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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Randomized phase II study of atrasentan alone or in combination with zoledronic acid in men with metastatic prostate cancer.

BACKGROUND: Metastatic prostate cancer is characterized by the presence of osteoblastic bone metastases.

Bone metastases account for most of the morbidity from this disease.

METHODS: The effects of atrasentan alone versus combination therapy with atrasentan and zoledronic acid were investigated on bone turnover markers in men with bone metastases from prostate cancer.

There was minimal clinical efficacy, with no objective responses and only 1 prostate-specific antigen (PSA) response.

CONCLUSIONS: There is no evidence for additive or synergistic effects of combination therapy with atrasentan and zoledronic acid on bone turnover markers in men with metastatic prostate cancer.

[MeSH-minor] Aged. Aged, 80 and over. Alkaline Phosphatase / analysis. Biomarkers, Tumor / analysis. Bone Density Conservation Agents / administration & dosage. Bone Density Conservation Agents / adverse effects. Bone Neoplasms / metabolism. Bone Neoplasms / secondary. Bone and Bones / enzymology. Bone and Bones / metabolism. Disease Progression. Dyspnea / complications. Edema / complications. Humans. Male. Middle Aged. Neoplasm Metastasis. Treatment Outcome

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[Copyright] Copyright 2006 American Cancer Society.

(PMID = 16804927.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / 1K12CA87723

[Publication-type] Clinical Trial, Phase II; 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 / Biomarkers, Tumor; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 0 / Pyrrolidines; 6XC1PAD3KF / zoledronic acid; EC 3.1.3.1 / Alkaline Phosphatase; V6D7VK2215 / atrasentan

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Identification of enhancer of zeste homolog 2 expression in peripheral circulating tumor cells in metastatic prostate cancer patients: a preliminary study.

PURPOSE: Enhancer of zeste homolog 2 (EZH2), a kind of transcriptional repressor, is reportedly over-expressed in metastatic prostate cancer.

In this study, we analyzed EZH2 mRNA in circulating tumor cells (CTCs) in peripheral blood as a biomarker in patients with metastatic prostate cancer.

The sensitivity of this test for detection of EZH2 mRNA was determined by serial dilutions of a human prostate cancer cell line.

Blood samples were collected from 20 patients each with metastatic or localized prostate cancer and 10 healthy volunteers.

RESULTS: Sensitivity experiments showed that the test was highly sensitive as it could detect 10 tumor cells per 5 mL.

EZH2 mRNA expression density in the metastatic prostate cancer group was significantly higher than in the control (p=0.023) and localized prostate cancer groups (p=0.019).

There was no difference between the control and localized prostate cancer groups (p > 0.05).

CONCLUSION: EZH2 mRNA expression in circulating epithelial cells represents a promising marker for detecting early metastasis in prostate cancer.

[MeSH-minor] Aged. Humans. Male. Middle Aged. Neoplasm Metastasis. Polycomb Repressive Complex 2. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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[Cites] Clin Cancer Res. 2002 Jun;8(6):1794-9 [12060619.001]

[Cites] Prostate. 2007 Apr 1;67(5):547-56 [17252556.001]

[Cites] Urology. 2003 Feb;61(2):277-81 [12597930.001]

[Cites] J Natl Cancer Inst. 2003 May 7;95(9):661-8 [12734317.001]

[Cites] J Urol. 2000 Jun;163(6):2022-9 [10799250.001]

[Cites] J Urol. 2000 Jul;164(1):101-5 [10840432.001]

[Cites] J Urol. 2001 Aug;166(2):416-9 [11458039.001]

[Cites] Urology. 2001 Sep;58(3):386-92 [11549486.001]

[Cites] J Urol. 2002 Feb;167(2 Pt 1):528-34 [11792912.001]

[Cites] Br J Cancer. 2004 Jan 26;90(2):443-8 [14735191.001]

[Cites] Cancer Res. 1992 Nov 1;52(21):6110-2 [1382851.001]

[Cites] Urology. 1994 Jun;43(6):765-75 [7515202.001]

[Cites] Cancer Res. 1994 Dec 15;54(24):6306-10 [7527294.001]

[Cites] J Clin Oncol. 1994 Dec;12(12):2634-9 [7527455.001]

[Cites] J Clin Oncol. 1995 May;13(5):1195-200 [7537803.001]

[Cites] Cancer. 1996 Jul 1;78(1):10-6 [8646704.001]

[Cites] J Urol. 1996 Nov;156(5):1560-6 [8863538.001]

[Cites] Urology. 1997 Aug;50(2):184-8 [9255285.001]

[Cites] J Clin Oncol. 1997 Dec;15(12):3451-7 [9396397.001]

[Cites] Urology. 2005 Mar;65(3):616-21 [15780403.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Aug 23;102(34):12177-82 [16091473.001]

[Cites] Genes Chromosomes Cancer. 2006 Jul;45(7):639-45 [16575874.001]

[Cites] Nature. 2002 Oct 10;419(6907):624-9 [12374981.001]

(PMID = 18159594.001).

[ISSN] 0513-5796

[Journal-full-title] Yonsei medical journal

[ISO-abbreviation] Yonsei Med. J.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Korea (South)

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Polycomb Repressive Complex 2

[Other-IDs] NLM/ PMC2628187

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Immunotherapy for metastatic prostate cancer.

Chemotherapy with docetaxel is the standard treatment for men with metastatic prostate cancer, and results in statistically significant improvements in survival, as well as in quality of life.

More significantly, with the onset of early, PSA-based detection of prostate cancer and closer follow-up, many men present with metastatic disease that remains asymptomatic.

Immunotherapy represents one such approach; a number of clinical trials have suggested a survival benefit for immunotherapy in metastatic prostate cancer and confirmed that these agents are generally well-tolerated.

This review will discuss the mechanisms of action of several immunotherapy approaches for metastatic prostate cancer, focusing on active immunotherapy as opposed to administration of anti-tumor antibodies.

[MeSH-minor] Dendritic Cells / immunology. Granulocyte-Macrophage Colony-Stimulating Factor / genetics. Humans. Male. Neoplasm Metastasis

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(PMID = 18593624.001).

[ISSN] 1078-1439

[Journal-full-title] Urologic oncology

[ISO-abbreviation] Urol. Oncol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P30 CA006973

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor

[Number-of-references] 36

[Other-IDs] NLM/ NIHMS787032; NLM/ PMC4886229

   

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prognostic factors affecting progression and survival in metastatic prostate cancer.

PURPOSE: To evaluate the role of age, Gleason score, prostate-specific antigen (PSA), PSA doubling time (PSADT), and PSA half-time (PSAT(1/2)) as prognostic factors in metastatic prostate cancer to predict long-term outcome.

PATIENTS AND METHODS: 412 patients with metastatic prostate cancer diagnosed after January 1995, with at least 6 months of follow-up, were enrolled.

Serum PSA was determined at diagnosis and every 3-6 months thereafter.

Patients aged <or=65 years at diagnosis, high baseline PSA and high nadir PSA were associated with poor overall survival.

CONCLUSION: Prostate cancer is a common malignancy in the elderly population.

[MeSH-major] Prostate-Specific Antigen / blood. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / mortality

[MeSH-minor] Adult. Aged. Aged, 80 and over. Alkaline Phosphatase / metabolism. Disease Progression. Humans. Male. Medical Oncology / methods. Middle Aged. Neoplasm Metastasis. Prognosis. Proportional Hazards Models. Time Factors. Treatment Outcome

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[Copyright] Copyright (c) 2010 S. Karger AG, Basel.

(PMID = 20215819.001).

[ISSN] 1423-0399

[Journal-full-title] Urologia internationalis

[ISO-abbreviation] Urol. Int.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Switzerland

[Chemical-registry-number] EC 3.1.3.1 / Alkaline Phosphatase; EC 3.4.21.77 / Prostate-Specific Antigen

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Hypocalcemia and parathyroid function in metastatic prostate cancer.

OBJECTIVE: To report the occurrence of hypocalcemia in a patient with metastatic prostate cancer, discuss its pathogenesis, and review the related medical literature.

METHODS: An 82-year-old man with a known history of prostate cancer was found to have a serum calcium level of 5.4 mg/dL during an admission to the hospital for small bowel obstruction.

A thorough review of his medical history revealed a temporal relationship between the diagnosis of malignant disease and progressive hypocalcemia.

RESULTS: The patient had no history of hypocalcemia before the diagnosis of, and initiation of antiandrogen therapy for, advanced prostate cancer.

A 24-hour urine collection showed substantially reduced calcium excretion, and a whole-body bone scan revealed widespread metastatic deposits.

These findings were compatible with hypocalcemia related to prostate cancer and bone metastatic lesions.

CONCLUSION: This case serves as a reminder that hypocalcemia can be a manifestation of prostate cancer metastatic to bone.

In contrast to the occurrence of secondary hyperparathyroidism in this setting, however, this patient had normal levels of parathyroid hormone.

Review of similar previous reports and the causes and implications of a possible functional hypoparathyroid state are discussed.

[MeSH-major] Bone Neoplasms / secondary. Hypocalcemia / complications. Parathyroid Glands / physiopathology. Prostatic Neoplasms / blood. Prostatic Neoplasms / physiopathology

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(PMID = 16006299.001).

[ISSN] 1530-891X

[Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists

[ISO-abbreviation] Endocr Pract

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Parathyroid Hormone

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Collet-sicard syndrome: an uncommon manifestation of metastatic prostate cancer.

Metastatic spread of prostate adenocarcinoma to the temporal bone is very rare.

A case of metastatic prostate adenocarcinoma involving the temporal bone causing Collet-Sicard syndrome is presented.

This case highlights an uncommon manifestation of prostate adenocarcinoma causing symptoms referable to the occipital condyle of the temporal bone.

Few cases have been reported in the literature of Collet-Sicard syndrome due to metastatic prostate cancer.

[MeSH-major] Adenocarcinoma / secondary. Prostatic Neoplasms / pathology. Skull Neoplasms / secondary. Temporal Bone

[MeSH-minor] Deglutition Disorders / diagnosis. Deglutition Disorders / etiology. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Syndrome. Tomography, X-Ray Computed

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(PMID = 16929891.001).

[ISSN] 0038-4348

[Journal-full-title] Southern medical journal

[ISO-abbreviation] South. Med. J.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Novel tracers and their development for the imaging of metastatic prostate cancer.

There are presently no accurate methods of imaging prostate cancer metastases to bone.

We reviewed contemporary molecular imaging modalities that have been tested in humans with metastatic prostate cancer, with consideration of the studies' adherence to current prostate cancer clinical trial designs.

Articles from the years 2002 to 2008 on PET using (18)F-FDG, (11)C-choline, (18)F-choline, (18)F-flouride, (11)C-acetate, (11)C-methionine, and (18)F-fluoro-5alpha-dihydrotestosterone in patients with metastatic prostate cancer were reviewed.

Although these studies are encouraging, most focus on the rising population with prostate-specific antigen, and many involve small numbers of patients and do not adhere to consensus criteria for clinical trial designs in prostate cancer.

