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1
benign prostatic tumour 2005:2010[pubdate] *count=100
35809 results
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Items 1 to 100 of about 35809
1.
Karpf AR, Bai S, James SR, Mohler JL, Wilson EM:
Increased expression of androgen receptor coregulator MAGE-11 in prostate cancer by DNA hypomethylation and cyclic AMP.
Mol Cancer Res
; 2009 Apr;7(4):523-35
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[Title]
Increased expression of androgen receptor coregulator MAGE-11 in
prostate
cancer by DNA hypomethylation and cyclic AMP.
The present study investigated the regulatory mechanisms that control MAGE-11 expression during androgen deprivation therapy and
prostate
cancer progression.
Studies include the CWR22 xenograft model of human
prostate
cancer, clinical specimens of
benign
and malignant
prostate
, and
prostate
cancer cell lines.
MAGE-11 mRNA levels increased 100- to 1,500-fold during androgen deprivation therapy and
prostate
cancer progression, with highest levels in the castration-recurrent CWR22 xenograft and clinical specimens of castration-recurrent
prostate
cancer.
Pyrosequencing of genomic DNA from
prostate
cancer specimens and cell lines indicated the increase in MAGE-11 resulted from DNA hypomethylation of a CpG island in the 5' promoter of the MAGE-11 gene.
Sodium bisulfite sequencing of genomic DNA from
benign
and malignant
prostate
tumors and
prostate
cancer cell lines revealed DNA hypomethylation at individual CpG sites at the transcription start site were most critical for MAGE-11 expression.
Cyclic AMP (cAMP) also increased MAGE-11 expression and AR transcriptional activity in
prostate
cancer cell lines.
Increased expression of the AR coregulator MAGE-11 through promoter DNA hypomethylation and cAMP provides a novel mechanism for increased AR signaling in castration-recurrent
prostate
cancer.
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[Cites]
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[
17045745.001
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(PMID = 19372581.001).
[ISSN]
1541-7786
[Journal-full-title]
Molecular cancer research : MCR
[ISO-abbreviation]
Mol. Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA116674; United States / NCI NIH HHS / CA / P01-CA77739; United States / NCI NIH HHS / CA / R21 CA128062; United States / NICHD NIH HHS / HD / R01 HD016910-26; United States / NCI NIH HHS / CA / P01 CA077739; United States / NICHD NIH HHS / HD / R01-HD16910; United States / NCI NIH HHS / CA / R21-CA128062; United States / NCI NIH HHS / CA / P01 CA077739-090007; United States / NCI NIH HHS / CA / R01 CA116674-03; United States / NCI NIH HHS / CA / R01-CA11674; United States / NICHD NIH HHS / HD / R01 HD016910; United States / NCI NIH HHS / CA / CA077739-090007; United States / NICHD NIH HHS / HD / HD016910-26; United States / NCI NIH HHS / CA / CA116674-03
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / AR protein, human; 0 / Androgens; 0 / Antigens, Neoplasm; 0 / MAGEA11 protein, human; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Receptors, Androgen; E0399OZS9N / Cyclic AMP
[Other-IDs]
NLM/ NIHMS94772; NLM/ PMC2670465
2.
Barnard RJ:
Prostate cancer prevention by nutritional means to alleviate metabolic syndrome.
Am J Clin Nutr
; 2007 Sep;86(3):s889-93
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[Title]
Prostate
cancer prevention by nutritional means to alleviate metabolic syndrome.
When subjects were placed on the Pritikin Program, insulin fell and SHBG rose and it was suggested that
prostate
cancer might also be an aspect of MS.
A bioassay was developed with
tumor
cell lines grown in culture and stimulated with serum before and after a diet and exercise intervention.
Diet and exercise altered serum factors that slowed the growth rate and induced apoptosis in androgen-dependent
prostate
cancer cells.
Hyperinsulinemia stimulates liver production of IGF-I, plays a role in the promotion
of prostate
cancer, and thus is the cornerstone for both MS and
prostate
cancer.
Adopting a low-fat starch diet with daily exercise controls MS and should reduce the risk
of prostate
cancer.
[MeSH-major]
Diet, Fat-Restricted. Exercise / physiology. Metabolic Syndrome X / diet therapy. Nutritional Physiological Phenomena / physiology.
Prostatic
Neoplasms
/ prevention & control
[MeSH-minor]
Diet, Reducing. Humans. Insulin-Like Growth Factor Binding Protein 3 / metabolism. Insulin-Like Growth Factor Binding Protein 3 / physiology. Insulin-Like Growth Factor I / metabolism. Insulin-Like Growth Factor I / physiology. Male. Risk Factors.
Tumor
Cells, Cultured
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(PMID = 18265484.001).
[ISSN]
0002-9165
[Journal-full-title]
The American journal of clinical nutrition
[ISO-abbreviation]
Am. J. Clin. Nutr.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P50 CA-921310-01A1; United States / NCI NIH HHS / CA / R01 CA-100938
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Insulin-Like Growth Factor Binding Protein 3; 67763-96-6 / Insulin-Like Growth Factor I
[Number-of-references]
62
3.
Berry LJ, Au GG, Barry RD, Shafren DR:
Potent oncolytic activity of human enteroviruses against human prostate cancer.
Prostate
; 2008 May 1;68(6):577-87
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[Title]
Potent oncolytic activity of human enteroviruses against human
prostate
cancer.
BACKGROUND: Oncolytic virotherapy offers a unique treatment modality for
prostate
cancer, especially stages that are resistant to current therapies, with the additional benefit of preferentially targeting
tumor
cells amongst an environment of healthy tissue.
Herein, the low pathogenic enteroviruses; Coxsackievirus A21 (CVA21), as well as a bio-selected variant of Coxsackievirus A21 (CVA21-DAFv) and Echovirus 1 (EV1) are evaluated as novel oncolytic agents against human
prostate
cancer.
METHODS: The surface expression of viral receptors required for enterovirus cell attachment/entry, including intercellular adhesion molecule-1 (ICAM-1), decay-accelerating factor (DAF) and integrin alpha(2)beta(1) on a number of human
prostate
cancer lines was assessed by flow cytometry.
RESULTS: The majority
of prostate
cancer lines tested expressed surface ICAM-1 and/or DAF, or alpha(2)beta(1), facilitating significant degrees of oncolysis following in vitro viral challenge.
Systemic delivery of each of the three viruses induced reduction of xenograft
tumor
burdens in vivo, and a therapeutic dose-response was demonstrated for escalating doses of EV1 in the LNCaP animal model.
CONCLUSION: Enteroviruses CVA21, CVA21-DAFv, and EV1 are potentially potent oncolytic agents against human
prostate
cancer.
[MeSH-major]
Enterovirus A, Human / physiology. Enterovirus B, Human / physiology. Membrane Glycoproteins / metabolism. Oncolytic Virotherapy. Oncolytic Viruses / physiology.
Prostatic
Neoplasms
/ virology
[MeSH-minor]
Animals. Antigens, CD55 / metabolism. Cell Line,
Tumor
. Flow Cytometry. Humans. Integrin alpha2beta1 / metabolism. Intercellular Adhesion Molecule-1 / metabolism. Male. Mice. Mice, Inbred BALB C. Mice, SCID. Specific Pathogen-Free Organisms. Virus Replication. Xenograft Model Antitumor Assays
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(PMID = 18288643.001).
[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 / Antigens, CD55; 0 / Integrin alpha2beta1; 0 / Membrane Glycoproteins; 126547-89-5 / Intercellular Adhesion Molecule-1
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4.
Moretti RM, Montagnani Marelli M, Mai S, Cariboni A, Scaltriti M, Bettuzzi S, Limonta P:
Clusterin isoforms differentially affect growth and motility of prostate cells: possible implications in prostate tumorigenesis.
Cancer Res
; 2007 Nov 1;67(21):10325-33
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[Title]
Clusterin isoforms differentially affect growth and motility
of prostate
cells: possible implications in
prostate
tumorigenesis.
The possible differential roles played by the two clusterin forms in growth and motility of nonmalignant and malignant
prostate
cells are investigated here. sCLU or nCLU was transiently transfected in both androgen-independent
prostate
cancer cells (PC3 and DU 145) and immortalized
prostate
epithelial cells (PNT1A, a nontumoral control).
Thus, CLU gene expression might play a crucial role in
prostate
tumorigenesis by exerting differential biological effects on normal versus
tumor
cells through differential processing of CLU isoforms in the two cell systems.
[MeSH-major]
Clusterin / physiology.
Prostatic
Neoplasms
/ etiology
[MeSH-minor]
Actinin / analysis. Actins / analysis. Cell Line,
Tumor
. Cell Movement. Cell Proliferation. Fluorescent Antibody Technique. Humans. Male. Protein Isoforms
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(PMID = 17974975.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Actins; 0 / CLU protein, human; 0 / Clusterin; 0 / Protein Isoforms; 11003-00-2 / Actinin
5.
Mottet N, Bourmaud A, Droz JP:
[Prostate cancer screening and early diagnosis].
Rev Prat
; 2010 Feb 20;60(2):205-11
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[Title]
[
Prostate
cancer screening and early
diagnosis
].
[Transliterated title]
Dépistage et diagnostic précoce du cancer
de la prostate
.
Prostate
cancer is the first cancer by incidence in men.
This decision making strategy is also true for screening and early
diagnosis
.
The current recommendation is an individual early
diagnosis
procedure based on the measure of serum PSA level and Digital Rectal Examination.
[MeSH-major]
Early Detection of Cancer. Mass Screening.
Prostatic
Neoplasms
/
diagnosis
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(PMID = 20225559.001).
[ISSN]
0035-2640
[Journal-full-title]
La Revue du praticien
[ISO-abbreviation]
Rev Prat
[Language]
fre
[Publication-type]
English Abstract; Journal Article
[Publication-country]
France
6.
Bar-Shira A, Matarasso N, Rosner S, Bercovich D, Matzkin H, Orr-Urtreger A:
Mutation screening and association study of the candidate prostate cancer susceptibility genes MSR1, PTEN, and KLF6.
Prostate
; 2006 Jul 1;66(10):1052-60
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[Title]
Mutation screening and association study of the candidate
prostate
cancer susceptibility genes MSR1, PTEN, and KLF6.
BACKGROUND: MSR1, PTEN, and KLF6 have been implicated as candidate susceptibility genes for
prostate
tumorigenesis.
METHODS: Three hundred Jewish
prostate
cancer patients were screened for alterations in these genes.
The KLF6 IVS1-27G>A polymorphism, recently associated with
prostate
cancer risk, was detected in 11.9% of the patients and 17.3% of the controls (P = 0.043).
IVS1-27A allele frequency was significantly lower in
prostate
cancer patients (P = 0.030), specifically in Ashkenazi patients (P = 0.047) compared to controls.
CONCLUSIONS: We found no evidence that MSR1 and PTEN germline mutations are associated with
prostate
cancer risk in Jews.
The negative association between KLF6 IVS1-27A and
prostate
cancer risk supports a population-specific effect of susceptibility alleles in
prostate
tumorigenesis.
[MeSH-major]
Genetic Predisposition to Disease. Genetic Testing. Kruppel-Like Transcription Factors / genetics. PTEN Phosphohydrolase / genetics.
Prostatic
Neoplasms
/ genetics. Proto-Oncogene Proteins / genetics. Scavenger Receptors, Class A / genetics
[MeSH-minor]
Adult. DNA,
Neoplasm
/ genetics. Female. Gene Expression Regulation, Neoplastic. Gene Frequency. Genotype. Germ-Line Mutation. Humans. Israel. Male. Middle Aged. Mutation, Missense. Pedigree. Polymorphism, Genetic. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors
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[Copyright]
Copyright 2005 Wiley-Liss, Inc.
(PMID = 16598737.001).
[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 / DNA, Neoplasm; 0 / KLF6 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / MSR1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Scavenger Receptors, Class A; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
7.
Garbis SD, Tyritzis SI, Roumeliotis T, Zerefos P, Giannopoulou EG, Vlahou A, Kossida S, Diaz J, Vourekas S, Tamvakopoulos C, Pavlakis K, Sanoudou D, Constantinides CA:
Search for potential markers for prostate cancer diagnosis, prognosis and treatment in clinical tissue specimens using amine-specific isobaric tagging (iTRAQ) with two-dimensional liquid chromatography and tandem mass spectrometry.
J Proteome Res
; 2008 Aug;7(8):3146-58
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[Title]
Search for potential markers for
prostate
cancer
diagnosis
, prognosis and treatment in clinical tissue specimens using amine-specific isobaric tagging (iTRAQ) with two-dimensional liquid chromatography and tandem mass spectrometry.
This study aimed to identify candidate new
diagnosis
and prognosis markers and medicinal targets
of prostate
cancer (PCa), using state of the art proteomics.
A total of 20
prostate
tissue specimens from 10 patients with
benign prostatic
hyperplasia (BPH) and 10 with PCa (
Tumour
Node Metastasis [TNM] stage T1-T3) were analyzed by isobaric stable isotope labeling (iTRAQ) and two-dimensional liquid chromatography-tandem mass spectrometry (2DLC-MS/MS) approaches using a hybrid quadrupole time-of-flight system (QqTOF).
Selected findings were confirmed by immunohistochemical analysis
of prostate
tissue specimens.
[MeSH-major]
Biomarkers,
Tumor
/ metabolism.
Prostatic
Hyperplasia / metabolism.
Prostatic
Neoplasms
/ metabolism. Proteome / metabolism
[MeSH-minor]
Aged. Amino Acid Sequence. Biomarkers / metabolism. Chromatography, Liquid. Humans. Immunohistochemistry. Male. Middle Aged. Molecular Sequence Data. Prognosis.
Prostate
-Specific Antigen / metabolism. Reproducibility of Results. Tandem Mass Spectrometry
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(PMID = 18553995.001).
[ISSN]
1535-3893
[Journal-full-title]
Journal of proteome research
[ISO-abbreviation]
J. Proteome Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / Proteome; EC 3.4.21.77 / Prostate-Specific Antigen
8.
Holyoak JD, Crawford ED, Meacham RB:
Testosterone and the prostate: implications for the treatment of hypogonadal men.
Curr Urol Rep
; 2008 Nov;9(6):500-5
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[Title]
Testosterone and
the prostate
: implications for the treatment of hypogonadal men.
Because aging men are at risk for
benign prostatic
hyperplasia (BPH) and
prostate
cancer, elucidating the relationship between testosterone and these diseases is crucial to ensure its safe administration.
It is known that testosterone supplementation may worsen active
prostate
cancer and that its blockade or removal slows the disease's progression.
However, recent studies have attempted to show that, in individuals in whom
prostate
cancer has been ruled out, TRT may simply restore serum testosterone levels to within normal limits without significant adverse affects on
the prostate
.
Patients undergoing TRT should be monitored carefully for any evidence of
prostatic
disease.
[MeSH-major]
Hypogonadism / drug therapy.
Prostate
/ physiology. Testosterone / therapeutic use
[MeSH-minor]
Humans. Male.
Prostatic
Hyperplasia / etiology.
Prostatic
Neoplasms
/ etiology
Hazardous Substances Data Bank.
TESTOSTERONE
.
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[ISSN]
1534-6285
[Journal-full-title]
Current urology reports
[ISO-abbreviation]
Curr Urol Rep
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
3XMK78S47O / Testosterone
9.
Stachon A:
[Significance of the PSA-concentration for the detection of prostate cancer].
Pathologe
; 2005 Nov;26(6):469-72
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[Title]
[Significance of the PSA-concentration for the detection
of prostate
cancer].
Prostate
cancer among adult males is the most common
neoplasm
in western countries.
Prostate
specific antigen (PSA) is now a well established
tumor
marker that aids in the early detection of localized
prostate
cancer.
Increased PSA concentrations are found in the serum of patients with
benign prostatic
hyperplasia or patients with
prostate
cancer, respectively.
[MeSH-major]
Biomarkers,
Tumor
/ blood.
Prostate
-Specific Antigen / blood.
Prostatic
Neoplasms
/ pathology
[MeSH-minor]
Aged. Cell Transformation, Neoplastic / pathology.
Diagnosis
, Differential. Humans. Male. Middle Aged. Predictive Value of Tests.
Prostate
/ pathology.
Prostatic
Hyperplasia / blood.
Prostatic
Hyperplasia /
diagnosis
.
Prostatic
Hyperplasia / pathology.
Prostatic
Hyperplasia / surgery. Reference Values
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0172-8113
[Journal-full-title]
Der Pathologe
[ISO-abbreviation]
Pathologe
[Language]
ger
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
10.
Sun T, Lee GS, Oh WK, Pomerantz M, Yang M, Xie W, Freedman ML, Kantoff PW:
Single-nucleotide polymorphisms in p53 pathway and aggressiveness of prostate cancer in a Caucasian population.
Clin Cancer Res
; 2010 Nov 1;16(21):5244-51
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[Title]
Single-nucleotide polymorphisms in p53 pathway and aggressiveness
of prostate
cancer in a Caucasian population.
PURPOSE:
The tumor
suppressor p53 plays a crucial role in maintaining genomic stability and
tumor
prevention.
Despite the importance of the p53 pathway in
prostate
cancer development and progression, little is known about the association of functional single-nucleotide polymorphisms (SNP) in the p53 pathway genes and
prostate
cancer aggressiveness.
EXPERIMENTAL DESIGN: In this study, we analyze the association of SNPs in p53, Mdm2, Mdm4, and Hausp genes with
prostate
cancer clinicopathologic variables in a large hospital-based Caucasian
prostate
cancer cohort (N = 4,073).
RESULTS: We found that the Mdm2 SNP309 T allele was associated with earlier onset
prostate
cancer (P = 0.004), higher Gleason scores (P = 0.004), and higher stages in men undergoing a radical prostatectomy (P = 0.011).
Both the Mdm4 and Hausp SNPs (rs1380576 and rs1529916) were found to be associated with higher D'Amico risk
prostate
cancer category at the time
of diagnosis
(P = 0.023 and P = 0.046, respectively).
We did not observe any statistically significant association between the p53 Arg72Pro polymorphism and
prostate
cancer aggressiveness or pathologic variables.
CONCLUSIONS: These results suggested the importance of these p53 regulators in
prostate
cancer development and progression.
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[Copyright]
©2010 AACR.
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Mod Pathol. 2001 May;14(5):428-36
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11353053.001
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(PMID = 20855462.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50 CA090381; United States / NCI NIH HHS / CA / 2 P50 CA090381-06
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / MDM4 protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; EC 3.1.2.15 / USP7 protein, human; EC 3.1.2.15 / Ubiquitin Thiolesterase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
[Other-IDs]
NLM/ NIHMS225371; NLM/ PMC2970725
11.
Brasky TM, Velicer CM, Kristal AR, Peters U, Potter JD, White E:
Nonsteroidal anti-inflammatory drugs and prostate cancer risk in the VITamins And Lifestyle (VITAL) cohort.
Cancer Epidemiol Biomarkers Prev
; 2010 Dec;19(12):3185-8
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[Title]
Nonsteroidal anti-inflammatory drugs and
prostate
cancer risk in the VITamins And Lifestyle (VITAL) cohort.
INTRODUCTION: Chronic inflammation may be important in
prostate
carcinogenesis.
Several epidemiologic studies have reported inverse associations between nonsteroidal anti-inflammatory drugs (NSAIDs) and
prostate
cancer risk, although many studies are limited by assessment of short-term use only.
Cox proportional hazards models were used to estimate adjusted hazard ratios (HR) and 95% confidence intervals (95% CI) of 10-year average use of individual NSAIDs with total
prostate
cancer (n = 1,550) and
prostate
cancer by grade.
RESULTS: Low-dose aspirin, regular-strength aspirin, ibuprofen, and any nonaspirin NSAID (ibuprofen, naproxen, and COX-2 inhibitors) were not associated with
prostate
cancer risk.
CONCLUSION: NSAID use was not associated with
prostate
cancer risk in the VITAL cohort.
IMPACT: Our findings do not support the use of NSAIDs for chemoprevention
of prostate
cancer.
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[Copyright]
©2010 AACR.
[Cites]
Nat Rev Cancer. 2007 Apr;7(4):256-69
[
17384581.001
]
[Cites]
Int J Cancer. 2010 Oct 1;127(7):1680-91
[
20091856.001
]
[Cites]
Clin Cancer Res. 2004 Nov 15;10(22):7727-37
[
15570007.001
]
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14693663.001
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]
[Cites]
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10953162.001
]
(PMID = 20935064.001).
