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[Title] Androgen deprivation and stem cell markers in prostate cancers.

In our previous studies using human LNCaP xenografts and TRAMP (transgenic adenocarcinoma of mouse prostate) mice, androgen deprivation therapy (ADT) resulted in a temporary cessation of prostate cancer (PCa) growth, but then tumors grew faster with more malignant behaviour.

To understand whether cancer stem cells might play a role in PCa progression in these animal models, we investigated the expressions of stem cell-related markers in tumors at different time points after ADT.

[MeSH-major] Androgens / metabolism. Biomarkers, Tumor / metabolism. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. Stem Cells / metabolism

[MeSH-minor] Adenocarcinoma / pathology. Animals. Cell Line, Tumor. Disease Models, Animal. Humans. Immunohistochemistry. Male. Mice. Mice, SCID. Mice, Transgenic. Neoplasm Recurrence, Local / pathology. Neoplasm Transplantation. Orchiectomy. Time Factors

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(PMID = 20126580.001).

[ISSN] 1936-2625

[Journal-full-title] International journal of clinical and experimental pathology

[ISO-abbreviation] Int J Clin Exp Pathol

[Language] eng

[Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Androgens; 0 / Biomarkers, Tumor

[Other-IDs] NLM/ PMC2809992

[Keywords] NOTNLM ; Prostate cancer / TRAMP mice / androgen deprivation / stem-like cells / xenograft tumor

   

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[Title] Failure definition-dependent differences in outcome following radiation for localized prostate cancer: can one size fit all?

[MeSH-major] Adenocarcinoma / radiotherapy. Prostatic Neoplasms / radiotherapy

[MeSH-minor] Biomarkers, Tumor / blood. Disease-Free Survival. Follow-Up Studies. Humans. Male. Multicenter Studies as Topic. Neoplasm Staging. Outcome Assessment (Health Care) / statistics & numerical data. Prostate-Specific Antigen / blood. Radioisotope Teletherapy / mortality. Treatment Failure

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(PMID = 16093990.001).

[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] 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen

   

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[Title] [Gleason score 8-10 prostatic adenocarcinoma: prognostic influence in the biochemical progression free survival].

[Transliterated title] Adenocarcinoma de próstata gleason clínico 8-10: influencia pronóstica en la supervivencia libre de progresión bioquímica.

OBJECTIVE: Hereby, we analyze the characteristics of the clinical Gleason 8-10 group of patients with in our series diagnosed of Prostate Cancer and treated by means of radical prostatectomy, and we try to ascertain which are the influence factors within this group upon progression and progression free survival.

MATERIAL AND METHODS: From the global series of 781 patients with T1-T2 prostate cancer treated by means of radical prostatectomy between 1990 and 2004, we study 108 with a Gleason score on the biopsy of 8-10.

RESULTS: Actual State: 62.7% (490/781) are alive and free of biochemical progression, 24.8% (194/781) are alive with biochemical progression, 2.9% (23/781) are dead by cancer and 1.9% (15/781) are dead by other cause and 7.6% (59/781) are lost.

[MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Prostatic Neoplasms / pathology. Prostatic Neoplasms / surgery

[MeSH-minor] Biopsy. Disease-Free Survival. Humans. Male. Prognosis. Prostate-Specific Antigen / blood. Sensitivity and Specificity

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(PMID = 19013977.001).

[ISSN] 0210-4806

[Journal-full-title] Actas urologicas espanolas

[ISO-abbreviation] Actas Urol Esp

[Language] spa

[Publication-type] Comparative Study; English Abstract; Journal Article

[Publication-country] Spain

[Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen

   

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[Title] [Update of the treatment of advanced prostate cancer and management of its complications].

[Transliterated title] Actualización del tratamiento del cáncer de próstata avanzado y de sus complicaciones.

Prostate adenocarcinoma is the leading cause of cancer in Spain, among men older than 65.

1,200 new cases out of every 100,000 males are diagnosed with prostate cancer on an annual basis.

In the United States, this illness represents the second leading cause of death due to cancer in males.

In those patients whose prostate tumors progress after surgery or radiotherapy, or have metastatic disease when diagnosed, a systemic approach in order to improve their quality of life and overall survival is mandatory.

However, most of these tumors becomes androgen-independent over time and behave as a more aggressive cancer type.

The accurate knowledge of the symptoms due to disease spreading as well as treatment's side effects is necessary to provide an appropriate palliative management that contributes to an improvement of the quality of life in advanced prostate cancer patients.

[MeSH-major] Adenocarcinoma / therapy. Prostatic Neoplasms / therapy

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(PMID = 16324498.001).

[ISSN] 0025-7753

[Journal-full-title] Medicina clínica

[ISO-abbreviation] Med Clin (Barc)

[Language] spa

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Spain

[Number-of-references] 78

   

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[Title] Metastatic patterns in adenocarcinoma.

The authors analyzed clinical data from a large number of patients with histologically confirmed, distant-stage adenocarcinoma to evaluate metastatic patterns.

RESULTS: Three primary tumors had single, dominant metastatic sites: ovary to abdominal cavity (91%), prostate to bone (90%), and pancreas to liver (85%).

In a study of combinations of liver, abdominal cavity, and bone metastases, 86% of prostate primary tumors had only bone metastases, 80% of ovarian primary tumors had only abdominal cavity metastases, and 74% of pancreas primary tumors had only liver metastases.

A single organ was the dominant source of metastases in 7 sites: axillary lymph node from the breast (97%), intestinal lymph node from the colon (84%), thoracic lymph node from the lung (66%), brain from the lung (64%), mediastinal lymph node from the lung (62%), supraclavicular lymph node from the breast (51%), and adrenal gland from the lung (51%).

[MeSH-major] Adenocarcinoma / secondary. Algorithms. Neoplasm Metastasis. Registries / statistics & numerical data

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[Copyright] Copyright 2006 American Cancer Society.

(PMID = 16518827.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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BACKGROUND: Chronic inflammation is a risk factor for colorectal cancer (CRC) development.

Colonic adenocarcinoma developed after 20 weeks and a proteomics analysis based on two-dimensional gel electrophoresis and ultraflex TOF/TOF mass spectrometry was conducted in the cancerous and nontumorous tissue specimens.

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(PMID = 19491504.001).

[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/ PMC2699605

   

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[Title] Dose-escalated radiotherapy for high-risk prostate cancer: outcomes in modern era with short-term androgen deprivation therapy.

PURPOSE: Randomized data have supported the use of long-term androgen deprivation therapy (ADT) combined with radiotherapy (RT) for men with high-risk prostate cancer.

MATERIALS AND METHODS: A total of 184 men with any single risk factor of prostate-specific antigen >or=10 ng/mL, clinical Stage T2b or greater, or Gleason score >or=7 were treated with primary external beam RT for nonmetastatic adenocarcinoma of the prostate.

Univariate and multivariable analyses were performed for risk factors, including T stage, Gleason score, radiation dose, and prostate-specific antigen level.

On a subset analysis of high-risk patients (National Comprehensive Cancer Network criteria), those with clinical Stage T3 disease (4-year FFBF rate, 46% vs. 80%; p = .0303) and a radiation dose <74 Gy (4-year FFBF rate, 64% vs. 80%) had a poorer outcome on univariate analysis.

CONCLUSION: Short-term ADT and RT might be acceptable for men with intermediate- and high-risk prostate cancer, especially for clinically localized disease treated with doses of >or=74 Gy.

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(PMID = 19695789.001).

[ISSN] 1879-355X

[Journal-full-title] International journal of radiation oncology, biology, physics

[ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA090386-01; United States / NCI NIH HHS / CA / P50 CA090386; United States / NCI NIH HHS / CA / P50 CA090386-01

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Androgen Antagonists; EC 3.4.21.77 / Prostate-Specific Antigen

[Other-IDs] NLM/ NIHMS273199; NLM/ PMC3049990

   

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[Title] Complete loss of PTEN expression as a possible early prognostic marker for prostate cancer metastasis.

