enhancement / methods. Lymphatic
Metastasis
. Male. Middle Aged. Reproducibility of Results. Sensitivity and Specificity
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19624290.001).
[ISSN]
1754-9485
[Journal-full-title]
Journal of medical imaging and radiation oncology
[ISO-abbreviation]
J Med Imaging Radiat Oncol
[Language]
eng
[Grant]
United Kingdom / Cancer Research UK / / 10588; United Kingdom / Medical Research Council / / G0501019; United Kingdom / Cancer Research UK / / C46/A2131
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Australia
73.
Spahn M, Kneitz S, Scholz CJ, Stenger N, Rüdiger T, Ströbel P, Riedmiller H, Kneitz B:
Expression of microRNA-221 is progressively reduced in aggressive prostate cancer and metastasis and predicts clinical recurrence.
Int J Cancer
; 2010 Jul 15;127(2):394-403
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Expression of microRNA-221 is progressively reduced in aggressive
prostate
cancer
and
metastasis
and predicts clinical recurrence.
Emerging evidence shows that microRNAs (miR) are involved in the pathogenesis
of a
variety of cancers, including
prostate
carcinoma (PCa).
Little information is available regarding miR expression levels in lymph node
metastasis of
prostate
cancer
or the potential of miRs as prognostic markers in this disease.
Therefore, we analyzed the global expression of miRs in benign, hyperplastic
prostate
tissue (BPH), primary PCa
of a
high risk group of PCa patients, and corresponding
metastatic
tissues by microarray analysis.
Consistent with the proposal that some miRs are oncomirs, we found aberrant expression of several miRs, including the downregulation of miR-221, in PCa
metastasis
.
In a
large study cohort, the
prostate
-specific oncomir miR-221 was progressively downregulated in aggressive forms of PCa.
Kaplan-Meier estimates and Cox proportional hazard models showed that miR-221 downregulation was linked
to tumor
progression and recurrence
in a
high risk
prostate
cancer
cohort.
Our results showed that progressive miR-221 downregulation hallmarks
metastasis
and presents a novel prognostic marker in high risk PCa.
[MeSH-major]
Biomarkers,
Tumor
/ genetics. MicroRNAs / physiology.
Neoplasm
Recurrence, Local /
diagnosis
. Prostatic Neoplasms / genetics. Prostatic Neoplasms / pathology
[MeSH-minor]
Aged. Cohort Studies. Computational Biology. Disease Progression. Humans. Lymphatic
Metastasis
. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prostatic Hyperplasia / genetics. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19585579.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / MIRN221 microRNA, human; 0 / MicroRNAs; 0 / RNA, Messenger
74.
Kosari F, Munz JM, Savci-Heijink CD, Spiro C, Klee EW, Kube DM, Tillmans L, Slezak J, Karnes RJ, Cheville JC, Vasmatzis G:
Identification of prognostic biomarkers for prostate cancer.
Clin Cancer Res
; 2008 Mar 15;14(6):1734-43
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Identification of prognostic biomarkers for
prostate
cancer
.
PURPOSE: This paper describes a process for the identification of genes that can report on the aggressiveness of
prostate
tumors and thereby add to the information provided by current pathologic analysis.
MATERIALS AND METHODS: Expression profiling data from over 100 laser capture microdissection derived samples from nonneoplastic epithelium; Gleason patterns 3, 4, and 5 and node
metastasis
prostate
cancer
were used to identify genes at abnormally high levels in only some tumors.
Selected genes were validated
in a
case-control study in which cases (systemic progression within 5 years) and controls (no systemic progression at 7 years of follow-up) were matched for all clinical and pathologic criteria from time of prostatectomy (n = 175).
RESULTS: A number of candidate variably overexpressed genes selected for their association with aggressive
prostate
cancer
phenotype were evaluated in the case control study.
CONCLUSIONS: The process described here identified genes that add information not available from current clinical measures and can improve the prognosis of
prostate
cancer
.
[MeSH-major]
Biomarkers,
Tumor
/ genetics. Prostatic Neoplasms /
diagnosis
[MeSH-minor]
Antigens,
Neoplasm
/ genetics. Automatic Data Processing. Case-Control Studies. Cluster Analysis. DNA Topoisomerases, Type II / genetics. DNA-Binding Proteins / genetics. Follow-Up Studies. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Male.
Neoplasm
Invasiveness. Oligonucleotide Array Sequence Analysis. Prognosis. Prostatectomy. Receptors, Somatostatin / genetics
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18347174.001).
[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]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Validation Studies
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Receptors, Somatostatin; 0 / somatostatin receptor type 1; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
75.
Chua CW, Chiu YT, Yuen HF, Chan KW, Man K, Wang X, Ling MT, Wong YC:
Suppression of androgen-independent prostate cancer cell aggressiveness by FTY720: validating Runx2 as a potential antimetastatic drug screening platform.
Clin Cancer Res
; 2009 Jul 1;15(13):4322-35
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Suppression of androgen-independent
prostate
cancer
cell aggressiveness by FTY720: validating Runx2 as a potential antimetastatic drug screening platform.
PURPOSE: Previously, FTY720 was found to possess potent anticancer effects on various types
of cancer
.