[ISSN]
1538-7755
[Journal-full-title]
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
[ISO-abbreviation]
Cancer Epidemiol. Biomarkers Prev.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R25 CA094880-10; United States / NCI NIH HHS / CA / K05 CA154337; United States / NCI NIH HHS / CA / R25 CA094880; United States / NCI NIH HHS / CA / K05-CA154337; United States / NCI NIH HHS / CA / R25-CA94880
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal
[Other-IDs]
NLM/ NIHMS243668; NLM/ PMC3005534
12.
Macura KJ, Stoianovici D:
Advancements in magnetic resonance-guided robotic interventions in the prostate.
Top Magn Reson Imaging
; 2008 Dec;19(6):297-304
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[Title]
Advancements in magnetic resonance-guided robotic interventions in
the prostate
.
Magnetic resonance imaging (MRI) provides more detailed anatomical images of the
prostate
compared with the transrectal ultrasound imaging.
Therefore, for the purpose of intervention in
the prostate gland
, diagnostic or therapeutic, MRI guidance offers a possibility of more precise targeting that may be crucial to the success
of prostate
interventions.
Several systems have been already tested clinically for
prostate
biopsy and brachytherapy.
As technology matures, precise image guidance for
prostate
interventions performed or assisted by specialized MR-compatible robotic devices may provide a uniquely accurate solution for guiding the intervention directly based on MR findings and feedback.
Such an instrument would become a valuable clinical tool for biopsies directly targeting imaged
tumor
foci and delivering
tumor
-centered focal therapy.
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(PMID = 19512852.001).
[ISSN]
1536-1004
[Journal-full-title]
Topics in magnetic resonance imaging : TMRI
[ISO-abbreviation]
Top Magn Reson Imaging
[Language]
ENG
[Grant]
United States / NIBIB NIH HHS / EB / RC1 EB010936-01; United States / CCR NIH HHS / RC / EB010936-02; United States / NIBIB NIH HHS / EB / RC1 EB010936; United States / NIBIB NIH HHS / EB / RC1 EB010936-02; United States / CCR NIH HHS / RC / EB010936-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
57
[Other-IDs]
NLM/ NIHMS284671; NLM/ PMC3099454
13.
Raffoul JJ, Banerjee S, Che M, Knoll ZE, Doerge DR, Abrams J, Kucuk O, Sarkar FH, Hillman GG:
Soy isoflavones enhance radiotherapy in a metastatic prostate cancer model.
Int J Cancer
; 2007 Jun 1;120(11):2491-8
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[Title]
Soy isoflavones enhance radiotherapy in a metastatic
prostate
cancer model.
We previously reported that genistein, the bioactive isoflavone of soybeans, acts as a radiosensitizer for
prostate
cancer.
Pretreatment
of tumor
cells with genistein potentiated radiation-induced killing in vitro and in orthotopic models in vivo.
Soy isoflavones inhibited cell survival and potentiated radiation cell killing in PC-3
tumor
cells, in vitro.
In vivo, using the PC-3 orthotopic metastatic mouse model, soy isoflavones and
prostate tumor
irradiation led to enhanced control of primary
tumor
growth and metastasis, as observed with pure genistein and radiation.
Histologically
prostate
tumors, treated with soy isoflavones and radiation, showed
tumor
destruction and in situ tissue alterations, comparable with genistein and radiation effects.
However, genistein, but not soy isoflavones, caused induction of HIF1-alpha in
prostate
tumors, suggesting that induction of hypoxia by pure genistein could contribute to increased metastasis.
Our studies demonstrate the safety and potential role of soy isoflavones for enhancing the therapeutic effect of radiotherapy in
prostate
cancer.
[MeSH-major]
Genistein / pharmacology.
Prostatic
Neoplasms
/ radiotherapy. Radiotherapy. Soybeans / chemistry
[MeSH-minor]
Animals. Blotting, Western. Cell Line,
Tumor
. Humans. Male. Mice.
Neoplasm
Metastasis.
Neoplasm
Transplantation
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GENISTEIN
.
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(PMID = 17304503.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
DH2M523P0H / Genistein
14.
Shah SK, Lui PD, Baldwin DD, Ruckle HC:
Urothelial carcinoma after external beam radiation therapy for prostate cancer.
J Urol
; 2006 Jun;175(6):2063-6
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[Title]
Urothelial carcinoma after external beam radiation therapy for
prostate
cancer.
PURPOSE: We reviewed the clinical course of patients in whom urothelial carcinoma developed following radiation therapy for
prostate
cancer.
MATERIALS AND METHODS: A retrospective review of all patients between 1990 and 2005 with
the diagnosis
of bladder and
prostate
cancer was performed.
Of 125 total patients new onset urothelial carcinoma developed in 11 after undergoing external beam radiation therapy for
prostate
cancer.
RESULTS: Whole pelvis external beam radiation therapy with a proton boost to
the prostate
was the radiation modality in 7 of the 11 patients (64%), while the remaining 4 patients received standard external beam radiation only.
Average patient age at
diagnosis
was 72 years (range 64 to 84).
Of the 11 patients 10 (91%) were nonsmokers at the time of urothelial carcinoma
diagnosis
.
CONCLUSIONS: Urothelial carcinoma in patients with previous radiation therapy for
prostate
cancer is often high grade, and the majority of patients have cancer progression requiring cystectomy.
[MeSH-major]
Carcinoma, Transitional Cell / etiology.
Neoplasms
, Radiation-Induced / etiology.
Prostatic
Neoplasms
/ radiotherapy. Urinary Bladder
Neoplasms
/ etiology
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(PMID = 16697804.001).
[ISSN]
0022-5347
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
15.
Crocetti E, Ciatto S, Buzzoni C, Zappa M:
Prostate cancer incidence rates have started to decrease in central Italy.
J Med Screen
; 2010;17(1):50-1
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[Title]
Prostate
cancer incidence rates have started to decrease in central Italy.
The widespread use
of prostate
-specific antigen (PSA) testing has dramatically changed the epidemiology
of prostate
cancer.
Similar changes have been documented also in the area of the Tuscany Cancer Registry, central Italy, where
prostate
cancer incidence rates doubled from the early 1990s to 2003 and afterwards decreased.
This is the first evidence, to our knowledge, of a decline in
prostate
cancer incidence in Italy following the screening-related increase.
[MeSH-major]
Prostatic
Neoplasms
/ epidemiology
[MeSH-minor]
Humans. Italy / epidemiology. Male.
Prostate
-Specific Antigen / metabolism
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(PMID = 20356946.001).
[ISSN]
1475-5793
[Journal-full-title]
Journal of medical screening
[ISO-abbreviation]
J Med Screen
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
16.
Fritzsche FR, Jung M, Xu C, Rabien A, Schicktanz H, Stephan C, Dietel M, Jung K, Kristiansen G:
ADAM8 expression in prostate cancer is associated with parameters of unfavorable prognosis.
Virchows Arch
; 2006 Dec;449(6):628-36
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[Title]
ADAM8 expression in
prostate
cancer is associated with parameters of unfavorable prognosis.
Gene products of the A disintegrin and metalloprotease (ADAM) family are critically involved in carcinogenesis and
tumor
progression of various solid tumors.
Little is known about ADAM8 in
prostate
cancer.
In our quest for novel diagnostic tissue markers
of prostate
cancer, we aimed to evaluate the expression of ADAM8 in
prostate
cancer and to correlate it with clinicopathological parameters.
One hundred twenty-eight clinicopathologically characterized
prostate
cancer patients, with available follow-up data, were immunostained for ADAM8.
Still, a significant prognostic value for
the prostate
-specific antigen relapse-free survival of ADAM8 could not be demonstrated.
Therefore, despite of its significant association with conventional parameters of an unfavorable prognosis, ADAM8 adds only limited information to the conventional histopathological assessment
of prostate
cancer.
[MeSH-major]
ADAM Proteins / analysis. Membrane Proteins / analysis.
Prostatic
Neoplasms
/ chemistry
[MeSH-minor]
Aged. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis.
Prostate
/ chemistry. RNA, Messenger / analysis
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[ISSN]
0945-6317
[Journal-full-title]
Virchows Archiv : an international journal of pathology
[ISO-abbreviation]
Virchows Arch.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Membrane Proteins; 0 / RNA, Messenger; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / ADAM8 protein, human
17.
Flitsch J, Bernreuther C, Hagel C, Lüdecke DK:
Hypophysectomy for prostate cancer: a revival of old knowledge?
J Neurosurg
; 2008 Oct;109(4):760-4
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[Title]
Hypophysectomy for
prostate
cancer: a revival of old knowledge?
The growth
of prostate
cancer is controlled by several hormones and growth factors.
In cases of metastasized
prostate
cancer, antigonadotropic therapy is currently considered state-of-the-art treatment.
The authors present the case of a 63-year-old man with metastatic
prostate
cancer who presented with high serum
prostate
-specific antigen levels (1216 microg/L) and cavernous sinus syndrome.
Because of the elevated prolactin and high-normal IGF-I levels he was offered a hypophysectomy in addition to pituitary
tumor
removal.
Histological examination of the resected lesion confirmed a nonsecreting pituitary adenoma with infiltration
of prostate
cancer cells.
Postoperatively the patient's
prostate
-specific antigen levels dropped to 876 microg/L, his bone pain resolved, and the cavernous sinus syndrome improved.
A reduction of IGF-I levels even in the final stage metastasized
prostate
cancer may play a major role.
[MeSH-major]
Hypophysectomy. Pituitary
Neoplasms
/ secondary. Pituitary
Neoplasms
/ surgery.
Prostatic
Neoplasms
/ pathology
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(PMID = 18826367.001).
[ISSN]
0022-3085
[Journal-full-title]
Journal of neurosurgery
[ISO-abbreviation]
J. Neurosurg.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
67763-96-6 / Insulin-Like Growth Factor I
18.
Rodriguez C, Patel AV, Mondul AM, Jacobs EJ, Thun MJ, Calle EE:
Diabetes and risk of prostate cancer in a prospective cohort of US men.
Am J Epidemiol
; 2005 Jan 15;161(2):147-52
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[Title]
Diabetes and risk
of prostate
cancer in a prospective cohort of US men.
One previous study has suggested that diabetes may decrease risk
of prostate
cancer but only several years after
diagnosis of
diabetes.
The authors examined the role of timing of diabetes
diagnosis
in relation to risk
of prostate
cancer among men in the Cancer Prevention Study II Nutrition Cohort.
The authors documented 5,318 cases of incident
prostate
cancer through August 31, 2001, among 72,670 men.
Results from Cox proportional hazards models showed that diabetes was associated with a lower incidence
of prostate
cancer (rate ratio (RR) = 0.67, 95% confidence interval (CI): 0.60, 0.75).
This association differed significantly by time since
diagnosis of
diabetes (p < 0.0002); risk
of prostate
cancer was slightly increased during the first 3 years after
diagnosis of
diabetes (RR = 1.23, 95% CI: 0.92, 1.65) but was reduced among men diagnosed 4 or more years before (RR = 0.63, 95% CI: 0.56, 0.71).
Study results are consistent with the hypothesis that diabetes is associated with reduced risk
of prostate
cancer but only several years after
diagnosis of
diabetes.
[MeSH-major]
Diabetes Mellitus, Type 2 / complications.
Prostatic
Neoplasms
/ etiology
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(PMID = 15632264.001).
[ISSN]
0002-9262
[Journal-full-title]
American journal of epidemiology
[ISO-abbreviation]
Am. J. Epidemiol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
19.
Chuu CP, Kokontis JM, Hiipakka RA, Liao S:
Modulation of liver X receptor signaling as novel therapy for prostate cancer.
J Biomed Sci
; 2007 Sep;14(5):543-53
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[Title]
Modulation of liver X receptor signaling as novel therapy for
prostate
cancer.
Recently we observed that LXR agonists suppressed proliferation
of prostate
and breast cancer cells in vitro and treatment of mice with the LXR agonist T0901317 suppressed the growth
of prostate tumor
xenografts.
T0901317 induced expression of ATP-binding cassette transporter A1 (ABCA1) and delayed the progression of androgen-dependent human
prostate tumor
xenografts towards androgen-independency in mice.
Phytosterols, the plant equivalent of mammalian cholesterol, have recently been shown to be agonists for LXRs. beta-Sitosterol and campesterol, the two most common phytosterols, suppressed proliferation
of prostate
and breast cancer cells.
This review examines the potential use of LXR signaling as a therapeutic target in
prostate
and other cancers.
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(PMID = 17372849.001).
[ISSN]
1021-7770
[Journal-full-title]
Journal of biomedical science
[ISO-abbreviation]
J. Biomed. Sci.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA058073; United States / NCI NIH HHS / CA / CA58073
[Publication-type]
Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Orphan Nuclear Receptors; 0 / Receptors, Cytoplasmic and Nuclear; 0 / liver X receptor
[Number-of-references]
88
20.
Guo CC, Pisters LL, Troncoso P:
Prostate cancer invading the rectum: a clinicopathological study of 18 cases.
Pathology
; 2009;41(6):539-43
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[Title]
Prostate
cancer invading the rectum: a clinicopathological study of 18 cases.
AIMS:
Prostate
cancer may involve the rectum and cause severe perineal pain.
The aim of this study was to understand the rectal involvement by
prostate
cancer and its clinical significance.
METHODS: We evaluated pathological and clinical features of 18 cases
of prostate
cancer with rectal involvement.
Twelve patients received rectal biopsies, which revealed poorly differentiated
prostatic
adenocarcinoma (n = 6), squamous cell carcinoma (n = 3), angiosarcoma (n = 1), or no
tumour
(n = 2).
All patients received palliative total pelvic exenteration, which demonstrated
prostate
cancer invading the rectal wall.
In these resection specimens, the
tumour
consisted of poorly differentiated
prostatic
adenocarcinoma (n = 16), squamous cell carcinoma (n = 1), or angiosarcoma (n = 1).
In addition, six cases of
prostatic
adenocarcinomas also showed focal squamous (n = 3) or high-grade neuroendocrine (n = 3) differentiation.
CONCLUSIONS:
Prostate
cancer with rectal involvement often develops heterogeneous differentiation and carries a dismal prognosis.
[MeSH-major]
Adenocarcinoma / pathology. Carcinoma, Squamous Cell / pathology. Hemangiosarcoma / pathology.
Prostatic
Neoplasms
/ pathology. Rectal
Neoplasms
/ pathology
[MeSH-minor]
Aged. Biopsy. Combined Modality Therapy. Fatal Outcome. Humans. Male. Middle Aged.
Neoplasm
Invasiveness. Prognosis
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(PMID = 19900102.001).
[ISSN]
1465-3931
[Journal-full-title]
Pathology
[ISO-abbreviation]
Pathology
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
21.
de Muga S, Hernández S, Agell L, Salido M, Juanpere N, Lorenzo M, Lorente JA, Serrano S, Lloreta J:
Molecular alterations of EGFR and PTEN in prostate cancer: association with high-grade and advanced-stage carcinomas.
Mod Pathol
; 2010 May;23(5):703-12
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[Title]
Molecular alterations of EGFR and PTEN in
prostate
cancer: association with high-grade and advanced-stage carcinomas.
Prostate
cancer is the second cause of cancer-related death in men of the Western world.
The potential prognostic role of the combined alterations in EGFR and PTEN in
prostate
cancer is not well established.
Prevalence of EGFR and PTEN somatic mutations, EGFR amplification and EGFR protein expression were investigated in a series
of prostate
adenocarcinomas, classified according to the current Gleason grading system.
Mutational analysis revealed eight EGFR and three PTEN mutations in 98 (8%) and 92 (3%)
prostate
adenocarcinomas, respectively.
In 35% of adenocarcinomas we found some type of EGFR-PTEN alteration, with a tendency to be associated with advanced-stage
prostate
adenocarcinomas (P=0.04).
The IVS18+19 polymorphism was also associated with more advanced
prostate
adenocarcinomas.
This is the first study reporting mutations of EGFR and PTEN in the same series
of prostate
adenocarcinomas.
Mutations in EGFR and PTEN genes are a minor event, although
prostate
cancer represents the third
neoplasm
in which the EGFR gene mutations are more prevalent.
Alterations in the EGFR-PTEN signaling pathway are present in a third
of prostate
adenocarcinomas, particularly affecting the more advanced cases.
[MeSH-major]
Adenocarcinoma / genetics. PTEN Phosphohydrolase / genetics.
Prostatic
Neoplasms
/ genetics. Receptor, Epidermal Growth Factor / genetics
[MeSH-minor]
DNA Mutational Analysis. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Mutation.
Neoplasm
Staging. Polymerase Chain Reaction. Polymorphism, Genetic. Severity of Illness Index. Signal Transduction / genetics
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(PMID = 20208477.001).
[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; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.67 / PTEN Phosphohydrolase
22.
Hoffman RM, Barry MJ, Stanford JL, Hamilton AS, Hunt WC, Collins MM:
Health outcomes in older men with localized prostate cancer: results from the Prostate Cancer Outcomes Study.
Am J Med
; 2006 May;119(5):418-25
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[Title]
Health outcomes in older men with localized
prostate
cancer: results from
the Prostate
Cancer Outcomes Study.
PURPOSE: We compared health-related quality-of-life (HRQOL) outcomes and survival of men with localized
prostate
cancer who received aggressive treatment with those receiving conservative management.
We used medical record abstractions and patient surveys to obtain clinical and HRQOL data at
diagnosis
and 24-month follow-up.
RESULTS: At 24 months following
diagnosis
, aggressively treated men were more likely to report daily urinary leakage (odds ratio [OR] = 2.9, 95% confidence interval [CI] 1.2-7.0) and to be bothered by urinary problems (OR = 5.1, 95% CI, 1.3-9.1) and sexual problems (OR = 2.8, 95% CI, 1.2-6.3).
However, men who were aggressively treated for localized cancer had a minimally reduced absolute risk of dying from
prostate
cancer.
[MeSH-major]
Prostatic
Neoplasms
/ pathology.
Prostatic
Neoplasms
/ therapy. Quality of Life
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(PMID = 16651054.001).
[ISSN]
1555-7162
[Journal-full-title]
The American journal of medicine
[ISO-abbreviation]
Am. J. Med.
[Language]
eng
[Grant]
United States / NCI NIH HHS / PC / N01-PC-67000; United States / NCI NIH HHS / PC / N01-PC-67005; United States / NCI NIH HHS / PC / N01-PC-67006; United States / NCI NIH HHS / PC / N01-PC-67007; United States / NCI NIH HHS / PC / N01-PC-67010; United States / PHS HHS / / N01-PCN-67009
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
23.
Stamatiou K, Skolarikos A, Heretis I, Papadimitriou V, Alevizos A, Ilias G, Karanasiou V, Mariolis A, Sofras F:
Does educational printed material manage to change compliance with prostate cancer screening?
World J Urol
; 2008 Aug;26(4):365-73
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[Title]
Does educational printed material manage to change compliance with
prostate
cancer screening?
The aim of our study was to evaluate the impact of similar printed educational material on
prostate
cancer screening by PSA and DRE.
MATERIAL AND METHODS: Thousand five hundred men aged between 50 and 86 years of age, who attended our institutions for various medical conditions except
prostate
-related conditions, were randomly assigned to two study groups.
Men in the informed group, received an educational leaflet with simple, general information on
prostate
cancer screening methods given by their physician along with treatment and other regular recommendations, while men in the non-informed group, were only informed by their physician in the examination room during an interview.
CONCLUSIONS: A single, one-shift distribution of printed educational material on
prostate
cancer screening, changed their attitude regarding
prostate
cancer screening only in favour of PSA testing, while did not manage to change the DRE acceptance behavior.
However, since the combination of the two tests is more sensitive for
diagnosis
than either one alone, there is a need of introducing intervention strategies, in the efforts of ameliorating
the prostate
cancer screening behavior.
[MeSH-major]
Mass Screening / methods. Pamphlets. Patient Compliance. Patient Education as Topic / methods.
Prostatic
Neoplasms
/
diagnosis
[MeSH-minor]
Aged. Aged, 80 and over. Digital Rectal Examination. Health Behavior. Humans. Male. Middle Aged.