The EGF/IGF growth factors are potent mitogens that regulate cell proliferation and cell survival and are involved in prostate cancer development.

Using laser microdissection technology and real-time PCR, together with immunohistochemistry, we have explored the growth factor and integrin dependent PI3-kinase/PTEN/Akt signalling pathway in prostate cell lines and tumour samples by analysing EGF-R, IGF1-R, ILK, beta3 integrin, PTEN and p-Akt protein expression.

We provide evidence that loss of PTEN expression rather than upregulated EGF/IGF1 receptor expression was responsible for increased p-Akt in neoplastic prostate cells.

We therefore compared PTEN expression in patient biopsies at first time diagnosis recruited prospectively (Study I, 112 patients) and patients with confirmed metastasis recruited retrospectively from the Luxembourg cancer registry (Study II, 42 patients).

In Study I, loss of PTEN expression at first time diagnosis was found in 26 of 112 patients (23%).

In Study II, 25 of the 42 patients (59%) with lymph node metastasis had complete loss of PTEN expression in both the neoplastic glands of the prostate and the invasive prostate cancer cells in the lymph node, and of these 13 (52%) exhibited already loss of PTEN expression at first diagnosis.

These findings demonstrate that loss of PTEN expression is an important factor in progression towards metastatic disease and could potentially serve as an early prognostic marker for prostate cancer metastasis.

[MeSH-major] Adenocarcinoma / secondary. Biomarkers, Tumor / analysis. PTEN Phosphohydrolase / analysis. Prostate / pathology. Prostatic Neoplasms / pathology

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[Copyright] (c) 2006 Wiley-Liss, Inc.

(PMID = 17163422.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Integrin beta3; 0 / RNA, Messenger; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase

   

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[Title] Diet, vegetarian food and prostate carcinoma among men in Taiwan.

In a case-control study in a veterans hospital in Taiwan, we compared 237 histology-confirmed prostate carcinoma cases with 481 controls, frequency matched by age, for their consumption of vegetarian food, namely soybean products, rice, wheat protein and other vegetables.

The OR of prostate carcinoma for men with BMI < or =25 kg m(-2) was 1.74 (95% CI=1.21, 2.51), compared with men with higher BMI (>25 kg m(-2)).

This study suggests that the intake of the low fat local vegetarian food has a protective effect against prostate carcinoma for thin men in this study population.

[MeSH-major] Adenocarcinoma / epidemiology. Diet, Vegetarian. Prostatic Neoplasms / epidemiology

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(PMID = 16205693.001).

[ISSN] 0007-0920

[Journal-full-title] British journal of cancer

[ISO-abbreviation] Br. J. Cancer

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Other-IDs] NLM/ PMC2361673

   

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[Title] Induction of apoptosis in prostate cancer cells by pachymic acid from Poria cocos.

PLA(2) is elevated in prostatic adenocarcinoma and conversion of AA to prostaglandins leads to AKT pro-survival activity.

In this study, we investigated the effect of PA on the growth of human prostate cancer cells.

PA significantly reduced cell proliferation and induced apoptosis in a dose- and time-dependent fashion, with androgen-insensitive DU145 prostate cancer cells showing greater growth inhibition relative to androgen-responsive LNCaP.

[MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. Polyporales / metabolism. Prostatic Neoplasms / pathology. Triterpenes / metabolism

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[ErratumIn] Biochem Biophys Res Commun. 2006 Jan 6;339(1):457

(PMID = 15913545.001).

[ISSN] 0006-291X

[Journal-full-title] Biochemical and biophysical research communications

[ISO-abbreviation] Biochem. Biophys. Res. Commun.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BAD protein, human; 0 / Carrier Proteins; 0 / Coloring Agents; 0 / Prostaglandins; 0 / Proto-Oncogene Proteins; 0 / Terpenes; 0 / Triterpenes; 0 / bcl-Associated Death Protein; 29070-92-6 / pachymic acid; EC 2.7.11.1 / AKT1 protein, human; 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, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases

   

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[Title] Residual tumor potentially left behind after local ablation therapy in prostate adenocarcinoma.

PURPOSE: We examined contralateral prostate cancer potentially left behind by focal therapy.

There were 13 cases in which more than 0.5 cm(3) cancer was contralateral to the positive biopsy and 7 with predominantly anterior tumor.

CONCLUSIONS: In a highly selected population with limited unilateral biopsy cancer, tumor contralateral to the positive biopsy side at radical prostatectomy is typically small.

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[Cites] Technol Cancer Res Treat. 2004 Aug;3(4):365-70 [15270587.001]

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[CommentIn] J Urol. 2008 Jun;179(6):2091 [18423729.001]

(PMID = 18423736.001).

[ISSN] 1527-3792

[Journal-full-title] The Journal of urology

[ISO-abbreviation] J. Urol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P50 CA058236; United States / NCI NIH HHS / CA / CA 58236

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Other-IDs] NLM/ NIHMS374261; NLM/ PMC3353270

   

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Human prostate adenocarcinoma tumors implanted in mice were used as a system model.

[MeSH-major] Adenocarcinoma / diagnosis. Ferrosoferric Oxide / analysis. Fiber Optic Technology / methods. Fluorescent Dyes / analysis. Metal Nanoparticles / analysis. Microscopy, Confocal / methods. Microscopy, Fluorescence / methods. Prostatic Neoplasms / diagnosis. Rhodamines / analysis

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(PMID = 17445508.001).

[ISSN] 1535-3508

[Journal-full-title] Molecular imaging

[ISO-abbreviation] Mol Imaging

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Fluorescent Dyes; 0 / Liposomes; 0 / Rhodamines; 30IQX730WE / Polyethylene Glycols; XM0M87F357 / Ferrosoferric Oxide

   

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[Title] Activity and content of antioxidant enzymes in prostate tumors.

AIM: To investigate the antioxidant enzyme system in blood of men with benign hyperplasia of prostate (BHP) and with prostate adenocarcinoma (CaP).

Blood plasma and erythrocytes of men with prostate tumors served as the material for the studies; n = 15 for each group.

[MeSH-major] Antioxidants / metabolism. Erythrocytes / enzymology. Oxidoreductases / metabolism. Prostatic Hyperplasia / enzymology. Prostatic Neoplasms / enzymology

[MeSH-minor] Adenocarcinoma / blood. Adenocarcinoma / enzymology. Adenocarcinoma / pathology. Aged. Catalase / metabolism. Ceruloplasmin / metabolism. Glutathione / metabolism. Glutathione Peroxidase / metabolism. Glutathione Reductase / metabolism. Humans. Lipid Peroxidation. Male. Middle Aged. Superoxide Dismutase / metabolism. Thiobarbituric Acid Reactive Substances

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(PMID = 18806750.001).

[ISSN] 1812-9269

[Journal-full-title] Experimental oncology

[ISO-abbreviation] Exp. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Ukraine

[Chemical-registry-number] 0 / Antioxidants; 0 / Thiobarbituric Acid Reactive Substances; EC 1.- / Oxidoreductases; EC 1.11.1.6 / Catalase; EC 1.11.1.9 / Glutathione Peroxidase; EC 1.15.1.1 / Superoxide Dismutase; EC 1.16.3.1 / Ceruloplasmin; EC 1.8.1.7 / Glutathione Reductase; GAN16C9B8O / Glutathione

   

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[Title] The sphingosine kinase-1 survival pathway is a molecular target for the tumor-suppressive tea and wine polyphenols in prostate cancer.

The sphingosine kinase-1/sphingosine 1-phosphate (SphK1/S1P) pathway has been associated with cancer promotion and progression and resistance to treatments in a number of cancers, including prostate adenocarcinoma.

Here we provide the first evidence that dietary agents, namely, epigallocatechin gallate (EGCg, IC(50)≈75 μM), resveratrol (IC(50)≈40 μM), or a mixture of polyphenols from green tea [polyphenon E (PPE), IC(50)≈70 μM] or grapevine extract (vineatrol, IC(50)≈30 μM), impede prostate cancer cell growth in vitro and in vivo by inhibiting the SphK1/S1P pathway.