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[Cites] Cancer Res. 1997 Sep 1;57(17):3629-34 [9288760.001]

[Cites] Clin Cancer Res. 1998 Jul;4(7):1765-72 [9676853.001]

[Cites] Cancer. 1998 Aug 15;83(4):739-47 [9708939.001]

[Cites] Urology. 1998 Oct;52(4):637-40 [9763084.001]

[Cites] J Urol. 1998 Dec;160(6 Pt 2):2393-5 [9817390.001]

[Cites] Clin Cancer Res. 1997 Jan;3(1):81-5 [9815541.001]

[Cites] J Clin Oncol. 1999 Mar;17(3):948-57 [10071289.001]

[Cites] Cancer. 1999 Apr 1;85(7):1586-92 [10193950.001]

[Cites] Cancer Res. 1999 Jul 1;59(13):3192-8 [10397265.001]

[Cites] J Urol. 1999 Oct;162(4):1322-8 [10492189.001]

[Cites] J Urol. 2005 Jan;173(1):66-9; discussion 69 [15592030.001]

[Cites] J Clin Oncol. 2005 Mar 20;23(9):1962-8 [15774789.001]

[Cites] Eur J Nucl Med Mol Imaging. 2005 Mar;32(3):344-50 [15726353.001]

[Cites] J Clin Oncol. 1999 Nov;17(11):3461-7 [10550143.001]

[Cites] NMR Biomed. 1999 Nov;12(7):413-39 [10654290.001]

[Cites] Urology. 2000 Mar;55(3):323-7 [10699601.001]

[Cites] Cancer Res. 2001 Jan 1;61(1):110-7 [11196147.001]

[Cites] Semin Nucl Med. 2001 Jan;31(1):50-61 [11200205.001]

[Cites] J Nucl Med. 2001 Dec;42(12):1805-14 [11752077.001]

[Cites] J Nucl Med. 2002 Jan;43(1):46-55 [11801702.001]

[Cites] J Nucl Med. 2002 Jan;43(1):92-6 [11801711.001]

[Cites] Radiology. 2005 May;235(2):623-8 [15858102.001]

[Cites] Eur Urol. 2007 Aug;52(2):423-9 [17397992.001]

[Cites] Eur J Nucl Med Mol Imaging. 2007 Aug;34(8):1316-7; author reply 1318-9 [17476505.001]

[Cites] BJU Int. 2007 Oct;100(4):786-93 [17822459.001]

[Cites] Clin Cancer Res. 2005 May 1;11(9):3210-6 [15867215.001]

[Cites] Clin Cancer Res. 2005 Jul 1;11(13):4761-9 [16000572.001]

[Cites] Clin Cancer Res. 2005 Jul 15;11(14):5223-32 [16033840.001]

[Cites] J Clin Oncol. 2005 Jul 20;23(21):4591-601 [15837970.001]

[Cites] Clin Cancer Res. 2005 Oct 15;11(20):7454-61 [16243819.001]

[Cites] J Clin Oncol. 2005 Nov 10;23(32):8253-61 [16278481.001]

[Cites] J Nucl Med. 2006 Feb;47(2):287-97 [16455635.001]

[Cites] Urology. 2006 May;67(5):996-1000 [16698359.001]

[Cites] J Clin Oncol. 2006 Jun 1;24(16):2513-9 [16636343.001]

[Cites] Eur J Nucl Med Mol Imaging. 2006 Dec;33(12):1387-98 [16865395.001]

[Cites] J Nucl Med. 2007 Jan;48(1):56-63 [17204699.001]

[Cites] Eur J Nucl Med Mol Imaging. 2007 Feb;34(2):185-96 [16832632.001]

[Cites] Mol Cancer Ther. 2007 Oct;6(10):2609-17 [17938257.001]

[Cites] Eur J Nucl Med Mol Imaging. 2008 Jan;35(1):18-23 [17891394.001]

[Cites] J Clin Oncol. 2008 Mar 1;26(7):1148-59 [18309951.001]

[Cites] J Clin Oncol. 2008 May 1;26(13):2147-54 [18362364.001]

[Cites] Eur Urol. 2008 Aug;54(2):392-401 [18456393.001]

[Cites] BJU Int. 2008 Aug;102(4):446-51 [18410442.001]

[Cites] Eur J Nucl Med Mol Imaging. 2008 Oct;35(10):1766-74 [18465129.001]

[Cites] J Nucl Med. 2002 Feb;43(2):181-6 [11850482.001]

[Cites] J Nucl Med. 2002 Feb;43(2):187-99 [11850483.001]

[Cites] Urology. 2002 Jun;59(6):913-8 [12031380.001]

[Cites] J Urol. 2002 Dec;168(6):2439-43 [12441935.001]

[Cites] J Clin Oncol. 2003 Feb 15;21(4):679-89 [12586806.001]

[Cites] Nuklearmedizin. 2003 Feb;42(1):25-30 [12601451.001]

[Cites] J Nucl Med. 2003 Mar;44(3):331-5 [12620996.001]

[Cites] Urol Int. 2003;70(4):311-5 [12740497.001]

[Cites] BJU Int. 2003 Jul;92(1):24-7 [12823377.001]

[Cites] J Clin Oncol. 2004 Feb 1;22(3):537-56 [14752077.001]

[Cites] J Nucl Med. 2004 Mar;45(3):366-73 [15001675.001]

[Cites] J Clin Oncol. 2004 Jul 1;22(13):2522-31 [15173215.001]

[Cites] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213.001]

[Cites] Cancer. 1973 Nov;32(5):1131-40 [4271302.001]

[Cites] AJR Am J Roentgenol. 1979 Jun;132(6):927-31 [108971.001]

[Cites] J Clin Oncol. 1985 Jul;3(7):1013-21 [3894584.001]

[Cites] Circulation. 1990 May;81(5):1594-605 [2110037.001]

[Cites] Clin Nucl Med. 1990 Jul;15(7):485-7 [2116949.001]

[Cites] Cancer. 1990 Sep 1;66(5 Suppl):1009-16 [2144203.001]

[Cites] J Urol. 1994 Dec;152(6 Pt 1):1952-5 [7966649.001]

[Cites] J Nucl Med. 1995 Sep;36(9):1595-601 [7658216.001]

[Cites] Urology. 1996 Aug;48(2):326-34 [8753752.001]

[Cites] Clin Nucl Med. 1996 Sep;21(9):704-13 [8879871.001]

(PMID = 18997047.001).

[ISSN] 0161-5505

[Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine

[ISO-abbreviation] J. Nucl. Med.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / T32 CA009207; United States / NCI NIH HHS / CA / K23CA102544; United States / NCI NIH HHS / CA / T32 CA009207-35; United States / NCI NIH HHS / CA / T-32CA09207; United States / NCI NIH HHS / CA / K23 CA102544; United States / NCI NIH HHS / CA / K23 CA102544-05

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

[Publication-country] United States

[Chemical-registry-number] 0 / Radiopharmaceuticals

[Number-of-references] 71

[Other-IDs] NLM/ NIHMS324605; NLM/ PMC3310891

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Integrative microarray analysis of pathways dysregulated in metastatic prostate cancer.

Microarrays have been used to identify genes involved in cancer progression.

Integrative microarray analysis of pathways (IMAP) was done using existing expression array data from localized and metastatic prostate cancer.

Comparison of metastatic cancer and localized disease in multiple expression array profiling studies using the IMAP approach yielded a list of about 100 pathways that were significantly dysregulated (P < 0.05) in prostate cancer metastasis.

Our results indicate that this pathway is especially dysregulated in hormone-refractory prostate cancer.

[MeSH-minor] Gene Expression Regulation, Neoplastic. Humans. Male. NF-kappa B / physiology. NF-kappa B p50 Subunit / physiology. Neoplasm Metastasis. nef Gene Products, Human Immunodeficiency Virus / physiology

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(PMID = 17974971.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / NF-kappa B; 0 / NF-kappa B p50 Subunit; 0 / NFKB1 protein, human; 0 / nef Gene Products, Human Immunodeficiency Virus; 0 / nef protein, Human immunodeficiency virus 1

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pharmacoeconomics of available treatment options for metastatic prostate cancer.

The resources devoted to managing metastatic prostate cancer are enormous, yet little attention has been given to directly measuring the economic consequences of treatment alternatives.

The purpose of this article was to evaluate the pharmacoeconomics of available treatments for metastatic prostate cancer, including hormone-sensitive disease, androgen-independent prostate cancer and locally advanced/progressive disease.

We identified 58 articles addressing economic issues related to metastatic prostate cancer.

Survival remains poor for metastatic disease, thus QOL is the primary consideration for many therapies.

However, QOL for treatment of metastatic disease is poorly measured and, in most analyses, the impact of therapy on QOL was inferred based on speculation by the authors.

The economic studies of advanced prostate cancer highlight several aspects of clinical care that are filled with considerable uncertainty and remain guided by forces other than optimal resource allocation.

It is essential that we address the weaknesses in our understanding of the economic consequences of therapies for prostate cancer, and find ways to include economic information into the process of determining optimal therapy.

[MeSH-minor] Clinical Trials as Topic. Combined Modality Therapy / methods. Economics, Pharmaceutical. Humans. Male. Neoplasm Metastasis. Neoplasm Staging

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(PMID = 17402804.001).

[ISSN] 1170-7690

[Journal-full-title] PharmacoEconomics

[ISO-abbreviation] Pharmacoeconomics

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] New Zealand

[Number-of-references] 100

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Molecular pathways in the progression of hormone-independent and metastatic prostate cancer.

Once prostate cancer becomes castration resistant, cancer cells may rapidly gain the ability to invade and to metastasize to lymph nodes and distant organs.

The progression through hormone-dependent to hormone-independent/castration-resistant and metastatic PCa is poorly understood.

In this review paper, we provide an overview on the cellular and molecular mechanisms underlying the process of tumor cell invasion and metastasis in prostate cancer.

We specifically present the most recent findings on the role of multiple cellular signaling pathways including androgen receptor (AR), mitogen-activated protein kinases (MAPK), Akt, transforming growth factor b (TGFb interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) in the development of hormone-independent/castration-resistant prostate cancer.

In addition, we also discuss the recent findings on signatures of gene expression during prostate cancer progression.

Our overviews on the novel findings will help to gain better understanding of the complexity of molecular mechanisms that may play an essential role in the development of castration-resistant and metastatic prostate cancer.

[MeSH-major] Androgens / physiology. Neoplasm Metastasis. Prostatic Neoplasms / genetics

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(PMID = 20384583.001).

[ISSN] 1873-5576

[Journal-full-title] Current cancer drug targets

[ISO-abbreviation] Curr Cancer Drug Targets

[Language] eng

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Androgens

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prostate cancer metastatic to the external auditory canals.

A 58-year-old white man with prostate-specific antigen (PSA) level of 6 ng/mL, a Gleason score of 6 (3+3), and T2a adenocarcinoma of the prostate underwent prostatectomy.

The PSA continued to increase, and the patient developed bone-only metastatic disease.

Six months later, he presented with bilateral hearing loss and was found to have pathologic and radiographic evidence of metastatic prostate cancer to the external auditory canals.

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

[MeSH-minor] Fatal Outcome. Humans. Male. Middle Aged. Prostate-Specific Antigen / blood. Prostatectomy

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(PMID = 17645833.001).

[ISSN] 1558-7673

[Journal-full-title] Clinical genitourinary cancer

[ISO-abbreviation] Clin Genitourin Cancer

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Surgical management of prostate cancer metastatic to the spine.

OBJECT: Significant improvements in neurological function and pain relief are the benefits of aggressive surgical management of spinal metastatic disease.

In this study, a series of patients undergoing spinal surgery for metastatic prostate cancer were reviewed to identify predictors of survival and functional outcome.

METHODS: The authors retrospectively reviewed the records of all patients who were treated with surgery for prostate cancer metastases to the spine between 1993 and 2005 at a single institution.

The median age at spinal metastasis was 66 years (range 50-84 years).

Gleason score (p = 0.002), total number of metastases (p = 0.001), and the degree of spinal canal compression (p = 0.001) were independent predictors of survival.

Age > or = 65 years at the time of surgery was an independent predictor of a postoperative complication (p = 0.005).

CONCLUSIONS: In selected patients with prostate cancer metastases to the spine, aggressive surgical decompression and spinal reconstruction is a useful treatment option.

Gleason score, metastatic burden, and degree of spinal canal compression may be associated with survival following surgery, and thus should be considered carefully prior to opting for surgical management.

[MeSH-major] Prostatic Neoplasms / pathology. Spinal Neoplasms / secondary. Spinal Neoplasms / surgery

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(PMID = 19442002.001).

[ISSN] 1547-5654

[Journal-full-title] Journal of neurosurgery. Spine

[ISO-abbreviation] J Neurosurg Spine

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Narcotics; 0 / Steroids

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Severe hypophosphatemic osteomalacia in hormone-refractory prostate cancer metastatic to the skeleton: natural history and pitfalls in management.

We report the case of a severe symptomatic hypophosphatemic osteomalacia in a 66-year-old patient with hormone-refractory prostate cancer metastatic to the skeleton.

A follow-up of 2 years from diagnosis to development of hormone refractoriness and death allowed us to study the natural history of this uncommon disturbance of mineral homeostasis in this common malignancy.

Relevant to the difficult management of the late stages of prostate cancer is the failure of hypophosphatemia to respond to conventional therapeutic approaches and the favorable outcome of antitumor therapy suggesting that this group of patients, although having a poor prognosis, could still benefit from aggressive second line therapy.

In this malignancy in which metastases have a predilection for bone, failure to recognize osteomalacia can only result in significantly increasing the burden of skeletal complications.

[MeSH-major] Bone Neoplasms / secondary. Hypophosphatemia / complications. Osteomalacia / complications. Prostatic Neoplasms / pathology

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(PMID = 15663996.001).

[ISSN] 8756-3282

[Journal-full-title] Bone

[ISO-abbreviation] Bone

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Leptomeningeal carcinomatosis in a patient with metastatic prostate cancer: case report and literature review.

BACKGROUND: Leptomeningeal metastasis is discovered at autopsy in approximately 5% of patients with systemic cancer.

Until recently with the introduction of magnetic resonance imaging (MRI), premorbid diagnosis was extremely difficult.

Leptomeningeal metastasis in metastatic prostate cancer has been reported in only 14 patients previously.

CASE DESCRIPTION: We recently studied such a patient and were able to establish a correct diagnosis based solely on the MRI and the presence of an elevated cerebrospinal fluid (CSF) prostate-specific antigen (PSA).

Only 3 previous patients with leptomeningeal prostate metastasis have undergone CSF PSA evaluations.