In the present study, we aimed to first verify the role of Runx2 in
prostate
cancer
progression and
metastasis
, and, subsequently, assessed if FTY720 could modulate Runx2 expression, thus interfering downstream events regulated by this protein.
EXPERIMENTAL DESIGN: First, the association between Runx2 and
prostate
cancer
progression was assessed using localized
prostate
cancer
specimens and mechanistic investigation of Runx2-induced
cancer
aggressiveness was then carried out.
Last, the involvement of Runx2 in FTY720-induced anticancer effects was evaluated by modulating Runx2 expression in various
prostate
cancer
cell lines.
RESULTS: Runx2 nuclear expression was found to be up-regulated in
prostate
cancer
and its expression could be used as a predictor
of metastasis
in
prostate
cancer
.
Further mechanistic studies indicated that Runx2 accelerated
prostate
cancer
aggressiveness through promotion of cadherin switching, invasion toward collagen I, and Akt activation.
CONCLUSION: This study provided a novel mechanism for the anticancer effect of FTY720 on advanced
prostate
cancer
, thus highlighting the therapeutic potential of this drug in treating this disease.
[MeSH-major]
Core Binding Factor Alpha 1 Subunit / physiology. Drug Screening Assays, Antitumor / methods. Propylene Glycols / therapeutic use. Prostatic Intraepithelial
Neoplasia
/ pathology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Sphingosine / analogs & derivatives
[MeSH-minor]
Aged. Aged, 80 and over. Androgens / pharmacology. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Case-Control Studies. Down-Regulation / drug effects. Down-Regulation / genetics. Drug Resistance,
Neoplasm
/ drug effects. Drug Resistance,
Neoplasm
/ genetics. Fingolimod Hydrochloride. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Middle Aged.
Neoplasm
Invasiveness.
Neoplasm Metastasis
.
Tumor
Cells, Cultured
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19509141.001).
[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]
Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgens; 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 1 Subunit; 0 / Propylene Glycols; 0 / RUNX2 protein, human; G926EC510T / Fingolimod Hydrochloride; NGZ37HRE42 / Sphingosine
76.
Fujii M, Abe K, Hayashi K, Kosuda S, Yano F, Watanabe S, Katagiri S, Ka WJ, Tominaga S:
Honda sign and variants in patients suspected of having a sacral insufficiency fracture.
Clin Nucl Med
; 2005 Mar;30(3):165-9
[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.
PURPOSE: The purpose of this study was to reassess whether the Honda sign (HS) and its variants on bone scans can be used to differentiate an insufficiency fracture (IF) of the sacrum from
a metastasis
and to evaluate extrapelvic tracer accumulation in patients suspected of having a sacral IF.
RESULTS: Twenty-four of the patients had a sacral IF and 1 had a sacral
metastasis
from
prostate
cancer
and another from lung
cancer
.
One of the 2 patients with
metastasis
exhibited the HS and the other exhibited a variant.
The most common site was the pubic bone (50%, 12 of 24), and the second most common site was the spine (46%, 11 of 24), where the accumulation was the result
of a
compression fracture or degenerative joint disease of the spine.
CONCLUSIONS: A "Honda sign or variation" with evidence of fractures elsewhere or no evidence of other
metastatic
disease should be strong evidence for a sacral insufficiency fracture.
The likelihood of having a solitary
metastasis to
the sacrum is small.
[MeSH-major]
Sacrum / injuries. Sacrum / radionuclide imaging. Spinal Fractures / radionuclide imaging. Spinal Neoplasms / radionuclide imaging. Spinal Neoplasms /
secondary
. Technetium Tc 99m Medronate
[MeSH-minor]
Aged. Aged, 80 and over.
Diagnosis
, Differential. Female. Humans. Male. Middle Aged. Radiopharmaceuticals / pharmacokinetics. Reproducibility of Results. Retrospective Studies. Sensitivity and Specificity
MedlinePlus Health Information.
consumer health - Spine Injuries and Disorders
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15722819.001).
[ISSN]
0363-9762
[Journal-full-title]
Clinical nuclear medicine
[ISO-abbreviation]
Clin Nucl Med
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Radiopharmaceuticals; X89XV46R07 / Technetium Tc 99m Medronate
77.
Hövels AM, Heesakkers RA, Adang EM, Barentsz JO, Jager GJ, Severens JL:
Cost-effectiveness of MR lymphography for the detection of lymph node metastases in patients with prostate cancer.
Radiology
; 2009 Sep;252(3):729-36
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Cost-effectiveness of MR lymphography for the detection of lymph node
metastases in
patients with
prostate
cancer
.
PURPOSE: To apply a decision analytic model to determine whether the addition of magnetic resonance (MR) lymphography to the diagnostic workup of patients with intermediate or high probability of lymph node
metastases
is cost effective from a health care perspective.
Probabilistic sensitivity analysis showed that in 63% of simulations, MR lymphography was cost saving and resulted in better patient outcome for patients with
prostate
cancer
and intermediate or high probability of lymph node
metastases
.
CONCLUSION: MR lymphography is an efficient strategy in the detection of lymph node
metastases of
prostate
cancer
when compared with the PLND strategy.