These results provide the first demonstration that the prosurvival, antiapoptotic SphK1/S1P pathway represents a target of dietary green tea and wine polyphenols in cancer.

[MeSH-major] Phosphotransferases (Alcohol Group Acceptor) / physiology. Prostatic Neoplasms / pathology. Tea / chemistry. Wine / analysis

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(PMID = 20522783.001).

[ISSN] 1530-6860

[Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology

[ISO-abbreviation] FASEB J.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Tea; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.- / sphingosine kinase

   

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[Title] The Swedish family-cancer database: update, application to colorectal cancer and clinical relevance.

The Swedish Family-Cancer Database has been used for almost 10 years in the study of familial risks at all common sites.

Cancer cases were retrieved from the Swedish Cancer Registry from 1958-2002, including over 1.2 million first and multiple primary cancers and in situ tumours.

Compared to previous versions, only 6.0% of deceased offspring with a cancer diagnosis lack any parental information.

We show one application of the Database in the study of familial risks in colorectal adenocarcinoma, with defined age-group and anatomic site specific analyses.

Familial standardized incidence ratios (SIRs) were determined for offspring when parents or sibling were diagnosed with colon or rectal cancer.

The excess risk was limited to colon cancer and particularly to right-sided colon cancer.

The SIRs for colon cancer in age matched populations were 2.58 when parents were probands and 3.81 when siblings were probands; for right-sided colon cancer the SIRs were 3.66 and 7.53, respectively.

Thus the familial excess (SIR-1.00) was more than two fold higher for right-sided colon cancer.

Useful risk estimates have been developed for familial breast and prostate cancers.

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(PMID = 20223029.001).

[ISSN] 1897-4287

[Journal-full-title] Hereditary cancer in clinical practice

[ISO-abbreviation] Hered Cancer Clin Pract

[Language] eng

[Publication-type] Journal Article

[Publication-country] Poland

[Other-IDs] NLM/ PMC2837068

   

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[Title] Immunohistochemical analysis of NF-kappaB signaling proteins IKKepsilon, p50/p105, p52/p100 and RelA in prostate cancers.

Activation of nuclear factor-kappa B (NF-kappaB) signaling is considered an important mechanism in the development of prostate cancers.

Expression of NF-kappaB members has been reported in prostate cancer tissues, but expression of IKKepsilon has not yet been studied in prostate cancers.

In this study, we attempted to explore as to whether expressions of IKKepsilon and NF-kappaB members p50/105, p52/p100 and RelA are altered in prostate cancers.

We analyzed the expression of IKKepsilon, p50/105, p52/p100 and RelA in 107 prostate adenocarcinoma tissues by immunohistochemistry using a tissue microarray (TMA) method.

In the TMA, IKKepsilon is expressed in basal cells, but not in alveolar cells in normal prostate glands.

IKKepsilon is expressed in 60.0% of prostate intraepithelial neoplasm (PIN) and 70.1% of the prostate cancers in the cytoplasm.

The increased cytoplasmic expression of IKKepsilon as well as the increased nuclear expressions of p50/105, p52/p100 and RelA in the prostate cancers compared to normal alveolar cells suggested that overexpression of these proteins may be related to activation of the NF-kappaB pathway and might play a role in tumorigenesis of prostate cancers.

[MeSH-major] Adenocarcinoma / pathology. I-kappa B Kinase / biosynthesis. NF-kappa B p50 Subunit / biosynthesis. NF-kappa B p52 Subunit / biosynthesis. Prostatic Neoplasms / pathology. Transcription Factor RelA / biosynthesis

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(PMID = 19664134.001).

[ISSN] 1600-0463

[Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica

[ISO-abbreviation] APMIS

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Denmark

[Chemical-registry-number] 0 / NF-kappa B p50 Subunit; 0 / NF-kappa B p52 Subunit; 0 / Transcription Factor RelA; EC 2.7.11.10 / I-kappa B Kinase

   

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[Title] [A case of prostate cancer diagnosed pathologically by bone metastatic site biopsy].

A 61-year-old man consulted our hospital complaining of high prostate specific antigen (PSA) value and difficulty to urinate.

Prostate biopsy had been performed at another hospital, but did not reveal cancer.

Transrectal ultrasound-guided prostate biopsy was performed, but cancer was not detected.

A repeat prostate biopsy was performed, but cancer was not detected from the prostate.

On right pubic bone biopsy, poorly to moderately differentiated adenocarcinoma was detected.

PSA immunohistochemical staining was positive, and the diagnosis was bone metastasis from prostate cancer.

[MeSH-major] Adenocarcinoma / diagnosis. Bone Neoplasms / secondary. Bone and Bones / pathology. Prostatic Neoplasms / diagnosis. Pubic Bone

[MeSH-minor] Biomarkers, Tumor / blood. Biopsy. Humans. Male. Middle Aged. Prostate-Specific Antigen / blood

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(PMID = 15948412.001).

[ISSN] 0021-5287

[Journal-full-title] Nihon Hinyōkika Gakkai zasshi. The japanese journal of urology

[ISO-abbreviation] Nippon Hinyokika Gakkai Zasshi

[Language] jpn

[Publication-type] English Abstract; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen

   

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[Title] S-100A1 is a reliable marker in distinguishing nephrogenic adenoma from prostatic adenocarcinoma.

In addition to its uncertain origin, there can be diagnostic difficulty in distinguishing nephrogenic adenoma from prostatic adenocarcinoma, particularly with lesions arising in the prostatic urethra.

Alpha-methylacyl-CoA racemase (AMACR), a recently identified prostate cancer marker, has also been found to be expressed in renal tubules and in some renal epithelial neoplasms.

In this study, we investigated the expression of S100A1 and AMACR in 18 nephrogenic adenomas and in 100 prostatic adenocarcinomas.

A strong and distinct cytoplasmic or nucleocytoplasmic staining of S100A1 was found in 17 out of 18 cases of nephrogenic adenoma (94%), but never in prostatic adenocarcinoma.

In contrast, AMACR expression was detected in 14 of 18 nephrogenic adenomas (78%) and in 96 of 100 prostatic adenocarcinomas (96%).

We conclude that (1) S100A1 is a specific and sensitive immunohistochemical marker to differentiate nephrogenic adenoma from prostatic adenocarcinoma;.

[MeSH-major] Adenocarcinoma / diagnosis. Adenoma / diagnosis. Prostatic Neoplasms / diagnosis. S100 Proteins / biosynthesis. Urogenital Neoplasms / diagnosis

[MeSH-minor] Biomarkers, Tumor / analysis. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Racemases and Epimerases / biosynthesis. Sensitivity and Specificity

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(PMID = 19384190.001).

[ISSN] 1532-0979

[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 / Biomarkers, Tumor; 0 / S100 Proteins; 0 / S100A1 protein; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase

   

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[Title] Differential expression of metallothioneins (MTs) 1, 2, and 3 in response to zinc treatment in human prostate normal and malignant cells and tissues.

BACKGROUND: The disturbance of zinc homeostasis featured with a significant decrease of cellular zinc level was well documented to associate with the development and progression of human prostate malignancy.

We have previously reported that zinc treatment induces prostate malignant cell apoptosis through mitochondrial pathway.

However, the studies on the expression of MT in association with the prostate pathological and malignant status are very limited, and the zinc regulation of MT isoform expression in prostate cells remains elusive.

The goals of this study were to define the expression of endogenous MTs, the isoforms of MT 1, 2, 3 at both messenger ribonucleic acid (mRNA) and protein levels; and to investigate the zinc effect on MT expression in normal prostate, benign prostatic hyperplasia (BPH) and malignant PC-3 cells, and in relevant human tissues.

RESULTS: Our results demonstrated a significant suppression of endogenous levels of MT1/2 in malignant PC-3 cells (95% reduction compared to the normal prostate cells) and in human adenocarcinoma tissues (73% MT1/2 negative).

