BioMedLib Search Engine
[ goto HOMEPAGE ]
Save time; Find better answers!
Skip to content
Advanced Search
Search History
MeSH Query
Page Format
Query is expanded
Login
Skip to content
Export Citations
Search Results
RSS
Email
Articles' Details
Start new query
Reset All
Refine your query
(more in Advanced-Search):
Search all of MEDLINE
Focus on the recent 5 years
Focus on the current year
Focus on the last 30 days
More choices ...
Focus on articles with free fulltexts
More choices ...
Do simple 'keyword' search (no query expansion)
[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click
here to
RESET
all values
Click
here to
GO BACK
without resetting any value
Advanced Search
Submit one or more of the following items, and they will be searched along with your query in the search box above.
Any submit button will submit all of the items you have changed.
+
Publication-Date
Published in the last:
30 days
60 days
90 days
6 months
12 months
this year
2 years
3 years
5 years
10 years
Or published in the following date range: From (yyyy/mm/dd - month and day are optional)
to ('to' is optional)
+
Full Text
Retrieve articles with hyperlinks to:
full text (either free or subscription)
free full text
subscription full text
no full text link
+
Sort-Order
Sort the retrieved articles by:
relevance
publication date
+
Language
And with languages:
English
French
German
Italian
Japanese
Russian
Spanish
More languages:
Afrikaans
Albanian
Amharic
Arabic
Armenian
Azerbaijani
Bengali
Bosnian
Bulgarian
Catalan
Chinese
Czech
Danish
Dutch
Esperanto
Estonian
Finnish
Georgian
Scottish Gaelic
Greek, Modern
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Kinyarwanda
Korean
Latin
Latvian
Lithuanian
Macedonian
Malayalam
Maori
Malay
Multiple languages
Norwegian
Persian
Polish
Portuguese
Pushto
Romanian
Sanskrit
Serbian
Croatian
Slovak
Slovenian
Swedish
Thai
Turkish
Ukrainian
Undetermined
Urdu
Vietnamese
Welsh
+
Publication-Type
And with publication types:
Clinical Trial
Editorial
Letter
Meta-Analysis
Practice Guideline
Randomized Controlled Trial
Review
More publication types:
Addresses
Bibliography
Biography
Case Reports
Classical Article
Clinical Conference
Clinical Trial, Phase I
Clinical Trial, Phase II
Clinical Trial, Phase III
Clinical Trial, Phase IV
Comment
Comparative Study
Congresses
Consensus Development Conference
Consensus Development Conference, NIH
Controlled Clinical Trial
Corrected and Republished Article
Dictionary
Directory
Duplicate Publication
English Abstract
Evaluation Studies
Festschrift
Government Publications
Guideline
Historical Article
Interactive Tutorial
Interview
Introductory Journal Article
In Vitro
Journal Article
Lectures
Legal Cases
Legislation
Multicenter Study
News
Newspaper Article
Overall
Patient Education Handout
Periodical Index
Portraits
Published Erratum
Retracted Publication
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
Retraction of Publication
Scientific Integrity Review
Technical Report
Twin Study
Validation Studies
+
Species
And for:
Humans
Animals
+
Gender
And for:
Male
Female
+
Age
And for these age groups:
Newborn: birth to 1 month
Infant: 1 to 23 months
Preschool child: 2 to 5 years
Child: 6 to 12 years
Adolescent: 13 to 18 years
Adult: 19 to 44 years
Middle aged: 45 to 64 years
Aged: 65+ years
80 and over: 80+ years
+
Title
And for this query matching the titles:
+
Transliterated-Title
And for this query matching the title in original language:
+
Abstract
And for this query matching the abstratcs:
+
Major-Mesh
And for this query matching the MeSH-Major terms:
+
Mesh
And for this query matching any MeSH terms:
+
Journal
And for one or more of these journal abbreviated names:
OR
OR
(see
title abbreviations
)
+
Volume
And with journal volume number:
+
Issue
And with journal issue number:
+
Page
And with page number:
+
ISSN
And with ISSN:
+
Publication-Place
And with journal's country of publication:
+
Author
And for...
all these author names:
AND
AND
(see
help
)
one or more of these author names:
OR
OR
but not having any of these unwanted author names:
NOT
NOT
+
Affiliation
And with affiliation to:
+
Has-Abstract
Find MEDLINE records with the abstract status:
has abstract
does not have abstract
include both record types
include both record types but rank higher the records having abstract (the default BML behavior)
+
PMID
Show me only articles for these PMIDs (PubMed IDs):
+
Semantic-Type
And with semantic types:
A. Entity
A1. Physical Object
A1.1. Organism
A1.1.1. Archaeon
A1.1.2. Bacterium
A1.1.3. Eukaryote
A1.1.3.1. Animal
A1.1.3.1.1. Vertebrate
A1.1.3.1.1.1. Amphibian
A1.1.3.1.1.2. Bird
A1.1.3.1.1.3. Fish
A1.1.3.1.1.4. Mammal
A1.1.3.1.1.4.1. Human
A1.1.3.1.1.5. Reptile
A1.1.3.2. Fungus
A1.1.3.3. Plant
A1.1.4. Virus
A1.2. Anatomical Structure
A1.2.1. Embryonic Structure
A1.2.2. Anatomical Abnormality
A1.2.2.1. Congenital Abnormality
A1.2.2.2. Acquired Abnormality
A1.2.3. Fully Formed Anatomical Structure
A1.2.3.1. Body Part, Organ, or Organ Component
A1.2.3.2. Tissue
A1.2.3.3. Cell
A1.2.3.4. Cell Component
A1.2.3.5. Gene or Genome
A1.3. Manufactured Object
A1.3.1. Medical Device
A1.3.1.1. Drug Delivery Device
A1.3.2. Research Device
A1.3.3. Clinical Drug
A1.4. Substance
A1.4.1. Chemical
A1.4.1.1. Chemical Viewed Functionally
A1.4.1.1.1. Pharmacologic Substance
A1.4.1.1.1.1. Antibiotic
A1.4.1.1.2. Biomedical or Dental Material
A1.4.1.1.3. Biologically Active Substance
A1.4.1.1.3.1. Neuroreactive Substance or Biogenic Amine
A1.4.1.1.3.2. Hormone
A1.4.1.1.3.3. Enzyme
A1.4.1.1.3.4. Vitamin
A1.4.1.1.3.5. Immunologic Factor
A1.4.1.1.3.6. Receptor
A1.4.1.1.4. Indicator, Reagent, or Diagnostic Aid
A1.4.1.1.5. Hazardous or Poisonous Substance
A1.4.1.2. Chemical Viewed Structurally
A1.4.1.2.1. Organic Chemical
A1.4.1.2.1.5. Nucleic Acid, Nucleoside, or Nucleotide
A1.4.1.2.1.6. Organophosphorus Compound
A1.4.1.2.1.7. Amino Acid, Peptide, or Protein
A1.4.1.2.1.8. Carbohydrate
A1.4.1.2.1.9. Lipid
A1.4.1.2.1.9.1. Steroid
A1.4.1.2.1.9.2. Eicosanoid
A1.4.1.2.2. Inorganic Chemical
A1.4.1.2.3. Element, Ion, or Isotope
A1.4.2. Body Substance
A1.4.3. Food
A2. Conceptual Entity
A2.1. Idea or Concept
A2.1.1. Temporal Concept
A2.1.2. Qualitative Concept
A2.1.3. Quantitative Concept
A2.1.4. Functional Concept
A2.1.4.1. Body System
A2.1.5. Spatial Concept
A2.1.5.1. Body Space or Junction
A2.1.5.2. Body Location or Region
A2.1.5.3. Molecular Sequence
A2.1.5.3.1. Nucleotide Sequence
A2.1.5.3.2. Amino Acid Sequence
A2.1.5.3.3. Carbohydrate Sequence
A2.1.5.4. Geographic Area
A2.2. Finding
A2.2.1. Laboratory or Test Result
A2.2.2. Sign or Symptom
A2.3. Organism Attribute
A2.3.1. Clinical Attribute
A2.4. Intellectual Product
A2.4.1. Classification
A2.4.2. Regulation or Law
A2.5. Language
A2.6. Occupation or Discipline
A2.6.1. Biomedical Occupation or Discipline
A2.7. Organization
A2.7.1. Health Care Related Organization
A2.7.2. Professional Society
A2.7.3. Self-help or Relief Organization
A2.8. Group Attribute
A2.9. Group
A2.9.1. Professional or Occupational Group
A2.9.2. Population Group
A2.9.3. Family Group
A2.9.4. Age Group
A2.9.5. Patient or Disabled Group
B. Event
B1. Activity
B1.1. Behavior
B1.1.1. Social Behavior
B1.1.2. Individual Behavior
B1.2. Daily or Recreational Activity
B1.3. Occupational Activity
B1.3.1. Health Care Activity
B1.3.1.1. Laboratory Procedure
B1.3.1.2. Diagnostic Procedure
B1.3.1.3. Therapeutic or Preventive Procedure
B1.3.2. Research Activity
B1.3.2.1. Molecular Biology Research Technique
B1.3.3. Governmental or Regulatory Activity
B1.3.4. Educational Activity
B1.4. Machine Activity
B2. Phenomenon or Process
B2.1. Human-caused Phenomenon or Process
B2.1.1. Environmental Effect of Humans
B2.2. Natural Phenomenon or Process
B2.2.1. Biologic Function
B2.2.1.1. Physiologic Function
B2.2.1.1.1. Organism Function
B2.2.1.1.1.1. Mental Process
B2.2.1.1.2. Organ or Tissue Function
B2.2.1.1.3. Cell Function
B2.2.1.1.4. Molecular Function
B2.2.1.1.4.1. Genetic Function
B2.2.1.2. Pathologic Function
B2.2.1.2.1. Disease or Syndrome
B2.2.1.2.1.1. Mental or Behavioral Dysfunction
B2.2.1.2.1.2. Neoplastic Process
B2.2.1.2.2. Cell or Molecular Dysfunction
B2.2.1.2.3. Experimental Model of Disease
B2.3. Injury or Poisoning
Page Format
Any submit button will submit all of the items you have changed.
[theme]
Use this page design theme:
original
twenty ten
[shown]
Results per page:
5
10
20
50
100
200
500
[expand/collapse]
show these sections expanded by default:
Advanced search
MeSH query
Search history
Page format
Query expansion
Articles details
Export citations
Email
[text size]
use this font size for text:
25%
50%
75%
100%
125%
150%
200%
or enter your choice of font size:
[page width]
use this page width (relative to the default initial value):
25%
50%
75%
100%
125%
150%
200%
or enter your choice of page width:
[highlight color]
use this color to highlight query words in the articles:
red
green
blue
black
purple
yellow
orange
navy
olive
maroon
none
[query history]
maximum number of queries shown in the history section:
[annotate]
Annotate these parts of each article:
title
abstract
both
none
Reset all values
Find best MeSH terms for
Search History
1
adenocarcinoma of the prostate metastatic 2005:2010[pubdate] *count=100
526 results
Searchbox
Export
PDF
RSS
Email
Delete
Email this search result to the following email address:
[X] Close
Expand the query
'
adenocarcinoma of the prostate metastatic
' 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 526
1.
Zellweger T, Ninck C, Bloch M, Mirlacher M, Koivisto PA, Helin HJ, Mihatsch MJ, Gasser TC, Bubendorf L:
Expression patterns of potential therapeutic targets in prostate cancer.
Int J Cancer
; 2005 Feb 10;113(4):619-28
[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 patterns of potential therapeutic targets in
prostate
cancer.
Androgen withdrawal is the only effective therapy for patients with advanced
prostate
cancer, but progression to androgen independence ultimately occurs in almost all patients.
Here, we aimed to evaluate the expression of potential therapeutic targets in advanced
prostate
cancer.
A tissue microarray (TMA) containing samples from 535 tissue blocks was constructed, including benign
prostatic
hyperplasia as controls (n = 65),
prostatic
intraepithelial neoplasia (PIN; n = 78), clinically localized
prostate
cancers (n = 181), as well as hormone-refractory local recurrences (n = 120) and distant metastases (n = 91).
Significant overexpression in hormone-refractory
prostate
cancer and
metastatic
tissue compared to localized
prostate
cancer was found for Ki67 (64% vs. 9%), Bcl-2 (11% vs. 1%), p53 (35% vs. 4%), Syndecan-1 (38% vs. 3%), EGFR (16% vs. 1%) and HER2/neu (16% vs. 0%).
Taken together, p53, Bcl-2, Syndecan-1, EGFR and HER2/neu are preferentially expressed in hormone-refractory and
metastatic prostate
cancer.
Treatment decisions should not be based on findings in primary tumors but rather on tissues from recurrent or
metastatic
lesions.
[MeSH-major]
Adenocarcinoma
/ metabolism. Biomarkers, Tumor / metabolism. Gene Expression Regulation, Neoplastic. Neoplasm Proteins / metabolism. Neoplasms, Hormone-Dependent / metabolism.
Prostatic
Neoplasms / metabolism
[MeSH-minor]
Humans. Immunoenzyme Techniques. Male. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology.
Prostate
/ metabolism.
Prostate
/ pathology.
Prostatic
Hyperplasia / metabolism.
Prostatic
Hyperplasia / pathology.
Prostatic
Intraepithelial Neoplasia / metabolism.
Prostatic
Intraepithelial Neoplasia / pathology
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15472903.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
2.
Schmitz M, Grignard G, Margue C, Dippel W, Capesius C, Mossong J, Nathan M, Giacchi S, Scheiden R, Kieffer N:
Complete loss of PTEN expression as a possible early prognostic marker for prostate cancer metastasis.
Int J Cancer
; 2007 Mar 15;120(6):1284-92
[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]
Complete loss of PTEN expression as a possible early prognostic marker for
prostate
cancer metastasis.
The EGF/IGF growth factors are potent mitogens that regulate cell proliferation and cell survival and are involved in
prostate
cancer development.
Using laser microdissection technology and real-time PCR, together with immunohistochemistry, we have explored the growth factor and integrin dependent PI3-kinase/PTEN/Akt signalling pathway in
prostate
cell lines and tumour samples by analysing EGF-R, IGF1-R, ILK, beta3 integrin, PTEN and p-Akt protein expression.
We provide evidence that loss of PTEN expression rather than upregulated EGF/IGF1 receptor expression was responsible for increased p-Akt in neoplastic
prostate
cells.
In Study II, 25 of the 42 patients (59%) with lymph node metastasis had complete loss of PTEN expression in both the neoplastic glands of the
prostate
and the invasive
prostate
cancer cells in the lymph node, and of these 13 (52%) exhibited already loss of PTEN expression at first diagnosis.
These findings demonstrate that loss of PTEN expression is an important factor in progression towards
metastatic
disease and could potentially serve as an early prognostic marker for
prostate
cancer metastasis.
[MeSH-major]
Adenocarcinoma
/ secondary. Biomarkers, Tumor / analysis. PTEN Phosphohydrolase / analysis.
Prostate
/ pathology.
Prostatic
Neoplasms / pathology
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
(c) 2006 Wiley-Liss, Inc.
(PMID = 17163422.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Integrin beta3; 0 / RNA, Messenger; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
3.
Tan WW:
Novel agents and targets in managing patients with metastatic prostate cancer.
Cancer Control
; 2006 Jul;13(3):194-8
[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]
Novel agents and targets in managing patients with
metastatic prostate
cancer.
BACKGROUND: Docetaxel has recently been found to improve survival in patients with
metastatic
androgen-independent
prostate
cancer (AIPC).
METHODS: Clinically relevant articles focusing on chemotherapy drugs for
metastatic prostate
cancer and their mechanism of action and efficacy were reviewed from January 2004 through April 2006.
CONCLUSIONS: Docetaxel should be considered for first-line treatment
of metastatic
AIPC.
[MeSH-major]
Adenocarcinoma
/ therapy. Bone Neoplasms / therapy.
Prostatic
Neoplasms / therapy
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
(PMID = 16885915.001).
[ISSN]
1073-2748
[Journal-full-title]
Cancer control : journal of the Moffitt Cancer Center
[ISO-abbreviation]
Cancer Control
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
33
Advertisement
4.
Boyiadzis M, Nam M, Dahut W:
Fulminant hepatic failure secondary to metastatic prostate cancer.
Urol Int
; 2005;74(2):185-7
[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]
Fulminant hepatic failure secondary to
metastatic prostate
cancer.
The most common sites
of metastatic
disease from
prostate
cancer include the bones, lymph nodes and less commonly the lungs, adrenal glands, brain and kidneys.
We describe a case of fatal liver failure in a 71-year-old male due to metastases to the liver from a
prostatic
adenocarcinoma
.
Thus in patients with
metastatic
cancer and elevated liver function tests, the possibility of hepatic involvement by the cancer should be considered as a possible cause of hepatic failure.
[MeSH-major]
Adenocarcinoma
/ complications. Liver Failure, Acute / etiology. Liver Neoplasms / complications.
Prostatic
Neoplasms / pathology
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Liver 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
(PMID = 15756074.001).
[ISSN]
0042-1138
[Journal-full-title]
Urologia internationalis
[ISO-abbreviation]
Urol. Int.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
5.
Mimeault M, Johansson SL, Henichart JP, Depreux P, Batra SK:
Cytotoxic effects induced by docetaxel, gefitinib, and cyclopamine on side population and nonside population cell fractions from human invasive prostate cancer cells.
Mol Cancer Ther
; 2010 Mar;9(3):617-30
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Cytotoxic effects induced by docetaxel, gefitinib, and cyclopamine on side population and nonside population cell fractions from human invasive
prostate
cancer cells.
The present study has been undertaken to establish the therapeutic benefit of cotargeting epidermal growth factor receptor (EGFR) and sonic hedgehog pathways by using gefitinib and cyclopamine, respectively, for improving the efficacy of the current chemotherapeutic drug docetaxel to counteract
the prostate
cancer progression from locally invasive to
metastatic
and recurrent disease stages.
The data from immuofluorescence analyses revealed that EGFR/Tyr(1173)-pEGFR, sonic hedgehog ligand, smoothened coreceptor, and GLI-1 were colocalized with the CD133(+) stem cell-like marker in a small subpopulation
of prostate
cancer cells.
These signaling molecules were also present in the bulk tumor mass of CD133(-)
prostate
cancer cells with a luminal phenotype detected in patient's
adenocarcinoma
tissues.
Altogether, these observations suggest that EGFR and sonic hedgehog cascades may represent the potential therapeutic targets of great clinical interest to eradicate the total
prostate
cancer cell mass and improve the current docetaxel-based therapies against locally advanced and invasive
prostate
cancers, and thereby prevent metastases and disease relapse.
[MeSH-major]
Adenocarcinoma
/ pathology.
Prostate
/ drug effects.
Prostate
/ pathology.
Prostatic
Neoplasms / pathology. Quinazolines / pharmacology. Taxoids / pharmacology. Veratrum Alkaloids / pharmacology
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
DOCETAXEL
.
Hazardous Substances Data Bank.
CYCLOPAMINE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Endocrinology. 2004 Aug;145(8):3961-70
[
15132968.001
]
[Cites]
Cancer Res. 2007 May 15;67(10):4807-15
[
17510410.001
]
[Cites]
N Engl J Med. 2004 Oct 7;351(15):1502-12
[
15470213.001
]
[Cites]
N Engl J Med. 2004 Oct 7;351(15):1513-20
[
15470214.001
]
[Cites]
Nature. 2004 Oct 7;431(7009):707-12
[
15361885.001
]
[Cites]
Am J Respir Cell Mol Biol. 1992 Dec;7(6):574-81
[
1449805.001
]
[Cites]
Hum Pathol. 1998 Sep;29(9):1005-12
[
9744319.001
]
[Cites]
Mol Cancer. 2004 Oct 13;3:29
[
15482598.001
]
[Cites]
Int J Cancer. 2005 Feb 10;113(4):619-28
[
15472903.001
]
[Cites]
Prostate. 2005 Feb 1;62(2):187-99
[
15389789.001
]
[Cites]
J Pathol. 2005 Mar;205(4):522-9
[
15685688.001
]
[Cites]
Cancer Res. 2005 Apr 15;65(8):2990-2
[
15833820.001
]
[Cites]
Cancer Res. 2005 Dec 1;65(23):10946-51
[
16322242.001
]
[Cites]
Carcinogenesis. 2006 Jan;27(1):1-22
[
16195239.001
]
[Cites]
Int J Cancer. 2006 Feb 15;118(4):1022-31
[
16108016.001
]
[Cites]
Oncogene. 2006 Mar 16;25(12):1696-708
[
16449977.001
]
[Cites]
Cell Mol Life Sci. 2006 Feb;63(4):435-48
[
16389455.001
]
[Cites]
Endocr Relat Cancer. 2006 Mar;13(1):197-210
[
16601288.001
]
[Cites]
J Urol. 2006 Aug;176(2):532-7
[
16813883.001
]
[Cites]
Prostate. 2006 Sep 15;66(13):1437-44
[
16741920.001
]
[Cites]
Int J Cancer. 2007 Jan 1;120(1):160-9
[
17013895.001
]
[Cites]
Mol Cancer Ther. 2007 Mar;6(3):967-78
[
17363490.001
]
[Cites]
Cancer Res. 2007 Apr 1;67(7):3153-61
[
17409422.001
]
[Cites]
Lab Invest. 2000 Aug;80(8):1243-50
[
10950115.001
]
[Cites]
Clin Cancer Res. 2000 Dec;6(12):4885-92
[
11156248.001
]
[Cites]
Bioorg Med Chem Lett. 2001 Jul 23;11(14):1911-4
[
11459659.001
]
[Cites]
J Cell Sci. 2001 Nov;114(Pt 21):3865-72
[
11719553.001
]
[Cites]
J Pathol. 2001 Dec;195(5):563-70
[
11745692.001
]
[Cites]
Int J Oncol. 2002 Apr;20(4):681-9
[
11894110.001
]
[Cites]
Clin Cancer Res. 2002 May;8(5):1253-64
[
12006546.001
]
[Cites]
J Immunol Methods. 2002 Jul 1;265(1-2):39-47
[
12072177.001
]
[Cites]
Clin Cancer Res. 2002 Nov;8(11):3438-44
[
12429632.001
]
[Cites]
Clin Cancer Res. 2002 Dec;8(12):3870-6
[
12473602.001
]
[Cites]
J Cancer Res Clin Oncol. 2003 Mar;129(3):165-74
[
12712332.001
]
[Cites]
Cytometry A. 2003 Aug;54(2):89-99
[
12879455.001
]
[Cites]
Nature. 2003 Oct 23;425(6960):851-6
[
14520413.001
]
[Cites]
Br J Cancer. 2004 Jan 26;90(2):449-54
[
14735192.001
]
[Cites]
Pancreas. 2004 May;28(4):401-12
[
15097858.001
]
[Cites]
J Cell Sci. 2004 Jul 15;117(Pt 16):3539-45
[
15226377.001
]
[Cites]
Biochem Biophys Res Commun. 2007 Jun 15;357(4):1084-9
[
17466949.001
]
[Cites]
Cancer. 2007 Jun 1;109(11):2239-47
[
17455209.001
]
[Cites]
Cancer Res. 2007 Jul 15;67(14):6796-805
[
17638891.001
]
[Cites]
Prostate. 2007 Sep 15;67(13):1384-96
[
17639507.001
]
[Cites]
J Urol. 2007 Sep;178(3 Pt 2):S30-5
[
17644121.001
]
[Cites]
Cancer Lett. 2007 Oct 8;255(2):300-6
[
17602833.001
]
[Cites]
Cancer Biol Ther. 2007 May;6(5):763-8
[
17592251.001
]
[Cites]
Ernst Schering Found Symp Proc. 2006;(5):155-79
[
17939301.001
]
[Cites]
J Cell Mol Med. 2007 Sep-Oct;11(5):981-1011
[
17979879.001
]
[Cites]
Mo Med. 2007 Sep-Oct;104(5):408-13; quiz 413-4
[
18018527.001
]
[Cites]
CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96
[
18287387.001
]
[Cites]
Growth Factors. 2007 Dec;25(6):400-16
[
18365871.001
]
[Cites]
Endocr Rev. 2008 Apr;29(2):234-52
[
18292464.001
]
[Cites]
Prostate. 2008 Jun 15;68(9):1007-24
[
18398820.001
]
[Cites]
J Cell Physiol. 2008 Sep;216(3):571-5
[
18481259.001
]
[Cites]
Genome Biol. 2008;9(5):R83
[
18492237.001
]
[Cites]
Cancer Res. 2008 Oct 1;68(19):7905-14
[
18829547.001
]
[Cites]
Proc Natl Acad Sci U S A. 2009 Jan 6;106(1):268-73
[
19116269.001
]
[Cites]
Ageing Res Rev. 2009 Apr;8(2):94-112
[
19114129.001
]
[Cites]
Cancer Genomics Proteomics. 2008 Nov-Dec;5(6):301-10
[
19287071.001
]
[Cites]
Clin Exp Metastasis. 2009;26(5):433-46
[
19221883.001
]
[Cites]
Methods Mol Biol. 2009;568:139-49
[
19582424.001
]
[Cites]
Stem Cells Dev. 2009 Dec;18(10):1515-22
[
19260804.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12561-6
[
15314219.001
]
(PMID = 20179163.001).
[ISSN]
1538-8514
[Journal-full-title]
Molecular cancer therapeutics
[ISO-abbreviation]
Mol. Cancer Ther.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA138791; United States / NCI NIH HHS / CA / R01 CA138791-03
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Cytotoxins; 0 / GLI1 protein, human; 0 / Quinazolines; 0 / Taxoids; 0 / Transcription Factors; 0 / Veratrum Alkaloids; 15H5577CQD / docetaxel; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib; ZH658AJ192 / cyclopamine
[Other-IDs]
NLM/ NIHMS173400; NLM/ PMC3228252
6.
Moura FM, Garcia LT, Castro LP, Ferrari TC:
Prostate adenocarcinoma manifesting as generalized lymphadenopathy.
Urol Oncol
; 2006 May-Jun;24(3):216-9
[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]
Prostate adenocarcinoma
manifesting as generalized lymphadenopathy.
Generalized lymphadenopathy is a rare manifestation
of metastatic prostate
cancer.
There were no urinary symptoms, and the serum
prostate
-specific antigen (PSA) was only mildly increased with a normal free PSA.
A biopsy of the supraclavicular lymph node was compatible with
adenocarcinoma
, whose
prostatic
origin was shown by immunohistochemical staining with PSA.
The origin of the primary tumor was confirmed by directed
prostate
biopsy.
We emphasize that a suspicion
of prostate
cancer in men with
adenocarcinoma of
undetermined origin is important for an adequate diagnostic and therapeutic approach.
[MeSH-major]
Adenocarcinoma
/ diagnosis. Lymphatic Diseases / diagnosis.
Prostatic
Neoplasms / diagnosis
[MeSH-minor]
Aged. Diagnosis, Differential. Humans. Male.
Prostate
-Specific Antigen / analysis. Tomography, X-Ray Computed
MedlinePlus Health Information.
consumer health - Lymphatic Diseases
.
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 = 16678051.001).
[ISSN]
1078-1439
[Journal-full-title]
Urologic oncology
[ISO-abbreviation]
Urol. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
7.
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
8.
Haidar A, Yassin A, Saad F, Shabsigh R:
Effects of androgen deprivation on glycaemic control and on cardiovascular biochemical risk factors in men with advanced prostate cancer with diabetes.
Aging Male
; 2007 Dec;10(4):189-96
[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 androgen deprivation on glycaemic control and on cardiovascular biochemical risk factors in men with advanced
prostate
cancer with diabetes.
INTRODUCTION AND OBJECTIVE: Androgen deprivation therapy
of prostate
cancer with luteinizing hormone releasing hormone agonists may result in loss of bone mass, changes in body composition and a deterioration of arterial stiffness.
All men had insulin-dependent diabetes mellitus prior to being diagnosed with
metastatic prostate
cancer.
[MeSH-major]
Adenocarcinoma
/ drug therapy.
Adenocarcinoma
/ epidemiology. Blood Glucose / analysis. Diabetes Mellitus, Type 2 / epidemiology. Gonadotropin-Releasing Hormone / agonists.
Prostatic
Neoplasms / drug therapy.
Prostatic
Neoplasms / epidemiology
Genetic Alliance.
consumer health - Diabetes
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Blood Sugar
.
MedlinePlus Health Information.
consumer health - Diabetes Type 2
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
CHOLESTEROL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18033628.001).
[ISSN]
1368-5538
[Journal-full-title]
The aging male : the official journal of the International Society for the Study of the Aging Male
[ISO-abbreviation]
Aging Male
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Blood Glucose; 0 / Hemoglobin A, Glycosylated; 0 / Triglycerides; 33515-09-2 / Gonadotropin-Releasing Hormone; 9001-32-5 / Fibrinogen; 9007-41-4 / C-Reactive Protein; 97C5T2UQ7J / Cholesterol
9.
Hainsworth JD, Meluch AA, Spigel DR, Yost K, Meng C, Greco FA:
Weekly docetaxel/estramustine phosphate in patients with increasing serum prostate- specific antigen levels after primary treatment for prostate cancer: a phase II trial of the Minnie Pearl Cancer Research Network.
Clin Genitourin Cancer
; 2006 Mar;4(4):287-92
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Weekly docetaxel/estramustine phosphate in patients with increasing serum
prostate
- specific antigen levels after primary treatment for
prostate
cancer: a phase II trial of the Minnie Pearl Cancer Research Network.
PURPOSE: Docetaxel alone or in combination with estramustine prolongs survival in patients with
metastatic
hormone-refractory
prostate
cancer.
The role of chemotherapy is undefined in the treatment of patients who develop an increasing serum
prostate
-specific antigen (PSA) level after primary therapy but have no detectable metastases.
This phase II study was performed as a preliminary evaluation of the feasibility and efficacy of weekly docetaxel/estramustine in patients with
prostate
cancer and increasing serum PSA levels.
All patients had biopsy-proven
adenocarcinoma of the prostate
and had increasing PSA levels but no clinically or radiographically detected metastases after primary therapy.
CONCLUSION: Treatment with weekly docetaxel and estramustine is feasible and active in patients with
prostate
cancer and increasing serum PSA levels.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / administration & dosage.
Prostate
-Specific Antigen / blood.