[MeSH-major]
Lymphatic
Metastasis
/ pathology. Magnetic Resonance Imaging / economics. Prostatic Neoplasms / pathology
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19717752.001).
[ISSN]
1527-1315
[Journal-full-title]
Radiology
[ISO-abbreviation]
Radiology
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
78.
Ananias HJ, van den Heuvel MC, Helfrich W, de Jong IJ:
Expression of the gastrin-releasing peptide receptor, the prostate stem cell antigen and the prostate-specific membrane antigen in lymph node and bone metastases of prostate cancer.
Prostate
; 2009 Jul 1;69(10):1101-8
[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]
Expression of the gastrin-releasing peptide receptor, the
prostate
stem cell antigen and the
prostate
-specific membrane antigen in lymph node and bone
metastases of
prostate
cancer
.
OBJECTIVE: Cell membrane antigens like the gastrin-releasing peptide receptor (GRPR), the
prostate
stem cell antigen (PSCA), and the
prostate
-specific membrane antigen (PSMA), expressed in
prostate
cancer
, are attractive targets for new therapeutic and diagnostic applications.
Therefore, we investigated in this study whether these antigens are expressed in metastasized
prostate
cancer
.
METHODS: Formalin-fixed, paraffin-embedded specimens of 15 patients with uni- or bilateral lymph node
metastases of
prostate
cancer
(totaling 21 cases) and 17 patient-cases of bone
metastases
were processed for immunohistochemistry with anti-GRPR, anti-PSCA, and anti-PSMA antibodies.
RESULTS: GRPR staining in lymph node
metastases
was seen in 85.7% of cases (18 of 21 cases), PSCA in 95.2% (20/21), and PSMA in 100% (21/21).
GRPR in bone
metastases
was seen in 52.9% of cases (9/17), PSCA in 94.1% (16/17), and PSMA in 100% (17/17).
CONCLUSION: We have shown for the first time that GRPR is expressed in the vast majority of lymph node
metastases
and in 52.9% of bone
metastases of
prostate
cancer
.
PSCA and PSMA are both highly expressed in lymph node and bone
metastases
.
Although PSCA and PSMA are mostly expressed in
prostate
cancer metastases
, GRPR offers an interesting alternative target as it can be targeted relatively easy with peptide-based (radio)pharmaceuticals.
[MeSH-major]
Antigens,
Neoplasm
/ biosynthesis. Antigens, Surface / biosynthesis. Bone Neoplasms / metabolism. Bone Neoplasms /
secondary
. Glutamate Carboxypeptidase II / biosynthesis. Membrane Glycoproteins / biosynthesis.
Neoplasm
Proteins / biosynthesis. Prostatic Neoplasms / metabolism. Receptors, Bombesin / biosynthesis
[MeSH-minor]
Biomarkers,
Tumor
/ biosynthesis. GPI-Linked Proteins. Gene Expression Regulation, Neoplastic / physiology. Humans. Lymph Nodes / metabolism. Lymph Nodes / pathology. Lymphatic
Metastasis
. Male. Retrospective Studies
Genetic Alliance.
consumer health - Bone Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
(c) 2009 Wiley-Liss, Inc.
(PMID = 19343734.001).
[ISSN]
1097-0045
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Antigens, Surface; 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / PSCA protein, human; 0 / Receptors, Bombesin; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human
79.
Zhao P, Luo R, Wu J, Xie F, Li H, Xiao X, Fu L, Zhu X, Liu R, Zhu Y, Liang Z, Huang W:
E10A, an adenovirus carrying human endostatin gene, in combination with docetaxel treatment inhibits prostate cancer growth and metastases.
J Cell Mol Med
; 2010 Jan;14(1-2):381-91
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
E10A, an adenovirus carrying human endostatin gene, in combination with docetaxel treatment inhibits
prostate
cancer
growth and
metastases
.
We assessed whether the combination of E10A with docetaxel would enhance antiangiogenic activities and inhibit
prostate
cancer
growth and
metastases
.
Combination use of conditioned medium from
prostate
cancer
cells infected by E10A and docetaxel exerted synergistic inhibition of HUVECs proliferation, migration and tube formation, compared with either agent alone.
In
prostate
cancer
s.c. xenograft models, combined therapy resulted in significant
tumor
growth inhibition and survival improvement.
The antitumoral effect was tightly correlated with a remarkable decrease
in tumor
cell proliferation, microvessel, especially immature vasculature and significant increase in apoptosis induction.
Systemic administration of E10A and docetaxel also effectively inhibited orthotopic growth and
metastases of
prostate
cancer
and achieved better in vivo antiangiogenic effects than either agent alone.
Our data indicate that E10A in combination with docetaxel exert enhanced antiangiogenic activities and inhibit
prostate
cancer
growth and
metastases
.
Therefore, this approach may be an effective treatment for advanced
prostate
cancer
and deserves more extensive investigation.
[MeSH-minor]
Adenoviridae / genetics. Animals. Apoptosis. Cell Line,
Tumor
. Cell Proliferation. Combined Modality Therapy. Genetic Vectors. Human Umbilical Vein Endothelial Cells. Humans. Male. Mice. Mice, Nude.