Prostate
-Specific Antigen / blood. Surveys and Questionnaires
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0724-4983
[Journal-full-title]
World journal of urology
[ISO-abbreviation]
World J Urol
[Language]
eng
[Publication-type]
Journal Article; Randomized Controlled Trial
[Publication-country]
Germany
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
24.
Pal P, Xi H, Kaushal R, Sun G, Jin CH, Jin L, Suarez BK, Catalona WJ, Deka R:
Variants in the HEPSIN gene are associated with prostate cancer in men of European origin.
Hum Genet
; 2006 Sep;120(2):187-92
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[Title]
Variants in the HEPSIN gene are associated with
prostate
cancer in men of European origin.
There is considerable evidence that genetic factors are involved in
prostate
cancer susceptibility.
We have studied the association of 11 single nucleotide polymorphisms (SNPs) in the HEPSIN gene (HPN) with
prostate
cancer in men of European ancestry.
HPN is a likely candidate in
prostate
cancer susceptibility, as it encodes a transmembrane cell surface serum protease, which is overexpressed in
prostate
cancer; HPN is also located on 19q11-q13.2, where linkage is found with
prostate
cancer susceptibility.
In this case-control association study (590 men with histologically verified
prostate
cancer and 576 unrelated controls, all of European descent), we find significant allele frequency differences between cases and controls at five SNPs that are located contiguously within the gene.
A major 11-locus haplotype is significantly associated, which provides further support that HPN is a potentially important candidate gene involved in
prostate
cancer susceptibility.
Association of one of the SNPs with Gleason score is also suggestive of a plausible role of HPN in
tumor
aggressiveness.
[MeSH-major]
European Continental Ancestry Group / genetics. Genetic Predisposition to Disease. Polymorphism, Single Nucleotide.
Prostatic
Neoplasms
/ genetics. Serine Endopeptidases / genetics
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[ISSN]
0340-6717
[Journal-full-title]
Human genetics
[ISO-abbreviation]
Hum. Genet.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / hepsin
25.
Liu P, Ramachandran S, Ali Seyed M, Scharer CD, Laycock N, Dalton WB, Williams H, Karanam S, Datta MW, Jaye DL, Moreno CS:
Sex-determining region Y box 4 is a transforming oncogene in human prostate cancer cells.
Cancer Res
; 2006 Apr 15;66(8):4011-9
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[Title]
Sex-determining region Y box 4 is a transforming oncogene in human
prostate
cancer cells.
Prostate
cancer is the most commonly diagnosed noncutaneous
neoplasm
and second most common cause of cancer-related mortality in western men.
To investigate the mechanisms
of prostate
cancer development and progression, we did expression profiling of human
prostate
cancer and
benign
tissues.
We show that the SOX4 is overexpressed in
prostate tumor
samples compared with
benign
tissues by microarray analysis, real-time PCR, and immunohistochemistry.
Silencing of SOX4 by small interfering RNA transfection induced apoptosis
of prostate
cancer cells, suggesting that SOX4 could be a therapeutic target for
prostate
cancer.
Stable transfection of SOX4 into nontransformed
prostate
cells enabled colony formation in soft agar, suggesting that, in the proper cellular context, SOX4 can be a transforming oncogene.
[MeSH-major]
Cell Transformation, Neoplastic / genetics. High Mobility Group Proteins / genetics. Oncogenes.
Prostatic
Neoplasms
/ genetics. Trans-Activators / genetics
[MeSH-minor]
Apoptosis / genetics. Cell Growth Processes / physiology. Cell Line, Transformed. Cell Line,
Tumor
. Gene Expression Profiling. Humans. Male. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction. SOXC Transcription Factors. Transfection
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(PMID = 16618720.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / NIGMS NIH HHS / GM / T32 GM008169; United States / NCI NIH HHS / CA / CA91435; United States / NCI NIH HHS / CA / K22-CA96560; United States / NIDDK NIH HHS / DK / DK60647; United States / NIGMS NIH HHS / GM / T32 GM008490; United States / NCI NIH HHS / CA / R01-CA106826
[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 / High Mobility Group Proteins; 0 / RNA, Small Interfering; 0 / SOX4 protein, human; 0 / SOXC Transcription Factors; 0 / Trans-Activators
26.
Krejcarek SC, Chen MH, Renshaw AA, Loffredo M, Sussman B, D'Amico AV:
Prediagnostic prostate-specific antigen velocity and probability of detecting high-grade prostate cancer.
Urology
; 2007 Mar;69(3):515-9
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[Title]
Prediagnostic
prostate
-specific antigen velocity and probability of detecting high-grade
prostate
cancer.
OBJECTIVES: Men with high-grade
prostate
cancer experience a survival benefit when androgen suppression therapy is combined with radiotherapy (RT) compared with RT alone.
We evaluated whether an association exists between the pretreatment
prostate
-specific antigen (PSA) velocity and high-grade
prostate
cancer at
diagnosis
, controlling for known predictors of high-grade disease.
METHODS: The study cohort consisted of 358 men with Stage T1c-T4
prostate
cancer treated with external beam RT from 1989 to 2002.
Univariate and multivariate logistic regression analyses were used to assess whether an association exists between the pretreatment PSA velocity, PSA level, age, clinical T stage, and Gleason score 4+3 or greater compared with Gleason score 3+4 or less
prostate
cancer.
On multivariate analysis, the PSA velocity (odds ratio 1.06, 95% confidence interval 1.02 to 1.10, P = 0.004), age (odds ratio 1.07, 95% confidence interval 1.02 to 1.13, P = 0.008), and clinical T stage (odds ratio 2.17, 95% confidence interval 1.21 to 3.92, P = 0.01) were significantly associated with the detection of Gleason score 4+3 or greater
prostate
cancer.
CONCLUSIONS: The prediagnostic PSA velocity, patient age, and clinical T stage were significantly associated with high-grade
prostate
cancer at
diagnosis
.
Because a biopsy Gleason score of 4+3 or greater is associated with a prostatectomy Gleason score of 7 or greater in the vast majority of cases, these parameters can identify men at high risk of harboring occult high-grade
prostate
cancer, permitting improved selection of RT fields and the use of androgen suppression therapy.
[MeSH-major]
Prostate
-Specific Antigen / blood.
Prostatic
Neoplasms
/
diagnosis
.
Prostatic
Neoplasms
/ pathology
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(PMID = 17382156.001).
[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]
EC 3.4.21.77 / Prostate-Specific Antigen
27.
Xu RS, Michailovich O, Salama M:
Information tracking approach to segmentation of ultrasound imagery of the prostate.
IEEE Trans Ultrason Ferroelectr Freq Control
; 2010 Aug;57(8):1748-61
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[Title]
Information tracking approach to segmentation of ultrasound imagery of the
prostate
.
The volume of the
prostate
is known to be a pivotal quantity used by clinicians to assess the condition of the
gland
during
prostate
cancer screening.
As an alternative to palpation, an increasing number of methods for estimation of the volume of the
prostate
are based on using imagery data.
In particular, the use of transrectal ultrasound (TRUS) imaging in
prostate
cancer screening seems to be becoming a standard clinical practice because of the high benefit-to-cost ratio of this imaging modality.
Unfortunately, the segmentation of TRUS images is still hampered by relatively low contrast and reduced SNR of the images, thereby requiring the segmentation algorithms to incorporate prior knowledge about the geometry of the
gland
.
The proposed approach is based on the concept of distribution tracking, which provides a unified framework for modeling and fusing image-related and morphological features of the
prostate
.
[MeSH-major]
Prostate
/ ultrasonography. Signal Processing, Computer-Assisted. Ultrasonography / methods
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(PMID = 20679005.001).
[ISSN]
1525-8955
[Journal-full-title]
IEEE transactions on ultrasonics, ferroelectrics, and frequency control
[ISO-abbreviation]
IEEE Trans Ultrason Ferroelectr Freq Control
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
28.
Koga N, Noguchi M, Moriya F, Ohshima K, Yoshitake N, Matsuoka K:
A case of primary mucosa-associated lymphoid tissue lymphoma of the prostate.
Rare Tumors
; 2009;1(2):e55
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[Title]
A case of primary mucosa-associated lymphoid tissue lymphoma of the
prostate
.
We report a case of primary mucosa-associated lymphoid tissue (MALT) lymphoma of the
prostate
.
A 67-year-old man presented with urinary obstruction and an elevated
prostate
-specific antigen (PSA) level.
A physical examination revealed mild
prostate
enlargement and no lymphadenopathy.
A needle biopsy and immunohistochemical studies of the
prostate
were performed, which revealed marginal zone B-cell MALT-type lymphoma.
The patient was diagnosed and staged as extranodal marginal zone B-cell MALT-type lymphoma of the
prostate
, low grade and stage I.
The patient received external beam radiation therapy to
the prostate
with a total dose of 3600cGy in 22 fractions, and became free of disease within the following 15 months.
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(PMID = 21139934.001).
[ISSN]
2036-3613
[Journal-full-title]
Rare tumors
[ISO-abbreviation]
Rare Tumors
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Other-IDs]
NLM/ PMC2994450
[Keywords]
NOTNLM ; mucosa-associated lymphoid tissue lymphoma / prostate / prostate-specific antigen / radiation therapy.
29.
Petrovics G, Liu A, Shaheduzzaman S, Furusato B, Sun C, Chen Y, Nau M, Ravindranath L, Chen Y, Dobi A, Srikantan V, Sesterhenn IA, McLeod DG, Vahey M, Moul JW, Srivastava S:
Frequent overexpression of ETS-related gene-1 (ERG1) in prostate cancer transcriptome.
Oncogene
; 2005 May 26;24(23):3847-52
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[Title]
Frequent overexpression of ETS-related gene-1 (ERG1) in
prostate
cancer transcriptome.
This study, analysing laser microdissected paired
benign
and malignant
prostate
epithelial cells from
prostate
cancer (CaP) patients (n=114; 228 specimen) by GeneChip and quantitative real-time RT-PCR, identifies ETS-related gene (ERG), a member of the ETS transcription factor family, as the most frequently overexpressed proto-oncogene in the transcriptome of malignant
prostate
epithelial cells.
Comprehensive evaluation of quantitative ERG1 expression with clinicopathological features also suggested that ERG1 expression level in
prostate tumor
cells relative to
benign
epithelial cells is indicator of disease-free survival after radical prostatectomy.
[MeSH-major]
DNA-Binding Proteins / genetics.
Prostatic
Neoplasms
/ genetics. Trans-Activators / genetics
[MeSH-minor]
Antigens,
Neoplasm
/ genetics. Glutathione S-Transferase pi. Glutathione Transferase / genetics. Humans. Isoenzymes / genetics. Male. Racemases and Epimerases / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic
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[ErratumIn]
Oncogene. 2007 Oct 11;26(46):6684. Furasato, Bungo [corrected to Furusato, Bungo]
(PMID = 15750627.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / R01 DK065977
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / Isoenzymes; 0 / Trans-Activators; 0 / prostate cancer antigen 3, human; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
30.
Tang J, Yang JC, Li Y, Li J, Shi H:
Peripheral zone hypoechoic lesions of the prostate: evaluation with contrast-enhanced gray scale transrectal ultrasonography.
J Ultrasound Med
; 2007 Dec;26(12):1671-9
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[Title]
Peripheral zone hypoechoic lesions of the
prostate
: evaluation with contrast-enhanced gray scale transrectal ultrasonography.
OBJECTIVE: The purpose of this study was to evaluate the efficacy of contrast-enhanced gray scale transrectal ultrasonography (TRUS) for detection
of prostate
cancer in peripheral zone hypoechoic lesions of the
prostate
.
The lesions were evaluated with contrast-enhanced TRUS to differentiate
prostate
cancer from
benign
lesions, and the results were compared with color Doppler ultrasonographic findings.
RESULTS: Transrectal ultrasonographically guided biopsy of the hypoechoic lesions revealed
prostate
cancer in 30 patients and
benign prostatic
diseases in 36.
Flow signals within the lesions were classified as no, increased, equal, and decreased flow compared with surrounding peripheral zone tissue as follows: 1, 16, 12, and 1, respectively, in
the prostate
cancer group and 10, 12, 10, and 4 in the
benign
disease group.
If we considered an increased flow signal within a peripheral hypoechoic lesion as a sign
of prostate
cancer, color Doppler ultrasonography had low sensitivity and specificity (55.2% and 53.8%, respectively).
The enhancement intensity within the lesions was classified as no, increased, equal, and decreased enhancement compared with surrounding peripheral zone tissue as follows: 2, 20, 3, and 5 in
the prostate
cancer group and 14, 8, 4, and 10 in the
benign
disease group.
CONCLUSIONS: Contrast-enhanced TRUS could reveal the presence of vasculature within peripheral zone hypoechoic lesions more objectively than color Doppler ultrasonography and could be promising in guidance
of prostate
biopsy.
[MeSH-major]
Phospholipids.
Prostate
/ ultrasonography.
Prostatic
Neoplasms
/ ultrasonography. Rectum / ultrasonography. Sulfur Hexafluoride. Ultrasonography / methods
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SULFUR HEXAFLUORIDE
.
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(PMID = 18029918.001).
[ISSN]
0278-4297
[Journal-full-title]
Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine
[ISO-abbreviation]
J Ultrasound Med
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Contrast Media; 0 / Phospholipids; 0 / contrast agent BR1; WS7LR3I1D6 / Sulfur Hexafluoride
31.
Marks LS, Fradet Y, Deras IL, Blase A, Mathis J, Aubin SM, Cancio AT, Desaulniers M, Ellis WJ, Rittenhouse H, Groskopf J:
PCA3 molecular urine assay for prostate cancer in men undergoing repeat biopsy.
Urology
; 2007 Mar;69(3):532-5
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[Title]
PCA3 molecular urine assay for
prostate
cancer in men undergoing repeat biopsy.
OBJECTIVES: Men with elevated serum
prostate
-specific antigen (PSA) levels and negative
prostate
biopsy findings present a dilemma because of the lack of an accurate diagnostic test.
We evaluated the potential utility of the investigational
prostate
cancer gene 3 (PCA3) urine assay to predict the repeat biopsy outcome.
Repeat biopsy revealed
prostate
cancer in 60 (27%) of the of 226 remaining subjects.
At PCA3 scores of less than 5, only 12% of men had
prostate
cancer on repeat biopsy; at PCA3 scores greater than 100, the risk of positive biopsy was 50%.
CONCLUSIONS: In men undergoing repeat
prostate
biopsy to rule out cancer, the urinary PCA3 score was superior to serum PSA determination for predicting the biopsy outcome.
The high specificity and informative rate suggest that the PCA3 assay could have an important role in
prostate
cancer
diagnosis
.
[MeSH-major]
Antigens,
Neoplasm
/ urine.
Prostatic
Neoplasms
/
diagnosis
[MeSH-minor]
Aged. Aged, 80 and over. Biopsy, Needle. Gene Expression. Humans. Immunoassay / methods. Male. Middle Aged.
Prostate
-Specific Antigen / genetics. RNA, Messenger / analysis. ROC Curve. Sensitivity and Specificity
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(PMID = 17382159.001).
[ISSN]
1527-9995
[Journal-full-title]
Urology
[ISO-abbreviation]
Urology
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / RNA, Messenger; 0 / prostate cancer antigen 3, human; EC 3.4.21.77 / Prostate-Specific Antigen
32.
Chang CH, Chiu CF, Wu HC, Tseng HC, Wang CH, Lin CC, Tsai CW, Liang SY, Wang CL, Bau DT:
Significant association of XRCC4 single nucleotide polymorphisms with prostate cancer susceptibility in Taiwanese males.
Mol Med Rep
; 2008 Jul-Aug;1(4):525-30
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[Title]
Significant association of XRCC4 single nucleotide polymorphisms with
prostate
cancer susceptibility in Taiwanese males.
In this case-control study, several novel polymorphic variants of XRCC4, including C-1622T (rs7727691), G-1394T (rs6869366), C-571T (rs2075686) and intron3 DIP (rs28360071), were investigated, and the correlation of these variants to
prostate
cancer susceptibility in a Taiwanese population was observed.
A total of 134
prostate
cancer patients were recruited along with 134 age-matched healthy controls, and the association of their selected genotypes with susceptibility to
prostate
cancer was determined.
The G-1394T variant of XRCC4 proved, after analysis of the frequencies of each variant in
the prostate
cancer and control groups, to be a significant single nucleotide polymorphism (SNP) in
prostate
carcinogenesis.
Our data clearly indicate that the heterogeneous G of G-1394T increases the risk of suceptibility to
prostate
cancer (P=0.0106), while no difference in distribution of XRCC4 C-1622T (rs7727691), C-571T (rs2075686) or intron3 DIP (rs28360071) between
the prostate
cancer and control groups was found.
In conclusion, our findings suggest that the G allele of XRCC4 G-1394T may be responsible for
prostate
carcinogenesis, and could be useful in the early detection and prevention of the disease.
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(PMID = 21479444.001).
[ISSN]
1791-2997
[Journal-full-title]
Molecular medicine reports
[ISO-abbreviation]
Mol Med Rep
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
33.
Liu X, Cicek MS, Plummer SJ, Jorgenson E, Casey G, Witte JS:
Association of testis derived transcript gene variants and prostate cancer risk.
J Urol
; 2007 Mar;177(3):894-8
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[Title]
Association of testis derived transcript gene variants and
prostate
cancer risk.
PURPOSE: The testis derived transcript gene has been suggested as a
tumor
suppressor gene for
prostate
cancer at 7q31.
To investigate this concept we evaluated the effects of 7 tagging single nucleotide polymorphisms that comprehensively captured the common genetic variants in TES on aggressive
prostate
cancer in a case-control study.
MATERIALS AND METHODS: A total of 506 cases diagnosed with aggressive
prostate
cancer, and an equal number of age, institute and ethnicity matched controls, were recruited from the major medical institutions in Cleveland, Ohio.
A logistic regression model was used to evaluate the association between SNPs/multimarker haplotypes and
prostate
cancer.
CONCLUSIONS: Our findings suggest that the variants in TES, or in a nearby gene, may be associated with
prostate
cancer in black men.
[MeSH-major]
African Americans / genetics. European Continental Ancestry Group / genetics. Homeodomain Proteins / genetics. Polymorphism, Single Nucleotide / genetics.
Prostatic
Neoplasms
/ ethnology.
Prostatic
Neoplasms
/ genetics.
Tumor
Suppressor Proteins / genetics
[MeSH-minor]
Aged. Case-Control Studies. Cytoskeletal Proteins. Genotype. Humans. LIM Domain Proteins. Male. Middle Aged.
Neoplasm
Staging
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(PMID = 17296370.001).
[ISSN]
0022-5347
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA88164; United States / NCI NIH HHS / CA / CA94211; United States / NCI NIH HHS / CA / CA98683
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Cytoskeletal Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / TES protein, human; 0 / Tumor Suppressor Proteins
34.
Escaff S, Fernández JM, González LO, Suárez A, González-Reyes S, González JM, Vizoso FJ:
Study of matrix metalloproteinases and their inhibitors in prostate cancer.
Br J Cancer
; 2010 Mar 2;102(5):922-9
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[Title]
Study of matrix metalloproteinases and their inhibitors in
prostate
cancer.
BACKGROUND: Extracellular matrix metalloproteases (MMPs) have raised an extraordinary interest in cancer research because of their potential role in basal membrane and extracellular matrix degradation, consequently facilitating
tumour
invasion and metastases development.
More than 2600 determinations on cancer specimens from 133 patients with clinically localised
prostate
carcinoma, 20 patients with
prostatic
intraepithelial
neoplasia
and 50 patients with
benign
prostate
hyperplasia and controls, were performed.
RESULTS: When compared with
benign
pathologies,
prostate
carcinomas had higher expression of all MMPs and TIMPs.
CONCLUSION: The expression of MMPs and TIMPs seems to have an important role in the molecular biology
of prostate
carcinomas, and their expression by tumours may be of clinical interest to used as indicators of
tumour
aggressiveness.
[MeSH-major]
Adenocarcinoma / metabolism. Matrix Metalloproteinases / metabolism.
Prostatic
Hyperplasia / metabolism.
Prostatic
Intraepithelial
Neoplasia
/ metabolism.
Prostatic
Neoplasms
/ metabolism. Tissue Inhibitor of Metalloproteinases / metabolism
[MeSH-minor]
Aged. Biomarkers,
Tumor
/ metabolism. Follow-Up Studies. Humans. Immunoenzyme Techniques. Male. Middle Aged.
Neoplasm
Recurrence, Local / metabolism.
Neoplasm
Recurrence, Local / pathology. Prognosis. Survival Rate. Tissue Array Analysis
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Prostate Cancer Prostatic Dis. 2004;7(4):327-32
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]
(PMID = 20160732.001).
[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
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Tissue Inhibitor of Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases
[Other-IDs]
NLM/ PMC2833257
35.
Trock BJ, Han M, Freedland SJ, Humphreys EB, DeWeese TL, Partin AW, Walsh PC:
Prostate cancer-specific survival following salvage radiotherapy vs observation in men with biochemical recurrence after radical prostatectomy.
JAMA
; 2008 Jun 18;299(23):2760-9
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[Title]
Prostate
cancer-specific survival following salvage radiotherapy vs observation in men with biochemical recurrence after radical prostatectomy.
OBJECTIVES: To quantify the relative improvement in
prostate
cancer-specific survival of salvage radiotherapy vs no therapy after biochemical recurrence following prostatectomy, and to identify subgroups for whom salvage treatment is most beneficial.
MAIN OUTCOME MEASURE:
Prostate
cancer-specific survival defined from time of recurrence until death from disease.
RESULTS: With a median follow-up of 6 years after recurrence and 9 years after prostatectomy, 116 men (18%) died from
prostate
cancer, including 89 (22%) who received no salvage treatment, 18 (11%) who received salvage radiotherapy alone, and 9 (12%) who received salvage radiotherapy and hormonal therapy.
Salvage radiotherapy alone was associated with a significant 3-fold increase in
prostate
cancer-specific survival relative to those who received no salvage treatment (hazard ratio [HR], 0.32 [95% confidence interval {CI}, 0.19-0.54]; P<.001).
Addition of hormonal therapy to salvage radiotherapy was not associated with any additional increase in
prostate
cancer-specific survival (HR, 0.34 [95% CI, 0.17-0.69]; P = .003).
The increase in
prostate
cancer-specific survival associated with salvage radiotherapy was limited to men with a
prostate
-specific antigen doubling time of less than 6 months and remained after adjustment for pathological stage and other established prognostic factors.
Salvage radiotherapy initiated more than 2 years after recurrence provided no significant increase in
prostate
cancer-specific survival.
Men whose
prostate
-specific antigen level never became undetectable after salvage radiotherapy did not experience a significant increase in
prostate
cancer-specific survival.
CONCLUSIONS: Salvage radiotherapy administered within 2 years of biochemical recurrence was associated with a significant increase in
prostate
cancer-specific survival among men with a
prostate
-specific antigen doubling time of less than 6 months, independent of other prognostic features such as pathological stage or Gleason score.
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Eur Urol. 2009 Jan;55(1):247
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]
(PMID = 18560003.001).
[ISSN]
1538-3598
[Journal-full-title]
JAMA
[ISO-abbreviation]
JAMA
[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 CA058236-13; United States / NCI NIH HHS / CA / CA58236
[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 / Antineoplastic Agents, Hormonal; EC 3.4.21.77 / Prostate-Specific Antigen
[Other-IDs]
NLM/ NIHMS283299; NLM/ PMC3076799
36.
Lindström S, Ma J, Altshuler D, Giovannucci E, Riboli E, Albanes D, Allen NE, Berndt SI, Boeing H, Bueno-de-Mesquita HB, Chanock SJ, Dunning AM, Feigelson HS, Gaziano JM, Haiman CA, Hayes RB, Henderson BE, Hunter DJ, Kaaks R, Kolonel LN, Le Marchand L, Martínez C, Overvad K, Siddiq A, Stampfer M, Stattin P, Stram DO, Thun MJ, Trichopoulos D, Tumino R, Virtamo J, Weinstein SJ, Yeager M, Kraft P, Freedman ML:
A large study of androgen receptor germline variants and their relation to sex hormone levels and prostate cancer risk. Results from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium.
J Clin Endocrinol Metab
; 2010 Sep;95(9):E121-7
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[Title]
A large study of androgen receptor germline variants and their relation to sex hormone levels and
prostate
cancer risk. Results from the National Cancer Institute Breast and
Prostate
Cancer Cohort Consortium.
BACKGROUND: Androgens are key regulators
of prostate gland
maintenance and
prostate
cancer growth, and androgen deprivation therapy has been the mainstay of treatment for advanced
prostate
cancer for many years.
A long-standing hypothesis has been that inherited variation in the androgen receptor (AR) gene plays a role in
prostate
cancer initiation.
OBJECTIVE AND METHODS: We investigated the association of AR sequence variants with circulating sex hormone levels and
prostate
cancer risk in 6058
prostate
cancer cases and 6725 controls of Caucasian origin within the Breast and
Prostate
Cancer Cohort Consortium.
We genotyped a highly polymorphic CAG microsatellite in exon 1 and six haplotype tagging single nucleotide polymorphisms and tested each genetic variant for association with
prostate
cancer risk and with sex steroid levels.
RESULTS: We observed no association between AR genetic variants and
prostate
cancer risk.
CONCLUSIONS: This study is the largest to date investigating AR sequence variants, sex steroid levels, and
prostate
cancer risk.
Although we observed no association between AR sequence variants and
prostate
cancer risk, our results support earlier findings of a relation between the number of CAG repeats and circulating levels of testosterone and estradiol.
[MeSH-major]
Carcinoma / genetics. Gonadal Steroid Hormones / blood.
Prostatic
Neoplasms
/ genetics. Receptors, Androgen / genetics
[MeSH-minor]
Aged. Breast
Neoplasms
/ genetics. Case-Control Studies. Cohort Studies. Female. Genetic Association Studies. Genetic Predisposition to Disease. Germ-Line Mutation / physiology. Humans. Male. Middle Aged. National Cancer Institute (U.S.). Risk. Trinucleotide Repeats / genetics. United States
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Hum Mol Genet. 2009 Oct 1;18(19):3749-57
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(PMID = 20534771.001).
[ISSN]
1945-7197
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / UO1-CA98758; United Kingdom / Cancer Research UK / / A10123; United States / NCI NIH HHS / CA / U01 CA098216; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / UO1-CA98233; United States / NCI NIH HHS / CA / UO1-CA98216; United States / NCI NIH HHS / CA / U01 CA098233; United States / NCI NIH HHS / CA / U01 CA098758; United States / NCI NIH HHS / CA / UO1-CA98710; United States / NCI NIH HHS / CA / R01 CA097193; United States / NCI NIH HHS / CA / U01 CA098710
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
[Publication-country]
United States
[Chemical-registry-number]
0 / AR protein, human; 0 / Gonadal Steroid Hormones; 0 / Receptors, Androgen
[Other-IDs]
NLM/ PMC2936075
37.
Tomlins SA, Mehra R, Rhodes DR, Cao X, Wang L, Dhanasekaran SM, Kalyana-Sundaram S, Wei JT, Rubin MA, Pienta KJ, Shah RB, Chinnaiyan AM:
Integrative molecular concept modeling of prostate cancer progression.
Nat Genet
; 2007 Jan;39(1):41-51
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[Title]
Integrative molecular concept modeling
of prostate
cancer progression.
Despite efforts to profile
prostate
cancer, the genetic alterations and biological processes that correlate with the observed histological progression are unclear.
Using laser-capture microdissection to isolate 101 cell populations, we have profiled
prostate
cancer progression from
benign
epithelium to metastatic disease.
Of note, relative to low-grade
prostate
cancer (Gleason pattern 3), high-grade cancer (Gleason pattern 4) shows an attenuated androgen signaling signature, similar to metastatic
prostate
cancer, which may reflect dedifferentiation and explain the clinical association of grade with prognosis.
[MeSH-major]
Gene Expression Profiling. Models, Theoretical.
Prostatic
Neoplasms
/ genetics.
Prostatic
Neoplasms
/ pathology
[MeSH-minor]
Androgens / metabolism. Disease Progression. Humans. Male.
Neoplasm
Metastasis.
Prostatic
Hyperplasia / genetics.
Prostatic
Hyperplasia / pathology.
Prostatic
Intraepithelial
Neoplasia
/ genetics.
Prostatic
Intraepithelial
Neoplasia
/ pathology. Signal Transduction. Systems Integration
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(PMID = 17173048.001).
[ISSN]
1061-4036
[Journal-full-title]
Nature genetics
[ISO-abbreviation]
Nat. Genet.
[Language]
eng
[Databank-accession-numbers]
GEO/ GSE6099
[Grant]
United States / NCI NIH HHS / CA / 5P30 CA46592; United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / R01 CA102872; United States / NIDA NIH HHS / DA / U54 DA021519-01A1; United States / NCI NIH HHS / CA / UO1 CA111275-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgens
38.
Rayford W:
Managing the low-socioeconomic-status prostate cancer patient.
J Natl Med Assoc
; 2006 Apr;98(4):521-30
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[Title]
Managing the low-socioeconomic-status
prostate
cancer patient.
Management of patients with low socioeconomic status and/or low literacy who have
prostate
cancer presents a challenge to healthcare professionals.
Improving treatment outcomes for these men requires specific educational programs to provide a better understanding
of prostate
cancer including careful posttreatment follow-up to ensure they have recovered well, that the cancer is not progressing and that complications are not proving troublesome.
Education and knowledgeable advice can lead to earlier
diagnosis of prostate
cancer, improved patient participation in the treatment decision-making process and effective management of posttreatment complications.
[MeSH-major]
Decision Making.
Prostatic
Neoplasms
/ therapy. Social Class
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[ISSN]
1943-4693
[Journal-full-title]
Journal of the National Medical Association
[ISO-abbreviation]
J Natl Med Assoc
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
34
[Other-IDs]
NLM/ PMC2569254
39.
Chapel-Fernandes S, Jordier F, Lauro F, Maitland N, Chiaroni J, de Micco P, Mannoni P, Bagnis C:
Use of the PSA enhancer core element to modulate the expression of prostate- and non-prostate-specific basal promoters in a lentiviral vector context.
Cancer Gene Ther
; 2006 Oct;13(10):919-29
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[Title]
Use of the PSA enhancer core element to modulate the expression
of prostate
- and non-
prostate
-specific basal promoters in a lentiviral vector context.
Composite promoters combining
the prostate
-specific antigen (PSA) enhancer core element with promoter elements derived from gene coding for human
prostate
-specific transglutaminase gene,
prostate
-specific membrane antigen gene,
prostate
-specific antigen, rat probasin or phosphoglycerate kinase were characterized for their ability to specifically express the enhanced green fluorescent protein (EGFP) gene in
prostate
versus non-
prostate
cancer cell lines when transferred with a human immunodeficiency virus-1-based lentiviral vector.
By themselves minimal proximal promoter elements were found to inefficiently promote relevant tissue-specific expression; in all the vectors tested, addition of the PSA enhancer core element markedly improved EGFP expression in LnCaP, a cancer
prostate
cell line used as a model for
prostate
cancer.
The composite promoter was inactive in HuH7, a hepatocarcinoma cell line used as a model of neighboring non-
prostate
cancer cells.
Our data suggest that composite
prostate
-specific promoters constructed by combining key elements from various promoters can improve and/or confer tissue specific expression in a lentiviral vector context.
[MeSH-major]
Enhancer Elements, Genetic. Genetic Vectors. Lentivirus / genetics. Promoter Regions, Genetic.
Prostate
/ metabolism.
Prostate
-Specific Antigen / genetics
[MeSH-minor]
Cell Line,
Tumor
. Green Fluorescent Proteins / genetics. Humans. Male
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(PMID = 16741521.001).
[ISSN]
0929-1903
[Journal-full-title]
Cancer gene therapy
[ISO-abbreviation]
Cancer Gene Ther.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins; EC 3.4.21.77 / Prostate-Specific Antigen
40.
Urba WJ, Nemunaitis J, Marshall F, Smith DC, Hege KM, Ma J, Nguyen M, Small EJ:
Treatment of biochemical recurrence of prostate cancer with granulocyte-macrophage colony-stimulating factor secreting, allogeneic, cellular immunotherapy.
J Urol
; 2008 Nov;180(5):2011-7; discussion 2017-8
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[Title]
Treatment of biochemical recurrence
of prostate
cancer with granulocyte-macrophage colony-stimulating factor secreting, allogeneic, cellular immunotherapy.
PURPOSE: This phase I-II study evaluated the safety, clinical activity and immunogenicity of an immunotherapy developed from human
prostate
cancer cell lines (PC-3 and LNCaP) modified to secrete granulocyte-macrophage colony-stimulating factor.
MATERIALS AND METHODS: Patients with noncastrate
prostate
cancer (19) with biochemical (
prostate
specific antigen) recurrence following prostatectomy or radiation therapy and no radiological evidence of metastasis were enrolled in the study.
The adverse event profile,
prostate
specific antigen response, changes in
prostate
specific antigen kinetics and immunogenicity were assessed.
A negative deflection in
prostate
specific antigen slope was observed in 84% of patients after treatment with a significant increase in median
prostate
specific antigen doubling time from 28.7 weeks before treatment to 57.1 weeks after treatment (p = 0.0095).
Median time to
prostate
specific antigen progression was 9.7 months.
Induction of antibody responses reactive against PC-3 in general, and to the PC-3 associated filamin-B protein specifically, were positively associated with treatment associated changes in
prostate
specific antigen kinetics.
CONCLUSIONS: Granulocyte-macrophage colony-stimulating factor secreting cellular immunotherapy has a favorable toxicity profile with signals of clinical and immunological activity against hormone naïve
prostate
cancer.
An association between immune response and
prostate
specific antigen changes was observed.
Phase 3 trials in patients with advanced, metastatic, hormone refractory
prostate
cancer are under way.
[MeSH-major]
Cancer Vaccines / administration & dosage. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Immunotherapy / methods.
Neoplasm
Recurrence, Local / therapy.
Prostate
-Specific Antigen / blood.
Prostatic
Neoplasms
/ therapy
[MeSH-minor]
Aged. Aged, 80 and over. Dose-Response Relationship, Drug. Drug Administration Schedule. Humans. Injections, Subcutaneous. Male. Middle Aged.
Neoplasm
Staging. Probability. Prognosis. Prostatectomy / methods. Radiotherapy, Conformal / methods. Risk Assessment. Statistics, Nonparametric. Survival Rate. Treatment Outcome
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(PMID = 18801509.001).
[ISSN]
1527-3792
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[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 / Cancer Vaccines; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 3.4.21.77 / Prostate-Specific Antigen
41.
Wu GJ, Fu P, Chiang CF, Huss WJ, Greenberg NM, Wu MW:
Increased expression of MUC18 correlates with the metastatic progression of mouse prostate adenocarcinoma in the TRAMP model.
J Urol
; 2005 May;173(5):1778-83
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[Title]
Increased expression of MUC18 correlates with the metastatic progression of mouse
prostate
adenocarcinoma in the TRAMP model.
PURPOSE: The transgenic adenocarcinoma mouse
prostate
(TRAMP) model is a paradigm that closely mimics the progression of clinical
prostate
cancer.
We have previously reported that MUC18, a cell adhesion molecule in the Ig gene superfamily, is a marker as well as an important mediator for the metastatic potential of human
prostate
cancer cells.
In this study we investigated the possible correlation of increased MUC18 expression with the malignant progression
of prostate
cancer in the TRAMP model.
MATERIALS AND METHODS: We used immunohistochemistry, Western blot and reverse transcriptase-polymerase chain reaction analyses to determine MUC18 expression in
the prostate gland of
178 to 282-day-old TRAMP positive males with a
prostate tumor
size of 0.4 to 12.7 gm.
Eight normal prostates, 10 prostates with high grade
prostatic
intraepithelial
neoplasia
(PIN), 24 prostates with primary
prostate
cancer, 10 metastatic lesions from 50 pure C57BL/6 TRAMP mice (Wu colony) and 2 normal prostates, 2 prostates with high grade PIN, 6 prostates with primary
prostate
cancer and 4 metastatic lesions from 10 [C57BL/6 TRAMP x FVB] F1 mice (NMG colony) were used.
All mice bearing primary
prostate
tumors had
prostate
cancer metastatic to the peri-aortic lymph nodes and some had it to other organs (liver, lung, kidney, testes, seminal vesicles and abdominal cavity).
CONCLUSIONS: MUC18 expression is up-regulated in the TRAMP model and it correlates with the malignant progression of mouse
prostate
adenocarcinoma in this transgenic model.
This further strengthens the hypothesis that MUC18 has an important role in increasing the metastatic potential
of prostate
cancer cells.
[MeSH-major]
Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Antigens, CD / biosynthesis. Biomarkers,
Tumor
/ biosynthesis. Neural Cell Adhesion Molecules / biosynthesis.
Prostatic
Neoplasms
/ metabolism.
Prostatic
Neoplasms
/ pathology
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Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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(PMID = 15821586.001).
[ISSN]
0022-5347
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD146; 0 / Biomarkers, Tumor; 0 / Mcam protein, mouse; 0 / Neural Cell Adhesion Molecules
42.
Fujimoto N, Miyamoto H, Mizokami A, Harada S, Nomura M, Ueta Y, Sasaguri T, Matsumoto T:
Prostate cancer cells increase androgen sensitivity by increase in nuclear androgen receptor and androgen receptor coactivators; a possible mechanism of hormone-resistance of prostate cancer cells.
Cancer Invest
; 2007 Feb;25(1):32-7
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[Title]
Prostate
cancer cells increase androgen sensitivity by increase in nuclear androgen receptor and androgen receptor coactivators; a possible mechanism of hormone-resistance
of prostate
cancer cells.
Although androgen-hypersensitivity is one of the possible pathways of hormone-resistance in
prostate
cancer, the mechanisms of androgen-hypersensitivity are still largely unknown.
Using androgen-hypersensitive
prostate
cancer cells LN-TR2, established from androgen-sensitive LNCaP cells by the long term treatment with
tumor
necrosis factor alpha, we explored the mechanisms of androgen-hypersensitivity in
prostate
cancer cells which may thus play a role in hormone-resistance.
In 2 of 6 patients, the expression level of ARA55 was higher in cancer cells in hormone-resistant
tumor
than those in hormone-sensitive
tumor
.
Taken together, our results suggest that
prostate
cancer cells change androgen-sensitivity by an overexpression of nuclear AR and AR coactivators, thus, resulting in transition from androgen-dependent to androgen-independent
prostate
cancer cells.
An increase in nuclear AR and AR coactivators may cause androgen-hypersensitivity
of prostate
cancer cells and thus play a role in hormone-resistance, at least in some patients with
prostate
cancer.
[MeSH-major]
Drug Resistance,
Neoplasm
/ physiology.
Neoplasms
, Hormone-Dependent / metabolism.
Prostatic
Neoplasms
/ metabolism. Receptors, Androgen / metabolism
[MeSH-minor]
Androgen Antagonists / pharmacology. Antineoplastic Agents, Hormonal / pharmacology. Blotting, Western. Cell Line,
Tumor
. Cell Nucleus / metabolism. Humans. Immunohistochemistry. Intracellular Signaling Peptides and Proteins / metabolism. LIM Domain Proteins. Male. Nuclear Receptor Coactivator 2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection.
Tumor
Necrosis Factor-alpha / metabolism
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(PMID = 17364555.001).
[ISSN]
0735-7907
[Journal-full-title]
Cancer investigation
[ISO-abbreviation]
Cancer Invest.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Intracellular Signaling Peptides and Proteins; 0 / LIM Domain Proteins; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Receptors, Androgen; 0 / TGFB1I1 protein, human; 0 / Tumor Necrosis Factor-alpha
43.
Kalender ME, Sevinc A, Kucukdurmaz Z, Balik A, Sari I, Camci C:
Gastric and prostate adenocarcinoma in a patient with metastatic gastrointestinal stromal tumor.
Onkologie
; 2007 Nov;30(11):568-70
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[Title]
Gastric and
prostate
adenocarcinoma in a patient with metastatic gastrointestinal stromal
tumor
.
BACKGROUND: Gastrointestinal stromal
tumor
(GIST) is the most common mesenchymal malignancy of the gastrointestinal tract.
Gastric cancer is the second most common
neoplasm
worldwide.
Prostate
cancer is the most common non-cutaneous cancer.
The most frequently encountered second malignancies in patients with
prostate
adenocarcinoma include carcinomas of the bladder, stomach, and colon, followed by cutaneous and hematolymphoid malignancies.
At followup 6 months later,
prostate
-specific antigen (PSA) levels were elevated, and a
prostate
biopsy showed a
prostate
adenocarcinoma.
CONCLUSION: This is the second report of metachronous
prostate
cancer, gastric cancer, and GIST in the English language literature.
[MeSH-major]
Gastrointestinal Stromal Tumors /
diagnosis
.
Prostatic
Neoplasms
/
diagnosis
.
Prostatic
Neoplasms
/ secondary. Stomach
Neoplasms
/
diagnosis
. Stomach
Neoplasms
/ secondary
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(PMID = 17992028.001).
[ISSN]
1423-0240
[Journal-full-title]
Onkologie
[ISO-abbreviation]
Onkologie
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
44.
Zeliadt SB, Ramsey SD:
Cost-effectiveness of prostate cancer chemoprevention among high-risk men.
Expert Rev Pharmacoecon Outcomes Res
; 2010 Oct;10(5):505-8
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[Title]
Cost-effectiveness
of prostate
cancer chemoprevention among high-risk men.
Cost effectiveness of 5-α reductase inhibitors for the prevention
of prostate
cancer in multiple patient populations.
Chemoprevention with 5-α reductase inhibitors (5ARIs) has been shown in clinical trials to reduce the incidence
of prostate
cancer.
Although avoiding or delaying a
diagnosis of prostate
cancer through chemoprevention is attractive, it is unknown whether 5ARI chemoprevention reduces the number
of prostate
cancer deaths.
The current study examines the cost-effectiveness of 5ARIs for men with multiple risk factors, including an elevated
prostate
-specific antigen and a prior negative biopsy.
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[CommentOn]
Pharmacoeconomics. 2010;28(6):489-505
[
20196623.001
]
(PMID = 20950065.001).
[ISSN]
1744-8379
[Journal-full-title]
Expert review of pharmacoeconomics & outcomes research
[ISO-abbreviation]
Expert Rev Pharmacoecon Outcomes Res
[Language]
eng
[Publication-type]
Comment; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
England
45.
Han B, Mehra R, Suleman K, Tomlins SA, Wang L, Singhal N, Linetzky KA, Palanisamy N, Zhou M, Chinnaiyan AM, Shah RB:
Characterization of ETS gene aberrations in select histologic variants of prostate carcinoma.
Mod Pathol
; 2009 Sep;22(9):1176-85
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[Title]
Characterization of ETS gene aberrations in select histologic variants
of prostate
carcinoma.
Histologic variants
of prostate
carcinoma account for 5-10% of the disease and are typically seen in association with conventional acinar carcinoma.
Recently, recurrent gene fusions between the androgen-regulated gene TMPRSS2 and the ETS transcription factors ERG, ETV1, ETV4, or ETV5 have been identified in a majority of conventional
prostate
carcinomas.
However, the frequency and significance of this critical molecular event is unknown in the histologic variants
of prostate
carcinoma.
Here, we used break-apart fluorescence in situ hybridization to assess TMPRSS2 and ETS aberrations in a series of select histologic variants: foamy
gland
carcinoma (N=17), ductal adenocarcinoma (N=18), mucinous carcinoma (N=18), and small cell carcinoma (N=7).
TMPRSS2:ERG fusion was identified in 83% (15/18), 71% (5/7), 50% (9/18), 33% (3/9), and 29% (5/17) of mucinous, small cell, ductal, glomeruloid, and foamy
gland prostate
carcinomas, respectively.
Previously, we reported that 100% of androgen-independent metastatic
prostate
carcinomas harboring TMPRSS2:ERG gene fusion were associated with interstitial deletion (Edel).
SPINK1, a biomarker expressed exclusively in a subset of ETS negative
prostate
carcinomas, was expressed in 6% of ETS negative histologic variants, specifically in ductal adenocarcinoma.
Overall, our data provide insight into the origin, molecular mechanism, and phenotypic association of ETS fusions in histologic variants
of prostate
carcinoma.
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[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 / P50 CA069568-110020; United States / NCI NIH HHS / CA / U01 CA111275-01; United States / NCI NIH HHS / CA / R01 CA102872; United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / CA069568-110020; United States / NCI NIH HHS / CA / UO1 CA111275-01; United States / NCI NIH HHS / CA / P50 CA069568; United States / NCI NIH HHS / CA / U01 CA111275
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / SPINK1 protein, human; 0 / TMPRSS2-ERG fusion protein, human; 0 / TMPRSS2-ETV1 fusion protein, human
[Other-IDs]
NLM/ NIHMS148618; NLM/ PMC2760291
46.
van der Wielen GJ, Mutanga TF, Incrocci L, Kirkels WJ, Vasquez Osorio EM, Hoogeman MS, Heijmen BJ, de Boer HC:
Deformation of prostate and seminal vesicles relative to intraprostatic fiducial markers.
Int J Radiat Oncol Biol Phys
; 2008 Dec 1;72(5):1604-1611.e3
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[Title]
Deformation
of prostate
and seminal vesicles relative to intraprostatic fiducial markers.
PURPOSE: To quantify the residual geometric uncertainties after on-line corrections with intraprostatic fiducial markers, this study analyzed the deformation of the
prostate
and, in particular, the seminal vesicles relative to such markers.
PATIENTS AND METHODS: A planning computed tomography (CT) scan and three repeat CT scans were obtained for 21
prostate
cancer patients who had had three to four cylindrical gold markers placed.
The prostate
and whole seminal vesicles (clinical target volume [CTV]) were delineated on each scan at a slice thickness of 1.5 mm.
Prostate
deformation was small (standard deviation </=1 mm).
CONCLUSION: Although
prostate
deformation with respect to implanted fiducial markers was small, the corresponding deformation of the seminal vesicles was considerable.
[MeSH-major]
Prostate
/ abnormalities.
Prostate
/ radiography.
Prostatic
Neoplasms
/ radiotherapy. Seminal Vesicles / pathology. Seminal Vesicles / radiography
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(PMID = 19028284.001).
[ISSN]
1879-355X
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers
47.
Chodak GW, Warren KS:
Watchful waiting for prostate cancer: a review article.
Prostate Cancer Prostatic Dis
; 2006;9(1):25-9
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[Title]
Watchful waiting for
prostate
cancer: a review article.
As earlier detection
of prostate
cancer increases because
of prostate
-specific antigen (PSA) testing, appropriate use for watchful waiting warrants re-evaluation.
Watchful waiting has the potential to play an increasingly important role in
prostate
cancer as less advanced disease is detected and methods are refined for identifying low-risk patients.
[MeSH-major]
Prostate
-Specific Antigen / blood.
Prostatic
Neoplasms
/ therapy
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(PMID = 16402090.001).
[ISSN]
1365-7852
[Journal-full-title]
Prostate cancer and prostatic diseases
[ISO-abbreviation]
Prostate Cancer Prostatic Dis.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
[Number-of-references]
22
48.
Breyer JP, McReynolds KM, Yaspan BL, Bradley KM, Dupont WD, Smith JR:
Genetic variants and prostate cancer risk: candidate replication and exploration of viral restriction genes.
Cancer Epidemiol Biomarkers Prev
; 2009 Jul;18(7):2137-44
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[Title]
Genetic variants and
prostate
cancer risk: candidate replication and exploration of viral restriction genes.
The genetic variants underlying the strong heritable component
of prostate
cancer remain largely unknown.
Genome-wide association studies
of prostate
cancer have yielded several variants that have significantly replicated across studies, predominantly in cases unselected for family history
of prostate
cancer.
Additional candidate gene variants have also been proposed, many evaluated within familial
prostate
cancer study populations.
Such variants hold great potential value for risk stratification, particularly for early-onset or aggressive
prostate
cancer, given the comorbidities associated with current therapies.
Here, we investigate a Caucasian study population of 523 independent familial
prostate
cancer cases and 523 age-matched controls without a personal or family history
of prostate
cancer.
[MeSH-major]
Chromosomes, Human, X / genetics. European Continental Ancestry Group / genetics. Genetic Predisposition to Disease / genetics. Polymorphism, Single Nucleotide / genetics.
Prostatic
Neoplasms
/ genetics
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(PMID = 19567509.001).
[ISSN]
1538-7755
[Journal-full-title]
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
[ISO-abbreviation]
Cancer Epidemiol. Biomarkers Prev.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA068485; United States / NCI NIH HHS / CA / P30 CA068485; United States / NCI NIH HHS / CA / P30 CA068485-13; United States / NCI NIH HHS / CA / T32 CA009592
[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
[Other-IDs]
NLM/ NIHMS154795; NLM/ PMC2813685
49.
Miyagawa T, Tsutsumi M, Matsumura T, Kawazoe N, Ishikawa S, Shimokama T, Miyanaga N, Akaza H:
Real-time elastography for the diagnosis of prostate cancer: evaluation of elastographic moving images.
Jpn J Clin Oncol
; 2009 Jun;39(6):394-8
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[Title]
Real-time elastography for
the diagnosis of prostate
cancer: evaluation of elastographic moving images.
We applied elastography for
the diagnosis of prostate
cancer and evaluated the usefulness of elastography for
prostate
biopsy.
METHODS: The subjects of this study were 311 patients who underwent elastography during
prostate
needle biopsy at Hitachi General Hospital.
Strain images obtained during compression of the
prostate
tissue were displayed on a monitor and recorded on the computer.
RESULTS: The median patient age was 67 years (range 50-85 years), the median serum level
of prostate
-specific antigen was 8.4 ng/ml (range 0.3-82.5 ng/ml) and the median
prostate
volume was 42.6 ml (range 12-150 ml).
Among the 311 patients,
prostate
cancer was detected in 95 patients (30%) by biopsy.
Elastography-positive EMIs with negative biopsies were eventually determined to be due to
benign prostatic
hyperplasia.
CONCLUSION: Elastography has a significantly higher sensitivity for the detection
of prostate
cancer than the conventionally used examinations including DRE and TRUS.
[MeSH-major]
Diagnostic Imaging / methods. Elasticity Imaging Techniques / methods.
Prostatic
Neoplasms
/
diagnosis
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(PMID = 19359330.001).
[ISSN]
1465-3621
[Journal-full-title]
Japanese journal of clinical oncology
[ISO-abbreviation]
Jpn. J. Clin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
50.
Yang TH, Leung SK, Phipps S, Reuben RL, McNeill SA, Habib FK, Schnieder A, Stevens R:
In-vitro dynamic micro-probing and the mechanical properties of human prostate tissues.
Technol Health Care
; 2006;14(4-5):281-96
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[Title]
In-vitro dynamic micro-probing and the mechanical properties of human
prostate
tissues.
In vitro macro- and micro-indentation test systems have been designed to measure the dynamic micro-mechanical properties of human
prostate
tissues at actuation frequencies between 5 Hz and 30 Hz, and 0.5 Hz and 20 Hz, respectively.
The development of in vitro test systems was aimed at assessing the capacity of such an in vivo medical probe to provide information useful for
the diagnosis
of various
prostate
diseases.
The macro-indentation test system is an established one, which we have used to determine structure-property relationships in human and canine
prostate
tissues and here we use it to validate a newly-developed micro-indentation test system using a tissue phantom.
Mechanical testing was also carried out on sections
of prostate
tissue harvested from cystectomy and radical prostatectomy, diagnosed with bladder cancer and
benign prostatic
hyperplasia.
Dynamic probing under displacement control was carried at pre-strains between 5% and 8% for macro-probing and at 5% pre-strain for micro-probing, and the general effect of pre-strain on the dynamic mechanical properties (described by the amplitude ratio between stress and strain, and the phase lag between strain and stress) of phantom and
prostate
tissues is presented.
[MeSH-major]
Biomechanical Phenomena.
Prostatic
Hyperplasia / physiopathology.
Prostatic
Neoplasms
/ physiopathology. Silicones / analysis
[MeSH-minor]
Compressive Strength.
Diagnosis
, Differential. Epithelial Cells / pathology. Humans. Immunohistochemistry. Male. Phantoms, Imaging.
Prostate
/ chemistry.
Prostate
/ pathology. Stromal Cells / pathology. Tissue Engineering
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(PMID = 17065751.001).
[ISSN]
0928-7329
[Journal-full-title]
Technology and health care : official journal of the European Society for Engineering and Medicine
[ISO-abbreviation]
Technol Health Care
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Silicones
51.
Garrison JB, Shaw YJ, Chen CS, Kyprianou N:
Novel quinazoline-based compounds impair prostate tumorigenesis by targeting tumor vascularity.
Cancer Res
; 2007 Dec 1;67(23):11344-52
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[Title]
Novel quinazoline-based compounds impair
prostate
tumorigenesis by targeting
tumor
vascularity.
Previous evidence showed the ability of the quinazoline-based alpha(1)-adrenoreceptor antagonist doxazosin to suppress
prostate tumor
growth via apoptosis.
Confocal microscopy revealed a significantly reduced ability
of tumor
cells to attach to extracellular matrix and migrate through endothelial cells in the presence of DZ-50.
In vivo tumorigenicty studies using two androgen-independent human
prostate
cancer xenografts, PC-3 and DU-145, showed that DZ-50 treatment leads to significant suppression of tumorigenic growth.
Exposure to the drug at the time
of tumor
cell inoculation led to prevention
of prostate
cancer initiation.
Furthermore, DZ-50 resulted in a reduced formation
of prostate
-
tumor
derived metastatic lesions to the lungs in an in vivo spontaneous metastasis assay.
Thus, our drug discovery approach led to the development of a class of lead (quinazoline-based) compounds with higher potency than doxazosin in suppressing
prostate
growth by targeting tissue vascularity.
This new class of quinazoline-based compounds provides considerable promise as antitumor drugs for the treatment of advanced
prostate
cancer.
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(PMID = 18056461.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA107575; United States / NCI NIH HHS / CA / R01 CA107575-01; United States / NCI NIH HHS / CA / CA112250-02; United States / NCI NIH HHS / CA / CA112250; United States / NCI NIH HHS / CA / R01 CA112250; United States / NCI NIH HHS / CA / CA107575-01; United States / NCI NIH HHS / CA / R01 CA112250-02
[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 / 2-(4-(biphenyl-4-sulfonyl)-piperazin-1-yl)-6,7-dipropoxyquinazolin-4-yl-amine; 0 / Adrenergic alpha-Antagonists; 0 / Antigens, CD29; 0 / Quinazolines; NW1291F1W8 / Doxazosin
[Other-IDs]
NLM/ NIHMS19064; NLM/ PMC2194658
52.
Seki N, Tatsugami K, Naito S:
Holmium laser enucleation of the prostate: comparison of outcomes according to prostate size in 97 Japanese patients.
J Endourol
; 2007 Feb;21(2):192-6
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[Title]
Holmium laser enucleation of the
prostate
: comparison of outcomes according to
prostate
size in 97 Japanese patients.
PURPOSE: To review the outcomes associated with holmium laser enucleation of the
prostate
(HoLEP) to identify the efficacy and safety in relation to
the prostate
size in subjects with symptomatic
benign prostatic
hyperplasia (BPH).
The morbidity and improvement in the outcome variables were compared in groups classified according to the baseline
prostate
volume: <50 cm3 (group 1), >or=50 cm3-<100 cm3 (group 2), and >or=100 cm3 (group 3).
RESULTS: The peak urinary flow rate (Qmax), postvoiding residual urine volume (PVR), International
Prostate
Symptom Score (IPSS) and quality of life (QoL) score all improved significantly after HoLEP, and no significant differences were observed among the groups.
CONCLUSIONS: Holmium laser enucleation is an effective treatment for symptomatic BPH independent
of prostate
size.
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(PMID = 17338621.001).
[ISSN]
0892-7790
[Journal-full-title]
Journal of endourology
[ISO-abbreviation]
J. Endourol.
[Language]
ENG
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
W1XX32SQN1 / Holmium
53.
Sadetsky N, Hubbard A, Carroll PR, Satariano W:
Predictive value of serial measurements of quality of life on all-cause mortality in prostate cancer patients: data from CaPSURE (cancer of the prostate strategic urologic research endeavor) database.
Qual Life Res
; 2009 Oct;18(8):1019-27
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[Title]
Predictive value of serial measurements of quality of life on all-cause mortality in
prostate
cancer patients: data from CaPSURE (cancer of the
prostate
strategic urologic research endeavor) database.
In light of the longer survival in patients with
prostate
cancer and importance of quality of life, we seek to evaluate the association between HRQOL and survival using traditional and novel techniques.
METHODS: Patients from CaPSURE (Cancer of the
Prostate
Strategic Urologic Research Endeavor) who were treated within 6 months
of diagnosis
and had pre-treatment and sufficient post-treatment follow-up information constituted the study population.
Association between HRQOL and survival (defined by all-cause mortality) in patients with
prostate
cancer was evaluated using Cox proportional hazards models controlling for age at
diagnosis
, type of treatment received, clinical risk classification, and number of comorbidities.
CONCLUSION: This study demonstrated that several domains of HRQOL were significantly associated with survival in a large group of patients with localized
prostate
cancer.
[MeSH-major]
Prostatic
Neoplasms
/
diagnosis
. Quality of Life
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J Clin Oncol. 2003 May 1;21(9):1660-8
[
12721239.001
]
(PMID = 19697155.001).
[ISSN]
1573-2649
[Journal-full-title]
Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation
[ISO-abbreviation]
Qual Life Res
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
[Other-IDs]
NLM/ PMC2744792
54.
Heitzer MD, DeFranco DB:
Hic-5/ARA55, a LIM domain-containing nuclear receptor coactivator expressed in prostate stromal cells.
Cancer Res
; 2006 Jul 15;66(14):7326-33
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[Title]
Hic-5/ARA55, a LIM domain-containing nuclear receptor coactivator expressed in
prostate
stromal cells.
Prostate gland
development and growth requires both androgen action and epithelial-stromal communications.
In fact, androgen signaling through the androgen receptor (AR) may be important in both stromal and epithelial cells of the
prostate
.
Because interaction of AR with the coactivator, Hic-5/ARA55, results in enhanced androgen-induced transcription, we analyzed Hic-5/ARA55 expression in
prostate
tissue sections from normal human donors and
prostate
cancer patients.
In each sample, Hic-5/ARA55 expression was confined to the stromal compartment of the
prostate
.
Furthermore, a
prostate
stromal cell line, WPMY-1 cells, expresses Hic-5/ARA55, which is localized both at focal adhesion complexes and within the soluble cytoplasmic compartment.
These data provide the first demonstration of a stromal-specific AR coactivator that has an effect on an androgen-regulated growth factor that is essential for stromal/epithelial cell communication in
the prostate
.
[MeSH-major]
Cytoskeletal Proteins / biosynthesis. DNA-Binding Proteins / biosynthesis.
Prostate
/ metabolism.
Prostatic
Neoplasms
/ metabolism
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(PMID = 16849583.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA43037
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / LIM Domain Proteins; 0 / Receptors, Androgen; 0 / TGFB1I1 protein, human; 126469-10-1 / Fibroblast Growth Factor 7
55.
Jackson MD, McFarlane-Anderson ND, Simon GA, Bennett FI, Walker SP:
Urinary phytoestrogens and risk of prostate cancer in Jamaican men.
Cancer Causes Control
; 2010 Dec;21(12):2249-57
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[Title]
Urinary phytoestrogens and risk
of prostate
cancer in Jamaican men.
We evaluated the relationship of spot urinary concentrations of phytoestrogens with total
prostate
cancer and
tumor
grade in a hospital-based case-control study in Jamaica.
Compared with non-producers of equol (reference tertile), men who produced equol were at decreased risk of total
prostate
cancer (tertile 2: OR, 0.42; CI, 0.23-0.75) (tertile 3: OR, 0.48; CI, 0.26-0.87) (p (trend), 0.020) and high-grade disease (tertile 2: OR, 0.31; CI, 0.15-0.61) (tertile 3: OR, 0.29; CI, 0.13-0.60) (p (trend), 0.001).
Higher concentrations of enterolactone were positively related to total
prostate
cancer (OR, 1.85; CI, 1.01-3.44; p (trend), 0.027) as well as high-grade disease (OR, 2.46; CI, 1.11-5.46; p (trend), 0.023).
There were no associations between urinary excretion of genistein and daidzein with risk
of prostate
cancer.
Producers of equol (isoflavone) may be at reduced risk of total- and high-grade
prostate
cancer whereas enterolactone may increase the likelihood of disease.
[MeSH-major]
Carcinoma / etiology. Phytoestrogens / urine.
Prostatic
Neoplasms
/ etiology
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(PMID = 20924663.001).
[ISSN]
1573-7225
[Journal-full-title]
Cancer causes & control : CCC
[ISO-abbreviation]
Cancer Causes Control
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / 4',7-dihydroxy-3,4-dihydroisoflavone; 0 / Isoflavones; 0 / Lignans; 0 / Phytoestrogens; 531-95-3 / Equol; 6287WC5J2L / daidzein; DH2M523P0H / Genistein
56.
Nagata Y, Sonoda T, Mori M, Miyanaga N, Okumura K, Goto K, Naito S, Fujimoto K, Hirao Y, Takahashi A, Tsukamoto T, Akaza H:
Dietary isoflavones may protect against prostate cancer in Japanese men.
J Nutr
; 2007 Aug;137(8):1974-9
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[Title]
Dietary isoflavones may protect against
prostate
cancer in Japanese men.
We examined associations between nutritional and other lifestyle factors and the prevalence
of prostate
cancer in a case-control study of Japanese men.
BMI, physical activity, occupation, family history
of prostate
cancer, and medical history were not associated with
prostate
cancer risk.
On the other hand, isoflavone significantly decreased the risk
of prostate
cancer regardless of adjustment by PUFA, (n-6) fatty acids or magnesium.
In conclusion, our findings indicate that isoflavones might be an effective dietary protective factor against
prostate
cancer in Japanese men.
[MeSH-major]
Diet. Isoflavones / pharmacology.
Prostatic
Neoplasms
/ prevention & control
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(PMID = 17634273.001).
[ISSN]
0022-3166
[Journal-full-title]
The Journal of nutrition
[ISO-abbreviation]
J. Nutr.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Isoflavones
57.
Saeki N, Gu J, Yoshida T, Wu X:
Prostate stem cell antigen: a Jekyll and Hyde molecule?
Clin Cancer Res
; 2010 Jul 15;16(14):3533-8
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[Title]
Prostate
stem cell antigen: a Jekyll and Hyde molecule?
Prostate
stem cell antigen (PSCA) is a glycosylphosphatidylinositol (GPI)-anchored cell surface protein.
It is up-regulated in several major cancers including
prostate
, bladder, and pancreatic cancers.
The expression of PSCA is positively correlated with advanced clinical stage and metastasis in
prostate
cancers and is also associated with malignant progression of premalignant
prostate
lesions.
Therefore, PSCA has been proposed as a biomarker
of diagnosis
and prognosis, as well as a target of therapy for these cancers.
In addition, PSCA has also shown clinical potential in immunotherapy as a
prostate
-specific antigen, which, when presented by dendritic cells, may elicit strong
tumor
-specific immunity.
In contrast, PSCA is down-regulated in esophageal and gastric cancer and may have a
tumor
-suppressing function in the gastric epithelium.
PSCA seems to be a Jekyll and Hyde molecule that plays differential roles,
tumor
promoting or suppressing, depending on the cellular context.
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.
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.
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[Copyright]
Copyright 2010 AACR.
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(PMID = 20501618.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50 CA091846; United States / NCI NIH HHS / CA / R01 CA074880; United States / NCI NIH HHS / CA / U01 CA127615; United States / NCI NIH HHS / CA / CA127615-02; United States / NCI NIH HHS / CA / R01CA74880; United States / NCI NIH HHS / CA / R01 CA131335; United States / NCI NIH HHS / CA / P50CA91846; United States / NCI NIH HHS / CA / R01 CA131335-02; United States / NCI NIH HHS / CA / R01 CA074880-10; United States / NCI NIH HHS / CA / CA091846-090007; United States / NCI NIH HHS / CA / U01 CA127615-02; United States / NCI NIH HHS / CA / R01CA131335; United States / NCI NIH HHS / CA / P50 CA091846-090007; United States / NCI NIH HHS / CA / U01CA127615; United States / NCI NIH HHS / CA / CA074880-10; United States / NCI NIH HHS / CA / R01 CA111922; United States / NCI NIH HHS / CA / CA131335-02
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Neoplasm Proteins; 0 / PSCA protein, human
[Other-IDs]
NLM/ NIHMS204237; NLM/ PMC2905486
58.
Wong PF, Abubakar S:
Comparative transcriptional study of the effects of high intracellular zinc on prostate carcinoma cells.
Oncol Rep
; 2010 Jun;23(6):1501-16
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[Title]
Comparative transcriptional study of the effects of high intracellular zinc on
prostate
carcinoma cells.
The normally high concentration of zinc in normal
prostate gland
is significantly reduced in malignant
prostate
tissues, but its precise role in
prostate
tumorigenesis remains unclear.
The present study investigates the growth and transcriptional responses of LNCaP
prostate
cancer cells to prolonged high Zn2+ treatment.
FBL and CD164 were responsive to the treatment with Zn2+ in PNT2
prostate
normal cells and were further overexpressed in the prolonged Zn2+-treated LNCaP cells.
These observations suggest that in general high Zn2+ has suppressive effects on
prostate
cancer cell growth but continuous exposure to an environment of high Zn2+ can lead to the overexpression of cancer promoting genes such as FBL and CD164.
These findings support a potential detrimental role of Zn2+ in
prostate
cancer.
[MeSH-major]
Biomarkers,
Tumor
/ genetics.
Prostatic
Neoplasms
/ metabolism. RNA, Messenger / genetics. Trace Elements / pharmacology. Transcription, Genetic / drug effects. Zinc / pharmacology
[MeSH-minor]
Cell Proliferation / drug effects. Colony-Forming Units Assay. Gene Expression Profiling. Humans. Male. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction.
Tumor
Cells, Cultured
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ZINC, ELEMENTAL
.
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(PMID = 20428803.001).
[ISSN]
1791-2431
[Journal-full-title]
Oncology reports
[ISO-abbreviation]
Oncol. Rep.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Trace Elements; J41CSQ7QDS / Zinc
59.
Frattaroli J, Weidner G, Dnistrian AM, Kemp C, Daubenmier JJ, Marlin RO, Crutchfield L, Yglecias L, Carroll PR, Ornish D:
Clinical events in prostate cancer lifestyle trial: results from two years of follow-up.
Urology
; 2008 Dec;72(6):1319-23
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[Title]
Clinical events in
prostate
cancer lifestyle trial: results from two years of follow-up.
OBJECTIVES: Previous research has demonstrated that patients with
prostate
cancer participating in
the Prostate
Cancer Lifestyle Trial had a reduction in
prostate
-specific antigen (PSA) levels, inhibition of LNCaP cell growth, and fewer
prostate
cancer-related clinical events at the end of 1 year compared with controls.
METHODS:
The Prostate
Cancer Lifestyle Trial was a 1-year randomized controlled clinical trial of 93 patients with early-stage
prostate
cancer (Gleason score <7, PSA 4-10 ng/mL) undergoing active surveillance.
RESULTS: By 2 years of follow-up, 13 of 49 (27%) control patients and 2 of 43 (5%) experimental patients had undergone conventional
prostate
cancer treatment (radical prostatectomy, radiotherapy, or androgen deprivation, P < .05).
CONCLUSIONS: Patients with early-stage
prostate
cancer choosing active surveillance might be able to avoid or delay conventional treatment for at least 2 years by making changes in their diet and lifestyle.
[MeSH-major]
Life Style.
Prostatic
Neoplasms
/ therapy
[MeSH-minor]
Aged. Biopsy. Cell Line,
Tumor
. Diet. Exercise. Follow-Up Studies. Humans. Male. Medical Oncology / methods. Middle Aged.
Prostate
-Specific Antigen / biosynthesis. Self-Help Groups. Treatment Outcome
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(PMID = 18602144.001).
[ISSN]
1527-9995
[Journal-full-title]
Urology
[ISO-abbreviation]
Urology
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / 5P50CA089520-02; United States / PHS HHS / / C76HF00803
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
60.
Thompson IM, Ankerst DP:
Prostate-specific antigen in the early detection of prostate cancer.
CMAJ
; 2007 Jun 19;176(13):1853-8
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[Title]
Prostate
-specific antigen in the early detection
of prostate
cancer.
Throughout Canada, the United States and much of Europe,
prostate
-specific antigen (PSA) screening for
prostate
cancer has proliferated over the past 2 decades, leading to dramatic increases in detection rates
of prostate
cancer.
Although it has unquestionably led to increased detection of cancer and a migration to lower-stage and -volume tumours, it is still unknown whether PSA screening significantly reduces mortality from
prostate
cancer.
The recently developed risk calculator from
the Prostate
Cancer Prevention Trial, which integrates family history
of prostate
cancer, digital rectal examination findings, PSA test result, age, ethnicity, and history of a prior
prostate
biopsy with a negative result, allows clinicians to assess a patient's individual risk of cancer.
This risk should be examined in the context of a patient's life expectancy and comorbidity as well as his concern about the possibility
of prostate
cancer.
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J Urol. 2004 Jul;172(1):94-7
[
15201745.001
]
(PMID = 17576986.001).
[ISSN]
1488-2329
[Journal-full-title]
CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne
[ISO-abbreviation]
CMAJ
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U01 CA086402; United States / NCI NIH HHS / CA / UO1 CA 86402
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
Canada
[Chemical-registry-number]
0 / Biomarkers; EC 3.4.21.77 / Prostate-Specific Antigen
[Number-of-references]
48
[Other-IDs]
NLM/ PMC1891131
61.
Phan TP, Syed AM, Puthawala A, Sharma A, Khan F:
High dose rate brachytherapy as a boost for the treatment of localized prostate cancer.
J Urol
; 2007 Jan;177(1):123-7; discussion 127
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[Title]
High dose rate brachytherapy as a boost for the treatment of localized
prostate
cancer.
PURPOSE: We report the outcome and toxicities of high dose rate brachytherapy as a boost for localized
prostate
cancer.
MATERIALS AND METHODS: Between 1996 and 2003, 309 patients with
prostate
carcinoma were treated with external beam radiation therapy and high dose rate brachytherapy.
Group 1 of 67 patients had Gleason score 6 or less, pretreatment
prostate
specific antigen 10 ng/ml or less and clinical stage T2a or less.
Group 2 of 109 patients had Gleason score 7 or greater, pretreatment
prostate
specific antigen greater than 10 ng/ml and clinical stage T2b or greater.
On univariate analysis risk group, pretreatment
prostate
specific antigen and Gleason score were significant predictors of biochemical control.
However, on multivariate analysis only risk group and pretreatment
prostate
specific antigen were significant.
CONCLUSIONS: External beam radiation therapy and high dose rate brachytherapy for
prostate
cancer resulted in excellent biochemical control, cause specific survival and overall survival with minimal severe acute or late complications.
[MeSH-major]
Adenocarcinoma / radiotherapy. Brachytherapy / methods.
Prostatic
Neoplasms
/ radiotherapy
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(PMID = 17162020.001).
[ISSN]
0022-5347
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
62.
Marcu M, Radu E, Sajin M:
Neuroendocrine transdifferentiation of prostate carcinoma cells and its prognostic significance.
Rom J Morphol Embryol
; 2010;51(1):7-12
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[Title]
Neuroendocrine transdifferentiation
of prostate
carcinoma cells and its prognostic significance.
Neuroendocrine (
NE
) cells are a distinct epithelial cell compartment of the normal human
prostate gland
.
Their phenotype and range of endocrine secretion products are similar, but not identical to those
of NE
-like cells from
prostate
carcinoma.
Neuroendocrine differentiation (NED) is a feature commonly seen in
prostate
carcinoma and a number of studies pointed out that its extent is associated to hormone therapy refractory and aggressive disease.
However, less information is available on the significance of NED in organ-confined
prostate
cancer, although identification of early predictors of aggressive disease would obviously allow for more adequate therapy.
[MeSH-major]
Carcinoma /
diagnosis
. Carcinoma / pathology. Cell Transdifferentiation / physiology. Neuroendocrine Cells / physiology.
Prostatic
Neoplasms
/
diagnosis
.
Prostatic
Neoplasms
/ pathology
[MeSH-minor]
Biomarkers,
Tumor
. Humans. Male.
Neoplasm
Invasiveness. Prognosis
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(PMID = 20191113.001).
[ISSN]
1220-0522
[Journal-full-title]
Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
[ISO-abbreviation]
Rom J Morphol Embryol
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article; Review
[Publication-country]
Romania
[Chemical-registry-number]
0 / Biomarkers, Tumor
[Number-of-references]
53
63.
Adhami VM, Mukhtar H:
Anti-oxidants from green tea and pomegranate for chemoprevention of prostate cancer.
Mol Biotechnol
; 2007 Sep;37(1):52-7
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[Title]
Anti-oxidants from green tea and pomegranate for chemoprevention
of prostate
cancer.
Among males,
prostate
cancer has become the second leading cause of cancer-related deaths in North America, with similar trends in many Western and developing countries.
One way to control
prostate
cancer is through chemoprevention, which refers to the administration of synthetic or naturally occurring agents to block, reverse, or delay the process of carcinogenesis.
Prostate
cancer is an ideal candidate disease for chemopreventive intervention, because it grows very slowly, likely for decades, before symptoms arise and a
diagnosis
is finally established, it has a long latency period, and it is typically diagnosed in men >50 years of age.
We have been defining the usefulness of dietary anti-oxidants for chemoprevention
of prostate
and other cancers.
This review will focus on
prostate
cancer chemopreventive effects of polyphenolic anti-oxidants derived from green tea and pomegranate.
It is a challenge to custom-tailor these gift molecules as cocktails in concentrations that can easily be consumed by humans for delaying
prostate
and other cancers.
[MeSH-major]
Antioxidants / administration & dosage. Camellia sinensis / chemistry. Flavonoids / administration & dosage. Phenols / administration & dosage.
Prostatic
Neoplasms
/ prevention & control. Punicaceae / chemistry. Tea / chemistry
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.
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.
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Cancer Surv. 1995;23:43-62
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(PMID = 17914164.001).
[ISSN]
1073-6085
[Journal-full-title]
Molecular biotechnology
[ISO-abbreviation]
Mol. Biotechnol.
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / P50 DK065303-019; United States / NCI NIH HHS / CA / R01 CA 101039; United States / NCI NIH HHS / CA / R01 CA 120451; United States / NCI NIH HHS / CA / R01 CA 78809
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antioxidants; 0 / Flavonoids; 0 / Phenols; 0 / Polyphenols; 0 / Tea
[Number-of-references]
52
64.
Setlur SR, Mertz KD, Hoshida Y, Demichelis F, Lupien M, Perner S, Sboner A, Pawitan Y, Andrén O, Johnson LA, Tang J, Adami HO, Calza S, Chinnaiyan AM, Rhodes D, Tomlins S, Fall K, Mucci LA, Kantoff PW, Stampfer MJ, Andersson SO, Varenhorst E, Johansson JE, Brown M, Golub TR, Rubin MA:
Estrogen-dependent signaling in a molecularly distinct subclass of aggressive prostate cancer.
J Natl Cancer Inst
; 2008 Jun 4;100(11):815-25
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[Title]
Estrogen-dependent signaling in a molecularly distinct subclass of aggressive
prostate
cancer.
BACKGROUND: The majority
of prostate
cancers harbor gene fusions of the 5'-untranslated region of the androgen-regulated transmembrane protease serine 2 (TMPRSS2) promoter with erythroblast transformation-specific transcription factor family members.
The common fusion between TMPRESS2 and v-ets erythroblastosis virus E26 oncogene homolog (avian) (ERG) is associated with a more aggressive clinical phenotype, implying the existence of a distinct subclass
of prostate
cancer defined by this fusion.
METHODS: We used complementary DNA-mediated annealing, selection, ligation, and extension to determine the expression profiles of 6144 transcriptionally informative genes in archived biopsy samples from 455
prostate
cancer patients in the Swedish Watchful Waiting cohort (1987-1999) and the United States-based Physicians(') Health Study cohort (1983-2003).
A gene expression signature for
prostate
cancers with the TMPRSS2-ERG fusion was determined using partitioning and classification models and used in computational functional analysis.
Cell proliferation and TMPRSS2-ERG expression in androgen receptor-negative (NCI-H660)
prostate
cancer cells after treatment with vehicle or estrogenic compounds were assessed by viability assays and quantitative polymerase chain reaction, respectively.
RESULTS: We identified an 87-gene expression signature that distinguishes TMPRSS2-ERG fusion
prostate
cancer as a discrete molecular entity (area under the curve = 0.80, 95% confidence interval [CI] = 0.792 to 0.81; P < .001).
CONCLUSIONS: TMPRSS2-ERG fusion
prostate
cancer is a distinct molecular subclass.
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(PMID = 18505969.001).
[ISSN]
1460-2105
[Journal-full-title]
Journal of the National Cancer Institute
[ISO-abbreviation]
J. Natl. Cancer Inst.
[Language]
ENG
[Grant]
United States / NIA NIH HHS / AG / R01AG21404; United States / NCI NIH HHS / CA / P50 CA090381; United States / NIA NIH HHS / AG / R01 AG021404; United States / NIA NIH HHS / AG / R01 AG021404-05; United States / NCI NIH HHS / CA / P50 CA090381-10; United States / NIA NIH HHS / AG / AG021404-05
[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 / 1,3,5-tris(4-hydroxyphenyl)-4-propyl-1H-pyrazole; 0 / Antineoplastic Agents, Hormonal; 0 / DNA, Complementary; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Estrogens; 0 / Nitriles; 0 / Oncogene Proteins, Fusion; 0 / Phenols; 0 / Propionates; 0 / Pyrazoles; 0 / TMPRSS2-ERG fusion protein, human; 0 / diarylpropionitrile; 4TI98Z838E / Estradiol; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / TMPRSS2 protein, human
[Other-IDs]
NLM/ NIHMS272096; NLM/ PMC3073404
65.
Nishiyama T, Suzuki K, Yamana K, Tonegawa E, Wako K, Takahashi K:
Stepping-stones to the further advancement of androgen-deprivation therapy for prostate cancer.
Expert Rev Anticancer Ther
; 2006 Feb;6(2):259-68
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[Title]
Stepping-stones to the further advancement of androgen-deprivation therapy for
prostate
cancer.
Androgen-deprivation therapy has remained the critical therapeutic option for patients with advanced
prostate
cancer for over 60 years.
Patients with poorly differentiated
prostate
cancer have low dihydrotestosterone levels in
the prostate
.
After androgen-deprivation therapy, dihydrotestosterone levels in
the prostate
remain at approximately 25% of the level measured before therapy.
The biologically aggressive
prostate
cancer cells may have an androgen receptor with heightened sensitivity to low dihydrotestosterone levels from the early stage of androgen-dependent disease.
It is necessary to consider the androgen environment and the status of the androgen receptor in
the prostate
in order to improve the clinical efficacy of androgen-deprivation therapy and the quality of life of patients.
[MeSH-major]
Androgen Antagonists / therapeutic use.
Prostatic
Neoplasms
/ drug therapy. Receptors, Androgen / physiology
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(PMID = 16445378.001).
[ISSN]
1744-8328
[Journal-full-title]
Expert review of anticancer therapy
[ISO-abbreviation]
Expert Rev Anticancer Ther
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Androgen Antagonists; 0 / Androgens; 0 / Receptors, Androgen; 08J2K08A3Y / Dihydrotestosterone
[Number-of-references]
71
66.
Bruxvoort KJ, Charbonneau HM, Giambernardi TA, Goolsby JC, Qian CN, Zylstra CR, Robinson DR, Roy-Burman P, Shaw AK, Buckner-Berghuis BD, Sigler RE, Resau JH, Sullivan R, Bushman W, Williams BO:
Inactivation of Apc in the mouse prostate causes prostate carcinoma.
Cancer Res
; 2007 Mar 15;67(6):2490-6
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[Title]
Inactivation of Apc in the mouse
prostate
causes
prostate
carcinoma.
Alterations of the Wnt/beta-catenin signaling pathway are positively associated with the development and progression of human cancer, including carcinoma of the
prostate
.
To determine the role of activated Wnt/beta-catenin signaling in mouse
prostate
carcinogenesis, we created a mouse
prostate tumor
model using probasin-Cre-mediated deletion of Apc.
Prostate
tumors induced by the deletion of Apc have elevated levels of beta-catenin protein and are highly proliferative.
Tumor
formation is fully penetrant and follows a consistent pattern of progression.
Continued
tumor
growth usually necessitated sacrifice between 12 and 15 months of age.
Surgical castration of 6-week-old mice inhibited
tumor
formation, and castration of mice with more advanced tumors resulted in the partial regression of specific
prostate
glands.
We conclude that
the prostate
-specific deletion of Apc and the increased expression of beta-catenin associated with
prostate
carcinoma suggests a role for beta-catenin in
prostate
cancer and offers an appropriate animal model to investigate the interaction of Wnt signaling with other genetic and epigenetic signals in
prostate
carcinogenesis.
[MeSH-major]
Cell Transformation, Neoplastic / genetics. Genes, APC.
Prostatic
Neoplasms
/ genetics
[MeSH-minor]
Alleles. Androgens / deficiency. Androgens / metabolism. Animals. Cell Nucleus / metabolism. Female. Gene Deletion. Gene Expression Regulation, Neoplastic. Gene Silencing. Immunohistochemistry. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic.
Neoplasms
, Hormone-Dependent / genetics.
Neoplasms
, Hormone-Dependent / metabolism. Organ Specificity.
Prostatic
Hyperplasia / genetics.
Prostatic
Hyperplasia / metabolism. beta Catenin / metabolism
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gene/protein/disease-specific - Gene Ontology annotations from this paper
.
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gene/protein/disease-specific - KOMP Repository
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Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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(PMID = 17363566.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01CA59705
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgens; 0 / beta Catenin
67.
Biundo B:
Hormonal influences in prostate cancer: an update of a complex subject.
Int J Pharm Compd
; 2010 Mar-Apr;14(2):100-4
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[Title]
Hormonal influences in
prostate
cancer: an update of a complex subject.
Pharmacists who are involved with patients and physicians have a tremendous opportunity to serve in the realm
of prostate
cancer, and there are numerous compounding opportunities.
Nutraceuticals such as omega-3 fatty acids, vitamin D, zinc, and selenium all play an important role in
prostate
health, as these agents have 5a-reductase inhibiting and anti-inflammatory properties.
More than anything else, we see that the pathophysiology
of prostate
cancer, although quite complex, is being explored at an amazing rate.
The author believes that hormonal balance is critical, and that it is largely hormonal imbalance that is involved in
prostate
disease.
In that regard, the author concludes that the levels of testosterone, estradiol, and drotestosterone, experienced at a more youthful age are vital if we are to improve
prostate
health.
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(PMID = 23965417.001).
[ISSN]
1092-4221
[Journal-full-title]
International journal of pharmaceutical compounding
[ISO-abbreviation]
Int J Pharm Compd
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
United States
68.
Crook J, Patil N, Wallace K, Borg J, Zhou D, Ma C, Pond G:
A phase III randomized trial of the timing of meloxicam with iodine-125 prostate brachytherapy.
Int J Radiat Oncol Biol Phys
; 2010 Jun 1;77(2):496-501
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[Title]
A phase III randomized trial of the timing of meloxicam with iodine-125
prostate
brachytherapy.
PURPOSE: Nonsteroidal anti-inflammatory medication is used to reduce
prostate
edema and urinary symptoms following
prostate
brachytherapy.
Prostate
volume obtained by MR imaging at 1 month was compared to baseline
prostate
volume obtained by TRUS planimetry and expressed as an edema factor.
The trial endpoints were
prostate
edema at 1 month, International
Prostate
Symptom Score (IPSS) questionnaire results at 1 and 3 months, and any need for catheterization.
Median age was 61 (range, 45-79 years), and median TRUS
prostate
volume was 35.7 cc (range, 18.1-69.5 cc).
Baseline
prostate
volume remained the primary predictor of postimplant urinary retention.
[MeSH-minor]
Administration, Oral. Aged. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Drug Administration Schedule. Edema / drug therapy. Edema / etiology. Humans. Male. Middle Aged. Ontario.
Prostatic
Diseases / drug therapy.
Prostatic
Diseases / etiology
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Meloxicam
.
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[Copyright]
Copyright 2010 Elsevier Inc. All rights reserved.
(PMID = 20350785.001).
[ISSN]
1879-355X
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00152919
[Publication-type]
Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Iodine Radioisotopes; 0 / Thiazines; 0 / Thiazoles; 71125-38-7 / meloxicam
69.
Famili P, Cauley JA, Greenspan SL:
The effect of androgen deprivation therapy on periodontal disease in men with prostate cancer.
J Urol
; 2007 Mar;177(3):921-4
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[Title]
The effect of androgen deprivation therapy on periodontal disease in men with
prostate
cancer.
PURPOSE: We tested the hypothesis that men undergoing androgen deprivation therapy as treatment for
prostate
cancer are at greater risk for periodontitis and tooth loss.
MATERIALS AND METHODS: A total of 81 men with a mean age of 68.5 years who had
prostate
cancer were consecutively recruited among 325 enrolled in an academic osteoporosis study.
The prevalence of periodontal disease in 41 men with
prostate
cancer undergoing androgen deprivation for a mean of 1.5 years was compared to that in 27 with
prostate
cancer not undergoing androgen deprivation, who served as controls.
The prevalence of periodontal disease was examined in relation to bone mineral density in men with
prostate
cancer with and without androgen deprivation therapy.
Linear regression models were used to assess the association between periodontal disease and bone mineral density in the 2 groups with
prostate
cancer (treated/untreated).
CONCLUSIONS: Men with
prostate
cancer undergoing androgen deprivation therapy were more likely to have periodontal disease than men not on androgen deprivation therapy.
If confirmed in larger studies, this observation could have important public health implications, given the increasing use of androgen deprivation therapy to treat
prostate
cancer.
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[ISSN]
0022-5347
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[Language]
ENG
[Grant]
United States / NIA NIH HHS / AG / P30 AG024827; United States / NCATS NIH HHS / TR / UL1 TR000005; United States / NCRR NIH HHS / RR / M01-RR0056; United States / NCRR NIH HHS / RR / M01 RR000056; United States / NIDDK NIH HHS / DK / K24 DK062895; United States / NIDDK NIH HHS / DK / K24 DK 062895-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgen Antagonists
[Other-IDs]
NLM/ NIHMS19813; NLM/ PMC1934505
70.
Basu HS, Thompson TA, Church DR, Clower CC, Mehraein-Ghomi F, Amlong CA, Martin CT, Woster PM, Lindstrom MJ, Wilding G:
A small molecule polyamine oxidase inhibitor blocks androgen-induced oxidative stress and delays prostate cancer progression in the transgenic adenocarcinoma of the mouse prostate model.
Cancer Res
; 2009 Oct 1;69(19):7689-95
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[Title]
A small molecule polyamine oxidase inhibitor blocks androgen-induced oxidative stress and delays
prostate
cancer progression in the transgenic adenocarcinoma of the mouse
prostate
model.
High levels of reactive oxygen species (ROS) present in human
prostate
epithelia are an important etiologic factor in
prostate
cancer (CaP) occurrence, recurrence, and progression.
Androgen induces ROS production in
the prostate
by a yet unknown mechanism.
As
prostatic
epithelia produce a large excess of polyamines, the androgen-induced polyamine oxidation that produces H2O2 could be a major reason for the high ROS levels in
the prostate
epithelia.
These data show that polyamine oxidation is not only a major pathway for ROS production in
prostate
, but inhibiting this pathway also successfully delays CaP progression.
Genetic Alliance.
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.
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consumer health - Prostate Cancer
.
COS Scholar Universe.
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Hazardous Substances Data Bank.
Putrescine
.
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
.
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[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R03 CA121367-02; United States / NCI NIH HHS / CA / CA121367-02; United States / NCI NIH HHS / CA / R03 CA121367-01; United States / NCI NIH HHS / CA / CA121367-01; United States / NCI NIH HHS / CA / R03 CA121367; United States / NCI NIH HHS / CA / R01 CA085509
[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 / Androgens; 0 / Enzyme Inhibitors; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 93565-01-6 / MDL 72527; EC 1.5.- / Oxidoreductases Acting on CH-NH Group Donors; EC 1.5.3.- / polyamine oxidase; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.57 / diamine N-acetyltransferase; V10TVZ52E4 / Putrescine
[Other-IDs]
NLM/ NIHMS140232; NLM/ PMC2756327
71.
Schroeder JC, Bensen JT, Su LJ, Mishel M, Ivanova A, Smith GJ, Godley PA, Fontham ET, Mohler JL:
The North Carolina-Louisiana Prostate Cancer Project (PCaP): methods and design of a multidisciplinary population-based cohort study of racial differences in prostate cancer outcomes.
Prostate
; 2006 Aug 1;66(11):1162-76
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[Title]
The North Carolina-Louisiana
Prostate
Cancer Project (PCaP): methods and design of a multidisciplinary population-based cohort study of racial differences in
prostate
cancer outcomes.
BACKGROUND: The North Carolina-Louisiana
Prostate
Cancer Project (PCaP) is a multidisciplinary study of social, individual, and
tumor
-level causes of racial differences in
prostate
cancer aggressiveness.
METHODS: A population-based sample of incident
prostate
cancer cases from North Carolina and Louisiana will include 1,000 African Americans and 1,000 Caucasian Americans.
Prostate
cancer aggressiveness is classified based on PSA, clinical stage, and Gleason grade.
CONCLUSIONS: Preliminary data support the feasibility of this comprehensive study to help determine the focus of public health efforts to reduce racial disparities in
prostate
cancer mortality.
[MeSH-major]
Continental Population Groups.
Prostatic
Neoplasms
/ epidemiology
[MeSH-minor]
African Continental Ancestry Group. Cohort Studies. European Continental Ancestry Group. Humans. Louisiana / epidemiology. Male. Microarray Analysis. North Carolina / epidemiology. Patient Acceptance of Health Care.
Prostate
-Specific Antigen / blood. Surveys and Questionnaires. Survival Rate. Treatment Outcome
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.
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NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
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.
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[Copyright]
(c) 2006 Wiley-Liss, Inc.
(PMID = 16676364.001).
[ISSN]
0270-4137
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
72.
Lum AM, Wang BB, Beck-Engeser GB, Li L, Channa N, Wabl M:
Orphan receptor GPR110, an oncogene overexpressed in lung and prostate cancer.
BMC Cancer
; 2010 Feb 11;10:40
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[Title]
Orphan receptor GPR110, an oncogene overexpressed in lung and
prostate
cancer.
GPR110 transcript and protein levels were measured in lung and
prostate
cancer cell lines and clinical samples, respectively, by quantitative PCR and immunohistochemistry.
However, it had higher than average gene expression in normal kidney tissue and in
prostate
tissues originating from older donors.
Although identified as an oncogene in murine T lymphomas, GPR110 is greatly overexpressed in human lung and
prostate
cancers.
As detected by immunohistochemistry, GPR110 was overexpressed in 20 of 27 (74%) lung adenocarcinoma tissue cores and in 17 of 29 (59%)
prostate
adenocarcinoma tissue cores.
Additionally, staining with a GPR110 antibody enabled us to differentiate between
benign
prostate
hyperplasia and potential incipient malignancy.
CONCLUSION: Our work suggests a role for GPR110 in
tumor
physiology and supports it as a potential therapeutic candidate and disease marker for both lung and
prostate
cancer.
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[ISSN]
1471-2407
[Journal-full-title]
BMC cancer
[ISO-abbreviation]
BMC Cancer
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / R01AI041570
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
0 / Epitopes; 0 / GPR110 protein, human; 0 / Oncogene Proteins; 0 / Protein Isoforms; 0 / Receptors, Cell Surface; 0 / Receptors, G-Protein-Coupled
[Other-IDs]
NLM/ PMC2830182
73.
Pu H, Collazo J, Jones E, Gayheart D, Sakamoto S, Vogt A, Mitchell B, Kyprianou N:
Dysfunctional transforming growth factor-beta receptor II accelerates prostate tumorigenesis in the TRAMP mouse model.
Cancer Res
; 2009 Sep 15;69(18):7366-74
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[Title]
Dysfunctional transforming growth factor-beta receptor II accelerates
prostate
tumorigenesis in the TRAMP mouse model.
The contribution of a dysfunctional transforming growth factor-beta type II receptor (TGF beta RII) to
prostate
cancer initiation and progression was investigated in an in vivo mouse model.
Transgenic mice harboring the dominant-negative mutant TGF-beta type II receptor (DNTGF beta RII) in mouse epithelial cell were crossed with the TRAMP
prostate
cancer transgenic mouse to characterize the in vivo consequences of inactivated TGF-beta signaling on
prostate tumor
initiation and progression.
Histopathologic
diagnosis of prostate
specimens from the TRAMP+/DNTGF beta RII double transgenic mice revealed the appearance of early malignant changes and subsequently highly aggressive
prostate
tumors at a younger age, compared with littermates TRAMP+/Wt TGF beta RII mice.
A significant increase in the androgen receptor mRNA and protein levels was associated with the early onset
of prostate
tumorigenesis in TRAMP+/DNTGF beta RII mice.
Our results indicate that in vivo disruption of TGF-beta signaling accelerates the pathologic malignant changes in
the prostate
by altering the kinetics
of prostate
growth and inducing EMT.
The study also suggests that a dysfunctional TGF beta RII augments androgen receptor expression and promotes inflammation in early stage
tumor
growth, thus conferring a significant contribution by TGF-beta to
prostate
cancer progression.
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[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / DK053525-07; United States / NIEHS NIH HHS / ES / T32 ES007266; United States / NIDDK NIH HHS / DK / R01 DK053525; United States / NIDDK NIH HHS / DK / R01 DK053525-07; United States / NIDDK NIH HHS / DK / R01 DK5355-12
[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 / Receptors, Androgen; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
[Other-IDs]
NLM/ NIHMS135291; NLM/ PMC2747670
74.
Lawson DA, Zong Y, Memarzadeh S, Xin L, Huang J, Witte ON:
Basal epithelial stem cells are efficient targets for prostate cancer initiation.
Proc Natl Acad Sci U S A
; 2010 Feb 9;107(6):2610-5
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[Title]
Basal epithelial stem cells are efficient targets for
prostate
cancer initiation.
Prevailing theories suggest that luminal cells are the origin
of prostate
cancer because it is histologically defined by basal cell loss and malignant luminal cell expansion.
We introduced a series of genetic alterations into prospectively identified populations of murine basal/stem and luminal cells in an in vivo
prostate
regeneration assay.
Even though luminal cells fail to respond, basal/stem cells demonstrate efficient capacity for cancer initiation and can produce luminal-like disease characteristic of human
prostate
cancer in multiple models.
This finding provides evidence in support of basal epithelial stem cells as one target cell for
prostate
cancer initiation and demonstrates the propensity of primitive cells for tumorigenesis.
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[ISSN]
1091-6490
[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 / NCI NIH HHS / CA / R00 CA125937-03; United States / NCI NIH HHS / CA / 1K99/R00 CA125937; United States / NCI NIH HHS / PC / PC061456; United States / NCI NIH HHS / CA / R00 CA125937; United States / NICHD NIH HHS / HD / K12 HD001400; United States / NCI NIH HHS / CA / K99 CA125937; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / CA125937-03; United States / NICHD NIH HHS / HD / 5 K12HD001400
[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 / Fibroblast Growth Factor 10; 0 / Fli1 protein, mouse; 0 / Proto-Oncogene Protein c-fli-1; 0 / Receptors, Androgen; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Akt1 protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
[Other-IDs]
NLM/ PMC2823887
75.
Sartor O:
Prostate cancer. Saturation biopsy does not accurately localize tumors.
Nat Rev Urol
; 2010 Sep;7(9):479-80
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[Title]
Prostate
cancer. Saturation biopsy does not accurately localize tumors.
Precise localization
of prostate
cancer is essential for the success of focal therapies.
Despite suggestions that saturation biopsy might be useful in this regard, a new study implies it cannot accurately pinpoint
prostate
tumors. research efforts would perhaps be better focused on identifying which patients require treatment for clinically localized
prostate
cancer in the first place.
[MeSH-major]
Biopsy, Needle / methods.
Prostatic
Neoplasms
/ pathology
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(PMID = 20818322.001).
[ISSN]
1759-4820
[Journal-full-title]
Nature reviews. Urology
[ISO-abbreviation]
Nat Rev Urol
[Language]
eng
[Publication-type]
News
[Publication-country]
England
76.
Josifovski T, Radosević-Jelić L, Tulić C, Milosević A:
[Disease relapses after radical radiotherapy of prostate cancer--analysis of prognostic factors].
Srp Arh Celok Lek
; 2008 Jul-Aug;136(7-8):373-8
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[Title]
[Disease relapses after radical radiotherapy
of prostate
cancer--analysis of prognostic factors].
INTRODUCTION: Although there is no consensus on which is the best option in
prostate
cancer treatment, these patients could be successfully treated with radiotherapy.
Regarding some prognostic factors, it is possible today to classify
prostate
cancer patients into several risk groups for clinical and biochemical relapse, and therefore to choose the right treatment modality.
OBJECTIVE: The objective in our study was to analyze the impact of
tumour
stage and grade, previous transurethral resection of the
prostate
(TUR), initial
prostate
specific antigen (PSA) level and age on disease relapse after radical radiotherapy of the
prostate
cancer.
METHOD: Between January 1991 and December 2005, a clinical, retrospective study was performed at the Radiotherapy Department of the Institute for Oncology and Radiology of Serbia, which included 283 patients with
prostate
cancer treated only with radical radiotherapy.
RESULTS: After radical radiotherapy disease relapse more often occurred (with statistical significance) in patients with locally advanced
tumour
(stage C 35% vs. A 13% vs. B 19%), low
tumour
grade (grade III 38% vs. grade II 23% vs. grade I 17%), initial PSA level over 10 ng/ml (29%) and over 20 ng/ml (37%) compared to 11% in the patients with initial PSA level below 10 ng/ml, and patients of lower age (less than 55 years 50% vs. 16% in patients over 70 years).
CONCLUSION:
Tumour
stage C, low
tumour
grade (grade II-III), initial PSA level over 10 ng/ml (over 20 ng/ml) and younger age are poor prognostic factors for disease relapse.
[MeSH-major]
Carcinoma / radiotherapy. Carcinoma / secondary.
Neoplasm
Recurrence, Local.
Prostatic
Neoplasms
/ radiotherapy
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Humans. Male. Middle Aged. Prognosis.
Prostate
-Specific Antigen / blood
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(PMID = 18959172.001).
[ISSN]
0370-8179
[Journal-full-title]
Srpski arhiv za celokupno lekarstvo
[ISO-abbreviation]
Srp Arh Celok Lek
[Language]
srp
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Serbia
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
77.
Miller DC, Spencer BA, Ritchey J, Stewart AK, Dunn RL, Sandler HM, Wei JT, Litwin MS:
Treatment choice and quality of care for men with localized prostate cancer.
Med Care
; 2007 May;45(5):401-9
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[Title]
Treatment choice and quality of care for men with localized
prostate
cancer.
BACKGROUND: Variations in patterns of care and treatment outcomes suggest differences in the quality of care for men treated for localized
prostate
cancer.
OBJECTIVE: We sought to compare adherence with quality indicators for
prostate
cancer care among men treated with radical prostatectomy or external beam radiation therapy.
RESEARCH DESIGN AND SUBJECTS: We sampled 5230 men diagnosed in 2000 or 2001 with early-stage
prostate
cancer from 984 facilities reporting to the National Cancer Data Base.
MAIN OUTCOME MEASURE: Subject-level compliance with the RAND quality indicators for localized
prostate
cancer care, stratified by treatment.
CONCLUSIONS: Documented compliance with process of care quality indicators among men with localized
prostate
cancer appears superior for those treated with external beam radiation compared with those treated surgically.
[MeSH-major]
Choice Behavior. Guideline Adherence / statistics & numerical data.
Prostatic
Neoplasms
/ radiotherapy.
Prostatic
Neoplasms
/ surgery. Quality Indicators, Health Care
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(PMID = 17446826.001).
[ISSN]
0025-7079
[Journal-full-title]
Medical care
[ISO-abbreviation]
Med Care
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / 1-T-32 DK07782
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
78.
Kane CJ, Bassett WW, Sadetsky N, Silva S, Wallace K, Pasta DJ, Cooperberg MR, Chan JM, Carroll PR:
Obesity and prostate cancer clinical risk factors at presentation: data from CaPSURE.
J Urol
; 2005 Mar;173(3):732-6
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[Title]
Obesity and
prostate
cancer clinical risk factors at presentation: data from CaPSURE.
PURPOSE: We investigated the association of obesity with
prostate
cancer case demographics and clinical disease features at presentation.
MATERIALS AND METHODS: Data were abstracted from CaPSURE (Cancer of the
Prostate
Strategic Urologic Research Endeavor), a disease registry of 10,018 men with
prostate
cancer.
The overweight group had a lower serum
prostate
specific antigen (p = 0.010) and lower stage disease (p = 0.030) at
diagnosis
, but there was no association between Gleason score and obesity (p = 0.57).
However, among men with a BMI of 25 kg/m or greater there was a positive correlation between increasing BMI and risk of being in a worse prognostic group at
diagnosis
(p = 0.018).
CONCLUSIONS: Overweight and obese patients are more likely to be young at
diagnosis
and have multiple comorbidities.
Men in the overweight and obese groups presented with lower risk
prostate
cancer at
diagnosis
.
Among overweight and obese patients increased obesity is associated with a slightly increased chance of having high risk
prostate
cancer at
diagnosis
.
[MeSH-major]
Adenocarcinoma / complications. Obesity / complications.
Prostatic
Neoplasms
/ complications
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(PMID = 15711258.001).
[ISSN]
0022-5347
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P50-CA089520-0
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
79.
Qu Y, Zhang L, Mao M, Zhao F, Huang X, Yang C, Xiong Y, Mu D:
Effects of DNAzymes targeting Aurora kinase A on the growth of human prostate cancer.
Cancer Gene Ther
; 2008 Aug;15(8):517-25
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[Title]
Effects of DNAzymes targeting Aurora kinase A on the growth of human
prostate
cancer.
Aurora kinase A has been demonstrated to be involved in the malignant progression of many types of cancer including
prostate
cancer, we therefore hypothesized that Aurora kinase A might work as a valuable target for
prostate
cancer treatment.
To test this hypothesis, we used DNAzyme technology to inhibit Aurora kinase A expression and evaluated the effects of DNAzymes as therapeutic agents to treat
prostate
cancer.
When transfected into
the prostate
cancer cell line PC3, DZ2 was found to strongly inhibit the expression of Aurora kinase A examined by western blot analysis, and thus suppressed cell growth, arrested the progression of cell cycle, induced cell apoptosis and attenuated cell migration, as measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium assay, flow cytometry and Boyden chamber assay.
Through in vivo study, we also found that DZ2 could significantly inhibit the growth of human
prostate
cancer xenografts in nude mice.
In conclusion, DZ2 could effectively attenuate malignant progression
of prostate
cancer both in vitro and in vivo, suggesting that DNAzyme targeting Aurora kinase A may be used as a valuable therapy to treat
prostate
cancer.
[MeSH-major]
DNA, Catalytic / pharmacology.
Prostatic
Neoplasms
/ pathology. Protein-Serine-Threonine Kinases / antagonists & inhibitors
[MeSH-minor]
Animals. Aurora Kinase A. Aurora Kinases. Base Sequence. Blotting, Western. Cell Cycle. Cell Line,
Tumor
. Cell Proliferation. Cloning, Molecular. DNA Primers. DNA, Complementary. Humans. Male. Mice. Mice, Nude
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(PMID = 18404163.001).
[ISSN]
1476-5500
[Journal-full-title]
Cancer gene therapy
[ISO-abbreviation]
Cancer Gene Ther.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA Primers; 0 / DNA, Catalytic; 0 / DNA, Complementary; EC 2.7.11.1 / AURKA protein, human; EC 2.7.11.1 / Aurka protein, mouse; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
80.
Drouin SJ, Rouprêt M:
[Epidemiology, diagnosis and prognosis of localized prostate cancer: what's new?].
Prog Urol
; 2009 Apr;19 Suppl 1:S3-7
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[Title]
[Epidemiology,
diagnosis
and prognosis of localized
prostate
cancer: what's new?].
[Transliterated title]
Epidemiologie, diagnostic et pronostic du cancer
de prostate
localisé : état des lieux.
Detection and
diagnosis of prostate
cancer has challenged researchers and clinicians for several years, particularly with the increase of its incidence.
With the advent of optimal treatments for each patient,
diagnosis
and prognostic tools arouse more and more interest.
Effectively, it becomes necessary to assess even better the aggressiveness of the
tumour
in order to choose the most appropriate treatment and, thus to make a correlation between the phenotype and the genotype.
The optimization of MRI allows more precise
diagnosis of
local invasion and is usefull to optimize.
[MeSH-major]
Prostatic
Neoplasms
/ epidemiology
[MeSH-minor]
Antigens,
Neoplasm
/ genetics. Antigens,
Neoplasm
/ urine. Biopsy / methods. France / epidemiology. Genetic Markers. Humans. Incidence. Magnetic Resonance Imaging. Male. Phenotype. Prognosis. Reference Values
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.
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(PMID = 19465334.001).
[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
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Genetic Markers; 0 / prostate cancer antigen 3, human
81.
Moreira Leite KR, Camara-Lopes LH, Dall'Oglio MF, Cury J, Antunes AA, Sañudo A, Srougi M:
Upgrading the Gleason score in extended prostate biopsy: implications for treatment choice.
Int J Radiat Oncol Biol Phys
; 2009 Feb 1;73(2):353-6
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[Title]
Upgrading the Gleason score in extended
prostate
biopsy: implications for treatment choice.
PURPOSE: To determine the incidence of overestimation of Gleason score (GS) in extended
prostate
biopsy, and consequently circumventing unnecessary aggressive treatment.
METHODS AND MATERIALS: This is a retrospective study of 464 patients who underwent
prostate
biopsy and radical prostatectomy between January 2001 and November 2007.
The incidence of overestimation of GS in biopsies and
tumor
volume were studied.
Multivariate analysis was applied to find parameters that predict upgrading the GS in
prostate
biopsy.
RESULTS: The exact agreement of GS between
prostate
biopsy and radical prostatectomy occurred in 56.9% of cases.
One hundred and six (22.8%) patients received a
diagnosis of
high GS (8, 9, or 10) in a
prostate
biopsy.
In multivariate analysis, the total percentage
of tumor
was the only independent factor in overestimation of GS.
This should be remembered by professionals involved with
prostate
cancer to avoid overtreatment and undesirable side effects.
[MeSH-major]
Prostate
/ pathology.
Prostatic
Neoplasms
/ pathology
[MeSH-minor]
Adult. Aged. Biopsy, Needle. Chi-Square Distribution. Humans. Male. Middle Aged. Prostatectomy. Regression Analysis. Retrospective Studies. Statistics, Nonparametric.
Tumor
Burden
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(PMID = 18774658.001).
[ISSN]
1879-355X
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
82.
Reiner T, de Las Pozas A, Parrondo R, Perez-Stable C:
Progression of prostate cancer from a subset of p63-positive basal epithelial cells in FG/Tag transgenic mice.
Mol Cancer Res
; 2007 Nov;5(11):1171-9
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[Title]
Progression
of prostate
cancer from a subset of p63-positive basal epithelial cells in FG/Tag transgenic mice.
Transgenic mice that allow targeting of SV40 T antigen (Tag) to
the prostate
provide a unique model to identify cancer-initiating cells and follow their progression from a normal cell phenotype into
prostate
cancer cells.
We have developed the FG/Tag transgenic mouse model
of prostate
cancer using the human fetal globin (FG) promoter linked to Tag.
Immunohistochemistry results show that before the development
of prostate
intraepithelial
neoplasia
(PIN), a subset of p63(+) basal epithelial cells expresses Tag.
As in the case of human
prostate
cancer, there is a loss of p63(+) basal cells with neoplastic progression, and a long period of time is required for PIN lesions to develop into palpable
prostate
tumors.
Cell lines derived from primary
prostate
tumors showed characteristics of a neuroendocrine-epithelial intermediate cell type.
The FG promoter has high transcriptional activity in intermediate (DU 145, PC-3) and p63(+) basal epithelial (LHSR-AR)
prostate
cancer cells.
Therefore, the unexpected development
of prostate
cancer in the FG/Tag mice may be due to the presence of DNA elements in the FG promoter that can target Tag to specific basal or intermediate cells.
We conclude that FG/Tag mouse is a unique model
of prostate
cancer because the initiating cells are a subset of p63(+) basal (possibly stem cells), which may be the true cells of origin for carcinogenesis in aggressive human
prostate
cancer.
[MeSH-major]
Antigens, Polyomavirus Transforming / genetics. Disease Models, Animal. Mice, Transgenic.
Prostatic
Neoplasms
/ pathology
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.
MedlinePlus Health Information.
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.
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
.
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(PMID = 17982114.001).
[ISSN]
1541-7786
[Journal-full-title]
Molecular cancer research : MCR
[ISO-abbreviation]
Mol. Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Polyomavirus Transforming; 0 / Phosphoproteins; 0 / Trans-Activators; 0 / Trp63 protein, mouse; 9004-22-2 / Globins
83.
Zhang J, Dhakal I, Stone A, Ning B, Greene G, Lang NP, Kadlubar FF:
Plasma carotenoids and prostate cancer: a population-based case-control study in Arkansas.
Nutr Cancer
; 2007;59(1):46-53
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[Title]
Plasma carotenoids and
prostate
cancer: a population-based case-control study in Arkansas.
Carotenoids possess antioxidant properties and thus may protect against
prostate
cancer.
In this study, we aimed to investigate the relation between plasma concentrations of carotenoids and the risk
of prostate
cancer in a population-based case-control study in Arkansas.
Cases (n = 193) were men with
prostate
cancer diagnosed in 3 major hospitals, and controls (n = 197) were matched to cases by age, race, and county of residence.
After adjustment for confounders, plasma levels of lycopene, lutein/zeaxanthin, and beta-cryptoxanthin were inversely associated with
prostate
cancer risk.
Subjects in the highest quartile of plasma lycopene (513.7 microg/l) had a 55% lower risk
of prostate
cancer than those in the lowest quartile (140.5 microg/l; P trend = 0.042).
This study added to the emerging evidence that high circulating levels of lycopene, lutein/zeaxanthin, and beta-cryptoxanthin are associated with a low risk
of prostate
cancer.
[MeSH-major]
Antioxidants / metabolism. Carotenoids / blood.
Prostatic
Neoplasms
/ blood.
Prostatic
Neoplasms
/ epidemiology
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.
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.
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(PMID = 17927501.001).
[ISSN]
0163-5581
[Journal-full-title]
Nutrition and cancer
[ISO-abbreviation]
Nutr Cancer
[Language]
eng
[Grant]
United States / NIA NIH HHS / AG / 1 R01 AG15722
[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 / Antioxidants; 0 / Cryptoxanthins; 0 / Xanthophylls; 0 / Zeaxanthins; 01YAE03M7J / beta Carotene; 36-88-4 / Carotenoids; 45XWE1Z69V / alpha-carotene; SB0N2N0WV6 / lycopene; X72A60C9MT / Lutein
84.
Carver BS, Bianco FJ Jr, Scardino PT, Eastham JA:
Long-term outcome following radical prostatectomy in men with clinical stage T3 prostate cancer.
J Urol
; 2006 Aug;176(2):564-8
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[Title]
Long-term outcome following radical prostatectomy in men with clinical stage T3
prostate
cancer.
PURPOSE: We evaluated patients at our institution who underwent radical prostatectomy for clinical stage T3
prostate
cancer to determine their long-term clinical outcomes.
MATERIALS AND METHODS: We reviewed our prospective surgical database and identified 176 men who underwent radical retropubic prostatectomy for clinical stage T3
prostate
cancer from 1983 to 2003.
Clinical progression following biochemical recurrence was evaluated and clinical failure was defined as the development of clinical metastases or progression to hormone refractory
prostate
cancer.
RESULTS: Of the 176 patients with cT3
prostate
cancer 64 (36%) received neoadjuvant hormonal therapy.
On multivariate analysis biopsy Gleason score, pretreatment serum
prostate
specific antigen and year of surgery were independent predictors of biochemical recurrence.
Overall the 5, 10 and 15-year probabilities of death from
prostate
cancer were 6%, 15% and 24%, respectively.
Radical prostatectomy remains an integral component in the treatment of select patients with clinical stage T3
prostate
cancer.
[MeSH-major]
Prostatectomy.
Prostatic
Neoplasms
/ pathology.
Prostatic
Neoplasms
/ surgery
[MeSH-minor]
Follow-Up Studies. Humans. Male. Middle Aged.
Neoplasm
Recurrence, Local / blood.
Neoplasm
Staging. Prospective Studies.
Prostate
-Specific Antigen / blood. Time Factors. Treatment Outcome
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(PMID = 16813890.001).
[ISSN]
0022-5347
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
85.
Park H, Piert MR, Khan A, Shah R, Hussain H, Siddiqui J, Chenevert TL, Meyer CR:
Registration methodology for histological sections and in vivo imaging of human prostate.
Acad Radiol
; 2008 Aug;15(8):1027-39
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[Title]
Registration methodology for histological sections and in vivo imaging of human
prostate
.
Our objective is to register in vivo imaging with histologic sections of the human
prostate
so that histologic truth can be correlated with in vivo imaging features.
MATERIALS AND METHODS: In vivo imaging of the
prostate
included T2-weighted anatomic and diffusion weighted 3-T magnetic resonance imaging (MRI) as well as 11C-choline positron emission tomography (PET).
In addition, ex vivo 3-T MRI of the
prostate
specimen, histology, and associated block face photos of the
prostate
specimen were obtained.
An indirect validation of the registration accuracy has been proposed comparing
tumor
boundary markings found in diffusion MRI and histologic sections.
CONCLUSION: This proof of concept paper demonstrates a method based on intrinsic image information content for successfully registering in vivo imaging of the human
prostate
with its post-resection histology, which does not require the use of extrinsic fiducial markers.
The methodology is therefore the basis for a systematic comparison of in vivo imaging for staging of human
prostate
cancer.
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[Cites]
IEEE Trans Med Imaging. 1999 Aug;18(8):712-21
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10534053.001
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Med Phys. 1999 Oct;26(10):2151-60
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10535632.001
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(PMID = 18620123.001).
[ISSN]
1076-6332
[Journal-full-title]
Academic radiology
[ISO-abbreviation]
Acad Radiol
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P01 CA087634-01A2; United States / NCI NIH HHS / CA / P01 CA087634; United States / NCI NIH HHS / CA / P50 CA069568-05; United States / NCI NIH HHS / CA / CA087634-01A2; United States / NCI NIH HHS / CA / P50CA069568; United States / NCI NIH HHS / CA / 1P01CA87684; United States / NCI NIH HHS / CA / P50 CA069568; None / None / / P50 CA069568-05
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Carbon Radioisotopes
[Other-IDs]
NLM/ NIHMS60416; NLM/ PMC2646010
86.
Forootan SS, Foster CS, Aachi VR, Adamson J, Smith PH, Lin K, Ke Y:
Prognostic significance of osteopontin expression in human prostate cancer.
Int J Cancer
; 2006 May 01;118(9):2255-61
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[Title]
Prognostic significance of osteopontin expression in human
prostate
cancer.
To test the hypothesis that expression of osteopontin (OPN), an integrin-binding glycoprotein, can independently predict the potential aggressiveness
of prostate
cancer, the status of OPN expression in
benign
and malignant
prostate
cancer cell lines and tissues was analysed by Western blot and immunohistochemistry.
Amongst the four
prostate
cell lines analysed, the level of OPN expressed in the
benign
PNT-2 cells was set at 1, the relative level of OPN expressed in the weakly malignant cell line LNCaP was increased to 1.5.
An increased expression of OPN was also observed in
the prostate
tissue samples.
When the level of OPN in normal tissue was set at 1, its level in
benign
prostate
hyperplasia (BPH) was similar at 0.99 +/- 0.2, whereas the OPN level in the highly malignant carcinoma tissue was greatly increased by nearly 6-fold to 5.9 +/- 0.3.
The results in our study support our hypothesis and suggest that the increased OPN level may be involved in the malignant transformation
of prostate
epithelial cells and OPN expression level is an important determinant for patient survival.
[MeSH-major]
Prostatic
Neoplasms
/ pathology. Sialoglycoproteins / biosynthesis
[MeSH-minor]
Aged. Blotting, Western. Cell Transformation, Neoplastic. Epithelial Cells. Gene Expression Profiling. Humans. Immunohistochemistry. Male. Osteopontin. Predictive Value of Tests. Prognosis.
Prostate
/ cytology. Survival Analysis.
Tumor
Cells, Cultured
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[Copyright]
2005 Wiley-Liss, Inc.
(PMID = 16331611.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0501019
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / SPP1 protein, human; 0 / Sialoglycoproteins; 106441-73-0 / Osteopontin
87.
Antunes AA, Leite KR, Dall'Oglio MF, Cury J, Srougi M:
The effect of the number of biopsy cores on the concordance between prostate biopsy and prostatectomy Gleason score: a prostate volume-controlled study.
Arch Pathol Lab Med
; 2008 Jun;132(6):989-92
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[Title]
The effect of the number of biopsy cores on the concordance between
prostate
biopsy and prostatectomy Gleason score: a
prostate
volume-controlled study.
Some included 2 or more centers, used historical controls from the early
prostate
specific antigen era or lacked a clear definition of the biopsy schemes.
Furthermore, most did not control the results for
prostate
volume.
OBJECTIVE: To confirm whether prediction of RP Gleason score can be optimized by taking more biopsy cores in a contemporary series of patients, with pathologic samples analyzed by the same pathologist, and controlling these results for
prostate
volume.
DESIGN: The study comprised a retrospective case-control analysis of 393 patients with
prostate
cancer treated with RP.
When we analyzed patients with
prostate
volumes of less than 50 cm(3), concordance rates were 58.3%, 58.3%, and 65.1% for each group, respectively (P = .03).
Among patients with
prostate
volumes of 50 cm(3) or more, concordance rates were 70%, 58.1%, and 63.6%, respectively (P = .66).
CONCLUSIONS: Taking 10 or more cores can improve the prediction of RP Gleason score in patients with
prostate
volumes of less than 50 cm(3).
For patients with
prostate
volumes of 50 cm(3) or more, increasing the biopsy cores to 10 or more did not improve prediction of RP Gleason score.
[MeSH-major]
Biopsy. Prostatectomy.
Prostatic
Neoplasms
/ pathology.
Prostatic
Neoplasms
/ surgery
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(PMID = 18517284.001).
[ISSN]
1543-2165
[Journal-full-title]
Archives of pathology & laboratory medicine
[ISO-abbreviation]
Arch. Pathol. Lab. Med.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
88.
Raben A, Rusthoven KE, Sarkar A, Glick A, Benge B, Jacobs D, Raben D:
Favorable toxicity and biochemical control using real-time inverse optimization technique for prostate brachytherapy.
Brachytherapy
; 2009 Jul-Sep;8(3):297-303
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[Title]
Favorable toxicity and biochemical control using real-time inverse optimization technique for
prostate
brachytherapy.
PURPOSE: Favorable dosimetric results have been reported using intraoperative inverse optimization (IO) for permanent
prostate
brachytherapy.
METHODS AND MATERIALS: Between 2001 and 2007, 165 patients received permanent
prostate
implants using real-time IO and had >/=3 months of followup.
Dose constraints for inverse planning were:
the prostate
volume receiving 100% of the prescription dose [
prostate
V(100)] was >95%; the dose received by 90% of the
gland
[
prostate
D(90)] was within the 140-180 by dose range; the volume of urethra receiving 150% of the prescription dose [urethra V(150)] was <30%; and the volume of rectal wall receiving 110% of the prescription dose [rectal V(110)] was <1.0 cc.
Toxicity was prospectively scored using the Radiation Therapy Oncology Group toxicity scale and the International
Prostate
Symptom Score questionnaire.
The median number of seeds and total activity implanted were 61 and 999 MBq, respectively, for a median
prostate
volume of 33.6 cc.
CONCLUSIONS: IO technique for
prostate
brachytherapy is associated with low rates of late morbidity and excellent early biochemical control.
[MeSH-major]
Brachytherapy / adverse effects. Brachytherapy / methods.
Prostatic
Neoplasms
/ radiotherapy
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Humans. Iodine Radioisotopes. Male. Middle Aged. Palladium.
Prostate
-Specific Antigen / blood. Radioisotopes. Radiotherapy Dosage. Risk Assessment
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.