Prostatic
Neoplasms / blood.
Prostatic
Neoplasms / drug therapy
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer Screening
.
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 = 16729913.001).
[ISSN]
1558-7673
[Journal-full-title]
Clinical genitourinary cancer
[ISO-abbreviation]
Clin Genitourin Cancer
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel; 35LT29625A / Estramustine; EC 3.4.21.77 / Prostate-Specific Antigen
10.
Dorff TB, Shazer RL, Nepomuceno EM, Tucker SJ:
Successful treatment of metastatic androgen-independent prostate carcinoma in a transsexual patient.
Clin Genitourin Cancer
; 2007 Jun;5(5):344-6
[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]
Successful treatment
of metastatic
androgen-independent
prostate
carcinoma in a transsexual patient.
The occurrence
of prostate
carcinoma in transsexual patients has rarely been reported.
By definition, their disease is androgen-independent
prostate
cancer, and the role of local therapy is undefined.
We report on a male-to-female transsexual patient with
metastatic prostate
cancer treated successfully with combination chemotherapy after previous standard therapy failed.
[MeSH-major]
Adenocarcinoma
/ drug therapy.
Prostatic
Neoplasms / drug therapy. Salvage Therapy. Transsexualism / pathology
[MeSH-minor]
Aged. Androgen Antagonists / therapeutic use. Combined Modality Therapy. Female. Humans. Male.
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 = 17645834.001).
[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]
0 / Androgen Antagonists; EC 3.4.21.77 / Prostate-Specific Antigen
11.
Flannery T, Kano H, Niranjan A, Monaco EA 3rd, Flickinger JC, Lunsford LD, Kondziolka D:
Stereotactic radiosurgery as a therapeutic strategy for intracranial metastatic prostate carcinoma.
J Neurooncol
; 2010 Feb;96(3):369-74
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Stereotactic radiosurgery as a therapeutic strategy for intracranial
metastatic prostate
carcinoma.
Intracranial
metastatic prostate
carcinoma is rare.
We sought to determine the clinical outcomes after Gamma Knife stereotactic radiosurgery (GKSRS) for patients with intracranial
prostate
carcinoma metastases.
The primary pathology was
adenocarcinoma
(eight patients) and small cell carcinoma (two patients).
SRS was a well tolerated and effective therapy either alone or as a boost to fractionated radiation therapy in the management of patients with intracranial
prostate
carcinoma metastases.
[MeSH-minor]
Aged. Aged, 80 and over. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Magnetic Resonance Imaging / methods. Male. Middle Aged.
Prostatic
Neoplasms / pathology. Radiotherapy Dosage. Survival Rate
MedlinePlus Health Information.
consumer health - Brain Tumors
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Int J Radiat Oncol Biol Phys. 2005 Sep 1;63(1):37-46
[
16111570.001
]
[Cites]
Arch Neurol. 1988 Jul;45(7):741-4
[
3390029.001
]
[Cites]
Surg Neurol. 2003 Dec;60(6):506-14; discussion 514-5
[
14670663.001
]
[Cites]
Cancer. 1987 May 15;59(10):1803-9
[
3030528.001
]
[Cites]
Surg Neurol. 2008 Jun;69(6):641-6; discussion 646
[
18262258.001
]
[Cites]
Cancer. 1999 Dec 1;86(11):2301-11
[
10590371.001
]
[Cites]
Neurosurgery. 1997 Oct;41(4):776-83; discussion 783-5
[
9316038.001
]
[Cites]
J Neurooncol. 2004 Aug-Sep;69(1-3):125-37
[
15527085.001
]
[Cites]
Cancer. 2004 Oct 1;101(7):1639-43
[
15468187.001
]
[Cites]
Am J Med Sci. 1994 Sep;308(3):177-9
[
8074136.001
]
[Cites]
Neurosurgery. 2003 Jun;52(6):1318-26; discussion 1326
[
12762877.001
]
[Cites]
J Urol. 1992 Mar;147(3 Pt 2):935-7
[
1311396.001
]
[Cites]
Cancer. 1996 Oct 15;78(8):1781-8
[
8859192.001
]
[Cites]
Cancer. 2003 Jul 15;98(2):363-8
[
12872358.001
]
[Cites]
Virchows Arch. 2004 Feb;444(2):202-3
[
14652753.001
]
[Cites]
J Urol. 2002 Jun;167(6):2419-22
[
11992049.001
]
[Cites]
Can J Neurol Sci. 2002 Nov;29(4):375-7
[
12463494.001
]
[Cites]
Gynecol Oncol. 2001 May;81(2):196-200
[
11330949.001
]
(PMID = 19609490.001).
[ISSN]
1573-7373
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
12.
Zhang J, Wilkinson JE, Gonit M, Keck R, Selman S, Ratnam M:
Expression and sub-cellular localization of the CCAAT/enhancer binding protein alpha in relation to postnatal development and malignancy of the prostate.
Prostate
; 2008 Aug 1;68(11):1206-14
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Expression and sub-cellular localization of the CCAAT/enhancer binding protein alpha in relation to postnatal development and malignancy of the
prostate
.
There, is a paucity of information on the expression and sub-cellular localization of C/EBPalpha in normal mouse and human
prostate
and in
prostate
cancer.
RESULTS: In the mouse
prostate
epithelium, C/EBPalpha was present at 1 week postnatal localized in the cytosol, began to show nuclear localization at 8 weeks and continued to show prominent nuclear expression at 10 weeks and beyond; C/EBPalpha mRNA was expressed at all ages.
Most
prostate
adenocarcinomas expressed a range of levels of C/EBPalpha mRNA and protein that were relatively high in
metastatic
tumors in a manner that correlated with AR expression; however, most cells showed C/EBPalpha sequestered in the cytosol.
CONCLUSIONS: Temporal changes in sub-cellular localization of C/EBPalpha are consistent with a role in
prostate
differentiation and as a
prostate
tumor suppressor; the cytoplasmic sequestration of C/EBPalpha, unique to older human prostates, is arguably a permissive condition for the greater frequency of proliferative disorders of the
prostate
.
In malignant
prostate
C/EBPalpha may be available to regulate AR signaling through transient changes in its sub-cellular localization.
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 (c) 2008 Wiley-Liss, Inc.
[Cites]
Nucleic Acids Res. 1995 Nov 25;23(22):4726-33
[
8524667.001
]
[Cites]
Genes Dev. 1996 Apr 1;10(7):804-15
[
8846917.001
]
[Cites]
J Biol Chem. 1996 Feb 16;271(7):3891-6
[
8632009.001
]
[Cites]
Cancer Res. 1996 Mar 1;56(5):1063-7
[
8640762.001
]
[Cites]
J Biol Chem. 1996 Jul 26;271(30):17974-8
[
8663327.001
]
[Cites]
Mol Cell Biol. 1997 Dec;17(12):7353-61
[
9372966.001
]
[Cites]
Nat Genet. 2001 Mar;27(3):263-70
[
11242107.001
]
[Cites]
Nat Med. 2001 Apr;7(4):444-51
[
11283671.001
]
[Cites]
Prostate. 2001 Jun 15;48(1):54-65
[
11391687.001
]
[Cites]
Mol Cell Biol. 2001 Aug;21(16):5577-90
[
11463839.001
]
[Cites]
J Biol Chem. 2001 Aug 3;276(31):29200-9
[
11369759.001
]
[Cites]
Cell. 2001 Oct 19;107(2):247-58
[
11672531.001
]
[Cites]
Mol Cell. 2001 Oct;8(4):817-28
[
11684017.001
]
[Cites]
Cancer Res. 2002 Jan 15;62(2):528-34
[
11809705.001
]
[Cites]
Cancer Res. 2002 Feb 15;62(4):1008-13
[
11861374.001
]
[Cites]
EMBO J. 2002 Mar 1;21(5):930-41
[
11867521.001
]
[Cites]
Biochem J. 2002 Aug 1;365(Pt 3):561-75
[
12006103.001
]
[Cites]
J Biol Chem. 2004 Feb 20;279(8):7353-8
[
14660596.001
]
[Cites]
Genes Dev. 2004 Apr 15;18(8):912-25
[
15107404.001
]
[Cites]
J Clin Oncol. 2004 Jul 15;22(14):2790-9
[
15254046.001
]
[Cites]
Nature. 1990 Apr 12;344(6267):678-82
[
2157987.001
]
[Cites]
Science. 1991 Jan 18;251(4991):288-92
[
1987644.001
]
[Cites]
Chin Med J (Engl). 1994 Aug;107(8):596-9
[
7805444.001
]
[Cites]
Science. 1995 Aug 25;269(5227):1108-12
[
7652557.001
]
[Cites]
Mol Cell Biol. 1999 Apr;19(4):2936-45
[
10082561.001
]
[Cites]
Br J Cancer. 1999 Mar;79(7-8):1240-8
[
10098766.001
]
[Cites]
Nucleic Acids Res. 1999 Sep 1;27(17):3621-30
[
10446255.001
]
[Cites]
Mol Cell Biol. 2005 Feb;25(4):1325-38
[
15684384.001
]
[Cites]
Clin Cancer Res. 2005 May 1;11(9):3184-90
[
15867211.001
]
[Cites]
Mol Endocrinol. 2006 May;20(5):984-95
[
16455820.001
]
[Cites]
Biochim Biophys Acta. 2006 Aug;1766(1):88-103
[
16616425.001
]
[Cites]
BMC Cancer. 2006;6:158
[
16774685.001
]
[Cites]
Cancer Res. 2007 Jul 15;67(14):6768-76
[
17638888.001
]
(PMID = 18481268.001).
[ISSN]
0270-4137
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA103964; United States / NCI NIH HHS / CA / 5R01CA103964
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / RNA, Messenger; 0 / Receptors, Androgen
[Other-IDs]
NLM/ NIHMS546003; NLM/ PMC3911780
13.
Ruiz-Martín I, Rodríguez-Sánchez CA, Ocaña-Fernández A, del Valle-Zapico J, Soto de Prado-Otero D, Cruz-Hernández JJ:
Metastatic prostate cancer with a normal prostate-specific antigen level.
Clin Transl Oncol
; 2005 Oct;7(9):412-3
[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]
Metastatic prostate
cancer with a normal
prostate
-specific antigen level.
Prostate
-specific antigen (PSA) is the most commonly used tumour marker for
prostate
cancer, both in screening and in follow-up.
However, there are many false positive increases in the presence of other
prostate
diseases and, currently, there is no consensus regarding sensitivity and specificity of the PSA test, nor what constitutes the upper limit of normality.
We report a case of a 67-year-old patient with
metastatic prostate
cancer who, with increased level of alkaline phosphatase and normal PSA, showed clinical and radiological evidence of progression of the disease.
[MeSH-major]
Adenocarcinoma
/ blood. Bone Neoplasms / secondary.
Prostate
-Specific Antigen / blood.
Prostatic
Neoplasms / blood
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
.
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
[Cites]
Cancer. 2000 Jun 15;88(12 Suppl):2919-26
[
10898335.001
]
[Cites]
N Engl J Med. 2004 May 27;350(22):2239-46
[
15163773.001
]
[Cites]
JAMA. 1997 May 14;277(18):1452-5
[
9145717.001
]
[Cites]
J Am Board Fam Pract. 2003 Mar-Apr;16(2):95-101
[
12665174.001
]
[Cites]
J Urol. 1995 Aug;154(2 Pt 1):407-13
[
7541857.001
]
[Cites]
Urology. 1996 Mar;47(3):343-6
[
8633399.001
]
[Cites]
N Engl J Med. 1995 Nov 23;333(21):1401-5
[
7477122.001
]
[Cites]
J Clin Oncol. 2003 Jan 15;21(2):383-91
[
12525533.001
]
[Cites]
Urology. 2002 Sep;60(3):469-73; discussion 473-4
[
12350486.001
]
(PMID = 16238977.001).
[ISSN]
1699-048X
[Journal-full-title]
Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
[ISO-abbreviation]
Clin Transl Oncol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / Antineoplastic Agents; EC 3.4.21.77 / Prostate-Specific Antigen
14.
Kolias AG, Derham C, Mankad K, Hasegawa H, O'Kane R, Ismail A, Phillips NI:
Multiple cranial neuropathy as the initial presentation of metastatic prostate adenocarcinoma: case report and review of literature.
Acta Neurochir (Wien)
; 2010 Jul;152(7):1251-5
[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]
Multiple cranial neuropathy as the initial presentation
of metastatic prostate adenocarcinoma
: case report and review of literature.
The skull base is an atypical
metastatic
site for
prostate
carcinoma.
However, skull base involvement causing cranial nerve palsies may rarely be the presenting sign
of prostate
carcinoma.
Here, we describe an unusual case
of prostate adenocarcinoma
presenting as a central skull base tumour with multiple cranial neuropathy.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20379748.001).
[ISSN]
0942-0940
[Journal-full-title]
Acta neurochirurgica
[ISO-abbreviation]
Acta Neurochir (Wien)
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Austria
15.
Andreoiu M, Cheng L:
Multifocal prostate cancer: biologic, prognostic, and therapeutic implications.
Hum Pathol
; 2010 Jun;41(6):781-93
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Multifocal
prostate
cancer: biologic, prognostic, and therapeutic implications.
Prostatic
adenocarcinoma
is the most common cancer diagnosed in men and is often multifocal.
This review examines recent progress in the pathogenesis of multifocal
prostatic
adenocarcinoma
and its biologic, pathologic, prognostic, and therapeutic implications.
Prostatic
cancer multifocality makes accurate clinical staging difficult, and repeated revisions have been undertaken in an effort to optimize prognostic accuracy.
The clinical significance of smaller secondary tumors and the relationship between extent of chromosomal abnormalities and
the metastatic
potential of an individual tumor focus were reviewed.
[MeSH-major]
Adenocarcinoma
. Neoplasms, Multiple Primary.
Prostatic
Neoplasms
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
[Copyright]
Copyright 2010 Elsevier Inc. All rights reserved.
(PMID = 20466122.001).
[ISSN]
1532-8392
[Journal-full-title]
Human pathology
[ISO-abbreviation]
Hum. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
125
16.
Sciarra A, Lichtner M, Autran GA, Mastroianni C, Rossi R, Mengoni F, Cristini C, Gentilucci A, Vullo V, Di Silverio F:
Characterization of circulating blood dendritic cell subsets DC123+ (lymphoid) and DC11C+ (myeloid) in prostate adenocarcinoma patients.
Prostate
; 2007 Jan 1;67(1):1-7
[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]
Characterization of circulating blood dendritic cell subsets DC123+ (lymphoid) and DC11C+ (myeloid) in
prostate adenocarcinoma
patients.
PURPOSE: We verified whether
prostate adenocarcinoma
produces specific modifications in DC subsets count.
METHODS: Twenty-one untreated
prostate
adenocarcinomas were divided on the basis of clinical stage in localized and
metastatic
disease.
RESULTS: We showed a statistically significant reduction in pDCs count in
prostate
cancer population when compared to healthy controls (P = 0.002).
Comparing each clinical stage with healthy controls, significant differences were found between controls and
the metastatic
group in both pDCs and mDCs (P = 0.005 and P = 0.023 respectively) but not between controls and the localized group (P = 0.055 and P = 0.829 respectively).
CONCLUSIONS: We showed that DCs count in PB is significantly affected by
prostate adenocarcinoma
progression in a
metastatic
disease.
[MeSH-major]
Adenocarcinoma
/ pathology. Dendritic Cells / pathology.
Prostatic
Neoplasms / pathology
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]
(c) 2006 Wiley-Liss, Inc.
(PMID = 17075798.001).
[ISSN]
1097-0045
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
17.
Chua CW, Chiu YT, Yuen HF, Chan KW, Wang X, Ling MT, Wong YC:
Differential expression of MSX2 in nodular hyperplasia, high-grade prostatic intraepithelial neoplasia and prostate adenocarcinoma.
APMIS
; 2010 Dec;118(12):918-26
[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]
Differential expression of MSX2 in nodular hyperplasia, high-grade
prostatic
intraepithelial neoplasia and
prostate adenocarcinoma
.
One of the common features in advanced
prostate
cancer is bone metastasis.
In this study, we investigated the clinical relevance of a bone factor, MSX2, in predicting
the metastatic
ability
of prostate adenocarcinoma
.
Evaluation of MSX2 expression was performed using
prostate
cell lines as well as patient specimens.
A sharp decrease in MSX2 was found in primary
prostate
cancer cells, 22Rv1, when compared with the non-malignant counterparts, followed by a gradual increase in more aggressive
prostate
cancer cell lines.
Interestingly, the MSX2 protein was upregulated and predominantly expressed in the nucleus in aggressive
prostate
cancer cell line, C4-2b, compared with the less aggressive 22Rv1.
Consistent with the in vitro results, MSX2 nuclear expression was significantly higher in nodular hyperplasia when compared with high-grade
prostatic
intraepithelial neoplasia (PIN), while MSX2 nuclear expression in
prostate adenocarcinoma
was higher than that in high-grade PIN.
Taken together, MSX2 may serve as a potential biomarker in predicting primary
prostate
tumors with higher
metastatic
capability.
[MeSH-major]
Adenocarcinoma
/ metabolism. Homeodomain Proteins / biosynthesis.
Prostatic
Hyperplasia / metabolism.
Prostatic
Intraepithelial Neoplasia / metabolism.
Prostatic
Neoplasms / metabolism
MedlinePlus Health Information.
consumer health - Enlarged Prostate (BPH)
.
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
[Copyright]
© 2010 The Authors. Journal Compilation © 2010 APMIS.
(PMID = 21091772.001).
[ISSN]
1600-0463
[Journal-full-title]
APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
[ISO-abbreviation]
APMIS
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / MSX2 protein
18.
Chiosea S, Jelezcova E, Chandran U, Acquafondata M, McHale T, Sobol RW, Dhir R:
Up-regulation of dicer, a component of the MicroRNA machinery, in prostate adenocarcinoma.
Am J Pathol
; 2006 Nov;169(5):1812-20
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Up-regulation of dicer, a component of the MicroRNA machinery, in
prostate adenocarcinoma
.
In
prostate adenocarcinoma
, 39 microRNAs are up-regulated, and six microRNAs are down-regulated.
From a gene array analysis of 16 normal
prostate
tissue samples, 64 organ-confined, and four
metastatic prostate
adenocarcinomas, we identified an up-regulation of major components of the microRNA machinery, including Dicer, in
metastatic prostate adenocarcinoma
.
Immunohistochemical studies on a tissue microarray consisting of 232
prostate
specimens confirmed up-regulation of Dicer in
prostatic
intraepithelial neoplasia and in 81%
of prostate adenocarcinoma
.
The increased Dicer level in
prostate adenocarcinoma
correlated with clinical stage, lymph node status, and Gleason score.
Western blot analysis of benign and neoplastic
prostate
cell lines further confirmed Dicer up-regulation in
prostate adenocarcinoma
.
Dicer up-regulation may explain an almost global increase of microRNA expression in
prostate adenocarcinoma
.
The presence of up-regulated microRNA machinery may predict the susceptibility
of prostate adenocarcinoma
to RNA interference-based therapy.
[MeSH-major]
Adenocarcinoma
/ enzymology.
Adenocarcinoma
/ pathology. DEAD-box RNA Helicases / metabolism. Endoribonucleases / metabolism. MicroRNAs / metabolism.
Prostatic
Neoplasms / enzymology.
Prostatic
Neoplasms / pathology. Up-Regulation
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Blotting, Western. Cell Line, Tumor. Epithelium / pathology. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Microarray Analysis. Middle Aged.
Prostate
/ cytology.
Prostate
/ enzymology.
Prostate
/ pathology. Ribonuclease III
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]
Nat Cell Biol. 2004 Aug;6(8):784-91
[
15247924.001
]
[Cites]
Biochem Biophys Res Commun. 2004 Jan 16;313(3):552-4
[
14697225.001
]
[Cites]
Int J Cancer. 1978 Mar 15;21(3):274-81
[
631930.001
]
[Cites]
Genes Dev. 2003 Dec 15;17(24):3011-6
[
14681208.001
]
[Cites]
Nat Neurosci. 2004 Feb;7(2):113-7
[
14703574.001
]
[Cites]
Mol Biol Cell. 2004 Mar;15(3):1425-35
[
14699070.001
]
[Cites]
Cancer Res. 2004 Jun 1;64(11):3753-6
[
15172979.001
]
[Cites]
J Clin Oncol. 2004 Jul 15;22(14):2790-9
[
15254046.001
]
[Cites]
Eur Urol. 1996;30(2):201-5
[
8875201.001
]
[Cites]
Carcinogenesis. 1997 Jun;18(6):1215-23
[
9214605.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1735-40
[
9465086.001
]
[Cites]
Nat Cell Biol. 2004 Nov;6(11):1048-53
[
15516998.001
]
[Cites]
Cell. 2005 Jan 14;120(1):15-20
[
15652477.001
]
[Cites]
Cell. 2005 Jan 14;120(1):21-4
[
15652478.001
]
[Cites]
Cancer Gene Ther. 2005 Mar;12(3):217-27
[
15550938.001
]
[Cites]
Cancer Sci. 2005 Feb;96(2):111-5
[
15723655.001
]
[Cites]
Cell. 2005 Mar 11;120(5):635-47
[
15766527.001
]
[Cites]
Biochem J. 2005 May 1;387(Pt 3):561-71
[
15845026.001
]
[Cites]
Cancer Res. 2005 May 1;65(9):3509-12
[
15867338.001
]
[Cites]
Nature. 2005 Jun 9;435(7043):839-43
[
15944709.001
]
[Cites]
Curr Opin Struct Biol. 2005 Jun;15(3):331-41
[
15925505.001
]
[Cites]
BMC Cancer. 2005;5:45
[
15892885.001
]
[Cites]
Cell. 2005 Jul 15;122(1):6-7
[
16009126.001
]
[Cites]
J Exp Med. 2005 Jul 18;202(2):261-9
[
16009718.001
]
[Cites]
Nature. 2005 Aug 4;436(7051):740-4
[
15973356.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13944-9
[
16166262.001
]
[Cites]
Eur Urol. 2005 Nov;48(5):852-7
[
16230228.001
]
[Cites]
Pathol Int. 2005 Nov;55(11):688-93
[
16271080.001
]
[Cites]
Cancer Gene Ther. 2005 Dec;12(12):926-34
[
15956982.001
]
[Cites]
Cancer Cell. 2005 Nov;8(5):393-406
[
16286247.001
]
[Cites]
Curr Biol. 2005 Dec 6;15(23):2149-55
[
16289642.001
]
[Cites]
Differentiation. 2005 Dec;73(9-10):463-73
[
16351690.001
]
[Cites]
Genes Dev. 2005 Dec 15;19(24):2979-90
[
16357216.001
]
[Cites]
Curr Opin Genet Dev. 2006 Feb;16(1):4-9
[
16361094.001
]
[Cites]
Mol Cancer Ther. 2006 Jan;5(1):179-86
[
16432177.001
]
[Cites]
EMBO J. 2006 Feb 8;25(3):522-32
[
16424907.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61
[
16461460.001
]
[Cites]
Br J Cancer. 2006 Mar 27;94(6):776-80
[
16495913.001
]
[Cites]
Genome Biol. 2006;7(3):210
[
16584538.001
]
[Cites]
Science. 2002 Sep 20;297(5589):2056-60
[
12154197.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21
[
11309499.001
]
[Cites]
Cell. 2001 Jul 13;106(1):23-34
[
11461699.001
]
[Cites]
Science. 2001 Aug 3;293(5531):834-8
[
11452083.001
]
[Cites]
Prostate. 2002 May 1;51(2):98-107
[
11948964.001
]
[Cites]
Cancer Genet Cytogenet. 2002 Jun;135(2):177-81
[
12127403.001
]
[Cites]
Chin Med J (Engl). 2002 Apr;115(4):571-5
[
12133301.001
]
[Cites]
Science. 2002 Sep 13;297(5588):1833-7
[
12193640.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):16648-53
[
12482946.001
]
[Cites]
Genes Dev. 2003 Feb 15;17(4):438-42
[
12600936.001
]
[Cites]
Urology. 2003 Aug;62(2):378-84
[
12893368.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9779-84
[
12902540.001
]
[Cites]
EMBO J. 2004 Oct 13;23(20):4051-60
[
15372072.001
]
(PMID = 17071602.001).
[ISSN]
0002-9440
[Journal-full-title]
The American journal of pathology
[ISO-abbreviation]
Am. J. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MicroRNAs; EC 3.1.- / Endoribonucleases; EC 3.1.26.3 / DICER1 protein, human; EC 3.1.26.3 / Ribonuclease III; EC 3.6.4.13 / DEAD-box RNA Helicases
[Other-IDs]
NLM/ PMC1780192
19.
Gravdal K, Halvorsen OJ, Haukaas SA, Akslen LA:
Proliferation of immature tumor vessels is a novel marker of clinical progression in prostate cancer.
Cancer Res
; 2009 Jun 1;69(11):4708-15
[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]
Proliferation of immature tumor vessels is a novel marker of clinical progression in
prostate
cancer.
Including vascular endothelial growth factor (VEGF)-A and hypoxia-inducible factor-1alpha (HIF-1alpha) expression, we studied relation to disease progression in
prostate
cancer.
Sections from 104 radical prostatectomies with long follow-up, 33 castration-resistant
prostate
cancers, 28 nonskeletal metastases, 13 skeletal metastases, and 41 benign
prostatic
hyperplasias were immunostained for Nestin/Ki-67, VEGF-A, and HIF-1alpha.
Median vascular proliferation counts were 4- to 5-fold higher in castration-resistant
prostate
cancers and metastases versus localized cancers and
prostatic
hyperplasias (P < 0.0005).
Thus, vascular proliferation was of independent prognostic importance among
prostate
cancers.
When compared with localized cancers, vascular proliferation was significantly increased in castration-resistant cases and
metastatic
lesions.
These novel data might have an effect on clinical evaluation and treatment
of prostate
cancer patients.
[MeSH-major]
Adenocarcinoma
/ blood supply. Biomarkers, Tumor. Blood Vessels / pathology. Neovascularization, Pathologic / pathology.
Prostatic
Neoplasms / blood supply
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
[ErratumIn]
Cancer Res. 2009 Jul 15;69(14):6005
(PMID = 19487287.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Intermediate Filament Proteins; 0 / Ki-67 Antigen; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
20.
Azios NG, Krishnamoorthy L, Harris M, Cubano LA, Cammer M, Dharmawardhane SF:
Estrogen and resveratrol regulate Rac and Cdc42 signaling to the actin cytoskeleton of metastatic breast cancer cells.
Neoplasia
; 2007 Feb;9(2):147-58
[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]
Estrogen and resveratrol regulate Rac and Cdc42 signaling to the actin cytoskeleton
of metastatic
breast cancer cells.
Genetic Alliance.
consumer health - Breast Cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Breast Cancer
.
Hazardous Substances Data Bank.
ESTRADIOL
.
Hazardous Substances Data Bank.
RESVERATROL
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Carcinogenesis. 2005 Jan;26(1):1-10
[
15217905.001
]
[Cites]
Curr Biol. 2004 Nov 23;14(22):2052-6
[
15556869.001
]
[Cites]
J Biol Chem. 2005 Mar 4;280(9):7460-8
[
15615701.001
]
[Cites]
Int J Cancer. 2005 May 20;115(1):74-84
[
15688415.001
]
[Cites]
Int J Cancer. 2005 May 20;115(1):36-45
[
15688416.001
]
[Cites]
Neoplasia. 2005 Feb;7(2):128-40
[
15802018.001
]
[Cites]
Oncogene. 2005 May 5;24(20):3274-84
[
15735708.001
]
[Cites]
Free Radic Biol Med. 2005 Jul 1;39(1):118-32
[
15925284.001
]
[Cites]
Mol Endocrinol. 2005 Aug;19(8):1951-9
[
15705661.001
]
[Cites]
Biomed Pharmacother. 2005 Aug;59(7):359-64
[
16084059.001
]
[Cites]
Curr Opin Cell Biol. 2005 Oct;17(5):559-64
[
16098726.001
]
[Cites]
Breast Cancer Res Treat. 2005 Sep;93(2):101-10
[
16187229.001
]
[Cites]
Annu Rev Cell Dev Biol. 2005;21:247-69
[
16212495.001
]
[Cites]
Oncogene. 2005 Nov 24;24(53):7821-9
[
16027728.001
]
[Cites]
Curr Opin Cell Biol. 2006 Feb;18(1):18-25
[
16337369.001
]
[Cites]
Breast Cancer Res. 2005;7(6):R965-74
[
16280046.001
]
[Cites]
Endocrinology. 2006 Mar;147(3):1203-12
[
16339197.001
]
[Cites]
Curr Drug Targets. 2006 Apr;7(4):423-42
[
16611030.001
]
[Cites]
Int J Oncol. 2006 Jul;29(1):217-23
[
16773203.001
]
[Cites]
Biol Reprod. 2006 Jul;75(1):9-16
[
16571873.001
]
[Cites]
Mol Endocrinol. 2006 Aug;20(8):1756-71
[
16601072.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):14138-43
[
9391166.001
]
[Cites]
Histochem Cell Biol. 1999 Nov;112(5):341-50
[
10603073.001
]
[Cites]
Hepatology. 2000 Apr;31(4):922-31
[
10733549.001
]
[Cites]
J Cancer Res Clin Oncol. 2001 Apr;127(4):258-64
[
11315261.001
]
[Cites]
Semin Cancer Biol. 2001 Apr;11(2):119-28
[
11322831.001
]
[Cites]
J Cell Sci. 2001 May;114(Pt 10):1801-9
[
11329366.001
]
[Cites]
Int J Oncol. 2001 Jul;19(1):83-8
[
11408926.001
]
[Cites]
Cancer Res. 2001 Oct 15;61(20):7456-63
[
11606380.001
]
[Cites]
Mol Med. 2001 Dec;7(12):816-30
[
11844870.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Mar;87(3):1223-32
[
11889192.001
]
[Cites]
J Biol Chem. 2002 Jul 5;277(27):24753-63
[
11948177.001
]
[Cites]
Free Radic Biol Med. 2002 Aug 1;33(3):387-98
[
12126761.001
]
[Cites]
J Nutr. 2002 Nov;132(11 Suppl):3482S-3489S
[
12421874.001
]
[Cites]
Int J Oncol. 2003 Jul;23(1):17-28
[
12792772.001
]
[Cites]
Exp Cell Res. 2003 Jul 1;287(1):47-56
[
12799181.001
]
[Cites]
Science. 2003 Dec 5;302(5651):1704-9
[
14657486.001
]
[Cites]
Int J Cancer. 2004 Mar 20;109(2):167-73
[
14750165.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):2076-81
[
14764897.001
]
[Cites]
Breast Cancer Res Treat. 2004 Mar;84(1):13-9
[
14999150.001
]
[Cites]
Breast Cancer Res Treat. 2004 Mar;84(1):43-8
[
14999153.001
]
[Cites]
Breast Cancer Res Treat. 2004 Mar;84(1):49-60
[
14999154.001
]
[Cites]
Oncogene. 2004 Mar 11;23(10):1845-53
[
14661062.001
]
[Cites]
J Cell Sci. 2004 Mar 15;117(Pt 8):1301-12
[
15020670.001
]
[Cites]
Prostate. 2004 May 1;59(2):214-25
[
15042621.001
]
[Cites]
Biochem Soc Trans. 2004 Dec;32(Pt 6):1115-7
[
15506983.001
]
[Cites]
Neurosci Lett. 1999 Apr 2;264(1-3):141-4
[
10320034.001
]
[Cites]
Anticancer Res. 2004 Sep-Oct;24(5A):2783-840
[
15517885.001
]
[Cites]
Clin Exp Metastasis. 2004;21(5):445-51
[
15672869.001
]
(PMID = 17356711.001).