Neoplasm Metastasis
/ therapy. Xenograft Model Antitumor Assays
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Genes and Gene Therapy
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
DOCETAXEL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Clin Oncol. 2002 Sep 15;20(18):3792-803
[
12228199.001
]
[Cites]
Cancer Res. 2002 Oct 15;62(20):5720-6
[
12384530.001
]
[Cites]
FASEB J. 2002 Nov;16(13):1802-4
[
12354694.001
]
[Cites]
Mol Cancer Ther. 2002 Nov;1(13):1191-200
[
12479700.001
]
[Cites]
Int J Cancer. 2003 Mar 10;104(1):121-9
[
12532428.001
]
[Cites]
Clin Cancer Res. 2003 Oct 1;9(12):4619-26
[
14555538.001
]
[Cites]
Cancer Res. 2003 Dec 15;63(24):8890-8
[
14695206.001
]
[Cites]
Cancer Cell. 2004 Jan;5(1):13-7
[
14749122.001
]
[Cites]
Nat Rev Cancer. 2004 Jun;4(6):423-36
[
15170445.001
]
[Cites]
World J Gastroenterol. 2004 Jul 1;10(13):1867-71
[
15222025.001
]
[Cites]
Pharmacol Rev. 1989 Jun;41(2):93-141
[
2692037.001
]
[Cites]
J Natl Cancer Inst. 1992 Jun 17;84(12):951-7
[
1378502.001
]
[Cites]
Cell. 1997 Jan 24;88(2):277-85
[
9008168.001
]
[Cites]
Cancer Res. 1997 Sep 1;57(17):3847-51
[
9288798.001
]
[Cites]
Nature. 1998 Jul 16;394(6690):287-91
[
9685160.001
]
[Cites]
Clin Cancer Res. 1996 Nov;2(11):1843-9
[
9816139.001
]
[Cites]
APMIS. 2004 Jul-Aug;112(7-8):496-507
[
15563312.001
]
[Cites]
J Biol Chem. 2002 Aug 2;277(31):27872-9
[
12029087.001
]
[Cites]
Cancer Res. 2002 Feb 1;62(3):789-95
[
11830534.001
]
[Cites]
Nat Med. 2001 Sep;7(9):987-9
[
11533692.001
]
[Cites]
Nature. 2000 Sep 14;407(6801):249-57
[
11001068.001
]
[Cites]
Prostate. 2000 Sep 15;45(1):72-9
[
10960845.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4802-7
[
10758166.001
]
[Cites]
Cancer Cell. 2004 Dec;6(6):553-63
[
15607960.001
]
[Cites]
CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96
[
18287387.001
]
[Cites]
Gene Ther. 2008 Feb;15(4):247-56
[
18097470.001
]
[Cites]
Cancer Biol Ther. 2007 May;6(5):648-53
[
17426445.001
]
[Cites]
J Cell Mol Med. 2007 May-Jun;11(3):374-82
[
17635633.001
]
[Cites]
Adv Cancer Res. 2007;97:203-24
[
17419947.001
]
[Cites]
Hum Gene Ther. 2007 Mar;18(3):207-21
[
17346097.001
]
[Cites]
Clin Cancer Res. 2006 Aug 1;12(15):4702-13
[
16899621.001
]
[Cites]
Hepatology. 2005 Apr;41(4):879-86
[
15739185.001
]
[Cites]
Lancet Oncol. 2005 Apr;6(4):229-39
[
15811618.001
]
[Cites]
Clin Cancer Res. 2005 Jun 1;11(11):4217-24
[
15930360.001
]
[Cites]
Clin Exp Metastasis. 2005;22(1):31-8
[
16132576.001
]
[Cites]
Nat Rev Cancer. 2005 Sep;5(9):735-43
[
16079909.001
]
[Cites]
CA Cancer J Clin. 2005 Sep-Oct;55(5):300-18; quiz 323-5
[
16166075.001
]
[Cites]
Mol Ther. 2005 Dec;12(6):1091-100
[
16169279.001
]
[Cites]
Cancer Res. 2005 Dec 1;65(23):11044-50
[
16322254.001
]
[Cites]
J Cell Mol Med. 2005 Oct-Dec;9(4):777-94
[
16364190.001
]
[Cites]
Int J Cancer. 2006 Apr 15;118(8):2064-71
[
16287067.001
]
[Cites]
Lancet Oncol. 2006 Mar;7(3):199
[
16538782.001
]
[Cites]
Cancer Res. 2006 Apr 15;66(8):4319-28
[
16618757.001
]
[Cites]
Gastroenterology. 2006 Apr;130(4):1301-10
[
16618420.001
]
[Cites]
Science. 2006 May 26;312(5777):1171-5
[
16728631.001
]
(PMID = 26065034.001).
[ISSN]
1582-4934
[Journal-full-title]
Journal of cellular and molecular medicine
[ISO-abbreviation]
J. Cell. Mol. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Angiogenesis Inhibitors; 0 / Endostatins; 0 / Taxoids; 15H5577CQD / docetaxel
[Other-IDs]
NLM/ PMC3837610
80.