CONCLUSION: This study provided evidence of the association of attenuated MT1/2 with prostate tumor progression, and the zinc induction of MT1/2 expression resulting in cellular zinc restoration.

The results suggest the potential of MT1/2 as a candidate biomarker for prostate cancer and the utilization of zinc in prostate cancer prevention and treatment.

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(PMID = 18208603.001).

[ISSN] 1476-4598

[Journal-full-title] Molecular cancer

[ISO-abbreviation] Mol. Cancer

[Language] ENG

[Grant] United States / PHS HHS / / R01-116815

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Messenger; 9038-94-2 / Metallothionein; J41CSQ7QDS / Zinc

[Other-IDs] NLM/ PMC2265743

   

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[Title] Genome-wide analysis of histone H3 lysine 27 trimethylation by ChIP-chip in gastric cancer patients.

In gastric cancer (GC), global and gene-specific DNA methylation changes have been demonstrated to occur.

[MeSH-major] Adenocarcinoma / genetics. DNA Methylation. Genome. Stomach Neoplasms / genetics

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(PMID = 19267258.001).

[ISSN] 0944-1174

[Journal-full-title] Journal of gastroenterology

[ISO-abbreviation] J. Gastroenterol.

[Language] eng

[Publication-type] Journal Article; Validation Studies

[Publication-country] Japan

[Chemical-registry-number] 0 / Histones

   

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[Title] Improved prostate cancer detection using systematic 14-core biopsy for large prostate glands with normal digital rectal examination findings.

OBJECTIVES: To evaluate in a retrospective study the improvements in prostate cancer detection rates for patients with a prostate gland larger than 30 cm3 using a systematic 14-core biopsy strategy compared with a systematic 8-core biopsy.

METHODS: We retrospectively assessed 273 patients with screened prostate-specific antigen (PSA) levels of 3.0 to 50.0 ng/mL.

A total of 204 patients with a prostate volume of 30 cm3 or larger and with normal digital rectal examination findings were enrolled in this study.

Of the 204 patients, 110 underwent 8-core biopsy and 94 underwent 14-core biopsy of the prostate.

We compared the cancer detection rates of prostate biopsy between the 8 and 14-core groups using total PSA, free/total PSA ratio, PSA density, and PSA density adjusted by transition zone volume.

RESULTS: Of the 204 patients, 40 (19.5%) were identified as having prostate adenocarcinoma.

The cancer detection rate for the 8 and 14-core groups was 14.5% (16 of 110 patients) and 24.5% (23 of 94 patients), respectively.

The 14-core biopsy had a statistically significant greater cancer detection rate than did the 8-core group in patients with a prostate volume of 30 to 40 cm3 (36.7% versus 11.8%, respectively, P<0.05) and a PSA density adjusted by transition zone volume of 0.38 ng/mL/cm3 or greater (47.8% versus 20.0%, respectively, P <0.05).

CONCLUSIONS: The 14-core prostate needle biopsy is a recommended method for detecting prostate cancer in a large-volume prostate gland without increasing the risk of complications.

[MeSH-major] Adenocarcinoma / pathology. Prostate / pathology. Prostatic Neoplasms / pathology

[MeSH-minor] Adult. Biomarkers, Tumor / blood. Biopsy, Needle. Digital Rectal Examination. Humans. Male. Neoplasm Staging. Organ Size. Prostate-Specific Antigen / blood. Retrospective Studies

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(PMID = 17070359.001).

[ISSN] 1527-9995

[Journal-full-title] Urology

[ISO-abbreviation] Urology

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen

   

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[Title] Re: Hara et al.: Decline of the red cell blood count in patients receiving androgen deprivation therapy for localized prostate cancer: impact of ADT on insulin-like growth factor 1 and erythropoesis. (Urology 2010;75:1441-1445).

[MeSH-major] Adenocarcinoma / drug therapy. Androgen Antagonists / adverse effects. Anemia / chemically induced. Antineoplastic Agents, Hormonal / adverse effects. Erythrocyte Count. Erythropoiesis / drug effects. Insulin-Like Growth Factor I / physiology. Prostatic Neoplasms / drug therapy. Receptor, IGF Type 1 / physiology

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[CommentOn] Urology. 2010 Jun;75(6):1441-5 [20110105.001]

(PMID = 20932425.001).

[ISSN] 1527-9995

[Journal-full-title] Urology

[ISO-abbreviation] Urology

[Language] eng

[Publication-type] Comment; Letter

[Publication-country] United States

[Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Recombinant Proteins; 11096-26-7 / Erythropoietin; 3XMK78S47O / Testosterone; 67763-96-6 / Insulin-Like Growth Factor I; EC 2.7.10.1 / Receptor, IGF Type 1

   

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[Title] Interleukin-8 increases vascular endothelial growth factor and neuropilin expression and stimulates ERK activation in human pancreatic cancer.

Although up-regulation of IL-8 is indicated in many cancers, its function in pancreatic cancer has not been well characterized.

In this study we examined the expression of IL-8 on pancreatic cancer cells and clinical tissue specimens, and investigated the effect of exogenous IL-8 on gene expression, and signaling in human pancreatic cancer cells.

We found that pancreatic cancer cells expressed higher amount of IL-8 mRNA than normal human pancreatic ductal epithelium cells.

IL-8 mRNA was also substantially overexpressed in 11 of 14 (79%) clinical pancreatic-adenocarcinoma samples compared with that in their surrounding normal tissues.

Exogenous IL-8 up-regulated the expression of vascular endothelial growth factor(165), and neuropilin (NRP)-2 in BxPC-3 cells, one of human pancreatic cancer cell lines.

Our studies suggest that IL-8 might be a malignant factor in human pancreatic cancer by induction of vascular endothelial growth factor and NRP-2 expression and ERK activation.

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(PMID = 18307536.001).

[ISSN] 1349-7006

[Journal-full-title] Cancer science

[ISO-abbreviation] Cancer Sci.

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / R01 HL083471; United States / NIBIB NIH HHS / EB / R01 EB002436; United States / NHLBI NIH HHS / HL / HL083471-02; United States / NIBIB NIH HHS / EB / EB002436-02; United States / NCCIH NIH HHS / AT / R21 AT003094-01; United States / NHLBI NIH HHS / HL / HL08347; United States / NIDCR NIH HHS / DE / DE015543-02; United States / NIDCR NIH HHS / DE / R01 DE015543; United States / NIDCR NIH HHS / DE / R01 DE015543-02; United States / NIBIB NIH HHS / EB / R01 EB002436-02; United States / NHLBI NIH HHS / HL / R01 HL083471-02; United States / NCCIH NIH HHS / AT / R21 AT003094; United States / NIBIB NIH HHS / EB / EB002436; United States / NCCIH NIH HHS / AT / AT003094-01; United States / NIDCR NIH HHS / DE / R01 DE15543

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Interleukin-8; 0 / Neuropilin-2; 0 / Vascular Endothelial Growth Factor A; 3G0H8C9362 / Cobalt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EVS87XF13W / cobaltous chloride

[Other-IDs] NLM/ NIHMS228014; NLM/ PMC2930017

   

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In non-transformed tissues CRASH was only detected in testis, brain, esophagus, prostate and proliferating endometrium.

Twenty-eight out of 42 endometrium tumors expressed CRASH at high levels as did 5/41 prostate carcinomas, as well as ovary and breast cancers, indicating a regulation of CRASH expression by sex hormones.

[MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Amino Acid Sequence. Animals. Antibodies, Monoclonal / immunology. Blotting, Western. Carcinoma, Transitional Cell / metabolism. Carcinoma, Transitional Cell / secondary. Cell Line, Tumor. Cystadenocarcinoma / metabolism. Cystadenocarcinoma / secondary. Female. Humans. Immunoenzyme Techniques. Mice. Mice, Inbred BALB C. Molecular Sequence Data. Prognosis. RNA, Small Interfering / pharmacology. Sequence Homology, Amino Acid

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(PMID = 19414332.001).