[ISSN]
1476-5586
[Journal-full-title]
Neoplasia (New York, N.Y.)
[ISO-abbreviation]
Neoplasia
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / 5 F31 CA111486-02; United States / NCI NIH HHS / CA / R03 CA109913; United States / NCI NIH HHS / CA / CA109913-03; United States / NCI NIH HHS / CA / R03 CA109913-03; United States / NCI NIH HHS / CA / F31 CA111486; United States / NCRR NIH HHS / RR / 2G12RR003035; United States / NCI NIH HHS / CA / 5R03CA109913-03; United States / NCRR NIH HHS / RR / G12 RR003035
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Actins; 0 / Estrogens; 0 / Recombinant Fusion Proteins; 0 / Stilbenes; 4TI98Z838E / Estradiol; 62229-50-9 / Epidermal Growth Factor; EC 3.6.5.2 / cdc42 GTP-Binding Protein; EC 3.6.5.2 / rac GTP-Binding Proteins; Q369O8926L / resveratrol
[Other-IDs]
NLM/ PMC1813930
21.
McMorris TC, Chimmani R, Alisala K, Staake MD, Banda G, Kelner MJ:
Structure-activity studies of urea, carbamate, and sulfonamide derivatives of acylfulvene.
J Med Chem
; 2010 Feb 11;53(3):1109-16
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
The lead acylfulvene (4), irofulven (5), in a randomized phase IIB clinical trial significantly increased overall survival in patients with
metastatic
hormone-refractory
prostate
cancer who failed prior treatment with two different standard chemotherapeutic regimens.
[MeSH-major]
Adenocarcinoma
/ pathology. B-Lymphocytes / drug effects. Carbamates / chemistry. Lung Neoplasms / pathology. Sulfonamides / chemistry. Urea / chemistry
MedlinePlus Health Information.
consumer health - Lung Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
UREA
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20067264.001).
[ISSN]
1520-4804
[Journal-full-title]
Journal of medicinal chemistry
[ISO-abbreviation]
J. Med. Chem.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Carbamates; 0 / Sesquiterpenes; 0 / Spiro Compounds; 0 / Sulfonamides; 0 / acylfulvene; 8W8T17847W / Urea
22.
Rojiani MV, Alidina J, Esposito N, Rojiani AM:
Expression of MMP-2 correlates with increased angiogenesis in CNS metastasis of lung carcinoma.
Int J Clin Exp Pathol
; 2010;3(8):775-81
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Matrix metalloproteinases (MMP) have been implicated in increased invasive and
metastatic
potential of tumors, possibly via interactions with the extracellular matrix and angiogenesis.
This study investigates the relationship between MMP-2 immunoexpression and angiogenesis in a series of lung carcinomas
metastatic
to the central nervous system (CNS).
Twenty eight
metastatic
carcinoma cases with adequate brain-tumor interface were identified from the archives at the Moffitt Cancer Center.
Sixteen (57.14%)
metastatic
tumors were strongly immunoreac-tive for MMP-2, while 12 (42.86%) were negative.
[MeSH-major]
Adenocarcinoma
/ blood supply. Brain Neoplasms / blood supply. Lung Neoplasms / blood supply. Matrix Metalloproteinase 2 / metabolism. Neovascularization, Pathologic / enzymology
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Lung Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Prostate. 2000 Jan;42(1):18-25
[
10579795.001
]
[Cites]
Pediatr Nephrol. 1993 Feb;7(1):96-104
[
8439492.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):3884-9
[
10760260.001
]
[Cites]
Nat Cell Biol. 2000 Oct;2(10):737-44
[
11025665.001
]
[Cites]
Curr Opin Cell Biol. 2001 Oct;13(5):534-40
[
11544020.001
]
[Cites]
Science. 2002 Jun 7;296(5574):1883-6
[
11976409.001
]
[Cites]
Cancer. 2002 Nov 1;95(9):1902-10
[
12404284.001
]
[Cites]
Cell. 1985 Sep;42(2):469-77
[
2411423.001
]
[Cites]
Science. 1987 Jan 23;235(4787):442-7
[
2432664.001
]
[Cites]
Cancer. 1992 Dec 15;70(12):2747-53
[
1451050.001
]
[Cites]
Annu Rev Cell Biol. 1993;9:541-73
[
8280471.001
]
[Cites]
J Invest Dermatol. 1995 Aug;105(2):170-6
[
7543547.001
]
[Cites]
J Cell Physiol. 1995 Dec;165(3):475-83
[
7593226.001
]
[Cites]
Cancer Res. 1996 Jan 1;56(1):190-6
[
8548762.001
]
[Cites]
Int J Cancer. 1996 Feb 20;69(1):9-16
[
8600068.001
]
[Cites]
Br J Cancer. 1996 Apr;73(8):972-8
[
8611434.001
]
[Cites]
Br J Cancer. 1996 Aug;74(3):413-7
[
8695357.001
]
[Cites]
Pathol Int. 1997 Jul;47(7):461-9
[
9234385.001
]
[Cites]
Ann Thorac Surg. 1997 Oct;64(4):1204-11
[
9354565.001
]
[Cites]
Cancer. 1998 Feb 15;82(4):642-50
[
9477095.001
]
[Cites]
Cancer Res. 1998 Mar 1;58(5):1048-51
[
9500469.001
]
[Cites]
Cancer. 1998 Sep 15;83(6):1153-62
[
9740080.001
]
[Cites]
Curr Opin Cell Biol. 1998 Oct;10(5):602-8
[
9818170.001
]
[Cites]
Ann Med. 1999 Feb;31(1):34-45
[
10219712.001
]
[Cites]
Gynecol Oncol. 1999 Jun;73(3):372-82
[
10366463.001
]
[Cites]
Gynecol Oncol. 1999 Oct;75(1):91-8
[
10502432.001
]
[Cites]
Nat Rev Mol Cell Biol. 2007 Mar;8(3):221-33
[
17318226.001
]
[Cites]
Semin Cell Dev Biol. 2008 Feb;19(1):52-60
[
17625931.001
]
[Cites]
Cancer Metastasis Rev. 2008 Dec;27(4):679-90
[
18465089.001
]
[Cites]
Matrix Biol. 2009 Jan;28(1):3-10
[
19010413.001
]
[Cites]
Integr Biol (Camb). 2009 Jun;1(5-6):382-93
[
20023745.001
]
[Cites]
Biochim Biophys Acta. 2010 Jan;1803(1):3-19
[
19631700.001
]
[Cites]
Cell. 2010 Apr 2;141(1):52-67
[
20371345.001
]
[Cites]
Breast Cancer Res Treat. 1999 Dec;58(3):287-93
[
10718490.001
]
(PMID = 21151391.001).
[ISSN]
1936-2625
[Journal-full-title]
International journal of clinical and experimental pathology
[ISO-abbreviation]
Int J Clin Exp Pathol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD34; EC 3.4.24.24 / Matrix Metalloproteinase 2
[Other-IDs]
NLM/ PMC2993228
[Keywords]
NOTNLM ; CNS metastasis / Matrix metalloproteinases (MMP) / angiogenesis / lung cancer
23.
Prawettongsopon C, Asawakarn S, Suthiphongchai T:
Suppression of prometastatic phenotype of highly metastatic androgen-independent rat prostate cancer MLL cell line by PI3K inhibitor LY294002.
Oncol Res
; 2009;17(7):301-9
[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]
Suppression of prometastatic phenotype of highly
metastatic
androgen-independent rat
prostate
cancer MLL cell line by PI3K inhibitor LY294002.
Upregulation of the PI3K pathway has often been reported in androgen-independent
prostate
cancer and is implicated in cancer cell survival and proliferation in the absence of androgen.
Inhibition of PI3K by LY294002 suppressed cell invasion and motility of the highly
metastatic
androgen-independent Dunning rat
prostate
cancer MLL cell line with similar IC50 values and inhibition profile.
[MeSH-major]
Androgens / pharmacology. Chromones / pharmacology. Enzyme Inhibitors / pharmacology. Morpholines / pharmacology. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / secondary. Phosphatidylinositol 3-Kinases / antagonists & inhibitors.
Prostatic
Neoplasms / drug therapy
[MeSH-minor]
Adenocarcinoma
/ drug therapy.
Adenocarcinoma
/ metabolism.
Adenocarcinoma
/ secondary. Animals. Cell Movement / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Male. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 2 / metabolism. Phosphorylation / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Tumor Cells, Cultured. Urokinase-Type Plasminogen Activator / genetics. Urokinase-Type Plasminogen Activator / metabolism
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19408575.001).
[ISSN]
0965-0407
[Journal-full-title]
Oncology research
[ISO-abbreviation]
Oncol. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgens; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / RNA, Messenger; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; EC 3.4.24.24 / Matrix Metalloproteinase 2
24.
Schlomm T, Iwers L, Kirstein P, Jessen B, Köllermann J, Minner S, Passow-Drolet A, Mirlacher M, Milde-Langosch K, Graefen M, Haese A, Steuber T, Simon R, Huland H, Sauter G, Erbersdobler A:
Clinical significance of p53 alterations in surgically treated prostate cancers.
Mod Pathol
; 2008 Nov;21(11):1371-8
[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]
Clinical significance of p53 alterations in surgically treated
prostate
cancers.
Despite the high number of previous studies, the role of p53 alterations in
prostate
cancer is not clearly defined.
To address the role of p53 alterations in
prostate
cancer biology, a total of 2514 cancers treated by radical prostatectomy were successfully analyzed by immunohistochemistry in a tissue microarray format.
These data suggest a high sensitivity of our immunohistochemistry approach and confirm the overall low frequency of p53 alterations in clinically localized
prostate
cancer.
A higher rate of positive p53 immunostaining was detected in late-stage diseases including
metastatic prostate
cancer (P=0.0152) and hormone-refractory tumors (P=0.0003).
In summary, the results of this study show that p53 mutations characterize a small biologically aggressive subgroup
of prostate
cancers with a high risk of progression after prostatectomy.
The rate of p53 alterations increases with
prostate
cancer progression.
[MeSH-major]
Adenocarcinoma
/ metabolism. Biomarkers, Tumor / metabolism.
Prostatic
Neoplasms / metabolism. Tumor Suppressor Protein p53 / metabolism
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 = 18552821.001).
[ISSN]
1530-0285
[Journal-full-title]
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
[ISO-abbreviation]
Mod. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Tumor Suppressor Protein p53
25.
Kuttan NA, Flemming DK, Dane JN, Ang DB:
Metastatic lesion of the anterior mandible with an occult primary: a case report.
Spec Care Dentist
; 2006 Mar-Apr;26(2):76-80
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Metastatic
lesion of the anterior mandible with an occult primary: a case report.
Metastatic
tumors to the oral cavity are relatively uncommon and account for about 1% of all oral cancers.
The leading common primary sites for these lesions are the breast in females and the lung in males followed by the adrenals, kidneys,
prostate
, thyroid and colon.
In 30% of all cancers, a
metastatic
lesion could be the first sign of a primary tumor elsewhere in the body.
Metastatic
lesions to the jaws are known to simulate periodontal and pulpal disease and other radiolucent lesions that can occur in the jaws.
Microscopic evaluation with concurrent radiographic skeletal survey is warranted in patients where a
metastatic
lesion is suspected.
[MeSH-major]
Adenocarcinoma
/ secondary. Colonic Neoplasms / pathology. Mandibular Neoplasms / secondary. Neoplasms, Unknown Primary / pathology
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16681243.001).
[ISSN]
0275-1879
[Journal-full-title]
Special care in dentistry : official publication of the American Association of Hospital Dentists, the Academy of Dentistry for the Handicapped, and the American Society for Geriatric Dentistry
[ISO-abbreviation]
Spec Care Dentist
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
26.
Tollefson M, Magera J, Sebo T, Cohen J, Drauch A, Maier J, Frank I:
Raman spectral imaging of prostate cancer: can Raman molecular imaging be used to augment standard histopathology?
BJU Int
; 2010 Aug;106(4):484-8
[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]
Raman spectral imaging
of prostate
cancer: can Raman molecular imaging be used to augment standard histopathology?
OBJECTIVE: To evaluate whether Raman molecular imaging (RMI, which combines digital imaging and analytical spectroscopy to evaluate the biochemical composition of interrogated material) can be used to identify biochemical differences in patients with Gleason 7
prostate
cancer who progress to
metastatic
disease and die from
prostate
cancer.
PATIENTS AND METHODS: We identified 38 patients who had a radical prostatectomy for Gleason 7
adenocarcinoma of the prostate
.
Half progressed to
metastatic
disease and half had no evidence of disease after treatment.
Patients were matched for preoperative
prostate
-specific antigen level, surgical margin status, pathological stage, tumour volume, age at surgery, year of surgery and DNA ploidy.
In Gleason 7 disease, RMI shows distinctive chemical differences in patients who progress to
metastatic
disease in both Gleason pattern 3 and 4 regions.
This preliminary work lays the foundation for the further study of RMI for evaluating
prostate
tissue.
[MeSH-major]
Adenocarcinoma
/ pathology. Prostatectomy / methods.
Prostatic
Neoplasms / pathology. Spectrum Analysis, Raman
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 = 20201840.001).
[ISSN]
1464-410X
[Journal-full-title]
BJU international
[ISO-abbreviation]
BJU Int.
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article
[Publication-country]
England
27.
Comstock CE, Revelo MP, Buncher CR, Knudsen KE:
Impact of differential cyclin D1 expression and localisation in prostate cancer.
Br J Cancer
; 2007 Mar 26;96(6):970-9
[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]
Impact of differential cyclin D1 expression and localisation in
prostate
cancer.
Cyclin D1 is a critical regulator of androgen-dependent transcription and cell cycle progression in
prostate
cancer cells.
Despite the influence of D-type cyclins on
prostate
cancer proliferation, few studies have examined the expression of cyclin D1 in localised tumours or challenged its relevance to disease progression.
Cyclin D1 status was characterised using immunohistochemistry in 38 non-neoplastic
prostate
samples, 138 primary human
prostate
carcinomas, and three lymph node
metastatic
specimens.
Relevance of cyclin D1 to preoperative
prostate
-specific antigen (PSA) levels, Ki-67 index, and p21Cip1 status was also examined.
These data demonstrate that differential cyclin D1 status may influence clinicopathological parameters, and reveal new insight as to the regulation and potential consequence of cyclin D1 expression in
prostate
cancer.
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
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Biol Chem. 2004 Jan 9;279(2):1422-8
[
14530270.001
]
[Cites]
Prostate. 2004 Feb 15;58(3):269-76
[
14743466.001
]
[Cites]
J Cell Biochem. 2004 Feb 15;91(3):483-90
[
14755679.001
]
[Cites]
Clin Cancer Res. 2004 Feb 1;10(3):1032-40
[
14871982.001
]
[Cites]
Trends Mol Med. 2004 Apr;10(4):158-62
[
15059606.001
]
[Cites]
Oncogene. 1993 Aug;8(8):2127-33
[
8336939.001
]
[Cites]
Proc Natl Acad Sci U S A. 1993 Oct 1;90(19):9026-30
[
8415648.001
]
[Cites]
Mol Cell Biol. 1995 May;15(5):2600-11
[
7739541.001
]
[Cites]
Oncogene. 1996 Aug 15;13(4):797-802
[
8761301.001
]
[Cites]
Prostate. 1997 Jul 1;32(2):99-105
[
9215397.001
]
[Cites]
Cancer. 1997 Aug 15;80(4):753-63
[
9264360.001
]
[Cites]
Semin Cancer Biol. 1997 Feb;8(1):11-9
[
9299577.001
]
[Cites]
Mol Cell Biol. 1997 Dec;17(12):7362-74
[
9372967.001
]
[Cites]
Am J Surg Pathol. 1998 Feb;22(2):188-94
[
9500219.001
]
[Cites]
Curr Opin Genet Dev. 1998 Feb;8(1):21-7
[
9529601.001
]
[Cites]
Prostate. 1998 May;35(2):95-101
[
9568672.001
]
[Cites]
J Biol Chem. 1998 Aug 7;273(32):20213-22
[
9685369.001
]
[Cites]
Hum Pathol. 1998 Aug;29(8):778-83
[
9712417.001
]
[Cites]
Genes Dev. 1998 Nov 15;12(22):3499-511
[
9832503.001
]
[Cites]
Eur J Cancer. 1998 Sep;34(10):1575-81
[
9893631.001
]
[Cites]
Prostate. 1999 Jan 1;38(1):40-5
[
9973108.001
]
[Cites]
Prostate. 1999 Feb 15;38(3):175-82
[
10068341.001
]
[Cites]
Mol Cell Biol. 1999 Mar;19(3):1775-83
[
10022865.001
]
[Cites]
Cancer Res. 1999 Feb 15;59(4):803-6
[
10029066.001
]
[Cites]
Breast Cancer Res Treat. 1998;52(1-3):79-98
[
10066074.001
]
[Cites]
Adv Anat Pathol. 2006 Jan;13(1):57-9
[
16462155.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2190-5
[
16461912.001
]
[Cites]
CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30
[
16514137.001
]
[Cites]
Mol Cancer. 2006;5:7
[
16503970.001
]
[Cites]
Anat Histol Embryol. 2006 Apr;35(2):125-9
[
16542178.001
]
[Cites]
Mol Endocrinol. 1999 Mar;13(3):376-84
[
10076995.001
]
[Cites]
EMBO J. 1999 Mar 15;18(6):1571-83
[
10075928.001
]
[Cites]
Nature. 1999 Apr 1;398(6726):422-6
[
10201372.001
]
[Cites]
Cancer Res. 1999 May 15;59(10):2297-301
[
10344732.001
]
[Cites]
Int J Cancer. 1999 Jun 21;84(3):225-33
[
10371338.001
]
[Cites]
Endocrinology. 2004 Dec;145(12):5439-47
[
15331580.001
]
[Cites]
Genes Dev. 2004 Nov 15;18(22):2699-711
[
15545627.001
]
[Cites]
Oncogene. 2005 Jan 13;24(3):431-44
[
15558026.001
]
[Cites]
Mol Endocrinol. 2005 Mar;19(3):607-20
[
15539430.001
]
[Cites]
Clin Cancer Res. 2005 Jun 1;11(11):4117-27
[
15930347.001
]
[Cites]
Expert Opin Ther Targets. 2005 Apr;9(2):283-98
[
15934916.001
]
[Cites]
J Cancer Res Clin Oncol. 2005 Jul;131(7):479-85
[
15809880.001
]
[Cites]
J Clin Oncol. 2005 Jun 20;23(18):4215-24
[
15961768.001
]
[Cites]
J Steroid Biochem Mol Biol. 2005 Aug;96(3-4):251-8
[
15982869.001
]
[Cites]
Eur Urol. 2005 Oct;48(4):541-5
[
16139417.001
]
[Cites]
Chem Rev. 2005 Sep;105(9):3352-70
[
16159155.001
]
[Cites]
BMC Cancer. 2005;5:98
[
16086840.001
]
[Cites]
J Cell Biochem. 2005 Dec 1;96(5):906-13
[
16163738.001
]
[Cites]
Oncogene. 2005 Nov 14;24(50):7465-74
[
16288293.001
]
[Cites]
Biochem Biophys Res Commun. 2006 Feb 3;340(1):302-8
[
16364255.001
]
[Cites]
Br J Cancer. 1999 May;80(3-4):546-55
[
10408865.001
]
[Cites]
Prostate. 1999 Sep 1;40(4):256-60
[
10420154.001
]
[Cites]
J Gastroenterol. 1999 Aug;34(4):486-93
[
10452682.001
]
[Cites]
Clin Cancer Res. 1999 Aug;5(8):2082-8
[
10473090.001
]
[Cites]
Clin Cancer Res. 1999 Aug;5(8):2133-9
[
10473097.001
]
[Cites]
Cancer Treat Rev. 2006 Apr;32(2):90-100
[
16458434.001
]
[Cites]
Int J Colorectal Dis. 2006 May;21(4):291-300
[
16041507.001
]
[Cites]
J Surg Oncol. 2006 Aug 1;94(2):155-60
[
16847925.001
]
[Cites]
Cancer Res. 2006 Aug 1;66(15):7783-92
[
16885382.001
]
[Cites]
Endocr Relat Cancer. 2006 Dec;13(4):979-94
[
17158750.001
]
[Cites]
J Natl Cancer Inst. 1999 Nov 3;91(21):1869-76
[
10547394.001
]
[Cites]
Br J Cancer. 1999 Dec;81(7):1174-81
[
10584879.001
]
[Cites]
J Biol Chem. 2000 Apr 21;275(16):12074-9
[
10766840.001
]
[Cites]
Clin Cancer Res. 2000 May;6(5):1891-5
[
10815912.001
]
[Cites]
Mol Pathol. 2000 Feb;53(1):15-8
[
10884916.001
]
[Cites]
Cell Growth Differ. 2000 Jul;11(7):361-72
[
10939590.001
]
[Cites]
Int J Cancer. 2000 Oct 1;88(1):77-81
[
10964085.001
]
[Cites]
Genes Dev. 2000 Dec 15;14(24):3102-14
[
11124803.001
]
[Cites]
Br J Cancer. 2001 Jan;84(2):270-5
[
11161387.001
]
[Cites]
Prostate. 2001 Feb 15;46(3):184-90
[
11170146.001
]
[Cites]
Mol Endocrinol. 2001 May;15(5):797-811
[
11328859.001
]
[Cites]
J Cell Biochem. 2001;81(4):621-38
[
11329617.001
]
[Cites]
Carcinogenesis. 2001 Aug;22(8):1149-54
[
11470742.001
]
[Cites]
Int J Cancer. 2001 Sep 20;95(5):302-6
[
11494229.001
]
[Cites]
J Neurooncol. 2001 Sep;54(2):95-110
[
11761437.001
]
[Cites]
Prostate. 2001 Nov 1;49(3):191-9
[
11746264.001
]
[Cites]
Biochem Biophys Res Commun. 2002 Feb 8;290(5):1368-75
[
11820772.001
]
[Cites]
J Biol Chem. 2002 Mar 8;277(10):8517-23
[
11751903.001
]
[Cites]
Eur J Cancer. 2001 Oct;37 Suppl 7:S119-25
[
11887983.001
]
[Cites]
Clin Cancer Res. 2002 Mar;8(3):775-81
[
11895908.001
]
[Cites]
Nat Rev Cancer. 2001 Oct;1(1):34-45
[
11900250.001
]
[Cites]
J Biol Chem. 2002 Aug 9;277(32):28733-41
[
12048199.001
]
[Cites]
Gene. 2002 Oct 16;299(1-2):35-55
[
12459251.001
]
[Cites]
Virchows Arch. 2003 Jan;442(1):1-7
[
12536308.001
]
[Cites]
Urology. 2003 Apr;61(4):837
[
12670580.001
]
[Cites]
Mol Cell Biol. 2003 Sep;23(17):6139-49
[
12917336.001
]
[Cites]
Cancer Res. 2003 Aug 15;63(16):4903-13
[
12941814.001
]
[Cites]
Cancer Res. 2003 Nov 1;63(21):7056-61
[
14612495.001
]
[Cites]
Nat Med. 2004 Jan;10(1):33-9
[
14702632.001
]
(PMID = 17375037.001).
[ISSN]
0007-0920
[Journal-full-title]
British journal of cancer
[ISO-abbreviation]
Br. J. Cancer
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA099996; United States / NCI NIH HHS / CA / CA 099996
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Ki-67 Antigen; 136601-57-5 / Cyclin D1; EC 3.4.21.77 / Prostate-Specific Antigen
[Other-IDs]
NLM/ PMC2360090
28.
Carducci MA, Saad F, Abrahamsson PA, Dearnaley DP, Schulman CC, North SA, Sleep DJ, Isaacson JD, Nelson JB, Atrasentan Phase III Study Group Institutions:
A phase 3 randomized controlled trial of the efficacy and safety of atrasentan in men with metastatic hormone-refractory prostate cancer.
Cancer
; 2007 Nov 01;110(9):1959-66
[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]
A phase 3 randomized controlled trial of the efficacy and safety of atrasentan in men with
metastatic
hormone-refractory
prostate
cancer.
BACKGROUND: The objective of this study was to evaluate the efficacy and safety of atrasentan (Xinlay), a selective endothelin-A receptor antagonist, in patients with
metastatic
hormone-refractory
prostate
cancer (HRPC).
METHODS: This multinational, double-blind, placebo-controlled trial enrolled 809 men with
metastatic
HRPC.
In exploratory analyses, increases from baseline to final bone alkaline phosphatase (BAP) and
prostate
-specific antigen (PSA) levels were significantly lower with atrasentan treatment (P < .05 for each).
CONCLUSIONS: Atrasentan did not delay disease progression in men with
metastatic
HRPC despite evidence of biologic effects on PSA and BAP as markers of disease burden.
[MeSH-major]
Adenocarcinoma
/ drug therapy.
Adenocarcinoma
/ pathology. Antineoplastic Agents / therapeutic use.
Prostatic
Neoplasms / drug therapy.
Prostatic
Neoplasms / pathology. Pyrrolidines / therapeutic use
[MeSH-minor]
Aged. Aged, 80 and over. Alkaline Phosphatase / blood. Alkaline Phosphatase / drug effects. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Disease Progression. Double-Blind Method. Drug Resistance, Neoplasm. Humans. Kaplan-Meier Estimate. Male. Middle Aged.
Prostate
-Specific Antigen / blood.
Prostate
-Specific Antigen / drug effects
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
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
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Cancer. 2007 Nov 1;110(9):1877-9
[
17849427.001
]
(PMID = 17886253.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0501019
[Publication-type]
Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Pyrrolidines; EC 3.1.3.1 / Alkaline Phosphatase; EC 3.4.21.77 / Prostate-Specific Antigen; V6D7VK2215 / atrasentan
29.
Jantscheff P, Esser N, Graeser R, Ziroli V, Kluth J, Unger C, Massing U:
Liposomal gemcitabine (GemLip)-efficient drug against hormone-refractory Du145 and PC-3 prostate cancer xenografts.
Prostate
; 2009 Aug 1;69(11):1151-63
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Liposomal gemcitabine (GemLip)-efficient drug against hormone-refractory Du145 and PC-3
prostate
cancer xenografts.
BACKGROUND: Gemcitabine (Gemc) is an efficient chemotherapeutic drug in various cancer types (e.g., pancreas) but has only limited effects on hormone-refractory
prostate
cancer (HRPCa).
METHODS: Anti-tumoral and anti-
metastatic
activity of GemLip and Gemc were investigated in two luciferase-expressing, human hormone-refractory PC-3 and Du145 HRPCa xenograft models in immunodeficient mice.
Anti-
metastatic
effects of treatment were determined by in vitro luciferase assay of the tissues.
GemLip has, even at very low doses, a significant anti-tumoral and anti-
metastatic
therapeutic effect in HRPCa xenografts in vivo and was beneficial even when the conventional Gemc failed.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / therapeutic use. Deoxycytidine / analogs & derivatives.
Prostatic
Neoplasms / drug therapy. Transplantation, Heterologous
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 = 19399788.001).
[ISSN]
1097-0045
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 0 / Liposomes; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 1.13.12.- / Luciferases
30.
Jennbacken K, Gustavsson H, Welén K, Vallbo C, Damber JE:
Prostate cancer progression into androgen independency is associated with alterations in cell adhesion and invasivity.
Prostate
; 2006 Nov 1;66(15):1631-40
[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]
Prostate
cancer progression into androgen independency is associated with alterations in cell adhesion and invasivity.
BACKGROUND: Mortality in
prostate
cancer is primarily due to failure to cure hormone refractory patients with
metastatic
disease.
CONCLUSIONS: The results show that LNCaP-19 mimics hormone refractory
prostate
cancer and therefore is an excellent tool for studies on androgen-independent cancer and invasion.
[MeSH-major]
Adenocarcinoma
/ pathology. Androgens / metabolism. Cell Transformation, Neoplastic / pathology.
Prostatic
Neoplasms / pathology
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
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 = 16927303.001).
[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 / Androgens; 0 / Cell Adhesion Molecules
31.
Wong SY, Haack H, Crowley D, Barry M, Bronson RT, Hynes RO:
Tumor-secreted vascular endothelial growth factor-C is necessary for prostate cancer lymphangiogenesis, but lymphangiogenesis is unnecessary for lymph node metastasis.
Cancer Res
; 2005 Nov 1;65(21):9789-98
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Tumor-secreted vascular endothelial growth factor-C is necessary for
prostate
cancer lymphangiogenesis, but lymphangiogenesis is unnecessary for lymph node metastasis.
Dissemination to draining lymph nodes is a frequent first step in
prostate
cancer metastasis.
Here, we inhibit intratumoral lymphangiogenesis in s.c. and surgical orthotopic implantation mouse models of human
prostate
cancer using several strategies.