Maeda T, Tateishi U, Komiyama M, Fujimoto H, Watanabe S, Terauchi T, Moriyama N, Arai Y, Sugimura K, Kakizoe T:
Distant metastasis of prostate cancer: early detection of recurrent tumor with dual-phase carbon-11 choline positron emission tomography/computed tomography in two cases.
Jpn J Clin Oncol
; 2006 Sep;36(9):598-601
[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]
Distant
metastasis of
prostate
cancer
: early detection of recurrent
tumor
with dual-phase carbon-11 choline positron emission tomography/computed tomography in two cases.
Several types of recurrence may be detected by radiologic assessment after treatment in patients with
prostate
cancer
.
However, early detection of distant
metastasis
using positron emission tomography has so far never been published.
We report two patients who underwent hormone therapy or surgical resection for
prostate
cancer
.
They developed distant
metastases
which were detected on whole body [C-11] choline positron emission tomography/computed tomography with significant elevation of serum PSA level.
In one patient, recurrent
tumor of
the supraclavicular node (6 mm) diminished in size after subsequent hormone therapy.
Surgical resection of recurrent
tumor of
the lung (12 mm) was performed in the other patient, the pathology of which confirmed
the metastatic
adenocarcinoma derived from the
prostate
.
The recurrent
tumor
can be correctly detected by dual-phase whole body [C-11] choline positron emission tomography/computed tomography.
[MeSH-major]
Adenocarcinoma /
secondary
. Lung Neoplasms / radionuclide imaging. Lymph Nodes / pathology. Lymphatic
Metastasis
/ radionuclide imaging. Pelvic Neoplasms / radionuclide imaging. Positron-Emission Tomography. Prostatic Neoplasms / pathology
[MeSH-minor]
Aged. Antineoplastic Agents, Hormonal / therapeutic use. Carbon Radioisotopes. Choline. Early
Diagnosis
. Humans. Male.
Prostate
-Specific Antigen / blood. Tomography, X-Ray Computed
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Lung Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
CHOLINE CHLORIDE
.
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 = 16844733.001).
[ISSN]
0368-2811
[Journal-full-title]
Japanese journal of clinical oncology
[ISO-abbreviation]
Jpn. J. Clin. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / Carbon Radioisotopes; EC 3.4.21.77 / Prostate-Specific Antigen; N91BDP6H0X / Choline
81.
Kim HS, Sung W, Lee S, Chang SG, Park YK:
Lymphatic vessel densities of lymph node-negative prostate adenocarcinoma in Korea.
Pathol Res Pract
; 2009;205(4):249-54
[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]
Lymphatic vessel densities of lymph node-negative
prostate
adenocarcinoma in Korea.
Although lymphatic vessel density (LVD) is associated with regional lymph node (LN)
metastasis in
prostate
adenocarcinoma, no study is available that examines whether the LVD is correlated with prognostic factors other than LN
metastasis in
LN-negative
prostate
adenocarcinoma.
The aim of our study was to analyze intratumoral (IT), peritumoral (PT), and nontumoral (NT) LVDs, and to determine if there is a correlation between the LVD and the clinicopathological parameters in the Korean LN-negative
prostate
adenocarcinoma patients.
The IT-LVD was significantly lower in patients with larger
tumor
volume (P=0.029) and higher preoperative
prostate
-specific antigen level (P=0.008).
Our results suggest that IT- and PT-LVDs may increase in LN-negative
prostate
adenocarcinoma as a result of lymphangiogenesis, but IT lymphatics may decrease due to mechanical compression and destruction caused by proliferating
tumor
cells.
In addition, IT-LVD may be used as a prognostic factor in LN-negative
prostate
adenocarcinoma.
[MeSH-minor]
Aged. Humans. Immunohistochemistry. Korea. Lymph Nodes / pathology. Male. Middle Aged. Prognosis.
Prostate
-Specific Antigen / blood
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19058917.001).
[ISSN]
1618-0631
[Journal-full-title]
Pathology, research and practice
[ISO-abbreviation]
Pathol. Res. Pract.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
82.
Slavine NV, Antich PP:
Practical method for radioactivity distribution analysis in small-animal PET cancer studies.
Appl Radiat Isot
; 2008 Dec;66(12):1861-9
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Practical method for radioactivity distribution analysis in small-animal PET
cancer
studies.
We demonstrate reconstruction results for the amount of radioactivity within the scanned mouse
in a
sample study of osteolytic and osteoblastic bone
metastasis
from
prostate
cancer
xenografts.
Our method uses high-resolution images to determine the volume of organ or
tumor
and the amount of their radioactivity has the possibility of saving time, effort and the necessity to sacrifice animals.