[MeSH-major] Arachnoid / pathology. Carcinoma / secondary. Meningeal Neoplasms / secondary. Pia Mater / pathology. Prostatic Neoplasms / pathology

[MeSH-minor] Aged. Anti-Inflammatory Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms / secondary. Consciousness Disorders / etiology. Diagnostic Errors / prevention & control. Early Diagnosis. Fatal Outcome. Headache / etiology. Humans. Lymph Nodes / pathology. Magnetic Resonance Imaging. Male. Neoplasm Metastasis / drug therapy. Neoplasm Metastasis / pathology. Neoplasm Metastasis / physiopathology. Prostate-Specific Antigen / blood. Prostate-Specific Antigen / cerebrospinal fluid. Tomography, X-Ray Computed. Treatment Failure

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(PMID = 16531199.001).

[ISSN] 0090-3019

[Journal-full-title] Surgical neurology

[ISO-abbreviation] Surg Neurol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-Inflammatory Agents; EC 3.4.21.77 / Prostate-Specific Antigen

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pain and analgesic use in men with metastatic prostate cancer.

: e20515 Background: Pain is an important endpoint in metastatic prostate cancer and was the basis for the 1996 FDA approval of mitoxantrone.

The prevalence and distribution of pain severity at specific points in the prostate cancer disease continuum are not well defined.

METHODS: A questionnaire that includes the Brief Pain Inventory and additional pain/analgesia items was developed as a collaboration between the DOD/PCF-supported Prostate Cancer Clinical Trials Consortium (PCCTC) and FDA Study Endpoints and Labeling Design (SEALD) team.

RESULTS: Between August-December 2008, 325 men with prostate cancers representing different disease states being seen in outpatient clinics of participating centers were each queried once.

More than half (n=175) self-reported metastatic disease, including 129 with bone metastases.

Among those with bone metastases, 76 (59%) reported experiencing any level of pain in the last week; 49 (38%) reported a worst pain score ≥4/10 of which 38 (78%) used analgesics over the past week and 31 (63%) used daily analgesia.

Among the 49 patients with pain scores ≥4/10, current or past docetaxel use was reported by 32 (65%), androgen deprivation therapy by 47 (96%), and 28 (57%) had been or were currently enrolled in a clinical trial.

CONCLUSIONS: Pain is sufficiently prevalent in men with metastatic prostate cancer to enable prospective assessment of palliation endpoints in clinical trials.

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(PMID = 27960916.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Analyses of circulating tumor cell (CTC) dynamics and treatment response in prostate cancer using the CTC-chip microfluidic device.

: 5149 Background: The CTC-Chip reliably detects CTCs in patients with localized and metastatic prostate cancer.

In localized disease, CTCs may be indicative of tumor invasiveness.

In the metastatic setting, CTCs may be useful in monitoring response to therapy.

Molecular analyses of CTCs through this minimally invasive technique may provide insights into disease behavior, whereas sampling of metastatic deposits in bone (the predominant site of prostate metastasis) is not feasible.

Subgroups of patients (n) included: localized disease undergoing prostatectomy (25), and metastatic disease undergoing either androgen deprivation therapy (ADT) (12) or docetaxel chemotherapy (5).

In patients with metastatic disease undergoing either ADT or chemotherapy, CTC quantities generally corresponded with changes in serum PSA and radiographic assessments.

Molecular characterization of CTCs may provide new insights into prostate cancer biology, clinical behavior, and therapeutic targets.

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(PMID = 27964441.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Anaemia following initiation of androgen deprivation therapy for metastatic prostate cancer: a retrospective chart review.

We conducted a chart review of patients receiving ADT for metastatic prostate cancer to assess anaemia-related symptoms.

METHODS: 135 stage IV prostate cancer cases were reviewed for treatment type; haemoglobin values before and after treatment; and symptoms of anaemia.

CONCLUSIONS: The present study confirms that ADT results in a significant drop in haemoglobin levels into the anaemic range.

[MeSH-minor] Aged. Anilides / adverse effects. Anilides / therapeutic use. Combined Modality Therapy. Goserelin / adverse effects. Goserelin / therapeutic use. Hemoglobins / analysis. Humans. Leuprolide / adverse effects. Leuprolide / therapeutic use. Linear Models. Male. Neoplasm Metastasis. Nitriles / adverse effects. Nitriles / therapeutic use. Retrospective Studies. Tosyl Compounds / adverse effects. Tosyl Compounds / therapeutic use

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(PMID = 18937151.001).

[ISSN] 1473-0790

[Journal-full-title] The aging male : the official journal of the International Society for the Study of the Aging Male

[ISO-abbreviation] Aging Male

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antineoplastic Agents, Hormonal; 0 / Hemoglobins; 0 / Nitriles; 0 / Tosyl Compounds; 0F65R8P09N / Goserelin; A0Z3NAU9DP / bicalutamide; EFY6W0M8TG / Leuprolide

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [The survival analysis of metastatic prostate cancer].

OBJECTIVES: To analyze the clinical and pathological informations of metastatic prostate cancer patients to find the predictive factors of the survival.

METHODS: To filter 364 cases of metastatic prostate cancer in the 940 cases of prostate cancer that were treated in Cancer Hospital Fudan University in Shanghai from March 1998 to June 2009, the cases had hormonal therapy and full clinical and pathological records.

The median survival time of metastatic prostate cancer was 64 months, and the one-year, two-year, three-year, four-year, five-year survival rate was 92%, 78%, 66%, 60%, 54%.

The univariate analysis indicated that Gleason score (P = 0.033), clinical stage (P < 0.001), the effectiveness of hormonal therapy (P < 0.001), the prostate specific antigen (PSA) nadir during hormonal therapy (P < 0.001) and the time from the start of hormonal therapy to the PSA nadir (P = 0.002) were predictive factors for the survival time of metastatic prostate cancer.

The multivariate analysis indicated that the PSA nadir during hormonal therapy (P < 0.001) and the time from the start of hormonal therapy to the PSA nadir (P < 0.001) were independent factors that predict the survival time of metastatic prostate cancer.

CONCLUSION: The PSA nadir during hormonal therapy and the time from the start of hormonal therapy to the PSA nadir are independent factors that predict the survival time of metastatic prostate cancer.

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(PMID = 21055012.001).

[ISSN] 0529-5815

[Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]

[ISO-abbreviation] Zhonghua Wai Ke Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Hormone-refractory and metastatic prostate cancer - palliative radiotherapy.

Prostate cancer progression is commonly manifested by obstructive uropathy, regional lymphatic metastases and hematogenous metastases to the axial skeleton.

Radiotherapy is a mainstay in the palliation of symptomatic metastatic prostate cancer and is most often used for the palliation of painful metastatic bone lesions, resulting in a relief of pain in about 80-90% of patients and a reduction of analgesics.

In metastatic disease compromising the integrity of the spinal cord or a nerve root, radiotherapy can be used as an urgent intervention to minimize neurological dysfunction and local progression or as an adjunct to surgical decompression.

Symptoms of metastatic lymphadenopathy like leg edema and back discomfort caused by pelvic or paraaortic metastases are related to the immediate anatomic structures affected.

Radiotherapy for localized hormone-refractory prostate cancer has an excellent local control rate; nevertheless, the prognosis is poor, the majority of patients failing with distant metastasis within few years.

The role of radiotherapy in hormone-refractory and metastatic prostate cancer, considering the patient's individual situation, are presented and discussed.

[MeSH-major] Drug Resistance, Neoplasm. Neoplasm Metastasis / radiotherapy. Palliative Care / methods. Prostatic Neoplasms / radiotherapy

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(PMID = 18544993.001).

[ISSN] 0071-9676

[Journal-full-title] Frontiers of radiation therapy and oncology

[ISO-abbreviation] Front Radiat Ther Oncol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Androgen Antagonists

[Number-of-references] 26

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Role of hormonotherapy in the treatment of metastatic prostate cancer].

[Transliterated title] Place de l'hormonothérapie dans le traitement du cancer de prostate métastatique.

Androgen privation is considered as the referent first line treatment for metastatic prostate cancer.

Since metastasis is confirmed, immediate treatment with continue LHRH agonist is the French Association of Urology (AFU) AFU recommendations treatment for metastatic prostate cancer but intermittent treatment can be considered as an option.

[MeSH-minor] Gonadotropin-Releasing Hormone / analogs & derivatives. Humans. Male. Neoplasm Metastasis / drug therapy

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(PMID = 19070812.001).

[ISSN] 1166-7087

[Journal-full-title] Progrès en urologie : journal de l'Association française d'urologie et de la Société française d'urologie

[ISO-abbreviation] Prog. Urol.

[Language] fre

[Publication-type] English Abstract; Journal Article

[Publication-country] France

[Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Chemokine receptor CXCR4 expression and prognosis in patients with metastatic prostate cancer.

The chemokine receptor CXCR4 has been reported to be aberrantly expressed in human cancers and has also been shown to participate in the development of cancer metastasis.

The present study was carried out to assess immunohistochemically the pattern of CXCR4 expression in patients with metastatic prostate cancer.

We also evaluated the pathological grade, extent of bony metastasis, clinical response to hormonal therapy, and patient prognosis.

Its expression showed no association with pathological grade, extent of bony metastasis, or clinical response to hormonal therapy.

Patients with a high expression of CXCR4 in tumors had poorer cancer-specific survival than those with low expression of CXCR4.

CXCR4 expression is a useful prognostic factor for patients with metastatic prostate cancer treated with androgen-withdrawal therapy.

[MeSH-major] Biomarkers, Tumor / metabolism. Prostatic Neoplasms / pathology. Receptors, CXCR4 / metabolism

[MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Bone Neoplasms / pathology. Bone Neoplasms / secondary. Humans. Immunohistochemistry. Male. Middle Aged. Multivariate Analysis. Prognosis. Survival Analysis

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(PMID = 18201276.001).

[ISSN] 1349-7006

[Journal-full-title] Cancer science

[ISO-abbreviation] Cancer Sci.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Receptors, CXCR4

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Bone and prostate cancer cell interactions in metastatic prostate cancer.

The interplay in prostate cancer bone metastases between the 'seed' (the prostate cancer cells) and the 'soil' (the bone microenvironment) has been increasingly recognized as integral to the remarkable tropism for bone shown by prostate cancer.

Recent developments, including the use of bisphosphonates in metastatic disease, highlight the important role of bone cells in the development and progression of metastatic prostate cancer.

[MeSH-minor] Aging / physiology. Bone Density / physiology. Bone Remodeling / physiology. Hormones / physiology. Humans. Male. Neoplasm Proteins / metabolism

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(PMID = 17166237.001).

[ISSN] 1464-4096

[Journal-full-title] BJU international

[ISO-abbreviation] BJU Int.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Hormones; 0 / Neoplasm Proteins

[Number-of-references] 35

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Systemic treatment of metastatic prostate cancer].

Systemic treatment of advanced prostate cancer is multifaceted.

Chemotherapy is effective in hormone refractory (castration resistant) prostate cancer.

Use of bisphosphonates is standard in metastatic bone disease.

Treatment of patients with metastatic prostate cancer is palliative.

[MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Bone Neoplasms / secondary. Prostatic Neoplasms / drug therapy

[MeSH-minor] Androgen Antagonists / adverse effects. Androgen Antagonists / therapeutic use. Combined Modality Therapy. Diphosphonates / therapeutic use. Disease Progression. Humans. Male. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / mortality. Neoplasm Recurrence, Local / pathology. Neoplasm Staging. Orchiectomy. Palliative Care. Quality of Life. Survival Analysis

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[Cites] Aktuelle Urol. 2009 May;40(3):159-63 [19399720.001]

[Cites] J Clin Oncol. 2009 Feb 1;27(4):644-6 [19103725.001]

[Cites] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213.001]

[Cites] Cochrane Database Syst Rev. 2002;(4):CD003851 [12519611.001]

[Cites] BJU Int. 2008 Feb;101(4):440-3 [17941935.001]

[Cites] CMAJ. 2009 May 26;180(11):E62-71 [19407261.001]

[Cites] Urol Oncol. 2008 Jul-Aug;26(4):420-5 [18593621.001]

[Cites] Cancer. 2009 Aug 15;115(16):3670-9 [19536890.001]

[Cites] Scand J Urol Nephrol. 2006;40(6):441-52 [17130095.001]

[Cites] Oncologist. 2009 Apr;14(4):391-8 [19342474.001]

[Cites] N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214.001]

[Cites] Urol Oncol. 2008 Jul-Aug;26(4):426-9 [18593622.001]

[Cites] J Clin Endocrinol Metab. 2001 Aug;86(8):3467-77 [11502765.001]

[Cites] J Natl Cancer Inst. 2002 Oct 2;94(19):1458-68 [12359855.001]

[Cites] J Clin Oncol. 2007 Apr 20;25(12):1596-605 [17404365.001]

[Cites] J Clin Oncol. 2006 Apr 20;24(12):1868-76 [16622261.001]

[Cites] J Clin Oncol. 2004 Jul 15;22(14):2927-41 [15184404.001]

[Cites] BJU Int. 2007 Jun;99(6):1383-9 [17346269.001]

[Cites] N Engl J Med. 2009 Aug 20;361(8):745-55 [19671656.001]

[Cites] Cochrane Database Syst Rev. 2006 Oct 18;(4):CD006250 [17054286.001]

[Cites] J Clin Oncol. 2006 Aug 20;24(24):3984-90 [16921051.001]

[Cites] JAMA. 2009 Aug 26;302(8):866-73 [19706860.001]

[Cites] J Clin Oncol. 2009 Apr 20;27(12):2022-9 [19289629.001]

[Cites] Nucl Med Commun. 2007 Aug;28(8):623-30 [17625384.001]

[Cites] J Clin Oncol. 2001 Sep 15;19(18 Suppl):61S-63S [11560975.001]

[Cites] Urol Oncol. 2008 Jul-Aug;26(4):430-7 [18593623.001]

[Cites] CA Cancer J Clin. 2002 May-Jun;52(3):154-79 [12018929.001]

[Cites] Clin Prostate Cancer. 2002 Dec;1(3):163-71 [15046691.001]

[Cites] Lancet. 2000 Apr 29;355(9214):1491-8 [10801170.001]

[Cites] Urol Oncol. 2008 Jul-Aug;26(4):415-9 [18593620.001]

(PMID = 20180063.001).