Combination of soluble Flt4 and VEGF-C siRNA yielded >92% reduction of intratumoral lymphatics in orthotopic
prostate
tumors.
We also analyzed the lymphatics in spontaneous transgenic adenocarcinomas of the mouse
prostate
which metastasize to lymph nodes.
Progression from well-differentiated
prostate
intraepithelial neoplasia to
metastatic
, undifferentiated
adenocarcinoma
was accompanied by loss of lymphatics.
These results suggest that tumor-secreted VEGF-C and, to a lesser extent, VEGF-A, are important for inducing
prostate
cancer intratumoral lymphangiogenesis but are unnecessary for lymph node metastasis.
[MeSH-major]
Adenocarcinoma
/ pathology. Lymph Nodes / pathology.
Prostatic
Neoplasms / pathology. Vascular Endothelial Growth Factor C / physiology
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16267000.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01CA17007
[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 / RNA, Small Interfering; 0 / VEGFA protein, human; 0 / VEGFC protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C
32.
Plotnikov A, Niego B, Ophir R, Korenstein R, Keisari Y:
Effective treatment of mouse metastatic prostate cancer by low electric field enhanced chemotherapy.
Prostate
; 2006 Nov 1;66(15):1620-30
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Effective treatment of mouse
metastatic prostate
cancer by low electric field enhanced chemotherapy.
In the present study we investigated its efficacy against
prostate metastatic
transgenic
adenocarcinoma of
mice (TRAMP).
METHODS: Mice with 5, 10, and 13 mm in diameter intracutaneous tumors received Low Electric Field Cancer Treatment-Enhanced Chemotherapy (LEFCT-EC) with doxorubicin (10 mg/kg), and monitored for survival, and primary and
metastatic
tumors growth.
CONCLUSION: Our results suggest that LEFCT-EC is an effective method for the destruction
of metastatic prostate
tumors.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Antibiotics, Antineoplastic / therapeutic use. Doxorubicin / therapeutic use. Electrochemotherapy.
Prostatic
Neoplasms / drug therapy
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16941466.001).
[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 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
33.
Castellana D, Zobairi F, Martinez MC, Panaro MA, Mitolo V, Freyssinet JM, Kunzelmann C:
Membrane microvesicles as actors in the establishment of a favorable prostatic tumoral niche: a role for activated fibroblasts and CX3CL1-CX3CR1 axis.
Cancer Res
; 2009 Feb 1;69(3):785-93
[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]
Membrane microvesicles as actors in the establishment of a favorable
prostatic
tumoral niche: a role for activated fibroblasts and CX3CL1-CX3CR1 axis.
To elucidate their role in cancer-to-fibroblast cell communication, TMV obtained from two
prostate
carcinoma cell lines with high and weak
metastatic
potential (PC3 and LnCaP, respectively) have been characterized.
Moreover, TMV not only induce the activation of fibroblasts assessed through extracellular signal-regulated kinase 1/2 phosphorylation and MMP-9 up-regulation, increase motility and resistance to apoptosis but also promote MV shedding from activated fibroblasts able in turn to increase migration and invasion of highly
metastatic
PC3 cells but not LnCaP cells.
[MeSH-major]
Adenocarcinoma
/ pathology. Cell Communication / physiology. Chemokine CX3CL1 / metabolism.
Prostatic
Neoplasms / pathology. Receptors, Chemokine / metabolism
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 = 19155311.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / CX3CL1 protein, human; 0 / CX3CR1 protein, human; 0 / Chemokine CX3CL1; 0 / Receptors, Chemokine; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.24.35 / Matrix Metalloproteinase 9
34.
Grenader T, Shavit L, Lossos A, Pizov G, Wygoda M:
Brain metastases: a rare initial presentation of prostate cancer.
Int Urol Nephrol
; 2007;39(2):537-9
[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]
Brain metastases: a rare initial presentation
of prostate
cancer.
Although brain metastases are common in cancer patients, carcinoma of the
prostate
rarely metastasizes to the brain.
Cerebral metastases as an initial clinical presentation
of prostate
carcinoma are extremely rare.
The pathological diagnosis of the tumor was consistent with
metastatic prostate
carcinoma.
Further evaluation revealed widespread bony metastases by technetium 99 bone scan and high level
of prostate
-specific antigen.
[MeSH-major]
Adenocarcinoma
/ secondary. Brain Neoplasms / secondary.
Prostatic
Neoplasms / pathology
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
[Cites]
Cancer. 1999 Dec 1;86(11):2301-11
[
10590371.001
]
[Cites]
Cancer. 1976 Dec;38(6):2583-7
[
1000485.001
]
[Cites]
Cancer. 1994 Nov 1;74(9):2516-9
[
7923009.001
]
[Cites]
Urology. 1986 Oct;28(4):280-7
[
3765236.001
]
[Cites]
Cancer. 1992 Oct 15;70(8):2149-51
[
1394044.001
]
[Cites]
Cancer. 1984 Dec 15;54(12):3078-84
[
6498785.001
]
[Cites]
Urology. 1996 Nov;48(5):789-93
[
8911530.001
]
[Cites]
Am J Psychiatry. 1996 Aug;153(8):974-84
[
8678193.001
]
(PMID = 17308872.001).
[ISSN]
0301-1623
[Journal-full-title]
International urology and nephrology
[ISO-abbreviation]
Int Urol Nephrol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Netherlands
35.
Mackler NJ, Pienta KJ, Dunn RL, Cooney KA, Redman BG, Olson KB, Fardig JE, Smith DC:
Phase II evaluation of oral estramustine, oral etoposide, and intravenous paclitaxel in patients with hormone-sensitive prostate adenocarcinoma.
Clin Genitourin Cancer
; 2007 Jun;5(5):318-22
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Phase II evaluation of oral estramustine, oral etoposide, and intravenous paclitaxel in patients with hormone-sensitive
prostate adenocarcinoma
.
PURPOSE: The primary objective of this study was to assess the feasibility and efficacy of administering etoposide/estramustine/paclitaxel in hormone-sensitive
metastatic prostate
cancer responding to hormonal therapy.
PATIENTS AND METHODS: Eligible patients had
metastatic prostate
cancer and had received combined androgen blockade for 6-8 months with a > or = 80% decrease in
prostate
-specific antigen from pretreatment.
Although the TTF of 21.7 months by
prostate
-specific antigen criteria is similar to historical controls in the emergence of clinically evident androgen-independent disease after starting hormone therapy, direct comparisons cannot be made.
More trials are needed to investigate the timing of chemotherapy in patients with
prostate
cancer.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasms, Hormone-Dependent / drug therapy.
Prostatic
Neoplasms / drug therapy
[MeSH-minor]
Administration, Oral. Aged. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Disease Progression. Estramustine / administration & dosage. Etoposide / administration & dosage. Feasibility Studies. Humans. Injections, Intravenous. Male. Middle Aged. Paclitaxel / administration & dosage.
Prostate
-Specific Antigen / blood. Survival Rate. Treatment Outcome
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
TAXOL
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17645828.001).
[ISSN]
1558-7673
[Journal-full-title]
Clinical genitourinary cancer
[ISO-abbreviation]
Clin Genitourin Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / 5 P30 CA 46592
[Publication-type]
Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
35LT29625A / Estramustine; 6PLQ3CP4P3 / Etoposide; EC 3.4.21.77 / Prostate-Specific Antigen; P88XT4IS4D / Paclitaxel
36.
Chiappino I, Destefanis P, Addeo A, Galetto A, Cucchiarale G, Munoz F, Zitella A, Ferrando U, Fontana D, Ricardi U, Tizzani A, Bertetto O:
Activity of weekly paclitaxel in advanced hormone-refractory prostate cancer.
Am J Clin Oncol
; 2007 Jun;30(3):234-8
[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]
Activity of weekly paclitaxel in advanced hormone-refractory
prostate
cancer.
OBJECTIVE: We evaluated efficacy and toxicity of weekly paclitaxel in
metastatic
hormone-refractory
prostate
cancer (HRPC).
RESULTS: The study enrolled 43 patients with
metastatic
HRPC diagnosed a median of 10.5 months before.
Five had previous radioisotopes treatment for bone pain, 15 had previous treatment
of metastatic
hormone-refractory disease, mainly estramustine.
CONCLUSION: Docetaxel every 3 weeks is the standard of care for
metastatic
HRPC, but our results suggest some activity and an acceptable toxicity of weekly paclitaxel.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Antineoplastic Agents, Phytogenic / administration & dosage. Paclitaxel / administration & dosage.
Prostatic
Neoplasms / drug therapy
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
TAXOL
.
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 = 17551298.001).
[ISSN]
1537-453X
[Journal-full-title]
American journal of clinical oncology
[ISO-abbreviation]
Am. J. Clin. Oncol.
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Phytogenic; P88XT4IS4D / Paclitaxel
37.
Idelevich E, Kashtan H, Mavor E, Brenner B:
Small bowel obstruction caused by secondary tumors.
Surg Oncol
; 2006 Jul;15(1):29-32
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Linitis plastica caused by
metastatic
lobular carcinoma of the breast.
Small bowel intussusception due to
metastatic
malignant melanoma.
Rectal obstruction secondary to carcinoma of the
prostate
treated by transanal resection of the
prostate
.
Unusual presentation of rectal
adenocarcinoma
.
A case of jejunal intussusception with gastrointestinal bleeding caused by
metastatic
testicular germ cell cancer.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16905310.001).
[ISSN]
0960-7404
[Journal-full-title]
Surgical oncology
[ISO-abbreviation]
Surg Oncol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Netherlands
[Number-of-references]
22
38.
Inoue S, Oka K, Araki T, Yano A, Tacho T, Fujii M, Kimoto K, Murakami M, Ohshiro Y:
[Neuroendocrine carcinoma of the prostate effectively treated by cisplatin and irinotecan--a case report].
Gan To Kagaku Ryoho
; 2007 Aug;34(8):1323-5
[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]
[Neuroendocrine carcinoma of the
prostate
effectively treated by cisplatin and irinotecan--a case report].
Because the serum PSA was 2,9 39 ng/mL,we performed transabdominal
prostatic
needle biopsy.
Pathological examination of the
prostate
revealed conventional
adenocarcinoma
.
Follow-up CT revealed
prostate
and lymph node metastasis were reduced, but liver metastases, measuring 45 x 34 mm and 28 x 24 mm, respectively, were newly recognized in February 2006.
The NSE level was high at 88.5 ng/mL, so a percutaneous liver biopsy was performed,and pathological examination of the liver revealed
metastatic prostate
cancer which showed neuroendocrine differentiation.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymph Nodes / pathology.
Prostatic
Neoplasms / drug therapy
[MeSH-minor]
Aged. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Carcinoma, Neuroendocrine / pathology. Cisplatin / administration & dosage. Drug Administration Schedule. Humans. Liver Neoplasms / pathology. Liver Neoplasms / secondary. Lymphatic Metastasis. Male.
Prostate
-Specific Antigen / blood
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
CIS-DIAMINEDICHLOROPLATINUM
.
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 = 17687224.001).
[ISSN]
0385-0684
[Journal-full-title]
Gan to kagaku ryoho. Cancer & chemotherapy
[ISO-abbreviation]
Gan To Kagaku Ryoho
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
7673326042 / irinotecan; EC 3.4.21.77 / Prostate-Specific Antigen; Q20Q21Q62J / Cisplatin; XT3Z54Z28A / Camptothecin
39.
Tarján M:
Prognostic significance of focal neuroendocrine differentiation in prostate cancer: cases with autopsy-verified cause of death.
Indian J Urol
; 2010 Jan-Mar;26(1):41-5
[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]
Prognostic significance of focal neuroendocrine differentiation in
prostate
cancer: cases with autopsy-verified cause of death.
AIMS: This study was designed to evaluate the prognostic significance of focal chromogranin A (cgA) expression in
prostate
cancer in a series of cases with autopsy-verified cause of death.
METHODS AND RESULTS: Seventy seven autopsy-verified cases
of prostate
cancer were identified, 41 cases with
metastatic
disease and 36 with nonmetastatic disease at autopsy.
After exclusion of a single case of carcinoid tumor, 14 of the 18 (78%)
metastatic
and none of the 21 (0%) nonmetastatic tumors showed focal neuroendocrine differentiation (NED).
The Gleason score and focal cgA expression further increased the accuracy of the prediction of the outcome, as all the cases with focal NED associated with high Gleason score had
metastatic
disease in contrast to cases without cgA-expression and low Gleason score, all of which were non-
metastatic
.
CONCLUSIONS: Focal NED seems to be a powerful negative prognostic parameter in
prostate
adenocarcinomas.
The outcome of the disease in
prostate
cancer can be accurately predicted based on focal NED of the tumor cells either alone or in combination with Gleason score.
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 Endocrinol Invest. 2005;28(11 Suppl International):141-5
[
16625864.001
]
[Cites]
Urology. 2003 Mar;61(3):589-95
[
12639653.001
]
[Cites]
BJU Int. 2007 Jan;99(1):189-95
[
17034504.001
]
[Cites]
Prostate. 1991;19(2):91-8
[
1717965.001
]
[Cites]
Science. 1987 Jan 9;235(4785):177-82
[
3798106.001
]
[Cites]
Hum Pathol. 1994 Jan;25(1):42-6
[
7508883.001
]
[Cites]
Prostate. 1994;24(3):114-8
[
7509483.001
]
[Cites]
Prostate. 1997 May 1;31(2):91-7
[
9140121.001
]
[Cites]
Am J Clin Pathol. 2000 Mar;113(3):383-8
[
10705819.001
]
[Cites]
Am J Clin Pathol. 2001 Aug;116(2):234-9
[
11488070.001
]
[Cites]
Cancer Lett. 2002 Dec 10;187(1-2):1-7
[
12359344.001
]
[Cites]
Hum Pathol. 2005 May;36(5):562-70
[
15948124.001
]
[Cites]
Am J Surg Pathol. 2006 Aug;30(8):980-5
[
16861969.001
]
[Cites]
Cancer. 2007 Feb 1;109(3):477-86
[
17186531.001
]
[Cites]
J Urol. 1997 Jul;158(1):171-4
[
9186347.001
]
[Cites]
Nat Med. 1999 Mar;5(3):280-5
[
10086382.001
]
[Cites]
Urology. 2001 Feb;57(2):291-5
[
11182339.001
]
[Cites]
Am J Clin Pathol. 2002 Mar;117(3):471-7
[
11888088.001
]
[Cites]
Prostate. 2002 Oct 1;53(2):118-23
[
12242726.001
]
[Cites]
Hum Pathol. 2006 Sep;37(9):1137-44
[
16938518.001
]
(PMID = 20535283.001).
[ISSN]
1998-3824
[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/ PMC2878436
[Keywords]
NOTNLM ; Adenocarcinoma / neuroendocrine differentiation / prognosis / prostate
40.
Stein ME, Boehmer D, Kuten A:
Radiation therapy in prostate cancer.
Recent Results Cancer Res
; 2007;175:179-99
[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]
Radiation therapy in
prostate
cancer.
Adenocarcinoma of the prostate
is one of the most frequently diagnosed cancers of men in the Western hemisphere and is second only to lung cancer for male cancer mortality.
Innovative methods such as brachytherapy, three-dimensional conformal radiotherapy (3D-CRT), and IMRT (intensity modulated radiotherapy) are able to deliver very high tumoricidal doses to the diseased
prostate
, with minimal side effects to the surrounding tissue.
Radiation therapy is also very effective in alleviating symptoms
of metastatic prostate
cancer (bone metastases, spinal cord compression, and bladder outlet obstruction).
[MeSH-major]
Prostatic
Neoplasms / radiotherapy
Genetic Alliance.
consumer health - Prostate 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 = 17432560.001).
[ISSN]
0080-0015
[Journal-full-title]
Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
[ISO-abbreviation]
Recent Results Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Germany
[Number-of-references]
103
41.
Wong SY, Haack H, Kissil JL, Barry M, Bronson RT, Shen SS, Whittaker CA, Crowley D, Hynes RO:
Protein 4.1B suppresses prostate cancer progression and metastasis.
Proc Natl Acad Sci U S A
; 2007 Jul 31;104(31):12784-9
[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]
Protein 4.1B suppresses
prostate
cancer progression and metastasis.
In a screen for genes involved with
prostate
cancer metastasis, we found that 4.1B expression is reduced in highly
metastatic
tumors.
Down-regulation of 4.1B increased
the metastatic
propensity of poorly
metastatic
cells in an orthotopic model
of prostate
cancer.
Furthermore, 4.1B-deficient mice displayed increased susceptibility for developing aggressive, spontaneous
prostate
carcinomas.
Because expression of Protein 4.1B is frequently down-regulated in human clinical
prostate
cancer, as well as in a spectrum of other tumor types, these results suggest a more general role for Protein 4.1B as a negative regulator of cancer progression to
metastatic
disease.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
Jackson Laboratory JAX®Mice Database.
culture/stock collections - STOCK Epb41l3<tm1Jkis>/J
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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]
Genes Dev. 2005 Oct 1;19(19):2265-77
[
16204178.001
]
[Cites]
Invest Urol. 1979 Jul;17(1):16-23
[
447482.001
]
[Cites]
Mol Cell Biol. 2005 Nov;25(22):10052-9
[
16260618.001
]
[Cites]
Cancer Res. 2005 Nov 1;65(21):9789-98
[
16267000.001
]
[Cites]
Nat Genet. 2006 May;38(5):500-1
[
16642009.001
]
[Cites]
Cancer Res. 2006 May 15;66(10):5295-303
[
16707455.001
]
[Cites]
Proc Natl Acad Sci U S A. 1980 Jul;77(7):4113-7
[
6933460.001
]
[Cites]
Hum Mol Genet. 2000 Jun 12;9(10):1495-500
[
10888600.001
]
[Cites]
Neurobiol Dis. 2001 Apr;8(2):266-78
[
11300722.001
]
[Cites]
Breast Cancer Res. 2001;3(3):192-8
[
11305954.001
]
[Cites]
Cancer Res. 2001 Aug 15;61(16):5974-8
[
11507037.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13790-5
[
11707567.001
]
[Cites]
Mol Biol Cell. 2002 Jun;13(6):1929-39
[
12058060.001
]
[Cites]
Cancer Cell. 2002 Mar;1(2):203-9
[
12086878.001
]
[Cites]
Int J Cancer. 2002 Jul 10;100(2):181-8
[
12115567.001
]
[Cites]
Nat Rev Mol Cell Biol. 2002 Aug;3(8):586-99
[
12154370.001
]
[Cites]
J Cell Sci. 2002 Nov 1;115(Pt 21):3991-4000
[
12356905.001
]
[Cites]
J Clin Invest. 1981 Aug;68(2):454-60
[
6894932.001
]
[Cites]
Cancer Res. 1984 Aug;44(8):3522-9
[
6744277.001
]
[Cites]
Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3439-43
[
7724580.001
]
[Cites]
Neurology. 1997 Jul;49(1):267-70
[
9222206.001
]
[Cites]
Cancer Res. 1997 Aug 15;57(16):3325-30
[
9269988.001
]
[Cites]
Prostate. 1998 Feb 15;34(3):169-74
[
9492844.001
]
[Cites]
Genes Dev. 1998 Apr 15;12(8):1121-33
[
9553042.001
]
[Cites]
Cancer Res. 1999 Jan 1;59(1):35-43
[
9892180.001
]
[Cites]
Histochem Cell Biol. 2004 Dec;122(6):579-86
[
15517334.001
]
[Cites]
Oncogene. 2005 Mar 10;24(11):1946-57
[
15688033.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13479-83
[
16157875.001
]
[Cites]
Cell. 2003 Jul 25;114(2):241-53
[
12887925.001
]
[Cites]
Histochem Cell Biol. 2003 Oct;120(4):277-83
[
14574582.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Jan 20;101(3):811-6
[
14711987.001
]
[Cites]
Nat Med. 2004 Feb;10(2):175-81
[
14704789.001
]
[Cites]
Nat Med. 2004 Feb;10(2):182-6
[
14704791.001
]
[Cites]
Neoplasia. 2004 Jan-Feb;6(1):1-6
[
15068665.001
]
[Cites]
J Clin Oncol. 2004 Jul 15;22(14):2790-9
[
15254046.001
]
[Cites]
Science. 2005 Oct 28;310(5748):644-8
[
16254181.001
]
(PMID = 17640904.001).
[ISSN]
0027-8424
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
ENG
[Databank-accession-numbers]
GEO/ GSE7930
[Grant]
United States / NCI NIH HHS / CA / R01 CA017007; United States / NCI NIH HHS / CA / U54 CA112967; United States / NCI NIH HHS / CA / R01 CA 17007; United States / NCI NIH HHS / CA / U54 CA 112967
[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 / EPB41L3 protein, human; 0 / Epb4.1l3 protein, mouse; 0 / Membrane Proteins; 0 / Microfilament Proteins; 0 / Tumor Suppressor Proteins
[Other-IDs]
NLM/ PMC1924789
42.
Berezovska OP, Glinskii AB, Yang Z, Li XM, Hoffman RM, Glinsky GV:
Essential role for activation of the Polycomb group (PcG) protein chromatin silencing pathway in metastatic prostate cancer.
Cell Cycle
; 2006 Aug;5(16):1886-901
[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]
Essential role for activation of the Polycomb group (PcG) protein chromatin silencing pathway in
metastatic prostate
cancer.
Another PcG protein, Ezh2, was implicated in
metastatic prostate
and breast cancers, suggesting that PcG pathway activation is relevant for epithelial malignancies.
Here we demonstrate that activation of the BMI1 oncogene-associated PcG pathway plays an essential role in
metastatic prostate
cancer, thus mechanistically linking the pathogenesis of leukemia, self-renewal of stem cells, and
prostate
cancer metastasis.
To characterize the functional status of the PcG pathway in
metastatic prostate
cancer, we utilized advanced cell- and whole animal-imaging technologies, gene and protein expression profiling, stable siRNA-gene targeting, and tissue microarray (TMA) analysis in relevant experimental and clinical settings.
We demonstrate that in multiple experimental models
of metastatic prostate
cancer both BMI1 and Ezh2 genes are amplified and gene amplification is associated with increased expression of corresponding mRNAs and proteins.
For the first time, we provide images of human
prostate
carcinoma metastasis precursor cells isolated from blood and shown to overexpress both BMI1 and Ezh2 oncoproteins.
Consistent with the PcG pathway activation hypothesis, increased BMI1 and Ezh2 expression in
metastatic
cancer cells is associated with elevated levels of H2AubiK119 and H3metK27 histones.
Quantitative immunofluorescence colocalization analysis and expression profiling experiments documented increased BMI1 and Ezh2 expression in clinical
prostate
carcinoma samples and demonstrated that high levels of BMI1 and Ezh2 expression are associated with markedly increased likelihood of therapy failure and disease relapse after radical prostatectomy.
Gene-silencing analysis reveals that activation of the PcG pathway is mechanistically linked with highly malignant behavior of human
prostate
carcinoma cells and is essential for in vivo growth and metastasis of human
prostate
cancer.
We conclude that the results of experimental and clinical analyses indicate the important biological role of the PcG pathway activation in
metastatic prostate
cancer.
Our work suggests that the PcG pathway activation is a common oncogenic event in pathogenesis
of metastatic
solid tumors and provides justification for development of small molecule inhibitors of the PcG chromatin silencing pathway as a novel therapeutic modality for treatment
of metastatic prostate
cancer.
[MeSH-major]
Adenocarcinoma
/ metabolism. Chromatin Assembly and Disassembly. Gene Silencing. Neoplastic Cells, Circulating / metabolism.
Prostatic
Neoplasms / metabolism. Repressor Proteins / biosynthesis
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic 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 = 16963837.001).
[ISSN]
1551-4005
[Journal-full-title]
Cell cycle (Georgetown, Tex.)
[ISO-abbreviation]
Cell Cycle
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / 5R01 CA89827
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / BMI1 protein, human; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Polycomb-Group Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Repressor Proteins; 0 / Transcription Factors; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Polycomb Repressive Complex 2; EC 6.3.2.19 / Polycomb Repressive Complex 1
43.
Chen HL, Chang WH, Shih SC, Pang KK, Bair MJ:
Trismus and trigeminal neuralgia in one patient with colon cancer.
J Natl Med Assoc
; 2008 Jun;100(6):740-2
[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.
Metastatic
tumors to the oral cavity are relatively uncommon.
They are found most commonly in the mandible, and 70% of cases are
adenocarcinoma
-most commonly from breast and lung, followed by adrenals, kidneys,
prostate
, thyroid and colon.
[MeSH-major]
Adenocarcinoma
/ secondary. Colonic Neoplasms / pathology. Mandibular Neoplasms / secondary. Trigeminal Neuralgia / etiology. Trismus / etiology
Genetic Alliance.
consumer health - Trigeminal neuralgia
.
MedlinePlus Health Information.
consumer health - Trigeminal Neuralgia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18595580.001).
[ISSN]
1943-4693
[Journal-full-title]
Journal of the National Medical Association
[ISO-abbreviation]
J Natl Med Assoc
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
44.
Senzer N, Arsenau J, Richards D, Berman B, MacDonald JR, Smith S:
Irofulven demonstrates clinical activity against metastatic hormone-refractory prostate cancer in a phase 2 single-agent trial.
Am J Clin Oncol
; 2005 Feb;28(1):36-42
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Irofulven demonstrates clinical activity against
metastatic
hormone-refractory
prostate
cancer in a phase 2 single-agent trial.
BACKGROUND: The primary objective of this study was to assess the antitumor activity of irofulven in patients with hormone-refractory
prostate
cancer by measuring a sustained decrease of 50% or greater in serum
prostate
-specific antigen (PSA) levels.
Eligible patients had pathologically confirmed
metastatic
hormone-refractory
adenocarcinoma of the prostate
and had not received prior cytotoxic chemotherapy.
CONCLUSION: Irofulven shows activity in hormone-refractory
prostate
cancer and has an acceptable safety profile, warranting further investigation of this drug, particularly in combination therapies.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Antineoplastic Agents, Alkylating / therapeutic use.
Prostatic
Neoplasms / drug therapy. Sesquiterpenes / therapeutic use
[MeSH-minor]
Aged. Aged, 80 and over. Humans. Male. Middle Aged.
Prostate
-Specific Antigen / blood. Survival Analysis
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 = 15685033.001).
[ISSN]
1537-453X
[Journal-full-title]
American journal of clinical oncology
[ISO-abbreviation]
Am. J. Clin. Oncol.
[Language]
eng
[Publication-type]
Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Alkylating; 0 / Sesquiterpenes; 6B799IH05A / irofulven; EC 3.4.21.77 / Prostate-Specific Antigen
45.
Narayanan BA, Narayanan NK, Pttman B, Reddy BS:
Adenocarcina of the mouse prostate growth inhibition by celecoxib: downregulation of transcription factors involved in COX-2 inhibition.
Prostate
; 2006 Feb 15;66(3):257-65
[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]
Adenocarcina of the mouse
prostate
growth inhibition by celecoxib: downregulation of transcription factors involved in COX-2 inhibition.
BACKGROUND: Epidemiological studies have shown a decreased risk
of prostate
cancer among men who regularly take aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs).
In this study, we examined a dose-dependent effect of a cyclooxygenase-2 (COX-2) inhibitor, celecoxib against transgenic
adenocarcinoma of
the mouse
prostate
.
METHODS: Efficacy of four different doses in parts per million of celecoxib, such as 200 ppm, 400 ppm, 600 ppm, and 1,000 ppm representing very low, moderate, and high doses, respectively were tested against
adenocarcinoma of
the mouse
prostate
using a transgenic
adenocarcinoma of
the mouse
prostate
(TRAMP) model assay.
RESULTS: Dietary supplement of celecoxib at doses of 400 ppm, 600 ppm, and 1,000 ppm are most effective against mPIN (mouse
prostatic
intraepithelial neoplasia) and
adenocarcinoma of the prostate
.
At 1,000 ppm, a complete inhibition of the PIN lesions was extended to limit the growth
of adenocarcinoma
(from 85% to 15%) and metastasis of the mouse
prostate
.
CONCLUSIONS: Dietary supplementation of celecoxib at different doses provides evidence for the suppression
of prostate adenocarcinoma
tumor growth in a dose-dependent manner.
Suppression
of adenocarcinoma
by celecoxib further limits the growth
of metastatic prostate
cancer.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Cyclooxygenase 2 / metabolism. Cyclooxygenase Inhibitors / pharmacology.
Prostatic
Intraepithelial Neoplasia / drug therapy.
Prostatic
Neoplasms / drug therapy. Pyrazoles / pharmacology. Sulfonamides / pharmacology. Transcription Factor RelA / antagonists & inhibitors
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
CELECOXIB
.
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
[Copyright]
Copyright (c) 2005 Wiley-Liss, Inc.
(PMID = 16175586.001).
[ISSN]
0270-4137
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA107813-01
[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 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; 0 / Transcription Factor RelA; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib
46.
Higano CS, Corman JM, Smith DC, Centeno AS, Steidle CP, Gittleman M, Simons JW, Sacks N, Aimi J, Small EJ:
Phase 1/2 dose-escalation study of a GM-CSF-secreting, allogeneic, cellular immunotherapy for metastatic hormone-refractory prostate cancer.
Cancer
; 2008 Sep 1;113(5):975-84
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Phase 1/2 dose-escalation study of a GM-CSF-secreting, allogeneic, cellular immunotherapy for
metastatic
hormone-refractory
prostate
cancer.
BACKGROUND: This open-label, multicenter, dose-escalation study evaluated multiple dose levels of immunotherapy in patients with
metastatic
hormone-refractory
prostate
cancer (HRPC).
The immunotherapy, based on the GVAX platform, consisted of 2 allogeneic
prostate
-carcinoma cell lines modified to secrete granulocyte-macrophage-colony-stimulating factor (GM-CSF).
Endpoints included safety, immunogenicity, overall survival, radiologic response,
prostate
-specific antigen (PSA) kinetics, and serum GM-CSF pharmacokinetics.
Two phase 3 trials in patients with
metastatic
HRPC are underway.
[MeSH-major]
Adenocarcinoma
/ therapy. Cancer Vaccines / therapeutic use. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Immunotherapy / methods.
Prostatic
Neoplasms / therapy
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
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
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
(c) 2008 American Cancer Society.
(PMID = 18646045.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
47.