This method has utility for prognosis and quantitative analysis in small-animal
cancer
studies, and will enhance the assessment of characteristics
of tumor
growth, identifying
metastases
, and potentially determining the effectiveness
of cancer
treatment.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Nucl Med. 2006 Jan;47(1):113-21
[
16391195.001
]
[Cites]
Med Phys. 2006 Jan;33(1):61-8
[
16485410.001
]
[Cites]
J Nucl Med. 2006 Mar;47(3):393-403
[
16513607.001
]
[Cites]
J Nucl Med. 2006 Jul;47(7):1181-6
[
16818953.001
]
[Cites]
Phys Med Biol. 2006 Aug 7;51(15):R541-78
[
16861768.001
]
[Cites]
Clin Cancer Res. 2006 Oct 15;12(20 Pt 2):6213s-6216s
[
17062703.001
]
[Cites]
Phys Med Biol. 2008 Feb 7;53(3):719-36
[
18199911.001
]
[Cites]
Clin Cancer Res. 2008 Mar 1;14(5):1377-85
[
18316558.001
]
[Cites]
J Nucl Med. 2004 Sep;45(9):1519-27
[
15347719.001
]
[Cites]
J Nucl Med. 2008 Mar;49(3):347-53
[
18287260.001
]
[Cites]
N Engl J Med. 2004 Apr 15;350(16):1655-64
[
15084698.001
]
[Cites]
J Nucl Med. 2004 Feb;45(2):192-201
[
14960635.001
]
[Cites]
J Cell Biochem. 2004 Feb 15;91(3):528-39
[
14755683.001
]
[Cites]
Clin Exp Metastasis. 2003;20(2):171-80
[
12705638.001
]
[Cites]
J Nucl Med. 2003 Mar;44(3):341-6
[
12620998.001
]
[Cites]
IEEE Trans Med Imaging. 2001 Aug;20(8):804-14
[
11513031.001
]
[Cites]
Comput Med Imaging Graph. 2001 Mar-Apr;25(2):105-11
[
11137786.001
]
[Cites]
Nucl Med Biol. 2000 Oct;27(7):643-6
[
11091106.001
]
[Cites]
J Nucl Med. 2000 Oct;41(10):1664-72
[
11037996.001
]
[Cites]
J Clin Pharmacol. 2000 Jul;40(7):770-80
[
10883419.001
]
[Cites]
Prostate. 2000 Jun 1;43(4):263-71
[
10861745.001
]
[Cites]
J Immunol. 2004 Jun 15;172(12):7694-702
[
15187152.001
]
[Cites]
AJR Am J Roentgenol. 2004 Oct;183(4):1127-32
[
15385319.001
]
[Cites]
Phys Med Biol. 1984 Nov;29(11):1421-31
[
6334321.001
]
[Cites]
J Nucl Med. 1988 Sep;29(9):1603-4
[
3261788.001
]
[Cites]
Phys Med Biol. 1992 May;37(5):1065-76
[
1608996.001
]
[Cites]
J Nucl Med. 1995 Oct;36(10):1836-9
[
7562051.001
]
[Cites]
Prostate. 1997 Jun 1;31(4):264-81
[
9180937.001
]
[Cites]
Int J Cancer. 1998 Sep 11;77(6):887-94
[
9714059.001
]
[Cites]
Cancer Res. 2005 Feb 1;65(3):967-71
[
15705897.001
]
[Cites]
Clin Cancer Res. 2005 Jun 1;11(11):4022-8
[
15930336.001
]
[Cites]
Cancer Biother Radiopharm. 2005 Jun;20(3):310-5
[
15989476.001
]
[Cites]
Appl Radiat Isot. 2005 Sep;63(3):343-51
[
15955705.001
]
[Cites]
Invest New Drugs. 2005 Oct;23(5):429-36
[
16133794.001
]
[Cites]
Cancer Res. 2005 Sep 1;65(17):7554-60
[
16140917.001
]
[Cites]
J Nucl Med. 2005 Oct;46(10):1707-18
[
16204722.001
]
(PMID = 18667322.001).
[ISSN]
1872-9800
[Journal-full-title]
Applied radiation and isotopes : including data, instrumentation and methods for use in agriculture, industry and medicine
[ISO-abbreviation]
Appl Radiat Isot
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U24 CA126608; None / None / / U24 CA126608-02; United States / NCI NIH HHS / CA / U24 CA126608-02
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
[Other-IDs]
NLM/ NIHMS77452; NLM/ PMC2644068
83.
Williams SA, Singh P, Isaacs JT, Denmeade SR:
Does PSA play a role as a promoting agent during the initiation and/or progression of prostate cancer?
Prostate
; 2007 Feb 15;67(3):312-29
[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]
Does PSA play a role as a promoting agent during the initiation and/or progression of
prostate
cancer
?
Prostate
cancer
cells, like normal
prostate
epithelial cells, produce high levels of the differentiation marker and serine protease
prostate
-specific antigen (PSA).
PSA is used extensively as a biomarker to screen for
prostate
cancer
, to detect recurrence following local therapies, and to follow response to systemic therapies for
metastatic
disease.
While much is known about PSA's role as a biomarker, only a relatively few studies address the role played by PSA in the pathobiology of
prostate
cancer
.
Autopsy studies have documented that not only do
prostate
cancer
cells maintain production of high amounts of PSA but they also maintain the enzymatic machinery required to process PSA to an enzymatically active form.
A variety studies performed over the last 10 years have hinted at a role for PSA in growth, progression, and
metastases of
prostate
cancer
.
A fuller understanding of PSA's functional role in
prostate
cancer
biology, however, has been hampered by the lack of appropriate models and tools.