[ISSN] 1433-0563

[Journal-full-title] Der Urologe. Ausg. A

[ISO-abbreviation] Urologe A

[Language] ger

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

[Publication-country] Germany

[Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Diphosphonates

[Number-of-references] 36

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Trends and racial differences in the use of androgen deprivation therapy for metastatic prostate cancer.

CONTEXT: Androgen deprivation therapy (ADT) is widely used to manage the symptoms of advanced prostate cancer and has been shown to slow the progression of the disease.

OBJECTIVES: The purpose of this study was to assess use trends for ADT overall and by type (orchiectomy and luteinizing hormone-releasing hormone [LHRH] agonists) and the factors associated with time to receipt for metastatic prostate cancer.

METHODS: Data from the Surveillance, Epidemiology, and End Results (SEER) cancer registry and Medicare claims database were obtained for 5,273 men, aged 65 years and older and diagnosed with Stage IV prostate cancer during 1991-1999 from seven SEER regions.

RESULTS: African-American men were less likely than white men to receive any ADT after diagnosis (P<0.001).

CONCLUSION: African-American men with metastatic prostate cancer were significantly less likely to receive ADT and, when treated, had a slightly longer time to receipt than white men, which has implications for patients and physicians involved in the palliative management of metastatic prostate cancer.

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[Copyright] Copyright 2010. Published by Elsevier Inc.

[Cites] J Clin Oncol. 2001 Sep 1;19(17):3750-7 [11533098.001]

[Cites] J Natl Cancer Inst. 2001 Mar 7;93(5):388-95 [11238701.001]

[Cites] J Natl Cancer Inst. 2002 Mar 6;94(5):334-57 [11880473.001]

[Cites] J Urol. 2002 Jul;168(1):9-12 [12050481.001]

[Cites] Med Care. 2002 Aug;40(8 Suppl):IV-3-18 [12187163.001]

[Cites] Stat Med. 2002 Nov 30;21(22):3493-510 [12407686.001]

[Cites] J Natl Cancer Inst. 2003 Jul 2;95(13):981-9 [12837834.001]

[Cites] Urol Oncol. 2003 Jul-Aug;21(4):245-54 [12954493.001]

[Cites] J Natl Cancer Inst. 2003 Nov 19;95(22):1702-10 [14625261.001]

[Cites] J Gen Intern Med. 2004 Feb;19(2):146-55 [15009794.001]

[Cites] Med Care. 2004 Mar;42(3):239-50 [15076823.001]

[Cites] Bull N Y Acad Med. 1972 Jun;48(5):751-66 [4555718.001]

[Cites] Cancer. 1973 Nov;32(5):1126-30 [4585929.001]

[Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(5):1658-62 [6461861.001]

[Cites] Urology. 1989 May;33(5 Suppl):45-52 [2523611.001]

[Cites] Urology. 1989 May;33(5 Suppl):57-62 [2523612.001]

[Cites] Br J Urol. 1991 May;67(5):502-8 [1828183.001]

[Cites] Br J Urol. 1997 Feb;79(2):235-46 [9052476.001]

[Cites] Cancer. 1998 Jul 15;83(2):320-30 [9669815.001]

[Cites] Med Care. 1998 Sep;36(9):1337-48 [9749657.001]

[Cites] Cancer. 2005 Feb 1;103(3):538-45 [15612083.001]

[Cites] Cancer. 2005 Apr 15;103(8):1615-24 [15742331.001]

[Cites] JAMA. 2005 Jul 13;294(2):238-44 [16014598.001]

[Cites] J Natl Cancer Inst. 2006 Jun 21;98(12):839-45 [16788157.001]

[Cites] J Urol. 2006 Aug;176(2):526-31 [16813882.001]

[Cites] Int J Radiat Oncol Biol Phys. 2006 Oct 1;66(2):395-402 [16904843.001]

[Cites] J Clin Oncol. 2006 Sep 20;24(27):4448-56 [16983113.001]

[Cites] J Clin Oncol. 2007 Apr 20;25(12):1596-605 [17404365.001]

[Cites] J Urol. 2001 Jan;165(1):104-7 [11125375.001]

[Cites] J Clin Epidemiol. 2000 Dec;53(12):1258-67 [11146273.001]

[Cites] Cochrane Database Syst Rev. 2002;(1):CD003506 [11869665.001]

(PMID = 20471547.001).

[ISSN] 1873-6513

[Journal-full-title] Journal of pain and symptom management

[ISO-abbreviation] J Pain Symptom Manage

[Language] ENG

[Grant] United States / PHS HHS / / U55/CCR921930-02; United States / NCI NIH HHS / CA / 1U01CA114629; United States / NCI NIH HHS / PC / N01-PC-35139; United States / NCI NIH HHS / PC / N02 PC015105; United States / NIMHD NIH HHS / MD / P60MD000244; United States / NCI NIH HHS / CA / U01 CA114629; United States / NIMHD NIH HHS / MD / P60 MD000239; United States / NIMHD NIH HHS / MD / P60 MD000244; United States / NCI NIH HHS / CA / 2R25CA057726; United States / NCI NIH HHS / CA / N01PC35136; United States / NCI NIH HHS / CA / N01PC35139; United States / NCI NIH HHS / PC / N01-PC-35136; United States / NCI NIH HHS / CA / R25 CA057726

[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 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone

[Other-IDs] NLM/ NIHMS362675; NLM/ PMC3878612

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Local and systemic therapy for patients with metastatic prostate cancer: should the primary tumor be treated?

Data from well-designed, prospective clinical trials are lacking to support treatment of primary tumor in men diagnosed with metastatic prostate cancer.

However, a growing body of evidence suggests that treatment of the primary tumor may enhance cancer control and survival in some men.

This evidence is examined and recommendations are made for identifying patients with metastatic prostate cancer who may benefit from definitive treatment of the prostate tumor.

[MeSH-major] Neoplasm Metastasis / therapy. Prostatic Neoplasms / pathology. Prostatic Neoplasms / therapy

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(PMID = 15869722.001).

[ISSN] 1527-2737

[Journal-full-title] Current urology reports

[ISO-abbreviation] Curr Urol Rep

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Androgen Antagonists

[Number-of-references] 50

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Metronomic chemotherapy: principles and lessons learned from applications in the treatment of metastatic prostate cancer.

By frequent and protracted administration of conventional cytotoxic drugs without prolonged interruptions, the primary treatment target shifts from the tumor cell population to the tumor vasculature.

We outline the basic aspects of the metronomic concept, describe the results of clinical applications of such chemotherapy by focusing on studies in metastatic prostate cancer, and discuss certain shortcomings.

[MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials as Topic. Endothelial Cells / physiology. Humans. Male. Neoplasm Metastasis. Stem Cells / physiology

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(PMID = 20033383.001).

[ISSN] 0080-0015

[Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer

[ISO-abbreviation] Recent Results Cancer Res.

[Language] eng

[Grant] Canada / Canadian Institutes of Health Research / /

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

[Publication-country] Germany

[Chemical-registry-number] 0 / Angiogenesis Inhibitors

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Use of androgen deprivation therapy for metastatic prostate cancer in older men.

OBJECTIVE: To assess factors associated with early or delayed androgen deprivation therapy (ADT) among men diagnosed with metastatic prostate cancer, and to assess the relationship between ADT and overall survival, as there is uncertainty about the ideal timing for initiating ADT in men with metastatic prostate cancer.

PATIENTS AND METHODS: We studied a population-based cohort of American men aged >or=66 years diagnosed with metastatic prostate cancer during 1992-2002 and followed to 2003.

We assessed the receipt of ADT early (<or=4 months from diagnosis), delayed (>4 months), or not at all, using multinomial logistic regression to identify factors associated with treatment, and Cox proportional-hazard models to assess whether treatment was associated with survival.

CONCLUSIONS: A large minority of men with metastatic prostate cancer, particularly black men, receive delayed or no ADT.

After controlling for patient and tumour characteristics, survival did not differ by race, and receipt of ADT did not contribute to racial differences in survival.

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[Cites] J Urol. 2000 Jan;163(1):137-42 [10604331.001]

[Cites] J Clin Oncol. 2006 Sep 20;24(27):4448-56 [16983113.001]

[Cites] J Urol. 2002 Jul;168(1):9-12 [12050481.001]

[Cites] Med Care. 2002 Aug;40(8 Suppl):IV-3-18 [12187163.001]

[Cites] J Natl Cancer Inst. 2003 Jul 2;95(13):981-9 [12837834.001]

[Cites] Soc Sci Med. 2003 Dec;57(11):2137-47 [14512244.001]

[Cites] Health Serv Res. 2003 Oct;38(5):1253-62 [14596389.001]

[Cites] J Clin Oncol. 2004 Jul 15;22(14):2927-41 [15184404.001]

[Cites] J Chronic Dis. 1987;40(5):373-83 [3558716.001]

[Cites] Am J Epidemiol. 1991 Apr 1;133(7):672-82 [2018022.001]

[Cites] Cancer. 1993 Apr 15;71(8):2569-73 [8453581.001]

[Cites] Med Care. 1993 Aug;31(8):732-48 [8336512.001]

[Cites] JAMA. 1995 Nov 22-29;274(20):1599-605 [7474244.001]

[Cites] Health Care Financ Rev. 1996 Spring;17(3):101-28 [10172666.001]

[Cites] BJU Int. 2006 Nov;98(5):973-8 [16879443.001]

[Cites] J Urol. 2007 Feb;177(2):535-9 [17222628.001]

[Cites] J Clin Oncol. 2007 Apr 20;25(12):1596-605 [17404365.001]

[Cites] J Natl Cancer Inst. 2002 Mar 6;94(5):334-57 [11880473.001]

[Cites] Br J Urol. 1997 Feb;79(2):235-46 [9052476.001]

[Cites] J Urol. 1997 Jul;158(1):150-4 [9186343.001]

[Cites] Med Care. 1998 Sep;36(9):1337-48 [9749657.001]

[Cites] J Urol. 1998 Nov;160(5):1685-8 [9783932.001]

[Cites] Urology. 1999 May;53(5):898-902; discussion 902-3 [10223480.001]

[Cites] Prostate. 1999 Sep 1;40(4):218-24 [10420149.001]

[Cites] Urology. 2004 Dec;64(6):1171-6 [15596192.001]

[Cites] Cancer. 2005 Apr 15;103(8):1615-24 [15742331.001]

[Cites] JAMA. 2005 Jul 13;294(2):238-44 [16014598.001]

[Cites] J Clin Oncol. 2006 Jan 1;24(1):85-94 [16382117.001]

[Cites] CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30 [16514137.001]

[Cites] Cancer. 2006 Mar 15;106(6):1276-85 [16475208.001]

[Cites] J Urol. 2006 Aug;176(2):526-31 [16813882.001]

[Cites] Med Care. 2006 Aug;44(8):745-53 [16862036.001]

[CommentIn] Eur Urol. 2008 Nov;54(5):1201-2 [19051382.001]

(PMID = 18190632.001).

[ISSN] 1464-410X

[Journal-full-title] BJU international

[ISO-abbreviation] BJU Int.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P50 CA090381; United States / NCI NIH HHS / CA / K24 CA121990; United States / NCI NIH HHS / CA / K24 CA121990-02; United States / NCI NIH HHS / CA / P50CA90381; United States / NCI NIH HHS / CA / CA121990-02

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

[Publication-country] England

[Chemical-registry-number] 0 / Androgen Antagonists; 33515-09-2 / Gonadotropin-Releasing Hormone

[Other-IDs] NLM/ NIHMS204636; NLM/ PMC2900629

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Current status of cytotoxic chemotherapy in patients with metastatic prostate cancer.

Despite efforts at early detection with prostate specific antigen-based screening, more than 25,000 patients in the United States will die this year of metastatic prostate cancer.

As a consequence both of screening and increased use of androgen deprivation therapy, patients commonly present with low volume, asymptomatic, metastatic disease.

Over the past 2 decades chemotherapy for advanced prostate cancer has evolved from a frightful, toxic experience to one that frequently provides clinically meaningful palliation and a modest, but real survival benefit.

[MeSH-minor] Humans. Male. Mitoxantrone / therapeutic use. Neoplasm Metastasis. Taxoids / therapeutic use

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(PMID = 18593622.001).

[ISSN] 1078-1439

[Journal-full-title] Urologic oncology

[ISO-abbreviation] Urol. Oncol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Taxoids; 15H5577CQD / docetaxel; BZ114NVM5P / Mitoxantrone

[Number-of-references] 25

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Phenoxodiol inhibits growth of metastatic prostate cancer cells.

BACKGROUND: Phenoxodiol, a synthetic analog of Genistein, is being assessed in several clinical studies against a range of cancer types and was shown to have a good efficacy and safety profile.

In this study we tested the effects of Phenoxodiol against prostate cancer cell lines.

METHODS: Cell-cycle analysis, plasmatic membrane damage, clonogenic assay, comet assay, and Western blot methodologies were employed to assess the effects of Phenoxodiol on prostate cancer cell lines.

An in vivo model confirmed the potential therapeutic efficacy of Phenoxodiol when administered orally to tumor bearing mice.

RESULTS: Phenoxodiol treatment promoted a marked inhibition of proliferation and loss of colony formation in LNCaP cells in a dose- and time-dependent manner.

Similar effects were also observed in the metastatic prostate cell lines PC3 and DU145.

Oral administration of Phenoxodiol induced a considerable growth inhibition of malignant tumors generated by inoculation of LNCaP cells into Balb/c nu/nu athymic mice.

CONCLUSIONS: These data demonstrated that Phenoxodiol promotes apoptosis, as determined by PARP-1 degradation, via mitochondrial depolarization and G1/S cell-cycle arrest thereby confirming that it is active against androgen-dependent and independent prostate cancer cells.

Although a precise target for Phenoxodiol has not been identified, these data contribute to our understanding of the mechanism by which this drug promotes cell death in prostate cancer cells, and warrants the continued clinical development of Phenoxodiol as a therapeutic for the treatment of metastatic prostate cancer.

[MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Comet Assay. DNA Damage. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / genetics. Neoplasms, Hormone-Dependent / metabolism. Neoplasms, Hormone-Dependent / pathology. Poly(ADP-ribose) Polymerase Inhibitors. Poly(ADP-ribose) Polymerases / metabolism. Xenograft Model Antitumor Assays

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[Copyright] 2010. (c) 2010 Wiley-Liss, Inc.

(PMID = 20564423.001).

[ISSN] 1097-0045

[Journal-full-title] The Prostate

[ISO-abbreviation] Prostate

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Isoflavones; 0 / Poly(ADP-ribose) Polymerase Inhibitors; 995FT1W541 / phenoxodiol; EC 2.4.2.30 / PARP1 protein, human; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Current status of thalidomide and CC-5013 in the treatment of metastatic prostate cancer.

Thalidomide is emerging as a potentially important therapeutic option in the treatment of metastatic prostate cancer.

Although the mechanism of action of this agent remains elusive in malignancies of the prostate, recent data has indicated that thalidomide may play a role in inflammation, immunomodulation, and anti-angiogenesis.

Lenalidomide (CC-5013), a thalidomide analogue with improved activity and safety profile in certain disease contexts, is in the early stages of development in prostate cancer.

This review will provide the current status of the history, mechanism, metabolism, and clinical use of thalidomide in metastatic prostate cancer.

It will also describe the mechanism and clinical use of lenalidomide as it pertains to malignancies of the prostate.

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(PMID = 19719457.001).

[ISSN] 1875-5992

[Journal-full-title] Anti-cancer agents in medicinal chemistry

[ISO-abbreviation] Anticancer Agents Med Chem

[Language] eng

[Grant] United States / PHS HHS / / HHSN261200800001E; United States / Intramural NIH HHS / /

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antineoplastic Agents; 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide

[Number-of-references] 95

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Use of hormonal therapy in men with metastatic prostate cancer.

PURPOSE: Bilateral orchiectomy or luteinizing hormone releasing hormone agonists represent the standard of care for metastatic prostate cancer.

In this population based study we assessed the use rates of these therapies in men who died of prostate cancer.

MATERIAL AND METHODS: A total of 9,110 men 65 years or older who died of prostate cancer in 1991 to 2000 were identified through the population based Surveillance, Epidemiology and End Results, and Medicare linked database to determine hormonal therapy use rates.

RESULTS: Approximately 38% of black and 25% of white men did not receive hormonal therapy before dying of prostate cancer.

After adjusting for cancer status at diagnosis and other potential confounding factors black race and residence in low income areas were associated with lower hormonal therapy use (relative risk 0.73, 95% CI 0.67 to 0.80 and 0.91, 95% CI 0.85 to 0.98, respectively).

CONCLUSIONS: A substantial number of men who die as a consequence of prostate cancer never receive hormonal therapy.

Further studies are warranted to determine factors that may be associated with the incomplete use of hormonal therapy for metastatic prostate cancer.

[MeSH-minor] Aged. Humans. Male. Neoplasm Metastasis. SEER Program

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(PMID = 16813882.001).

[ISSN] 0022-5347

[Journal-full-title] The Journal of urology

[ISO-abbreviation] J. Urol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Overexpression of E-cadherin and beta-catenin proteins in metastatic prostate cancer cells in bone.

BACKGROUND: The expression of E-cadherin in the intercellular adhesion of metastatic prostate cancer cells in bone, which is the most prevalent site of metastatic growth, remains elusive.

METHODS: The aim of the study was to compare the concurrent membranous expression of E-cadherin and beta-catenin proteins, the state which is known to be associated with the cellular adhesion function of E-cadherin, in prostate biopsy tissue specimens by immunohistochemical staining method.

RESULTS: Benign prostate hyperplasia cells exhibited homogeneous expression of both E-cadherin and beta-catenin in 9 of 11 (82%), whereas the primary prostate cancer cells were homogeneously positive for both proteins only in 4 of 22 (18%) of the cases.

However, in contrast to the primary cancer, a significantly increased frequency of the metastatic prostate cancer cells in bone exhibited homogeneous expression of E-cadherin and beta-catenin in 12 of 17 (71%) of the cases.

A statistically significant association was observed between the overexpression of both proteins and the metastatic prostate cancer cells in bone (Fisher's exact P < 0.001).

CONCLUSIONS: The result of the study demonstrated for the first time that the membranous overexpression of E-cadherin and beta-catenin are significantly associated with the metastatic prostate cancer cells in bone and that the high frequency of expression suggest their involvement in the intercellular adhesion of the metastatic cells in bone.

[MeSH-major] Bone Neoplasms / metabolism. Bone Neoplasms / secondary. Cadherins / metabolism. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. beta Catenin / metabolism

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[Copyright] (c) 2007 Wiley-Liss, Inc.

(PMID = 18008331.001).

[ISSN] 0270-4137

[Journal-full-title] The Prostate

[ISO-abbreviation] Prostate

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Cadherins; 0 / beta Catenin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Metastatic prostate cancer-does treatment of the primary tumor matter?

PURPOSE: In recent years there has been increased interest in adjuvant therapy for prostate cancer.

This trend has engendered a tendency toward overlooking the issue of therapy to the primary tumor in advanced disease.

We reviewed the effect of treating the principal disease bulk on overall treatment outcome in patients with advanced and metastatic cancer.

Specifically we evaluated the role of surgical tumor cytoreduction.

MATERIALS AND METHODS: We performed a comprehensive literature review to evaluate the role of surgical debulking on the outcome of advanced cancer, including any published evidence supporting a benefit of this therapy for prostate cancer.

The beneficial role of maximal surgical cytoreduction has been clearly demonstrated in advanced ovarian cancer and gastrointestinal carcinomatosis.

Maximal debulking of brain, liver and lung metastasis has translated into longer survival.

Removal of the primary tumor has been proved to increase survival in randomized trials of metastatic renal cell cancer.

It appears that patients with node positive and possibly metastatic prostate cancer have a better response to androgen ablation with surgical removal of the gland.

CONCLUSIONS: Surgical cytoreduction of cancer results in a more favorable and durable response to systemic therapy.

It is reasonable to explore aggressive surgical therapy for advanced prostate cancer.

[MeSH-major] Neoplasm Metastasis / prevention & control. Prostatic Neoplasms / pathology. Prostatic Neoplasms / therapy

[MeSH-minor] Female. Humans. Male. Neoplasm Staging. Survival Rate

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[CommentIn] Eur Urol. 2007 Mar;51(3):852-3 [17421064.001]

(PMID = 16952615.001).

[ISSN] 0022-5347

[Journal-full-title] The Journal of urology

[ISO-abbreviation] J. Urol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 49

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Influence of BMPs on the formation of osteoblastic lesions in metastatic prostate cancer.

The purpose of this study was to evaluate the role of BMPs on the formation of metastatic prostate cancer lesions to bone.

INTRODUCTION: Prostate adenocarcinoma is the leading cause of cancer in North American men.

The formation of skeletal metastases affects approximately 70% of patients with advanced disease, and a majority of these patients have osteoblastic lesions.

Although BMPs have been found to be expressed in multiple oncogenic cell lines, their role in the formation of metastatic osteoblastic lesions remains uncharacterized.

We hypothesized that BMPs influence the development of metastatic osteoblastic lesions associated with prostate cancer.

MATERIALS AND METHODS: Western blot analysis and RT-PCR was used to determine BMP receptor expression on osteoblastic prostate cancer cell lines LAPC-4 and LAPC-9.

Tumor size was determined by radiographs and direct measurement.

RESULTS: We determined that BMP receptor mRNA and protein was expressed on osteoblastic prostate cancer cell lines LAPC-4 and LAPC-9.

In vitro studies showed that BMP-2 and -7 stimulated cellular migration and invasion of prostate cancer cells in a dose-dependent fashion, although BMP-4 had no effect.

Formation of osteoblastic lesions was inhibited by overexpression of noggin by prostate cancer cells transduced with a retrovirus containing the cDNA for noggin.

CONCLUSIONS: BMPs are critical in the formation of the osteoblastic lesions associated with prostate cancer metastases, and future treatment strategies that inhibit local BMP activity may reduce the formation and progression of osteoblastic lesions.

[MeSH-minor] Animals. Blotting, Western. Bone Morphogenetic Protein 2. Bone Morphogenetic Protein 4. Bone Morphogenetic Protein 7. Bone Morphogenetic Protein Receptors, Type I / genetics. Bone Morphogenetic Protein Receptors, Type I / metabolism. Bone Morphogenetic Protein Receptors, Type II / genetics. Bone Morphogenetic Protein Receptors, Type II / metabolism. Bone Neoplasms / genetics. Bone Neoplasms / metabolism. Bone Neoplasms / secondary. Carrier Proteins / genetics. Carrier Proteins / pharmacology. Cell Line. Cell Line, Tumor. Cell Movement / drug effects. Cell Proliferation / drug effects. Gene Expression / genetics. Humans. Male. Mice. Mice, SCID. Neoplasm Invasiveness / pathology. Neoplasm Transplantation. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tibia / pathology. Transfection. Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta / pharmacology. Xenograft Model Antitumor Assays / methods

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(PMID = 16294272.001).

[ISSN] 0884-0431

[Journal-full-title] Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

[ISO-abbreviation] J. Bone Miner. Res.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA 10303901

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

[Publication-country] United States

[Chemical-registry-number] 0 / BMP2 protein, human; 0 / BMP4 protein, human; 0 / BMP7 protein, human; 0 / Bmp2 protein, mouse; 0 / Bmp4 protein, mouse; 0 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Protein 7; 0 / Bone Morphogenetic Proteins; 0 / Carrier Proteins; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 148294-77-3 / noggin protein; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type I; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type II

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Analysis of complications in metastatic prostate cancer patients submitted to bilateral orchiectomy].

[Transliterated title] Análise de complicações em pacientes portadores de câncer de próstata metastático submetidos à orquiectomia bilateral.

METHODS: That's an analytical transversal study with a sample of 25 patients, between 58 to 82 years, carriers of metastatic prostate cancer, submitted to the bilateral orchiectomy in the Professor Alberto Antunes University Hospital 's (HUPAA-UFAL), in the period of January of 2003 to December of 2008.

CONCLUSION: The bilateral orchiectomy constitutes in a good alternative for metastatic prostate cancer patients, in a way that it is observed satisfaction of the majority of the patients in relation to the improvement of the symptoms and the presented complications had not great impact in the daily life of the same ones.

[MeSH-minor] Aged. Aged, 80 and over. Cross-Sectional Studies. Humans. Male. Middle Aged. Neoplasm Metastasis. Postoperative Complications / epidemiology. Postoperative Complications / etiology

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(PMID = 21085843.001).

[ISSN] 1809-4546

[Journal-full-title] Revista do Colégio Brasileiro de Cirurgiões

[ISO-abbreviation] Rev Col Bras Cir

[Language] por

[Publication-type] English Abstract; Journal Article

[Publication-country] Brazil

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Eliciting patient preferences for hormonal therapy options in the treatment of metastatic prostate cancer.

Treatment choices for metastatic prostate cancer are complex and can involve men balancing survival versus quality of life.

The present study aims to elicit patient preferences with respect to the attributes of treatments for metastatic prostate cancer through a discrete choice experiment (DCE) questionnaire.

Men with recently diagnosed localized prostate cancer were asked to envisage that they had metastatic disease when completing a survey.

As expected, men with prostate cancer placed considerable importance on gains in survival; however, avoiding side effects of treatment was also clearly important.

Survival gains should be considered alongside side effects when discussing treatment options in metastatic disease.

[MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / secondary. Androgen Antagonists / therapeutic use. Anilides / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Flutamide / therapeutic use. Nitriles / therapeutic use. Patient Satisfaction. Prostatic Neoplasms / drug therapy. Tosyl Compounds / therapeutic use

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(PMID = 17637761.001).

[ISSN] 1476-5608

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

[ISO-abbreviation] Prostate Cancer Prostatic Dis.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antineoplastic Agents, Hormonal; 0 / Nitriles; 0 / Tosyl Compounds; 76W6J0943E / Flutamide; A0Z3NAU9DP / bicalutamide

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Essential role for activation of the Polycomb group (PcG) protein chromatin silencing pathway in metastatic prostate cancer.

Another PcG protein, Ezh2, was implicated in metastatic prostate and breast cancers, suggesting that PcG pathway activation is relevant for epithelial malignancies.

Here we demonstrate that activation of the BMI1 oncogene-associated PcG pathway plays an essential role in metastatic prostate cancer, thus mechanistically linking the pathogenesis of leukemia, self-renewal of stem cells, and prostate cancer metastasis.

To characterize the functional status of the PcG pathway in metastatic prostate cancer, we utilized advanced cell- and whole animal-imaging technologies, gene and protein expression profiling, stable siRNA-gene targeting, and tissue microarray (TMA) analysis in relevant experimental and clinical settings.

We demonstrate that in multiple experimental models of metastatic prostate cancer both BMI1 and Ezh2 genes are amplified and gene amplification is associated with increased expression of corresponding mRNAs and proteins.

For the first time, we provide images of human prostate carcinoma metastasis precursor cells isolated from blood and shown to overexpress both BMI1 and Ezh2 oncoproteins.

Consistent with the PcG pathway activation hypothesis, increased BMI1 and Ezh2 expression in metastatic cancer cells is associated with elevated levels of H2AubiK119 and H3metK27 histones.

Quantitative immunofluorescence colocalization analysis and expression profiling experiments documented increased BMI1 and Ezh2 expression in clinical prostate carcinoma samples and demonstrated that high levels of BMI1 and Ezh2 expression are associated with markedly increased likelihood of therapy failure and disease relapse after radical prostatectomy.

Gene-silencing analysis reveals that activation of the PcG pathway is mechanistically linked with highly malignant behavior of human prostate carcinoma cells and is essential for in vivo growth and metastasis of human prostate cancer.

We conclude that the results of experimental and clinical analyses indicate the important biological role of the PcG pathway activation in metastatic prostate cancer.

Our work suggests that the PcG pathway activation is a common oncogenic event in pathogenesis of metastatic solid tumors and provides justification for development of small molecule inhibitors of the PcG chromatin silencing pathway as a novel therapeutic modality for treatment of metastatic prostate cancer.

[MeSH-minor] Animals. Anoikis. Cell Line, Tumor. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / genetics. Gene Amplification. Humans. Male. Mice. Mice, Nude. Neoplasm Metastasis. Neoplasm Transplantation. Nuclear Proteins / biosynthesis. Nuclear Proteins / genetics. Polycomb Repressive Complex 1. Polycomb Repressive Complex 2. Polycomb-Group Proteins. Prognosis. Proto-Oncogene Proteins / biosynthesis. Proto-Oncogene Proteins / genetics. RNA, Messenger / biosynthesis. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Tissue Array Analysis. Transcription Factors / biosynthesis. Transcription Factors / genetics

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(PMID = 16963837.001).

[ISSN] 1551-4005

[Journal-full-title] Cell cycle (Georgetown, Tex.)

[ISO-abbreviation] Cell Cycle

[Language] eng

[Grant] United States / NCI NIH HHS / CA / 5R01 CA89827

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

[Publication-country] United States

[Chemical-registry-number] 0 / BMI1 protein, human; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Polycomb-Group Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Repressor Proteins; 0 / Transcription Factors; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Polycomb Repressive Complex 2; EC 6.3.2.19 / Polycomb Repressive Complex 1

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Tumor-stroma interactions of metastatic prostate cancer cell lines: analyses using microarrays.

Tumor-stroma interactions are of great importance not only for the development and progression of primary prostate carcinoma but probably also for the establishment of metastasis.

Fibroblasts are an important stromal cell type encountered by metastatic tumor cells at different sites.

In previous investigations, we had found that media conditioned by three metastatic prostate cancer cell lines (LNCaP, PC-3, and DU-145) induced cultured nonprostatic fibroblasts to proliferate or to express matrix-metalloproteinase-1 considered important for tumor invasion.

Both tumor cells and fibroblasts secrete VEGF suggesting that not only metastatic but also stromal cells at metastatic sites contribute to the vascularization of metastasis necessary for continuous growth.

In order to better understand the reciprocal tumor-stroma cross-talk in molecular terms we used the mRNA extracted from stimulated and unstimulated neoplastic and fibroblastic stromal cells for cDNA array hybridization using Affymetrix chips.

The three prostate cell lines influenced the fibroblasts nearly in the same manner.

In contrast, fibroblasts affected every prostate cancer cell line in different ways, which may be because of the different origin of the metastatic prostate cancer cell lines.

[MeSH-major] Fibroblasts / pathology. Gene Expression Profiling / methods. Neoplasm Proteins / metabolism. Oligonucleotide Array Sequence Analysis / methods. Prostatic Neoplasms / pathology. Stromal Cells / pathology

[MeSH-minor] Cell Communication. Culture Media, Conditioned / pharmacology. Humans. Male. Neoplasm Invasiveness. Tumor Cells, Cultured

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(PMID = 18220234.001).

[ISSN] 1064-3745

[Journal-full-title] Methods in molecular biology (Clifton, N.J.)

[ISO-abbreviation] Methods Mol. Biol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Neoplasm Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] An oncogene-tumor suppressor cascade drives metastatic prostate cancer by coordinately activating Ras and nuclear factor-kappaB.

Metastasis is responsible for the majority of prostate cancer-related deaths; however, little is known about the molecular mechanisms that underlie this process.

Here we identify an oncogene-tumor suppressor cascade that promotes prostate cancer growth and metastasis by coordinately activating the small GTPase Ras and nuclear factor-kappaB (NF-kappaB).

Specifically, we show that loss of the Ras GTPase-activating protein (RasGAP) gene DAB2IP induces metastatic prostate cancer in an orthotopic mouse tumor model.

Notably, DAB2IP functions as a signaling scaffold that coordinately regulates Ras and NF-kappaB through distinct domains to promote tumor growth and metastasis, respectively.

DAB2IP is suppressed in human prostate cancer, where its expression inversely correlates with tumor grade and predicts prognosis.

Moreover, we report that epigenetic silencing of DAB2IP is a key mechanism by which the polycomb-group protein histone-lysine N-methyltransferase EZH2 activates Ras and NF-kappaB and triggers metastasis.

These studies define the mechanism by which two major pathways can be simultaneously activated in metastatic prostate cancer and establish EZH2 as a driver of metastasis.

[MeSH-major] Genes, Tumor Suppressor / physiology. Genes, ras / physiology. NF-kappa B / pharmacology. Oncogenes / physiology. Prostatic Neoplasms / physiopathology. ras GTPase-Activating Proteins / physiology

[MeSH-minor] Animals. Cell Line, Tumor. DNA-Binding Proteins / physiology. Gene Expression Regulation, Neoplastic. Humans. Male. Mice. Neoplasm Invasiveness / physiopathology. Neoplasm Metastasis / physiopathology. Neoplasm Transplantation. Polycomb Repressive Complex 2. Signal Transduction / physiology. Transcription Factors / physiology. Transcriptional Activation

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[Cites] Mol Cell Biol. 2000 Nov;20(21):8084-92 [11027278.001]

[Cites] Nature. 2009 Nov 5;462(7269):108-12 [19847166.001]

[Cites] Mol Carcinog. 2002 Jan;33(1):25-35 [11807955.001]

[Cites] Clin Cancer Res. 2002 Apr;8(4):1168-71 [11948129.001]

[Cites] Trends Genet. 2002 May;18(5):S1-5 [12047956.001]

[Cites] Nat Rev Cancer. 2002 Jun;2(6):442-54 [12189386.001]

[Cites] Nature. 2002 Oct 10;419(6907):624-9 [12374981.001]

[Cites] Cancer Cell. 2002 Nov;2(5):349-50 [12450788.001]

[Cites] J Biol Chem. 2003 Jan 31;278(5):3121-30 [12446720.001]

[Cites] Cancer Res. 2003 Jul 15;63(14):3877-82 [12873976.001]

[Cites] N Engl J Med. 2003 Jul 24;349(4):366-81 [12878745.001]

[Cites] Cancer Cell. 2003 Sep;4(3):209-21 [14522255.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Jan 20;101(3):811-6 [14711987.001]

[Cites] Genes Chromosomes Cancer. 2004 Apr;39(4):324-34 [14978793.001]

[Cites] Clin Cancer Res. 2004 Mar 15;10(6):2082-9 [15041729.001]

[Cites] Cell. 2004 Jun 25;117(7):927-39 [15210113.001]

[Cites] J Biol Chem. 2004 Oct 22;279(43):44955-65 [15310755.001]

[Cites] Cancer Res. 1990 Nov 1;50(21):6830-2 [2208148.001]

[Cites] Cancer Res. 1991 Mar 15;51(6):1632-7 [1998954.001]

[Cites] Int J Urol. 1996 Sep;3(5):373-8 [8886914.001]

[Cites] Science. 1997 Dec 5;278(5344):1812-5 [9388187.001]

[Cites] Cancer Res. 1999 Jan 15;59(2):279-84 [9927031.001]

[Cites] Int J Cancer. 2005 Jan 1;113(1):59-66 [15386433.001]

[Cites] Cancer Res. 2004 Dec 15;64(24):8867-75 [15604246.001]

[Cites] Cell Cycle. 2004 Dec;3(12):1477-80 [15539952.001]

[Cites] Br J Cancer. 2005 Mar 28;92(6):1117-25 [15770214.001]

[Cites] J Biol Chem. 2005 Jun 10;280(23):22437-44 [15817459.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8573-8 [15937108.001]

[Cites] Growth Factors. 2005 Jun;23(2):143-9 [16019436.001]

[Cites] Curr Opin Urol. 2006 May;16(3):173-8 [16679855.001]

[Cites] Int J Cancer. 2006 Oct 15;119(8):1858-62 [16721785.001]

[Cites] Cancer Res. 2007 Jul 15;67(14):6535-8 [17638861.001]

[Cites] Cancer Res. 2007 Nov 15;67(22):10657-63 [18006806.001]

[Cites] Annu Rev Pathol. 2006;1:243-71 [18039115.001]

[Cites] Cancer Res. 2007 Dec 15;67(24):11476-9; discussion 11479-80 [18089773.001]

[Cites] Growth Factors. 2007 Oct;25(5):355-61 [18236214.001]

[Cites] Cell. 2008 Feb 8;132(3):344-62 [18267068.001]

[Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]

[Cites] Curr Opin Genet Dev. 2008 Feb;18(1):19-26 [18440219.001]

[Cites] Nat Genet. 2008 Jun;40(6):741-50 [18488029.001]

[Cites] Nature. 2008 Oct 23;455(7216):1061-8 [18772890.001]

[Cites] Nature. 2008 Oct 23;455(7216):1069-75 [18948947.001]

[Cites] Mutat Res. 2008 Dec 1;647(1-2):21-9 [18723033.001]

[Cites] PLoS One. 2008;3(12):e3949 [19079609.001]

[Cites] PLoS One. 2009;4(3):e4687 [19262738.001]

[Cites] Nat Rev Cancer. 2009 Apr;9(4):239-52 [19279573.001]

[Cites] Cancer Cell. 2009 Jul 7;16(1):44-54 [19573811.001]

[Cites] N Engl J Med. 2000 Dec 21;343(25):1846-50 [11117976.001]

(PMID = 20154697.001).

[ISSN] 1546-170X

[Journal-full-title] Nature medicine

[ISO-abbreviation] Nat. Med.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / K08 CA122833; United States / NCI NIH HHS / CA / K08 CA122833-05

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

[Publication-country] United States

[Chemical-registry-number] 0 / DAB2IP protein, human; 0 / DNA-Binding Proteins; 0 / NF-kappa B; 0 / Transcription Factors; 0 / ras GTPase-Activating Proteins; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Polycomb Repressive Complex 2

[Other-IDs] NLM/ NIHMS211415; NLM/ PMC2903662

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Impact of IGF-I and CYP19 gene polymorphisms on the survival of patients with metastatic prostate cancer.

PURPOSE: The prognosis of metastatic prostate cancer significantly differs among individuals.

In this study, we evaluated genetic polymorphisms as prognostic predictors of metastatic prostate cancer.

PATIENTS AND METHODS: One hundred eleven prostate cancer patients with bone metastasis at the diagnosis were enrolled in this study.

RESULTS: Among the polymorphisms, the long allele (over 18 [CA] repeats) of insulin-like growth factor-I (IGF-I) and the long allele (over seven [TTTA] repeats) of cytochrome P450 (CYP) 19 were significantly associated with a worse cancer-specific survival (P = .016 and .025 by logrank test, respectively).

CONCLUSION: The prognosis of metastatic prostate cancer patients is suggested to be influenced by intrinsic genetic factors.

The IGF-I (CA) repeat and CYP19 (TTTA) repeat polymorphisms may be novel predictors in prostate cancer patients with bone metastasis at the diagnosis.

[MeSH-minor] Aged. Aged, 80 and over. Humans. Male. Middle Aged. Neoplasm Metastasis. Prognosis. Repetitive Sequences, Nucleic Acid

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[CommentIn] J Clin Oncol. 2006 May 1;24(13):1972-4 [16648495.001]

(PMID = 16648498.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I; EC 1.14.14.1 / Aromatase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Alterations in the serum glycome due to metastatic prostate cancer.

Glycomic profiles derived from human blood sera of 10 healthy males were compared to those from 24 prostate cancer patients.

The first principal component distinguished the 24 prostate cancer patients from the healthy individuals.

It was determined that fucosylation of glycan structures is generally higher in cancer samples (ANOVA test p-value of 0.0006).

Ten of these structures had significantly higher relative intensities in the case of the cancer samples, while the other two were less abundant in the cancer samples.

Accordingly, these structures can be considered as cancer-specific glycans and potential prostate cancer biomarkers.

Therefore, serum glycomic profiling appears worthy of further investigation to define its role in cancer early detection and prognostication.

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[Cites] Cancer Res. 2000 Mar 1;60(5):1410-6 [10728707.001]

[Cites] Biomarkers. 2006 Sep-Oct;11(5):406-16 [16966158.001]

[Cites] Proteomics. 2001 Feb;1(2):311-28 [11680878.001]

[Cites] Proteomics. 2001 Oct;1(10):1264-70 [11721637.001]

[Cites] Glycobiology. 2002 Jan;12(1):47-63 [11825886.001]

[Cites] J Cancer Res Clin Oncol. 2002 Apr;128(4):189-96 [11935309.001]

[Cites] Glycobiology. 2002 Mar;12(3):153-62 [11971859.001]

[Cites] Oncol Rep. 2002 Nov-Dec;9(6):1251-5 [12375029.001]

[Cites] Anal Sci. 2003 Jan;19(1):85-92 [12558029.001]

[Cites] Biol Chem. 2003 Feb;384(2):321-7 [12675527.001]

[Cites] Glycobiology. 2003 Jun;13(6):457-70 [12626390.001]

[Cites] Biochimie. 2003 Jan-Feb;85(1-2):207-18 [12765790.001]

[Cites] Science. 2003 Jul 11;301(5630):159-60 [12855785.001]

[Cites] Korean J Radiol. 2004 Jan-Mar;5(1):11-8 [15064554.001]

[Cites] Clin Chem. 2004 Jun;50(6):1017-25 [15054080.001]

[Cites] Radiology. 1982 Apr;143(1):29-36 [7063747.001]

[Cites] Science. 1988 Jun 3;240(4857):1285-93 [3287615.001]

[Cites] Neoplasma. 1988;35(6):691-705 [3265486.001]

[Cites] Eur J Cancer Clin Oncol. 1989 Jan;25(1):65-72 [2920769.001]

[Cites] J Urol. 1994 Jun;151(6):1571-4 [7514690.001]

[Cites] J Chromatogr A. 1996 Jan 12;720(1-2):429-46 [8601205.001]

[Cites] Cancer Res. 1996 Dec 1;56(23):5309-18 [8968075.001]

[Cites] Anal Chem. 1998 Feb 1;70(3):455-63 [9470483.001]

[Cites] Mol Cell Proteomics. 2007 Jan;6(1):43-55 [16847285.001]

[Cites] Glycobiology. 2007 Apr;17(4):411-22 [17223647.001]

[Cites] Clin Chem. 2008 Jul;54(7):1166-75 [18487288.001]

[Cites] Glycoconj J. 2009 Feb;26(2):117-31 [18752066.001]

[Cites] J Clin Lab Anal. 1998;12(1):6-13 [9484663.001]

[Cites] Clin Chim Acta. 1998 Mar 23;271(2):191-202 [9565334.001]

[Cites] Glycobiology. 1998 Jun;8(6):605-13 [9592127.001]

[Cites] Glycoconj J. 1998 Apr;15(4):323-31 [9613818.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1597-602 [9990070.001]

[Cites] Gan To Kagaku Ryoho. 2005 Feb;32(2):275-80 [15751649.001]

[Cites] Curr Opin Urol. 2005 May;15(3):151-6 [15815190.001]

[Cites] Clin Cancer Res. 2005 Apr 15;11(8):2969-73 [15837749.001]

[Cites] Int J Oncol. 2005 Nov;27(5):1289-97 [16211224.001]

[Cites] Rapid Commun Mass Spectrom. 2005;19(23):3421-8 [16252310.001]

[Cites] Biochemistry. 2005 Nov 29;44(47):15619-35 [16300412.001]

[Cites] Mol Cell Proteomics. 2005 Dec;4(12):1977-89 [16170054.001]

[Cites] Glycobiology. 2006 Feb;16(2):132-45 [16177264.001]

[Cites] Biometrics. 2006 Mar;62(1):221-9 [16542249.001]

[Cites] Electrophoresis. 2006 Apr;27(8):1609-16 [16550497.001]

[Cites] Urol Oncol. 2006 May-Jun;24(3):231-6 [16678055.001]

[Cites] J Proteome Res. 2006 Jul;5(7):1626-35 [16823970.001]

[Cites] CA Cancer J Clin. 1999 Sep-Oct;49(5):264-81 [11198954.001]

(PMID = 17432893.001).

[ISSN] 1535-3893

[Journal-full-title] Journal of proteome research

[ISO-abbreviation] J. Proteome Res.

[Language] ENG

[Grant] United States / NCRR NIH HHS / RR / P41 RR018942; United States / NIGMS NIH HHS / GM / R01 GM024349; United States / NIGMS NIH HHS / GM / GM24349; United States / NCRR NIH HHS / RR / RR018942

[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 / Blood Proteins; 0 / Glycoproteins; 0 / Polysaccharides

[Other-IDs] NLM/ NIHMS62933; NLM/ PMC3685170

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Population based study of hormonal therapy and survival in men with metastatic prostate cancer.

PURPOSE: Although the palliative benefits of hormonal therapy for metastatic prostate cancer are widely recognized, little information is available regarding the effect of hormonal therapy on cancer specific and overall survival, and the types of patients who might benefit the most or least from hormonal therapy.

MATERIALS AND METHODS: Prostate cancer specific and overall survival according to hormonal therapy use was determined by the Kaplan-Meier method in 6,098 men 65 years or older diagnosed with metastatic prostate cancer in 1991 to 1999 who were identified through the population based Surveillance, Epidemiology, and End Results, and Medicare linked database.

Effects were most evident in patients with poorly differentiated cancer (cancer specific mortality in favor of treatment HR 0.60, 95% CI 0.53-0.69, p <0.001).

Benefit was not found in patients with well differentiated cancer (cancer specific mortality in favor of no treatment HR 1.92, 95% CI 0.90-4.10, p = 0.09).

CONCLUSIONS: Hormonal therapy is associated with improved prostate cancer specific and overall survival in men with poorly differentiated cancer.

[MeSH-minor] Aged. Humans. Male. Neoplasm Metastasis. Survival Rate

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(PMID = 17222628.001).

[ISSN] 0022-5347

[Journal-full-title] The Journal of urology

[ISO-abbreviation] J. Urol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone; 731DCA35BT / Diethylstilbestrol

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Tumour-stroma interactions between metastatic prostate cancer cells and fibroblasts.

Previous work has shown the importance of tumour-stroma interactions for prostate cancer development at the primary site.

The aim of the present study was to find out whether evidence can be found for a tumour-stroma cross- talk also between metastatic prostate cancer cell lines and non-prostatic stromal fibroblasts which are encountered by metastatic cells at most sites.

We addressed this issue in cell culture systems using 3 metastatic human prostate cancer cell lines (LnCaP, PC-3 and DU-145) on the one hand, and a human fibroblast line (HFF, human foreskin fibroblasts) on the other.

We incubated fibroblasts with tumour cell- and tumour cells with fibroblast-conditioned media and evaluated several parameters important for the establishment of metastases such as cell proliferation, migration and expression of matrix degrading proteases.

We found that media conditioned by all 3 metastatic prostate cancer cell lines stimulated fibroblast proliferation which corresponds to fibrous stroma induction in vivo.

DU-145 cell conditioned media induced in fibroblasts expression of mmp-1 mRNA known to be important for tumour invasion.

ELISA assays revealed that tumour cells secrete bFGF, PDGF and TNFalpha known to stimulate fibroblast proliferation and/or MMP-1 expression.

KGF (able to stimulate proliferation of normal and neoplastic prostate epithelial cells) was secreted by fibroblasts at higher concentrations than by all 3 tumour cell lines.

In addition, fibroblasts secreted TNFalpha, bFGF, PDGF, HGF and also VEGF, the most important factor for tumour vascularization.

Our results provide evidence that tumour-stroma interactions do not only exist at the primary site but also between metastatic prostate cancer cell lines and their fibroblastic microenvironment.

These interactions, which are mediated through secreted factors, affect several steps of the metastatic cascade including proliferation, anchorage-independent growth, migration and the secretion of matrix-degrading proteases.

[MeSH-minor] Cell Line, Tumor. Cell Movement. Culture Media, Conditioned / pharmacology. Cytokines / metabolism. Growth Substances / metabolism. Humans. Male. Matrix Metalloproteinase 1 / metabolism. Neoplasm Invasiveness. Peptide Hydrolases / metabolism

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(PMID = 17016625.001).

[ISSN] 1107-3756

[Journal-full-title] International journal of molecular medicine

[ISO-abbreviation] Int. J. Mol. Med.

[Language] eng

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

[Publication-country] Greece

[Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Cytokines; 0 / Growth Substances; EC 3.4.- / Peptide Hydrolases; EC 3.4.24.7 / Matrix Metalloproteinase 1

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Novel agents and targets in managing patients with metastatic prostate cancer.

BACKGROUND: Docetaxel has recently been found to improve survival in patients with metastatic androgen-independent prostate cancer (AIPC).

METHODS: Clinically relevant articles focusing on chemotherapy drugs for metastatic prostate cancer and their mechanism of action and efficacy were reviewed from January 2004 through April 2006.

CONCLUSIONS: Docetaxel should be considered for first-line treatment of metastatic AIPC.

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(PMID = 16885915.001).

[ISSN] 1073-2748

[Journal-full-title] Cancer control : journal of the Moffitt Cancer Center

[ISO-abbreviation] Cancer Control

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 33

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Circulating tumor cells predict survival in patients with metastatic prostate cancer.

OBJECTIVES: To determine whether circulating tumor cells (CTCs) predict for survival in patients with metastatic prostate cancer (PCa) and to compare its prognostic abilities with other clinical factors.

METHODS: Blood samples from 37 patients with metastatic PCa were analyzed for CTCs.

CONCLUSIONS: In this pilot study, the presence of 5 or more CTCs in 7.5 mL blood was associated with poor overall survival in patients with metastatic PCa.

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(PMID = 15833514.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prognostic grouping of metastatic prostate cancer using conventional pretreatment prognostic factors.

OBJECTIVE: To develop three prognostic groups for disease specific mortality based on the binary classified pretreatment variables age, haemoglobin concentration (Hb), erythrocyte sedimentation rate (ESR), alkaline phosphatase (ALP), prostate-specific antigen (PSA), plasma testosterone and estradiol level in hormonally treated patients with metastatic prostate cancer (PCa).

CONCLUSION: Patients with metastatic PCa can be divided into three statistically significantly different prognostic risk groups for PCa-specific mortality by using the binary classified pretreatment variables ALP, PSA, ESR and age.