Whang PG, Schwarz EM, Gamradt SC, Dougall WC, Lieberman JR:
The effects of RANK blockade and osteoclast depletion in a model of pure osteoblastic prostate cancer metastasis in bone.
J Orthop Res
; 2005 Nov;23(6):1475-83
[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]
The effects of RANK blockade and osteoclast depletion in a model of pure osteoblastic
prostate
cancer metastasis in bone.
Adenocarcinoma of the prostate
exhibits a clear propensity for bone and is associated with the formation of osteoblastic metastases.
Here we investigate the effects of complete in vivo osteoclast depletion via the blockade of receptor activator of NF:kappaB (RANK) on the establishment and progression of purely osteoblastic (LAPC-9 cells) bone lesions induced by human
prostate
cancer cells using a SCID mouse intratibial injection model.
These results indicate that in vivo RANK blockade may not be effective for the prevention of osteoblastic metastasis but may potentially represent a novel therapy that limits the growth of established
metastatic
CaP lesions in bone.
[MeSH-major]
Bone Neoplasms / pathology. Bone Neoplasms / secondary. Glycoproteins / antagonists & inhibitors. Osteoblasts / pathology. Osteoclasts / physiology.
Prostatic
Neoplasms / pathology. Receptors, Cytoplasmic and Nuclear / antagonists & inhibitors. Receptors, Tumor Necrosis Factor / antagonists & inhibitors. Recombinant Fusion Proteins / therapeutic use
MedlinePlus Health Information.
consumer health - Bone 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 = 16005175.001).
[ISSN]
0736-0266
[Journal-full-title]
Journal of orthopaedic research : official publication of the Orthopaedic Research Society
[ISO-abbreviation]
J. Orthop. Res.
[Language]
eng
[Grant]
United States / NIAMS NIH HHS / AR / R01 AR46789-01A1
[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 / Glycoproteins; 0 / Immunoglobulin Fc Fragments; 0 / Osteoprotegerin; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Fusion Proteins; 0 / TNFRSF11B protein, human; 0 / Tnfrsf11b protein, mouse
48.
You YN, Wolff BG, Boardman LA, Riegert-Johnson DL, Qin R:
Peutz-Jeghers syndrome: a study of long-term surgical morbidity and causes of mortality.
Fam Cancer
; 2010 Dec;9(4):609-16
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Two malignancies were found intra-operatively (duodenal and rectal
adenocarcinoma
).
Twenty-one additional cancers were treated in 19 patients: gynecologic (11), lung (3), and
prostate
(2) being the most common.
The cause of death was unknown in 4 patients, but was due exclusively to malignancies in all other patients, most commonly due to
metastatic
gynecologic cancer (5).
Genetic Alliance.
consumer health - Peutz Jeghers syndrome
.
MedlinePlus Health Information.
consumer health - Cancer in Children
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Clin Cancer Res. 2008 Feb 15;14(4):1167-71
[
18281551.001
]
[Cites]
Gut. 2002 Oct;51 Suppl 5:V21-7
[
12221036.001
]
[Cites]
Arch Surg. 1969 Apr;98(4):509-17
[
4887290.001
]
[Cites]
J R Soc Med. 2003 Oct;96(10):505-6
[
14519733.001
]
[Cites]
Ann Intern Med. 1998 Jun 1;128(11):896-9
[
9634427.001
]
[Cites]
Gastrointest Endosc. 2000 Oct;52(4):552-4
[
11023581.001
]
[Cites]
Gut. 1989 Nov;30(11):1588-90
[
2599445.001
]
[Cites]
Colorectal Dis. 2004 Sep;6(5):332-5
[
15335366.001
]
[Cites]
Clin Gastroenterol Hepatol. 2006 Apr;4(4):408-15
[
16616343.001
]
[Cites]
Clin Cancer Res. 2006 May 15;12(10):3209-15
[
16707622.001
]
[Cites]
Cancer. 1982 Mar 1;49(5):971-83
[
7059931.001
]
[Cites]
J Laparoendosc Adv Surg Tech A. 2007 Feb;17(1):140-2
[
17362193.001
]
[Cites]
N Engl J Med. 1987 Jun 11;316(24):1511-4
[
3587280.001
]
[Cites]
Surg Laparosc Endosc. 1998 Feb;8(1):17-20
[
9488564.001
]
[Cites]
Br J Surg. 1990 Mar;77(3):301-2
[
2322793.001
]
[Cites]
Arch Surg. 1981 Sep;116(9):1182-4
[
7283716.001
]
[Cites]
J Pediatr Gastroenterol Nutr. 2004 Aug;39(2):219-20
[
15269641.001
]
[Cites]
Clin Cancer Res. 2003 Aug 1;9(8):3065-72
[
12912958.001
]
[Cites]
Surg Laparosc Endosc Percutan Tech. 2003 Aug;13(4):280-2
[
12960794.001
]
[Cites]
Can J Surg. 1994 Jun;37(3):231-6
[
8199943.001
]
[Cites]
Br J Surg. 1995 Oct;82(10):1311-4
[
7489151.001
]
[Cites]
Dig Dis Sci. 1983 Nov;28(11):1047-51
[
6628153.001
]
[Cites]
Fam Cancer. 2001;1(2):121-5
[
14574008.001
]
[Cites]
Am Surg. 1990 May;56(5):331-3
[
2334077.001
]
[Cites]
Surg Endosc. 2000 Dec;14(12):1185-7
[
11148795.001
]
[Cites]
Physiol Rev. 2009 Jul;89(3):777-98
[
19584313.001
]
[Cites]
J Med Genet. 2005 May;42(5):428-35
[
15863673.001
]
[Cites]
Am J Surg Pathol. 1987 Oct;11(10):743-9
[
3661821.001
]
[Cites]
Hum Mutat. 2005 Oct;26(4):291-7
[
16110486.001
]
[Cites]
Gut. 2007 Oct;56(10):1475-6
[
17872577.001
]
[Cites]
Dis Colon Rectum. 2003 Jan;46(1):48-50
[
12544521.001
]
[Cites]
Gastroenterology. 2000 Dec;119(6):1447-53
[
11113065.001
]
[Cites]
Int J Colorectal Dis. 1994;9(4):177-9
[
7876718.001
]
(PMID = 20571886.001).
[ISSN]
1573-7292
[Journal-full-title]
Familial cancer
[ISO-abbreviation]
Fam. Cancer
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
Netherlands
49.
Pallini R, Sabatino G, Doglietto F, Lauretti L, Fernandez E, Maira G:
Clivus metastases: report of seven patients and literature review.
Acta Neurochir (Wien)
; 2009 Apr;151(4):291-6; discussion 296
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
The primary tumours associated were lung
adenocarcinoma
(n = 2),
prostate
carcinoma (n = 2), skin melanoma (n = 1), hepatocarcinoma (n = 1) and lung squamous cell carcinoma (n = 1).
Including our series, the most common primary tumours were
prostate
cancer (26.4%), thyroid carcinoma (11.7%) and hepatocarcinoma (11.7%).
The metastatic
lesion might be a late and single expression of the primary tumour.
[MeSH-minor]
Abducens Nerve Diseases / etiology. Adult. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Liver Neoplasms / pathology. Lung Neoplasms / pathology. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Metastasis. Prognosis.
Prostatic
Neoplasms / pathology. Skin Neoplasms / pathology. Survival Rate. Tomography, X-Ray Computed
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19259614.001).
[ISSN]
0942-0940
[Journal-full-title]
Acta neurochirurgica
[ISO-abbreviation]
Acta Neurochir (Wien)
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Austria
[Number-of-references]
30
50.
Kasper S:
Survey of genetically engineered mouse models for prostate cancer: analyzing the molecular basis of prostate cancer development, progression, and metastasis.
J Cell Biochem
; 2005 Feb 1;94(2):279-97
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Survey of genetically engineered mouse models for
prostate
cancer: analyzing the molecular basis
of prostate
cancer development, progression, and metastasis.
Genetically engineered mouse models have been generated to study the molecular basis
of prostate
cancer (PCa) development, progression, and metastasis.
Selection of a
prostate
-specific promoter, such as the probasin (PB) and
prostate
specific antigen (PSA) promoters, is critical for generating sufficient levels of transgene expression to elicit a phenotypic response.
Furthermore, the effects of gene disruption on promoting low- and high-grade intraepithelial neoplasia (LGPIN and HGPIN, respectively), locally invasive carcinoma and
metastatic
lesions will be discussed.
To date, the PB-Cre4 x PTENloxp/loxp model appears to be the only model that represents the entire continuum
of prostate adenocarcinoma
development, tumor progression, and metastasis, although models that develop
prostatic
neuroendocrine (NE) cancer can be generated by disrupting one genetic event.
Indeed, analysis of bigenic mouse models indicates that two genetic events are generally required for progression from HGPIN to locally invasive
adenocarcinoma
and that two to five genetic events can promote metastasis to distant sites.
[MeSH-major]
Adenocarcinoma
/ secondary. Disease Models, Animal. Mice, Transgenic.
Prostatic
Neoplasms / genetics.
Prostatic
Neoplasms / pathology
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
2004 Wiley-Liss, Inc.
(PMID = 15565647.001).
[ISSN]
0730-2312
[Journal-full-title]
Journal of cellular biochemistry
[ISO-abbreviation]
J. Cell. Biochem.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
110
51.
Hainsworth JD, Meluch AA, Spigel DR, Barton J Jr, Simons L, Meng C, Gould B, Greco FA:
Weekly docetaxel and bortezomib as first-line treatment for patients with hormone-refractory prostate cancer: a Minnie Pearl Cancer Research Network phase II trial.
Clin Genitourin Cancer
; 2007 Mar;5(4):278-83
[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]
Weekly docetaxel and bortezomib as first-line treatment for patients with hormone-refractory
prostate
cancer: a Minnie Pearl Cancer Research Network phase II trial.
BACKGROUND: Docetaxel is currently the standard first-line treatment in patients with hormone-refractory
prostate
cancer (HRPC).
Bortezomib, the first proteasome inhibitor in clinical use, demonstrated activity against
prostate
cancer in phase I trials.
All patients had
metastatic adenocarcinoma
of the
prostate
that had progressed on hormonal therapy.
Fifteen patients (25%; 95% confidence interval, 15%-38%) had a > 50% decrease in serum
prostate
-specific antigen level with treatment; the median response duration was 8 months.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Antineoplastic Agents / administration & dosage. Boronic Acids / administration & dosage.
Prostatic
Neoplasms / drug therapy. Pyrazines / administration & dosage. Taxoids / administration & dosage
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
Hazardous Substances Data Bank.
DOCETAXEL
.
Hazardous Substances Data Bank.
BORTEZOMIB
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17553208.001).
[ISSN]
1558-7673
[Journal-full-title]
Clinical genitourinary cancer
[ISO-abbreviation]
Clin Genitourin Cancer
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgens; 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Pyrazines; 0 / Taxoids; 15H5577CQD / docetaxel; 69G8BD63PP / Bortezomib
52.
Hu SY, Liu T, Liu ZZ, Ledet E, Velasco-Gonzalez C, Mandal DM, Koochekpour S:
Identification of a novel germline missense mutation of the androgen receptor in African American men with familial prostate cancer.
Asian J Androl
; 2010 May;12(3):336-43
[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 a novel germline missense mutation of the androgen receptor in African American men with familial
prostate
cancer.
Race, family history and age are the unequivocally accepted risk factors for
prostate
cancer (PCa).
Androgen receptor (AR)-dependent signaling is an important element in
prostate
carcinogenesis and its progression to
metastatic
disease.
Genetic Alliance.
consumer health - Familial Prostate Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Epidemiol Biomarkers Prev. 2004 Nov;13(11 Pt 1):1765-71
[
15533905.001
]
[Cites]
Am J Hum Genet. 1999 Mar;64(3):776-87
[
10053012.001
]
[Cites]
BJU Int. 2005 Dec;96(9):1380-5
[
16287462.001
]
[Cites]
J Urol. 2007 Feb;177(2):444-9
[
17222606.001
]
[Cites]
Asian J Androl. 2007 Mar;9(2):147-79
[
17334586.001
]
[Cites]
Carcinogenesis. 2007 May;28(5):1032-9
[
17151093.001
]
[Cites]
Prostate Cancer Prostatic Dis. 2008;11(3):274-9
[
18268528.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2008 Sep;17(9):2451-7
[
18768516.001
]
[Cites]
Br J Cancer. 2008 Nov 18;99(10):1743-7
[
18827812.001
]
[Cites]
Br J Cancer. 1999 Oct;81(4):672-6
[
10574254.001
]
[Cites]
Eur J Cancer. 1999 Aug;35(8):1248-57
[
10615237.001
]
[Cites]
Am J Hum Genet. 2000 Mar;66(3):1161-7
[
10712229.001
]
[Cites]
Cancer Res. 2000 Nov 15;60(22):6479-81
[
11103816.001
]
[Cites]
J Urol. 2003 Sep;170(3):990-3
[
12913756.001
]
[Cites]
J Urol. 2004 Jan;171(1):431-3
[
14665948.001
]
[Cites]
Endocr Rev. 2004 Apr;25(2):276-308
[
15082523.001
]
[Cites]
Hum Mutat. 2004 Jun;23(6):527-33
[
15146455.001
]
[Cites]
Proc Natl Acad Sci U S A. 1989 Dec;86(23):9534-8
[
2594783.001
]
[Cites]
Am J Hum Genet. 1991 Jan;48(1):22-5
[
1985459.001
]
[Cites]
Nat Genet. 1995 Jun;10(2):224-8
[
7663520.001
]
[Cites]
Cancer Res. 1995 Sep 15;55(18):3973-5
[
7664265.001
]
[Cites]
Prostate. 1996 Mar;28(3):162-71
[
8628719.001
]
[Cites]
Science. 1996 Nov 22;274(5291):1371-4
[
8910276.001
]
[Cites]
J Clin Endocrinol Metab. 1996 Dec;81(12):4400-5
[
8954049.001
]
[Cites]
J Natl Cancer Inst. 1997 Jan 15;89(2):109-11
[
8998174.001
]
[Cites]
J Natl Cancer Inst. 1997 Jan 15;89(2):166-70
[
8998186.001
]
[Cites]
J Urol. 1997 Oct;158(4):1599-601
[
9302181.001
]
[Cites]
Am J Hum Genet. 1998 Jun;62(6):1416-24
[
9585607.001
]
[Cites]
Am J Hum Genet. 1998 Dec;63(6):1839-51
[
9837836.001
]
[Cites]
Int J Cancer. 1999 Feb 19;84(1):19-23
[
9988226.001
]
[Cites]
Prostate. 2005 Jun 1;63(4):309-15
[
15599941.001
]
(PMID = 20173765.001).
[ISSN]
1745-7262
[Journal-full-title]
Asian journal of andrology
[ISO-abbreviation]
Asian J. Androl.
[Language]
ENG
[Grant]
United States / NCRR NIH HHS / RR / 1P20 RR021970; United States / NCI NIH HHS / CA / R21 CA149137; United States / NCI NIH HHS / CA / R21 CA120625; United States / NIMHD NIH HHS / MD / R01 MD005824-01; United States / NCI NIH HHS / CA / R21 CA149137-01; United States / NCRR NIH HHS / RR / RR021970-056085; United States / NCI NIH HHS / CA / CA120625-01; United States / NIMHD NIH HHS / MD / R01 MD005824; United States / NCRR NIH HHS / RR / P20 RR021970; United States / NCI NIH HHS / CA / R03 CA097778; United States / NIMHD NIH HHS / MD / MD005824-01; United States / NCI NIH HHS / CA / 1 R03 CA97778-01; United States / NCRR NIH HHS / RR / P20 RR021970-056085; United States / NCI NIH HHS / CA / R21 CA143589; United States / NCI NIH HHS / CA / CA149137-01; United States / NCI NIH HHS / CA / R21 CA120625-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Receptors, Androgen
[Other-IDs]
NLM/ NIHMS224601; NLM/ PMC3008322
53.
Morris MJ, Pandit-Taskar N, Carrasquillo J, Divgi CR, Slovin S, Kelly WK, Rathkopf D, Gignac GA, Solit D, Schwartz L, Stephenson RD, Hong C, Delacruz A, Curley T, Heller G, Jia X, O'Donoghue J, Larson S, Scher HI:
Phase I study of samarium-153 lexidronam with docetaxel in castration-resistant metastatic prostate cancer.
J Clin Oncol
; 2009 May 20;27(15):2436-42
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Phase I study of samarium-153 lexidronam with docetaxel in castration-resistant
metastatic prostate
cancer.
PURPOSE: Early studies of patients with castration-resistant
metastatic prostate
cancer (CRMPC) suggest that chemotherapy administered with a dose of a bone-seeking radiopharmaceutical is superior to chemotherapy alone.
Fifteen patients demonstrated a more than 50% decline in
prostate
-specific antigen.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Prostatic
Neoplasms / drug therapy
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Analgesics, Non-Narcotic / administration & dosage. Analgesics, Non-Narcotic / adverse effects. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Bone and Bones / drug effects. Drug Resistance, Neoplasm. Humans. Male. Maximum Tolerated Dose. Middle Aged. Organometallic Compounds / administration & dosage. Organometallic Compounds / adverse effects. Organophosphorus Compounds / administration & dosage. Organophosphorus Compounds / adverse effects.
Prostate
-Specific Antigen / blood.
Prostate
-Specific Antigen / drug effects. Radiopharmaceuticals / administration & dosage. Radiopharmaceuticals / adverse effects. Taxoids / administration & dosage. Taxoids / adverse effects
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
DOCETAXEL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Natl Cancer Inst. 2000 Feb 2;92(3):205-16
[
10655437.001
]
[Cites]
Lancet. 2001 Feb 3;357(9253):336-41
[
11210994.001
]
[Cites]
Int J Cancer. 2004 Sep 20;111(5):783-91
[
15252851.001
]
[Cites]
N Engl J Med. 2004 Oct 7;351(15):1502-12
[
15470213.001
]
[Cites]
N Engl J Med. 2004 Oct 7;351(15):1513-20
[
15470214.001
]
[Cites]
J Clin Oncol. 2005 Aug 1;23(22):4925-35
[
15983391.001
]
[Cites]
Clin Cancer Res. 2006 Jun 1;12(11 Pt 1):3361-7
[
16740758.001
]
[Cites]
Cancer. 2007 Feb 1;109(3):637-43
[
17167764.001
]
[Cites]
J Clin Oncol. 2008 Mar 1;26(7):1148-59
[
18309951.001
]
[Cites]
Clin Genitourin Cancer. 2008 Mar;6(1):40-5
[
18501082.001
]
[CommentIn]
J Clin Oncol. 2009 May 20;27(15):2417-8
[
19364953.001
]
[ErratumIn]
J Clin Oncol. 2011 Oct 10;29(29):3947-8
(PMID = 19364960.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / K23 CA102544; United States / NCI NIH HHS / CA / CA102544
[Publication-type]
Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Analgesics, Non-Narcotic; 0 / Organometallic Compounds; 0 / Organophosphorus Compounds; 0 / Radiopharmaceuticals; 0 / Taxoids; 15H5577CQD / docetaxel; 745X144DZY / samarium Sm-153 lexidronam; EC 3.4.21.77 / Prostate-Specific Antigen
[Other-IDs]
NLM/ PMC2684850
54.
Morey SR, Smiraglia DJ, James SR, Yu J, Moser MT, Foster BA, Karpf AR:
DNA methylation pathway alterations in an autochthonous murine model of prostate cancer.
Cancer Res
; 2006 Dec 15;66(24):11659-67
[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]
DNA methylation pathway alterations in an autochthonous murine model
of prostate
cancer.
We examined the DNA methylation pathway in an autochthonous murine
prostate
cancer model, transgenic
adenocarcinoma of
mouse
prostate
(TRAMP).
We observed that, compared with strain-matched normal prostates, primary and
metastatic
TRAMP tumors display increased cytosine DNA methyltransferase (Dnmt) activity, Dnmt1 and Dnmt3b protein expression, and Dnmt1, Dnmt3a, and Dnmt3b mRNA expression.
In summary, our data reveal a systemic DNA methylation pathway defect in TRAMP reminiscent of human
prostate
cancer, supporting the use of this model to investigate the functional role of DNA methylation pathway alterations in
prostate
cancer development.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17178860.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / 5T32CA009072-31; United States / NCI NIH HHS / CA / R21 CA128062-01; United States / NCI NIH HHS / CA / R21 CA121216; United States / NCI NIH HHS / CA / P30 CA016056; United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / R21 CA128062; United States / NCI NIH HHS / CA / CA128062-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA Primers; 0 / Neoplasm Proteins; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase
55.
Kundranda MN, Muslimani A, Daw HA, Spiro TP:
Complete remission of metastatic carcinoma of the prostate with bicalutamide withdrawal.
Clin Genitourin Cancer
; 2007 Sep;5(6):401-2
[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]
Complete remission
of metastatic
carcinoma of the
prostate
with bicalutamide withdrawal.
An 83-year-old man was diagnosed with stage 4
prostate
cancer with a Gleason score of 7 (3+4).
His initial
prostate
-specific antigen (PSA) level was 965 ng/dL, and he demonstrated extensive
metastatic
disease of the thoracic spine.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Androgen Antagonists / administration & dosage. Anilides / administration & dosage. Nitriles / administration & dosage.
Prostatic
Neoplasms / drug therapy. Tosyl Compounds / administration & dosage
[MeSH-minor]
Aged. Aged, 80 and over. Humans. Male.
Prostate
-Specific Antigen / blood. Remission Induction. Retrospective Studies
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
BICALUTAMIDE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17956714.001).
[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]
0 / Androgen Antagonists; 0 / Anilides; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide; EC 3.4.21.77 / Prostate-Specific Antigen
56.
Hizli F, Berkmen F:
Penile metastasis from other malignancies. A study of ten cases and review of the literature.
Urol Int
; 2006;76(2):118-21
[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.
Furthermore, isolated
metastatic
penile carcinomas are exceptionally rare.
The rarity of the event prompted this study, which describes 10 cases
of metastatic
tumors of the penis including 7 cases with transitional cell carcinoma of the bladder, and in 1 case each of squamous cell carcinoma of the lung,
adenocarcinoma of the prostate
and leukemia.
Genetic Alliance.
consumer health - TEN
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16493210.001).
[ISSN]
0042-1138
[Journal-full-title]
Urologia internationalis
[ISO-abbreviation]
Urol. Int.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Switzerland
[Number-of-references]
26
57.
Ide H, Hatake K, Terado Y, Tsukino H, Okegawa T, Nutahara K, Higashihara E, Horie S:
Serum level of macrophage colony-stimulating factor is increased in prostate cancer patients with bone metastasis.
Hum Cell
; 2008 Feb;21(1):1-6
[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]
Serum level of macrophage colony-stimulating factor is increased in
prostate
cancer patients with bone metastasis.
Recent evaluation of human
prostate
tissues has shown predominantly high expression of the macrophage colony-stimulating factor receptor in
prostatic
intra-epithelial neoplasia or
prostate
cancer.
However, the expression of its ligand, the macrophage colony-stimulating factor (M-CSF), and the biological role of this signaling in
prostate
cancer has not been analyzed.
In this research we determined the relationship of serum M-CSF level to clinical parameters
of prostate
cancer progression.
We measured the serum level of M-CSF in 170 patients with histologically confirmed
prostatic
adenocarcinoma
and in 54 patients in whom
prostate
cancer was not detected.
We also investigated the M-CSF expression in
prostate
cancer tissues by immunohistochemistry.
The serum levels of M-CSF in bone
metastatic prostate
cancer patients was significantly higher than those in non-
metastatic
patients, while M-CSF did not differ with regards to histological grade, Gleason score or local tumor progression.
M-CSF expression was detected in
prostate
cancer cells themselves by immunohistochemistry.
These results suggest that M-CSF may have a functional role in
prostate
cancer progression.
[MeSH-major]
Adenocarcinoma
/ secondary. Bone Neoplasms / secondary. Macrophage Colony-Stimulating Factor / blood. Macrophage Colony-Stimulating Factor / physiology.
Prostatic
Neoplasms / etiology.
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
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Proc Natl Acad Sci U S A. 1989 Oct;86(20):7924-7
[
2554296.001
]
[Cites]
Prostate. 1998 Feb 1;34(2):80-91
[
9465939.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14404-9
[
12381783.001
]
[Cites]
Blood. 2001 Jul 1;98(1):74-84
[
11418465.001
]
[Cites]
Biochem Biophys Res Commun. 1985 Oct 30;132(2):548-54
[
3904752.001
]
[Cites]
Mol Reprod Dev. 1997 Jan;46(1):75-83; discussion 83-4
[
8981367.001
]
[Cites]
Clin Chem Lab Med. 2002 Apr;40(4):351-5
[
12059074.001
]
[Cites]
Am J Med. 1987 Feb 23;82(2A):6-28
[
3548343.001
]
[Cites]
Br J Cancer. 1999 Jan;79(1):40-6
[
10408691.001
]
[Cites]
Cancer Metastasis Rev. 1998-1999;17(4):443-7
[
10453289.001
]
[Cites]
Nature. 1990 May 31;345(6274):442-4
[
2188141.001
]
[Cites]
Curr Top Microbiol Immunol. 1992;181:141-67
[
1424779.001
]
[Cites]
Cancer Res. 2004 Aug 1;64(15):5378-84
[
15289345.001
]
[Cites]
Proc Soc Exp Biol Med. 1999 Jan;220(1):1-8
[
9893162.001
]
[Cites]
Neoplasma. 2004;51(5):375-8
[
15640942.001
]
[Cites]
Am J Obstet Gynecol. 1995 Jul;173(1):112-9
[
7631667.001
]
[Cites]
Eur Cytokine Netw. 2002 Jan-Mar;13(1):121-7
[
11956031.001
]
[Cites]
Mol Reprod Dev. 1997 Jan;46(1):54-60; discussion 60-1
[
8981364.001
]
[Cites]
Mol Reprod Dev. 1997 Jan;46(1):71-4
[
8981366.001
]
[Cites]
Cell. 1985 Jul;41(3):665-76
[
2408759.001
]
[Cites]
Prostate. 2000 Feb 1;42(2):150-60
[
10617873.001
]
[Cites]
J Soc Gynecol Investig. 1999 Jan-Feb;6(1):41-9
[
10065425.001
]
[Cites]
EMBO J. 1987 Aug;6(8):2261-5
[
3499313.001
]
[Cites]
Br J Haematol. 1999 Jun;105(3):613-5
[
10354120.001
]
[Cites]
J Exp Med. 2001 Mar 19;193(6):727-40
[
11257139.001
]
[Cites]
Prostate. 2004 Jun 15;60(1):1-17
[
15129424.001
]
(PMID = 18190394.001).
[ISSN]
0914-7470
[Journal-full-title]
Human cell
[ISO-abbreviation]
Hum. Cell
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Biomarkers, Tumor; 81627-83-0 / Macrophage Colony-Stimulating Factor
58.
Wang SQ, Mecca PS, Myskowski PL, Slovin SF:
Scrotal and penile papules and plaques as the initial manifestation of a cutaneous metastasis of adenocarcinoma of the prostate: case report and review of the literature.
J Cutan Pathol
; 2008 Jul;35(7):681-4
[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]
Scrotal and penile papules and plaques as the initial manifestation of a cutaneous metastasis
of adenocarcinoma
of the
prostate
: case report and review of the literature.
Cutaneous metastasis of
prostatic
adenocarcinoma
is a rare phenomenon.
We present a 56-year-old African American man with
metastatic
disease in the skin and subcutis of the suprapubic and scrotal area 2 years after his initial diagnosis presenting as scrotal and penile edema and plaque like scrotal rash.
[MeSH-major]
Adenocarcinoma
/ secondary. Genital Neoplasms, Male / secondary. Lymphedema / etiology. Penis / pathology.
Prostatic
Neoplasms / pathology. Scrotum / pathology. Skin Neoplasms / secondary
MedlinePlus Health Information.
consumer health - Lymphedema
.
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 = 18201228.001).
[ISSN]
1600-0560
[Journal-full-title]
Journal of cutaneous pathology
[ISO-abbreviation]
J. Cutan. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Biomarkers, Tumor
[Number-of-references]
45
59.
Adley BP, Maxwell K, Dalton DP, Yang XJ:
Urothelial-type adenocarcinoma of the prostate mimicking metastatic colorectal adenocarcinoma.
Int Braz J Urol
; 2006 Nov-Dec;32(6):681-7; discussion 687-8
[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]
Urothelial-type
adenocarcinoma of the prostate
mimicking
metastatic
colorectal
adenocarcinoma
.
Adenocarcinoma
arising in urinary bladder or
prostatic
urethra is uncommon.
When they occur, the tumor can be mistaken for
metastatic
lesions, especially from the colon.
Here we report the fifth case of a primary urothelial-type
adenocarcinoma
arising in
the prostate
which showed enteric differentiation.
The patient was a 55 year-old male whose
prostatic
needle core biopsy showed a high grade
adenocarcinoma
which was initially thought to be
metastatic
colon cancer.
Subsequent prostatectomy revealed a high grade
adenocarcinoma
which was positive for cytokeratins 7 and 20, carcinoembryonic antigen, CDX2, and high molecular weight cytokeratin, and negative for
prostate
specific antigen,
prostate
specific acid phosphatase and AMACR.
A diagnosis of urothelial-type
adenocarcinoma of the prostate
was rendered.
[MeSH-major]
Adenocarcinoma
, Mucinous / pathology. Colorectal Neoplasms / pathology.
Prostatic
Neoplasms / pathology
MedlinePlus Health Information.
consumer health - Colorectal 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
(PMID = 17201946.001).
[ISSN]
1677-5538
[Journal-full-title]
International braz j urol : official journal of the Brazilian Society of Urology
[ISO-abbreviation]
Int Braz J Urol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Brazil
60.
Sonpavde G, Hutson TE, Berry WR, Boehm KA, Asmar L:
Phase II trial of sunitinib for the therapy of progressive metastatic castration-refractory prostate cancer after previous docetaxel chemotherapy.
Clin Genitourin Cancer
; 2008 Sep;6(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]
Phase II trial of sunitinib for the therapy of progressive
metastatic
castration-refractory
prostate
cancer after previous docetaxel chemotherapy.
Effective options are lacking for progressive castration-refractory
prostate
cancer (CRPC) after conventional chemotherapy.
A phase II trial was conducted to examine the efficacy and toxicities of sunitinib in
metastatic
CRPC progressing after 1-2 previous chemotherapy regimens including docetaxel.
Secondary objectives included
prostate
-specific antigen (PSA) response, modulation of PSA kinetics, objective response, quality of life, pain, survival, and toxicities.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Antineoplastic Agents / therapeutic use. Indoles / therapeutic use.
Prostatic
Neoplasms / drug therapy. Pyrroles / therapeutic use
[MeSH-minor]
Androgen Antagonists / therapeutic use. Castration. Disease-Free Survival. Humans. Male. Neoplasm Metastasis.
Prostate
-Specific Antigen / analysis. Quality of Life
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
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 = 18824440.001).
[ISSN]
1558-7673
[Journal-full-title]
Clinical genitourinary cancer
[ISO-abbreviation]
Clin Genitourin Cancer
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgen Antagonists; 0 / Antineoplastic Agents; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib; EC 3.4.21.77 / Prostate-Specific Antigen
61.
Gasco J, Kew Y, Livingston A, Rose J, Zhang YJ:
Dissemination of prostate adenocarcinoma to the skull base mimicking giant trigeminal schwannoma: anatomic relevance of the extradural neural axis component.
Skull Base
; 2009 Nov;19(6):425-30
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Dissemination
of prostate adenocarcinoma
to the skull base mimicking giant trigeminal schwannoma: anatomic relevance of the extradural neural axis component.
We report an unusual case of a large
metastatic
lesion from
prostate adenocarcinoma
with its epicenter located in Meckel's cave.
The anatomic relevance the extradural neural axis component in the process of dissemination
of prostate adenocarcinoma
to the skull base is highlighted.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
MedGenMed. 2006;8(1):53
[
16915183.001
]
[Cites]
Cancer. 1999 Dec 1;86(11):2301-11
[
10590371.001
]
[Cites]
Neurologist. 2006 Jan;12(1):48-52
[
16547447.001
]
[Cites]
Australas Radiol. 2005 Dec;49(6):497-500
[
16351616.001
]
[Cites]
J Exp Clin Cancer Res. 2005 Jun;24(2):203-7
[
16110752.001
]
[Cites]
J Neurosurg. 1953 Sep;10(5):546-9
[
13097217.001
]
[Cites]
Arq Neuropsiquiatr. 1993 Jun;51(2):251-2
[
8274090.001
]
[Cites]
Cancer. 1984 Oct 15;54(8):1723-5
[
6478410.001
]
[Cites]
Neurosurgery. 1983 Nov;13(5):584-6
[
6646385.001
]
[Cites]
Surg Neurol. 1979 Sep;12(3):253-8
[
515927.001
]
[Cites]
Prog Clin Cancer. 1967;3:1-18
[
4966305.001
]
[Cites]
Neurosurgery. 2004 Feb;54(2):492-8; discussion 498-9
[
14744296.001
]
[Cites]
Cancer. 2003 Jul 15;98(2):363-8
[
12872358.001
]
[Cites]
Am Fam Physician. 2002 May 1;65(9):1834-40
[
12018806.001
]
[Cites]
Surg Neurol. 2000 Dec;54(6):422-31
[
11240168.001
]
[Cites]
J Neurosurg. 2000 Apr;92(4):585-8
[
10761646.001
]
[Cites]
Rev Neurol. 1999 Nov 16-30;29(10):929-32
[
10637842.001
]
[Cites]
Neurol Neurochir Pol. 2006 May-Jun;40(3):173-8
[
16794955.001
]
(PMID = 20436844.001).
[ISSN]
1532-0065
[Journal-full-title]
Skull base : official journal of North American Skull Base Society ... [et al.]
[ISO-abbreviation]
Skull Base
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2793894
[Keywords]
NOTNLM ; EDNAC / Meckel's cave / Prostate / brain metastases / schwannoma
62.
Jonsson E, Sigbjarnarson HP, Tomasson J, Benediktsdottir KR, Tryggvadottir L, Hrafnkelsson J, Olafsdottir EJ, Tulinius H, Jonasson JG:
Adenocarcinoma of the prostate in Iceland: a population-based study of stage, Gleason grade, treatment and long-term survival in males diagnosed between 1983 and 1987.
Scand J Urol Nephrol
; 2006;40(4):265-71
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Adenocarcinoma of the prostate
in Iceland: a population-based study of stage, Gleason grade, treatment and long-term survival in males diagnosed between 1983 and 1987.
OBJECTIVE: To investigate
adenocarcinoma of the prostate
in a single population with an extended follow-up period.
MATERIAL AND METHODS: Using the Icelandic Cancer Registry, we identified all Icelandic men diagnosed with
prostate
cancer between 1983 and 1987.
A critical evaluation was made of the accuracy of the death certificates regarding
prostate
cancer.
RESULTS: A total of 414 men were diagnosed with
adenocarcinoma of the prostate
.
Four stage groups were defined: focal incidental (n=50); localized (n=164); local advanced (n=32); and
metastatic
disease (n=124).
A total of 334 patients died during the follow-up period, of whom 168 (50%) died
of prostate
cancer.
Prostate
cancer-specific survival at 10 and 15 years was 100% and 90.6%, respectively for focal incidental cancer; 73.1% and 60.8% for men with localized disease; 23.4% and 11.7% for local advanced disease; and 6.81% and 5.45% for
metastatic
disease.
A Cox multivariate analysis showed age, stage and Gleason score to be independent predictors
of prostate
cancer death.
Death certificates were judged to be accurate with regard to
prostate
cancer in nearly all instances (96%).
CONCLUSIONS: During an extended follow-up period, half of all patients with
prostate
cancer died from the disease.
However, a higher stage and grade were associated with substantial
prostate
cancer mortality.
Death certificates were accurate as far as
prostate
cancer was concerned.
[MeSH-major]
Adenocarcinoma
/ pathology.
Adenocarcinoma
/ therapy.
Prostatic
Neoplasms / pathology.
Prostatic
Neoplasms / therapy
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16916765.001).
[ISSN]
0036-5599
[Journal-full-title]
Scandinavian journal of urology and nephrology
[ISO-abbreviation]
Scand. J. Urol. Nephrol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Sweden
63.
Mannweiler S, Amersdorfer P, Trajanoski S, Terrett JA, King D, Mehes G:
Heterogeneity of prostate-specific membrane antigen (PSMA) expression in prostate carcinoma with distant metastasis.
Pathol Oncol Res
; 2009 Jun;15(2):167-72
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Heterogeneity
of prostate
-specific membrane antigen (PSMA) expression in
prostate
carcinoma with distant metastasis.
Prostate
-specific membrane antigen (PSMA) is a transmembrane protein that is overexpressed in advanced stage
prostate
adenocarcinomas.
As a novel target for in vivo prognostic and therapeutic approaches, the distribution pattern of PSMA in primary and
metastatic
tumors is of significant interest.
Paraffin-embedded sections of 51 patients with primary
prostate
carcinoma and distant metastases were evaluated.
A significant number of the primary tumors (7/51) and metastases (6/51) presented with highly heterogeneous PSMA expression and in further 2 primary, and 8
metastatic
tumors the staining was in the negative range (<10% positive tumor cells).
Our findings clearly support the feasibility but also direct to potential failures of PSMA-targeted in vivo diagnostic and therapeutic approaches in
prostate
cancer patients with distant metastasis.
[MeSH-major]
Adenocarcinoma
/ metabolism. Antigens, Surface / metabolism. Cell Membrane / metabolism. Cytoplasm / metabolism. Glutamate Carboxypeptidase II / metabolism.
Prostatic
Neoplasms / metabolism
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
[Cites]
Prostate. 2006 Sep 15;66(13):1359-70
[
16894535.001
]
[Cites]
Virchows Arch. 2006 Feb;448(2):111-8
[
16328356.001
]
[Cites]
Anticancer Res. 1987 Sep-Oct;7(5B):927-35
[
2449118.001
]
[Cites]
Semin Nucl Med. 2007 Jan;37(1):17-28
[
17161036.001
]
[Cites]
Clin Cancer Res. 2003 Dec 15;9(17):6357-62
[
14695135.001
]
[Cites]
Urology. 1996 Aug;48(2):326-34
[
8753752.001
]
[Cites]
Clin Cancer Res. 1997 Jan;3(1):81-5
[
9815541.001
]
[Cites]
World J Surg Oncol. 2004 May 10;2:13
[
15132743.001
]
[Cites]
Cancer Immunol Immunother. 2008 Jan;57(1):43-52
[
17579857.001
]
[Cites]
Clin Cancer Res. 1996 Sep;2(9):1445-51
[
9816319.001
]
[Cites]
Hum Pathol. 2007 May;38(5):696-701
[
17320151.001
]
[Cites]
Cancer. 1998 Jun 1;82(11):2256-61
[
9610707.001
]
[Cites]
Nat Clin Pract Urol. 2006 Apr;3(4):216-25
[
16607370.001
]
[Cites]
Clin Cancer Res. 1999 Oct;5(10):2674-81
[
10537328.001
]
[Cites]
Cancer Res. 1992 Nov 1;52(21):6110-2
[
1382851.001
]
[Cites]
Rev Urol. 2004;6 Suppl 10:S13-8
[
16985927.001
]
(PMID = 18802790.001).
[ISSN]
1219-4956
[Journal-full-title]
Pathology oncology research : POR
[ISO-abbreviation]
Pathol. Oncol. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antigens, Surface; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human
64.
Karanikolas BD, Figueiredo ML, Wu L:
Comprehensive evaluation of the role of EZH2 in the growth, invasion, and aggression of a panel of prostate cancer cell lines.
Prostate
; 2010 May 1;70(6):675-88
[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]
Comprehensive evaluation of the role of EZH2 in the growth, invasion, and aggression of a panel
of prostate
cancer cell lines.
BACKGROUND: Although most
prostate
cancers respond well to initial treatments, a fraction
of prostate
cancers are more aggressive and will recur and metastasize.
Polycomb Group protein enhancer of zeste 2 (EZH2) was found to be overexpressed in
metastatic prostate
tumors, and is considered an excellent candidate for such a biomarker.
Scattered studies have found that EZH2 overexpression causes neoplastic transformation, invasion, and growth
of prostate
cells.
METHODS: In this study, a comprehensive evaluation of the phenotypic effects of EZH2 in a panel of five
prostate
cancer cell lines was performed.
By using multiple cell lines, and examining overexpression and knockdown of EZH2 concurrently, a broad view of EZH2's role in
prostate
cancer was achieved.
RESULTS: Overexpression of EZH2 led to more aggressive behaviors in all
prostate
cell lines tested.
In contrast, downregulation of EZH2 reduced invasion and tumorigenicity of androgen-independent (AI) cell lines CWR22Rv1, PC3, and DU145, but not of androgen-dependent (
AD
) cell lines LAPC4 and LNCaP.
CONCLUSIONS: Findings from this study suggest that AI
prostate
tumors are more dependent on EZH2 expression than
AD
tumors.
Our observations provide an explanation for the strong correlation between EZH2 overexpression and advanced stage, aggressive
prostate
cancers.
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
[Cites]
BJU Int. 2000 May;85(7):932-44
[
10792179.001
]
[Cites]
Mol Cancer Res. 2009 Sep;7(9):1456-65
[
19723877.001
]
[Cites]
Genes Dev. 2000 Oct 1;14(19):2410-34
[
11018010.001
]
[Cites]
J Clin Oncol. 2001 Jan 15;19(2):551-7
[
11208850.001
]
[Cites]
Curr Opin Genet Dev. 2001 Apr;11(2):175-81
[
11250141.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):377-82
[
11752410.001
]
[Cites]
Nature. 2002 Oct 10;419(6907):624-9
[
12374981.001
]
[Cites]
Science. 2002 Nov 1;298(5595):1039-43
[
12351676.001
]
[Cites]
J Natl Cancer Inst. 2003 May 7;95(9):661-8
[
12734317.001
]
[Cites]
Mol Biol Cell. 2003 Jul;14(7):2728-43
[
12857860.001
]
[Cites]
Hum Gene Ther. 2003 Aug 10;14(12):1207-12
[
12908971.001
]
[Cites]
Neoplasia. 2003 Nov-Dec;5(6):481-8
[
14965441.001
]
[Cites]
Oncogene. 2004 Jun 17;23(28):4930-7
[
15077161.001
]
[Cites]
Mol Cell. 2004 Jul 2;15(1):57-67
[
15225548.001
]
[Cites]
Genes Dev. 2004 Jul 1;18(13):1592-605
[
15231737.001
]
[Cites]
EMBO J. 2004 Oct 13;23(20):4061-71
[
15385962.001
]
[Cites]
Int J Cancer. 1978 Mar 15;21(3):274-81
[
631930.001
]
[Cites]
Natl Cancer Inst Monogr. 1978 Dec;(49):17-21
[
571045.001
]
[Cites]
Invest Urol. 1979 Jul;17(1):16-23
[
447482.001
]
[Cites]
Cancer Res. 1983 Apr;43(4):1809-18
[
6831420.001
]
[Cites]
Cancer Chemother Pharmacol. 1989;24(3):148-54
[
2544306.001
]
[Cites]
Mol Cell Biol. 1994 Mar;14(3):1721-32
[
7906858.001
]
[Cites]
Cancer Res. 1994 Dec 1;54(23):6049-52
[
7525052.001
]
[Cites]
Nucleic Acids Res. 1995 Feb 25;23(4):628-33
[
7899083.001
]
[Cites]
In Vitro Cell Dev Biol Anim. 1995 Jan;31(1):14-24
[
7535634.001
]
[Cites]
J Biol Chem. 1997 Feb 21;272(8):5007-15
[
9030563.001
]
[Cites]
Nat Med. 1997 Apr;3(4):402-8
[
9095173.001
]
[Cites]
EMBO J. 1997 Jun 2;16(11):3219-32
[
9214638.001
]
[Cites]
Mol Cell Biol. 1998 Jun;18(6):3586-95
[
9584199.001
]
[Cites]
J Virol. 1998 Nov;72(11):8463-71
[
9765382.001
]
[Cites]
Anal Biochem. 1999 May 15;270(1):41-9
[
10328763.001
]
[Cites]
In Vitro Cell Dev Biol Anim. 1999 Jul-Aug;35(7):403-9
[
10462204.001
]
[Cites]
Cancer Res. 2004 Dec 15;64(24):9209-16
[
15604294.001
]
[Cites]
Curr Biol. 2005 May 24;15(10):942-7
[
15916951.001
]
[Cites]
Science. 2005 Oct 14;310(5746):306-10
[
16224021.001
]
[Cites]
Oncogene. 2005 Nov 14;24(50):7465-74
[
16288293.001
]
[Cites]
J Clin Oncol. 2006 Jan 10;24(2):268-73
[
16330673.001
]
[Cites]
Nature. 2006 Feb 16;439(7078):871-4
[
16357870.001
]
[Cites]
Clin Cancer Res. 2006 Feb 15;12(4):1168-74
[
16489070.001
]
[Cites]
Cell. 2006 May 5;125(3):467-81
[
16603238.001
]
[Cites]
Genes Chromosomes Cancer. 2006 Jul;45(7):639-45
[
16575874.001
]
[Cites]
Mol Ther. 2006 Oct;14(4):494-504
[
16844419.001
]
[Cites]
Genes Dev. 2007 Jan 1;21(1):49-54
[
17210787.001
]
[Cites]
Prostate. 2007 Apr 1;67(5):547-56
[
17252556.001
]
[Cites]
Cancer Res. 2007 Jun 1;67(11):5097-102
[
17545586.001
]
[Cites]
Cancer Res. 2007 Nov 15;67(22):10657-63
[
18006806.001
]
[Cites]
Clin Cancer Res. 2007 Nov 15;13(22 Pt 1):6579-84
[
18006757.001
]
[Cites]
Int J Cancer. 2008 Feb 1;122(3):595-602
[
17943722.001
]
[Cites]
Prostate. 2008 Jan 1;68(1):78-84
[
18008331.001
]
[Cites]
Am J Surg Pathol. 2008 Feb;32(2):205-9
[
18223322.001
]
[Cites]
PLoS Comput Biol. 2008 Feb;4(2):e28
[
18282083.001
]
[Cites]
Cancer Res. 2008 Oct 1;68(19):7828-37
[
18829538.001
]
[Cites]
Nature. 2000 Aug 10;406(6796):593-9
[
10949293.001
]
(PMID = 20087897.001).
[ISSN]
1097-0045
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / AI028697-17; United States / NCI NIH HHS / CA / CA092131-080007; United States / NIAID NIH HHS / AI / P30 AI028697-17; United States / NCI NIH HHS / CA / P50 CA092131; United States / NCI NIH HHS / CA / P30 CA016042; United States / NIAID NIH HHS / AI / P30 AI028697; United States / NCI NIH HHS / CA / R01 CA101904-07; United States / NCI NIH HHS / CA / P30 CA016042-34; United States / NCI NIH HHS / CA / R01 CA101904; United States / NCI NIH HHS / CA / P50 CA092131-080007; United States / NCI NIH HHS / CA / CA016042-34; United States / NCI NIH HHS / CA / CA101904-07
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgens; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Transcription Factors; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Polycomb Repressive Complex 2
[Other-IDs]
NLM/ NIHMS179057; NLM/ PMC2848714
65.
Patil S, Veron A, Hosseini P, Bates R, Brown B, Guthikonda B, DeSouza R:
Metastatic prostate cancer mimicking chronic subdural hematoma: a case report and review of the literature.
J La State Med Soc
; 2010 Jul-Aug;162(4):203-5
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Metastatic prostate
cancer mimicking chronic subdural hematoma: a case report and review of the literature.
Cancer of the
prostate
is extremely common and is well known to metastasize to the pelvic lymph nodes and axial skeleton (vertebral column, pelvis, cranium, and proximal femur).
Moreover,
metastatic
lesions mimicking subdural hematoma are extremely rare and are uncommonly reported in the literature.
We present a unique case
of metastatic prostate
cancer presenting with headaches after head trauma with classic radiologic findings of subdural hematoma.
[MeSH-major]
Adenocarcinoma
/ secondary. Hematoma, Subdural, Chronic / diagnosis. Meningeal Neoplasms / secondary.
Prostatic
Neoplasms / pathology
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 = 20882812.001).
[ISSN]
0024-6921
[Journal-full-title]
The Journal of the Louisiana State Medical Society : official organ of the Louisiana State Medical Society
[ISO-abbreviation]
J La State Med Soc
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
66.
Mavis CK, Morey Kinney SR, Foster BA, Karpf AR:
Expression level and DNA methylation status of glutathione-S-transferase genes in normal murine prostate and TRAMP tumors.
Prostate
; 2009 Sep 1;69(12):1312-24
[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]
Expression level and DNA methylation status of glutathione-S-transferase genes in normal murine
prostate
and TRAMP tumors.
BACKGROUND: Glutathione-S-transferase (Gst) genes are downregulated in human
prostate
cancer, and GSTP1 silencing is mediated by promoter DNA hypermethylation in this malignancy.
We examined Gst gene expression and Gst promoter DNA methylation in normal murine prostates and Transgenic
Adenocarcinoma of
Mouse
Prostate
(TRAMP) tumors.
METHODS: Primary and
metastatic
tumors were obtained from TRAMP mice, and normal prostates were obtained from strain-matched WT mice (n = 15/group).
RESULTS: Of the genes analyzed, GstM1 and GstP1 were expressed at highest levels in normal
prostate
.
All five Gst genes showed greatly reduced expression in primary tumors compared to normal
prostate
, but not in tumor metastases.
Gst promoter methylation was unchanged in TRAMP tumors compared to normal
prostate
.
CONCLUSIONS: Gst genes are extensively downregulated in primary but not
metastatic
TRAMP tumors.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
AZACITIDINE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Clin Cancer Res. 2004 Dec 15;10(24):8472-8
[
15623627.001
]
[Cites]
Cancer. 2004 Nov 15;101(10 Suppl):2371-490
[
15495199.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Mar 1;102(9):3336-41
[
15728362.001
]
[Cites]
Annu Rev Pharmacol Toxicol. 2005;45:51-88
[
15822171.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):15785-90
[
16243968.001
]
[Cites]
Prostate. 2006 Jan 1;66(1):57-69
[
16114064.001
]
[Cites]
Cancer Res. 2006 Jan 1;66(1):385-92
[
16397253.001
]
[Cites]
Ann N Y Acad Sci. 2006 Sep;1075:235-43
[
17108217.001
]
[Cites]
Cancer Res. 2006 Dec 15;66(24):11659-67
[
17178860.001
]
[Cites]
J Nutr. 2007 Jan;137(1 Suppl):223S-228S
[
17182830.001
]
[Cites]
Nat Rev Cancer. 2007 Apr;7(4):256-69
[
17384581.001
]
[Cites]
Clin Cancer Res. 2007 Apr 1;13(7):2136-43
[
17404097.001
]
[Cites]
Pathology. 2007 Jun;39(3):299-304
[
17558856.001
]
[Cites]
Hum Pathol. 2007 Sep;38(9):1394-401
[
17555796.001
]
[Cites]
Cancer Res. 2007 Sep 1;67(17):8065-80
[
17804718.001
]
[Cites]
Genes Cells. 2007 Dec;12(12):1305-14
[
18076568.001
]
[Cites]
N Engl J Med. 2008 Mar 13;358(11):1148-59
[
18337604.001
]
[Cites]
Cancer Res. 2008 Jun 1;68(11):4173-82
[
18519676.001
]
[Cites]
Oncogene. 2008 Jul 17;27(31):4353-62
[
18372916.001
]
[Cites]
Mol Cancer Res. 2008 Aug;6(8):1365-74
[
18667590.001
]
[Cites]
Gut. 2009 Jan;58(1):5-15
[
18664505.001
]
[Cites]
Genomics. 2009 Feb;93(2):130-9
[
18952162.001
]
[Cites]
J Biol Chem. 2000 Jan 28;275(4):2727-32
[
10644736.001
]
[Cites]
Biochem Soc Trans. 2000 Feb;28(2):33-41
[
10816095.001
]
[Cites]
J Biochem Biophys Methods. 2000 Nov 20;46(1-2):69-81
[
11086195.001
]
[Cites]
Am J Pathol. 2001 Nov;159(5):1815-26
[
11696442.001
]
[Cites]
Genes Dev. 2002 Jan 1;16(1):6-21
[
11782440.001
]
[Cites]
Clin Cancer Res. 2002 Feb;8(2):514-9
[
11839671.001
]
[Cites]
Oncogene. 2002 Aug 12;21(35):5496-503
[
12154410.001
]
[Cites]
Int J Cancer. 2003 Sep 1;106(3):382-7
[
12845678.001
]
[Cites]
Nat Rev Cancer. 2004 Feb;4(2):143-53
[
14732866.001
]
[Cites]
J Pathol. 2004 Feb;202(2):233-40
[
14743506.001
]
[Cites]
J Cell Biochem. 2004 Feb 15;91(3):540-52
[
14755684.001
]
[Cites]
Cancer Res. 2004 Mar 15;64(6):1975-86
[
15026333.001
]
[Cites]
Prostate. 2004 Jun 15;60(1):25-31
[
15129426.001
]
[Cites]
Oncol Rep. 2004 Sep;12(3):631-7
[
15289848.001
]
[Cites]
Cell. 1980 May;20(1):85-93
[
6156004.001
]
[Cites]
J Biol Chem. 1990 Oct 5;265(28):17174-9
[
2211619.001
]
[Cites]
J Biol Chem. 1993 Jun 5;268(16):11475-8
[
8505281.001
]
[Cites]
Proc Natl Acad Sci U S A. 1994 Nov 22;91(24):11733-7
[
7972132.001
]
[Cites]
Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3439-43
[
7724580.001
]
[Cites]
Crit Rev Biochem Mol Biol. 1995;30(6):445-600
[
8770536.001
]
[Cites]
Cancer Res. 1997 Aug 15;57(16):3325-30
[
9269988.001
]
[Cites]
Adv Cancer Res. 1998;72:141-96
[
9338076.001
]
[Cites]
Cancer Res. 1997 Nov 1;57(21):4687-91
[
9354422.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):5275-80
[
9560266.001
]
[Cites]
Nat Genet. 1999 Jan;21(1):103-7
[
9916800.001
]
[Cites]
J Natl Cancer Inst. 2005 Jan 19;97(2):103-15
[
15657340.001
]
(PMID = 19444856.001).
[ISSN]
1097-0045
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R21 CA128062-01; United States / NCI NIH HHS / CA / P30 CA016056; United States / NCI NIH HHS / CA / R21CA128062; United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / R21 CA128062; United States / NCI NIH HHS / CA / R21 CA128062-02; United States / NCI NIH HHS / CA / CA128062-02; United States / NCI NIH HHS / CA / CA128062-01; United States / NCI NIH HHS / CA / 5T32CA009072; United States / NCI NIH HHS / CA / T32 CA009072
[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 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 0 / Hydroxamic Acids; 0 / RNA, Messenger; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / Gstp1 protein, mouse; M801H13NRU / Azacitidine
[Other-IDs]
NLM/ NIHMS182170; NLM/ PMC2836025
67.
Kaplan-Lefko PJ, Sutherland BW, Evangelou AI, Hadsell DL, Barrios RJ, Foster BA, Demayo F, Greenberg NM:
Enforced epithelial expression of IGF-1 causes hyperplastic prostate growth while negative selection is requisite for spontaneous metastogenesis.
Oncogene
; 2008 May 1;27(20):2868-76
[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]
Enforced epithelial expression of IGF-1 causes hyperplastic
prostate
growth while negative selection is requisite for spontaneous metastogenesis.
The insulin-like growth factor-1 (IGF-1) signaling axis is important for cell growth, differentiation and survival and increased serum IGF is a risk factor for
prostate
and other cancers.
To study IGF-1 action on
the prostate
, we created transgenic (PB-Des) mice that specifically express human IGF-1(des) in
prostate
epithelial cells.
Expression of IGF-1(des) was sufficient to cause hyperplastic lesions in all mice, however the well-differentiated lesions did not progress to
adenocarcinoma
within a year.
Remarkably, crossing the PB-Des mice to an established model
of prostate
cancer delayed progression of organ-confined tumors and emergence
of metastatic
lesions in young mice.
While dissemination
of metastatic
lesions was widespread in old bigenic mice we did not detect IGF-1(des) in poorly differentiated primary tumors or
metastatic
lesions.
[MeSH-major]
Insulin-Like Growth Factor I / biosynthesis. Insulin-Like Growth Factor I / genetics.
Prostate
/ metabolism.
Prostate
/ pathology.
Prostatic
Hyperplasia / pathology.
Prostatic
Neoplasms / metabolism.
Prostatic
Neoplasms / pathology
[MeSH-minor]
Adenocarcinoma
/ secondary. Animals. Brain Neoplasms / secondary. Cell Differentiation / physiology. Epithelium / metabolism. Epithelium / pathology. Heart Neoplasms / secondary. Humans. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Male. Mice. Mice, Transgenic. Splenic Neoplasms / secondary. Thymus Neoplasms / secondary. Urologic Neoplasms / secondary
MedlinePlus Health Information.
consumer health - Enlarged Prostate (BPH)
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
Jackson Laboratory JAX®Mice Database.
culture/stock collections - FVB-Tg(Pbsn-IGF1*)5305Ng/J
(subscription/membership/fee required).
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
SciCrunch.
Marmoset Gene list: Data: Gene Annotation
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18026134.001).
[ISSN]
1476-5594
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA74589; United States / NCI NIH HHS / CA / CA82807; United States / NCI NIH HHS / CA / CA84296
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
67763-96-6 / Insulin-Like Growth Factor I
68.
Massoud W, Paparel P, Lopez JG, Perrin P, Daumont M, Ruffion A:
Discovery of a pituitary adenoma following treatment with a gonadotropin-releasing hormone agonist in a patient with prostate cancer.
Int J Urol
; 2006 Jan;13(1):87-8
[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]
Discovery of a pituitary adenoma following treatment with a gonadotropin-releasing hormone agonist in a patient with
prostate
cancer.
We report the case of a T3
prostate
cancer in a 70-year-old white man.
Hormone therapy represents a prominent branch in the treatment of locally advanced and
metastatic prostate
cancer.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Adenoma / chemically induced. Antineoplastic Agents, Hormonal / adverse effects. Gonadotropin-Releasing Hormone / agonists. Leuprolide / adverse effects. Pituitary Neoplasms / chemically induced.
Prostatic
Neoplasms / drug therapy
Genetic Alliance.
consumer health - Pituitary cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
LEUPROLIDE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16448441.001).
[ISSN]
0919-8172
[Journal-full-title]
International journal of urology : official journal of the Japanese Urological Association
[ISO-abbreviation]
Int. J. Urol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Australia
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone; EFY6W0M8TG / Leuprolide
69.
Yagihashi Y, Okinami T, Fukuzawa S, Kuriki K:
[Pericardial effusion due to metastatic prostate cancer: a case report].
Hinyokika Kiyo
; 2008 May;54(5):369-72
[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]
[Pericardial effusion due to
metastatic prostate
cancer: a case report].
We describe a patient whose complaints were related to pericardial effusion due to
prostatic
carcinoma.
Cytologic study suggested
metastatic adenocarcinoma
or malignant mesothelioma.
At autopsy, the major finding was poorly differentiated
adenocarcinoma of the prostate
with metastases to the mediastinum.
[MeSH-major]
Adenocarcinoma
/ pathology. Mediastinal Neoplasms / secondary. Pericardial Effusion / etiology.
Prostatic
Neoplasms / pathology
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Pericardial Disorders
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18546864.001).
[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
70.
Lee DK:
Prostate cancer metastases to the leg, ankle, and foot.
J Am Podiatr Med Assoc
; 2008 May-Jun;98(3):242-5
[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]
Prostate
cancer metastases to the leg, ankle, and foot.
Metastases to the bones of the lower extremities from
prostate
carcinomas are rare and are usually associated with diffuse
metastatic
disease or primary tumors of the abdomen and lungs.
I present the case of a patient who presented with lower leg pain and had undiagnosed
prostate
carcinoma.
Unlike previous reports
of prostate
carcinoma, this rare case includes magnetic resonance imaging, histology, and medical management.
[MeSH-major]
Adenocarcinoma
/ secondary. Lower Extremity.
Prostatic
Neoplasms / pathology
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 = 18487599.001).
[ISSN]
8750-7315
[Journal-full-title]
Journal of the American Podiatric Medical Association
[ISO-abbreviation]
J Am Podiatr Med Assoc
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
71.
Ajani JA, Safran H, Bokemeyer C, Shah MA, Lenz HJ, Van Cutsem E, Burris HA 3rd, Lebwohl D, Mullaney B:
A multi-center phase II study of BMS-247550 (Ixabepilone) by two schedules in patients with metastatic gastric adenocarcinoma previously treated with a taxane.
Invest New Drugs
; 2006 Sep;24(5):441-6
[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]
A multi-center phase II study of BMS-247550 (Ixabepilone) by two schedules in patients with
metastatic
gastric
adenocarcinoma
previously treated with a taxane.
With the primary endpoint of assessing ixabepilone's response rate against
metastatic
gastric cancer previously treated with a taxane, we performed a multi-center phase II trial.
PATIENTS AND METHODS: Patients with histologically documented
metastatic
gastric or gastroesophageal
adenocarcinoma
, who had previously received a taxane, were eligible.
CONCLUSIONS: Ixabepilone, on a once every 21-day schedule, is modestly active against
metastatic
gastric cancer previously treated with a taxane.
The results of this study suggest that once every 21-day ixabepilone schedule should be pursued further in untreated gastric or gastroesophageal
adenocarcinoma
patients.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Antineoplastic Agents / therapeutic use. Epothilones / therapeutic use. Stomach Neoplasms / drug therapy
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
Ixabepilone
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Clin Oncol. 2005 Mar 1;23(7):1439-46
[
15735119.001
]
[Cites]
J Natl Cancer Inst. 2000 Feb 2;92 (3):205-16
[
10655437.001
]
[Cites]
Prostate Cancer Prostatic Dis. 1999 Jan;2(1):41-52
[
12496865.001
]
[Cites]
Control Clin Trials. 1989 Mar;10(1):1-10
[
2702835.001
]
[Cites]
Clin Cancer Res. 2001 May;7(5):1429-37
[
11350914.001
]
[Cites]
Cancer Chemother Pharmacol. 2001 Oct;48(4):319-26
[
11710633.001
]
[Cites]
J Clin Oncol. 2005 Apr 20;23(12):2726-34
[
15837987.001
]
[Cites]
Cancer Res. 1995 Jun 1;55(11):2325-33
[
7757983.001
]
(PMID = 16586011.001).
[ISSN]
0167-6997
[Journal-full-title]
Investigational new drugs
[ISO-abbreviation]
Invest New Drugs
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Bridged-Ring Compounds; 0 / Epothilones; 0 / Taxoids; 1605-68-1 / taxane; K27005NP0A / ixabepilone
72.
Sung MT, Jiang Z, Montironi R, MacLennan GT, Mazzucchelli R, Cheng L:
Alpha-methylacyl-CoA racemase (P504S)/34betaE12/p63 triple cocktail stain in prostatic adenocarcinoma after hormonal therapy.
Hum Pathol
; 2007 Feb;38(2):332-41
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Alpha-methylacyl-CoA racemase (P504S)/34betaE12/p63 triple cocktail stain in
prostatic
adenocarcinoma
after hormonal therapy.
Alpha-methylacyl-CoA racemase (AMACR) has recently been shown to be a highly sensitive marker for the diagnosis
of prostate
cancer.
However, there is limited information concerning its utility as a marker for
prostate
carcinoma after hormonal therapy.
Our current investigation was conducted to evaluate the expression of AMACR in patients with
prostate
carcinoma after hormonal therapy and assess its diagnostic utility in combination with p63 and high molecular weight cytokeratin (34betaE12) staining.
Prostate
tissues from 49 patients who had been treated with hormonal therapy were immunohistochemically analyzed for AMACR, 34betaE12, and p63 expression by a triple antibody cocktail stain.
The correlations between AMACR expression and
metastatic
status, associated hormonal therapy regimens, and the extent of hormone therapy effect were analyzed.
alpha-methylacyl-CoA racemase expression may be substantially diminished or entirely lost in
prostate
carcinoma after hormonal therapy.
This variation in AMACR expression does not correlate with
the metastatic
status, the modality of hormonal therapy, or the extent of therapy-related effect.
It is important that pathologists be aware that some hormonally treated
prostate
carcinomas do not express AMACR, and that immunostaining in such cases must be interpreted with caution.
A triple cocktail stain using AMACR, 34betaE12, and p63 can be helpful in evaluating
prostate
specimens for the presence of residual or recurrent carcinoma after hormonal therapy for cancer.
[MeSH-major]
Adenocarcinoma
/ pathology. DNA-Binding Proteins / analysis. Keratins / analysis.
Prostatic
Neoplasms / pathology. Racemases and Epimerases / analysis. Trans-Activators / analysis. Tumor Suppressor Proteins / analysis
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 = 17134736.001).
[ISSN]
0046-8177
[Journal-full-title]
Human pathology
[ISO-abbreviation]
Hum. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / CK-34 beta E12; 0 / DNA-Binding Proteins; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 68238-35-7 / Keratins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
73.
Deb P, Chander Y, Rai RS:
Testicular metastasis from carcinoma of prostate: report of two cases.
Prostate Cancer Prostatic Dis
; 2007;10(2):202-4
[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]
Testicular metastasis from carcinoma
of prostate
: report of two cases.
Despite the high incidence of
prostatic
adenocarcinoma
and its ability for wide dissemination,
metastatic
involvement of testis is rather uncommon.
We report two cases (aged 76 and 55 years, respectively), where unilateral testicular metastasis was incidentally discovered after bilateral orchiectomy following detection
of adenocarcinoma prostate
in six-quadrant trucut specimen.
Both patients had obstructive voiding symptoms, hard nodular
prostate
on direct rectal examination and raised serum
prostate
-specific antigen levels, without associated systemic or testicular symptoms.
[MeSH-major]
Adenocarcinoma
/ pathology.
Prostatic
Neoplasms / pathology. Testicular Neoplasms / secondary
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
MedlinePlus Health Information.
consumer health - Testicular Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17224911.001).
[ISSN]
1365-7852
[Journal-full-title]
Prostate cancer and prostatic diseases
[ISO-abbreviation]
Prostate Cancer Prostatic Dis.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
74.
Heebøll S, Borre M, Ottosen PD, Andersen CL, Mansilla F, Dyrskjøt L, Orntoft TF, Tørring N:
SMARCC1 expression is upregulated in prostate cancer and positively correlated with tumour recurrence and dedifferentiation.
Histol Histopathol
; 2008 09;23(9):1069-76
[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]
SMARCC1 expression is upregulated in
prostate
cancer and positively correlated with tumour recurrence and dedifferentiation.
BACKGROUND: The identification of new prognostic markers in
prostate
cancer (PC) is essential to improve patient treatment and management.
MATERIALS: Expression of SMARCC1 immunostaining was analysed on a tissue microarray containing specimens from 327 patients with
prostate
cancer and clinical follow-up information.
Furthermore, 30 specimens from patients with benign
prostate
hyperplasia were included as controls as well as 30 specimens of benign
prostate
tissue from PC patients.
In contrast, 20% of the specimens from patients with non-
metastatic
and non-recurrent disease showed moderate to marked staining.
In 31% of the patients with recurrent disease and in 31% of the patients with
metastatic
disease we found moderate to strong SMARCC1 immunostaining.
In a logistic regression analysis, patients with a marked SMARCC1 immunostaining had a significantly elevated odds ratio (OR) of 16 for recurrent cancer and an OR of 4.5 for
metastatic
disease.
Conclusions. Our present results demonstrate an increased expression of SMARCC1 protein in
prostate
cancer and reveal a positive correlation with tumour dedifferentiation, progression, metastasis and time to recurrence.
[MeSH-major]
Adenocarcinoma
/ metabolism.
Prostatic
Neoplasms / metabolism. Transcription Factors / metabolism
[MeSH-minor]
Animals. Biomarkers, Tumor / metabolism. COS Cells. Cell Dedifferentiation. Cell Nucleus / metabolism. Cell Nucleus / pathology. Cercopithecus aethiops. Fluorescent Antibody Technique, Direct. Humans. Immunoenzyme Techniques. Lymph Nodes / metabolism. Lymph Nodes / pathology. Lymphatic Metastasis. Male. Neoplasm Recurrence, Local. Odds Ratio.
Prostate
/ metabolism.
Prostate
/ pathology.
Prostatic
Hyperplasia / metabolism.
Prostatic
Hyperplasia / pathology. Tissue Array Analysis. Up-Regulation
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 = 18581278.001).
[ISSN]
1699-5848
[Journal-full-title]
Histology and histopathology
[ISO-abbreviation]
Histol. Histopathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Spain
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / SMARCC1 protein, human; 0 / Transcription Factors
75.
Hardie C, Parker C, Norman A, Eeles R, Horwich A, Huddart R, Dearnaley D:
Early outcomes of active surveillance for localized prostate cancer.
BJU Int
; 2005 May;95(7):956-60
[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]
Early outcomes of active surveillance for localized
prostate
cancer.
OBJECTIVE: To describe the preliminary clinical outcomes of active surveillance (AS), a new strategy aiming to individualize the management of early
prostate
cancer by selecting only those men with significant cancers for curative therapy, and illustrate the contrast with a policy of watchful waiting (WW).
PATIENTS AND METHODS: Eighty men with early
prostate
cancer began AS at the authors' institution between 1993 and 2002.
Eligibility included histologically confirmed
prostatic
adenocarcinoma
, fitness for radical treatment, clinical stage T1/T2, N0/X, M0/X, a
prostate
specific antigen (PSA) level of < or = 20 ng/mL, and a Gleason score of < or = 7.
During the same period, 32 men with localized
prostate
cancer (any T stage, N0/X, M0/X, any PSA, Gleason score < or = 7) were managed by WW; hormonal treatment was indicated for symptomatic
prostate
cancer progression.
No patient developed evidence
of metastatic
disease, none started palliative hormone therapy, and there were no deaths from
prostate
cancer.
Twenty (62%) of the 32 patients on WW remained on observation, eight (25%) received palliative hormonal therapy and four (12%) died, including one from
prostate
cancer.
CONCLUSIONS: AS is feasible in selected men with early
prostate
cancer.
[MeSH-major]
Adenocarcinoma
/ therapy.
Prostatic
Neoplasms / therapy
[MeSH-minor]
Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Clinical Protocols. Disease-Free Survival. Feasibility Studies. Follow-Up Studies. Humans. Male. Middle Aged. Prognosis.
Prostate
-Specific Antigen / blood. Prostatectomy / methods
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
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 = 15839912.001).
[ISSN]
1464-4096
[Journal-full-title]
BJU international
[ISO-abbreviation]
BJU Int.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; EC 3.4.21.77 / Prostate-Specific Antigen
76.
Taplin ME, George DJ, Halabi S, Sanford B, Febbo PG, Hennessy KT, Mihos CG, Vogelzang NJ, Small EJ, Kantoff PW:
Prognostic significance of plasma chromogranin a levels in patients with hormone-refractory prostate cancer treated in Cancer and Leukemia Group B 9480 study.
Urology
; 2005 Aug;66(2):386-91
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Prognostic significance of plasma chromogranin a levels in patients with hormone-refractory
prostate
cancer treated in Cancer and Leukemia Group B 9480 study.
OBJECTIVES: To test the hypothesis that chromogranin A (CgA) levels are prognostic in patients with
metastatic
hormone-refractory
prostate
cancer (HRPC).
The extent of neuroendocrine differentiation in
prostate
cancer correlates with aggressive disease and with progression to HRPC.
Plasma CgA levels in patients with
prostate
cancer may reflect the extent of the tumor neuroendocrine phenotype.
METHODS: Pretreatment plasma was collected from 390 patients with
metastatic
HRPC enrolled in the Cancer and Leukemia Group B (CALGB) 9480 trial, a study of three different doses of suramin.
In multivariate models (adjusting for performance status,
prostate
-specific antigen, and lactate dehydrogenase), the plasma CgA levels remained predictive of overall survival.
[MeSH-major]
Adenocarcinoma
/ blood.
Adenocarcinoma
/ mortality. Chromogranins / blood.
Prostatic
Neoplasms / blood.
Prostatic
Neoplasms / mortality
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
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 = 16098367.001).
[ISSN]
1527-9995
[Journal-full-title]
Urology
[ISO-abbreviation]
Urology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / CHGA protein, human; 0 / Chromogranin A; 0 / Chromogranins; 0 / Hormones
77.
Théodore C:
[Chemotherapy indications in the treatment of metastases from urological malignancies].
Prog Urol
; 2008 Nov;18 Suppl 7:S219-22
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Transliterated title]
Indications
de la
chimiothérapie dans le traitement des cancers urologiques métastatiques.
Chemotherapy is useful for many
metastatic
urological cancer treatments.
Very efficient for testis tumors, it is at present the best weapon against
metastatic
urothelial tumors, especially for transitional cell carcinoma of the bladder.
For
prostate
cancer, chemotherapy is used when
metastatic adenocarcinoma
has become refractory to hormonal treatment.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19070795.001).
[ISSN]
1166-7087
[Journal-full-title]
Progrès en urologie : journal de l'Association française d'urologie et de la Société française d'urologie
[ISO-abbreviation]
Prog. Urol.
[Language]
fre
[Publication-type]
English Abstract; Journal Article
[Publication-country]
France
78.
Bonkhoff H:
[Differential diagnosis of prostate cancer: impact of pattern analysis and immunohistochemistry].
Pathologe
; 2005 Nov;26(6):405-21
[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]
[Differential diagnosis
of prostate
cancer: impact of pattern analysis and immunohistochemistry].
[Transliterated title]
Differenzialdiagnose des Prostatakarzinoms. Rolle
der
Mustererkennung und
der
Immunhistochemie.
Prostate
cancer offers a wide range of growth patterns depicted in the classical Gleason diagram.
For each Gleason pattern exist a number of benign and malignant mimickers that can simulate
prostatic
adenocarcinoma
.
In the present review, the use of immunohistochemical markers is discussed with emphasis to a pattern-based approach to differential diagnosis in
prostate
pathology.
AMACR (P504 s) is helpful not only in identifying small amount of cancer in needle biopsies but also in the diagnosis of high grade
prostatic
intra epithelial neoplasia (HGPIN).
A number of lesions which may be confused with small acinar
adenocarcinoma
(Cowper's gland, nephrogenic metaplasia, mesonephric glands) and poorly differentiated
prostate
cancer (urothelial neoplasia, mucinous colon cancer and other
metastatic
lesions) lacks convincing PSA immunoreactivity.
Basal cell markers and the nuclear androgen receptors are important markers to differentiate Gleason grade 5 A und 5 B patterns from
prostatic
involvement by transitional cell carcinoma.
Finally, a selected panel of markers is useful to classify
prostatic
stromal lesions.
[MeSH-major]
Biomarkers, Tumor / analysis.
Prostate
/ pathology.
Prostatic
Neoplasms / pathology
[MeSH-minor]
Carcinoma, Basal Cell / pathology. Cell Division / physiology. Diagnosis, Differential. Humans. Male.
Prostatic
Hyperplasia / pathology.
Prostatic
Intraepithelial Neoplasia / pathology
Genetic Alliance.
consumer health - Prostate 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]
Mod Pathol. 2004 Mar;17(3):328-48
[
14976539.001
]
[Cites]
Pathologe. 1998 Jan;19(1):1-11
[
9541937.001
]
[Cites]
J Urol. 2004 Apr;171(4):1419-23
[
15017188.001
]
[Cites]
Mod Pathol. 2004 Mar;17(3):307-15
[
14739905.001
]
[Cites]
Hum Pathol. 2003 Aug;34(8):792-6
[
14506641.001
]
[Cites]
Am J Surg Pathol. 2004 Jul;28(7):928-34
[
15223964.001
]
[Cites]
Virchows Arch. 2002 Sep;441(3):231-7
[
12242519.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 Jun;14(6):1424-32
[
15941951.001
]
[Cites]
Mod Pathol. 2002 Dec;15(12):1302-8
[
12481011.001
]
[Cites]
Hum Pathol. 2004 Dec;35(12):1462-8
[
15619204.001
]
[Cites]
Hum Pathol. 2004 Aug;35(8):1008-13
[
15297968.001
]
[Cites]
Am J Surg Pathol. 2002 Jul;26(7):926-31
[
12131161.001
]
[Cites]
Am J Surg Pathol. 2003 Aug;27(8):1128-33
[
12883245.001
]
[Cites]
Am J Clin Pathol. 1994 Jan;101(1):48-64
[
7506479.001
]
[Cites]
Pathologe. 1998 Jan;19(1):21-32
[
9541939.001
]
[Cites]
Mod Pathol. 2004 Mar;17(3):316-27
[
14976541.001
]
[Cites]
Am J Surg Pathol. 2005 May;29(5):579-87
[
15832080.001
]
[Cites]
Am J Surg Pathol. 2004 Feb;28(2):239-43
[
15043314.001
]
[Cites]
Am J Surg Pathol. 2004 Jun;28(6):701-5
[
15166661.001
]
[Cites]
Am J Clin Pathol. 2004 Oct;122(4):517-23
[
15487448.001
]
(PMID = 16205899.001).
[ISSN]
0172-8113
[Journal-full-title]
Der Pathologe
[ISO-abbreviation]
Pathologe
[Language]
ger
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Biomarkers, Tumor
[Number-of-references]
20
79.
Roca Edreira A, Aguilera Tubet C, Villanueva Peña A, Ballestero Diego R, Zubillaga Guerrero S:
[Mediastinal lymph nodes during the course of a metastatic prostate cancer].
Actas Urol Esp
; 2007 Jun;31(6):693-5; discussion 695
[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]
[Mediastinal lymph nodes during the course of a
metastatic prostate
cancer].
[Transliterated title]
Adenopatías mediastínicas en
la
evolución
de
un cancer
de
próstata metastásico.
Prostate
carcinoma is one of the most frecuent cancers in men.
We report the case of a patient with
prostate
cancer who develops mediastinal lymphadenopathy, pulmonary nodules and cutaneous metastases 8 years after the diagnosis.
[MeSH-major]
Adenocarcinoma
/ secondary. Androgens. Lymphatic Metastasis. Mediastinum / pathology. Neoplasms, Hormone-Dependent / secondary.
Prostatic
Neoplasms / pathology
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
KETOCONAZOLE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17896567.001).
[ISSN]
0210-4806
[Journal-full-title]
Actas urologicas españolas
[ISO-abbreviation]
Actas Urol Esp
[Language]
spa
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Spain
[Chemical-registry-number]
0 / Androgen Antagonists; 0 / Androgens; 0 / Diphosphonates; 0 / Imidazoles; 35LT29625A / Estramustine; 57773-63-4 / Triptorelin Pamoate; 6XC1PAD3KF / zoledronic acid; 76W6J0943E / Flutamide; E61Q31EK2F / Cyproterone; R9400W927I / Ketoconazole
80.
Merrick GS, Butler WM, Wallner KE, Galbreath RW, Allen Z, Lief JH, Adamovich E:
Influence of body mass index on biochemical outcome after permanent prostate brachytherapy.
Urology
; 2005 Jan;65(1):95-100
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Influence of body mass index on biochemical outcome after permanent
prostate
brachytherapy.
OBJECTIVES: To evaluate the impact of body mass index (BMI) on the 8-year biochemical outcome after permanent
prostate
brachytherapy with or without the addition of supplemental external beam radiotherapy and/or androgen deprivation therapy (ADT).
METHODS: From April 1995 through February 2001, 686 consecutive patients underwent brachytherapy using either palladium-103 or iodine-125 for clinical Stage T1b-T3aNxM0 (2002 American Joint Committee on Cancer)
prostate
cancer.
Biochemical progression-free survival was defined by a
prostate
-specific antigen (PSA) level of 0.4 ng/mL or less after a nadir.
The clinical, treatment, and dosimetric parameters evaluated for biochemical progression-free survival included BMI, patient age, clinical T stage, Gleason score, preimplant PSA level, risk group, percentage of positive biopsies, isotope, use of supplemental external beam radiotherapy, use of ADT,
prostate
volume, planning volume, percentage of target volume receiving 100%, 150%, and 200% of the prescribed dose, minimal percentage of dose covering 90% of the target volume, tobacco use, and the presence of hypertension and diabetes.
At last follow-up, 5 patients (0.7%) had died
of metastatic prostate
cancer.
CONCLUSIONS:
Prostate
brachytherapy results in a high probability of 8-year biochemical progression-free survival for low, intermediate, and high-risk patients.
[MeSH-major]
Adenocarcinoma
/ radiotherapy. Body Mass Index. Brachytherapy.
Prostatic
Neoplasms / radiotherapy
[MeSH-minor]
Aged. Antineoplastic Agents, Hormonal / therapeutic use. Biomarkers, Tumor / blood. Combined Modality Therapy. Disease-Free Survival. Follow-Up Studies. Humans. Life Tables. Male. Middle Aged. Neoplasm Proteins / blood. Obesity / complications. Proportional Hazards Models.
Prostate
-Specific Antigen / blood. Radiotherapy, High-Energy. Risk. Treatment Outcome
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 = 15667872.001).
[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 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; EC 3.4.21.77 / Prostate-Specific Antigen
81.
Balanathan P, Williams ED, Wang H, Pedersen JS, Horvath LG, Achen MG, Stacker SA, Risbridger GP:
Elevated level of inhibin-alpha subunit is pro-tumourigenic and pro-metastatic and associated with extracapsular spread in advanced prostate cancer.
Br J Cancer
; 2009 Jun 2;100(11):1784-93
[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]
Elevated level of inhibin-alpha subunit is pro-tumourigenic and pro-
metastatic
and associated with extracapsular spread in advanced
prostate
cancer.
The biological function of inhibin-alpha subunit (INH alpha) in
prostate
cancer (PCa) is currently unclear.
This prompted us to use clinical specimens and functional studies to investigate the pro-tumourigenic and pro-
metastatic
function of INH alpha.
This study is the first to demonstrate a pro-tumourigenic and pro-
metastatic
function for INH alpha associated with androgen-independent stage
of metastatic prostate
disease.
Our results also suggest that INH alpha expression in the primary
prostate
tumour can be used as a predictive factor for prognosis of PCa.
[MeSH-major]
Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Inhibins / metabolism.
Prostatic
Neoplasms / metabolism.
Prostatic
Neoplasms / pathology
[MeSH-minor]
Adenocarcinoma
/ metabolism.
Adenocarcinoma
/ pathology. Cell Line, Tumor. Cell Separation. Gene Expression Regulation, Neoplastic. Humans. Male. Neoplasm Metastasis / genetics. Neoplasm Metastasis / pathology. Neoplasm Staging
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
[Cites]
Endocrinology. 1999 Nov;140(11):5303-9
[
10537161.001
]
[Cites]
J Clin Endocrinol Metab. 1999 Jun;84(6):2163-9
[
10372726.001
]
[Cites]
Cancer. 2001 Jan 1;91(1):66-73
[
11148561.001
]
[Cites]
EMBO J. 2001 Feb 15;20(4):672-82
[
11179212.001
]
[Cites]
Trends Endocrinol Metab. 2000 Oct;11(8):309-14
[
10996525.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Jan;86(1):330-6
[
11232020.001
]
[Cites]
Cancer Res. 2001 Mar 1;61(5):1786-90
[
11280723.001
]
[Cites]
Endocrinology. 2001 Jun;142(6):2458-67
[
11356695.001
]
[Cites]
Am J Pathol. 2001 Sep;159(3):893-903
[
11549582.001
]
[Cites]
Endocr Rev. 2001 Dec;22(6):836-58
[
11739336.001
]
[Cites]
Nat Cell Biol. 2002 Jan;4(1):E2-5
[
11780131.001
]
[Cites]
Mol Endocrinol. 2002 Feb;16(2):213-20
[
11818495.001
]
[Cites]
Int J Cancer. 2002 Apr 20;98(6):946-51
[
11948478.001
]
[Cites]
Biol Reprod. 2003 Jan;68(1):230-5
[
12493718.001
]
[Cites]
J Biol Chem. 2003 Mar 7;278(10):7934-41
[
12493742.001
]
[Cites]
Cell. 2003 Jun 13;113(6):685-700
[
12809600.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8621-3
[
12861075.001
]
[Cites]
J Urol. 2004 Jan;171(1):192-6
[
14665874.001
]
[Cites]
Prostate. 2004 Feb 1;58(2):193-9
[
14716745.001
]
[Cites]
J Mol Endocrinol. 2004 Feb;32(1):55-67
[
14765992.001
]
[Cites]
Clin Exp Metastasis. 2004;21(1):19-29
[
15065599.001
]
[Cites]
Gastroenterology. 2004 Jun;126(7):1828-43
[
15188178.001
]
[Cites]
Clin Cancer Res. 2004 Aug 1;10(15):5137-44
[
15297417.001
]
[Cites]
Cytokine Growth Factor Rev. 2004 Oct;15(5):291-6
[
15450247.001
]
[Cites]
Mol Cell Endocrinol. 2004 Oct 15;225(1-2):73-6
[
15451570.001
]
[Cites]
Invest Urol. 1979 Jul;17(1):16-23
[
447482.001
]
[Cites]
Prog Clin Biol Res. 1980;37:115-32
[
7384082.001
]
[Cites]
Cancer Res. 1983 Apr;43(4):1809-18
[
6831420.001
]
[Cites]
N Engl J Med. 1989 Sep 21;321(12):790-3
[
2770810.001
]
[Cites]
Prostate. 1989;15(1):1-12
[
2798227.001
]
[Cites]
Nature. 1992 Nov 26;360(6402):313-9
[
1448148.001
]
[Cites]
Br J Cancer. 1999 Apr;80(1-2):309-13
[
10390013.001
]
[Cites]
J Urol. 2005 Jan;173(1):10-20
[
15592017.001
]
[Cites]
Prostate. 2005 Sep 15;65(1):35-43
[
15800936.001
]
[Cites]
Prostate. 2005 Nov 1;65(3):222-30
[
15948136.001
]
[Cites]
Nature. 2005 Sep 22;437(7058):497-504
[
16177780.001
]
[Cites]
J Urol. 2005 Dec;174(6):2181-5
[
16280760.001
]
[Cites]
Endocrinology. 2006 Jul;147(7):3462-71
[
16601134.001
]
[Cites]
Int J Biol Markers. 2006 Apr-Jun;21(2):88-95
[
16847811.001
]
[Cites]
J Cell Biochem. 2006 Aug 15;98(6):1380-90
[
16598746.001
]
[Cites]
Cancer Res. 2006 Oct 1;66(19):9566-75
[
17018613.001
]
[Cites]
Prostate. 2007 Feb 15;67(3):301-11
[
17192875.001
]
[Cites]
Cancer Res. 2007 Feb 1;67(3):1090-8
[
17283142.001
]
[Cites]
Endocrinology. 2007 Nov;148(11):5355-68
[
17656464.001
]
[Cites]
J Mol Endocrinol. 2007 Nov;39(5):329-32
[
17975259.001
]
[Cites]
Curr Cancer Drug Targets. 2008 Sep;8(6):490-7
[
18781895.001
]
[Cites]
Endocrinology. 1996 Dec;137(12):5476-83
[
8940374.001
]
[Cites]
J Endocrinol. 1997 Sep;154(3):535-45
[
9379131.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Mar;83(3):969-75
[
9506758.001
]
[Cites]
Hum Pathol. 1998 Aug;29(8):856-62
[
9712429.001
]
[Cites]
Front Neuroendocrinol. 1998 Oct;19(4):287-322
[
9799587.001
]
[Cites]
J Cell Biol. 1999 Feb 22;144(4):789-801
[
10037799.001
]
[Cites]
Cancer. 1999 Nov 1;86(9):1775-82
[
10547551.001
]
(PMID = 19436293.001).
[ISSN]
1532-1827
[Journal-full-title]
British journal of cancer
[ISO-abbreviation]
Br. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / inhibin-alpha subunit; 57285-09-3 / Inhibins
[Other-IDs]
NLM/ PMC2695696
82.
Saleem M, Kweon MH, Johnson JJ, Adhami VM, Elcheva I, Khan N, Bin Hafeez B, Bhat KM, Sarfaraz S, Reagan-Shaw S, Spiegelman VS, Setaluri V, Mukhtar H:
S100A4 accelerates tumorigenesis and invasion of human prostate cancer through the transcriptional regulation of matrix metalloproteinase 9.
Proc Natl Acad Sci U S A
; 2006 Oct 3;103(40):14825-30
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
S100A4 accelerates tumorigenesis and invasion of human
prostate
cancer through the transcriptional regulation of matrix metalloproteinase 9.
We previously showed that the calcium-binding protein S100A4 is overexpressed during the progression
of prostate
cancer (CaP) in humans and in the TRAMP (transgenic
adenocarcinoma of
the mouse
prostate
) mouse model.
We tested a hypothesis that the S100A4 gene plays a role in the invasiveness of human CaP and may be associated with its
metastatic
spread.
We evaluated the mechanism through which the S100A4 gene controls invasiveness of cells by using a macroarray containing 96 well characterized
metastatic
genes.
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
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Pediatr Surg. 2001 Jul;36(7):1040-4
[
11431772.001
]
[Cites]
CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30
[
16514137.001
]
[Cites]
Br J Cancer. 2002 Feb 1;86(3):409-16
[
11875708.001
]
[Cites]
Cancer Res. 2002 Mar 15;62(6):1910-4
[
11912173.001
]
[Cites]
J Clin Oncol. 2003 Jan 1;21(1):106-12
[
12506178.001
]
[Cites]
Cancer Res. 2003 Jan 1;63(1):140-8
[
12517790.001
]
[Cites]
Clin Exp Metastasis. 2003;20(8):701-11
[
14713104.001
]
[Cites]
Curr Opin Urol. 2004 May;14(3):143-9
[
15069304.001
]
[Cites]
Oncogene. 2004 Jul 15;23(32):5487-95
[
15122322.001
]
[Cites]
Cancer Res. 2004 Aug 1;64(15):5311-21
[
15289337.001
]
[Cites]
BMC Cancer. 2004 Aug 3;4:42
[
15291964.001
]
[Cites]
Biochem Biophys Res Commun. 2004 Oct 29;323(4):1241-5
[
15451430.001
]
[Cites]
Oncol Res. 1996;8(2):69-75
[
8859777.001
]
[Cites]
Int J Cancer. 1997 May 29;71(5):832-7
[
9180153.001
]
[Cites]
Cancer. 1998 Sep 15;83(6):1180-8
[
9740084.001
]
[Cites]
Cell Tissue Res. 1999 Feb;295(2):287-96
[
9931375.001
]
[Cites]
Brain Pathol. 1999 Jan;9(1):1-19
[
9989446.001
]
[Cites]
Cancer Res. 1999 Sep 15;59(18):4702-8
[
10493528.001
]
[Cites]
Tumour Biol. 2004 Jul-Aug;25(4):188-92
[
15557756.001
]
[Cites]
Cancer Res. 2004 Dec 1;64(23):8715-22
[
15574782.001
]
[Cites]
Clin Cancer Res. 2005 Jan 1;11(1):147-53
[
15671539.001
]
[Cites]
Cancer Res. 2005 Dec 1;65(23):11203-13
[
16322271.001
]
[Cites]
J Biol Chem. 2006 Jan 13;281(2):677-80
[
16243835.001
]
[Cites]
Clin Cancer Res. 2006 Feb 15;12(4):1192-200
[
16489073.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):217-27
[
16492908.001
]
[Cites]
Methods Mol Biol. 2002;172:69-80
[
11833360.001
]
(PMID = 16990429.001).
[ISSN]
0027-8424
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / P50 DK065303; United States / NCI NIH HHS / CA / R01 CA 101039; United States / NCI NIH HHS / CA / R01 CA078809; United States / NCI NIH HHS / CA / R01 CA 78809; United States / NCI NIH HHS / CA / R01 CA101039; United States / NIDDK NIH HHS / DK / P50 DK 65303
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / S100 Proteins; 0 / Tissue Inhibitor of Metalloproteinase-1; 142662-27-9 / S100A4 protein, human; EC 3.4.24.35 / Matrix Metalloproteinase 9
[Other-IDs]
NLM/ PMC1595436
83.
Veshapidze N, Alibegashvili M, Gabunia N, Ramishvili L, Kotrikadze N:
Erythrocyte membrane permeability in the men with metastatic adenocarcinoma of the prostate.
Georgian Med News
; 2009 Jan;(166):9-12
[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]
Erythrocyte membrane permeability in the men with
metastatic adenocarcinoma
of the
prostate
.
The aim of our study was to investigate the alterations of the erythrocyte membrane permeability in the men with
metastatic adenocarcinoma
of the
prostate
before and six months after castration.
For experimental research were used the erythrocytes of 15 men with
metastatic prostate
cancer (Pca) (before and after 6 months from castration) and of the 15 practically healthy men (control group).
Investigations revealed the changes of Na(+)/K(+)-ATP-ase activity and the changes of Na(+) and K(+) ions concentration in
metastatic
Pca patients before and six months after castration.
[MeSH-major]
Adenocarcinoma
/ metabolism. Cell Membrane Permeability / physiology. Erythrocyte Membrane / metabolism.
Prostatic
Neoplasms / metabolism. Sodium-Potassium-Exchanging ATPase / metabolism
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
POTASSIUM, ELEMENTAL
.
Hazardous Substances Data Bank.
SODIUM
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19202209.001).
[ISSN]
1512-0112
[Journal-full-title]
Georgian medical news
[ISO-abbreviation]
Georgian Med News
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
Georgia (Republic)
[Chemical-registry-number]
9NEZ333N27 / Sodium; EC 3.6.3.9 / Sodium-Potassium-Exchanging ATPase; RWP5GA015D / Potassium
84.
Müller Arteaga C, Egea Camacho J, Alvarez Gago T, Cortiñas González JR, Gonzalo Rodríguez V, Fernández del Busto E:
[Spermatic cord liposarcoma. Association with prostate cancer. Report of a case and review of literature].
Actas Urol Esp
; 2005 Jul-Aug;29(7):700-3
[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]
[Spermatic cord liposarcoma. Association with
prostate
cancer. Report of a case and review of literature].
[Transliterated title]
Liposarcoma
de
cordón espermático. Asociación con carcinoma
de
próstata. Comunicación
de
un caso y revisión
de la
literatura.
We describe and relation between liposarcoma and
prostate
cancer in a 66 years old patient who had a left paratesticular tumor with low speed growth and 12 cm of length; nodule in
prostate
gland was detected.
Ecography demostrate an hipoecoic tumor in the spermatic cord;
Prostate
Specific Antigen (PSA) was 1276 ng.
/ml. and bone gammagraphy reported
metastatic
lesions.
[MeSH-major]
Adenocarcinoma
/ complications. Liposarcoma / complications.
Prostatic
Neoplasms / complications. Spermatic Cord / pathology
Genetic Alliance.
consumer health - Liposarcoma
.
Genetic Alliance.
consumer health - Prostate 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 = 16180322.001).
[ISSN]
0210-4806
[Journal-full-title]
Actas urologicas espanolas
[ISO-abbreviation]
Actas Urol Esp
[Language]
spa
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Spain
85.
Gurel B, Iwata T, Koh CM, Jenkins RB, Lan F, Van Dang C, Hicks JL, Morgan J, Cornish TC, Sutcliffe S, Isaacs WB, Luo J, De Marzo AM:
Nuclear MYC protein overexpression is an early alteration in human prostate carcinogenesis.
Mod Pathol
; 2008 Sep;21(9):1156-67
[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]
Nuclear MYC protein overexpression is an early alteration in human
prostate
carcinogenesis.
A region on chromosome 8q24 encompassing the MYC locus is amplified in
prostate
cancer, but this occurs mostly in advanced disease suggesting that MYC alterations occur late in
prostate
cancer.
In contrast, MYC mRNA is elevated in most
prostate
cancers, even those of relatively low stage and grade (eg Gleason score 6) suggesting that MYC plays a role in initiation.
Thus, it is critical to determine whether MYC protein is elevated in human
prostate
cancer, and if so, at what stage of the disease this elevation occurs.
We utilized a new anti-MYC antibody coupled with genetically defined control experiments to localize MYC protein within human tissue microarrays consisting of normal, atrophy, PIN, primary
adenocarcinoma
, and
metastatic adenocarcinoma
.
Nuclear overexpression of MYC protein occurred frequently in luminal cells of PIN, as well as in most primary carcinomas and
metastatic
disease.
These results provide evidence that upregulation of nuclear MYC protein expression is a highly prevalent and early change in
prostate
cancer and suggest that increased nuclear MYC may be a critical oncogenic event driving human
prostate
cancer initiation and progression.
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]
Mol Cell Biol. 1987 May;7(5):1697-709
[
3299053.001
]
[Cites]
Cancer Res. 1986 Mar;46(3):1535-8
[
2417706.001
]
[Cites]
Cancer Res. 1992 Nov 15;52(22):6182-7
[
1384957.001
]
[Cites]
J Urol. 1993 Aug;150(2 Pt 1):490-4
[
8326591.001
]
[Cites]
Cancer Res. 1997 Feb 1;57(3):524-31
[
9012485.001
]
[Cites]
Mod Pathol. 1997 Nov;10(11):1113-9
[
9388062.001
]
[Cites]
J Urol. 1998 Dec;160(6 Pt 2):2381-92
[
9817389.001
]
[Cites]
Am J Pathol. 1999 Jun;154(6):1777-83
[
10362802.001
]
[Cites]
Oncogene. 1999 May 13;18(19):3004-16
[
10378696.001
]
[Cites]
J Natl Cancer Inst. 1999 Sep 15;91(18):1574-80
[
10491435.001
]
[Cites]
J Cell Biochem. 2004 Dec 15;93(6):1282-96
[
15503302.001
]
[Cites]
Cell Cycle. 2004 Sep;3(9):1133-7
[
15467447.001
]
[Cites]
FASEB J. 2005 Feb;19(2):243-5
[
15548588.001
]
[Cites]
Cancer. 2005 Mar 15;103(6):1186-94
[
15712208.001
]
[Cites]
Prostate. 2005 Jun 1;63(4):369-84
[
15937962.001
]
[Cites]
Nat Rev Mol Cell Biol. 2005 Aug;6(8):635-45
[
16064138.001
]
[Cites]
Science. 2005 Oct 28;310(5748):644-8
[
16254181.001
]
[Cites]
Cancer Cell. 2005 Nov;8(5):393-406
[
16286247.001
]
[Cites]
Nature. 2006 Aug 17;442(7104):818-22
[
16862118.001
]
[Cites]
Semin Cancer Biol. 2006 Aug;16(4):253-64
[
16904903.001
]
[Cites]
Am J Pathol. 2006 Nov;169(5):1843-54
[
17071605.001
]
[Cites]
Cancer Res. 2006 Nov 15;66(22):10683-90
[
17108105.001
]
[Cites]
Nat Genet. 2007 Jan;39(1):41-51
[
17173048.001
]
[Cites]
Neoplasia. 2007 Feb;9(2):166-80
[
17356713.001
]
[Cites]
Nat Rev Cancer. 2007 Apr;7(4):256-69
[
17384581.001
]
[Cites]
Nat Med. 2007 Jul;13(7):820-7
[
17589519.001
]
[Cites]
Cancer Cell. 2007 Sep;12(3):230-8
[
17785204.001
]
[Cites]
Nat Biotechnol. 2007 Oct;25(10):1177-81
[
17724450.001
]
[Cites]
Cell Stem Cell. 2008 Jan 10;2(1):18-21
[
18371417.001
]
[Cites]
Cell Stem Cell. 2008 Apr 10;2(4):333-44
[
18397753.001
]
[Cites]
Curr Biol. 1999 Nov 4;9(21):1255-8
[
10556095.001
]
[Cites]
Genes Chromosomes Cancer. 2000 Jan;27(1):95-103
[
10564591.001
]
[Cites]
Prostate. 2000 Jun 1;43(4):278-85
[
10861747.001
]
[Cites]
Lab Invest. 2000 Aug;80(8):1251-8
[
10950116.001
]
[Cites]
Genes Dev. 2000 Oct 1;14(19):2410-34
[
11018010.001
]
[Cites]
Am J Pathol. 2001 Dec;159(6):2089-94
[
11733359.001
]
[Cites]
Am J Pathol. 2002 May;160(5):1799-806
[
12000731.001
]
[Cites]
Cancer Cell. 2002 Aug;2(2):113-6
[
12204531.001
]
[Cites]
Cancer Res. 2002 Nov 15;62(22):6405-9
[
12438224.001
]
[Cites]
Am J Pathol. 2003 May;162(5):1529-37
[
12707036.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Jul;88(7):2972-82
[
12843129.001
]
[Cites]
Cancer Cell. 2003 Sep;4(3):223-38
[
14522256.001
]
[Cites]
Genes Chromosomes Cancer. 2004 Jan;39(1):1-10
[
14603436.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Jan 20;101(3):811-6
[
14711987.001
]
[Cites]
J Clin Oncol. 2004 Jul 15;22(14):2790-9
[
15254046.001
]
[Cites]
Prostate. 2004 Nov 1;61(3):215-27
[
15368473.001
]
[Cites]
Nature. 1983 Nov 17-23;306(5940):274-7
[
6316149.001
]
[Cites]
Science. 1984 Aug 17;225(4663):718-21
[
6463648.001
]
[Cites]
Prostate. 1987;11(4):327-37
[
2446300.001
]
(PMID = 18567993.001).
[ISSN]
1530-0285
[Journal-full-title]
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
[ISO-abbreviation]
Mod. Pathol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P50 CA058236; United States / NCI NIH HHS / CA / P50 CA058236-11; United States / NCI NIH HHS / CA / P50CA58236
[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 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger
[Other-IDs]
NLM/ NIHMS285485; NLM/ PMC3170853
86.
Lin S, Shen YH, Zhang ZX, Li HL, Shan L, Liu RH, Xu XK, Zhang WD:
Revision of the Structures of 1,5-Dihydroxy-3,8-epoxyvalechlorine, Volvaltrate B, and Valeriotetrate C from Valeriana jatamansi and V. officinalis.
J Nat Prod
; 2010 Oct 22;73(10):1723-6
[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.
Volvaltrate B (6) showed cytotoxic activity against the lung
adenocarcinoma
(A549),
metastatic prostate
cancer (PC-3M), colon cancer (HCT-8), and hepatoma (Bel7402) cell lines, with IC50 values of 8.5, 2.0, 3.2, and 6.1 μM, respectively.
[MeSH-minor]
Colonic Neoplasms. Drug Screening Assays, Antitumor. Humans. Male. Molecular Structure. Nuclear Magnetic Resonance, Biomolecular. Plant Roots / chemistry.
Prostatic
Neoplasms / drug therapy
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20853876.001).
[ISSN]
1520-6025
[Journal-full-title]
Journal of natural products
[ISO-abbreviation]
J. Nat. Prod.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Phytogenic; 0 / Drugs, Chinese Herbal; 0 / Iridoids; 0 / valeriotetrate C; 0 / volvaltrate B
87.
Knight D, Peterson AC, Rini BI, Harlin H, Gajewski TF, Stadler WM:
The HLA-A2-restricted PSMA peptide LLHETDSAV is poorly immunogenic in patients with metastatic prostate cancer.
Prostate
; 2009 Feb 1;69(2):142-8
[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]
The HLA-A2-restricted PSMA peptide LLHETDSAV is poorly immunogenic in patients with
metastatic prostate
cancer.
BACKGROUND: Increasing evidence suggests that
prostate
cancer is visible to the immune system and is potentially responsive to immunotherapeutic interventions.
Previous work has identified
prostate
-specific membrane antigen (PSMA) as a potential antigen for T-cell recognition, and specific PSMA epitopes presented by HLA-A2 have been described.
METHODS: HLA-A2(+) patients with castrate-resistant
prostate
cancer and normal organ function were considered.
CONCLUSIONS: Our results suggest that the PSMA peptide LLHETDSAV is poorly immunogenic in humans and that alternative
prostate
cancer antigens should be pursued.
[MeSH-major]
Adenocarcinoma
/ immunology. Antigens, Surface / immunology. Glutamate Carboxypeptidase II / immunology. Peptide Fragments / immunology.
Prostatic
Neoplasms / immunology
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic 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 = 18942640.001).
[ISSN]
1097-0045
[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 / Antigens, Surface; 0 / Cancer Vaccines; 0 / Epitopes; 0 / HLA-A2 Antigen; 0 / Peptide Fragments; 0 / Recombinant Proteins; 187348-17-0 / Interleukin-12; 82115-62-6 / Interferon-gamma; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human
88.
Hansel DE, Epstein JI:
Sarcomatoid carcinoma of the prostate: a study of 42 cases.
Am J Surg Pathol
; 2006 Oct;30(10):1316-21
[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]
Sarcomatoid carcinoma of the
prostate
: a study of 42 cases.
Sarcomatoid carcinoma of the
prostate
is a rare type of
prostatic
cancer.
We examined transurethral resection, needle biopsy, and radical prostatectomy specimens from 42 patients with sarcomatoid carcinoma of the
prostate
, all of which were received in consultation.
Prior
prostatic
adenocarcinoma
: The majority of patients (n=21; 66%) had a prior history of acinar
adenocarcinoma of the prostate
.
Of the remaining patients for whom this information was known, 11 patients presented with
de
novo sarcomatoid carcinoma.
The time between the original diagnosis of acinar
adenocarcinoma
and diagnosis of sarcomatoid carcinoma ranged from 6 months to 16 years (mean 6.8 y).
Concurrent
adenocarcinoma
: The majority of patients demonstrated a concurrent high grade acinar carcinoma of Gleason score 7 (n=3), 8 (n=9), 9 (n=10), and 10 (n=10).
A subset of patients contained an admixed ductal
adenocarcinoma
(n=4), small cell carcinoma (n=3), squamous cell carcinoma (n=3), or other unusual pattern
of prostate
carcinoma (n=3).
In 1 case, the diagnosis was based on immunohistochemical evidence of epithelial differentiation along with the history of prior
adenocarcinoma
.
Of the 12 cases with received immunostains of the sarcomatoid component, 5/7 cases were at least focally positive for cytokeratin, 1/1 case was focally positive for Cam5.2, and 3/6 cases were focally positive for
prostate
acid phosphatase.
The sarcomatoid component did not demonstrate immunoreactivity for
prostate
-specific antigen in 8 cases.
PROGNOSIS: approximately half of all patients developed
metastatic
disease either at time of presentation or subsequently.
No correlation was identified between patient survival and morphologic features, before radiation or hormone therapy, or concurrent high-grade
prostate
cancer.
The epithelial component is typically high-grade acinar
adenocarcinoma
, yet other aggressive tumor subtypes such as ductal
adenocarcinoma
and small cell carcinoma may also be seen.
Sarcomatoid carcinoma is an aggressive form
of prostate
cancer, the prognosis of which is dismal regardless of other histologic or clinical findings.
[MeSH-major]
Carcinosarcoma / secondary.
Prostatic
Neoplasms / pathology
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 = 17001164.001).
[ISSN]
0147-5185
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor
89.
Yang S, Zhong C, Frenkel B, Reddi AH, Roy-Burman P:
Diverse biological effect and Smad signaling of bone morphogenetic protein 7 in prostate tumor cells.
Cancer Res
; 2005 Jul 1;65(13):5769-77
[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]
Diverse biological effect and Smad signaling of bone morphogenetic protein 7 in
prostate
tumor cells.
We found that bone morphogenetic protein (BMP) 7, a member of the BMP family, was strikingly up-regulated during the development of primary
prostatic
adenocarcinoma
in the conditional Pten deletion mouse model.
To determine the relevance of this finding to human
prostate
cancer, we examined the expression of BMPs and BMP receptors (BMPR) as well as the responsiveness to recombinant human BMP7 in a series of human
prostate
tumor cell lines.
All
prostatic
cell lines tested expressed variable levels of BMP2, BMP4, and BMP7 and at least two of each type I and II BMPRs.
BPH-1, a cell line representing benign
prostatic
epithelial hyperplasia, was growth arrested at G1.
In the bone metastasis-derived PC-3
prostate
cancer cells, BMP7 induced epithelial-mesenchymal transdifferentiation with classic changes in morphology, motility, invasiveness, and molecular markers.
Finally, BMP7 inhibited serum starvation-induced apoptosis in the LNCaP
prostate
cancer cell line and more remarkably in its bone
metastatic
variant C4-2B line.
Taken together, these findings suggest that BMPs are able to modulate the biological behavior
of prostate
tumor cells in diverse and cell type-specific manner and point to certain mechanisms by which these secreted signaling molecules may contribute to
prostate
cancer growth and metastasis.
[MeSH-major]
Adenocarcinoma
/ pathology. Bone Morphogenetic Proteins / physiology. DNA-Binding Proteins / physiology.
Prostatic
Neoplasms / pathology. Trans-Activators / physiology. Transforming Growth Factor beta / physiology
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15994952.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA59705
[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 / BMP7 protein, human; 0 / Bone Morphogenetic Protein 7; 0 / Bone Morphogenetic Proteins; 0 / DNA-Binding Proteins; 0 / Recombinant Proteins; 0 / Smad Proteins; 0 / Trans-Activators; 0 / Transforming Growth Factor beta
90.
Pommier P, Chabaud S, Lagrange JL, Richaud P, Lesaunier F, Le Prise E, Wagner JP, Hay MH, Beckendorf V, Suchaud JP, Pabot du Chatelard PM, Bernier V, Voirin N, Perol D, Carrie C:
Is there a role for pelvic irradiation in localized prostate adenocarcinoma? Preliminary results of GETUG-01.
J Clin Oncol
; 2007 Dec 1;25(34):5366-73
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Is there a role for pelvic irradiation in localized
prostate adenocarcinoma
? Preliminary results of GETUG-01.
PURPOSE: To assess the benefit and toxicity and quality-of-life (QOL) outcomes of pelvic nodes irradiation in nonmetastatic
prostate
carcinoma patients.
PATIENTS AND METHODS: Between December 1998 and June 2004, 444 patients with T1b-T3, N0 pNx, M0
prostate
carcinoma were randomly assigned to either pelvic and
prostate
radiotherapy or
prostate
radiotherapy only.
The total dose recommended to
the prostate
was changed during the course of the study from 66 Gy to 70 Gy.
Criteria for progression-free survival (PFS) included biologic
prostate
-specific antigen recurrences or a local or
metastatic
evolution.
The QOL outcome was recorded with the European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire C30, the International
Prostatic
Symptom Score, and the Sexual Function Index scales.
[MeSH-major]
Adenocarcinoma
/ radiotherapy.
Prostatic
Neoplasms / radiotherapy
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
J Clin Oncol. 2008 Apr 20;26(12):2055-6; author reply 2056-7
[
18421061.001
]
(PMID = 18048817.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Publication-type]
Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
91.
Barrisford GW, Sartor O, Richie JP:
Solitary adrenal metastatic lesion in a patient with a history of prostate cancer.
Clin Genitourin Cancer
; 2009 Jan;7(1):64-6
[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]
Solitary adrenal
metastatic
lesion in a patient with a history
of prostate
cancer.
Prostate
cancer is the most commonly diagnosed malignancy among American men.
Although
prostate
cancer-related death approximates only 3%, advanced disease can become widely disseminated.
Metastatic
disease is often found in a number of common sites.
[MeSH-major]
Adenocarcinoma
/ secondary. Adrenal Gland Neoplasms / secondary.
Prostatic
Neoplasms / pathology
[MeSH-minor]
Adult. Humans. Male.
Prostate
-Specific Antigen / blood. Tomography, X-Ray Computed
Genetic Alliance.
consumer health - Adrenal Cancer
.
Genetic Alliance.
consumer health - Prostate cancer
.
Genetic Alliance.
consumer health - Metastatic cancer
.
MedlinePlus Health Information.
consumer health - Adrenal Gland 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
(PMID = 19213672.001).
[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
92.
Yeh IT, Reddick RL, Kumar AP:
Malignancy arising in seminal vesicles in the transgenic adenocarcinoma of mouse prostate (TRAMP) model.
Prostate
; 2009 May 15;69(7):755-60
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Malignancy arising in seminal vesicles in the transgenic
adenocarcinoma of
mouse
prostate
(TRAMP) model.
BACKGROUND: Transgenic
adenocarcinoma of
mouse
prostate
(TRAMP) mice, derived by
prostate
specific expression of SV40 large T antigen using the rat probasin promoter, all develop
prostate
tumors akin to human
prostate
cancers.
Immunostains (cytokeratin, vimentin, desmin, and MIB-1) and electron microscopy were performed on selected blocks of the genitourinary system and
metastatic
tumor nodules.
In some cases, the stromal cells become large mass lesions that overgrow
the prostate
.
Some
metastatic
tumors have characteristics similar to the seminal vesicle ES tumor.
CONCLUSIONS:
Metastatic
tumors in TRAMP mice show three patterns:.
(1) A definite
adenocarcinoma
pattern
metastatic
from
the prostate
;.
[MeSH-major]
Adenocarcinoma
/ pathology.
Prostatic
Neoplasms / pathology. Seminal Vesicles / pathology
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 Wiley-Liss, Inc.
(PMID = 19170049.001).
[ISSN]
1097-0045
[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
93.
Xuan Q, Yang X, Mo L, Huang F, Pang Y, Qin M, Chen Z, He M, Wang Q, Mo ZN:
Expression of the serine protease kallikrein 7 and its inhibitor antileukoprotease is decreased in prostate cancer.
Arch Pathol Lab Med
; 2008 Nov;132(11):1796-801
[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 serine protease kallikrein 7 and its inhibitor antileukoprotease is decreased in
prostate
cancer.
Antileukoprotease overexpression is commonly associated with aggressive, high-risk, or
metastatic
cancer originating from various organs.
OBJECTIVE: To investigate the expression and potential role of hK7 and its inhibitor ALP in
prostate
cancer.
DESIGN: The mRNA expression of KLK7 and ALP transcript in benign
prostate
epithelial cells and
prostate
cancers was evaluated by semiquantitative reverse transcription-polymerase chain reaction.
We examined hK7 and ALP protein expression by immunohistochemistry in 20 normal
prostate
tissues, 50 benign
prostatic
hyperplasia tissues, and 103
prostate
cancers.
Western blot examination showed protein expression of hK7 and ALP in benign
prostate
epithelial cells and
prostate
cancer cell lines.
RESULTS: Semiquantitative polymerase chain reaction examination revealed that the mRNA level of KLK7 and ALP was significantly decreased in
prostate
cancers compared with that in benign
prostate
epithelial cells (P < .001).
Immunohistochemical expression of hK7 was observed in
prostate
epithelial cells, whereas little or no staining was observed in
prostate
cancer.
Western blot analysis revealed that hK7 and ALP were decreased in malignant
prostate
epithelium.
CONCLUSIONS: Like hK7, ALP is down-regulated in
prostate
cancers, which begs the question of whether it remains an effective inhibitor of hK7 or whether it is discordant in time or space and is ineffective as an inhibitor of hK7.
The function of KLK7 and ALP in
prostate
cancer should be further studied.
[MeSH-major]
Adenocarcinoma
/ metabolism. Kallikreins / metabolism.
Prostatic
Neoplasms / metabolism. Secretory Leukocyte Peptidase Inhibitor / metabolism
[MeSH-minor]
Case-Control Studies. Cell Line, Tumor. Down-Regulation. Epithelial Cells / metabolism. Epithelial Cells / pathology. Humans. Male.
Prostate
/ cytology.
Prostate
/ metabolism.
Prostatic
Hyperplasia / metabolism.
Prostatic
Hyperplasia / pathology. 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 = 18976018.001).
[ISSN]
1543-2165
[Journal-full-title]
Archives of pathology & laboratory medicine
[ISO-abbreviation]
Arch. Pathol. Lab. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / RNA, Messenger; 0 / Secretory Leukocyte Peptidase Inhibitor; EC 3.4.21.- / KLK7 protein, human; EC 3.4.21.- / Kallikreins
94.
Chung AC, Zhou S, Liao L, Tien JC, Greenberg NM, Xu J:
Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice.
Cancer Res
; 2007 Jun 15;67(12):5965-75
[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]
Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous
prostate
cancer progression in mice.
Although the amplified-in-breast cancer 1 (AIB1; SRC-3, ACTR, or NCoA3) was defined as a coactivator for androgen receptor (AR) by in vitro studies, its role in AR-mediated
prostate
development and
prostate
cancer remained unexplored.
AIB1 deficiency only slightly delayed
prostate
growth and had no effect on androgen-dependent
prostate
regeneration, suggesting an unessential role of AIB1 in AR function in
the prostate
.
Surprisingly, when
prostate
tumorigenesis was induced by the SV40 transgene in transgenic
adenocarcinoma of
the mouse
prostate
(TRAMP) mice, AIB1 expression was observed in certain epithelial cells of the
prostate
intraepithelial neoplasia (PIN) and well-differentiated carcinoma and in almost all cells of the poorly differentiated carcinoma.
After AIB1 was genetically inactivated in AIB1-/-/TRAMP mice, the progression
of prostate
tumorigenesis in most AIB1-/-/TRAMP mice was arrested at the well-differentiated carcinoma stage.
Wild-type (WT)/TRAMP mice developed progressive, multifocal, and
metastatic prostate
tumors and died between 25 and 34 weeks.
Our results indicate that induction of AIB1 expression in partially transformed epithelial cells is essential for progression
of prostate
tumorigenesis into poorly differentiated carcinoma.
Inhibition of AIB1 expression or function in
the prostate
epithelium may be a potential strategy to suppress
prostate
cancer initiation and progression.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
COS Scholar Universe.
author profiles
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Clin Sci (Lond). 2005 Apr;108(4):293-308
[
15603554.001
]
[Cites]
Clin Cancer Res. 2005 Mar 15;11(6):2111-22
[
15788656.001
]
[Cites]
J Biol Chem. 2005 Jul 1;280(26):25134-45
[
15802273.001
]
[Cites]
Cancer Res. 2005 Sep 1;65(17):7976-83
[
16140970.001
]
[Cites]
Cancer Res. 2005 Sep 1;65(17):7993-8002
[
16140972.001
]
[Cites]
J Clin Oncol. 2005 Nov 10;23(32):8146-51
[
16278465.001
]
[Cites]
Acta Pharmacol Sin. 2006 Apr;27(4):387-94
[
16539836.001
]
[Cites]
Mol Cell Biol. 2006 May;26(10):3810-23
[
16648476.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Nov 7;103(45):16716-21
[
17065319.001
]
[Cites]
Mol Cell Biol. 2004 Jun;24(12):5157-71
[
15169882.001
]
[Cites]
J Biol Chem. 2004 Jul 23;279(30):31105-12
[
15145939.001
]
[Cites]
Prostate. 2004 Oct 1;61(2):142-52
[
15305337.001
]
[Cites]
Cancer Cell. 2004 Sep;6(3):263-74
[
15380517.001
]
[Cites]
Biol Reprod. 1986 Jun;34(5):961-71
[
3730488.001
]
[Cites]
Biol Reprod. 1986 Jun;34(5):973-83
[
3730489.001
]
[Cites]
Cancer Res. 1996 Sep 15;56(18):4096-102
[
8797572.001
]
[Cites]
Nature. 1997 Jun 12;387(6634):677-84
[
9192892.001
]
[Cites]
Science. 1997 Aug 15;277(5328):965-8
[
9252329.001
]
[Cites]
Clin Cancer Res. 1998 Dec;4(12):2925-9
[
9865902.001
]
[Cites]
Am J Pathol. 1999 Feb;154(2):525-36
[
10027410.001
]
[Cites]
Urology. 1999 Apr;53(4):707-13
[
10197845.001
]
[Cites]
J Steroid Biochem Mol Biol. 1999 Apr-Jun;69(1-6):3-12
[
10418975.001
]
[Cites]
Clin Cancer Res. 2004 Nov 15;10(22):7727-37
[
15570007.001
]
[Cites]
Clin Sci (Lond). 2005 Jan;108(1):1-11
[
15384949.001
]
[Cites]
Mol Endocrinol. 2006 Dec;20(12):3105-19
[
16916939.001
]
[Cites]
Mol Endocrinol. 1999 Nov;13(11):1924-33
[