Instead, by reviewing what is known about the genetics, biochemistry, and biology of PSA in normal and
malignant
prostate
tissue, insights may be gained into the role PSA may be playing in the pathobiology of
prostate
cancer
that can connect measurement of this biomarker to an understanding of the underlying etiology and progression of the disease.
[MeSH-major]
Neoplasms, Hormone-Dependent / enzymology.
Prostate
-Specific Antigen / metabolism. Prostatic Neoplasms / enzymology. Prostatic Neoplasms / pathology
[MeSH-minor]
Adult. Animals. Bone Neoplasms / metabolism. Bone Neoplasms /
secondary
. Enzyme Activation. Humans. Male. Middle Aged. Models, Molecular
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer Screening
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
(c) 2006 Wiley-Liss, Inc.
(PMID = 17143882.001).
[ISSN]
0270-4137
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P50CA58236
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
[Number-of-references]
114
84.
Lamoureux F, Ory B, Battaglia S, Pilet P, Heymann MF, Gouin F, Duteille F, Heymann D, Redini F:
Relevance of a new rat model of osteoblastic metastases from prostate carcinoma for preclinical studies using zoledronic acid.
Int J Cancer
; 2008 Feb 15;122(4):751-60
[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]
Relevance
of a
new rat model of osteoblastic
metastases
from
prostate
carcinoma for preclinical studies using zoledronic acid.
Animal models that mimic osteoblastic
metastases
associated with
prostate
carcinoma are required to improve the therapeutic options in humans.
Rat AT6-1
prostate
tumor
cells were characterized in vitro at the transcriptional (bone and epithelial markers) and functional (induction of mineralized nodules) levels.
The tumor
itself is associated with bone formation as revealed by SEM analysis and polarized light microscopy.
ZOL prevents the development of such osteoblastic lesions, related
to a
direct inhibitory effect on
tumor
cell proliferation independent of caspase 3 activation, but associated with cell cycle arrest.
A new rat model of osteoblastic bone
metastases
was validated in immunocompetent rats and used to show the relevance of using ZOL in such lesions, as this compound shows bifunctional effects on both bone remodelling and
tumor
cell proliferation.
[MeSH-minor]
Animals. Apoptosis / drug effects. Bone Marrow Cells / drug effects. Bone Remodeling / drug effects. Cell Cycle / drug effects. Cell Proliferation / drug effects. Humans. Male. Mice. Mice, Inbred C3H. Osteoblasts / drug effects. Osteoblasts / metabolism. Osteogenesis / drug effects. Rats. Rats, Sprague-Dawley.
Tumor
Cells, Cultured / drug effects
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
(c) 2007 Wiley-Liss, Inc.
(PMID = 17960623.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
85.
Lerner I, Baraz L, Pikarsky E, Meirovitz A, Edovitsky E, Peretz T, Vlodavsky I, Elkin M:
Function of heparanase in prostate tumorigenesis: potential for therapy.
Clin Cancer Res
; 2008 Feb 1;14(3):668-76
[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]
Function of heparanase in
prostate
tumorigenesis: potential for therapy.
Whereas the role of heparanase in sustaining the pathology of human
cancer
is well documented, its association with
prostate
carcinoma remains uncertain.
Our research was undertaken to elucidate the significance of heparanase in
prostate
tumorigenesis and bone
metastasis
.
EXPERIMENTAL DESIGN: We applied immunohistochemical analysis of tissue microarray, in vitro adhesion and invasion assays, as well as mouse models of intraosseous growth and spontaneous
metastasis of
prostate
cancer
, monitored by whole-body bioluminescent imaging.
RESULTS: We report a highly statistically significant (P < 0.0001) prevalence of heparanase overexpression in
prostate
carcinomas versus noncancerous tissue, as well as strong correlation between
tumor
grade and the extent of heparanase expression.
We observed >5-fold increase in the
metastatic
potential of PC-3
prostate
carcinoma cells engineered to overexpress heparanase.
Notably, overexpression
of a
secreted form of the enzyme also led
to a
dramatic increase in intraosseous
prostate
tumor
growth.
Local in vivo silencing of heparanase resulted
in a
4-fold inhibition of
prostate
tumor
growth, representing the first successful application of anticancer therapy based on heparanase small interfering RNA and validating the potential of heparanase as a target for
prostate
cancer
treatment.
CONCLUSIONS: Heparanase directly contributes to
prostate
tumor
growth in bone and its ability to metastasize to distant organs.
Thus, anti-heparanase strategy may become an important modality in the treatment of
prostate
cancer
patients, particularly those with bone
metastases
.
[MeSH-minor]
Biopsy. Bone Neoplasms / enzymology. Bone Neoplasms / pathology. Bone Neoplasms /
secondary
. Cell Adhesion. Cell Division. Cell Line,
Tumor
. Cloning, Molecular. Collagen. Drug Combinations. Gene Expression Regulation, Neoplastic. Humans. Laminin. Male.
Neoplasm
Invasiveness. Oligonucleotide Array Sequence Analysis.
Prostate
/ enzymology. Proteoglycans. Reference Values. Reverse Transcriptase Polymerase Chain Reaction. Transfection
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18212251.001).