[MeSH-major] Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / secondary

[MeSH-minor] Age Factors. Aged. Aged, 80 and over. Alkaline Phosphatase / blood. Biomarkers, Tumor / blood. Blood Sedimentation. Bone Neoplasms / pathology. Bone Neoplasms / radiography. Estradiol / blood. Hemoglobins / metabolism. Humans. Male. Middle Aged. Prognosis. Prospective Studies. Prostate-Specific Antigen / blood. Retrospective Studies. Risk Factors. Testosterone / blood

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(PMID = 19382005.001).

[ISSN] 1651-2065

[Journal-full-title] Scandinavian journal of urology and nephrology

[ISO-abbreviation] Scand. J. Urol. Nephrol.

[Language] eng

[Publication-type] Journal Article; Multicenter Study

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Hemoglobins; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; EC 3.1.3.1 / Alkaline Phosphatase; EC 3.4.21.77 / Prostate-Specific Antigen

[Investigator] Ala-Opas M; Hansson E; Juusela H; Nurmi M; Permi J; Puolakka VM; Rintala E; Saarialho M; Talja M; Viitanen J; Wuokko E

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Disseminated intravascular coagulation as the presenting sign of metastatic prostate cancer.

Disseminated intravascular coagulation (DIC) is an acquired coagulation disorder that may occur in a wide variety of clinical conditions.

Suspicion of DIC should lead to a differential diagnosis that includes primary fibrinolysis and other bleeding diatheses such as thrombocytopenias of diverse etiology.

Confirmation of the diagnosis of DIC should always prompt a search for an underlying medical disorder, including sepsis, severe trauma, solid and hematological malignancies, obstetrical complications, and vascular disorders.

Here, we describe an unusual case of acute bleeding and DIC as the presenting manifestation of metastatic prostate cancer in a 60-year-old man.

Treatment with a luteinizing hormone-releasing hormone (LHRH) agonist and a short course of an antiandrogen, together with supportive measures (i.e., clotting factors, heparin, and platelets), led to normalization of all coagulation parameters within 1 week, and to clinical improvement and decline in the serum level of prostate-specific antigen (PSA).

We discuss the pathogenesis, differential diagnosis, and association of DIC with prostate cancer along with the management of this condition.

[MeSH-major] Disseminated Intravascular Coagulation / diagnosis. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / pathology

[MeSH-minor] Diagnosis, Differential. Hormone Antagonists / therapeutic use. Humans. Male. Middle Aged

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[Cites] CMAJ. 1986 Oct 1;135(7):775-6 [3756704.001]

[Cites] Am J Med. 1985 Oct;79(4):423-30 [4050830.001]

[Cites] Br J Urol. 1987 Apr;59(4):363-4 [3580784.001]

[Cites] JAMA. 1988 Nov 4;260(17):2507 [3172421.001]

[Cites] Br Dent J. 1989 Apr 22;166(8):295-6 [2785811.001]

[Cites] N Engl J Med. 1999 Aug 19;341(8):586-92 [10451465.001]

[Cites] CMAJ. 1987 Mar 15;136(6):570 [3815225.001]

[Cites] Clin Nucl Med. 1999 Nov;24(11):852-4 [10551466.001]

[Cites] J Urol. 2000 Jan;163(1):248 [10604368.001]

[Cites] Urology. 1999 Dec;54(6A Suppl):8-14 [10606278.001]

[Cites] Thromb Haemost. 1999 Aug;82(2):713-7 [10605772.001]

[Cites] Cancer Invest. 2000;18(3):191-6 [10754987.001]

[Cites] J Urol. 2000 Sep;164(3 Pt 1):782 [10953152.001]

[Cites] Scand J Urol Nephrol. 2000 Jun;34(3):215-6 [10961481.001]

[Cites] Thromb Haemost. 2001 Sep;86(3):828-33 [11583315.001]

[Cites] Semin Thromb Hemost. 2001 Dec;27(6):569-75 [11740680.001]

[Cites] Haemostasis. 2001;31 Suppl 1:47-8 [11990477.001]

[Cites] An Med Interna. 2002 Jan;19(1):54-5 [11989088.001]

[Cites] J Urol. 2002 Oct;168(4 Pt 1):1496 [12352431.001]

[Cites] Neth J Med. 2003 Nov;61(11):347-54 [14768717.001]

[Cites] Blood. 1982 Aug;60(2):284-7 [7046845.001]

[Cites] Lancet. 1984 Aug 25;2(8400):433-5 [6147504.001]

[CommentIn] J Gen Intern Med. 2007 Jul;22(7):1062 [17458572.001]

(PMID = 17026724.001).

[ISSN] 1525-1497

[Journal-full-title] Journal of general internal medicine

[ISO-abbreviation] J Gen Intern Med

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Hormone Antagonists

[Other-IDs] NLM/ PMC1831660

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Transfusion-dependent anemia after initiation of androgen deprivation therapy for metastatic prostate cancer.

Androgen deprivation therapy (ADT) is a commonly used treatment for metastatic prostate cancer.

A 78-year-old patient with metastatic prostate cancer had transfusion-dependent anemia develop while on ADT.

[MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / secondary. Androgen Antagonists / adverse effects. Anemia / chemically induced. Antineoplastic Agents, Hormonal / adverse effects. Blood Transfusion. Leuprolide / adverse effects. Prostatic Neoplasms / pathology

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(PMID = 17991572.001).

[ISSN] 1527-9995

[Journal-full-title] Urology

[ISO-abbreviation] Urology

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Hemoglobins; EFY6W0M8TG / Leuprolide

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A polycomb repression signature in metastatic prostate cancer predicts cancer outcome.

The Polycomb Group (PcG) protein EZH2 is a critical component of a multiprotein complex that methylates Lys(27) of histone 3 (H3K27), which consequently leads to the repression of target gene expression.

We have previously reported that EZH2 is overexpressed in metastatic prostate cancer and is a marker of aggressive diseases in clinically localized solid tumors.

However, the global set of genes directly regulated by PcG in tumors is largely unknown, and thus how PcG mediates tumor progression remains unclear.

Herein we mapped genome-wide H3K27 methylation in aggressive, disseminated human prostate cancer tissues.

By stepwise cross-validation, we developed a "Polycomb repression signature" composed of 14 direct targets of PcG in metastatic tumors.

Notably, solid tumor subtypes in which this gene signature is repressed show poor clinical outcome in multiple microarray data sets of tumors including breast and prostate cancer.

Taken together, our results show a fingerprint of PcG-mediated transcriptional repression in metastatic prostate cancer that is reminiscent of stem cells and associated with cancer progression.

Therefore, PcG proteins play a central role in the epigenetic silencing of target genes and functionally link stem cells, metastasis, and cancer survival.

[MeSH-minor] Biomarkers, Tumor / metabolism. Cell Line, Tumor. DNA Methylation. Disease Progression. Disease-Free Survival. Epigenesis, Genetic. Gene Silencing. Humans. Male. Neoplasm Metastasis. Polycomb-Group Proteins. Stem Cells / metabolism. Treatment Outcome

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(PMID = 18006806.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P50 CA69568; United States / NCI NIH HHS / CA / R01 CA102872; United States / NCI NIH HHS / CA / R01 CA97063; United States / NCI NIH HHS / CA / U01 CA111275

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

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Polycomb-Group Proteins; 0 / Repressor Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Metronomic chemotherapy for metastatic prostate cancer: a 'young' concept for old patients?

Prostate cancer is a common disease in the elderly, and the number of older prostate cancer patients will probably increase with both the aging of the population and the increased rate of screening.

In elderly patients with several co-morbidities, cancer management can be complex, and the risk of administering toxic therapy in this setting should be carefully evaluated.

Metronomic chemotherapy, i.e. low-dose, long-term, frequently administered chemotherapy, has been shown to have a significant stabilizing effect on cancer and a positive impact on the quality of life of patients, including those with prostate cancer.

Moreover, the possibility of patients being able to spend more time at home is an important component of a palliative treatment such as metronomic chemotherapy.

However, retrospective analyses conducted in a small cohort of patients have been published and, notwithstanding their limitations, indicate that novel metronomic schedules are well tolerated, safe and show potentially interesting activity in elderly, 'unfit' (poor performance status) patients with metastatic prostate cancer.

Therefore, evaluation of metronomic chemotherapy strategies in prospective, randomized, phase II/III clinical studies of elderly patients with metastatic prostate cancer appears to be warranted.

[MeSH-minor] Aged. Aged, 80 and over. Drug Administration Schedule. Humans. Male. Neoplasm Metastasis

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(PMID = 20809660.001).

[ISSN] 1179-1969

[Journal-full-title] Drugs & aging

[ISO-abbreviation] Drugs Aging

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] New Zealand

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Immunohistochemical staining of precursor forms of prostate-specific antigen (proPSA) in metastatic prostate cancer.

Precursors of prostate-specific antigen (proPSA) have been previously shown to be more concentrated in prostate cancer tissue.

This study characterizes the immunohistochemical staining (IHS) of proPSA forms in metastatic prostate cancer compared with prostate specific antigen (PSA) and prostatic acid phosphatase (PAP).

A tissue microarray, consisting of 74 cases of metastatic prostate carcinoma and control tissues, was used.

The monoclonal antibodies were specific for both benign and malignant prostatic glandular tissue.

[-5/-7]pPSA (native proPSA) may be a better marker than PSA and PAP in characterizing metastatic prostate adenocarcinoma, with most of the cases showing positivity for the marker.

Such enhanced detection is particularly important in poorly differentiated carcinomas involving metastatic sites where prostate carcinoma is a consideration.

A panel of markers, including proPSA, should be performed when metastatic prostate carcinoma is in the differential diagnosis.

[MeSH-major] Adenocarcinoma / chemistry. Immunoenzyme Techniques / methods. Prostate-Specific Antigen / analysis. Prostatic Neoplasms / chemistry. Protein Precursors / analysis. Protein Tyrosine Phosphatases / analysis

[MeSH-minor] Acid Phosphatase. Biomarkers, Tumor / analysis. Humans. Male. Tissue Array Analysis

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(PMID = 17001152.001).

[ISSN] 0147-5185

[Journal-full-title] The American journal of surgical pathology

[ISO-abbreviation] Am. J. Surg. Pathol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Protein Precursors; EC 3.1.3.2 / Acid Phosphatase; EC 3.1.3.2 / prostatic acid phosphatase; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.4.21.77 / Prostate-Specific Antigen

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Screening with prostate specific antigen and metastatic prostate cancer risk: a population based case-control study.

PURPOSE: Screening of asymptomatic men with prostate specific antigen (PSA) remains a controversial issue.

There is limited evidence that screening is effective in reducing mortality from prostate cancer.

In the current study we determined if screening with PSA reduces the risk of metastatic prostate cancer.

Data were obtained from 236 cases of metastatic prostate cancer and 462 controls randomly sampled from the source population and frequency matched to cases for age and area of residence.

The association between PSA screening and metastatic prostate cancer was measured by the Mantel-Haenszel odds ratio stratified by exposure observation time and other potential confounding factors.

CONCLUSIONS: In this case-control study screening of asymptomatic men with PSA was associated with a significantly reduced risk of metastatic prostate cancer.

[MeSH-major] Prostate-Specific Antigen / blood. Prostatic Neoplasms / pathology

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[CommentIn] J Urol. 2005 Aug;174(2):413-4 [16006854.001]

(PMID = 16006879.001).

[ISSN] 0022-5347

[Journal-full-title] The Journal of urology

[ISO-abbreviation] J. Urol.

[Language] eng

[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] EC 3.4.21.77 / Prostate-Specific Antigen

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Systemic inflammatory response, prostate-specific antigen and survival in patients with metastatic prostate cancer.

BACKGROUND: It is increasingly recognised that, in cancer patients, disease progression is dependent on a complex interaction of the tumour and the host inflammatory response and that the systemic inflammatory response, as evidenced by an elevated C-reactive protein (CRP) concentration, may be a useful prognostic factor.

MATERIALS AND METHODS: The prognostic value of CRP compared with prostate-specific antigen (PSA) was examined in 62 patients with metastatic prostate cancer receiving androgen-deprivation therapy.

On univariate survival analysis, PSA (p < 0.05) and CRP (p < 0.05) were significant predictors of cancer-specific survival.

On multivariate analysis, both PSA (HR 1.96, 95% CI 1.00-3.83, p = 0.049) and CR (HR 1.97, 95% CI 0.99-3.92, p = 0.052) were independent predictors of cancer-specific survival.

CONCLUSION: The results of the present study suggest that, in patients with metastatic prostate cancer, the presence of an elevated CRP concentration predicts poor outcome, independent of PSA.

[MeSH-major] Inflammation / etiology. Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / mortality

[MeSH-minor] Aged. Humans. Male. Neoplasm Metastasis. Survival Rate

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(PMID = 16888416.001).

[ISSN] 0042-1138

[Journal-full-title] Urologia internationalis

[ISO-abbreviation] Urol. Int.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Switzerland

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