[ISSN] 0250-7005

[Journal-full-title] Anticancer research

[ISO-abbreviation] Anticancer Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Greece

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Autoantigens; 0 / RNA, Small Interfering; EC 3.5.1.- / ASRGL1 protein, human; EC 3.5.1.1 / Asparaginase

   

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Our study examines the relevance of serum serotonin levels to urinary bladder, prostate, renal, and testicular carcinoma when it comes to prognosis and occurrence of these oncological conditions.

MATERIALS AND METHODS: Serotonin levels were obtained in 109 patients presenting with urothelial carcinoma to the urinary bladder, adenocarcinoma of the prostate and renal cell carcinoma, as well as presenting with seminomatous and non-seminomatous testicular tumors.

In prostate carcinoma, serotonin levels showed a tendency with organ exceeding growth, Grading/Gleason Score, PSA values >100 ng/ml, and the presence of distant metastases.

CONCLUSION: Serotonin levels are suitable for prognostic evaluation of urothelial carcinoma in the urinary bladder, adenocarcinoma of the prostate, and renal cell carcinoma, especially taking into account the lab cost of 25<euro> per test.

[MeSH-minor] Adult. Aged. Aged, 80 and over. Carcinoma, Renal Cell / blood. Female. Humans. Male. Middle Aged. Prognosis. Prostatic Neoplasms / blood. Testicular Neoplasms / blood. Urinary Bladder Neoplasms / blood. Young Adult

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[Cites] Int J Immunopathol Pharmacol. 2007 Oct-Dec;20(4):765-70 [18179749.001]

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(PMID = 18581119.001).

[ISSN] 0724-4983

[Journal-full-title] World journal of urology

[ISO-abbreviation] World J Urol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Biomarkers, Tumor; 333DO1RDJY / Serotonin

   

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[Title] Second-line chemotherapy for prostate cancer: patient characteristics and survival.

PURPOSE: First-line chemotherapy with docetaxel in patients with progressive castrate metastatic prostate cancer has been shown to improve overall survival compared with mitoxantrone-based therapies.

PATIENTS AND METHODS: Patients with progressive castrate metastatic prostate cancer enrolled on an antimicrotubule-based protocol for treatment were followed to determine their baseline characteristics and outcomes with second- or third-line systemic therapy.

Corresponding prostate-specific antigen (PSA) decreases > or = 50% were observed in 72%, 15%, and 22% of patients.

[MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Prostatic Neoplasms / drug therapy

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(PMID = 16197608.001).

[ISSN] 1540-0352

[Journal-full-title] Clinical prostate cancer

[ISO-abbreviation] Clin Prostate Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / K30 CA05826

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / LSM4 protein, S cerevisiae; 0 / Ribonucleoprotein, U4-U6 Small Nuclear; 0 / Saccharomyces cerevisiae Proteins

   

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[Title] Epithelial-stromal tumor of the seminal vesicles in the transgenic adenocarcinoma mouse prostate model.

The transgenic adenocarcinoma mouse prostate (TRAMP) model, designed for researching human prostatic cancer, was genetically engineered to harbor a transgene composed of the simian virus 40 Large-T/small-t antigen promoted by the rat probasin gene.

In addition to prostatic neoplasms, the TRAMP mouse develops tumors in the seminal vesicles.

Some of the larger papillary, polypoid lesions exhibited a phyllodes pattern resembling that seen in mixed epithelial-stromal tumors of the breast, prostate, and seminal vesicles of humans.

Our recommended diagnosis of this lesion in the seminal vesicles is epithelial-stromal tumor.

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(PMID = 15872376.001).

[ISSN] 0300-9858

[Journal-full-title] Veterinary pathology

[ISO-abbreviation] Vet. Pathol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; 0 / Desmin; G34N38R2N1 / Bromodeoxyuridine

   

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[Title] The possibility of 'de novo' cancer in the prostate.

BACKGROUND: To investigate the possibility of 'de novo' prostate cancer by analyzing the relationship between high grade prostatic intraepithelial neoplasia (HGPIN) and latent prostate cancer.

MATERIALS AND METHODS: Latent prostate cancers found at autopsy were examined and 55 cancer foci with a poorly (Gleason grade 4 and 5) or moderately (Gleason grade 3) differentiated component were selected.

High grade intraepithelial neoplasia was defined as positive if it was observed within 2 mm from the edge of the cancer focus and the relationship between HGPIN and the two groups was investigated.

RESULTS: The MDG had 39 cancer foci (71.0%) and there were 16 in the SDG (29.0%).

In the MDG, 13 small-volume cancer foci were HGPIN positive, but in the SDG, none of the small-volume cancers were HGPIN positive.

CONCLUSIONS: Small-volume cancer foci without HGPIN in the SDG may be candidates for de novo prostate cancers.

[MeSH-major] Adenocarcinoma / pathology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology

[MeSH-minor] Aged. Aged, 80 and over. Autopsy. Diagnosis, Differential. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Retrospective Studies. Severity of Illness Index

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(PMID = 15948722.001).

[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

[Publication-country] Australia

   

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[Title] [Testicular metastasis of prostatic adenocarcinoma: a case report].

Metastasis of prostate adenocarcinoma to testis is an extremely rare occurrence.

Orchiectomy is necessary to confirm histopathological diagnosis.

Metastatic carcinoma of the prostate to the testis is a commonly accepted as a sign of disseminated disease.

We report a case of a 62-year-old patient who presented a prostatic carcinoma with a testicular metastasis.

[MeSH-major] Adenocarcinoma / secondary. Prostatic Neoplasms / pathology. Testicular Neoplasms / secondary

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(PMID = 17489329.001).

[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] Case Reports; English Abstract; Journal Article

[Publication-country] France

   

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[Title] Evaluation of the frequency of putative prostate cancer stem cells in primary and metastatic prostate cancer.

BACKGROUND: Tumour cells with a stem cell-like phenotype have recently been identified in prostate tumors and it has been suggested that this population may be responsible for the diversity of cell types within tumors and also for the initiation of metastases.

In this study we have, for the first time, assessed matched primary and bone marrow biopsies from prostate cancer patients for the distribution of cells carrying these and a number of other putative stem cell markers.

METHODS: Eleven matched (primary and bone metastasis) specimens from prostate cancer patients were assessed for the presence of cd133, cd44, alpha2beta1 integrin, CXCR4, c-met, alpha6 integrin, and nestin using immunohistochemistry and stain intensity and distribution scored.

[MeSH-major] Adenocarcinoma / secondary. Bone Neoplasms / secondary. Neoplastic Stem Cells / cytology. Prostatic Neoplasms / pathology

[MeSH-minor] Antigens, CD / metabolism. Biomarkers, Tumor / metabolism. Bone and Bones / metabolism. Bone and Bones / pathology. Cell Count. Humans. Immunohistochemistry. Integrins / metabolism. Intermediate Filament Proteins / metabolism. Male. Nerve Tissue Proteins / metabolism. Nestin. Prostate / metabolism. Prostate / pathology

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(PMID = 20127735.001).

[ISSN] 1097-0045

[Journal-full-title] The Prostate

[ISO-abbreviation] Prostate

[Language] eng

[Grant] United Kingdom / Medical Research Council / / G0900871

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / Integrins; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin

   

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[Title] Endoglin (CD105) expression in angiogenesis of colon cancer: analysis using tissue microarrays and comparison with other endothelial markers.

Some markers of angiogenic endothelial cells are emerging as targets of cancer therapy.

The present study compares the expression of CD105 with that of other endothelial markers in all tissue layers during the development of colon cancer.

We examined sections from endoscopic mucosal resection and surgical resection of tubular adenoma (n=31), carcinoma in adenoma (n=11), and adenocarcinoma (n=34).

In contrast, cancer-associated blood vessels (up to 80%) and cancer cells themselves expressed high levels of CD105.

In normal mucosa, CD105 was weakly expressed in endothelial cells of capillaries (< or =21%), and significant differences in its expression in endothelial cells between the normal mucosa and adenoma, carcinoma in adenoma, and adenocarcinoma were found.

Flt-1, Flk-1, transforming growth factor-beta1, transforming growth factor-beta receptor II, and CD44 were strongly expressed in the cancer cells but were not expressed in the blood vessels.

The present study shows that de novo blood vessels of colon cancer specifically express CD105.

These findings provide the basis for novel antiangiogenic cancer therapies.

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(PMID = 16177881.001).

[ISSN] 0945-6317

[Journal-full-title] Virchows Archiv : an international journal of pathology

[ISO-abbreviation] Virchows Arch.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD31; 0 / Biomarkers, Tumor; 0 / ENG protein, human; 0 / Endoglin; 0 / Receptors, Cell Surface

   

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[Title] Immunohistochemical analysis of Fas and FLIP in prostate cancers.

Fas-mediated apoptosis is considered a principal pathway for apoptosis induction in normal and cancer cells.

Expression of Fas has been reported in prostate tissues several times, but the data were not consistent.

Expression of FLICE-like inhibitory protein (FLIP), an inhibitor of Fas-mediated apoptosis, has not been studied by immunohistochemistry in prostate tissues.

The aim of this study is to explore whether alterations of Fas and FLIP expression occur in prostate cancer tissues.

We analyzed the expression of Fas and FLIP in 107 prostate adenocarcinoma tissues by immunohistochemistry using a tissue microarray approach.

Prostate intraepithelial neoplasm also showed a strong Fas immunoreactivity.

The decreased expression of Fas in a large fraction of prostate cancers compared with their normal cells suggested that loss of Fas expression might play a role in tumorigenesis in some prostate cancers possibly by inhibiting apoptosis mediated by Fas.

[MeSH-major] Adenocarcinoma / metabolism. Antigens, CD95 / metabolism. CASP8 and FADD-Like Apoptosis Regulating Protein / metabolism. Prostate / metabolism. Prostatic Neoplasms / metabolism

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(PMID = 19161534.001).

[ISSN] 1600-0463

[Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica

[ISO-abbreviation] APMIS

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Denmark

[Chemical-registry-number] 0 / Antigens, CD95; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein

   

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[Title] Identification of genes potentially involved in the acquisition of androgen-independent and metastatic tumor growth in an autochthonous genetically engineered mouse prostate cancer model.

BACKGROUND: A major focus of prostate cancer research has been to identify genes that are deregulated during tumor progression, potentially providing diagnostic markers and therapeutic targets.

METHODS: We have employed serial analysis of gene expression (SAGE) and microarray hybridization to identify alterations that occur during malignant transformation in the Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) model.

CONCLUSIONS: Our analyses identified well-characterized genes that were previously known to be involved in prostate cancer, validating our study, and also uncovered transcripts that had not previously been implicated in prostate cancer progression.

[MeSH-major] Adenocarcinoma / genetics. Androgens / genetics. Disease Models, Animal. Gene Expression Profiling. Genes, Neoplasm / physiology. Genetic Engineering / methods. Oligonucleotide Array Sequence Analysis. Prostatic Neoplasms / genetics

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[Copyright] (c) 2006 Wiley-Liss, Inc.

(PMID = 17013881.001).

[ISSN] 1097-0045

[Journal-full-title] The Prostate

[ISO-abbreviation] Prostate

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA73747; United States / NCI NIH HHS / CA / CA84296

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Validation Studies

[Publication-country] United States

[Chemical-registry-number] 0 / Androgens

   

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[Title] A genome-wide screen for promoter methylation in lung cancer identifies novel methylation markers for multiple malignancies.

However, DNA methylation markers that are highly specific and sensitive for common tumors would be useful for the early detection of cancer, and those required for the malignant phenotype would identify pathways important as therapeutic targets.

METHODS AND FINDINGS: In an effort to identify new cancer-specific methylation markers, we employed a high-throughput global expression profiling approach in lung cancer cells.

We identified 132 genes that have 5' CpG islands, are induced from undetectable levels by 5-aza-2'-deoxycytidine in multiple non-small cell lung cancer cell lines, and are expressed in immortalized human bronchial epithelial cells.

Methylation analysis of a subset (45/132) of these promoter regions in primary lung cancer (n = 20) and adjacent nonmalignant tissue (n = 20) showed that 31 genes had acquired methylation in the tumors, but did not show methylation in normal lung or peripheral blood cells.

We studied the eight most frequently and specifically methylated genes from our lung cancer dataset in breast cancer (n = 37), colon cancer (n = 24), and prostate cancer (n = 24) along with counterpart nonmalignant tissues.

CONCLUSIONS: By using a systematic biological screen we identified multiple genes that are methylated with high penetrance in primary lung, breast, colon, and prostate cancers.

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[CommentIn] PLoS Med. 2006 Dec;3(12):e479 [17194184.001]

(PMID = 17194187.001).

[ISSN] 1549-1676

[Journal-full-title] PLoS medicine

[ISO-abbreviation] PLoS Med.

[Language] ENG

[Databank-accession-numbers] GEO/ GSE5816

[Grant] United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / U01 CA084971; United States / NCI NIH HHS / CA / P50CA70907; United States / NCI NIH HHS / CA / U01CA84971

[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 / CCNA1 protein, human; 0 / Cyclin A; 0 / Cyclin A1; 0 / DNA-Binding Proteins; 0 / MSX1 Transcription Factor; 0 / MSX1 protein, human; 0 / Transcription Factors; 148814-46-4 / BNC1 protein, human; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; EC 3.4.- / Cathepsins; EC 3.4.22.38 / CTSK protein, human; EC 3.4.22.38 / Cathepsin K; M801H13NRU / Azacitidine

[Other-IDs] NLM/ PMC1716188

   

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[Title] Radical prostatectomy for prostatic adenocarcinoma: a matched comparison of open retropubic and robot-assisted techniques.

PATIENTS AND METHODS: From August 2002 to December 2005 we identified 294 patients undergoing RARP for clinically localized prostate cancer.

A comparison RRP group of 588 patients from the same period was matched 2:1 for surgical year, age, preoperative prostate-specific antigen level, clinical stage and biopsy Gleason grade.

[MeSH-major] Adenocarcinoma / surgery. Intraoperative Complications / etiology. Postoperative Complications / etiology. Prostatectomy / methods. Prostatic Neoplasms / surgery. Robotics

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(PMID = 18778350.001).

[ISSN] 1464-410X

[Journal-full-title] BJU international

[ISO-abbreviation] BJU Int.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] England

   

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[Title] Sorafenib's inhibition of prostate cancer growth in transgenic adenocarcinoma mouse prostate mice and its differential effects on endothelial and pericyte growth during tumor angiogenesis.

OBJECTIVE: To evaluate Sorafenib's efficacy (60 mg/kg/d per os) in preventing the transformation of high grade prostate intraepithelial neoplasia (HGPIN) into adenocarcinoma (ADC) and in inhibiting the onset and progression of poorly differentiated carcinoma (PDC) in transgenic adenocarcinoma mouse prostate (TRAMP) mice.

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(PMID = 20701066.001).

[ISSN] 0884-6812

[Journal-full-title] Analytical and quantitative cytology and histology

[ISO-abbreviation] Anal. Quant. Cytol. Histol.

[Language] ENG

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib

   

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Our understanding of cancer has largely come from the analysis of aberrations within the tumor cell population.

We demonstrate that this indeed occurs in a mouse model of prostate cancer where epithelial cell cycle disruption via cell-specific inhibition of pRb function induces a paracrine p53 response that suppresses fibroblast proliferation in associated stroma.

[MeSH-minor] Actins / analysis. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Animals. Antigens, Polyomavirus Transforming / genetics. Cell Proliferation. Connective Tissue / pathology. Disease Models, Animal. Gene Deletion. Genotype. Keratin-8. Keratins / analysis. Loss of Heterozygosity / genetics. Male. Mice. Mice, Knockout. Mice, Transgenic. Models, Biological. Paracrine Communication. Prostate / metabolism. Prostate / pathology. Prostatic Neoplasms / genetics. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. Retinoblastoma Protein / metabolism. S100 Proteins / analysis

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[CommentIn] Cell. 2005 Dec 16;123(6):985-7 [16360028.001]

(PMID = 16360031.001).

[ISSN] 0092-8674

[Journal-full-title] Cell

[ISO-abbreviation] Cell

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01-CA046283; United States / NCI NIH HHS / CA / U01-CA84294

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Actins; 0 / Antigens, Polyomavirus Transforming; 0 / Keratin-8; 0 / Krt8 protein, mouse; 0 / Retinoblastoma Protein; 0 / S100 Proteins; 0 / S100a4 protein, mouse; 0 / Tumor Suppressor Protein p53; 68238-35-7 / Keratins

   

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[Title] Down-regulation of p57Kip2 induces prostate cancer in the mouse.

However, little is known about the role of p57(Kip2) in tumorigenesis and cancer progression.

Here, we show that the expression of p57(Kip2) is significantly decreased in human prostate cancer, and the overexpression of p57(Kip2) in prostate cancer cells significantly suppressed cell proliferation and reduced invasive ability.

In addition, overexpression of p57(Kip2) in LNCaP cells inhibited tumor formation in nude mice, resulting in well-differentiated squamous tumors rather than adenocarcinoma.

Furthermore, the prostates of p57(Kip2) knockout mice developed prostatic intraepithelial neoplasia and adenocarcinoma.

Remarkably, this mouse prostate cancer is pathologically identical to human prostate adenocarcinoma.

Therefore, these results strongly suggest that p57(Kip2) is an important gene in prostate cancer tumorigenesis, and the p57(Kip2) pathway may be a potential target for prostate cancer prevention and therapy.

[MeSH-major] Cyclin-Dependent Kinase Inhibitor p57 / biosynthesis. Down-Regulation. Gene Expression Regulation, Neoplastic. Prostatic Neoplasms / metabolism

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(PMID = 18483241.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01-CA116097; United States / NCI NIH HHS / CA / R01-CA76142

[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 / Cdkn1c protein, mouse; 0 / Cyclin D; 0 / Cyclin-Dependent Kinase Inhibitor p57; 0 / Cyclins; 0 / Retinoblastoma Protein; EC 2.7.11.22 / Cdk2 protein, mouse; EC 2.7.11.22 / Cdk4 protein, mouse; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 2.7.11.22 / Cyclin-Dependent Kinase 4

   

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[Title] The dual 5-alpha-reductase inhibitor dutasteride induces atrophic changes and decreases relative cancer volume in human prostate.

OBJECTIVES: To perform the first evaluation of the effects of the 5-alpha-reductase inhibitor class of drugs on cancer histopathologic features at radical prostatectomy in a placebo-controlled multicenter trial.

The histopathologic features of benign epithelium, high-grade prostatic intraepithelial neoplasia, and cancer were recorded, and the treatment effect was scored.

Digital imaging analysis was used to measure the stroma/epithelium ratio and epithelial height, as well as the nuclear area in cancer.

In cancer tissue, the tumor volume was significantly lower in the dutasteride-treated men than in the placebo-treated men (mean 15% versus 24%, respectively, P = 0.025), the percentage of atrophic epithelium was increased (P = 0.041), and the stroma/gland ratio was doubled (P = 0.046).

CONCLUSIONS: After short-term dutasteride treatment, benign epithelium showed involution and epithelial shrinkage, and prostate cancer tissue demonstrated a decrease in epithelium relative to stroma.

These findings indicate that dutasteride induces significant phenotypic alterations in both the benign and the neoplastic prostate, supportive of a chemopreventive or chemoactive role.

[MeSH-major] 5-alpha Reductase Inhibitors. Adenocarcinoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Azasteroids / therapeutic use. Neoplasm Proteins / antagonists & inhibitors. Prostate / drug effects. Prostatic Neoplasms / drug therapy

[MeSH-minor] Aged. Atrophy. Combined Modality Therapy. Double-Blind Method. Dutasteride. Epithelial Cells / drug effects. Epithelial Cells / pathology. Humans. Image Processing, Computer-Assisted. Male. Middle Aged. Neoadjuvant Therapy. Pilot Projects. Prostatectomy. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Intraepithelial Neoplasia / enzymology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Intraepithelial Neoplasia / surgery. Stromal Cells / drug effects. Stromal Cells / pathology

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(PMID = 15667867.001).

[ISSN] 1527-9995

[Journal-full-title] Urology

[ISO-abbreviation] Urology

[Language] eng

[Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] United States

[Chemical-registry-number] 0 / 5-alpha Reductase Inhibitors; 0 / Antineoplastic Agents, Hormonal; 0 / Azasteroids; 0 / Neoplasm Proteins; O0J6XJN02I / Dutasteride

   

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All patients had undergone extrafascial perineal prostatectomy for Stage cT1-cT3N0M0 prostate cancer.

[MeSH-minor] Adenocarcinoma / complications. Adenocarcinoma / radiotherapy. Adenocarcinoma / surgery. Aged. Anal Canal / innervation. Anal Canal / physiopathology. Humans. Incidence. Male. Middle Aged. Perineum / surgery. Prospective Studies. Prostatic Neoplasms / complications. Prostatic Neoplasms / radiotherapy. Prostatic Neoplasms / surgery. Radiotherapy, Adjuvant. Surveys and Questionnaires

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(PMID = 15708049.001).

[ISSN] 1527-9995

[Journal-full-title] Urology

[ISO-abbreviation] Urology

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Lysosomal and prostasomal hydrolytic enzymes and redox processes and initiation of prostate cancer.

Lysosomes, lysosomal enzymes and oxidant processes are known to be involved in cancer processes.

However, integrated biochemical and cell biology studies are necessary to understand how lysosomal enzymes and prostasomal enzymes combined with oxidant processes could initiate cancer.

Most prostate cancer is likely to be initiated in the prostate duct system.

The lysosomal enzymes acid phosphatase and glucosidase and prostasomal proteins and enzymes are found in human semen and therefore have come through prostate ducts.

The hypothesis presented here is that the lysosomal enzymes and prostasomes are exocytosed from prostate cells into the duct system of the prostate where their hydrolytic enzymes and oxidative processes, for example, the iron from the iron-sulfur clusters of the prostasomal dehydrogenases, damage proteins and other components of cells leading to the initiation of cancer.

Risk factors for prostate cancer are known to initiate activity of lysosomal enzymes and could initiate activity of prostasomal enzymes.

Other dietary components in fruits and vegetables protect against prostate cancer and can be hypothesized as decreasing cellular output of lysosomal or protasomal enzymes or inhibiting lysosomal and prostasomal enzymes in the duct system.

Measurements of multiple lysosomal and prostasomal enzyme activities and their biochemical pathways are vital to the understanding of protectors to inhibit lysosomal or prostasomal enzyme activities that might be leading to prostate cancer.

Lysosomal enzyme activities may be precursors to the onset of other kinds of cancer with other similar non-invasive screening techniques possible.

This overall hypothesis suggests protection against prostate cancer by inhibitors of lipid peroxidation including the dietary antioxidants selenium, vitamin E and lycopene and also cysteine glutathione.

[MeSH-major] Adenocarcinoma / etiology. Cell Transformation, Neoplastic / metabolism. Lysosomes / enzymology. Models, Biological. Prostatic Neoplasms / etiology

[MeSH-minor] Animals. Anticarcinogenic Agents / therapeutic use. Antioxidants / therapeutic use. Cocarcinogenesis. Diet. Enzyme Activation. Enzyme Inhibitors / therapeutic use. Exocytosis. Humans. Hydrolysis. Lipid Peroxidation. Male. Organelles / enzymology. Oxidation-Reduction. Prostate / ultrastructure. Risk Factors

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(PMID = 15823710.001).

[ISSN] 0306-9877

[Journal-full-title] Medical hypotheses

[ISO-abbreviation] Med. Hypotheses

[Language] eng

[Publication-type] Journal Article

[Publication-country] Scotland

[Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antioxidants; 0 / Enzyme Inhibitors

   

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[Title] Overexpression of Pim-1 during progression of prostatic adenocarcinoma.

Recently, evidence has shown Pim-1 to be important in prostatic carcinogenesis.

In order to further our understanding of its role in prostate cancer, we investigated Pim-1 expression in normal, premalignant, and malignant prostate tissue.

METHODS: Using immunohistochemistry, Pim-1 expression was analysed in prostate tissue from 120 radical prostatectomy specimens.

In each case, Pim-1 staining was evaluated in benign prostatic epithelium, high grade prostatic intraepithelial neoplasia (PIN), and prostatic adenocarcinoma.

RESULTS: Pim-1 immunoreactivity was identified in 120 cases (100%) of adenocarcinoma, 120 cases (100%) of high grade PIN, and 62 cases (52%) of benign glands.

The number of cells staining in benign epithelium (mean 34%) was much lower than that in high grade PIN (mean 80%; p<0.0001) or adenocarcinoma (mean, 84%; p<0.0001).

There was no significant difference between high grade PIN and adenocarcinoma in the percentage of cells staining positively for Pim-1 (p = 0.34).

The staining intensity for Pim-1 was significantly lower in benign prostatic epithelium than in PIN and adenocarcinoma (p<0.001).

CONCLUSIONS: Pim-1 expression is elevated in PIN and prostatic adenocarcinoma compared with benign prostatic epithelium.

This finding suggests that upregulation of Pim-1 may play a role in prostatic neoplasia.

[MeSH-major] Adenocarcinoma / chemistry. Biomarkers, Tumor / analysis. Prostatic Neoplasms / chemistry. Proto-Oncogene Proteins c-pim-1 / analysis

[MeSH-minor] Aged. Analysis of Variance. Disease Progression. Humans. Male. Middle Aged. Neoplasm Staging. Prostatectomy. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / surgery. Prostatic Intraepithelial Neoplasia / chemistry. Prostatic Intraepithelial Neoplasia / surgery. Sensitivity and Specificity

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(PMID = 16505280.001).

[ISSN] 0021-9746

[Journal-full-title] Journal of clinical pathology

[ISO-abbreviation] J. Clin. Pathol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.11.1 / Proto-Oncogene Proteins c-pim-1

[Other-IDs] NLM/ PMC1860332

   

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[Title] Toxicity and early treatment outcomes in low- and intermediate-risk prostate cancer managed by high-dose-rate brachytherapy as a monotherapy.

METHODS AND MATERIALS: Between October 2003 and June 2006, 36 patients with low (28) and intermediate (8) risk prostate cancer (PCA) were treated by HDR-B monotherapy.

[MeSH-major] Adenocarcinoma / radiotherapy. Brachytherapy / adverse effects. Iridium Radioisotopes / adverse effects. Prostatic Neoplasms / radiotherapy. Urethra / radiation effects

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(PMID = 19038584.001).

[ISSN] 1538-4721

[Journal-full-title] Brachytherapy

[ISO-abbreviation] Brachytherapy

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Iridium Radioisotopes

   

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Comparing the yield of parasagittal biopsies during initial saturation biopsy to the yield during repeat saturation biopsy for detection of prostate cancer.

Office-based saturation biopsy (24 cores) with periprostatic lidocaine block was performed in 139 consecutive men who had never previously undergone prostate biopsy.

Indication for biopsy was elevated prostate-specific antigen >2.5 ng/dl.

Subanalysis of patients from this unique study was performed to compare the location of saturation biopsy cancer detection in these patients to a cohort of 100 patients who had previously undergone biopsy with nonmalignant findings.

In the initial biopsy group, cancer was detected in 62/139 patients (44.6%).

Breakdown of cancer location demonstrated unique parasagittal cancers in 9/62 patients (14.5%).

Laterally base cancer was found exclusively in 22/62 patients (35.5%).

For the repeat biopsy population, cancer was found in 25 patients (25%); no patients (0%) had exclusive parasagittal cancer.

The exclusive parasagittal cancer detection rate decreases significantly in the repeat biopsy population when using the same biopsy method.

Our findings support including traditional template parasagittal sampling of the prostate on first-time biopsy in addition to lateral cores typical of extended field biopsies for a total of 10-12 cores.

[MeSH-major] Adenocarcinoma / pathology. Prostate / pathology. Prostatic Neoplasms / pathology

[MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy. Cohort Studies. Early Diagnosis. Humans. Male. Middle Aged. Prospective Studies

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(PMID = 17420763.001).

[ISSN] 1476-5608

[Journal-full-title] Prostate cancer and prostatic diseases

[ISO-abbreviation] Prostate Cancer Prostatic Dis.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

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[Title] Flexible sigmoidoscopy in the PLCO cancer screening trial: results from the baseline screening examination of a randomized trial.

BACKGROUND: The Prostate, Lung, Colorectal and Ovarian (PLCO) cancer screening trial is a randomized clinical trial to test the effectiveness of cancer screening, including the effect of flexible sigmoidoscopy screening on colorectal cancer mortality.

The yields per 1000 screened, depending on 5-year age group, were as follows: for colorectal cancer, 1.1-2.5 in women and 2.4-5.6 in men; for advanced adenoma, 18.0-30.4 in women and 36.1-49.1 in men; and for colorectal cancer or any adenoma, 50.6-79.6 in women and 101.9-128.6 in men.

Approximately 77% (130/169) of the colorectal adenocarcinoma patients were stage I or II at diagnosis.

Diagnostic follow-up varied according to polyp size, yet cancer or adenoma detection rates met expectations.

[MeSH-major] Colorectal Neoplasms / diagnosis. Colorectal Neoplasms / mortality. Mass Screening / methods. Sigmoidoscopy

[MeSH-minor] Adenoma / diagnosis. Adenoma / mortality. Age Distribution. Aged. Carcinoma / diagnosis. Carcinoma / mortality. Colonic Polyps / diagnosis. Colonic Polyps / mortality. Female. Humans. Male. Middle Aged. Sex Distribution. Surveys and Questionnaires. United States / epidemiology

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(PMID = 15998952.001).

[ISSN] 1460-2105

[Journal-full-title] Journal of the National Cancer Institute

[ISO-abbreviation] J. Natl. Cancer Inst.

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

   

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Using the final diagnosis as the reference standard, we evaluated the diagnostic usefulness of each investigation.

The primary was located in the lung in 37 patients, prostate in 26, breast or female genital tract in 24, urinary system in 11, gastrointestinal tract in 11, head and neck in 6, and other organs in 4.

The histological biopsy findings indicated adenocarcinoma in 58 cases, epidermoid carcinoma in 28 cases, undifferentiated carcinoma in 2 cases, and other histological patterns in 9 cases.

Tumor marker assays were of limited value for determining the site of the primary, with the exception of prostate-specific antigen.

[MeSH-major] Bone Neoplasms / diagnosis. Bone Neoplasms / secondary. Neoplasms, Unknown Primary / diagnosis

[MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor. Biopsy. Bone and Bones / pathology. Breast Neoplasms / diagnosis. Breast Neoplasms / pathology. Cohort Studies. Diagnostic Imaging. Female. Humans. Lung Neoplasms / diagnosis. Lung Neoplasms / pathology. Male. Middle Aged. Retrospective Studies. Sensitivity and Specificity. Urogenital Neoplasms / diagnosis. Urogenital Neoplasms / pathology

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[CommentIn] Joint Bone Spine. 2008 Jan;75(1):100; author reply 100-1 [18083617.001]

(PMID = 17218141.001).

[ISSN] 1778-7254

[Journal-full-title] Joint, bone, spine : revue du rhumatisme

[ISO-abbreviation] Joint Bone Spine

[Language] eng

[Publication-type] Evaluation Studies; Journal Article

[Publication-country] France

[Chemical-registry-number] 0 / Biomarkers, Tumor