[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 / NCI NIH HHS / CA / R01 CA106456-01
[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 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
86.
Shiraishi J, Li Q, Appelbaum D, Pu Y, Doi K:
Development of a computer-aided diagnostic scheme for detection of interval changes in successive whole-body bone scans.
Med Phys
; 2007 Jan;34(1):25-36
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Development
of a
computer-aided diagnostic scheme for detection of interval changes in successive whole-body bone scans.
It is a well-established imaging modality for
the diagnosis
of osseous
metastasis
and for monitoring osseous
tumor
response to chemotherapy and radiation therapy.
Although the sensitivity of bone scan examinations for detection of bone abnormalities has been considered to be relatively high, it is time consuming to identify multiple lesions such as bone
metastases of
prostate
and breast cancers.
Therefore, we developed a new computer-aided diagnostic (CAD) scheme for the detection of interval changes in successive whole-body bone scans by use
of a
temporal subtraction image which was obtained with a nonlinear image-warping technique.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17278486.001).
[ISSN]
0094-2405
[Journal-full-title]
Medical physics
[ISO-abbreviation]
Med Phys
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA62625; United States / NCI NIH HHS / CA / CA98119
[Publication-type]
Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
87.
Varghese S, Rabkin SD, Nielsen PG, Wang W, Martuza RL:
Systemic oncolytic herpes virus therapy of poorly immunogenic prostate cancer metastatic to lung.
Clin Cancer Res
; 2006 May 1;12(9):2919-27
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Systemic oncolytic herpes virus therapy of poorly immunogenic
prostate
cancer metastatic
to lung.
PURPOSE: Our goal was to evaluate whether systemic administration of NV1042, an interleukin-12 (IL-12)-expressing oncolytic herpes simplex virus, and its noncytokine parental vector NV1023 are effective against preexisting
metastatic
prostate
cancer in
an immunocompetent mice model.
EXPERIMENTAL DESIGN:
Metastatic
TRAMP-C2 lung tumors established in C57Bl/6 or nude mice were treated on day 21 with four i.v. administrations of NV1042 or NV1023 and sacrificed on day 42 to assess virus efficacy and the potential mechanism of efficacy.
However, NV1042 was further effective compared with NV1023 in controlling the growth of lung tumors (as determined by mean surface
tumor
nodule number, lung weights, and surface
tumor
burden) and in extending survival.
NV1042-treated mice exhibited a transient increase of serum IL-12 1 day posttreatment, whereas IL-12 levels
in tumor
bearing lungs persisted a further 2 days at least.
The IL-12-mediated enhancement observed with NV1042 in the syngeneic model was abrogated in athymic mice treated
in a
similar manner, thus indicating a role for T cells in the augmented efficacy of NV1042 virus.
CONCLUSIONS: Systemic administration of the IL-12-expressing NV1042 virus is more effective than its noncytokine parent, NV1023, against preestablished
metastatic
lung tumors.
Given the clinical safety profile of NV1020, the parental vector of NV1023, and NV1042's enhanced efficacy and ability to activate the host immune system, NV1042 merits clinical consideration for treating
metastatic
prostate
cancers.
[MeSH-major]
Lung Neoplasms / drug therapy. Lung Neoplasms /
secondary
. Oncolytic Virotherapy. Prostatic Neoplasms / pathology
[MeSH-minor]
Animals. Cell Line,
Tumor
. Male. Mice. Mice, Inbred C57BL.
Neoplasm
Transplantation. Organ Size / drug effects
MedlinePlus Health Information.
consumer health - Lung Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16675589.001).
[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 / NCI NIH HHS / CA / 1R01CA102139
[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.
[Publication-country]
United States
88.
Walz J, Chun FK, Klein EA, Reuther A, Saad F, Graefen M, Huland H, Karakiewicz PI:
Nomogram predicting the probability of early recurrence after radical prostatectomy for prostate cancer.
J Urol
; 2009 Feb;181(2):601-7; discussion 607-8
[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]
Nomogram predicting the probability of early recurrence after radical prostatectomy for
prostate
cancer
.
PURPOSE: We developed a nomogram predicting the probability of early biochemical recurrence after radical prostatectomy because early recurrence predisposes to distant
metastasis
and
prostate
cancer
related mortality.
MATERIALS AND METHODS: From January 1992 to December 2005, 2,911 patients underwent radical prostatectomy for localized
prostate
cancer
.
Age,
prostate
specific antigen, pathological Gleason sum, surgical margin, extracapsular extension, seminal vesicle invasion and lymph node invasion were considered.
[MeSH-major]
Neoplasm
Recurrence, Local / pathology. Nomograms. Prostatectomy / methods. Prostatic Neoplasms / pathology. Prostatic Neoplasms / surgery
[MeSH-minor]
Age Factors. Aged. Aged, 80 and over. Biopsy, Needle. Cohort Studies. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged.
Neoplasm
Staging. Predictive Value of Tests. Probability. Prognosis. Proportional Hazards Models. Retrospective Studies. Risk Assessment. Sensitivity and Specificity. Survival Analysis. Time Factors
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address: