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1
benign tumor of prostate 2005:2010[pubdate] *count=100
35842 results
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Items 1 to 100 of about 35842
1.
Walz J, Chun FK, Klein EA, Reuther A, Saad F, Graefen M, Huland H, Karakiewicz PI:
Nomogram predicting the probability of early recurrence after radical prostatectomy for prostate cancer.
J Urol
; 2009 Feb;181(2):601-7; discussion 607-8
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[Title]
Nomogram predicting the probability of early recurrence after radical prostatectomy for
prostate
cancer.
PURPOSE: We developed a nomogram predicting the probability of early biochemical recurrence after radical prostatectomy because early recurrence predisposes to distant metastasis and
prostate
cancer related mortality.
MATERIALS AND METHODS: From January 1992 to December 2005, 2,911 patients underwent radical prostatectomy for localized
prostate
cancer.
Age,
prostate
specific antigen, pathological Gleason sum, surgical margin, extracapsular extension, seminal vesicle invasion and lymph node invasion were considered.
[MeSH-major]
Neoplasm
Recurrence, Local / pathology. Nomograms. Prostatectomy / methods.
Prostatic Neoplasms
/ pathology.
Prostatic Neoplasms
/ surgery
[MeSH-minor]
Age Factors. Aged. Aged, 80 and over. Biopsy, Needle. Cohort Studies. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged.
Neoplasm
Staging. Predictive Value of Tests. Probability. Prognosis. Proportional Hazards Models. Retrospective Studies. Risk Assessment. Sensitivity and Specificity. Survival Analysis. Time Factors
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[CommentIn]
Eur Urol. 2009 Nov;56(5):885-6
[
20965035.001
]
(PMID = 19084864.001).
[ISSN]
1527-3792
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
2.
Bolla M, Artignan X, Fourneret P, Brochon D, Ringeisen F, Descotes JL:
[Neoadjuvant hormonal treatment combined with external irradiation in the management of prostate cancer].
Bull Cancer
; 2006 Nov;93(11):1101-5
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[Title]
[Neoadjuvant hormonal treatment combined with external irradiation in the management
of prostate
cancer].
[Transliterated title]
L'association hormonothérapie néoadjuvante et irradiation externe dans les cancers
de la
prostate
.
Very high risk
prostate
cancers, T3-4 N0 M0 or pelvic lymph node involvement (c or pN1) whatever the UICC T stage, need a long term androgen suppression of 3 years or more.
[MeSH-major]
Antineoplastic Agents, Hormonal / therapeutic use. Neoadjuvant Therapy / methods.
Neoplasms
, Hormone-Dependent / drug therapy.
Neoplasms
, Hormone-Dependent / radiotherapy.
Prostatic Neoplasms
/ drug therapy.
Prostatic Neoplasms
/ radiotherapy
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(PMID = 17145579.001).
[ISSN]
1769-6917
[Journal-full-title]
Bulletin du cancer
[ISO-abbreviation]
Bull Cancer
[Language]
fre
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
France
[Chemical-registry-number]
0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal
[Number-of-references]
23
3.
Elabbady AA, Khedr MM:
Free/total PSA ratio can help in the prediction of high gleason score prostate cancer in men with total serum prostate specific antigen (PSA) of 3-10 ng/ml.
Int Urol Nephrol
; 2006;38(3-4):553-7
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[Title]
Free/total PSA ratio can help in the prediction of high gleason score
prostate
cancer in men with total serum
prostate
specific antigen (PSA) of 3-10 ng/ml.
PURPOSE: We evaluate the use of free/total
prostate
specific antigen (PSA) ratio in improving the prediction of cancers of higher Gleason scores.
The mean age for the 62 patients with histologically proven
prostate
cancer was 62.3+/-5.5 years (49-73).
In the 20 patients with free PSA ratio>20%, 1 patient (5%), had
prostate
cancer of high Gleason score and the remaining 19 (95%) patients had low Gleason scores.
CONCLUSIONS: In this study, men with
prostate
cancer and lower F/T PSA ratio were at a higher risk of having higher Gleason scores (7-10) and those with higher F/T PSA ratio were more likely to have lower Gleason scores.
[MeSH-major]
Prostate
-Specific Antigen / blood.
Prostatic Neoplasms
/ blood.
Prostatic Neoplasms
/ pathology
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[Cites]
CA Cancer J Clin. 1999 Jan-Feb;49(1):8-31, 1
[
10200775.001
]
[Cites]
J Urol. 2002 Mar;167(3):1306-9
[
11832719.001
]
[Cites]
J Urol. 1998 Apr;159(4):1238-42
[
9507844.001
]
[Cites]
J Urol. 2004 Dec;172(6 Pt 1):2224-6
[
15538236.001
]
[Cites]
Urology. 2002 Feb;59(2):256-60
[
11834398.001
]
[Cites]
Eur Urol. 2005 Apr;47(4):427-32
[
15774237.001
]
[Cites]
Urology. 1998 Aug;52(2):230-6
[
9697787.001
]
[Cites]
Lancet. 1994 Dec 10;344(8937):1594-8
[
7527116.001
]
[Cites]
BJU Int. 2004 Mar;93(4):499-502
[
15008717.001
]
[Cites]
Urology. 1996 Dec;48(6A Suppl):55-61
[
8973701.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1995 May 15;32(2):479-82
[
7751188.001
]
[Cites]
Eur Urol. 1998;33(3):261-70
[
9555550.001
]
[Cites]
Br J Urol. 1997 Jun;79(6):920-3
[
9202560.001
]
[Cites]
Urology. 1996 Dec;48(6A Suppl):33-9
[
8973697.001
]
[Cites]
Urology. 2001 May;57(5):936-42
[
11337298.001
]
(PMID = 17171424.001).
[ISSN]
0301-1623
[Journal-full-title]
International urology and nephrology
[ISO-abbreviation]
Int Urol Nephrol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
Advertisement
4.
Grainger EM, Schwartz SJ, Wang S, Unlu NZ, Boileau TW, Ferketich AK, Monk JP, Gong MC, Bahnson RR, DeGroff VL, Clinton SK:
A combination of tomato and soy products for men with recurring prostate cancer and rising prostate specific antigen.
Nutr Cancer
; 2008;60(2):145-54
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[Title]
A combination of tomato and soy products for men with recurring
prostate
cancer and rising
prostate
specific antigen.
Tomato and soy products are hypothesized to reduce the risk
of prostate
cancer or enhance efficacy of therapy.
A study was completed to determine if men with active
prostate
cancer will adhere to a dietary intervention rich in tomato products and a soy protein supplement men (n = 41) with recurrent, asymptomatic
prostate
cancer were randomized among 2 groups: Group A (n = 20) consumed tomato products (no soy) for Weeks 0 through 4, targeting a minimum of 25 mg of lycopene/day.
Serum
prostate
-specific antigen decreased between Weeks 0 and 8 for 14 / 41 men (34%).
In conclusion,
prostate
cancer patients will consume diets rich in tomato products and soy with excellent compliance and bioavailability of phytochemicals.
Further studies combining tomato and soy foods to determine efficacy for
prostate
cancer prevention or management are encouraged.
[MeSH-major]
Carotenoids / therapeutic use.
Neoplasm
Recurrence, Local / prevention & control.
Prostate
-Specific Antigen / blood.
Prostate
-Specific Antigen / drug effects.
Prostatic Neoplasms
/ blood.
Prostatic Neoplasms
/ drug therapy. Soybean Proteins / therapeutic use
[MeSH-minor]
Administration, Oral. Aged. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Biological Availability. Biomarkers,
Tumor
/ blood. Cross-Over Studies. Dietary Supplements. Disease Progression. Drug Therapy, Combination. Humans. Lycopersicon esculentum / chemistry. Male. Patient Compliance. Soybeans / chemistry. Treatment Outcome
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(PMID = 18444145.001).
[ISSN]
0163-5581
[Journal-full-title]
Nutrition and cancer
[ISO-abbreviation]
Nutr Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / R01 CA112632
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Soybean Proteins; 36-88-4 / Carotenoids; EC 3.4.21.77 / Prostate-Specific Antigen; SB0N2N0WV6 / lycopene
5.
Ryan CJ, Harzstark AH, Rosenberg J, Lin A, Claros C, Goldfine ID, Kerner JF, Small EJ, Youngren JF:
A pilot dose-escalation study of the effects of nordihydroguareacetic acid on hormone and prostate specific antigen levels in patients with relapsed prostate cancer.
BJU Int
; 2008 Feb;101(4):436-9
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[Title]
A pilot dose-escalation study of the effects of nordihydroguareacetic acid on hormone and
prostate
specific antigen levels in patients with relapsed
prostate
cancer.
OBJECTIVE: To assess the tolerability of the effects of nordihydroguareacetic acid (NDGA) and its effect on
prostate
-specific antigen (PSA) kinetics in patients with relapsed
prostate
cancer, as among the many biological effects of NDGA is the inhibition of the insulin-like growth factor 1 receptor (IGF-1R) tyrosine kinase.
PATIENTS AND METHODS: Eligible patients were those with an increasing PSA level after definitive local therapy, in either the non-castrate (androgen-dependent
prostate
cancer, ADPC) or the castrate state (castration-resistant
prostate
cancer, CRPC) with no evidence of metastatic disease by bone scan or computed tomography of the abdomen or pelvis.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Masoprocol / therapeutic use.
Neoplasm
Recurrence, Local / drug therapy.
Prostate
-Specific Antigen / drug effects.
Prostatic Neoplasms
/ drug therapy
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[ErratumIn]
BJU Int. 2008 Jun;101(11):1483. Youngren, Jack F [added]
(PMID = 18234062.001).
[ISSN]
1464-410X
[Journal-full-title]
BJU international
[ISO-abbreviation]
BJU Int.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / K23 CA115775-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 7BO8G1BYQU / Masoprocol; EC 2.7.10.1 / Receptor, IGF Type 1; EC 3.4.21.77 / Prostate-Specific Antigen
6.
Odedina FT, Kumar N:
Prostate cancer disparities in Black men of African descent: a comparative literature review of prostate cancer burden among Black men in the United States, Caribbean, United Kingdom, and West Africa.
Infect Agent Cancer
; 2009 Feb 10;4 Suppl 1:S2
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[Title]
Prostate
cancer disparities in Black men of African descent: a comparative literature review
of prostate
cancer burden among Black men in the United States, Caribbean, United Kingdom, and West Africa.
BACKGROUND: African American men have the highest
prostate
cancer morbidity and mortality rates than any other racial or ethnic group in the US.
Although the overall incidence of and mortality from
prostate
cancer has been declining in White men since 1991, the decline in African American men lags behind White men.
Of particular concern is the growing literature on the disproportionate burden
of prostate
cancer among other Black men of West African ancestry in the Caribbean Islands, United Kingdom and West Africa.
This higher incidence
of prostate
cancer observed in populations of African descent may be attributed to the fact that these populations share ancestral genetic factors.
To better understand the burden
of prostate
cancer among men of West African Ancestry, we conducted a review of the literature on
prostate
cancer incidence, prevalence, and mortality in the countries connected by the Transatlantic Slave Trade.
RESULTS: Several published studies indicate high
prostate
cancer burden in Nigeria and Ghana.
Prostate
cancer morbidity and/or mortality data from the Caribbean Islands and the United Kingdom also provided comparable or worse
prostate
cancer burden to that of US Blacks.
CONCLUSION: The growing literature on the disproportionate burden
of prostate
cancer among other Black men of West African ancestry follows the path of the Transatlantic Slave Trade.
To better understand and address the global
prostate
cancer disparities seen in Black men of West African ancestry, future studies should explore the genetic and environmental risk factors for
prostate
cancer among this group.
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[ISSN]
1750-9378
[Journal-full-title]
Infectious agents and cancer
[ISO-abbreviation]
Infect. Agents Cancer
[Language]
eng
[Grant]
United States / NCRR NIH HHS / RR / G12 RR003020
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC2638461
7.
Kilbridge KL, Fraser G, Krahn M, Nelson EM, Conaway M, Bashore R, Wolf A, Barry MJ, Gong DA, Nease RF Jr, Connors AF:
Lack of comprehension of common prostate cancer terms in an underserved population.
J Clin Oncol
; 2009 Apr 20;27(12):2015-21
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[Title]
Lack of comprehension of common
prostate
cancer terms in an underserved population.
PURPOSE: To assess the comprehension of common medical terms used in
prostate
cancer in patient education materials to obtain informed consent, and to measure outcomes after
prostate
cancer treatment.
PATIENTS AND METHODS: We reviewed patient education materials and
prostate
-specific quality-of-life instruments to identify technical terms describing sexual, urinary, and bowel function.
Prostate
cancer knowledge was poor.
CONCLUSION: Limited comprehension
of prostate
cancer terms and low literacy create barriers to obtaining informed consent for treatment and to measuring
prostate
cancer outcomes accurately in our study population.
In addition, the level
of prostate
cancer knowledge was poor.
These results highlight the need for
prostate
cancer education efforts and outcomes measurements that consider literacy and use nonmedical language.
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[CommentIn]
J Clin Oncol. 2009 Apr 20;27(12):1938-40
[
19307497.001
]
(PMID = 19307512.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / K07 CA085754; United States / NCI NIH HHS / CA / KO7CA085754
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2669763
8.
Pruthi RS, Swords K, Schultz H, Carson CC 3rd, Wallen EM:
The impact of obesity on the diagnosis of prostate cancer using a modern extended biopsy scheme.
J Urol
; 2009 Feb;181(2):574-7; discussion 578
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[Title]
The impact of obesity on
the diagnosis
of prostate
cancer using a modern extended biopsy scheme.
PURPOSE: The effect of obesity on
prostate
cancer detection and behavior remains uncertain.
MATERIALS AND METHODS: We retrospectively reviewed the records of a consecutive series of 500 men who underwent transrectal ultrasound guided
prostate
biopsy using a 10 to 12 core biopsy scheme.
Variables, including patient age,
prostate
specific antigen,
prostate
specific antigen density, digital rectal examination findings, transrectal ultrasound
prostate
volume and biopsy outcome, including grade, were compared to anthropometric measures, including body mass index.
Obese men were younger (62.0 vs 63.8 years), had a larger
prostate
(57.7 vs 47.8 cc) and were less likely to have any abnormality on digital rectal examination (19.6% vs 30.8%).
On statistical modeling for the OR in nonobese vs obese men there was a trend toward lower detection based on crude and age adjusted ORs but not on multivariate OR controlling for age,
prostate
specific antigen and
prostate
volume.
In men with negative biopsies those who were obese vs nonobese had a larger
prostate
volume and trended toward a higher median
prostate
specific antigen and age.
CONCLUSIONS: Of men undergoing
prostate
biopsy using a modern extended biopsy scheme obese men were younger, had a larger
prostate
and were less likely to have abnormal digital rectal examinations.
Although some trends toward a lower detection rate in obese men were observed, such differences were not observed on multivariate analysis, nor were any differences observed in the incidence of higher grade tumors, thus questioning the effect of obesity on
prostate
cancer detection and behavior in our cases series.
[MeSH-major]
Biopsy, Needle / methods. Obesity / complications.
Prostatic Neoplasms
/ pathology. Ultrasound, High-Intensity Focused, Transrectal
[MeSH-minor]
Age Factors. Aged. Analysis of Variance. Body Mass Index. Case-Control Studies. Humans. Immunohistochemistry. Logistic Models. Male. Middle Aged.
Neoplasm
Staging. Odds Ratio.
Prostate
-Specific Antigen / blood. Reference Values. Retrospective Studies. Risk Assessment. Sensitivity and Specificity.
Tumor
Burden
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(PMID = 19084847.001).
[ISSN]
1527-3792
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
9.
Loblaw DA, Cheung P:
External beam irradiation for localized prostate cancer--the promise of hypofractionation.
Can J Urol
; 2006 Feb;13 Suppl 1:62-6
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[Title]
External beam irradiation for localized
prostate
cancer--the promise of hypofractionation.
Within the field of radiation oncology in the last 10 years, there have been two major thematic advances in the understanding and treatment
of prostate
cancer.
The second important discovery was that
prostate
cancer reacts differently than other tumors to radiation whereby higher doses of radiation per day ("hypofractionated radiation") seem to be more effective in killing
prostate
cancer cells.
The early experience of two hypofractionated trials in intermediate- and high-risk
prostate
cancer where the equivalent of > 80 Gy (in 2 Gy per day fractions) delivered in 5-6 weeks is reported.
In summary, hypofractionated radiation coupled with high-precision techniques may allow for better
prostate
cancer control rates, shorter treatment times and less toxicity.
[MeSH-major]
Dose Fractionation.
Prostatic Neoplasms
/ radiotherapy
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(PMID = 16526985.001).
[ISSN]
1195-9479
[Journal-full-title]
The Canadian journal of urology
[ISO-abbreviation]
Can J Urol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Canada
[Number-of-references]
11
10.
Cha TL, Qiu L, Chen CT, Wen Y, Hung MC:
Emodin down-regulates androgen receptor and inhibits prostate cancer cell growth.
Cancer Res
; 2005 Mar 15;65(6):2287-95
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[Title]
Emodin down-regulates androgen receptor and inhibits
prostate
cancer cell growth.
Hormone-refractory relapse is an inevitable and lethal event for advanced
prostate
cancer patients after hormone deprivation.
A growing body of evidence indicates that hormone deprivation may promote this aggressive
prostate
cancer phenotype.
Notably, androgen receptor (AR) not only mediates the effect of androgen on the
tumor
initiation but also plays the major role in the relapse transition.
This provides a strong rationale for searching new effective agents targeting the down-regulation of AR to treat or prevent advanced
prostate
cancer progression.
Here, we show that emodin, a natural compound, can directly target AR to suppress
prostate
cancer cell growth in vitro and prolong the survival of C3(1)/SV40 transgenic mice in vivo.
Our work indicates a new mechanism for the emodin-mediated anticancer effect and justifies further investigation of emodin as a therapeutic and preventive agent for
prostate
cancer.
[MeSH-major]
Androgen Receptor Antagonists. Emodin / pharmacology.
Prostatic Neoplasms
/ drug therapy.
Prostatic Neoplasms
/ pathology. Receptors, Androgen / metabolism
[MeSH-minor]
Animals. COS Cells. Cell Growth Processes / drug effects. Cell Line,
Tumor
. Cell Nucleus / metabolism. Cercopithecus aethiops. Down-Regulation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. HSP90 Heat-Shock Proteins / metabolism. Humans. Male. Mice. Mice, Transgenic. Nuclear Proteins / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-mdm2. Transcriptional Activation / drug effects. Transfection. Ubiquitin / metabolism. Xenograft Model Antitumor Assays
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(PMID = 15781642.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P01 CA099031; United States / NCI NIH HHS / CA / R01 CA109311
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgen Receptor Antagonists; 0 / HSP90 Heat-Shock Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Androgen; 0 / Ubiquitin; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Mdm2 protein, mouse; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2; KA46RNI6HN / Emodin
11.
Seitz M, Schlenker B, Gratzke C, Weidlich P, Stief CG, Reich O:
[Standards for the punch biopsy of the prostate].
MMW Fortschr Med
; 2007 Jan 25;149(4):35-6
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[Title]
[Standards for the punch biopsy of the
prostate
].
If, within the framework of screening examinations for the early detection of cancer of the
prostate
, the patient wishes a PSA test, the physician should accommodate him, but only after providing comprehensive information about the possible consequences and complications.
If a certain threshold value is exceeded, a punch biopsy of the
prostate
is recommended.
This procedure must be performed in accordance with accepted standards to enable, within the diagnostic chain, the reliable detection of a carcinoma of the
prostate
[MeSH-major]
Biomarkers,
Tumor
/ blood. Patient Education as Topic.
Prostate
/ pathology.
Prostate
-Specific Antigen / blood.
Prostatic Neoplasms
/
diagnosis
[MeSH-minor]
Biopsy, Needle. Early
Diagnosis
. Germany. Humans. Informed Consent. Male. Mass Screening. Postoperative Complications / etiology. Practice Guidelines as Topic
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(PMID = 17615715.001).
[ISSN]
1438-3276
[Journal-full-title]
MMW Fortschritte der Medizin
[ISO-abbreviation]
MMW Fortschr Med
[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
12.
Newmark HL, Heaney RP:
Dairy products and prostate cancer risk.
Nutr Cancer
; 2010;62(3):297-9
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[Title]
Dairy products and
prostate
cancer risk.
Increased calcium intake from dairy products has been suggested as a risk factor for
prostate
cancer.
Several epidemiologic correlations have indicated an increased risk
of prostate
cancer with long-term, high intake of dairy products in male U.S. physicians and males in Sweden.
We propose, however, that the high dietary phosphate of dairy products affects much larger fluctuation in serum phosphate and may be a more likely source
of prostate
cancer risk from high dietary intake of dairy products.
[MeSH-major]
Dairy Products / adverse effects.
Prostatic Neoplasms
/ etiology
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.
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(PMID = 20358466.001).
[ISSN]
1532-7914
[Journal-full-title]
Nutrition and cancer
[ISO-abbreviation]
Nutr Cancer
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Calcium, Dietary; 0 / Phosphates; SY7Q814VUP / Calcium
[Number-of-references]
14
13.
Merrick GS, Butler WM, Wallner KE, Galbreath RW, Adamovich E:
Monotherapeutic brachytherapy for clinically organ-confined prostate cancer.
W V Med J
; 2005 Jul-Aug;101(4):168-71
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[Title]
Monotherapeutic brachytherapy for clinically organ-confined
prostate
cancer.
Since the mid-1980s, permanent
prostate
brachytherapy has been utilized increasingly as a potentially curative treatment for patients of all ages with clinically localized
prostate
cancer To determine the 8-year biochemical progression-free survival rate for patients who had undergone monotherapeutic brachytherapy for clinically organ-confined
prostate
cancer, we conducted a study of 202 patients at Schiffler Cancer Center at Wheeling Hospital in Wheeling, W.Va.
These patients had undergone brachytherapy without supplemental external beam radiation therapy or androgen deprivation therapy for clinical T1b-T2c NxM0 (2002 AJCC)
prostate
cancer from April 1995 through May 2001.
Clinical, treatment and dosimetric parameters evaluated for biochemical progression-free survival included patient age, clinical T-stage, Gleason score, pretreatment PSA, risk group, percent positive biopsies, isotope,
prostate
volume, brachytherapy planning volume, V100/150/200, D90, tobacco status, hypertension and diabetes.
[MeSH-major]
Brachytherapy / methods.
Prostatic Neoplasms
/ pathology.
Prostatic Neoplasms
/ radiotherapy. Radiotherapy Planning, Computer-Assisted
[MeSH-minor]
Aged. Analysis of Variance. Cohort Studies. Dose-Response Relationship, Radiation. Follow-Up Studies. Humans. Male. Middle Aged. Multivariate Analysis.
Neoplasm
Staging. Proportional Hazards Models.
Prostate
-Specific Antigen / blood. Radiotherapy Dosage. Retrospective Studies. Risk Assessment. Survival Analysis. Treatment Outcome
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(PMID = 16296198.001).
[ISSN]
0043-3284
[Journal-full-title]
The West Virginia medical journal
[ISO-abbreviation]
W V Med J
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
14.
Perner S, Schmidt FH, Hofer MD, Kuefer R, Rubin M:
[TMPRSS2-ETS gene fusion in prostate cancer].
Urologe A
; 2007 Jul;46(7):754-60
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[Title]
[TMPRSS2-ETS gene fusion in
prostate
cancer].
By analogy, fusion status in
prostate
cancer may determine clinical outcome and secondary genetic alterations as witnessed in Ewing's tumors.
MATERIAL: These novel gene fusions occur in the majority
of prostate
cancers identified by PSA screening and are the driving mechanism for overexpression of the three members of the ETS transcription factor family, either ERG (21q22.3), ETV1 (7p21.2), or ETV4 (17q21).
Considering the high incidence
of prostate
cancer and the high frequency of this gene fusion, the TMPRSS2-ETS gene fusion is the most common genetic aberration so far described in human malignancies.
Also similar to the Philadelphia chromosome in chronic myelogenous leukemia (CML), the gene fusion in
prostate
cancer has potential as an important candidate for the development of targeted therapy.
[MeSH-major]
Biomarkers,
Tumor
/ genetics.
Neoplasm
Proteins / genetics. Oncogene Fusion / genetics.
Prostatic Neoplasms
/ epidemiology.
Prostatic Neoplasms
/ genetics. Proto-Oncogene Proteins c-ets / genetics. Serine Endopeptidases / genetics
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[Cites]
Am J Surg Pathol. 2007 Jun;31(6):882-8
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17527075.001
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(PMID = 17458530.001).
[ISSN]
0340-2592
[Journal-full-title]
Der Urologe. Ausg. A
[ISO-abbreviation]
Urologe A
[Language]
ger
[Publication-type]
English Abstract; Journal Article; Meta-Analysis; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-ets; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / TMPRSS2 protein, human
[Number-of-references]
24
15.
Lawson DA, Xin L, Lukacs R, Xu Q, Cheng D, Witte ON:
Prostate stem cells and prostate cancer.
Cold Spring Harb Symp Quant Biol
; 2005;70:187-96
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[Title]
Prostate
stem cells and
prostate
cancer.
Understanding
prostate
stem cells (PSCs) may provide insight for the design of therapeutics for
prostate
cancer.
We have developed a quantitative in vivo colony-forming assay and have demonstrated that the Sca-1 antigen is present on the surface of a
prostate
cell subpopulation that possesses multiple stem cell properties.
Immunofluorescent analysis demonstrates that Sca-1 is expressed by both basal and luminal cells in the proximal region of the adult
prostate
, but is not expressed by either lineage in more distal regions.
Sca-1 is also expressed by nearly all cells within fetal
prostate
epithelial chords, suggesting Sca-1 may be conserved on PSCs throughout development.
Malignant epithelial cells from TRAMP mice, as well as normal
prostate
cells with lentiviral-mediated alteration of the PTEN/AKT signaling pathway, give rise to PIN lesions and
prostate
cancer in vivo.
Alteration of PTEN/AKT signaling in Sca-1-enriched PSCs also results in PIN lesions, suggesting that PSCs can serve as one target for
prostate
carcinogenesis.
[MeSH-major]
Neoplastic Stem Cells / pathology.
Prostate
/ cytology.
Prostatic Neoplasms
/ pathology. Stem Cells / cytology
[MeSH-minor]
Animals. Antigens, Ly / metabolism. Colony-Forming Units Assay. Male. Membrane Proteins / metabolism. Mice. Mice, Inbred C57BL. Mice, Transgenic. Models, Biological. PTEN Phosphohydrolase / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction. Transforming Growth Factor beta / metabolism.
Tumor
Stem Cell Assay
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(PMID = 16869753.001).
[ISSN]
0091-7451
[Journal-full-title]
Cold Spring Harbor symposia on quantitative biology
[ISO-abbreviation]
Cold Spring Harb. Symp. Quant. Biol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / T32 CA09056
[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 / Antigens, Ly; 0 / Ly6a protein, mouse; 0 / Membrane Proteins; 0 / Transforming Growth Factor beta; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
16.
Davidson DD, Koch MO, Lin H, Jones TD, Biermann K, Cheng L:
Does the size matter?: Prostate weight does not predict PSA recurrence after radical prostatectomy.
Am J Clin Pathol
; 2010 Apr;133(4):662-8
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[Title]
Does the size matter?:
Prostate
weight does not predict PSA recurrence after radical prostatectomy.
Previous studies suggest that low
prostate
weight is a significant negative prognostic factor for
prostate
cancer.
In the current study, the data for 431 men who underwent radical retropubic prostatectomy between 1990 and 1998 were analyzed for association between
prostate
weight and various clinical and pathologic parameters.
These included age, preoperative
prostate
-specific antigen (PSA) level, PSA recurrence, pathologic stage, Gleason grade, extraprostatic extension, positive surgical margins,
tumor
volume, associated high-grade
prostatic
intraepithelial
neoplasia
, perineural invasion, and lymph node metastasis.
A significant positive correlation was found between
prostate
weight and increasing patient age or increasing preoperative PSA level.
There was no significant independent association between
prostate
weight and any of the other variables examined.
No association was found between
prostate
weight and PSA recurrence.
Although increasing
prostate
weight correlates with increased patient age and higher preoperative PSA level, it does not independently predict postoperative cancer recurrence.
[MeSH-major]
Prostate
/ pathology.
Prostate
-Specific Antigen / blood.
Prostatic Neoplasms
/ pathology
[MeSH-minor]
Aged. Humans. Male. Middle Aged.
Neoplasm
Recurrence, Local / pathology.
Neoplasm
Staging. Organ Size. Postoperative Period. Prognosis. Prostatectomy. Regression Analysis. Treatment Outcome
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(PMID = 20231620.001).
[ISSN]
1943-7722
[Journal-full-title]
American journal of clinical pathology
[ISO-abbreviation]
Am. J. Clin. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
17.
Finne P, Fallah M, Hakama M, Ciatto S, Hugosson J, de Koning H, Moss S, Nelen V, Auvinen A:
Lead-time in the European Randomised Study of Screening for Prostate Cancer.
Eur J Cancer
; 2010 Nov;46(17):3102-8
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[Title]
Lead-time in the European Randomised Study of Screening for
Prostate
Cancer.
BACKGROUND: Lead-time is defined as the time by which screening advances
the diagnosis
compared with absence of screening.
MATERIAL AND METHODS: In the first screening round, a total of 56,294 men aged 55-74 years were screened with serum
prostate
specific antigen (PSA) in five countries of the European Randomised Study of Screening for
Prostate
Cancer (ERSPC) with an overall detection rate (prevalence) of 2.8% (1972
prostate
cancers).
Prostate
cancer incidence among 92,142 men randomly allocated to the control arm of the trial was also assessed.
Lead-time was estimated as the time required to accumulate a similar cumulative risk
of prostate
cancer in the control arm to the detection rate in the intervention arm, i.e. from the ratio of detection rate (prevalence of screen-detected cases) and expected incidence (cumulative risk).
Lead-time based on advanced
prostate
cancer only was slightly shorter, mean 5.3 years (95% CI 4.6-6.0).
CONCLUSION: The lead-time for
prostate
cancer found in ERSPC substantially exceeded that found for breast, cervical and colorectal cancer screening.
One round
of prostate
cancer screening can advance clinical
diagnosis
by 4-8 years.
[MeSH-major]
Prostatic Neoplasms
/
diagnosis
[MeSH-minor]
Aged. Clinical Protocols. Early Detection of Cancer / methods. Europe / epidemiology. Humans. Incidence. Male. Middle Aged.
Prostate
-Specific Antigen / blood. Risk Assessment. Time Factors
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[Copyright]
Copyright © 2010. Published by Elsevier Ltd.
(PMID = 21047593.001).
[ISSN]
1879-0852
[Journal-full-title]
European journal of cancer (Oxford, England : 1990)
[ISO-abbreviation]
Eur. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
18.
Butler LM, Wang R, Wong AS, Koh WP, Yu MC:
Cigarette smoking and risk of prostate cancer among Singapore Chinese.
Cancer Causes Control
; 2009 Dec;20(10):1967-74
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[Title]
Cigarette smoking and risk
of prostate
cancer among Singapore Chinese.
Prospective epidemiologic studies conducted in Western populations support an association between current smoking and aggressive subtypes
of prostate
cancer.
In Singapore, where
prostate
-specific antigen is not used for population-wide screening,
prostate
cancer incidence has tripled within the past two decades.
Using Cox regression methods, we examined the relationship between smoking and
prostate
cancer established between 1993 and 1998 in a cohort of 27,293 Singapore Chinese men.
As of December 2006, 250 incident
prostate
cancer cases were diagnosed.
Smoking was not a major risk factor for
prostate
cancer in our Singapore Chinese cohort, a traditionally low risk population with parallel increases in incidence and mortality.
[MeSH-major]
Asian Continental Ancestry Group / ethnology. Carcinoma / etiology.
Prostatic Neoplasms
/ etiology. Smoking / adverse effects
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(PMID = 19579052.001).
[ISSN]
1573-7225
[Journal-full-title]
Cancer causes & control : CCC
[ISO-abbreviation]
Cancer Causes Control
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA55069; United States / NCI NIH HHS / CA / R35 CA53890
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
Netherlands
19.
Fowler JF:
The radiobiology of prostate cancer including new aspects of fractionated radiotherapy.
Acta Oncol
; 2005;44(3):265-76
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[Title]
The radiobiology
of prostate
cancer including new aspects of fractionated radiotherapy.
These differences work the opposite way round for
prostate
tumors versus late complications compared with most other types
of tumor
.
Using the Linear-Quadratic formula it is aimed to explain these differences, especially for treatments
of prostate
cancer.
The unusually slow growth rate
of prostate
cancers is associated with their high sensitivity to increased fraction size, so a large number of small fractions, such as 35 or 40 "daily" doses of 2 Gy, is not an optimum treatment.
Theoretical modeling shows a stronger enhancement
of tumor
effect than of late complications for larger (and fewer) fractions, in
prostate
tumors uniquely.
Biologically Effective Doses and Normalized Total Doses (in 2 Gy fraction equivalents) are given for
prostate tumor
, late rectal reactions, and--a new development--acute rectal mucosa.
Tables showing the change of fraction-size sensitivity (the alpha/beta ratio) with proliferation rates of tissues lead to the association of slow cell doubling times in
prostate
tumors with small alpha/beta ratios.
The alpha/beta ratios
of prostate
tumors appear to be as low as 1.5 Gy (95% confidence interval 1.3-1.8 Gy), in contrast with the value of about 10 Gy for most other types
of tumor
.
From this important difference stems the superior schedules of, for example, 20 fractions of 3 Gy, or 10 fractions of 4.7 Gy, or 5 fractions of 7 Gy, which can all give
tumor
results equivalent to 80-90 Gy in 2 Gy fractions, while keeping late complications equivalent to only 72 Gy in 2 Gy fractions.
Combination treatments of external beam (EBRT) and brachytherapy boost doses (25F x 2 Gy plus 2 x 10 Gy) can give higher biological
tumor
effects than any EBRT using daily 2 Gy doses, and with acceptable late complications.
Monotherapy by brachytherapy for low-risk cancer
prostate
using two to four fractions in a few days can give even higher biological effects on the tumors.
[MeSH-major]
Dose Fractionation.
Prostatic Neoplasms
/ radiotherapy
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(PMID = 16076699.001).
[ISSN]
0284-186X
[Journal-full-title]
Acta oncologica (Stockholm, Sweden)
[ISO-abbreviation]
Acta Oncol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Norway
[Number-of-references]
31
20.
Levin TG, Powell AE, Davies PS, Silk AD, Dismuke AD, Anderson EC, Swain JR, Wong MH:
Characterization of the intestinal cancer stem cell marker CD166 in the human and mouse gastrointestinal tract.
Gastroenterology
; 2010 Dec;139(6):2072-2082.e5
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Although the presence of CD166 at the
tumor
cell surface has been correlated with shortened survival, little is known about its function and expression in normal intestinal epithelia.
CD166-positive cells were also detected in
benign
adenomas in mice; rare cells coexpressed CD166 and CD44 or epithelial-specific antigen.
CD166-positive cells appear at multiple stages of intestinal carcinoma progression, including
benign
and metastatic tumors.
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[Copyright]
Copyright © 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
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19427292.001
]
[Cites]
Nature. 2009 May 14;459(7244):262-5
[
19329995.001
]
[Cites]
Am J Physiol Gastrointest Liver Physiol. 2010 May;298(5):G590-600
[
20185687.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8
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12629218.001
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Am J Pathol. 2000 Mar;156(3):769-74
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10702391.001
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Cancer Metastasis Rev. 2000;19(3-4):I-XI, 193-383
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11394186.001
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Blood. 2001 Oct 1;98(7):2134-42
[
11568000.001
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[Cites]
J Exp Med. 2002 Jun 17;195(12):1549-63
[
12070283.001
]
[Cites]
Prostate. 2003 Jan 1;54(1):34-43
[
12481253.001
]
[Cites]
Blood. 1997 Apr 15;89(8):2706-16
[
9108388.001
]
(PMID = 20826154.001).
[ISSN]
1528-0012
[Journal-full-title]
Gastroenterology
[ISO-abbreviation]
Gastroenterology
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA118235; United States / NIDDK NIH HHS / DK / U01 DK085525-02; United States / NHLBI NIH HHS / HL / T32 HL007781; United States / NCI NIH HHS / CA / CA106195-06A1; United States / NCI NIH HHS / CA / CA118235-05; United States / NICHD NIH HHS / HD / T32 HD049309-05; United States / NCI NIH HHS / CA / CA106195; United States / NCI NIH HHS / CA / T32 CA106195; United States / NICHD NIH HHS / HD / HD049309; United States / NICHD NIH HHS / HD / T32 HD049309; United States / NCI NIH HHS / CA / T32 CA106195-06A1; United States / NHLBI NIH HHS / HL / T32 HL007781-14; United States / NIDDK NIH HHS / DK / R01 DK068326; United States / NCI NIH HHS / CA / CA118235; United States / NIDDK NIH HHS / DK / R01 DK068326-05; United States / NIDDK NIH HHS / DK / DK068326; United States / NIDDK NIH HHS / DK / DK085525-02; United States / NICHD NIH HHS / HD / HD049309-05; United States / NHLBI NIH HHS / HL / HL007781-14; United States / NHLBI NIH HHS / HL / HL007781; United States / NIDDK NIH HHS / DK / U01 DK085525; United States / NIDDK NIH HHS / DK / DK085525; United States / NIDDK NIH HHS / DK / DK068326-05; United States / NCI NIH HHS / CA / R01 CA118235-05
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / ALCAM protein, human; 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules, Neuronal; 0 / Fetal Proteins
[Other-IDs]
NLM/ NIHMS234467; NLM/ PMC2997177
21.
Surapaneni KM, Venkata GR:
Lipid peroxidation and antioxidant status in patients with carcinoma of prostate.
Indian J Physiol Pharmacol
; 2006 Oct-Dec;50(4):350-4
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[Title]
Lipid peroxidation and antioxidant status in patients with carcinoma
of prostate
.
Prostate
cancer is the most prevalent cancer found in men above the age of fifty years and is frequently diagnosed in men between 45 and 89 years of age with a median age of 72 years.
This work was undertaken to assess oxidative stress and anti oxidant status in patients with carcinoma
of prostate
.
Glutathione (GSH), Malondialdehyde (MDA), Super Oxide Dismutase (SOD) levels in Erythrocytes and plasma Glutathione-S-Transferase (GST) levels were estimated in patients with carcinoma
of prostate
and compared to controls.
It was observed that Erythrocyte GSH levels were significantly lower and Erythrocyte MDA & SOD levels were significantly higher in patients with carcinoma
of prostate
compared to controls.
Oxidative stress may be involved in
prostate
cancer as evidenced by the higher MDA levels and lower GSH levels.
[MeSH-major]
Antioxidants / metabolism. Lipid Peroxidation / physiology.
Prostatic Neoplasms
/ metabolism
MedlinePlus Health Information.
consumer health - Antioxidants
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
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MALONALDEHYDE
.
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(PMID = 17402264.001).
[ISSN]
0019-5499
[Journal-full-title]
Indian journal of physiology and pharmacology
[ISO-abbreviation]
Indian J. Physiol. Pharmacol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
[Chemical-registry-number]
0 / Antioxidants; 0 / Thiobarbituric Acid Reactive Substances; 4Y8F71G49Q / Malondialdehyde; EC 1.15.1.1 / Superoxide Dismutase; EC 2.5.1.18 / Glutathione Transferase; GAN16C9B8O / Glutathione
22.
Lowe JF, Frazee LA:
Update on prostate cancer chemoprevention.
Pharmacotherapy
; 2006 Mar;26(3):353-9
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[Title]
Update on
prostate
cancer chemoprevention.
BACKGROUND:
Prostate
cancer is the most common type of cancer and the second leading cause of cancer-related deaths in American men.
Its high rate of occurrence and long lead time to clinically significant disease make
prostate
cancer an ideal disease for pharmacologic or nutritional chemoprevention.
METHODS: To identify the various chemoprevention strategies for
prostate
cancer, a MEDLINE search (from 1967-2005) and bibliographic search of the English-language literature were conducted.
RESULTS: Epidemiologic and retrospective studies have assessed the effect of carotenoids (e.g., lycopene), vitamins, selenium, and nonsteroidal antiinflammatory drugs (NSAIDs) on the rate of occurrence
of prostate
cancer.
The few published prospective trials evaluated
prostate
cancer as a secondary end point.
Lycopene (as beta-carotene) and selenium supplementation have been associated with a reduced risk
of prostate
cancer in nested case-control studies, but only in subgroups of men with low baseline plasma lycopene (or beta-carotene) and selenium levels respectively.
The
Prostate
Cancer Prevention Trial prospectively evaluated finasteride, a 5-alpha-reductase inhibitor, as chemoprevention.
The results showed a 25% relative risk reduction in
prostate
cancer, albeit at an increased risk of invasive tumors.
CONCLUSION: Data regarding lycopene, vitamin E, and selenium as chemoprevention for
prostate
cancer appear promising.
Prospective trials such as the Selenium and Vitamin E Cancer Prevention Trial (SELECT) will clarify the role of these agents in
prostate
cancer prevention.
Although finasteride has decreased overall
prostate
cancer occurrence, the risk of invasive tumors may outweigh the benefit of this agent.
The continuing Reduction by Dutasteride
of Prostate
Cancer Events (REDUCE) trial may help define a role for the 5-alpha-reductase inhibitors in cancer chemoprevention.
At this time, nothing has been proven effective as chemoprevention against clinically significant
prostate
cancer.
[MeSH-major]
Prostatic Neoplasms
/ prevention & control
Genetic Alliance.
consumer health - Prostate cancer
.
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consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
SELENIUM, ELEMENTAL
.
Hazardous Substances Data Bank.
FINASTERIDE
.
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[CommentIn]
Pharmacotherapy. 2006 Oct;26(10):1533; author reply 1533
[
16999665.001
]
(PMID = 16503715.001).
[ISSN]
0277-0008
[Journal-full-title]
Pharmacotherapy
[ISO-abbreviation]
Pharmacotherapy
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / 5-alpha Reductase Inhibitors; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Azasteroids; 0 / Enzyme Inhibitors; 0 / Vitamins; 1406-18-4 / Vitamin E; 36-88-4 / Carotenoids; 57GNO57U7G / Finasteride; H6241UJ22B / Selenium; O0J6XJN02I / Dutasteride
[Number-of-references]
48
23.
Ishkanian AS, Zafarana G, Thoms J, Bristow RG:
Array CGH as a potential predictor of radiocurability in intermediate risk prostate cancer.
Acta Oncol
; 2010 Oct;49(7):888-94
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[Title]
Array CGH as a potential predictor of radiocurability in intermediate risk
prostate
cancer.
Prostate
cancer is the most common male cancer and up to one fifth of diagnosed patients will die of their disease.
Current prognostic variables including T-category (of the TNM staging), the absolute or kinetics of
prostatic
specific antigen (PSA) and the pathologic Gleason score (GS) are utilized to place men in low, intermediate and high-risk
prostate
cancer risk groupings.
Somatic alterations in
prostate
cancer.
Herein, we review the potential for somatic alterations in
tumor
-associated genes (based on comparative genomic hybridization (CGH) in
prostate
cancers to be novel prognostic, and possibly predictive, factors for
prostate
cancer radiotherapy response.
Intermediate risk
prostate
cancers show alterations in a number of genes thought to be involved in radiosensitivity, DNA repair, cell death and stem cell renewal.
Conclusions. The use of high-resolution CGH for fine-mapping of deletions and amplifications in pre-radiotherapy
prostate
cancer biopsies is feasible.
Genetic alterations may delineate localized
prostate
cancer from systemic disease and be used as a predictive factor in that patients would be individually triaged to local (surgery versus radiotherapy) and/or adjuvant (adjuvant androgen ablation or post-operative radiotherapy) therapies in a prospective fashion to improve outcome.
[MeSH-major]
Carcinoma /
diagnosis
. Carcinoma / radiotherapy. Comparative Genomic Hybridization / methods.
Prostatic Neoplasms
/
diagnosis
.
Prostatic Neoplasms
/ radiotherapy
[MeSH-minor]
Algorithms. Animals. Humans. Male.
Neoplasm
Staging. Prognosis. Risk. Treatment Outcome
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
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author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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.
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(PMID = 20590366.001).
[ISSN]
1651-226X
[Journal-full-title]
Acta oncologica (Stockholm, Sweden)
[ISO-abbreviation]
Acta Oncol
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
24.
Braeckman J, Autier P, Garbar C, Marichal MP, Soviany C, Nir R, Nir D, Michielsen D, Bleiberg H, Egevad L, Emberton M:
Computer-aided ultrasonography (HistoScanning): a novel technology for locating and characterizing prostate cancer.
BJU Int
; 2008 Feb;101(3):293-8
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[Title]
Computer-aided ultrasonography (HistoScanning): a novel technology for locating and characterizing
prostate
cancer.
OBJECTIVE: To assess the extent to which
prostate
HistoScanning (PHS), a new ultrasound-based technology that uses computer-aided analysis to quantify tissue disorganization induced by malignant processes, can identify and characterize foci
of prostate
cancer compared with step-sectioned radical prostatectomy (RP) specimens.
In 13 men the histology was examined on sections of the whole-mount
prostate
onto which a grid of 5 x 5 mm squares was applied.
On a test set of 14 of the 29 patients, PHS analysis was used before knowing the histology results (blinded data), to predict the maximum
tumour
diameter, focality, laterality and extraprostatic extension (EPE).
RESULTS: Identification and characterization by PHS of the index
tumour
in the 14 patients in the test set correlated closely (r = 0.95, P < 0.001) with the reference test.
In the same set of data, EPE was attributed to one
prostate
cancer that on pathological inspection was deemed to be organ-confined (pT2b).
CONCLUSIONS: PHS has the potential to identify and characterize
prostate
cancer foci noninvasively.
The precision appears to be sufficient to suggest that PHS might be useful as a triage test for men deemed to be at risk
of prostate
cancer and who wish to avoid
prostate
biopsy.
[MeSH-major]
Image Interpretation, Computer-Assisted / standards.
Prostate
/ pathology.
Prostate
-Specific Antigen / blood.
Prostatic Neoplasms
/ ultrasonography
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer Screening
.
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author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
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[CommentIn]
BJU Int. 2009 Jan;103(1):115; author reply 115-6
[
19076972.001
]
(PMID = 17922870.001).
[ISSN]
1464-410X
[Journal-full-title]
BJU international
[ISO-abbreviation]
BJU Int.
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article
[Publication-country]
England
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
25.
Nair TM:
On selecting mRNA isoform features for profiling prostate cancer.
Comput Biol Chem
; 2009 Dec;33(6):421-8
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[Title]
On selecting mRNA isoform features for profiling
prostate
cancer.
In our earlier study we had used mRNA isoforms expression to identify biomarkers for
prostate
cancer (Li et. al, 2006.
Further, we have rigorously analyzed the isoform expression data to understand the variability and heterogeneity associated with the expression levels between (i)
prostate
cancer cell lines and non-
prostate
cancer cell lines and (ii) normal
prostate
tissue and
prostate
cancer tissue.
[MeSH-major]
Gene Expression Profiling.
Prostatic Neoplasms
/ genetics. RNA, Messenger / genetics
Genetic Alliance.
consumer health - Prostate cancer
.
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
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(PMID = 19889581.001).
[ISSN]
1476-928X
[Journal-full-title]
Computational biology and chemistry
[ISO-abbreviation]
Comput Biol Chem
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / Protein Isoforms; 0 / RNA, Messenger
26.
Bradley SV, Oravecz-Wilson KI, Bougeard G, Mizukami I, Li L, Munaco AJ, Sreekumar A, Corradetti MN, Chinnaiyan AM, Sanda MG, Ross TS:
Serum antibodies to huntingtin interacting protein-1: a new blood test for prostate cancer.
Cancer Res
; 2005 May 15;65(10):4126-33
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[Title]
Serum antibodies to huntingtin interacting protein-1: a new blood test for
prostate
cancer.
Huntingtin-interacting protein 1 (HIP1) is frequently overexpressed in
prostate
cancer.
In addition to human cancers, HIP1 is also overexpressed in
prostate
tumors from the transgenic adenocarcinoma of the mouse
prostate
(TRAMP) mouse model.
Here we provide evidence that HIP1 plays an important role in mouse
tumor
development, as
tumor
formation in the TRAMP mice was impaired in the Hip1null/null background.
In addition, we report that autoantibodies to HIP1 developed in the sera of TRAMP mice with
prostate
cancer as well as in the sera from human
prostate
cancer patients.
This led to the development of an anti-HIP1 serum test in humans that had a similar sensitivity and specificity to the anti-alpha-methylacyl CoA racemase (AMACR) and
prostate
-specific antigen tests for
prostate
cancer and when combined with the anti-AMACR test yielded a specificity of 97%.
These data suggest that HIP1 plays a functional role in tumorigenesis and that a positive HIP1 autoantibody test may be an important serum marker
of prostate
cancer.
[MeSH-major]
Adenocarcinoma / immunology. Autoantibodies / blood. DNA-Binding Proteins / immunology.
Prostatic Neoplasms
/ immunology
Genetic Alliance.
consumer health - Prostate cancer
.
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consumer health - Prostate Cancer
.
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.
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gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
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Mouse Genome Informatics (MGI)
.
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.
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(PMID = 15899803.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA098730-02; United States / NCI NIH HHS / CA / R01 CA82419-01; United States / NCI NIH HHS / CA / R01-CA82363-01A1
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Autoantibodies; 0 / DNA-Binding Proteins; 0 / HIP1 protein, human
27.
Nam RK, Reeves JR, Toi A, Dulude H, Trachtenberg J, Emami M, Daigneault L, Panchal C, Sugar L, Jewett MA, Narod SA:
A novel serum marker, total prostate secretory protein of 94 amino acids, improves prostate cancer detection and helps identify high grade cancers at diagnosis.
J Urol
; 2006 Apr;175(4):1291-7
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[Title]
A novel serum marker, total
prostate
secretory protein of 94 amino acids, improves
prostate
cancer detection and helps identify high grade cancers at
diagnosis
.
PURPOSE: New biomarkers for
prostate
cancer are needed.
MATERIALS AND METHODS: We conducted a case-control study of 1,212 men with no previous history
of prostate
cancer and who underwent a
prostate
biopsy from 1998 to 2000 because of an increased PSA or an abnormal DRE.
Cases were patients with
prostate
cancer, and controls were patients who had no evidence of cancer.
Multivariate logistic regression analysis was used to determine whether or not PSP94 levels improved the predictive value for
prostate
cancer.
The adjusted odds ratios for the presence
of prostate
cancer for patients with the lowest quartile of PSP94, compared to patients in the highest quartile was 2.70 (95% CI 1.8 - 4.0, p <0.0001).
CONCLUSIONS: Patients with low total PSP94 levels had a high probability for having
prostate
cancer detected at biopsy.
[MeSH-major]
Biomarkers,
Tumor
/ blood. Follicle Stimulating Hormone / blood.
Prostatic Neoplasms
/ blood.
Prostatic Neoplasms
/ pathology.
Prostatic
Secretory Proteins / blood
Genetic Alliance.
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.
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MENOTROPINS
.
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.
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.
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.
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[CommentIn]
J Urol. 2006 Apr;175(4):1199-200
[
16515959.001
]
(PMID = 16515983.001).
[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]
0 / Biomarkers, Tumor; 0 / Prostatic Secretory Proteins; 0 / beta-microseminoprotein; 9002-68-0 / Follicle Stimulating Hormone
28.
Chiang CF, Son EL, Wu GJ:
Oral treatment of the TRAMP mice with doxazosin suppresses prostate tumor growth and metastasis.
Prostate
; 2005 Sep 1;64(4):408-18
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[Title]
Oral treatment of the TRAMP mice with doxazosin suppresses
prostate tumor
growth and metastasis.
BACKGROUND: We used the TRAMP mouse model for testing the effect of oral doxazosin treatment on the in vivo
prostate tumor
growth and metastasis.
At the end of oral treatment,
tumor
weight was determined, and metastasis to multiple organs examined.
The levels of MUC18, Bcl-2, Bax, caspase-3, poly (ADP-ribose) polymerase (PARP), phospho (Ser473)-AKT, and Ki-67 in the mouse
prostate
tumors were determined.
RESULTS: Oral treatment of the TRAMP mice with doxazosin for 45-81 days did not decrease the size of preexisting
prostate
tumors, but it limited the metastasis to peri-aortic lymph nodes.
A prolonged treatment of TRAMP mice with doxazosin (156-196 days), if administered early, decreased the
prostate tumor
weight and completely suppressed metastasis.
The doxazosin treatment did not further decrease the expression of an already low level of Bcl-2 in all
prostate
tumors, but it increased the expression of Bax, and the activation of caspase-3, and the cleavage of a downstream substrate, PARP.
The treatment in the early phase appeared to promote
prostate tumor
growth and increased the expression of a proliferative index, Ki-67.
CONCLUSIONS: Doxazosin, if administered early, may be useful for preventing the
prostate tumor
formation, and also for limiting or completely suppressing the metastasis
of prostate
cancer in the TRAMP model.
[MeSH-major]
Adrenergic alpha-Antagonists / pharmacology. Doxazosin / pharmacology.
Prostatic Neoplasms
/ drug therapy.
Prostatic Neoplasms
/ secondary
MedlinePlus Health Information.
consumer health - Prostate Cancer
.
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DOXAZOSIN MESYLATE
.
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[Copyright]
Copyright 2005 Wiley-Liss, Inc.
(PMID = 15789364.001).
[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 / Adrenergic alpha-Antagonists; 0 / Androgen-Binding Protein; 0 / Antigens, CD; 0 / Antigens, CD146; 0 / Bax protein, mouse; 0 / Ki-67 Antigen; 0 / Mcam protein, mouse; 0 / Neural Cell Adhesion Molecules; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 0 / probasin; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; NW1291F1W8 / Doxazosin
29.
Zhang P, Zheng Y, Ran H, Leng Z, Wang Z:
Case report: gastric adenocarcinoma metastatic to the prostate gland.
J Radiol Case Rep
; 2010;4(3):35-8
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[Title]
Case report: gastric adenocarcinoma metastatic to the
prostate
gland
.
Metastasis to the
prostate
gland
from gastric cancer is exceedingly rare.
We have presented a rare case of gastric malignancy metastasizing to the
prostate
diagnosed by transrectal ultrasound guided
prostate
biopsy.
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(PMID = 22470718.001).
[ISSN]
1943-0922
[Journal-full-title]
Journal of radiology case reports
[ISO-abbreviation]
J Radiol Case Rep
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ PMC3303380
[Keywords]
NOTNLM ; gastric adenocarcinoma / metastases / secondary prostatic cancer / transrectal ultrasound
30.
Tamura K, Furihata M, Chung SY, Uemura M, Yoshioka H, Iiyama T, Ashida S, Nasu Y, Fujioka T, Shuin T, Nakamura Y, Nakagawa H:
Stanniocalcin 2 overexpression in castration-resistant prostate cancer and aggressive prostate cancer.
Cancer Sci
; 2009 May;100(5):914-9
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[Title]
Stanniocalcin 2 overexpression in castration-resistant
prostate
cancer and aggressive
prostate
cancer.
Prostate
cancer is usually androgen-dependent and responds well to androgen ablation therapy based on castration.
However, at a certain stage some
prostate
cancers eventually acquire a castration-resistant phenotype where they progress aggressively and show very poor response to any anticancer therapies.
To characterize the molecular features of these clinical castration-resistant
prostate
cancers, we previously analyzed gene expression profiles by genome-wide cDNA microarrays combined with microdissection and found dozens of trans-activated genes in clinical castration-resistant
prostate
cancers.
Among them, we report the identification of a new biomarker, stanniocalcin 2, as an overexpressed gene in castration-resistant
prostate
cancer cells.
Real-time polymerase chain reaction and immunohistochemical analysis confirmed overexpression of stanniocalcin 2, a 302-amino-acid glycoprotein hormone, specifically in castration-resistant
prostate
cancer cells and aggressive castration-naïve
prostate
cancers with high Gleason scores (8-10).
The gene was not expressed in normal
prostate
, nor in most indolent castration-naïve
prostate
cancers.
Knockdown of stanniocalcin 2 expression by short interfering RNA in a
prostate
cancer cell line resulted in drastic attenuation
of prostate
cancer cell growth.
Concordantly, stanniocalcin 2 overexpression in a
prostate
cancer cell line promoted
prostate
cancer cell growth, indicating its oncogenic property.
These findings suggest that stanniocalcin 2 could be involved in aggressive phenotyping
of prostate
cancers, including castration-resistant
prostate
cancers, and that it should be a potential molecular target for development of new therapeutics and a diagnostic biomarker for aggressive
prostate
cancers.
[MeSH-major]
Castration. Glycoproteins / metabolism. Intercellular Signaling Peptides and Proteins / metabolism.
Prostatic Neoplasms
/ metabolism.
Prostatic Neoplasms
/ pathology
[MeSH-minor]
Cell Line,
Tumor
. Disease Progression. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. RNA Interference
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(PMID = 19298603.001).
[ISSN]
1349-7006
[Journal-full-title]
Cancer science
[ISO-abbreviation]
Cancer Sci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Glycoproteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / STC2 protein, human
31.
Mann MJ, DeCastro GJ, Desai M, Benson MC, McKiernan JM:
Predictive significance of surgical margin status after prostatectomy for prostate cancer during PSA era.
Urology
; 2008 Dec;72(6):1203-7
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[Title]
Predictive significance of surgical margin status after prostatectomy for
prostate
cancer during PSA era.
OBJECTIVES: The presence of positive surgical margins (PSMs) after prostatectomy for
prostate
cancer has long been an indicator of poor survival outcomes.
However, with the downstaging of cancer occurring in the
prostate
-specific antigen testing era, we sought to determine whether the risk associated with PSMs retains the same effect on prognosis as before the
prostate
-specific antigen testing era.
RESULTS: The median age, preoperative
prostate
-specific antigen, and Gleason score was 61.6 years, 6 ng/mL, and 7, respectively, and >50% of patients had pathologic Stage T2 disease.
[MeSH-major]
Prostate
-Specific Antigen / blood. Prostatectomy / methods.
Prostatic Neoplasms
/
diagnosis
.
Prostatic Neoplasms
/ surgery
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Humans. Male. Medical Oncology / methods. Middle Aged.
Neoplasm
Recurrence, Local /
diagnosis
.
Neoplasm
Recurrence, Local / pathology. Predictive Value of Tests. Prognosis. Risk Factors. Treatment Outcome
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(PMID = 18674807.001).
[ISSN]
1527-9995
[Journal-full-title]
Urology
[ISO-abbreviation]
Urology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
32.
Hori J, Okuyama M, Azumi M, Kato Y, Saga Y, Hashimoto H, Tokumitsu M, Kakizaki H:
[Indication of repeat prostate biopsy for the diagnosis of prostate cancer].
Hinyokika Kiyo
; 2006 Nov;52(11):835-8; discussion 838-9
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[Title]
[Indication of repeat
prostate
biopsy for
the diagnosis
of prostate
cancer].
There is no standard criterion for repeat
prostate
biopsy in cases with a negative initial biopsy.
We retrospectively analyzed our experience of repeat
prostate
biopsy to establish its indication for
the diagnosis
of prostate
cancer.
From April 1997 to March 2005, 35 consecutive patients underwent repeat
prostate
biopsy at the department of Urology, Asahikawa Medical College Hospital because of clinically suspicious
prostate
cancer despite a negative initial biopsy.
We compared patients' age, number of cores obtained during repeat biopsy, digital rectal examination findings, total
prostate
volume, the time from the first to the last biopsy, total
prostate
specific antigen (PSA) value, free PSA/total PSA ratio, PSA density and PSA velocity between cancer-positive and cancer-negative groups.
Prostate
cancer was detected in 17 of 35 patients (49%).
Fifteen patients with
prostate
cancer were diagnosed by the first repeat biopsy and other 2 patients were diagnosed by the second repeat biopsy.
Persistently elevated total PSA and a higher PSA density in cases with a negative initial biopsy might be a good indication of repeat
prostate
biopsy for
the diagnosis
of prostate
cancer.
[MeSH-major]
Biopsy.
Prostate
/ pathology.
Prostatic Neoplasms
/ pathology
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(PMID = 17176864.001).
[ISSN]
0018-1994
[Journal-full-title]
Hinyokika kiyo. Acta urologica Japonica
[ISO-abbreviation]
Hinyokika Kiyo
[Language]
jpn
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Japan
33.
Wang LG, Chiao JW:
Prostate cancer chemopreventive activity of phenethyl isothiocyanate through epigenetic regulation (review).
Int J Oncol
; 2010 Sep;37(3):533-9
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[Title]
Prostate
cancer chemopreventive activity of phenethyl isothiocyanate through epigenetic regulation (review).
Prostate
cancer is one of the most commonly diagnosed cancers in men.
Therefore, finding strategies for the prevention
of prostate
cancer initiation and disease progression is a medical challenge.
Consumption of cruciferous vegetables has been reported to be associated with reduced incidence
of prostate
cancer cases.
In this review, we summarize the recent findings of PEITC on
prostate
cancer prevention with an emphasis on epigenetic mechanisms.
The gene for detoxifying enzyme pi-class glutathione S-transferase (GSTP1), silenced in the vast majority
of prostate tumor
cells, could be reactivated and the enzymatic function recovered.
The epigenetic regulation may play a critical role, along with interactive mechanisms including the disruption of microtubule polymerization, in
prostate
cancer prevention by PEITC.
[MeSH-major]
Anticarcinogenic Agents / pharmacology. Isothiocyanates / pharmacology.
Prostatic Neoplasms
/ genetics.
Prostatic Neoplasms
/ prevention & control
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(PMID = 20664922.001).
[ISSN]
1791-2423
[Journal-full-title]
International journal of oncology
[ISO-abbreviation]
Int. J. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Review
[Publication-country]
Greece
[Chemical-registry-number]
0 / Anticarcinogenic Agents; 0 / Isothiocyanates; 6U7TFK75KV / phenethyl isothiocyanate
34.
Ellinger J, Bastian PJ, Biermann K, Schmidt ME, Textor J, Bollmann D, Zhou H, Müller SC:
Prostate cancer tissue is masked by bicalutamide: a case report.
Eur J Med Res
; 2007 May 29;12(5):212-5
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[Title]
Prostate
cancer tissue is masked by bicalutamide: a case report.
Prostate
cancer is the most common malignant
tumor
in men.
Recently, a slightly decreased frequency of margin positivity following neoadjuvant bicalutamide treatment due to
tumor
shrinkage was reported.
In this case, local recurrence was confirmed by needle biopsy in a patient five years following radical prostatectomy for
prostate
adenocarcinoma.
After therapy with 50 mg bicalutamide for a month,
the tumour
was resected.
We think that bicalutamide may be capable of masking
prostate
cancer cells.
[MeSH-major]
Adenocarcinoma / drug therapy. Androgen Antagonists / adverse effects. Anilides / adverse effects.
Neoplasm
Recurrence, Local / pathology. Nitriles / adverse effects.
Prostatic Neoplasms
/ drug therapy. Tosyl Compounds / adverse effects
[MeSH-minor]
Biopsy, Needle. Humans. Immunohistochemistry. Male. Middle Aged. Neoadjuvant Therapy.
Prostate
/ drug effects.
Prostate
-Specific Antigen / blood. Prostatectomy
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(PMID = 17513193.001).
[ISSN]
0949-2321
[Journal-full-title]
European journal of medical research
[ISO-abbreviation]
Eur. J. Med. Res.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Androgen Antagonists; 0 / Anilides; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide; EC 3.4.21.77 / Prostate-Specific Antigen
35.
Drott JB, Alexeyev O, Bergström P, Elgh F, Olsson J:
Propionibacterium acnes infection induces upregulation of inflammatory genes and cytokine secretion in prostate epithelial cells.
BMC Microbiol
; 2010;10:126
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[Title]
Propionibacterium acnes infection induces upregulation of inflammatory genes and cytokine secretion in
prostate
epithelial cells.
BACKGROUND: The immune stimulating bacterium Propionibacterium acnes is a frequent colonizer
of benign
and malignant
prostate
tissue.
To understand the pathogenesis of the earliest phase of this infection, we examined the P. acnes triggered immune response in cultivated
prostate
epithelial cells.
RESULTS:
Prostate
epithelial cells are triggered to secrete IL-6, IL-8 and GM-CSF when infected with P. acnes.
CONCLUSIONS: P. acnes has potential to trigger a strong immune reaction in the
prostate
glandular epithelium.
Upon infection
of prostate
via the retrograde urethral route, the induced inflammatory reaction might facilitate bacterial colonization deeper in the
prostate
tissue where persistent inflammation may impact the development
of prostate
diseases as hyperplasia and/or malignancy.
[MeSH-major]
Cytokines / secretion. Epithelial Cells / immunology. Epithelial Cells / microbiology. Gram-Positive Bacterial Infections / immunology. Propionibacterium acnes / immunology.
Prostate
/ microbiology
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(PMID = 20420679.001).
[ISSN]
1471-2180
[Journal-full-title]
BMC microbiology
[ISO-abbreviation]
BMC Microbiol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Cytokines
[Other-IDs]
NLM/ PMC2867951
36.
Loeb S, Yu X, Nadler RB, Roehl KA, Han M, Hawkins SA, Catalona WJ:
Does body mass index affect preoperative prostate specific antigen velocity or pathological outcomes after radical prostatectomy?
J Urol
; 2007 Jan;177(1):102-6; discussion 106
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[Title]
Does body mass index affect preoperative
prostate
specific antigen velocity or pathological outcomes after radical prostatectomy?
PURPOSE: Several studies suggest that obesity may be associated with more aggressive
prostate
cancer.
Similarly the rate of serum
prostate
specific antigen change is associated with adverse
tumor
features and
prostate
cancer specific mortality rates after radical prostatectomy and radiation therapy.
We examined the associations among obesity,
prostate
specific antigen velocity and adverse
tumor
features in men treated with radical prostatectomy.
Prostate
specific antigen velocity and other clinicopathological features were compared among men with a body mass index of less than 25, 25 to 29.9 and 30 or greater.
RESULTS: Although Gleason score and
prostate
volume were similar among groups, there was a significantly lower proportion with organ confined disease and fewer low volume tumors as body mass index increased.
Of patients with a body mass index of 30 or greater 52% had a preoperative
prostate
specific antigen velocity of more than 2 ng/ml yearly compared to 34% with a body mass index of 25 to 29.9 and 26% with a body mass index of less than 25 (p = 0.04).
Although on univariate analysis body mass index was associated with adverse clinical and pathological
tumor
features, on multivariate analysis with other preoperative variables body mass index did not add significant independent predictive information concerning pathological stage (OR 1.02, 95% CI 0.96-1.08).
However, it did not provide independent predictive information concerning final pathological
tumor
stage.
Nevertheless, obesity was significantly associated with increased preoperative
prostate
specific antigen velocity.
Additional studies are needed to further clarify the links between body mass index,
prostate
specific antigen velocity and
prostate
cancer progression, and determine whether weight reduction could lead to improved outcomes.
[MeSH-major]
Body Mass Index.
Prostate
-Specific Antigen / blood. Prostatectomy.
Prostatic Neoplasms
/ blood.
Prostatic Neoplasms
/ pathology
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(PMID = 17162013.001).
[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
37.
Begley LA, Kasina S, MacDonald J, Macoska JA:
The inflammatory microenvironment of the aging prostate facilitates cellular proliferation and hypertrophy.
Cytokine
; 2008 Aug;43(2):194-9
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[Title]
The inflammatory microenvironment of the aging
prostate
facilitates cellular proliferation and hypertrophy.
Benign
Prostatic
Hypertrophy (BPH, also known as
benign
prostatic
hyperplasia or
benign
prostatic
enlargement), is one of the most common
benign
proliferative conditions associated with aging in men and is pathologically characterized by the proliferation of fibroblast/myofibroblast and epithelial cell types in the
prostate
.
Previous studies from our laboratory have shown that the CXC-type chemokines, CXCL5 and CXCL12, are secreted by aging
prostate
stroma and promote both proliferative and transcriptional responses from
prostate
epithelial cells.
Using array-based gene expression profiling and quantitative reverse-transcriptase polymerase chain reaction, we now show that the transcriptome of the aging
prostate
stroma is characterized by the up-regulation of several genes that encode secreted inflammatory mediators, including secreted CXC-type chemokines (CXCL1, CXCL2, CXCL5, CXCL6, CXCL12), interleukins (IL11, IL33), and transcripts with cytokine homology (CYTL1).
At the protein level, ELISA experiments demonstrated that CXCL1, CXCL5, and CXCL6 were secreted by primary
prostate
stromal fibroblasts explanted from aging
prostate
stroma.
Dose-response assays confirmed that, like CXCL5 and CXCL12, CXCL1 and CXCL6 promote low-level proliferative responses from both
prostate
stromal fibroblasts and epithelial cells.
Taken together, these data suggest that inflammatory mediators are secreted by
prostatic
stroma consequent to aging, that the levels of these mediators are sufficient to promote low-level increases in the proliferative rate of both epithelial and stromal fibroblast cell types.
Moreover, these processes may account for the low-level, but cumulative, proliferation of both epithelial and fibroblastic/myofibroblastic cell types that characterizes the aging-associated development
of benign
prostatic
hypertophy.
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Front Biosci. 1997 Jan 1;2:d12-26
[
9159205.001
]
[Cites]
J Immunol. 2004 Aug 15;173(4):2231-5
[
15294933.001
]
(PMID = 18572414.001).
[ISSN]
1096-0023
[Journal-full-title]
Cytokine
[ISO-abbreviation]
Cytokine
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / DK065313-010001; United States / NIDDK NIH HHS / DK / R01 DK081841; United States / NCI NIH HHS / CA / P30 CA046592; United States / NIDDK NIH HHS / DK / P50 DK065313; United States / NIDDK NIH HHS / DK / P50 DK065313-010001; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / P30 CA046592-159017; United States / NIDDK NIH HHS / DK / 1 P50 DK065313; United States / NCI NIH HHS / CA / CA046592-159017; United States / NIDDK NIH HHS / DK / R01 DK081841-04
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Other-IDs]
NLM/ NIHMS66226; NLM/ PMC2538565
38.
Vikram A, Jena GB, Ramarao P:
Increased cell proliferation and contractility of prostate in insulin resistant rats: linking hyperinsulinemia with benign prostate hyperplasia.
Prostate
; 2010 Jan 1;70(1):79-89
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[Title]
Increased cell proliferation and contractility
of prostate
in insulin resistant rats: linking hyperinsulinemia with
benign prostate
hyperplasia.
BACKGROUND: Obesity, dyslipidemia, Hyperinsulinemia, and insulin resistance (IR) are key features of metabolic syndrome and are considered as risk factors for
benign
prostatic
hyperplasia (BPH) as well as type 2 diabetes.
Effect of HFD feeding on the testosterone-induced
prostatic
growth was evaluated.
Pioglitazone (PG, 20 mg/kg) was used for the reversal of compensatory hyperinsulinemia and to examine the subsequent effect on
the prostatic
growth.
RESULTS:
Prostatic
enlargement was observed in the HFD-fed rats.
Significant increase in the cell proliferation markers confirmed the occurrence of cellular hyperplasia in the
prostate of
hyperinsulinemic rat.
Enhanced alpha-adrenoceptor mediated contraction in the
prostate of
HFD-fed rats indicates augmented contractility of
the gland
.
However, testosterone treatment further augmented
the prostatic
growth in HFD-fed rats.
PG treatment led to improved insulin sensitivity, decreased plasma insulin level and
prostate
weight, indicating the role of compensatory hyperinsulinemia in the
prostate
growth.
CONCLUSIONS: The present investigation reports that HFD-feeding induced hyperinsulinemic condition leads to increased cellular proliferation, enhanced alpha-adrenoceptor mediated contraction, and enlargement of the
prostate
in rats.
[MeSH-major]
Cell Proliferation. Hyperinsulinism / complications. Hyperinsulinism / pathology. Insulin Resistance.
Prostate
/ pathology.
Prostatic
Hyperplasia / etiology.
Prostatic
Hyperplasia / pathology
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[Copyright]
(c) 2009 Wiley-Liss, Inc.
(PMID = 19790233.001).
[ISSN]
1097-0045
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Dietary Fats
39.
Yazici S, Inci K, Yuksel S, Bilen CY, Ozen H:
Radical prostatectomy after previous prostate surgery: effects on surgical difficulty and pathologic outcomes.
Urology
; 2009 Apr;73(4):856-9
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[Title]
Radical prostatectomy after previous
prostate
surgery: effects on surgical difficulty and pathologic outcomes.
OBJECTIVES: To evaluate the surgical difficulty and pathologic outcomes of patients who had undergone radical prostatectomy after previous
prostate
surgery.
METHODS: A total of 45 patients with previous
prostate
surgery underwent radical retropubic prostatectomy for
prostate
cancer.
The surgical difficulty and pathologic outcomes for this group of patients (group 1) were compared with those for 50 consecutive patients who had undergone radical retropubic prostatectomy as their only
prostatic
surgery (group 2).
RESULTS: Radical prostatectomy was technically more challenging in the patients after previous
prostate
surgery compared with surgery-naive patients, with significantly more estimated blood loss (P <.05) and a longer operative time (P <.001).
CONCLUSIONS: Although radical retropubic prostatectomy is technically more difficult after previous
prostate
surgery, it can be performed safely with no difference in pathologic outcomes from those seen in patients with no history
of prostate
surgery.
[MeSH-major]
Prostate
/ surgery. Prostatectomy.
Prostatic Neoplasms
/ surgery
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(PMID = 19022487.001).
[ISSN]
1527-9995
[Journal-full-title]
Urology
[ISO-abbreviation]
Urology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
40.
Osunkoya AO, Hansel DE, Sun X, Netto GJ, Epstein JI:
Aberrant diffuse expression of p63 in adenocarcinoma of the prostate on needle biopsy and radical prostatectomy: report of 21 cases.
Am J Surg Pathol
; 2008 Mar;32(3):461-7
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[Title]
Aberrant diffuse expression of p63 in adenocarcinoma of the
prostate
on needle biopsy and radical prostatectomy: report of 21 cases.
Aberrant diffuse expression of p63 in
prostate
carcinoma cells is a rare and poorly understood phenomenon.
We studied 19 cases
of prostate
cancer with aberrant diffuse expression of p63 on needle biopsy and reviewed the subsequent radical prostatectomies in 6 cases.
Needle biopsy cases ranged from Gleason patterns 3 to 5 with
tumor
identified on one or more cores, ranging from a minute focus to 80% of the core.
In all 8 radical prostatectomies p63 positive cancer was present, with in 2/8 cases both p63 positive cancer and usual p63 negative acinar
prostate
cancer.
The presence of p63 positive atypical glands with an infiltrative pattern and perineural invasion on radical prostatectomy confirmed the needle biopsy
diagnosis
of carcinoma.
Rarely,
prostate
cancer can aberrantly express diffuse p63 staining in a nonbasal cell distribution leading to the erroneous
diagnosis
of atrophy or atypical basal cell proliferation.
The diagnosis
of prostate
cancer is based on the morphology and confirmed by the absence of high molecular weight cytokeratin staining and positivity for alpha-methylacyl-CoA racemase in the atypical glands.
Pathologists need to be aware of this rare and unusual phenomenon, which is a potential pitfall in
prostate
cancer
diagnosis
.
[MeSH-major]
Adenocarcinoma / chemistry. Biopsy, Needle. Membrane Proteins / analysis. Prostatectomy.
Prostatic Neoplasms
/ chemistry
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.
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(PMID = 18300803.001).
[ISSN]
0147-5185
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / CKAP4 protein, human; 0 / Membrane Proteins
41.
Cooper CS, Foster CS:
Concepts of epigenetics in prostate cancer development.
Br J Cancer
; 2009 Jan 27;100(2):240-5
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[Title]
Concepts of epigenetics in
prostate
cancer development.
Substantial evidence now supports the view that epigenetic changes have a role in the development of human
prostate
cancer.
Examination of cancer methylation patterns supports a stem cell origin
of prostate
cancer.
It is well established that methylation of GSTpi is a marker
of prostate
cancer, and global patterns of histone marking appear to be linked to cancer prognosis with levels of acetylated histones H3K9, H3K18, and H4K12, and of dimethylated H4R3 and H3K4, dividing low-grade
prostate
cancer (Gleason 6 or less) into two prognostically separate groups.
[MeSH-major]
Epigenesis, Genetic.
Prostatic Neoplasms
/ genetics
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[Cites]
Nat Genet. 2007 Feb;39(2):232-6
[
17200670.001
]
[Cites]
Nat Genet. 2007 Feb;39(2):237-42
[
17211412.001
]
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[
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]
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Oncogene. 2007 Jul 5;26(31):4590-5
[
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]
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[
17640892.001
]
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]
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[
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]
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[
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]
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Curr Top Microbiol Immunol. 2008;320:211-24
[
18268846.001
]
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[
18287625.001
]
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[
18371363.001
]
[Cites]
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[
18488029.001
]
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]
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]
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]
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[
16815976.001
]
[Cites]
Cancer Res. 2006 Nov 1;66(21):10242-6
[
17079440.001
]
(PMID = 19002169.001).
[ISSN]
1532-1827
[Journal-full-title]
British journal of cancer
[ISO-abbreviation]
Br. J. Cancer
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0501019
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Number-of-references]
31
[Other-IDs]
NLM/ PMC2634711
42.
Dos Reis ST, Pontes J Jr, Villanova FE, Borra PM, Antunes AA, Dall'oglio MF, Srougi M, Leite KR:
Genetic polymorphisms of matrix metalloproteinases: susceptibility and prognostic implications for prostate cancer.
J Urol
; 2009 May;181(5):2320-5
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[Title]
Genetic polymorphisms of matrix metalloproteinases: susceptibility and prognostic implications for
prostate
cancer.
PURPOSE:
Prostate
cancer is the most common
tumor
in males in Brazil.
We investigated the correlation between MMP1, 2, 7 and 9 polymorphisms with susceptibility to
prostate
cancer, and classic prognostic parameters
of prostate
cancer.
RESULTS: For the MMP1 gene the polymorphic allele was more common in the control group than in the
prostate
cancer group (p <0.001).
For the MMP9 gene the incidence of the polymorphic homozygote genotype was higher in the
prostate
cancer group (p <0.001).
CONCLUSIONS: MMP1 and MMP2 may protect against
prostate
cancer development and MMP9 may be related to higher risk.
[MeSH-major]
Genetic Predisposition to Disease / epidemiology. Matrix Metalloproteinases / genetics. Polymorphism, Genetic.
Prostatic Neoplasms
/ genetics
[MeSH-minor]
Aged. Biomarkers,
Tumor
/ genetics. Case-Control Studies. Chi-Square Distribution. Confidence Intervals. DNA,
Neoplasm
/ analysis. Gene Expression Regulation, Neoplastic. Humans. Male. Matrix Metalloproteinase 1 / genetics. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 9 / genetics. Middle Aged. Odds Ratio. Polymerase Chain Reaction. Probability. Prognosis. Sensitivity and Specificity
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.
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[CommentIn]
J Urol. 2010 Mar;183(3):1258
[
20097381.001
]
[ErratumIn]
J Urol. 2009 Jul;182(1):400
(PMID = 19303106.001).
[ISSN]
1527-3792
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.24.7 / Matrix Metalloproteinase 1
43.
Li TH, Zhao H, Peng Y, Beliakoff J, Brooks JD, Sun Z:
A promoting role of androgen receptor in androgen-sensitive and -insensitive prostate cancer cells.
Nucleic Acids Res
; 2007;35(8):2767-76
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[Title]
A promoting role of androgen receptor in androgen-sensitive and -insensitive
prostate
cancer cells.
Although the vital role of the androgen receptor (AR) has been well demonstrated in primary
prostate
cancers, its role in the androgen-insensitive
prostate
cancers still remains unclear.
Here, we used a small hairpin RNA approach to directly assess AR activity in
prostate
cancer cells.
Reduction of AR expression in the two androgen-sensitive
prostate
cancer cell lines, LNCaP and LAPC4, significantly decreased AR-mediated transcription and cell growth.
Intriguingly, in two androgen-insensitive
prostate
cell lines, LNCaP-C42B4 and CWR22Rv1, knockdown of AR expression showed a more pronounced effect on AR-induced transcription and cell growth than androgen depletion.
Finally, we demonstrated a direct role for AR in promoting
tumor
formation and growth in a xenograft model.
Taken together, our results elucidate an important role for the AR in androgen-insensitive
prostate
cancer cells, and suggest that AR can be used as a therapeutic target for androgen-insensitive
prostate
cancers.
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11018010.001
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(PMID = 17426117.001).
[ISSN]
1362-4962
[Journal-full-title]
Nucleic acids research
[ISO-abbreviation]
Nucleic Acids Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA070297-11A2; United States / NCI NIH HHS / CA / R01 CA070297-10; United States / NCI NIH HHS / CA / CA70297; United States / NCI NIH HHS / CA / R01 CA070297; United States / NCI NIH HHS / CA / K01 CA123532; United States / NIDDK NIH HHS / DK / R01 DK061002-05; United States / NCI NIH HHS / CA / CA070297-10; United States / NCI NIH HHS / CA / CA087767-05; United States / NCI NIH HHS / CA / R01 CA070297-11A2; United States / NCI NIH HHS / CA / CA087767-04; United States / NCI NIH HHS / CA / R01 CA070297-12; United States / NIDDK NIH HHS / DK / R01 DK061002-04; United States / NCI NIH HHS / CA / CA070297-12; United States / NCI NIH HHS / CA / R01 CA087767-05; United States / NIDDK NIH HHS / DK / DK061002-04; United States / NCI NIH HHS / CA / R29 CA070297; United States / NIDDK NIH HHS / DK / Z01 DK061002; United States / NCI NIH HHS / CA / CA123532-01; United States / NIDDK NIH HHS / DK / R56 DK061002; United States / NCI NIH HHS / CA / R01 CA087767; United States / NIDDK NIH HHS / DK / R01 DK061002; United States / NIDDK NIH HHS / DK / DK061002-05; United States / NIDDK NIH HHS / DK / DK61002; United States / NCI NIH HHS / CA / R01 CA087767-04; United States / NCI NIH HHS / CA / CA87767
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / Androgen Receptor Antagonists; 0 / Androgens; 0 / Receptors, Androgen; 08J2K08A3Y / Dihydrotestosterone
[Other-IDs]
NLM/ PMC1885678
44.
Thomas LN, Douglas RC, Lazier CB, Too CK, Rittmaster RS, Tindall DJ:
Type 1 and type 2 5alpha-reductase expression in the development and progression of prostate cancer.
Eur Urol
; 2008 Feb;53(2):244-52
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[Title]
Type 1 and type 2 5alpha-reductase expression in the development and progression
of prostate
cancer.
OBJECTIVES: Both normal and pathological growth of the
prostate
is dependent on dihydrotestosterone (DHT) synthesis, which is catalysed by two 5alpha-reductase (5alphaR) isoenzymes, 5alphaR1 and 5alphaR2, of which only 5alphaR2 has traditionally been viewed as important in the
prostate
.
The objective of this study was to evaluate the role of both isoenzymes during development/progression
of prostate
cancer.
METHODS: A thorough literature search was performed with the MEDLINE database to identify studies that have assessed expression of 5alphaR1/2 in
prostate
tissue.
RESULTS: DHT suppression data for the 5alphaR2-specific inhibitor, finasteride, and the dual 5alphaR1/2 inhibitor, dutasteride, show that both isoenzymes are active in
benign prostate
.
Furthermore, immunostaining studies have shown that 5alphaR1 expression increases and 5alphaR2 expression decreases in
prostatic
intraepithelial
neoplasia
(PIN) and
prostate
cancer, compared with nonmalignant
prostate
tissue.
Dual inhibition of both isoenzymes with dutasteride may, therefore, be effective in preventing or delaying the growth
of prostate
cancer.
The 4-yr REduction by DUtasteride
of prostate
Cancer Events (REDUCE) trial is underway to test this hypothesis.
Androgen-withdrawal therapy can reverse
prostate
tumour
growth by reducing circulating testosterone.
However, 5alphaR-catalysed DHT synthesis within the
prostate
can continue and most tumours eventually develop resistance to androgen-deprivation therapy.
CONCLUSIONS: The consensus of evidence to date shows that 5alphaR1 is present in the
prostate
, and that levels are higher in malignant compared with
benign prostate
hyperplasia tissue.
[MeSH-major]
3-Oxo-5-alpha-Steroid 4-Dehydrogenase / metabolism.
Prostatic Neoplasms
/ enzymology
Genetic Alliance.
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.
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consumer health - Prostate Cancer
.
Hazardous Substances Data Bank.
FINASTERIDE
.
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(PMID = 18006217.001).
[ISSN]
0302-2838
[Journal-full-title]
European urology
[ISO-abbreviation]
Eur. Urol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Azasteroids; 0 / Enzyme Inhibitors; 0 / Isoenzymes; 57GNO57U7G / Finasteride; EC 1.3.99.5 / 3-Oxo-5-alpha-Steroid 4-Dehydrogenase; O0J6XJN02I / Dutasteride
[Number-of-references]
59
45.
Benchikh El Fegoun A, Villers A, Moreau JL, Richaud P, Rebillard X, Beuzeboc P:
[PSA and follow-up after treatment of prostate cancer].
Prog Urol
; 2008 Mar;18(3):137-44
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[Title]
[PSA and follow-up after treatment
of prostate
cancer].
[Transliterated title]
PSA et suivi après traitement du cancer
de la
prostate
.
[MeSH-major]
Continuity of Patient Care.
Prostate
-Specific Antigen / blood.
Prostatic Neoplasms
/ blood.
Prostatic Neoplasms
/ therapy
[MeSH-minor]
Biomarkers,
Tumor
/ blood. Chemotherapy, Adjuvant. Humans. Male.
Neoplasm
Metastasis.
Neoplasm
Recurrence, Local / blood.
Neoplasm
Recurrence, Local /
diagnosis
. Prostatectomy. Radiotherapy, Adjuvant
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(PMID = 18472065.001).
[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; Review
[Publication-country]
France
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
[Number-of-references]
68
46.
Bastian PJ, Carter BH, Bjartell A, Seitz M, Stanislaus P, Montorsi F, Stief CG, Schröder F:
Insignificant prostate cancer and active surveillance: from definition to clinical implications.
Eur Urol
; 2009 Jun;55(6):1321-30
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[Title]
Insignificant
prostate
cancer and active surveillance: from definition to clinical implications.
CONTEXT: Due to early detection strategies,
prostate
cancer is diagnosed early in its natural history.
It remains unclear whether all patients diagnosed with
prostate
cancer warrant radical treatment or may benefit from delayed intervention following active surveillance.
EVIDENCE ACQUISITION: Medline was searched using the following terms:
prostate
cancer, active surveillance and expectant management for dates up to October 2008.
Once a patients requires active treatment, most patients still present with curable
prostate
cancer.
Furthermore, only few deaths due to
prostate
cancer have occurred.
CONCLUSIONS: Active surveillance is an alternative option to immediate treatment of men with presumed insignificant
prostate
cancer.
It seems that criteria used to identify men with low-risk
prostate
cancer are rather similar, and immediate treatment of men meeting these criteria may result in an unnecessary number of treatments in these highly selected patients.
[MeSH-major]
Monitoring, Physiologic / methods.
Prostate
-Specific Antigen / blood.
Prostatic Neoplasms
/
diagnosis
.
Prostatic Neoplasms
/ therapy
[MeSH-minor]
Aged. Disease Progression. Early Detection of Cancer. Evidence-Based Medicine. Follow-Up Studies. Humans. Male. Middle Aged.
Neoplasm
Invasiveness / pathology.
Neoplasm
Staging. Observation / methods. Patient Selection. Risk Assessment. Sensitivity and Specificity. Time Factors
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[CommentIn]
Eur Urol. 2009 Jun;55(6):1331-2
[
19286304.001
]
[CommentIn]
Eur Urol. 2009 Jun;55(6):1331
[
19286303.001
]
(PMID = 19286302.001).
[ISSN]
1873-7560
[Journal-full-title]
European urology
[ISO-abbreviation]
Eur. Urol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
[Number-of-references]
75
47.
Haworth A, Ebert M, St Clair S, Carey BM, Flynn A, Bottomley DM, Duchesne GM, Joseph D, Ash D:
Impact of selection of post-implant technique on dosimetry parameters for permanent prostate implants.
Brachytherapy
; 2005;4(2):146-53
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[Title]
Impact of selection of post-implant technique on dosimetry parameters for permanent
prostate
implants.
PURPOSE: To investigate the variability
of prostate
implant quality indices between three different methods of calculating the post-implant dose distribution.
METHODS AND MATERIALS: In a study of 9 permanent
prostate
implant patients, post-implant dosimetry was carried out using three methods of identifying seed positions within the
prostate
volume:.
(1)
prostate
volumes defined by transrectal ultrasound (TRUS) immediately following implant were registered with shift-film defined seed positions, (2) seeds were identified directly from the post-implant TRUS images, and (3) CT was used to define seed positions and
prostate
volumes from images acquired at 41-65 days post-implant.
For each method, the volume
of prostate
receiving 90%, 100%, and 150% of the prescribed dose (V90, V100, V150) and the dose delivered to 90% of the
prostate
volume (D90) were calculated.
CONCLUSIONS: There are many uncertainties in the calculation of parameters that are commonly used to describe the quality of a permanent
prostate
implant.
Differences in the parameters calculated were most likely a result of a combination of factors including uncertainties in delineating the
prostate
with different imaging modalities, differences in source identification techniques, and intraobserver variability.
[MeSH-major]
Brachytherapy / instrumentation.
Prostatic Neoplasms
/ radiotherapy. Prostheses and Implants
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(PMID = 15893269.001).
[ISSN]
1538-4721
[Journal-full-title]
Brachytherapy
[ISO-abbreviation]
Brachytherapy
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
48.
He M, Vanaja DK, Karnes RJ, Young CY:
Epigenetic regulation of Myc on retinoic acid receptor beta and PDLIM4 in RWPE1 cells.
Prostate
; 2009 Nov 1;69(15):1643-50
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Tumor
suppressor genes retinoic acid receptor beta (RARbeta) and PDLIM4 are hypermethylated and silenced in
prostate
cancer (PCa) tissues and PCa cell lines compared to normal
prostate
cells.
METHODS: In this study, a
benign prostate
epithelial cell line RWPE1 was used as a model to study the epigenetic regulation of Myc on the RARbeta and PDLIM4 promoters.
[MeSH-major]
DNA-Binding Proteins / genetics. Genes, myc.
Prostate
/ physiology. Receptors, Retinoic Acid / genetics
[MeSH-minor]
Blotting, Western. Cell Growth Processes / genetics. Cell Line. DNA / genetics. DNA (Cytosine-5-)-Methyltransferase / metabolism. DNA Methylation. Epigenesis, Genetic. Gene Expression Profiling. Humans. LIM Domain Proteins. Male. Polymerase Chain Reaction.
Prostatic Neoplasms
/ genetics.
Prostatic Neoplasms
/ pathology. Sequence Analysis, DNA. Transfection
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(PMID = 19623543.001).
[ISSN]
1097-0045
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA 91956
[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 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / PDLIM4 protein, human; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor beta; 9007-49-2 / DNA; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA methyltransferase 3A; EC 2.1.1.37 / DNA methyltransferase 3B
49.
Thompson IM, Ankerst DP, Chi C, Goodman PJ, Tangen CM, Lucia MS, Feng Z, Parnes HL, Coltman CA Jr:
Assessing prostate cancer risk: results from the Prostate Cancer Prevention Trial.
J Natl Cancer Inst
; 2006 Apr 19;98(8):529-34
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[Title]
Assessing
prostate
cancer risk: results from the
Prostate
Cancer Prevention Trial.
BACKGROUND:
Prostate
-specific antigen (PSA) testing is the primary method used to diagnose
prostate
cancer in the United States.
Methods to integrate other risk factors associated with
prostate
cancer into individualized risk prediction are needed.
We used
prostate
biopsy data from men who participated in the
Prostate
Cancer Prevention Trial (PCPT) to develop a predictive model
of prostate
cancer.
METHODS: We included 5519 men from the placebo group of the PCPT who underwent
prostate
biopsy, had at least one PSA measurement and a digital rectal examination (DRE) performed during the year before the biopsy, and had at least two PSA measurements performed during the 3 years before the
prostate
biopsy.
Logistic regression was used to model the risk
of prostate
cancer and high-grade disease associated with age at biopsy, race, family history
of prostate
cancer, PSA level, PSA velocity, DRE result, and previous
prostate
biopsy.
RESULTS: A total of 1211 (21.9%) men were diagnosed with
prostate
cancer by
prostate
biopsy.
Variables that predicted
prostate
cancer included higher PSA level, positive family history
of prostate
cancer, and abnormal DRE result, whereas a previous negative
prostate
biopsy was associated with reduced risk.
Higher PSA level, abnormal DRE result, older age at biopsy, and African American race were predictive for high-grade disease (Gleason score > or =7) whereas a previous negative
prostate
biopsy reduced this risk.
CONCLUSIONS: This predictive model allows an individualized assessment
of prostate
cancer risk and risk of high-grade disease for men who undergo a
prostate
biopsy.
[MeSH-major]
Biopsy, Needle.
Prostatic Neoplasms
/ epidemiology.
Prostatic Neoplasms
/ pathology
[MeSH-minor]
African Americans / statistics & numerical data. Age Factors. Aged. Confounding Factors (Epidemiology). Digital Rectal Examination. Genetic Predisposition to Disease. Humans. Logistic Models. Male. Predictive Value of Tests. Prognosis.
Prostate
-Specific Antigen / blood. Randomized Controlled Trials as Topic. Research Design. Risk Assessment. Risk Factors. Time Factors. United States / epidemiology
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[CommentIn]
J Natl Cancer Inst. 2006 Apr 19;98(8):506-7
[
16622114.001
]
(PMID = 16622122.001).
[ISSN]
1460-2105
[Journal-full-title]
Journal of the National Cancer Institute
[ISO-abbreviation]
J. Natl. Cancer Inst.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / 5UO1CA86402-04; United States / NCI NIH HHS / CA / CA35178; United States / NCI NIH HHS / CA / CA37429; United States / NCI NIH HHS / CA / CA45808
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
50.
Halpin M, Phillips M, Oliffe JL:
Prostate cancer stories in the Canadian print media: representations of illness, disease and masculinities.
Sociol Health Illn
; 2009 Mar;31(2):155-69
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[Title]
Prostate
cancer stories in the Canadian print media: representations of illness, disease and masculinities.
Despite the popularity of print media as an information source for men with
prostate
cancer, the representation
of prostate
cancer within this medium remains relatively understudied.
This article details the findings from an analysis
of prostate
cancer articles published in two Canadian national newspapers, The Globe and Mail and the National Post, from January 2001 through to December 2006.
The 817
prostate
cancer articles published during this period were retrieved and reviewed using manifest and latent analyses.
The latent analysis was guided by the connections between masculinities and
prostate
cancer in the newspapers' stories.
Findings indicated a low frequency of articles that substantively discussed
prostate
cancer and that the descriptive content reproduced hegemonic masculine ideals, such as competition and stoicism.
These findings support how representations
of prostate
cancer in Canadian newspapers predominately replicate detrimental ideologies and perspectives of men's health.
[MeSH-major]
Gender Identity. Health Knowledge, Attitudes, Practice. Men's Health. Newspapers as Topic / statistics & numerical data.
Prostatic Neoplasms
. Social Perception
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(PMID = 18983423.001).
[ISSN]
1467-9566
[Journal-full-title]
Sociology of health & illness
[ISO-abbreviation]
Sociol Health Illn
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
51.
Casciani E, Gualdi GF:
Prostate cancer: value of magnetic resonance spectroscopy 3D chemical shift imaging.
Abdom Imaging
; 2006 Jul-Aug;31(4):490-9
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[Title]
Prostate
cancer: value of magnetic resonance spectroscopy 3D chemical shift imaging.
The results of recent studies of magnetic resonance imaging (MRI) combined with three-dimensional magnetic resonance spectroscopic imaging (3D-MRSI) demonstrate that the MRI/3D-MRSI exam is a unique method by which to noninvasively study the cellular metabolism and anatomy of the
prostate
.
3D-MRSI is emerging as the most specificity tool for non-invasive evaluation of the
prostate
cancer.
Assessment of cancer spread outside the
prostate
can be significantly improved by combining MRI findings with estimates of metabolic abnormalities provided by 3D-MRSI.
Clinically, combined MRI/3D-MRSI has already demonstrated a potential for improved
diagnosis
, staging, and treatment planning for patients with
prostate
cancer.
This article reviewed the value of 3D-MRS imaging for
the diagnosis
, localization, staging, aggressiveness, and treatment planning
of prostate
cancer.
[MeSH-major]
Imaging, Three-Dimensional. Magnetic Resonance Spectroscopy.
Prostatic Neoplasms
/
diagnosis
. Prostatitis /
diagnosis
[MeSH-minor]
Biopsy, Needle. Humans. Male.
Neoplasm
Staging
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(PMID = 16955379.001).
[ISSN]
0942-8925
[Journal-full-title]
Abdominal imaging
[ISO-abbreviation]
Abdom Imaging
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
51
52.
Gallus S, Foschi R, Negri E, Talamini R, Franceschi S, Montella M, Ramazzotti V, Tavani A, Dal Maso L, La Vecchia C:
Dietary zinc and prostate cancer risk: a case-control study from Italy.
Eur Urol
; 2007 Oct;52(4):1052-6
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[Title]
Dietary zinc and
prostate
cancer risk: a case-control study from Italy.
OBJECTIVES: Zinc concentration is higher in the
prostate
than in most other tissues.
Since information on the role of zinc on
prostate
carcinogenesis is controversial, we analysed the issue in a case-control study.
METHODS: Between 1991 and 2002, we conducted a multicentre hospital-based case-control study on
prostate
cancer in Italy.
Cases included 1294 men with incident, histologically confirmed
prostate
cancer.
The trend in risk was significant for advanced cancers only, the OR being 2.02 (95% CI, 1.14-3.59) for
prostate
cancers with a high Gleason score.
CONCLUSIONS: In this large study we found a direct association between high zinc intake and
prostate
cancer risk, particularly for advanced cancers.
Our findings allow one to exclude a favourable effect of zinc on
prostate
carcinogenesis.
[MeSH-major]
Diet.
Prostatic Neoplasms
/ epidemiology. Zinc / adverse effects
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ZINC, ELEMENTAL
.
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[CommentIn]
Eur Urol. 2007 Oct;52(4):1056-7
[
17292534.001
]
[CommentIn]
Eur Urol. 2007 Oct;52(4):1262-3; author reply 1263-4
[
17445972.001
]
(PMID = 17292532.001).
[ISSN]
0302-2838
[Journal-full-title]
European urology
[ISO-abbreviation]
Eur. Urol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
[Chemical-registry-number]
J41CSQ7QDS / Zinc
53.
Gunes S, Bagci H, Sarikaya S, Bilen CY, Kara N:
Prostate-specific antigen and 17-hydroxylase polymorphic genotypes in patients with prostate cancer and benign prostatic hyperplasia.
DNA Cell Biol
; 2007 Dec;26(12):873-8
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[Title]
Prostate
-specific antigen and 17-hydroxylase polymorphic genotypes in patients with
prostate
cancer and
benign
prostatic
hyperplasia.
We investigated the association
of prostate
cancer (PCa) and
benign
prostatic
hyperplasia (BPH) with genetic polymorphisms in
prostate
-specific antigen (PSA) (-158 G/A) and 17-hydroxylase (CYP17) (-34 T/C) genes in a Turkish population.
[MeSH-major]
Polymorphism, Genetic.
Prostate
-Specific Antigen / genetics.
Prostatic
Hyperplasia / genetics.
Prostatic Neoplasms
/ genetics. Steroid 17-alpha-Hydroxylase / genetics
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.
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(PMID = 17961073.001).
[ISSN]
1044-5498
[Journal-full-title]
DNA and cell biology
[ISO-abbreviation]
DNA Cell Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA Primers; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; EC 3.4.21.77 / Prostate-Specific Antigen
54.
Ma S, Guan XY, Beh PS, Wong KY, Chan YP, Yuen HF, Vielkind J, Chan KW:
The significance of LMO2 expression in the progression of prostate cancer.
J Pathol
; 2007 Feb;211(3):278-85
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[Title]
The significance of LMO2 expression in the progression
of prostate
cancer.
This study has investigated LMO2 expression in human
prostatic
tissue specimens,
prostate
cancer cell lines, and xenografts; and has assessed the possible role and mechanism of LMO2 in
prostate
carcinogenesis.
Immunohistochemical analysis on a tissue microarray consisting of 91 human
prostate
specimens, including normal,
prostatic
hyperplasia, high-grade
prostatic
intraepithelial
neoplasia
, and invasive carcinoma, revealed that overexpression of LMO2 was significantly associated with advanced
tumour
stage, as measured by Gleason score (p = 0.012), as well as with the development of distant metastasis (p = 0.018).
These data were supported by quantitative real-time PCR experiments, where LMO2 mRNA levels were found to be significantly higher in
prostate
tumour
specimen than in normal epithelium (p = 0.037).
The expression of LMO2 in cell lines and xenografts representing androgen-dependent (AD) and androgen-independent (AI)
prostate
cancer stages was further studied.
Taken together, these findings provide the first evidence to support the hypothesis that LMO2 may play an important role in
prostate
cancer progression, possibly via repression of E-cadherin expression.
[MeSH-major]
Adenocarcinoma / pathology. DNA-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic. Metalloproteins / genetics.
Prostatic Neoplasms
/ pathology
[MeSH-minor]
Adaptor Proteins, Signal Transducing. Aged. Aged, 80 and over. Blotting, Western / methods. Cell Line,
Tumor
. Chi-Square Distribution. Gene Expression Profiling. Humans. Immunohistochemistry / methods. LIM Domain Proteins. Male. Middle Aged.
Neoplasm
Staging. Oligonucleotide Array Sequence Analysis. Prognosis. Proto-Oncogene Proteins. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction
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[Copyright]
Copyright 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
(PMID = 17167821.001).
[ISSN]
0022-3417
[Journal-full-title]
The Journal of pathology
[ISO-abbreviation]
J. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger
55.
Meyer P, Zuern C, Hermanns N, Haak T:
The association between paternal prostate cancer and type 2 diabetes.
J Carcinog
; 2007;6:14
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[Title]
The association between paternal
prostate
cancer and type 2 diabetes.
However, diabetes mellitus may be a protective factor for
prostate
cancer since both were found to be negatively associated.
Most notably, a lower number
of prostate
cancers was observed in fathers of diabetic patients (OR 0.47; 95% CI 0.22 to 0.94; p = 0.032).
Thus, the observed lower level of history
of prostate
cancer can be regarded as highly reliable.The analysis of 801 type 2 diabetics and 1267 controls showed that cancer of stomach was elevated among mothers of controls (OR 2.67; p = 0.0106).
In accordance with the previous investigation, we again obseved a lower number
of prostate
cancers in fathers of diabetic patients (OR 0.49; p = 0.0279).However, the application of the statistical method of Mantel-Haenszel showed no significant result concerning any of the cancer histories.
CONCLUSION: Fathers of patients suffering from type 2 diabetes were diagnosed less frequently with
prostate
cancer compared to fathers of non-diabetic controls.
As first-degree relatives, e.g. diabetic patients and their fathers, share 50% of their genes, it appears plausible that genetic factors may play an important role in the negative association between diabetes and
prostate
cancer.
However, different statistic analyses showed controversial results concerning the effect of type 2 diabetes on
prostate
cancers.
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[ISSN]
1477-3163
[Journal-full-title]
Journal of carcinogenesis
[ISO-abbreviation]
J Carcinog
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC2042980
56.
Kuo YF, Goodwin JS, Shahinian VB:
Gonadotropin-releasing hormone agonist use in men without a cancer registry diagnosis of prostate cancer.
BMC Health Serv Res
; 2008 Jul 14;8:146
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[Title]
Gonadotropin-releasing hormone agonist use in men without a cancer registry
diagnosis
of prostate
cancer.
BACKGROUND: Use of gonadotropin-releasing hormone (GnRH) agonists has become popular for virtually all stages
of prostate
cancer.
Such cases may be missed by
tumor
registries, leading to underestimates of the total extent of GnRH agonist use.
METHODS: We used linked Surveillance, Epidemiology and End-Results (SEER)-Medicare data from 1993 through 2001 to identify GnRH agonist use in men with either a
diagnosis
of prostate
cancer registered in SEER, or with a
diagnosis
of prostate
cancer based only on Medicare claims (from the 5% control sample of Medicare beneficiaries residing in SEER areas without a registered
diagnosis
of cancer).
The proportion of incident GnRH agonist users without a registry
diagnosis
of prostate
cancer was calculated.
Factors associated with lack of a registry
diagnosis
were examined in multivariable analyses.
RESULTS: Of incident GnRH agonist users, 8.9% had no
diagnosis
of prostate
cancer registered in SEER.
In a multivariable logistic regression model, lack of a registry
diagnosis
of prostate
cancer in GnRH agonist users was significantly more likely with increasing comorbidity, whereas it was less likely in men who had undergone either inpatient admission or procedures such as radical prostatectomy,
prostate
biopsy, or transurethral resection of the
prostate
.
CONCLUSION: Reliance solely on
tumor
registry data may underestimate the rate of GnRH agonist use in men with
prostate
cancer.
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consumer health - Prostate Cancer
.
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[ISSN]
1472-6963
[Journal-full-title]
BMC health services research
[ISO-abbreviation]
BMC Health Serv Res
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA116758-03; United States / NCI NIH HHS / CA / CA116758-04; United States / NCI NIH HHS / CA / CA116758-01; United States / NCI NIH HHS / CA / R01CA116758; United States / NCI NIH HHS / CA / R01 CA116758-04; United States / NCI NIH HHS / CA / R01 CA116758-01; United States / NCI NIH HHS / CA / R01 CA116758; United States / NCI NIH HHS / CA / CA116758-02; United States / NCI NIH HHS / CA / R01 CA116758-02; United States / NCI NIH HHS / CA / P50CA105631; United States / NCI NIH HHS / CA / P50 CA105631; United States / NCI NIH HHS / CA / CA116758-03
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
33515-09-2 / Gonadotropin-Releasing Hormone
[Other-IDs]
NLM/ PMC2483971
57.
Khamis ZI, Iczkowski KA, Sahab ZJ, Sang QX:
Protein profiling of isolated leukocytes, myofibroblasts, epithelial, Basal, and endothelial cells from normal, hyperplastic, cancerous, and inflammatory human prostate tissues.
J Cancer
; 2010;1:70-9
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[Title]
Protein profiling of isolated leukocytes, myofibroblasts, epithelial, Basal, and endothelial cells from normal, hyperplastic, cancerous, and inflammatory human
prostate
tissues.
In situ neoplastic
prostate
cells are not lethal unless they become invasive and metastatic.
For cells to become invasive, the
prostate
gland
must undergo degradation of the basement membrane and disruption of the basal cell layer underneath the luminal epithelia.
It is hypothesized that microenvironmental factors may affect the degradation of the basal cell layer, which if protected may prevent
tumor
progression and invasion.
In this study, we have revealed differential protein expression patterns between epithelial and stromal cells isolated from different
prostate
pathologies and identified several important epithelial and stromal proteins that may contribute to inflammation and malignant transformation of human
benign prostate
tissues to cancerous tissues using matrix-assisted laser desorption ionization time-of-flight mass spectrometry and proteomics methods.
Cellular retinoic acid-binding protein 2 was downregulated in basal cells
of benign prostate
.
Caspase-1 and interleukin-18 receptor 1 were highly expressed in leukocytes
of prostate
cancer.
Proto-oncogene Wnt-3 was downregulated in endothelial cells of prostatitis tissue and tyrosine phosphatase non receptor type 1 was only found in normal and
benign
endothelial cells.
Interestingly, integrin alpha-6 was upregulated in epithelial cells but not detected in myofibroblasts
of prostate
cancer.
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(PMID = 20842227.001).
[ISSN]
1837-9664
[Journal-full-title]
Journal of Cancer
[ISO-abbreviation]
J Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Australia
[Other-IDs]
NLM/ PMC2938068
[Keywords]
NOTNLM ; Prostate cancer / inflammation / magnetic bead cell separation / protein biomarkers / tumor microenvironment / tumorigenesis
58.
Gitenay D, Baron VT:
Is EGR1 a potential target for prostate cancer therapy?
Future Oncol
; 2009 Sep;5(7):993-1003
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[Source]
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[Title]
Is EGR1 a potential target for
prostate
cancer therapy?
Prostate
cancer is a major cause of cancer-related death in American men, for which finding new therapeutic strategies remains a challenge.
Although it has long been considered a
tumor
suppressor, a wealth of new evidence shows that EGR1 promotes the progression
of prostate
cancer.
While EGR1 mediates apoptosis in response to stress and DNA damage by regulating a
tumor
suppressor network, it also promotes the proliferation
of prostate
cancer cells by a mechanism that is not fully understood.
Thus, EGR1 might be targeted for
prostate
cancer therapy either by ectopic expression in combination with radiotherapy or chemotherapy, or by direct inhibition for systemic treatment.
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consumer health - Prostate cancer
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consumer health - Prostate Cancer
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[ISSN]
1744-8301
[Journal-full-title]
Future oncology (London, England)
[ISO-abbreviation]
Future Oncol
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA102688-05; United States / NCI NIH HHS / CA / R01 CA102688; United States / NCI NIH HHS / CA / R01 CA102688-05; United States / NCI NIH HHS / CA / R01-CA102688
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Early Growth Response Protein 1
[Number-of-references]
98
[Other-IDs]
NLM/ NIHMS155263; NLM/ PMC2776080
59.
Briganti A, Chun FK, Suardi N, Gallina A, Walz J, Graefen M, Shariat S, Ebersdobler A, Rigatti P, Perrotte P, Saad F, Montorsi F, Huland H, Karakiewicz PI:
Prostate volume and adverse prostate cancer features: fact not artifact.
Eur J Cancer
; 2007 Dec;43(18):2669-77
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[Title]
Prostate
volume and adverse
prostate
cancer features: fact not artifact.
PURPOSE: A recent
prostate
cancer finasteride chemoprevention trial showed a higher rate of sextant biopsy-detected high grade
prostate
cancer (HGPCa) in finasteride exposed men, whose prostates were significantly smaller than those of controls.
We investigated the association between
prostate
size and
prostate
cancer grade and stage in a large (n=3412) single center radical prostatectomy cohort, which was unexposed to any form of hormonal manipulation.
RESULTS: Small prostates were associated with higher rate of HGPCa at biopsy and at radical prostatectomy (both p<0.001), with higher rate of extracapsular extension (p<0.001), seminal vesicle invasion (p<0.001) and with
tumor
volume >3.4 cc, after accounting for age, PSA, clinical stage and year of surgery.
CONCLUSIONS: Our findings demonstrate that
prostate
cancers located in small glands are fundamentally more aggressive than those located within larger glands.
In consequence,
prostate
cancer detection and treatment strategies should account for
prostate
volume.
[MeSH-major]
Prostate
/ pathology. Prostatectomy / statistics & numerical data.
Prostatic Neoplasms
/ pathology
[MeSH-minor]
Adult. Aged. Biopsy. Humans. Male. Middle Aged.
Neoplasm
Invasiveness / pathology. Organ Size. Regression Analysis. Seminal Vesicles / pathology
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(PMID = 17996442.001).
[ISSN]
0959-8049
[Journal-full-title]
European journal of cancer (Oxford, England : 1990)
[ISO-abbreviation]
Eur. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
60.
Zhang P, Wang ZM, Chong T, Zhao LH:
[Analysis of reference range responsible to normal percent value of free prostate specific antigen from men without prostate disease].
Sichuan Da Xue Xue Bao Yi Xue Ban
; 2007 Sep;38(5):871-3, 903
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[Title]
[Analysis of reference range responsible to normal percent value of free
prostate
specific antigen from men without
prostate
disease].
OBJECTIVE: To study the effect of age on the percent value for free
prostate
specific antigen (fPSA) from men, and the relationships between the percent fPSA and the pathological grade or the clinical stage
of prostate
cancer (PCa), and also to determine appropriate reference value range for Chinese men.
Out of 713, 679 men without
prostate
disease were divided into 5 groups by age, and then the relationships were studied between man age and PSA, fPSA or percent fPSA, respectively.
With the help of the related data of men without
prostate
disease, the appropriate reference value range was established for Chinese men.
According to the data of our early studies and the reference value range of percent fPSA given by the test kit and the previously reported medical references, the data of 10%, 15% and 20% were selected as the percent fPSA threshold values to distinguish PCa or health men without
prostate
disease.
CONCLUSION: The percent fPSA may be more useful than PSA in the detection
of prostate
cancer.
The reference range of > or = 15% percent fPSA is more appropriate threshold value for diagnosing the
prostate
cancer in Chinese man population.
[MeSH-major]
Prostate
-Specific Antigen / blood
[MeSH-minor]
Adult. Age Factors. Aged. Biomarkers,
Tumor
/ blood. Humans. Male. Middle Aged.
Neoplasm
Staging.
Prostatic Neoplasms
/ blood.
Prostatic Neoplasms
/
diagnosis
.
Prostatic Neoplasms
/ pathology. Reference Values. Sensitivity and Specificity
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(PMID = 17953381.001).
[ISSN]
1672-173X
[Journal-full-title]
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
[ISO-abbreviation]
Sichuan Da Xue Xue Bao Yi Xue Ban
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
61.
Davis JW, Nakanishi H, Kumar VS, Bhadkamkar VA, McCormack R, Fritsche HA, Handy B, Gornet T, Babaian RJ:
Circulating tumor cells in peripheral blood samples from patients with increased serum prostate specific antigen: initial results in early prostate cancer.
J Urol
; 2008 Jun;179(6):2187-91; discussion 2191
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[Title]
Circulating
tumor
cells in peripheral blood samples from patients with increased serum
prostate
specific antigen: initial results in early
prostate
cancer.
PURPOSE: We evaluated the hypothesis that circulating
tumor
cells as determined using the CellSearch System would correlate with
tumor
volume, pathological stage and Gleason score in men with localized
prostate
cancer.
MATERIALS AND METHODS: Samples of blood (30 ml) were drawn from 97 men with localized
prostate
cancer before radical prostatectomy, on postoperative days 2 to 3 and at 6 weeks.
A control group consisted of 25 men with an increased
prostate
specific antigen and no
tumor
detected on extended
prostate
biopsy.
Samples were analyzed for circulating
tumor
cells using the CellSearch System.
RESULTS: Circulating
tumor
cells were detected in 21% of patients with cancer and 20% of controls (p = 0.946).
At 6 weeks after prostatectomy circulating
tumor
cells were detected in 16% and 11% (p = 0.51) of the men positive and negative for circulating
tumor
cells at baseline, respectively.
Of the 20 patients with cancer who had circulating
tumor
cells at baseline 18 showed no circulating
tumor
cells after surgery.
Circulating
tumor
cell values did not correlate with
tumor
volume, pathological stage or Gleason score.
Only 3.1% of the men with cancer and 8% of the control group had 3 or more circulating
tumor
cells per 22.5 ml blood at baseline.
CONCLUSIONS: In metastatic breast,
prostate
and other cancers more than 5 circulating
tumor
cells are often detected using the CellSearch System, and may correlate with prognosis.
However, in the setting of localized
prostate
cancer the number of detectable circulating
tumor
cells was low, with findings comparable to those in men who were biopsy negative for cancer.
We found no correlation between the number of circulating
tumor
cells and known prognostic factors in this population.
[MeSH-major]
Neoplastic Cells, Circulating.
Prostate
-Specific Antigen / blood.
Prostatic Neoplasms
/ blood.
Prostatic Neoplasms
/ pathology
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(PMID = 18423725.001).
[ISSN]
1527-3792
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
62.
Chiang CH, Hong CJ, Chang YH, Chang LS, Chen KK:
Human kallikrein-2 gene polymorphism is associated with the occurrence of prostate cancer.
J Urol
; 2005 Feb;173(2):429-32
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[Title]
Human kallikrein-2 gene polymorphism is associated with the occurrence
of prostate
cancer.
PURPOSE: Human glandular kallikrein, which is encoded by the human kallikrein-2 (KLK2) gene, is significantly associated with the occurrence
of prostate
cancer (PCa).
MATERIALS AND METHODS: Peripheral venous blood samples were obtained from 254 patients with PCa and 168 controls with
benign
prostatic
hyperplasia.
All control subjects had normal serum
prostate
specific antigen and proved to be free from malignancy on pathological examination of resected
prostatic
tissues.
Serum
prostate
specific antigen, testosterone, Gleason score, clinical and pathological stage,
tumor
and
prostate
volume of the patients were investigated.
[MeSH-major]
Polymorphism, Genetic.
Prostatic Neoplasms
/ genetics. Tissue Kallikreins / genetics
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(PMID = 15643194.001).
[ISSN]
0022-5347
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.35 / Tissue Kallikreins
63.
Toles CA:
Black men are dying from prostate cancer.
ABNF J
; 2008;19(3):92-5
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[Title]
Black men are dying from
prostate
cancer.
Prostate
cancer is the most frequently diagnosed cancer in the United States, accounting for 33% of all cancer cases among men (American Cancer Society, 2004).
In the United States the number of new cases
of prostate
cancer was estimated at 230,110 and 29,900 will die (American Cancer Society, 2004).
Black men (African-American) are 2.5 times more likely to die
of prostate
cancer than White men (Peters, 2005).
[MeSH-major]
African Americans / ethnology. African Americans / statistics & numerical data.
Prostatic Neoplasms
/ ethnology.
Prostatic Neoplasms
/ mortality
[MeSH-minor]
Attitude to Health / ethnology. Cause of Death. Digital Rectal Examination. European Continental Ancestry Group / ethnology. Food Habits / ethnology. Health Education. Health Knowledge, Attitudes, Practice. Health Planning Guidelines. Health Services Needs and Demand. Health Status Disparities. Healthcare Disparities. Humans. Male. Mass Screening. Primary Prevention.
Prostate
-Specific Antigen. Risk Factors. Social Class. United States / epidemiology
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(PMID = 18717207.001).
[ISSN]
1046-7041
[Journal-full-title]
The ABNF journal : official journal of the Association of Black Nursing Faculty in Higher Education, Inc
[ISO-abbreviation]
ABNF J
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
[Number-of-references]
32
64.
Hooker S, Bonilla C, Akereyeni F, Ahaghotu C, Kittles RA:
NAT2 and NER genetic variants and sporadic prostate cancer susceptibility in African Americans.
Prostate Cancer Prostatic Dis
; 2008;11(4):349-56
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[Title]
NAT2 and NER genetic variants and sporadic
prostate
cancer susceptibility in African Americans.
Prostate
cancer is a common malignancy that disproportionately affects African-American men.
Fourteen single nucleotide polymorphisms in NAT2 and four NER genes (ERCC1, XPF/ERCC4, XPG/ERCC5 and CSB/ERCC6) were genotyped in a case-control study of 254 African-American
prostate
cancer cases and 301 healthy controls from Washington, DC.
We found that individuals homozygous for the XPG/ERCC5 -72C/T promoter polymorphism had a significant reduction in risk, for
prostate
cancer (OR=0.12; 95% CI=0.03-0.48).
The protective effect of the promoter SNP on risk for
prostate
cancer was independent of smoking.
We note that there may be other factors, such as dietary exposures, which may modulate
prostate
cancer risk in combination with genetic variation within the NAT2 and NER genes.
Our results, in combination with previous observations of LOH for ERCC5 in
prostate
tumors, provide further evidence for a role of XPG/ERCC5 in the etiology
of prostate
cancer.
[MeSH-major]
African Americans / ethnology. African Americans / genetics. Arylamine N-Acetyltransferase / genetics. Polymorphism, Single Nucleotide / genetics.
Prostatic Neoplasms
/ ethnology.
Prostatic Neoplasms
/ genetics. Receptors, Cytoplasmic and Nuclear / genetics
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(PMID = 18026184.001).
[ISSN]
1476-5608
[Journal-full-title]
Prostate cancer and prostatic diseases
[ISO-abbreviation]
Prostate Cancer Prostatic Dis.
[Language]
eng
[Grant]
United States / NIGMS NIH HHS / GM / S06GM08016
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / Genetic Markers; 0 / Orphan Nuclear Receptors; 0 / Receptors, Cytoplasmic and Nuclear; 0 / liver X receptor; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / NAT2 protein, human
65.
Fernando HS, Sanders AJ, Kynaston HG, Jiang WG:
WAVE3 is associated with invasiveness in prostate cancer cells.
Urol Oncol
; 2010 May-Jun;28(3):320-7
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[Title]
WAVE3 is associated with invasiveness in
prostate
cancer cells.
We investigated the expression pattern and the effects of manipulating endogenous WAVE3 expression in
prostate
cancer cells.
MATERIALS AND METHODS: Reverse transcriptase-polymerase chain reaction (RT-PCR)
of prostate
cell lines and immunohistochemical staining of normal and cancer specimens for WAVE3 proteins were done.
Immunohistochemistry
of prostate
tissue specimens showed that the cytoplasm of cancer cells had stronger staining than normal epithelium.
CONCLUSIONS: This is the first report on the expression patterns and the functions of WAVE3 in
prostate
cancer cell lines.
This study shows that WAVE3 is pivotal in controlling the invasiveness
of prostate
cancer cells.
Further work is needed to assess WAVE3 as a potential marker for predicting
tumor
aggressiveness.
[MeSH-major]
Neoplasm
Invasiveness / genetics.
Prostatic Neoplasms
/ genetics.
Prostatic Neoplasms
/ pathology. Wiskott-Aldrich Syndrome Protein Family / biosynthesis
[MeSH-minor]
Blotting, Western. Cell Adhesion / genetics. Cell Line,
Tumor
. Cell Proliferation. Gene Expression. Gene Knockdown Techniques. Humans. Immunohistochemistry. Male. Reverse Transcriptase Polymerase Chain Reaction. Transfection
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[Copyright]
Copyright (c) 2010 Elsevier Inc. All rights reserved.
(PMID = 19395286.001).
[ISSN]
1873-2496
[Journal-full-title]
Urologic oncology
[ISO-abbreviation]
Urol. Oncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / WASF3 protein, human; 0 / Wiskott-Aldrich Syndrome Protein Family
66.
Kogan I, Goldfinger N, Milyavsky M, Cohen M, Shats I, Dobler G, Klocker H, Wasylyk B, Voller M, Aalders T, Schalken JA, Oren M, Rotter V:
hTERT-immortalized prostate epithelial and stromal-derived cells: an authentic in vitro model for differentiation and carcinogenesis.
Cancer Res
; 2006 Apr 1;66(7):3531-40
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[Title]
hTERT-immortalized
prostate
epithelial and stromal-derived cells: an authentic in vitro model for differentiation and carcinogenesis.
Prostate
cancer is the most commonly diagnosed type of cancer in men, and there is no available cure for patients with advanced disease.
In vitro model systems are urgently required to permit the study of human
prostate
cell differentiation and malignant transformation.
Unfortunately, human
prostate
cells are particularly difficult to convert into continuously growing cultures.
We report here the successful immortalization without viral oncogenes
of prostate
epithelial cells and, for the first time,
prostate
stromal cells.
These cells exhibit a significant pattern of authentic
prostate
-specific features.
In particular, the epithelial cell culture is able to differentiate into glandular buds that closely resemble the structures formed by primary
prostate
epithelial cells.
The stromal cells have typical characteristics
of prostate
smooth muscle cells.
These immortalized cultures may serve as a unique experimental platform to permit several research directions, including the study of cell-cell interactions in an authentic
prostate
microenvironment,
prostate
cell differentiation, and most significantly, the complex multistep process leading to
prostate
cell transformation.
[MeSH-major]
Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. DNA-Binding Proteins / physiology.
Prostate
/ cytology.
Prostate
/ metabolism.
Prostatic Neoplasms
/ metabolism.
Prostatic Neoplasms
/ pathology. Telomerase / physiology
[MeSH-minor]
Aged. Cell Differentiation / physiology. Cell Line,
Tumor
. Cells, Cultured. Cyclin-Dependent Kinase Inhibitor p16 / biosynthesis. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Epithelial Cells / cytology. Epithelial Cells / metabolism. Epithelial Cells / physiology. Humans. Male. Stromal Cells / cytology. Stromal Cells / metabolism. Stromal Cells / physiology. Transfection.
Tumor
Suppressor Protein p53 / biosynthesis.
Tumor
Suppressor Protein p53 / genetics
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(PMID = 16585177.001).
[ISSN]
0008-5472
[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 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA-Binding Proteins; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.7.7.49 / Telomerase
67.
Ross LE, Powe BD, Taylor YJ, Howard DL:
Physician-patient discussions with african american men about prostate cancer screening.
Am J Mens Health
; 2008 Jun;2(2):156-64
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[Title]
Physician-patient discussions with african american men about
prostate
cancer screening.
Prostate
cancer is the second leading cancer killer in men.
Men in general and African American men in particular face crucial decisions regarding
prostate
cancer screening and perhaps treatment for this disease.
Major health organizations agree that men should discuss
prostate
cancer screening with their physicians or other health care professionals.
The purpose of the study was to examine sociodemographic and other correlates of physician-patient discussions regarding the advantages and disadvantages of the
prostate
-specific antigen (PSA) test among African American men aged 40 or older.
A majority of African American men reported having discussed the advantages and disadvantages
of prostate
cancer screening and/or testing with their physicians before ordering it, and physician-patient discussions about the PSA test were associated with increased screening in African American men.
Inasmuch as African American men have greater
prostate
cancer incidence and mortality over other groups, future attempts should be made to find meaningful correlates of PSA screening and test use to help reduce the burden of this disease.
[MeSH-major]
African Americans / statistics & numerical data. Health Knowledge, Attitudes, Practice. Mass Screening / standards.
Prostatic Neoplasms
/ ethnology.
Prostatic Neoplasms
/ prevention & control
[MeSH-minor]
Adult. Age Factors. Aged. Communication. Confidence Intervals. Cross-Sectional Studies. Educational Status. Health Education / organization & administration. Humans. Male. Men's Health. Middle Aged. Multivariate Analysis. Odds Ratio. Physician-Patient Relations.
Prostate
-Specific Antigen / blood. Risk Assessment. Socioeconomic Factors. Survival Analysis. United States / epidemiology
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(PMID = 19477779.001).
[ISSN]
1557-9891
[Journal-full-title]
American journal of men's health
[ISO-abbreviation]
Am J Mens Health
[Language]
eng
[Grant]
United States / NIMHD NIH HHS / MD / P60 MD000239; United States / AHRQ HHS / HS / R24HS013353; United States / NIMHD NIH HHS / MD / R24MD000167
[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]
United States
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
68.
Chavarro JE, Stampfer MJ, Hall MN, Sesso HD, Ma J:
A 22-y prospective study of fish intake in relation to prostate cancer incidence and mortality.
Am J Clin Nutr
; 2008 Nov;88(5):1297-303
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[Title]
A 22-y prospective study of fish intake in relation to
prostate
cancer incidence and mortality.
BACKGROUND: Fish and seafood n-3 fatty acids may prevent or delay the progression
of prostate
cancer, but epidemiologic studies do not uniformly support this hypothesis.
OBJECTIVE: We examined the relation of fish and seafood n-3 fatty acid intakes with
prostate
cancer incidence and mortality.
RESULTS: During 382 144 person-years of follow-up, 2161 men were diagnosed with
prostate
cancer and 230 died
of prostate
cancer.
Fish intake was unrelated to
prostate
cancer incidence.
Survival analysis among the men diagnosed with
prostate
cancer revealed that those consuming fish >or=5 times/wk had a 48% lower risk
of prostate
cancer death than did men consuming fish less than once weekly [relative risk (RR) = 0.52; 95% CI: 0.30, 0.91; P for trend = 0.05].
A similar association was found between seafood n-3 fatty acid intake and
prostate
cancer mortality (RR(Q5 versus Q1) = 0.64; 95% CI: 0.42, 0.99; P for trend = 0.02).
CONCLUSION: These results suggest that fish intake is unrelated to
prostate
cancer incidence but may improve
prostate
cancer survival.
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[
9789062.001
]
(PMID = 18996866.001).
[ISSN]
1938-3207
[Journal-full-title]
The American journal of clinical nutrition
[ISO-abbreviation]
Am. J. Clin. Nutr.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA042182-20; United States / NCI NIH HHS / CA / CA042182-20; United States / NCI NIH HHS / CA / CA058684-13; United States / NCI NIH HHS / CA / R01 CA090598; United States / NCI NIH HHS / CA / R01 CA058684-13; United States / NCI NIH HHS / CA / CA090598-05S1; United States / NCI NIH HHS / CA / R01 CA058684; United States / NCI NIH HHS / CA / R01 CA042182; United States / NCI NIH HHS / CA / R01 CA090598-05S1
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Fatty Acids, Omega-3
[Other-IDs]
NLM/ NIHMS180899; NLM/ PMC2843087
69.
Albertsen PC:
Treatment of localized prostate cancer: when is active surveillance appropriate?
Nat Rev Clin Oncol
; 2010 Jul;7(7):394-400
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[Title]
Treatment of localized
prostate
cancer: when is active surveillance appropriate?
Testing for
prostate
-specific antigen (PSA) has caused a dramatic increase in the incidence
of prostate
cancer during the past two decades.
Data from a recently reported randomized trial indicate that as many as 48 men must undergo treatment to prevent one
prostate
cancer-related death.
To date,
prostate
cancer-specific survival is over 99%.
For men harboring tumors with a Gleason score >7, data from two recently reported Swedish trials suggest lower
prostate
cancer-related mortality for those men receiving either surgery or radiation.
[MeSH-major]
Prostatic Neoplasms
/
diagnosis
.
Prostatic Neoplasms
/ therapy
[MeSH-minor]
Digital Rectal Examination. Disease Progression. Humans. Male. Prognosis.
Prostate
-Specific Antigen / blood. Risk Assessment. Survival Rate
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(PMID = 20440282.001).
[ISSN]
1759-4782
[Journal-full-title]
Nature reviews. Clinical oncology
[ISO-abbreviation]
Nat Rev Clin Oncol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
EC 3.4.21.77 / Prostate-Specific Antigen
[Number-of-references]
44
70.
Pace G, Pomante R, Vicentini C:
Sarcoma of prostate: case report and review of the literature.
Arch Ital Urol Androl
; 2010 Jun;82(2):105-8
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[Title]
Sarcoma
of prostate
: case report and review of the literature.
OBJECTIVES:
Prostate
sarcomas are rare entity, the most common is leiomyosarcoma which account for 0.1% of all
prostate
malignancies.
The overall survival rate remains poor regardless of initial
tumour
size, grade or histological subtype.
Immunohistochemistry reveals
tumour
cells diffusely positive for vimentin, smooth muscle actin, focally positive for progesterone receptor, whilst keratins are usually negative.
MATERIALS AND METHODS: We describe a case of a patient affected by sarcoma
of prostate
.
Furthermore, we reviewed the cases
of prostate
sarcomas available in literature to clarify the best therapeutic options to be applied.
CONCLUSIONS:
Prostate
sarcomas are highly aggressive, with limited therapeutic options.
An early
diagnosis
and complete surgical excision with negative margins offer patients the long-term disease free survival.
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(PMID = 20812534.001).
[ISSN]
1124-3562
[Journal-full-title]
Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica
[ISO-abbreviation]
Arch Ital Urol Androl
[Language]
ENG
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Italy
[Number-of-references]
27
71.
Skaudickas D, Kondrotas AJ, Kevelaitis E, Venskutonis PR:
The effect of Echinacea purpurea (L.) Moench extract on experimental prostate hyperplasia.
Phytother Res
; 2009 Oct;23(10):1474-8
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[Title]
The effect of Echinacea purpurea (L.) Moench extract on experimental
prostate
hyperplasia.
Moench) on the
prostate
gland
of rats using an experimental model
of benign prostate
hyperplasia (BPH).
The animals were administered 50 mg/kg of extract preparation for 4 and 8 weeks and the
prostate
mass and structural degenerative changes were evaluated in the course of the experiment.
The administration of E. purpurea extract to rats with hyperplasia for 4 and 8 weeks gradually and significantly reduced the
prostate
mass and reversed the degenerative changes in the structure of the
prostate
gland
.
[MeSH-major]
Echinacea. Phytotherapy. Plant Extracts / therapeutic use.
Prostate
/ drug effects.
Prostatic
Hyperplasia / drug therapy
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.
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[Copyright]
(c) 2009 John Wiley & Sons, Ltd.
(PMID = 19288499.001).
[ISSN]
1099-1573
[Journal-full-title]
Phytotherapy research : PTR
[ISO-abbreviation]
Phytother Res
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Plant Extracts
72.
Knight SJ, Latini DM:
Sexual side effects and prostate cancer treatment decisions: patient information needs and preferences.
Cancer J
; 2009 Jan-Feb;15(1):41-4
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[Title]
Sexual side effects and
prostate
cancer treatment decisions: patient information needs and preferences.
Prostate
cancer treatment decision making requires complex trade-offs among treatment outcomes, and sexual function is a central consideration for most men.
Although sexual function is included in
prostate
cancer decision models, survival and fear of recurrence and cancer progression weigh more heavily in these decisions for many men than concerns about treatment impact on sexuality.
In this article, we discuss the importance of sexuality in men's treatment decisions for
prostate
cancer.
We focus on men's preferences for maintaining sexual function and their needs for information about the risk of sexual side effects with
prostate
cancer treatment.
Our review suggests that among men diagnosed with
prostate
cancer sexual function is less important to men than concerns about survival, but is more highly valued than other side effects and treatment characteristics.
However, there is evidence that concerns about sexuality are not in proportion with the associated risk for sexual problems with
prostate
cancer treatment and men acknowledge unmet needs for information about sexuality in making
prostate
cancer treatment decisions.
[MeSH-major]
Needs Assessment. Patient Education as Topic.
Prostatic Neoplasms
/ therapy. Sexual Dysfunction, Physiological / etiology
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(PMID = 19197172.001).
[ISSN]
1528-9117
[Journal-full-title]
Cancer journal (Sudbury, Mass.)
[ISO-abbreviation]
Cancer J
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
73.
Saito S, Murayama Y, Pan Y, Taima T, Fujimura T, Murayama K, Sadilek M, Egawa S, Ueno S, Ito A, Ishidoya S, Nakagawa H, Kato M, Satoh M, Endoh M, Arai Y:
Haptoglobin-beta chain defined by monoclonal antibody RM2 as a novel serum marker for prostate cancer.
Int J Cancer
; 2008 Aug 1;123(3):633-40
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[Title]
Haptoglobin-beta chain defined by monoclonal antibody RM2 as a novel serum marker for
prostate
cancer.
In our previous study, monoclonal antibody RM2, established toward the glycosyl epitope, reflected grade of malignancy
of prostate
cancer cells whereas RM2 reactivity to
benign
glands was negative or weak.
Then, we explored RM2 reactivity to sera of early
prostate
cancer.
We compared RM2 reactivity to sera between 62 patients with early
prostate
cancer and 43 subjects with
benign
prostatic
disease, and examined RM2 reactivity before and after radical prostatectomy in 15 patients by Western blotting.
RM2 reactivity was significantly enhanced on a serum glycoprotein with molecular mass approximately 40 kDa, hereby termed GPX, in the patients with early
prostate
cancer when compared with those with
benign
prostatic
disease (p < 0.0001).
Setting an appropriate cutoff level, RM2 reactivity to GPX for detection
of prostate
cancer had sensitivity of 87% and specificity of 84%, respectively.
The proteomics approach identified GPX as haptoglobin-beta chain and RM2 showed preferential reactivity toward haptoglobin-beta chain derived from
prostate
cancer when compared with polyclonal anti-haptoglobin antibody.
Haptoglobin-beta chain defined by RM2 is a novel serum marker that may be useful for detection of early
prostate
cancer when coupled with
prostate
-specific antigen because it is not specific to
prostate
cancer.
[MeSH-major]
Antigens,
Tumor
-Associated, Carbohydrate / blood. Biomarkers,
Tumor
/ blood. Haptoglobins / metabolism.
Prostatic Neoplasms
/ blood.
Prostatic Neoplasms
/ immunology
[MeSH-minor]
Aged. Antibodies, Monoclonal / blood. Blotting, Western. Electrophoresis, Polyacrylamide Gel. Humans. Immunohistochemistry. Male. Middle Aged.
Prostate
-Specific Antigen / blood. Prostatectomy.
Prostatic
Hyperplasia / blood.
Prostatic
Hyperplasia / immunology. Sensitivity and Specificity. Time Factors
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(PMID = 18464263.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / Biomarkers, Tumor; 0 / HP protein, human; 0 / Haptoglobins; 0 / RM2 antigen, human; EC 3.4.21.77 / Prostate-Specific Antigen
74.
Ruhayel Y, Giwercman A, Ulmert D, Rylander L, Bjartell A, Manjer J, Berglund G, Giwercman YL:
Male infertility and prostate cancer risk: a nested case-control study.
Cancer Causes Control
; 2010 Oct;21(10):1635-43
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[Title]
Male infertility and
prostate
cancer risk: a nested case-control study.
The pathogenesis
of prostate
cancer is unclear, although experimental evidence implicates androgens as playing an important role.
Infertile men frequently suffer from some degree of hypogonadism and may hence be hypothesized to be at lower risk of developing
prostate
cancer than fertile men.
To test this hypothesis, we conducted a case-control study nested within "the Malmö Diet and Cancer Study" cohort in Sweden, inviting 661
prostate
cancer cases and 661 age-matched controls to participate.
Thus, 891 men were included, providing 445
prostate
cancer cases and 446 controls.
Logistic regression showed that the infertile men were at significantly lower risk of being diagnosed with
prostate
cancer than the fertile men (odds ratio, 0.45; 95% confidence interval, 0.25-0.83).
We conclude that enduring male infertility is associated with a reduced
prostate
cancer risk, thus corroborating the theory that normal testicular function, and hence most probably sufficient steroidogenesis, is an important contributing factor to the later development of this malignancy.
[MeSH-major]
Fertility. Infertility, Male.
Prostatic Neoplasms
/ epidemiology
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(PMID = 20524053.001).
[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
75.
Rouvière O:
[MRI of the prostate: optimization of imaging protocols].
J Radiol
; 2006 Feb;87(2 Pt 2):210-21
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[Title]
[MRI of the
prostate
: optimization of imaging protocols].
[Transliterated title]
IRM
de la
prostate
: optimisation des protocoles techniques.
This article details the imaging protocols for
prostate
MRI and the influence on image quality of each particular setting: type of coils to be used (endorectal or external phased-array coils?
[MeSH-major]
Adenocarcinoma /
diagnosis
. Magnetic Resonance Imaging / methods.
Neoplasm
Recurrence, Local /
diagnosis
.
Prostatic Neoplasms
/
diagnosis
[MeSH-minor]
Aged. Artifacts. Biopsy. Clinical Protocols. Contrast Media. Follow-Up Studies. Humans. Image Enhancement. Lymphatic Metastasis /
diagnosis
. Male. Positron-Emission Tomography.
Prostate
/ pathology. Prostatectomy. Time Factors. Treatment Outcome. Ultrasonic Therapy
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(PMID = 16484946.001).
[ISSN]
0221-0363
[Journal-full-title]
Journal de radiologie
[ISO-abbreviation]
J Radiol
[Language]
fre
[Publication-type]
Case Reports; English Abstract; Journal Article; Review
[Publication-country]
France
[Chemical-registry-number]
0 / Contrast Media
[Number-of-references]
42
76.
Schostak M, Christoph F, Schrader M, Panick M, Lingnau A, Miller K:
[Prostate biopsy -- practical examination of the adequacy of Chen's virtual strategy].
Aktuelle Urol
; 2005 Apr;36(2):149-53
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[Title]
[
Prostate
biopsy -- practical examination of the adequacy of Chen's virtual strategy].
[Transliterated title]
Prostatabiopsie -- Chens virtuelles Schema in
der
Praxis.
INTRODUCTION:
Prostate
sextant biopsy is considered the gold standard of invasive
prostate
cancer diagnostics.
MATERIAL AND METHOD: Ultrasound-guided ten-core
prostate
biopsies are performed in our department.
Following the model of Chen, three
prostate
biopsies instead of on are taken from the middle plane.
RESULTS: Between July 2003 and February 2004, 191 patients scheduled for a 10-core
prostate
biopsy were included in the study.
Altogether, the
prostate
carcinoma was detected only by the additional biopsies in 6 patients (9.8 %).
[MeSH-major]
Biopsy, Needle / methods. Computer Simulation. Endosonography. Imaging, Three-Dimensional.
Prostate
/ pathology.
Prostatic Neoplasms
/ pathology. User-Computer Interface
[MeSH-minor]
Aged. Humans. Male. Middle Aged.
Neoplasm
Staging. Sensitivity and Specificity
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(PMID = 15902576.001).
[ISSN]
0001-7868
[Journal-full-title]
Aktuelle Urologie
[ISO-abbreviation]
Aktuelle Urol
[Language]
ger
[Publication-type]
Comparative Study; English Abstract; Journal Article
[Publication-country]
Germany
77.
Tomlins SA, Rhodes DR, Perner S, Dhanasekaran SM, Mehra R, Sun XW, Varambally S, Cao X, Tchinda J, Kuefer R, Lee C, Montie JE, Shah RB, Pienta KJ, Rubin MA, Chinnaiyan AM:
Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer.
Science
; 2005 Oct 28;310(5748):644-8
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[Title]
Recurrent fusion of TMPRSS2 and ETS transcription factor genes in
prostate
cancer.
Two ETS transcription factors, ERG and ETV1, were identified as outliers in
prostate
cancer.
We identified recurrent gene fusions of the 5' untranslated region of TMPRSS2 to ERG or ETV1 in
prostate
cancer tissues with outlier expression.
By using fluorescence in situ hybridization, we demonstrated that 23 of 29
prostate
cancer samples harbor rearrangements in ERG or ETV1.
Cell line experiments suggest that the androgen-responsive promoter elements of TMPRSS2 mediate the overexpression of ETS family members in
prostate
cancer.
These results have implications in the development of carcinomas and the molecular
diagnosis
and treatment
of prostate
cancer.
[MeSH-major]
DNA-Binding Proteins / genetics. Membrane Proteins / genetics.
Neoplasm
Proteins / genetics. Oncogene Proteins, Fusion / genetics.
Prostatic Neoplasms
/ genetics. Serine Endopeptidases / genetics. Trans-Activators / genetics. Transcription Factors / genetics
[MeSH-minor]
Androgens / metabolism. Cell Line,
Tumor
. Gene Expression Regulation, Neoplastic. Gene Rearrangement. Humans. In Situ Hybridization, Fluorescence. Male. Molecular Sequence Data. Polymerase Chain Reaction. Translocation, Genetic
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[CommentIn]
Science. 2005 Oct 28;310(5748):603
[
16254158.001
]
[CommentIn]
Eur Urol. 2007 May;51(5):1443-4
[
17494120.001
]
(PMID = 16254181.001).
[ISSN]
1095-9203
[Journal-full-title]
Science (New York, N.Y.)
[ISO-abbreviation]
Science
[Language]
eng
[Databank-accession-numbers]
GENBANK/ DQ204770/ DQ204771/ DQ204772/ DQ204773
[Grant]
United States / NCI NIH HHS / CA / 5P30 CA46592; United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / R01 CA97063; United States / NIA NIH HHS / AG / R01AG21404; 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.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Androgens; 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / ETV1 protein, human; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Trans-Activators; 0 / Transcription Factors; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / TMPRSS3 protein, human
78.
Yamashita S, Takahashi S, McDonell N, Watanabe N, Niwa T, Hosoya K, Tsujino Y, Shirai T, Ushijima T:
Methylation silencing of transforming growth factor-beta receptor type II in rat prostate cancers.
Cancer Res
; 2008 Apr 1;68(7):2112-21
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[Title]
Methylation silencing of transforming growth factor-beta receptor type II in rat
prostate
cancers.
To identify methylation-silenced genes in
prostate
cancers, a microarray analysis for genes up-regulated by treatment with a demethylating agent, 5-aza-2'-deoxycytidine, was performed using three rat
prostate
cancer cell lines.
From the eight genes, Tgfbr2, a key mediator of transforming growth factor-beta (TGF-beta) signaling that has been strongly implicated in human and rat
prostate
carcinogenesis, was selected, and its silencing in primary samples was analyzed further.
Tgfbr2 was methylated and markedly down-regulated in three of seven 3,2'-dimethyl-4-aminobiphenyl-induced invasive adenocarcinomas in the dorsolateral lobe of the rat
prostate
.
In humans, marked down-regulation of TGFBR2 protein was observed in 12 of 20 high-grade
prostatic
intraepithelial
neoplasia
and 36 of 60
prostate
cancers.
DNA methylation of the human TGFBR2 promoter CpG islands repressed transcription, if present, but neither methylation nor mutation were detected in 27 human
prostate
cancers analyzed.
The identification of methylation silencing of Tgfbr2 in rat
prostate
cancers, in accordance with TGFBR2 down-regulation in human
prostate
cancers, will enable us to analyze how aberrant methylation is induced in vivo and identify factors that promote and suppress the induction of aberrant methylation.
[MeSH-major]
Adenocarcinoma / genetics. DNA Methylation. Gene Silencing.
Prostatic Neoplasms
/ genetics. Protein-Serine-Threonine Kinases / genetics. Receptors, Transforming Growth Factor beta / genetics
[MeSH-minor]
Animals. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Cell Line,
Tumor
. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Histones / genetics. Humans. Male. Oligonucleotide Array Sequence Analysis. Rats. Rats, Inbred F344. Up-Regulation / drug effects
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(PMID = 18381416.001).
[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 / Histones; 0 / Receptors, Transforming Growth Factor beta; 776B62CQ27 / decitabine; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor; M801H13NRU / Azacitidine
79.
Bahn DK, Silverman P, Lee F Sr, Badalament R, Bahn ED, Rewcastle JC:
Focal prostate cryoablation: initial results show cancer control and potency preservation.
J Endourol
; 2006 Sep;20(9):688-92
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[Title]
Focal
prostate
cryoablation: initial results show cancer control and potency preservation.
BACKGROUND: Focal
prostate
cryoablation is the less-than-complete ablation of
the gland
with ice.
Known
tumor
is ablated aggressively, whereas contralateral
prostate
tissue and surrounding structures are spared.
This method offers targeted local cancer control aiming at sexual potency and urinary continence preservation in patients whose
prostate
cancer is believed to be unilateral.
PATIENTS AND METHODS: Patients who had a strong desire for preservation of sexual function and continence were informed of focal
prostate
cryoablation as an investigational treatment option for clinically organ-confined, unilateral
tumor
identified by color Doppler ultrasonography and confirmed by targeted and systematic biopsy.
Only stage, not preoperative serum
prostate
specific antigen concentration (PSA) or
tumor
differentiation, was considered a potential contraindication.
The one biopsy-positive patient was subsequently treated with full-
gland
cryoablation and remains disease free.
CONCLUSION: Focal cryoablation can provide biochemical and local control
of prostate
cancer while preserving potency and continence.
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(PMID = 16999628.001).
[ISSN]
0892-7790
[Journal-full-title]
Journal of endourology
[ISO-abbreviation]
J. Endourol.
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
United States
80.
Loeb S, Sutherland DE, D'Amico AV, Roehl KA, Catalona WJ:
PSA velocity is associated with gleason score in radical prostatectomy specimen: marker for prostate cancer aggressiveness.
Urology
; 2008 Nov;72(5):1116-20; discussion 1120
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[Title]
PSA velocity is associated with gleason score in radical prostatectomy specimen: marker for
prostate
cancer aggressiveness.
OBJECTIVES: Conflicting evidence has been reported on the association
of prostate
-specific antigen velocity (PSAV) with Gleason score in
prostate
needle biopsy specimens.
The Gleason score is an important prognostic indicator for men with
prostate
cancer, and, in modern practice, it frequently affects treatment decisions.
Statistical analysis was performed to examine the relationship between the preoperative PSAV and the prostatectomy Gleason score and other adverse
tumor
features.
CONCLUSIONS: Our results have further validated PSAV as a marker for
prostate
cancer aggressiveness.
Thus, PSAV could be useful in treatment decision-making and in assessing the likelihood of long-term cancer control in men with
prostate
cancer.
[MeSH-major]
Prostate
-Specific Antigen / blood. Prostatectomy.
Prostatic Neoplasms
/ blood.
Prostatic Neoplasms
/ pathology
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Cohort Studies. Humans. Male. Middle Aged.
Neoplasm
Invasiveness.
Neoplasm
Staging. Predictive Value of Tests. Reproducibility of Results. Retrospective Studies. Treatment Outcome
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(PMID = 18571700.001).
[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
81.
Ueda Y, Higuchii Y, Hashimoto T, Mitsui Y, Maruyamai T, Kondou N, Nojima M, Yamamoto S, Shincho M, Hirota S, Shima H:
[Prostate cancer diagnosed through the biopsy of the bone metastatic lesion; a case report].
Hinyokika Kiyo
; 2007 May;53(5):327-30
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[Title]
[
Prostate
cancer diagnosed through the biopsy of the bone metastatic lesion; a case report].
Although digital rectal examination was normal, a high serum
prostate
specific antigen (PSA) level (85.9 ng/ml) led us to perform sextant
prostate
biopsy, resulting in negative for cancer.
Twelve-core
prostate
biopsy was performed again, but the result was negative.
Pelvic magnetic resonance imaging (MRI) showed a metastatic lesion on the right pubic bone, which was biopsied, and turned out to be poorly differentiated
prostate
cancer in histology.
To our knowledge, there were only two case reports diagnosed as
prostate
cancer by biopsies of the metastatic lesions in Japanese literature, but none in the English literature.
These findings suggest that high serum levels of CEA and CA19-9 in patients with
prostate
cancer are indications of hormone-refractory
prostate
cancer resulting in poor prognosis.
[MeSH-major]
Bone
Neoplasms
/ secondary. Bone and Bones / pathology.
Prostatic Neoplasms
/
diagnosis
.
Prostatic Neoplasms
/ pathology
[MeSH-minor]
Aged, 80 and over. Biopsy. CA-19-9 Antigen / blood. Carcinoembryonic Antigen / blood. Humans. Male.
Prostate
/ pathology.
Prostate
-Specific Antigen / blood
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(PMID = 17561720.001).
[ISSN]
0018-1994
[Journal-full-title]
Hinyokika kiyo. Acta urologica Japonica
[ISO-abbreviation]
Hinyokika Kiyo
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen; EC 3.4.21.77 / Prostate-Specific Antigen
82.
Drewa T, Styczynski J:
Progenitor cells are responsible for formation primary epithelial cultures in the prostate epithelial model.
Int Urol Nephrol
; 2007;39(3):851-7
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[Title]
Progenitor cells are responsible for formation primary epithelial cultures in the
prostate
epithelial model.
We hypothesized
prostate
epithelial CD133-positive ASC to be responsible for establishing the primary cell culture.
The
prostate
epithelial stem cells were isolated using anti-CD133 microbeads in order to form different cell populations.
The morphology of cultures developed from CD133(+) and CD133(-)
prostate
epithelial cells were compared with
prostate
epithelium cell culture obtained after simple isolation procedure.
Double CD133(+) and CD133(-) cultures from two rats were established after enzymatic digestion and positive selection by SuperMACS device, and two non-selected CD133(+)/CD133(-) cultures were developed by simple
prostate
epithelial cell isolation from two other rats.
It was observed that growth of the CD133(+)/CD133(-) and CD133(+)culture resembled epithelial-like
prostate
cell culture.
We concluded that the epithelial progenitor cells are responsible for establishing primary
prostate
epithelial cultures in vitro.
[MeSH-major]
Neoplastic Stem Cells / metabolism.
Prostatic Neoplasms
/ metabolism
[MeSH-minor]
AC133 Antigen. Animals. Antigens, CD / metabolism. Cell Differentiation. Cells, Cultured. Epithelial Cells / metabolism. Glycoproteins / metabolism. Male. Microspheres. Models, Animal. Peptides / metabolism. Rats.
Tumor
Cells, Cultured
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[Cites]
Proc Natl Acad Sci U S A. 2003 Sep 30;100 Suppl 1:11896-903
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12909713.001
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Cell Prolif. 2005 Dec;38(6):363-74
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Lab Invest. 2000 Aug;80(8):1251-8
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Cell Cycle. 2006 Jan;5(2):138-41
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14999242.001
]
[Cites]
Cancer Res. 2001 Nov 15;61(22):8135-42
[
11719442.001
]
(PMID = 17318344.001).
[ISSN]
0301-1623
[Journal-full-title]
International urology and nephrology
[ISO-abbreviation]
Int Urol Nephrol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / AC133 Antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Peptides; 0 / Prom1 protein, rat
83.
Maresca KP, Hillier SM, Femia FJ, Keith D, Barone C, Joyal JL, Zimmerman CN, Kozikowski AP, Barrett JA, Eckelman WC, Babich JW:
A series of halogenated heterodimeric inhibitors of prostate specific membrane antigen (PSMA) as radiolabeled probes for targeting prostate cancer.
J Med Chem
; 2009 Jan 22;52(2):347-57
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[Title]
A series of halogenated heterodimeric inhibitors
of prostate
specific membrane antigen (PSMA) as radiolabeled probes for targeting
prostate
cancer.
Prostate
specific membrane antigen (PSMA) is a validated molecular marker for
prostate
cancer.
Two lead iodine compounds were radiolabeled with (123)I and (131)I and demonstrated specific PSMA binding on human
prostate
cancer cells, warranting evaluation as radioligands for the detection, staging, and monitoring
of prostate
cancer.
[MeSH-major]
Glutamate Carboxypeptidase II / antagonists & inhibitors. Halogens / chemistry.
Prostatic Neoplasms
/ drug therapy
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(PMID = 19111054.001).
[ISSN]
1520-4804
[Journal-full-title]
Journal of medicinal chemistry
[ISO-abbreviation]
J. Med. Chem.
[Language]
eng
[Grant]
United States / NIBIB NIH HHS / EB / 1R43EB004253
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Surface; 0 / Halogens; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human
84.
Denis LJ:
Europa Uomo: The European Prostate Cancer Coalition.
Arch Ital Urol Androl
; 2006 Dec;78(4):157-60
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[Title]
Europa Uomo: The European
Prostate
Cancer Coalition.
The European
Prostate
Cancer Coalition is an independent, international, non-profit association of patient led
prostate
cancer support groups.
The European survivors
of prostate
cancer, now about one million strong, have taken up their responsibility to get involved in the support the control of the disease and focus on prevention, optimal treatment and quality of life.
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(PMID = 17269623.001).
[ISSN]
1124-3562
[Journal-full-title]
Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica
[ISO-abbreviation]
Arch Ital Urol Androl
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
Italy
85.
Stock D, Groome PA, Siemens DR:
Inflammation and prostate cancer: a future target for prevention and therapy?
Urol Clin North Am
; 2008 Feb;35(1):117-30; vii
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[Title]
Inflammation and
prostate
cancer: a future target for prevention and therapy?
Given its long natural history,
prostate
cancer has become an ideal model for the clinical and basic science study of neoplastic disease in distinct pathologic phases:
tumor
initiation, progression, invasion, and metastasis.
Nonsteroidal anti-inflammatory drugs (NSAIDs), because of their ability to attenuate inflammation, as well as possibly direct anti-cancer properties associated with the inhibition of stromal cyclooxygenase-2, are potential candidates for clinical use in
prostate
cancer.
Though epidemiologic evidence indicating a reduced risk
of prostate
cancer for NSAID users supports a chemoprotective benefit, observational assessment and clinical trials of these agents among large cohorts
of prostate
cancer patients are needed to determine their value in
prostate
cancer management.
[MeSH-major]
Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Inflammation / drug therapy. Inflammation / pathology.
Prostatic Neoplasms
/ pathology.
Prostatic Neoplasms
/ prevention & control
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(PMID = 18061030.001).
[ISSN]
0094-0143
[Journal-full-title]
The Urologic clinics of North America
[ISO-abbreviation]
Urol. Clin. North Am.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal
[Number-of-references]
117
86.
Fang J, Zhou Q, Shi XL, Jiang BH:
Luteolin inhibits insulin-like growth factor 1 receptor signaling in prostate cancer cells.
Carcinogenesis
; 2007 Mar;28(3):713-23
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[Title]
Luteolin inhibits insulin-like growth factor 1 receptor signaling in
prostate
cancer cells.
Insulin-like growth factor 1 receptor (IGF-1R) activation is required for
prostate
cell proliferation.
Prostate
cancer is one of the most commonly diagnosed malignant tumors in Western countries.
Overexpression of IGF-1R in
prostate
cancer is associated with
tumor
growth.
With evidence accumulating for a chemopreventive role of flavonoids, the effects of luteolin, a bioactive flavonoid, on IGF-1R signaling in
prostate
cancer cells were examined.
Luteolin inhibited insulin-like growth factor 1 (IGF-1) induced activation of IGF-1R and AKT in
prostate
cancer PC-3 and DU145 cells.
As a result, luteolin suppressed proliferation and induced apoptosis
of prostate
cancer cells.
Knockdown of IGF-1R by siRNA led to inhibition of proliferation
of prostate
cancer cells.
Results of in vivo
tumor
growth assay indicated that luteolin inhibited PC-3
tumor
growth.
Immunoblotting of the extracts
of tumor
tissues showed that luteolin inhibited IGF-1R/AKT signaling.
[MeSH-major]
Anticarcinogenic Agents / pharmacology. Cell Cycle / drug effects. Luteolin / pharmacology.
Prostatic Neoplasms
/ pathology. Receptor, IGF Type 1 / antagonists & inhibitors
[MeSH-minor]
Animals. Cell Line,
Tumor
. Cyclin D1 / metabolism. Humans. Male. Mice. Mice, Inbred BALB C. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / genetics. Signal Transduction / drug effects. Transfection
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(PMID = 17065200.001).
[ISSN]
0143-3334
[Journal-full-title]
Carcinogenesis
[ISO-abbreviation]
Carcinogenesis
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Anticarcinogenic Agents; 0 / RNA, Small Interfering; 136601-57-5 / Cyclin D1; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; KUX1ZNC9J2 / Luteolin
87.
Brouwer IA:
Omega-3 PUFA: good or bad for prostate cancer?
Prostaglandins Leukot Essent Fatty Acids
; 2008 Sep-Nov;79(3-5):97-9
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[Title]
Omega-3 PUFA: good or bad for
prostate
cancer?
INTRODUCTION: The objective of this meta-analysis was to estimate quantitatively the associations between intake or status of omega-3 polyunsaturated (omega-3 PUFA) fatty acids and occurrence
of prostate
cancer in observational studies in humans.
RESULTS: The combined estimate showed an increased risk
of prostate
cancer in men with a high intake or blood level of alpha-linolenic acid (ALA) (combined relative risk (RR) 1.36; 95% CI 1.08-1.70).
Ecosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were not significantly associated with
prostate
cancer.
DISCUSSION: The association between high intake of ALA and
prostate
cancer is of concern and needs further study.
However, the fact that the prospective studies do not show a clear association makes a true effect of intake of ALA on
prostate
cancer less likely.
[MeSH-major]
Fatty Acids, Omega-3 / blood.
Prostatic Neoplasms
/ epidemiology
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(PMID = 18951003.001).
[ISSN]
0952-3278
[Journal-full-title]
Prostaglandins, leukotrienes, and essential fatty acids
[ISO-abbreviation]
Prostaglandins Leukot. Essent. Fatty Acids
[Language]
eng
[Publication-type]
Journal Article; Meta-Analysis; Review
[Publication-country]
Scotland
[Chemical-registry-number]
0 / Fatty Acids, Omega-3; 0RBV727H71 / alpha-Linolenic Acid; 25167-62-8 / Docosahexaenoic Acids
[Number-of-references]
20
88.
Marrari A, Iero M, Pilla L, Villa S, Salvioni R, Valdagni R, Parmiani G, Rivoltini L:
Vaccination therapy in prostate cancer.
Cancer Immunol Immunother
; 2007 Apr;56(4):429-45
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[Title]
Vaccination therapy in
prostate
cancer.
Radical prostatectomy and radiation therapy provide excellent localized
prostate
cancer (PC) control.
Although the majority
of prostate
carcinoma is nowadays diagnosed at early stages with favourable risk features, in patients up to 30-40% it recurs within 10 years.
Furthermore, the lack of effective therapies, once
prostate
carcinoma becomes refractory to androgen deprivation, mandates the development of alternative therapeutic options.
There is a growing interest in harnessing the potency and specificity of anti-
tumour
immunity through the generation of fully competent dendritic cells and
tumour
reactive effector lymphocytes.
In some cases clinical responses were achieved showing that vaccine-primed T cells induced anti-
tumour
activity in vivo.
[MeSH-major]
Cancer Vaccines / therapeutic use.
Prostatic Neoplasms
/ immunology.
Prostatic Neoplasms
/ therapy
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(PMID = 17031640.001).
[ISSN]
0340-7004
[Journal-full-title]
Cancer immunology, immunotherapy : CII
[ISO-abbreviation]
Cancer Immunol. Immunother.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Cancer Vaccines
[Number-of-references]
143
89.
Foley R, Marignol L, Thomas AZ, Cullen IM, Perry AS, Tewari P, O'Grady A, Kay E, Dunne B, Loftus B, Watson WR, Fitzpatrick JM, Woodson K, Lehman T, Hollywood D, Lynch TH, Lawler M:
The HIF-1alpha C1772T polymorphism may be associated with susceptibility to clinically localised prostate cancer but not with elevated expression of hypoxic biomarkers.
Cancer Biol Ther
; 2009 Jan;8(2):118-24
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[Title]
The HIF-1alpha C1772T polymorphism may be associated with susceptibility to clinically localised
prostate
cancer but not with elevated expression of hypoxic biomarkers.
We investigated the role of the C1772T polymorphisms in exon 12 of the Hypoxia-inducible factor-1 alpha (HIF-1alpha) gene C1772T genotype in
prostate
cancer (PCa) and amplification of the hypoxic response.
We identified the heterozygous germline CT genotype as an increased risk factor for clinically localised
prostate
cancer (Odds ratio = 6.2; p < 0.0001).
While immunostaining intensity for HIF-1alpha and VEGF was significantly enhanced in 75% of PCa specimens when compared to matched
benign
specimens (p < 0.0001), the CT genotype did not modulate the kinetics of HIF-1alpha protein expression in hypoxia in vitro, and was not associated with enhanced expression of hypoxic biomarkers.
This study provides the first evidence of an increased risk for clinically localised
prostate
cancer in men carrying the C1772T HIF-1alpha gene polymorphism.
[MeSH-major]
Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Polymorphism, Genetic.
Prostatic Neoplasms
/ genetics.
Prostatic Neoplasms
/ metabolism
[MeSH-minor]
Adult. Aged. Alleles. Biomarkers / metabolism. Case-Control Studies. Cell Line,
Tumor
. Chi-Square Distribution. Cohort Studies. DNA,
Neoplasm
/ analysis. DNA,
Neoplasm
/ genetics. Disease Susceptibility. Exons. Gene Frequency. Humans. Immunohistochemistry. Kinetics. Male. Middle Aged. Odds Ratio. Probability. Risk Factors
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(PMID = 19106642.001).
[ISSN]
1555-8576
[Journal-full-title]
Cancer biology & therapy
[ISO-abbreviation]
Cancer Biol. Ther.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers; 0 / DNA, Neoplasm; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit
90.
Ben Jemaa A, Bouraoui Y, Sallami S, Banasr A, Ben Rais N, Ouertani L, Nouira Y, Horchani A, Oueslati R:
Co-expression and impact of prostate specific membrane antigen and prostate specific antigen in prostatic pathologies.
J Exp Clin Cancer Res
; 2010;29:171
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[Title]
Co-expression and impact
of prostate
specific membrane antigen and
prostate
specific antigen in
prostatic
pathologies.
BACKGROUND: The present study was undertaken to relate the co-expression
of prostate
-associated antigens, PSMA and PSA, with the degree of vascularization in normal and pathologic (hyperplasia and cancer)
prostate
tissues to elucidate their possible role in
tumor
progression.
METHODS: The study was carried out in 6 normal, 44
benign
prostatic
hyperplastic and 39 cancerous human prostates.
RESULTS: In our study we found that in normal
prostate
tissue, PSMA and PSA were equally expressed (3.7 ± 0.18 and 3.07 ± 0.11).
Study
of prostate tumor
profiles showed that the profile (PSA+, PSMA-) expression levels decreased between normal
prostate
,
benign
prostatic
tissue and primary
prostate
cancer.
In the other hand, the profile (PSA-, PSMA+) expression levels increased from normal to
prostate tumor
tissues.
With regard to the duality PSMA-PSA, this implies the significance of their investigation together in normal and pathologic
prostate
tissues.
[MeSH-major]
Antigens, Surface / biosynthesis. Glutamate Carboxypeptidase II / biosynthesis.
Prostate
-Specific Antigen / biosynthesis.
Prostatic
Hyperplasia / metabolism.
Prostatic Neoplasms
/ metabolism
[MeSH-minor]
Aged. Aged, 80 and over. Biomarkers,
Tumor
. Humans. Immunohistochemistry. Male. Middle Aged
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Cancer Res. 2003 May 15;63(10):2645-8
[
12750292.001
]
(PMID = 21189143.001).
[ISSN]
1756-9966
[Journal-full-title]
Journal of experimental & clinical cancer research : CR
[ISO-abbreviation]
J. Exp. Clin. Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, Surface; 0 / Biomarkers, Tumor; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human; EC 3.4.21.77 / Prostate-Specific Antigen
[Other-IDs]
NLM/ PMC3023682
91.
Korkes F, Gasperini R, Korkes KL, Silva Neto DC, Castro MG:
Testicular metastases: a poor prognostic factor in patients with advanced prostate cancer.
World J Urol
; 2009 Feb;27(1):113-5
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[Title]
Testicular metastases: a poor prognostic factor in patients with advanced
prostate
cancer.
PURPOSE:
Prostate
cancer is the most frequently diagnosed
neoplasm
in men.
Testicular metastases from
prostate
cancer are rare events that have been previously reported; however, its frequency and clinical meaning are not well established.
PATIENTS AND METHODS: A review of patients who underwent androgen deprivation orchidectomy for
prostate
cancer between 1995 and 2007 was undertaken.
In such context, evaluation of testicular parenchyma of patients with advanced
prostate
cancer could be assessed.
RESULTS: Of the 1,693 orchidectomies performed during the period analysed, three cases of testicular metastases
of prostate
cancer (range 58-76 years) were diagnosed (0.18%).
All patients had very atypical
neoplasm
's behaviour and poor prognosis, dying within the first year.
CONCLUSION: In conclusion, testicular metastases from
prostate
cancer are a rare event, observed in 1.8 per 1,000 cases.
[MeSH-major]
Prostatic Neoplasms
/ pathology. Testicular
Neoplasms
/ secondary
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[Cites]
Int Braz J Urol. 2005 Jan-Feb;31(1):54-6
[
15763010.001
]
[Cites]
Urology. 1995 Sep;46(3 Suppl A):47-55
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7653020.001
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Cancer. 2002 May 15;94(10):2610-7
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]
(PMID = 18762947.001).
[ISSN]
1433-8726
[Journal-full-title]
World journal of urology
[ISO-abbreviation]
World J Urol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
92.
Wu YJ, Liang CH, Zhou FJ, Gao X, Chen LW, Liu Q:
[A case-control study of environmental and genetic factors and prostate cancer in Guangdong].
Zhonghua Yu Fang Yi Xue Za Zhi
; 2009 Jul;43(7):581-5
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[Title]
[A case-control study of environmental and genetic factors and
prostate
cancer in Guangdong].
OBJECTIVE: To explore the etiologic relationship
of prostate
cancer and environmental and genetic polymorphism in southern China METHODS: A hospital-based and 1:1 matched case-control study was conducted.
The blood samples were collected from 85 cases
of prostate
cancer and 82 controls of other diseases after informing consent.
RESULTS: An increased risk
of prostate
cancer development was observed with the early first spermatorrhea (age < 18) (OR = 2.90, 95% CI: 1.76 - 4.80), early first sexual intercourse (age < or = 24) (OR = 2.38, 95% CI: 1.14 - 4.96), frequent sexual intercourse before 35 year old (OR = 1.80, 95% CI: 1.19 - 2.70), family history of cancer (OR = 2.70, 95% CI: 1.31 - 5.58), more intake of pork (OR =2.27, 95% CI: 1.38 - 3.70).
CYP17 A1/A2 and CYP17 A2/A2 genotypes were related with a high risk
of prostate
cancer and OR values of 1.78 (95% CI: 0.70 - 4.53) and 2.57 (95% CI: 0.91 - 7.25) respectively.
Study also showed that there was an interaction between CYP17 polymorphisms and early first spermatorrhea and family cancer history related to the risk
of prostate
cancer with OR value at 13.35 (95% CI: 1.58 - 113.00) and 4.01 (95% CI: 1.22 - 13.17) respectively.
CONCLUSION: Sexual intercourse, dietary intake and family cancer history should be related to
prostate
cancer occurrence.
CYP17 polymorphism might be associated with a high risk
of prostate
cancer.
It suggests that there are multiple environmental and genetic factors to the
prostate
cancer.
[MeSH-major]
Environmental Exposure.
Prostatic Neoplasms
/ epidemiology.
Prostatic Neoplasms
/ genetics. Steroid 17-alpha-Hydroxylase / genetics
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(PMID = 19954068.001).
[ISSN]
0253-9624
[Journal-full-title]
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine]
[ISO-abbreviation]
Zhonghua Yu Fang Yi Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
EC 1.14.99.9 / CYP17A1 protein, human; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase
93.
Kato T, Suzuki H, Komiya A, Imamoto T, Naya Y, Tobe T, Ichikawa T:
Clinical significance of urinary white blood cell count and serum C-reactive protein level for detection of non-palpable prostate cancer.
Int J Urol
; 2006 Jul;13(7):915-9
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[Title]
Clinical significance of urinary white blood cell count and serum C-reactive protein level for detection of non-palpable
prostate
cancer.
AIM: The clinical significance of the urinary white blood cell (U-WBC) count and serum C-reactive protein (CRP) level was evaluated in an effort to improve the efficiency
of prostate
biopsies.
METHODS: We enrolled 228 consecutive patients with serum
prostate
-specific antigen (PSA) ranging from 3.0 to 20.0 ng/mL, normal digital rectal examination findings, and who underwent
prostate
biopsies between January 2001 and August 2004.
Of these, 157 patients had histologically confirmed
benign
prostatic
disease and the remaining 71 patients had
prostate
cancer.
CONCLUSION: The U-WBC count appears to be a reliable indicator of minute
prostatic
inflammation.
[MeSH-major]
Biomarkers,
Tumor
/ blood. C-Reactive Protein / metabolism.
Prostatic Neoplasms
. Urine / cytology
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Biopsy / methods.
Diagnosis
, Differential. Endosonography. Follow-Up Studies. Humans. Leukocyte Count. Male. Middle Aged. Palpation. Prognosis.
Prostate
-Specific Antigen / blood. Retrospective Studies
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(PMID = 16882055.001).
[ISSN]
0919-8172
[Journal-full-title]
International journal of urology : official journal of the Japanese Urological Association
[ISO-abbreviation]
Int. J. Urol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Australia
[Chemical-registry-number]
0 / Biomarkers, Tumor; 9007-41-4 / C-Reactive Protein; EC 3.4.21.77 / Prostate-Specific Antigen
94.
Salinas CA, Koopmeiners JS, Kwon EM, FitzGerald L, Lin DW, Ostrander EA, Feng Z, Stanford JL:
Clinical utility of five genetic variants for predicting prostate cancer risk and mortality.
Prostate
; 2009 Mar 1;69(4):363-72
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[Title]
Clinical utility of five genetic variants for predicting
prostate
cancer risk and mortality.
BACKGROUND: A recent report suggests that the combination of five single-nucleotide polymorphisms (SNPs) at 8q24, 17q12, 17q24.3 and a family history of the disease may predict risk
of prostate
cancer.
The present study tests the performance of these factors in prediction models for
prostate
cancer risk and
prostate
cancer-specific mortality.
Cox proportional hazards models estimated hazard ratios for
prostate
cancer-specific mortality according to genotypes.
RESULTS: The combination of SNP genotypes and family history was significantly associated with
prostate
cancer risk (p(trend) = 1.5 x 10(-20)).
Neither the individual nor combined risk factors was associated with
prostate
cancer-specific mortality.
CONCLUSION: Genotypes for five SNPs plus family history are associated with a significant elevation in risk for
prostate
cancer and may explain up to 45%
of prostate
cancer in our population.
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[Copyright]
2008 Wiley-Liss, Inc.
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(PMID = 19058137.001).
[ISSN]
1097-0045
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50 CA097186; United States / NCI NIH HHS / CA / R01 CA056678; United States / NCI NIH HHS / CA / R01 CA56678; United States / NCI NIH HHS / CA / R01 CA082664; United States / NCI NIH HHS / CA / R01 CA092579; United States / NCI NIH HHS / CA / R01 CA056678-05
[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
[Other-IDs]
NLM/ NIHMS105496; NLM/ PMC2788301
95.
Xie D, Gore C, Liu J, Pong RC, Mason R, Hao G, Long M, Kabbani W, Yu L, Zhang H, Chen H, Sun X, Boothman DA, Min W, Hsieh JT:
Role of DAB2IP in modulating epithelial-to-mesenchymal transition and prostate cancer metastasis.
Proc Natl Acad Sci U S A
; 2010 Feb 09;107(6):2485-90
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[Title]
Role of DAB2IP in modulating epithelial-to-mesenchymal transition and
prostate
cancer metastasis.
A single nucleotide polymorphism in the DAB2IP gene is associated with risk of aggressive
prostate
cancer (PCa), and loss of DAB2IP expression is frequently detected in metastatic PCa.
Here, we show that the loss of DAB2IP expression initiates epithelial-to-mesenchymal transition (EMT), which is visualized by repression of E-cadherin and up-regulation of vimentin in both human normal
prostate
epithelial and
prostate
carcinoma cells as well as in clinical
prostate
-cancer specimens.
In DAB2IP knockout mice,
prostate
epithelial cells exhibited elevated mesenchymal markers, which is characteristic of EMT.
Using a human
prostate
xenograft-mouse model, we observed that knocking down endogenous DAB2IP in human carcinoma cells led to the development of multiple lymph node and distant organ metastases.
[MeSH-major]
Epithelial Cells / pathology. Mesoderm / pathology.
Prostatic Neoplasms
/ pathology. ras GTPase-Activating Proteins / physiology
[MeSH-minor]
Animals. Blotting, Western. Cadherins / genetics. Cadherins / metabolism. Cell Line. Cell Line,
Tumor
. Cell Movement. Gene Expression. Humans. Immunohistochemistry. Male. Mice. Mice, Nude.
Neoplasm
Metastasis.
Neoplasms
, Experimental / genetics.
Neoplasms
, Experimental / metabolism.
Neoplasms
, Experimental / pathology. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction. TCF Transcription Factors / metabolism. Transfection. Transplantation, Heterologous. Vimentin / genetics. Vimentin / 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
(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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[CommentIn]
Proc Natl Acad Sci U S A. 2010 Feb 16;107(7):2731-2
[
20145111.001
]
(PMID = 20080667.001).
[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 / R01 CA102792; United States / NCI NIH HHS / CA / U24CA126608; United States / NCI NIH HHS / CA / P30 CA142543; United States / NIAID NIH HHS / AI / 5U19AI067773-04; United States / NIAID NIH HHS / AI / U19 AI067773; United States / NCI NIH HHS / CA / U24 CA126608; United States / NCI NIH HHS / CA / R01 CA139217
[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 / Cadherins; 0 / DAB2IP protein, human; 0 / RNA, Small Interfering; 0 / TCF Transcription Factors; 0 / Vimentin; 0 / beta Catenin; 0 / ras GTPase-Activating Proteins
[Other-IDs]
NLM/ PMC2823864
96.
Noel C, Parikh PJ, Roy M, Kupelian P, Mahadevan A, Weinstein G, Enke C, Flores N, Beyer D, Levine L:
Prediction of intrafraction prostate motion: accuracy of pre- and post-treatment imaging and intermittent imaging.
Int J Radiat Oncol Biol Phys
; 2009 Mar 1;73(3):692-8
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[Title]
Prediction of intrafraction
prostate
motion: accuracy of pre- and post-treatment imaging and intermittent imaging.
PURPOSE: To evaluate whether pre- and post-treatment imaging (immediately before and after a radiation therapy treatment fraction) and intermittent imaging (at intervals during a treatment fraction) are accurate predictors
of prostate
motion during the delivery of radiation.
METHODS AND MATERIALS: The Calypso 4D Localization System was used to continuously track the
prostate
during radiation delivery in 35
prostate
cancer patients, for a total of 1,157 fractions (28-45 per patient).
Predictions
of prostate
motion away from isocenter were modeled for a pre- and post-treatment imaging schedule and for multiple intermittent intrafraction imaging schedules and compared with the actual continuous tracking data.
The endpoint was drift of the
prostate
beyond a certain radial displacement for a duration of more than 30 s, 1 min, and 2 min.
Results were used to evaluate the sensitivity and specificity of these models as an evaluation of intrafraction
prostate
motion.
RESULTS: The sensitivity of pre- and post-treatment imaging in determining 30 s of intrafraction
prostate
motion greater than 3, 5, or 7 mm for all fractions was low, with values of 53%, 49%, and 39%, respectively.
CONCLUSIONS: These results suggest that pre- and post-treatment imaging is not a sensitive method of assessing intrafraction
prostate
motion, and that intermittent imaging is sufficiently sensitive only at a high sampling rate.
These findings support the value of continuous, real-time tracking in
prostate
cancer radiation therapy.
[MeSH-major]
Electromagnetic Fields. Movement.
Prostate
.
Prostatic Neoplasms
/ radiotherapy
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(PMID = 18692324.001).
[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]
Evaluation Studies; Journal Article
[Publication-country]
United States
97.
Hua LX, Wu HF, Sui YG, Zhang W, Qian LX, Song NH, Zhang JX:
[High intensity focused ultrasound combined with endocrine therapy in treating prostate cancer].
Zhonghua Nan Ke Xue
; 2005 Mar;11(3):195-7
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[Title]
[High intensity focused ultrasound combined with endocrine therapy in treating
prostate
cancer].
OBJECTIVE: To evaluate the clinical efficacy of high intensity focused ultrasound (HIFU) combined with endocrine therapy in the treatment of patients with
prostate
cancer.
METHODS: Twenty patients with
prostate
cancer were treated with extracorporeal HIFU device( model FEP-BY01 ) and androgen ablation, of whom 15 received orchiectomy and 5 LHRH-a.
Before and after the treatment, the
prostate
volume,
prostate
specific antigen (PSA), international
prostate
symptom score (IPSS) and maximal flow rate (Qmax) of the patients were (36.4 +/- 16.2) ml and (20.6 +/- 11.8) ml (P < 0.05), (32.2 +/- 10.4) ng/ml and (2.4 +/- 0.8) ng/ml (P < 0.01), 20.
CONCLUSION: HIFU combined with endocrine therapy is effective in the treatment
of prostate
canc-
[MeSH-major]
Prostatic Neoplasms
/ therapy. Ultrasound, High-Intensity Focused, Transrectal
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(PMID = 15804111.001).
[ISSN]
1009-3591
[Journal-full-title]
Zhonghua nan ke xue = National journal of andrology
[ISO-abbreviation]
Zhonghua Nan Ke Xue
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone; 76W6J0943E / Flutamide
98.
Vanaja DK, Grossmann ME, Cheville JC, Gazi MH, Gong A, Zhang JS, Ajtai K, Burghardt TP, Young CY:
PDLIM4, an actin binding protein, suppresses prostate cancer cell growth.
Cancer Invest
; 2009 Mar;27(3):264-72
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[Title]
PDLIM4, an actin binding protein, suppresses
prostate
cancer cell growth.
We investigated the molecular function of PDLIM4 in
prostate
cancer cells.
PDLIM4 mRNA and protein-expression levels were reduced in LNCaP, LAPC4, DU145, CWR22, and PC3
prostate
cancer cells.
The re-expression of PDLIM4 in
prostate
cancer cells has significantly reduced the cell growth and clonogenicity with G1 phase of cell-cycle arrest.
Restoration of PDLIM4 expression resulted in reduction
of tumor
growth in xenografts.
These results suggest that PDLIM4 may function as a
tumor
suppressor, involved in the control of cell proliferation by associating with actin in
prostate
cancer cells.
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[ISSN]
1532-4192
[Journal-full-title]
Cancer investigation
[ISO-abbreviation]
Cancer Invest.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA070892; United States / NCI NIH HHS / CA / CA070892-10; United States / NCI NIH HHS / CA / R01 CA070892-10; United States / NCI NIH HHS / CA / CA70892; United States / NIAMS NIH HHS / AR / R01 AR049277; United States / NIAMS NIH HHS / AR / AR049277-08; United States / NIAMS NIH HHS / AR / R01 AR049277-08
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
0 / Actins; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / Microfilament Proteins; 0 / PDLIM4 protein, human; 0 / Pdlim4 protein, mouse; 0 / Tumor Suppressor Proteins
[Other-IDs]
NLM/ NIHMS284933; NLM/ PMC3086358
99.
Cheng J, Bawa T, Lee P, Gong L, Yeh ET:
Role of desumoylation in the development of prostate cancer.
Neoplasia
; 2006 Aug;8(8):667-76
<